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xiii
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Preface
and how they may impact injury development and reha-
Athletic and Sport Issues bilitation including clinically relevant points.
Athletic and Sport Issues in Musculoskeletal Rehabilitation is • Management of Sports Injury and Illness focuses on
the 4th volume in our series Musculoskeletal Rehabilitation. non-musculoskeletal injury and management factors.
For this volume we have added a new editor, Robert • Special Populations and Epidemiology presents infor-
Manske. In this volume we have sought to provide the stu- mation on sport injury concerns based on gender, age or
dent and practicing clinician with a comprehensive source physical ability/disability. Also presented in this section is
of information for this topic area not addressed elsewhere in a comprehensive summary of the epidemiologic injury
this integrated series. Most texts on sports injuries have a data by specific sport.
primary focus on musculoskeletal pathology and interven- This volume is again liberally illustrated with multiple
tion. Information on these types of problems and condi- figures, tables and text boxes to allow the reader to quickly
tions are thoroughly addressed in Volumes 1 – Orthopaedic grasp the information being presented. A comprehensive
Physical Assessment, Volume 2 – Scientific Foundations and reference list is provided on an Evolve site with links to
Principles of Practice and Volume 3 – Pathology and Inter- MEDLINE abstracts where available.
vention. The advantage of Volume 4 – Athletic and Sport We firmly believe that with the addition of this volume
Issues in Musculoskeletal Rehabilitation being part of an in- the clinician who practices is the area of “sports medicine”
tegrated series is that the information the reader will find is will have a set of resources that provide them with compre-
summarized and presented in greater depth than most other hensive information on the management of this patient
texts. Because of this, we believe the reader will find this population.
textbook an exceptional resource for their practice. As we continue to develop this series we welcome the
Volume 4 is divided into four sections: readers’ feedback to allow us to continue to enhance the
• Preparation and Prevention in Sports Medicine focuses quality and comprehensiveness of the series.
on psychological, nutritional, environmental and pharma- David J. Magee
cologic factors associated with sport participation and Robert C. Manske
health. James E. Zachazewski
• Applied Biomechanics of Selected Sport Activities William S. Quillen
present in depth reviews of the biomechanics of activities
xv
Acknowledgments
We would like to gratefully acknowledge the ongoing pro- Kathy Falk – Executive Editor, Health Professions, Elsevier
fessional assistance of the following individuals who have Christie Hart –Senior Developmental Editor, Elsevier
steadfastly supported this series from its inception. Megan Fennell – Associate Developmental Editor, Elsevier
Bev Evjen – Editorial Assistant
Ted Huff – Artist
xvi
Contents
SECTION I: PREPARATION AND PREVENTION
IN SPORTS MEDICINE 16 APPLIED BIOMECHANICS OF COMMON WEIGHT TRAINING EXERCISES - 385
1
Michael P. Reiman, Rafael F. Escamilla,
ROLE OF THE SPORTS MEDICINE TEAM - Richard H. Leu, 1 Loren Z.F. Chiu
Robert C. Manske
2
SECTION III: MANAGEMENT OF SPORTS
PREPARTICIPATION EVALUATION AND PHYSICAL FITNESS PROFILING 9 INJURY AND ILLNESS
PART A: PREPARTICIPATION EVALUATION - David J. Magee,
William S. Quillen
PART B: PHYSICAL FITNESS PROFILING - William E. Amonette,
17 DELAYED-ONSET MUSCLE SORENESS - William T. Stauber,
Corrie A. Mancinelli
423
18
Barry A. Spiering
MEDICAL CONDITIONS IN SPORT - Dhiren J. Naidu
3
441
PSYCHOSOCIAL ASPECTS OF YOUTH SPORTS - Stephen A. Durant,
19
40
Richard D. Ginsburg, Michael S. Jellinek DERMATOLOGIC CONSIDERATIONS IN ATHLETICS - Donald W. Groot, 455
4
Patricia A. Johnston
NUTRITION COUNSELING AND ATHLETES - Heidi M. Wells
20
58
PROTECTIVE EQUIPMENT IN SPORTS - Michael R. Mirabella,
5
478
ENVIRONMENTAL CONSIDERATIONS FOR SPORTS - Travis L. Francis, 98 Timothy F. Tyler
21
Rich Bomgardner
TAPING FOR ATHLETICS AND REHABILITATION - Robert C. Manske,
6
515
USE OF ERGOGENIC AIDS IN SPORT - Jeffrey J. Zachwieja, 141 Justin Rohrberg
22
Elizabeth A. Mooradian, Kimberly M. White
SPORTS RELATED CONCUSSION - Alex M. Taylor,
7
536
SPORTS DRUG TESTING - Gary A. Green 174 Michael W. Collins
8
Francis Wang, Lars C. Richardson
APPLIED BIOMECHANICS OF CYCLING - Robert J. Gregor,
24
187
Eileen G. Fowler, W. Lee Childers MAXILLOFACIAL INJURIES - John P. Kelly 581
10 APPLIED BIOMECHANICS OF JUMPING - Scott A. Riewald 234 SECTION IV: SPECIAL POPULATIONS
11
AND EPIDEMIOLOGY
APPLIED BIOMECHANICS OF TENNIS - Todd S. Ellenbecker,
26
265
E. Paul Roetert, W. Ben Kibler, Mark S. Kovacs THE FEMALE ATHLETE - Janice Loudon, Lori A. Bolgla, 631
12
Steven A. Greer
APPLIED BIOMECHANICS OF SOCCER - Sérgio T. Fonseca,
27
287
Thales R. Souza, Juliana M. Ocarino, MUSCULOSKETAL DANCE MEDICINE AND SCIENCE - Jeffrey A. Russell 651
28
Gabriela P. Gonçalves, Natália F. Bittencourt
THE ATHLETE WITH DISABILITY - Duane G. Messner
13
681
APPLIED BIOMECHANICS OF RUNNING - Scott T. Miller
29
307
SELECTED REHABILITATION NEEDS OF THE MASTERS ATHLETE -
14
704
APPLIED BIOMECHANICS OF SWIMMING - Marilyn M. Pink, 331 James W. Matheson, Robert C. Manske
30
George T. Edelman, Russell Mark, Scott A. Rodeo
APPLIED SPORTS INJURY EPIDEMIOLOGY - Mitchell J. Rauh,
15
730
APPLIED BIOMECHANICS OF BASEBALL PITCHING - Glenn S. Fleisig, 350 Caroline A. Macera, Stephen W. Marshall
Rafael F. Escamilla, James R. Andrews
xvii
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1
CHAPTER
1
2 SECTION I • Preparation and Prevention in Sports Medicine
Figure 1-2
Sports physical therapist.
It is crucial that these various groups of physicians The team physician must always factor in the success and
are not competitors, but work to complement each other well-being of the entire team when dealing with an individual
and together treat common athletic conditions. There are athlete. It is imperative that the physician demonstrates the
multiple responsibilities when serving as a team physician. same degree of professionalism and understanding to each
Organized sports are a complex entity that requires multiple member of the team regardless of the athlete’s abilities.
interactions by the sports medicine team with a wide range The coaching staff is ultimately concerned with the success
of individuals including the athlete, team, coaching staff, of the team and must be informed and regularly updated
academic institution, and general management depending regarding an athlete’s injury in a timely manner. One of the
on the level of competition. roles of a team physician is to educate the coaching staff in
improvements in medical and preventive care for the team.
The team physician’s primary responsibility to an aca-
Some Responsibilities of the Team Physician demic institution or general management is protection
from liability by screening athletes prior to the start of
• Preparticipation physical examination
the competitive season. Furthermore, following injury, the
• Injury assessment and management
• “Return to play” decisions for injured athletes team physician should return an athlete to competition
• Medical coverage of athletic events only after the athlete has been adequately rehabilitated.
• Injury prevention This is accomplished by the team physician fulfilling his
• Strength training and conditioning or her responsibility to the individual athlete, which will
• Substance abuse assessment then translate into the success of the team.
• Special population assessment (i.e., youth, elderly, disabled) The effectiveness of the team physician is built around
• Educating and counseling on sports-related medical issues availability, competence, and the ability to communicate
with athletes, coaches, athletic trainers, and other members
of the sports medicine team. Obviously, a team physician
cannot be physically present at every practice or game
The team physician’s primary responsibility is to event, especially when covering multiple schools or a school
the individual athlete. “Do no harm” is one of the most with multiple sports.
important Hippocratic oaths medical professionals take
upon entering this profession. This must be constantly
remembered when athletes are injured during a season.
The physician, as do other members of the sports medi-
Clinical Point
cine team, has an ethical responsibility to allow the athlete
to participate, but must also balance this desire to allow To have an effective, efficient sports medicine team, communication
participation with the responsibility of making sure the is essential.
athlete has been adequately rehabilitated from injury
before a return to competition. This does not apply solely
to the physical needs of the athlete. The physician must
also be an effective communicator and demonstrate
empathy and concern toward the athlete; the team phy- The team physician or medical associate should always be
sician must be able to recognize the psychological aspects present for high-risk contact sports such as football, ice
of an injury (e.g., anxiety and depression) and be willing hockey, soccer, and wrestling. If a physician cannot be on-
to address these openly with the athlete. site, medical coverage should be provided by a certified
Injuries or illnesses of higher profile athletes at all athletic trainer or other appropriately trained individual.
levels of sports may create discussions in schools, universi- During these instances in which the team physician is not
ties, communities, and even at national levels. The team available on-site, he or she should be readily available by
physician must, as must all members of the sports medi- phone in case of suspected emergencies. Team physicians
cine team, maintain confidentiality regarding an athlete’s must be flexible and willing to adjust their schedules to
injury without compromising his or her responsibility evaluate athletes in the training room, the office, or after
to the coach, academic institution, general management, hours if that is when an injury occurs.
or the public. Event coverage and medical supervision of athletes is
the most time-consuming aspect of the role as a team
physician; however, the most difficult responsibility is the
Clinical Point decision on whether and when to return an athlete to
play. During event competition the physician must be able
The sports medicine team’s primary responsibility is to the athlete. to determine quickly if an athlete has full range of motion
and demonstrates 90% of normal strength after an injury
Role of the Sports Medicine Team • CHAPTER 1 5
Case Studies
The team approach can be examined and illustrated best by
looking at several case studies. These case studies describe
how the group of medical professionals can work together
as a cohesive “team” to facilitate appropriate medical care
for injured athletes.
Case Study 1
M.S. is a 17-year-old male high school soccer goalie who
injured his right knee during a game. The athlete was re-
ferred to the Sports Medicine Clinic by the high school’s
certified athletic trainer.
The athlete stated that his right knee was planted and he
sustained a blow to the upper torso; he felt his knee “pop”
twice. He stated that it felt like the patella was forced to
the lateral aspect of his knee and then “popped” back into
Figure 1-4 position. M.S. was unable to continue to participate in the
Preparticipation physical examination. game and noted immediate swelling of his right knee. Initial
Role of the Sports Medicine Team • CHAPTER 1 7
their close relationship and “team” approach the athlete to get a definitive diagnosis and implement a timely plan
was able to see the team physician first thing the next of care that was more realistic and appropriate for this form
day. The sports physician reviewed radiographs and of serious injury.
had additional images taken and determined that they
appeared negative at this point, but, because of the
classic symptoms, recommended casting the wrist for 7
Conclusion
to 14 days and scheduled the patient for a follow-up with Members of the sports medicine team clearly have the unique
possible computed tomography (CT) scan in 2 weeks opportunity to establish a relationship with young men
if symptoms were still present. The athlete continued and women participating in athletic activities. The team can
to have hand and wrist pain with active movements and positively influence these individuals by providing medical,
gripping 10 days later. He returned to the sports medicine philosophical, and psychological counseling to these athletes
physician’s office where a CT scan was ordered. To his regarding academic performance; use of supplements, drugs,
dismay, the athlete actually had a scaphoid fracture and alcohol; and the opposite sex. The implications of the
that went undetected by early conventional radiographic sports medicine team’s responsibility and its ability to change
technique (Figure 1-6). He was placed in a splint and these young athlete’s lives should not be taken lightly. There
started the arduous process of healing the wrist injury. is an opportunity for education and demonstration of
These two examples clearly illustrate the team approach positive role modeling in every interaction with athletes.
and the respect for each of the team members toward one The operative word in the sports medicine team is
another. Because of this team approach, the athlete was able team. In the Navy of old, the acronym TEAM stood for
to see the team physician in an expedited amount of time “Treat Everyone as Myself.”7 Another symbolic acronym
as it relates to sports is “Together Everyone Achieves
More.”8 The effectiveness of the team in enabling an
athlete to safely participate in his or her sport is pre-
dicated upon competency, mutual respect, and effective
communication.
References
1. Mellion MB, Walsh WM, Shelton GL: The team physician’s
handbook, ed 2, Philadelphia, 1997, Hanley & Belfus.
2. Fu FH, Tjoumakaris FP, Buoncristiani A: Building a sports medi-
cine team, Clin Sports Med 26:173–179, 2007.
3. Garfinkel D, Birrer RB: The team physician. In Birrer RB, editor:
Sports medicine for the primary care physician, ed 2, Boca Raton, FL,
1994, CRC Press.
4. Lyznicki JM, Rigg JA, Champion HC: Certified athletic
trainers in secondary schools: Report of the Council on Scientific
Affairs, American Medical Association, J Athl Train 34:272–276,
1999.
5. Prentice WE: Arnheim’s principles of athletic training. A competency-
based approach, ed 12, New York, 2006, McGraw Hill.
6. Matheson G: Role of preparticipation medical exam: Who can’t play.
The Puck Stops Here: Comprehensive Management of Hockey
Injuries, Chicago, IL, August 22–24, 2008.
Figure 1-6 7. Quillen WS: Personal communication, February 8, 2009.
Computed tomography scan of scaphoid fracture. 8. Accessed at www.acronymfinder.com/TEAM.html.
2
CHAPTER
PART A: PREPARTICIPATION EVALUATION sport, is to use a team physician who is familiar with the
activity requirements and demands. These evaluations are
Introduction often group efforts, using multiple health care professionals
The preparticipation evaluation (PPE), although generic (e.g., athletic trainer, sports physical therapist, nurse)
in some sense, is often designed for a particular activity, performing selected parts of a multistation evaluation.
sport, or age group.1-7 Each activity and sport is associated If properly organized, this method allows for many con-
with unique health concerns. For example, football players current screenings; however, some participants may find
and runners are at risk for different injuries. In addition, this method impersonal, confusing, and noisy.14,15 The PPE
the risks for each activity and sport vary by population, is often performed annually, and subsequent PPEs may be
age, and sex.3,8,9 The sophistication of a PPE can range less extensive, assessing only body systems affected during
from a limited physical examination to an extensive the preceding season.12,13,16-18 For example, strength and
evaluation that includes cardiac stress testing, fitness functional performance testing may be performed only for
profiling, diagnostic imaging, and other procedures, those joints affected by injury during the previous season;
depending on the practice situation; level of competition; these evaluations are used primarily to determine if the
institutional requirements; local, state, or national laws; athlete is ready to resume participation.
and insurance policies.10 Also, more strenuous activities McKeag19 describes five populations that deserve
and those involving contact or collision (Box 2-1) special attention during the PPE. In the prepubescent
commonly require a more extensive evaluation.11 Ideally, a athlete (i.e., 6 to 10 years old), physicians should examine
PPE should occur at least 6 weeks before the intended for previously undetected congenital abnormalities.
activity.12,13 This lead time allows for specialty consultation In pubescent athletes (i.e., 11 to 15 years old), the
and an opportunity to treat minor medical problems such examination should evaluate physical maturity and good
as skin disorders, muscle weakness, or acute infections health practices for safe participation. The postpubescent
before participation.10 and young adult groups (i.e., 16 to 30 years old) bring
PPEs are usually led by a family or team physician who is the widest variety of skills, levels, and motivation. For this
familiar with the athlete’s past medical history and family group, discussion of previous injuries and a sport-specific
history as this method is more likely to provide continuity examination are important. For adults (i.e., 30 to 65 years
of care. The physician should assess any congenital or old), the physician should address injury prevention
developmental problems, immunization status, and recent (e.g., overuse), previous injury patterns, and condition-
injuries or illnesses.12-14 However, many athletes do not ing. Elderly athletes (i.e., 65 years old or older) require an
have a family physician, or the physician may lack experience examination based on individual requirements because
or understanding of the proposed activity. Another method many elderly athletes increase exercise or physical activity
for assessing preparticipation health, especially for a specific following a medical illness.5
9
10 SECTION I • Preparation and Prevention in Sports Medicine
Box 2-1 Classification of Sports According Five Specific Populations for the Preparticipation
to Contact Evaluations
Contact Limited Contact Noncontact • Prepubescent athletes (6 to 10 years of age)
Basketball Adventure racinga Badminton • Pubescent athlete (11 to 15 years of age)
Boxingb Baseball Bodybuildingc • Young adult athlete (16 to 30 years of age)
Cheerleading Bicycling Bowling • Adult athlete (30 to 65 years of age)
Diving Canoeing or kayaking Canoeing or • Masters athlete ( 65 years of age)
Extreme sportsd (white water) kayaking (flat
Field hockey Fencing water)
Football, tackle Field events Crew or rowing
Gymnastics High jump Curling
Ice hockeye Pole vault Dance Objectives of the Preparticipation Evaluation
Lacrosse Floor hockey Field events
Martial artsf Football, flag or touch Discus • Act as a screening process
Rodeo Handball Javelin • Avoid misinterpretation of findings
Rugby Horseback riding Shot-put • Classify the athlete
Skiing, downhill Martial artsf Golf • Counsel the athlete
Ski jumping Racquetball Orienteeringg • Determine health status
Snowboarding Skating Power liftingc • Determine if disease is present
Soccer Ice Race walking • Determine if referral is necessary
Team handball In-line Riflery • Determine unsuspected correctable conditions
Ultimate Frisbee Roller Rope jumping • Develop a musculoskeletal profile
Water polo Skiing Running • Develop rapport with the athlete
Wrestling Cross-country Sailing • Ensure that previous treatments and injury rehabilitation have
Water Scuba diving been completed
Skateboarding Swimming • Establish baseline values
Softball Table tennis • Establish guidelines
Squash Tennis • Foster good health practices
Volleyball Track • Keep immunizations current
Weight lifting • Meet legal and insurance requirements
Windsurfing or surfing • Prevent injuries
• Uncover pre-existing conditions
From Rice SG, Council on Sports Medicine and Fitness: Medical conditions
affecting sports participation, Pediatrics 121(4):842, 2008. Available at
http://aappolicy.aappublications.org/cgi/reprint/pediatrics;121/4/841.pdf.
a
Adventure racing has been added since the previous statement was
published and is defined as a combination of two or more disciplines,
including orienteering and navigation, cross-country running, mountain Objectives of the Evaluation
biking, paddling, and climbing and rope skills.
b
The American Academy of Pediatrics opposes participation in boxing PPEs have many purposes.10,12,20,21 The examiner must re-
for children, adolescents, and young adults. member that the purpose is not to disqualify an athlete, but
c
The American Academy of Pediatrics recommends limiting bodybuilding to ensure the health and safety of all athletes.12 Therefore,
and power lifting until the adolescent achieves sexual maturity rating
5 (Tanner stage V). an athlete disqualified from specific activities should be
d
Extreme sports has been added since the previous statement was counseled to find other activities, exercises, or sports that
published. are more appropriate to the athlete’s needs and limitations.
e
The American Academy of Pediatrics recommends limiting the amount of
body checking allowed for hockey players 15 years and younger, to reduce Most organizations require PPEs for legal and insurance
injuries. reasons. PPEs provide some protection in case of litigation,
f
Martial arts can be subclassified as judo, jujitsu, karate, kung fu, and tae and many insurance companies require them prior to issu-
kwon do; some forms are contact sports and others are limited-contact
sports. ing an insurance policy.10 Often evaluations are performed
g
Orienteering is a race (contest) in which competitors use a map and a to uncover pre-existing conditions that could preclude
compass to find their way through unfamiliar territory. participation for health or safety reasons. These pre-existing
conditions range from physical immaturity to organ loss to
the presence of specific disease processes.
The PPE helps the sports medicine team develop a current
health profile, which is used to determine whether the athlete
has the physical attributes necessary for participation. Athletes
who have had surgery or an injury must be evaluated
physically and psychologically to ensure that they are prepared
to endure stresses typically encountered during their return to
exercise or sport.12 In developing a physical fitness profile
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 11
(PFP) (Part B of this chapter), the sports medicine team The evaluation can be used to establish guidelines
establishes a baseline for the athlete, against which any future for athletes, the health care team, coaches, and administra-
injuries may be assessed. The evaluation should not simply tors about health, safety, care, and issues related to
include “yes” or “no” answers, but should thoroughly de- performance. It also provides an opportunity to counsel the
scribe the athlete’s health and establish appropriate activity disabled athlete as to which sports or modified sports would
levels. This helps decrease the incidence of reinjury and provide suitable activity. The PPE enables a team or organi-
ensures that the athlete can participate at the desired level. zation to restrict from participation anyone whose
The PPE may be used to determine the athlete’s health physical limitations present undue risk. Finally, the PPE may
status before participation or competition. The PPE also help classify and direct participants by ability.
helps to identify any abnormalities, physical inadequacies,
or poor conditioning that may place the athlete at risk
for injury.22 The examiner may find unanticipated treatable
Structuring the Preparticipation Evaluation
conditions, as well as conditions that prevent safe partici- PPEs are structured in a variety of ways. Some participants
pation. In addition, the evaluation may uncover pre- visit a physician, often their family physician, to obtain
existing conditions. Past medical history and records “medical clearance” to participate in an activity. Group
should be reviewed to help establish the presence of evaluations are more likely when a large number of athletes
pre-existing conditions. need to be seen and in higher level sporting activities in
The PPE is important to ensure that previously diagnosed which injury is a bigger risk for unhealthy or unfit persons.
conditions have been properly treated and fully rehabilitated. These sports are also more likely to provide postseason
The PPE also provides an opportunity to diagnose serious or examinations. Detailed evaluations may include individual
life-threatening medical and surgical conditions so that they stations arranged in a space-available format or a straight-
may be addressed before participation. For example, those line format (Figure 2-1).12,23 In the space-available format,
with infectious mononucleosis must avoid contact sports athletes register, then proceed from station to station until
for several weeks because the athlete’s enlarged spleen may be all evaluations are complete. In the straight-line format,
easily injured or ruptured. The PPE also ensures that old athletes register, then proceed through each station in a
injuries have properly healed and that recovery and rehabili- predetermined order until all evaluations are complete.
tation are complete. Athletes may delay or forego treatment
for end-season injuries because they believe that the injuries
will heal spontaneously with time. The PPE can be used to
Station Examples for Preparticipation Evaluation
ensure proper treatment and recovery.
The PPE provides the medical team an opportunity to Check-In
promote good health practices and fitness. This evaluation • Athlete medical/injury history
allows health care providers to give guidance and to deter- • Vital signs
mine the athlete’s general state of health. For example, the • Temperature
provider can ensure that weight-class athletes (e.g., wrestlers, • Blood pressure
• Heart rate
weightlifters) maintain healthy weights. At the same time,
• Respiratory rate
health team members can discuss with athletes the dangers • Weight
associated with crash dieting and excessive dehydration. • Visual examination
The PPE enables the health team to bring immunizations • Musculoskeletal examination
up-to-date and to assess athletes for communicable diseases. • Neurological examination
The reader is referred to the Centers for Disease Control • Cardiovascular and pulmonary examination
and Prevention for the most up-to-date immunization infor- • Additional medical examination
mation (available at http://www.cdc.gov/vaccines/recs/ • Gastrointestinal examination
default.htm). Ideally, athletes should have the opportunity • Urogenital examination
to receive age-appropriate vaccinations for diphtheria, • Dermatological examination
tetanus, pertussis, polio, measles, mumps, rubella, varicella, • Heat illness examination
• Laboratory examination
meningococcus, and influenza at their PPE visits.
• Dental examination
The evaluation provides an opportunity for the physician • Physical fitness profile
and other health care team members to develop rapport
with the athlete. The examiners can learn what motivates
the athlete while building athlete confidence in the health
care team. Every institution or team has a moral and legal In group evaluations, each station is designed to evaluate
obligation to ensure safety and health care if it sponsors one or more organs or a body system. Not all stations require
particular programs or activities. Meeting this obligation a physician to conduct the examination. Often administrators
helps to protect the organization from litigation and helps or teachers may staff the check-in and check-out stations.
to fulfill insurance requirements. The check-in station is where participants complete all legal
12 SECTION I • Preparation and Prevention in Sports Medicine
Vital signs
Eye examination
General medical
examination
Check-in
History
H Dental examination
i
s Vital signs
Check-in Check-out
t
station o Musculoskeletal station
Eye examination
r examination
y
General medical examination
A Profiling B Check-out
Figure 2-1
Examples of traffic patterns for preparticipation examinations. A, Space-available station method.
B, Straight-line station method. (From Magee DJ: Orthopedic physical assessment, ed 4, p 964,
Philadelphia, 2002, WB Saunders.)
requirements for the organization and are directed to the both the athlete and the parent or guardian should provide
other stations. An athletic trainer, sports physical therapist, past medical history to ensure completeness. The history
nurse, or other trained health care provider can obtain vital provides details about health problems and injuries, which
signs, obtain height and weight data, and perform visual enables providers to focus on the most pertinent health
screening. Likewise, a dentist can provide on-site dental issues.10 Generally, the athlete’s history is initiated by asking
screening examinations. The maturity determination and a series of questions answerable in a “yes/no” format
medical examinations should be performed by physicians. (Figure 2-2). Affirmative responses lead to further questions
At the check-out station, the athlete’s file should be reviewed and investigations. It is important that negative answers also
by the team physician to ensure that the athlete has be checked for accuracy. Oral histories are ideal because of
satisfactorily passed all components of the examination, or to increased accuracy, but time may not allow for this approach.
determine if further tests or specialty consultation may be The history should include the athlete’s past medical history
required.12 The athlete should not be told at check-out and family history to assess for possible congenital, inherited,
whether he or she has passed the PPE. This decision should or injury problems. It is important that a complete and
be delayed until the athlete has an opportunity to discuss the careful health history be obtained, as athletes may try to
evaluation results and final participation decisions with the conceal past medical or injury information that may prevent
team physicians. participation in the desired activity.24
Preparticipation questions cover a wide range of health
issues, and specific organ or system evaluations should be
Preparticipation History performed to corroborate and further explore positive
The past medical history plays a central role in the PPE. responses. The following evaluation sections are related
A complete history can usually identify 60% to 75% of the to specific body systems with positive answers leading to
health issues affecting an athlete.7,10,24 For young persons, further examinations, tests, or interventions that may need
Figure 2-2
Preparticipation physical evaluation form. (Reprinted with permission of the Florida High School
Athletic Association.) Continued
14 SECTION I • Preparation and Prevention in Sports Medicine
From Magee DJ: Orthopedic physical assessment, ed 5, p 17, St Louis, 2007, Elsevier.
*
Ranges from 97.8°F to 99.1°F (36.5°C to 37.3°C).
Remember these points:
The patient’s normal range should always be taken into consideration.
Heart rate, blood pressure, and respiratory rate are expected to increase during times of fever or stress.
Respiratory rate for infants should be counted for a full 60 seconds.
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 17
Athletes presenting with joint asymmetry, weakness, in everyday situations, but also in stressful situations. For
or other abnormalities, or who have reported previous joint example, hyperventilation may precipitate epileptic sei-
injuries should undergo a more detailed examination of the zures, and seizures tend to occur after exercise, not during
specific injured area or joint. This evaluation should assess the event. It is also important to know if the extent or
active, passive, and resisted movements, as well as reflexes intensity of the participation poses a significant threat to
and sensation if neurological tissue is involved, and available the athlete’s physical condition.
joint play if a joint has been involved. The examiner may
also palpate the joint and may consider doing functional
or other special tests. Cardiovascular Examination
When assessing musculoskeletal health in the PPE, the Because the athlete needs to remove clothing to permit
examiner should consider whether the proposed activity will auscultation, the cardiovascular examination should be
exacerbate an existing disease or injury, increase an existing performed in a quiet, private area. The examiner should
deformity, or cause further bone or joint damage. In evalu- assess for subtle but important cardiac abnormalities to
ating orthopedic and musculoskeletal problems, the exam- reduce the incidence of sudden death during sports.13,30-36
iner may, depending on the activity or sport, measure the More than 90% of sudden deaths in exercise and sports
athlete’s flexibility as well as static and dynamic stability, participants younger than the age of 30 involve the
especially if there is the potential for a problem and the cardiovascular system.
problem is easily correctable. For example, spinal instability If the athlete has experienced dizziness, chest pain, high
(especially of the cervical or lumbar spine) or spondylolis- blood pressure, a heart murmur, raced or skipped beats,
thesis may preclude participation in contact, collision, or a positive cardiovascular family history, the examiner
or impact activities. Maturation level, previous injuries, must consider cardiomegaly, conduction abnormalities,
congenital problems, and growth abnormalities should be arrhythmias, valvular disease, coronary artery defects, and
evaluated for athletes who are still growing. lung or related problems.10,37 If cardiovascular problems
are suspected, the examiner may order further tests (e.g.,
electrocardiogram, treadmill stress tests) to detect any car-
Neurological Examination and Convulsive Disorders diac abnormalities.
The neurological examination is very important, especially
if the athlete has suffered a concussion or other head injury
or neurological injury. Such an examination is especially Abnormal Cardiovascular Findings
important prior to contact or collision activities.
• Heart rate faster than 120 beats per minute or inappropriately
When doing the neurological examination, the examiner
elevated heart rate for a specific activity
may assess head injury status, cranial nerve integrity,
• Arrhythmias or irregular beats
sensation, and reflexes if problems are suspected. Signs • Midsystolic clicks, indicative of a leaky valve or mitral valve
or symptoms suggesting recurrent concussions or nerve prolapse
palsies should prompt evaluation by a specialist and delay • Murmurs that are grade 3 or louder
clearance for further activity.
For participants with convulsive disorders, the sports
medicine team needs to know the frequency of episodes,
whether control of the disorder has been achieved, which The health care team should obtain the athlete’s history
medications are used, activating circumstances, and and perform a physical examination for congenital heart
whether the athlete understands the disorder, its hazards, abnormalities such as aortic coarctation (aortic stenosis),
and its predisposing factors. For example, athletes with which can be detected by differences in femoral and bra-
epilepsy should be discouraged from activities such as chial pulses. For athletes with aortic coarctation, strenuous
skiing, parachuting, and climbing water sports (e.g., swim- activity is contraindicated. Athletes with Marfan syndrome
ming alone, scuba diving), auto racing, or any activity in (an autosomal dominant disorder affecting connective
which recurrent head trauma or unexpected falls may tissue) have a 90% prevalence of cardiac abnormalities.
cause serious injury (e.g., mountain climbing, working at The health care team must be aware of atrial-septal defects
heights) because of their inherent dangers and the poten- (abnormal communications between the heart chambers),
tial of precipitating a convulsive event.10 Athletes should dextrocardia (heart position is left-to-right reversed within
be restricted from participation if they experience one or the thoracic cavity), and paroxysmal auricular tachycardia
more seizures per week, display bizarre forms of psycho- (characterized by short periods of abnormally increased
motor epilepsy, or experience prolonged postictal (period heart rate). Athletes with any of these conditions are dis-
after seizures) states or states marked by abnormal behav- qualified from competitive sports because of the possibility
ior. It is important to know if athletes can achieve good of fainting during physiological stress. The examiner must
control of their condition by using medications, not only be aware of heart enlargement resulting from exercise
18 SECTION I • Preparation and Prevention in Sports Medicine
(“athlete’s heart”). This condition should not necessarily Patient age 40 years or under
exclude athletes from participation, but should be investi-
gated further. If any cardiac abnormalities have been One or no CHD risk factor Two or more CHD risk factors
surgically corrected, the athlete should be evaluated by a
specialist for a decision about the safety of participating in
Health No health Health No health
the proposed activity. problem(s) problem(s) problem(s) problem(s)
Hypertrophic cardiomyopathy is the most common cause
of sudden death in athletes, followed by aortic rupture as-
CPE, EST, LPE, ECT,
sociated with Marfan syndrome, congenital coronary artery LPE, DLT* LPE
DLT MLT**
anomalies, and atherosclerotic coronary artery disease.10,38
If any of these conditions are present, strenuous activity
Patient age 41 years or older
should be avoided.
Other cardiovascular problems include thromboembolic
disease, heart rate abnormalities, valvular problems such No CHD risk factor One or more CHD risk factors
as mitral insufficiency or mitral valve prolapse, and hyper-
tension. A systolic pressure of 140 mm Hg on repeat mea- Health No health Health No health
problem(s) problem(s) problem(s) problem(s)
surement is considered abnormal.32 Athletes with labile
hypertension (unstable blood pressure characterized by
rapid changes) or organic hypertension caused by structural CPE, EST, LPE, ECG, CPE, EST, LPE, EST,
DLT MLT DLT MLT**
problems should undergo further evaluation. Athletes with
hypertension should be assessed for coronary artery disease Risk factors for Health problems
coronary heart disease
risk factors. Mild hypertension should not disqualify Cardiopulmonary disease
Hyperlipidemia Neurological disease
athletes from exercise or sports participation, but periodic Cigarette smoking Endocrinopathy
re-evaluation is indicated.10 Hypertension Musculoskeletal disorder
Hyperglycemia or diabetes Psychiatric disorder
If cardiovascular or cardiopulmonary disease is suspected, mellitus Renal or hepatic disease
an exercise stress test is often recommended.20 Figure 2-3 Hyperuricemia or gout Anemia
Obesity Current drug use
provides a flow chart of considerations before conducting Other acute or chronic disease
such a test. Of those with heart disease, 20% to 35% will have
* Exercise stress testing is recommended if patient has cardiopulmonary
normal stress tests, so it is important to remember that any disease.
stress test is only valid to the load at which the heart has been
** Diagnostic laboratory testing is indicated if CDH risk factors include
stressed during the test. For runners 40 years and older, 45% hyperlipidemia, hyperglycemia, or hyperuricemia.
have irregular electrocardiogram findings. Furthermore, dif-
Figure 2-3
ferent types of activity (e.g., static versus dynamic) create Pre-exercise evaluation flow sheet.
different stresses on the heart. Table 2-2 outlines a sports CDH, Coronary heart disease; CPE, comprehensive physical
classification based on peak dynamic and static stresses en- examination; DLT, diagnostic laboratory testing; ECG, resting
countered during sports competition.39 electrocardiogram; EST, exercise stress test; LPE, limited physical
examination; MLT, minimal laboratory testing. (Adapted with
permission from Taylor RB, Copyright 1983, Consultants,
UBM Medica. All rights reserved.)
Pulmonary Examination
The pulmonary examination is often performed concur-
rently with the cardiovascular examination in a quiet area to Urogenital Examination
determine if the athlete has had long periods of intermittent The urogenital examination is modified to fit the needs of
coughing, shortness of breath, or wheezing during or after the male and female athlete. In both males and females, the
activity, exercise, or sport. The examiner should auscultate examiner should determine if the athlete has any problems
the lungs to check for clear breath sounds and should with his or her kidneys or genitourinary organs, or has been
observe chest motion for symmetric diaphragmatic diagnosed as having sugar, albumin, or blood in his or
excursion.10 All pulmonary medications should be noted. her urine.
The ears, nose, and mouth may also be examined at The medical team must check for hernias, kidney
this station. Abnormalities may be further assessed by lung problems, albuminuria (excessive protein in the urine),
function tests or chest x-ray examination.40 Respiratory and sexually transmitted infections.43 Athletes with one
problems such as tuberculosis, uncontrolled asthma, exer- kidney should be warned of the danger of contact sports,
tional asthma, exercise-induced bronchospasm, pulmonary especially if the kidney is abnormally positioned or
insufficiency from a collapsed lung, or bronchial asthma diseased.28
deserve special attention and follow-up discussion and Females may be asked about their menstrual history
evaluation.20,41,42 (e.g., When did it begin? When was the last period?
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 19
Table 2-2
Classification of Sports Based on Peak Dynamic and Static Components During Competition
Low Dynamic Moderate Dynamic High Dynamic
From Mitchell JH, Haskell WL, Raven PB: Classification of sports, Med Sci Sports Exerc 26:S242-S245, 1994.
*
Danger of bodily collision.
†
Increased risk if syncope occurs.
Are there any abnormalities?) or about any gynecological blood in urine) are possible problems of the urogenital
problems. For females, it is important to assess for regular system.
menstruation, because exercise amenorrhea is a significant
problem that is associated with low bone density and
osteoporosis.20,44 Gastrointestinal Examination
For males, the examiner must ask about a history of The gastrointestinal questions and examination should ad-
undescended or atrophied testes or testicular torsion. Males dress digestion, eating habits, and nutrition.45 Questions
may be given a genital examination to check for abnormali- are related to eating regularly and having a well-balanced
ties, hernias, or absence of a testicle.10 diet; what food groups the athlete does not eat; whether the
A urinalysis should be performed if diabetes or kidney athlete has been on a diet or views himself or herself as too
disease is suspected. These conditions do not normally thin, too fat, or just right; and about weight control, heart
preclude activity, exercise, or sport, and may be amenable burn, and indigestion.
to treatment. The athlete and sponsoring organization The examiner should palpate the abdomen for masses
must be made aware of potential dangers caused by or organomegaly (enlarged organs).12 The health care team
these conditions. Dehydration, athletic pseudonephritis must ensure that there is no liver or spleen enlargement,
(false kidney inflammation), hemoglobinuria (abnormal especially for contact-sports participants.
presence of hemoglobin in the urine), nephroptosis For esthetic or weight-conscious sports (e.g., gymnastics,
(dropped kidney), and hematuria (abnormal presence of ballet, synchronized swimming, wrestling), the examiner
20 SECTION I • Preparation and Prevention in Sports Medicine
should check the athletes’ nutritional status, especially if usually require that the athlete be temporarily removed
there is a suspicion of an eating disorder such as anorexia or from participation, often to protect other participants.10
bulimia.46 This is best evaluated by asking the athlete to re- Febrile illness often causes dehydration, which can
cord his or her food intake for at least 3 days and ask a nu- predispose to heat disorders.
tritionist to determine if the calculated dietary intake is ap-
propriate for the athlete’s activity level (see Chapters 3 and
4 for more information). This also provides an opportunity
to find out about any banned or unsafe substances the ath- Examples of General Medical Problems Requiring
letes may be taking. Awareness of the Sports Medicine Team
• Athletes with systemic disease (e.g., diabetes)
Dermatological Examination • Female athlete triad (anorexia or bulimia, amenorrhea, osteoporosis)
• Athletes with progressive disease (e.g., muscular dystrophy,
The PPE is a good opportunity to identify skin conditions multiple sclerosis)
that may be amenable to treatment. Questions about acne, • Cancer
rashes, or itching, especially in areas covered by clothes, • Human immunodeficiency virus, acquired immune deficiency
equipment, or footwear, are appropriate and deal with skin syndrome
conditions that are usually easily treated. The examiner
must ensure that the athlete’s skin problems are addressed,
because many are contagious. Some common contagious
skin problems include bacteria (e.g., boils, impetigo),
fungus (e.g., athlete’s foot), and viruses (e.g., herpes Dental Examination
simplex, herpes gladiatorum, warts). The dental examination is commonly performed by a dentist.
The dentist should determine when the athlete last saw a
dentist, whether the athlete has had problems with his or her
Examination for Heat Disorders teeth or gums; whether the athlete has had any teeth knocked
Examination for prior history of heat disorders should be out, damaged, or extracted; whether the athlete wears a
included if the activity, exercise, or sport will occur in an mouthguard, smokes, or chews tobacco; or whether the
area with a high temperature, high humidity, or some athlete has ever had an injury to his or her face or jaw.27
combination of both. The examiner should determine if the When performing the dental examination, the dentist
athlete has ever suffered from a heat disorder or muscle should note the number of teeth the athlete has. This is
cramps; participated in an activity, exercise, or sport in a important because of the potential for liability if teeth are
high-temperature, high-humidity environment; ever passed avulsed (knocked out). It also provides an opportunity to fit
out or become dizzy in the heat; or is on any medications mouthguards and check dental appliances to ensure good
or drinks large quantities of caffeinated beverages. condition.
Use of antihistamines or excessive caffeine, as well as dehy-
dration (i.e., lack of fluids or electrolytes), can increase the risk
of heat disorders. If an athlete has a history of heat-related
disorders, the condition should be thoroughly investigated Examples of Dental Problems Requiring Awareness
because of the life-threatening potential of these disorders.
of the Sports Medicine Team
• Problems with teeth or gums
General Medical Problems • History of teeth knocked out, damaged, or extracted
In addition to the problems previously described, there • History of smoking or chewing tobacco
are general systemic medical problems that deserve • Previous injury to face or jaw
evaluation by the health care provider such as systemic
diseases, (e.g., diabetes), progressive diseases (e.g., mus-
cular dystrophy, multiple sclerosis, or cancer).
The examiner should be concerned about acute
infections, malignancies, and progressive diseases such as
Laboratory Tests
multiple sclerosis. Diabetes should not exclude someone Laboratory tests are not usually included in the PPE.
from participation, but the examiner must assess the However, the physician may request diagnostic laboratory
athlete’s disease status and control with medications. It tests for suspected problems. For example, if heart disease
must be determined whether the extent or intensity of the is suspected or an older athlete is being evaluated, the
activity poses a significant threat to the athlete’s physical examiner may order serum cholesterol, triglyceride, or
condition.47 Acute illnesses tend to be self-limited and high-density lipoprotein levels.
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 21
Table 2-3
Medical Conditions and Sports Participation
Condition Explanation Participation
Atlantoaxial instability (instability The athlete needs evaluation to assess the risk of spinal cord injury Qualified yes
of the joint between cervical during sports participation.
vertebrae 1 and 2)
Bleeding disorder The athlete needs an evaluation. Qualified yes
Carditis (inflammation of the Carditis may result in sudden death with exertion. No
heart)
Hypertension (high BP) Those athletes with significant essential (unexplained) hypertension Qualified yes
should avoid weight lifting and power lifting, body building, and
strength training. Those with secondary hypertension (hyperten-
sion caused by a previously identified disease) or severe essential
hypertension need evaluation.*
Congenital heart disease Those athletes with mild forms of congenital heart disease may Qualified yes
(structural heart defects present participate fully. Those with moderate or severe forms and those
at birth) who have undergone surgery need evaluation.†
Dysrhythmia (irregular heart The athlete needs evaluation because some types of cardiac dys- Qualified yes
rhythm) rhythmia require therapy, make certain sports dangerous, or both.
Mitral valve prolapse (abnormal Those athletes with symptoms (chest pain, symptoms of possible Qualified yes
heart valve) dysrhythmia) or evidence of mitral regurgitation (leaking) on physi-
cal examination need evaluation. All others may participate fully.
Heart murmur If the murmur is innocent (i.e., it does not indicate heart disease), Qualified yes
full participation is permitted. Otherwise, the athlete needs an eval-
uation (see “Congenital heart disease” and “Mitral valve prolapse”).
Cerebral palsy The athlete needs an evaluation. Qualified yes
Diabetes mellitus If the diabetes is well controlled, the athlete can play in all sports Yes
with proper attention to diet, hydration, and insulin therapy. Partic-
ular attention is needed for activities that last 30 minutes or more.
Diarrhea Unless the disease is mild, no participation is permitted because diarrhea Qualified no
may increase the risk of dehydration and heat illness. (See “Fever.”)
Anorexia nervosa, bulimia Patients need both medical and psychiatric assessments before Qualified yes
nervosa sports participation.
Functionally one-eyed athlete, A functionally one-eyed athlete has a BCVA of better than 20/40 Qualified yes
loss of an eye, detached retina, in the worse eye. These athletes could experience a significant
previous eye surgery, or serious disability if the better eye is seriously injured, as can those athletes
eye injury who have lost an eye. Athletes who have previously undergone
eye surgery or who have had a serious eye injury may be at
increased risk of injury because of weakened eye tissue. Use of eye
guards approved by ASTM International and other protective
equipment may allow the athlete to participate in most sports,
but this approach must be judged on an individual basis.
Fever Fever can increase cardiopulmonary effort, reduce maximum exercise No
capacity, make heat illness more likely, and increase orthostatic
hypotension during exercise. In rare cases, fever may accompany
myocarditis or other infections that may make exercise dangerous.
Heat illness, history of Because of the increased likelihood of the recurrence of heat illness, Qualified yes
the athlete needs an individual assessment to determine the presence
of predisposing conditions and to arrange a prevention strategy.
From American Academy of Pediatrics Committee on Sports Medicine and Fitness: Medical conditions affecting sports participation, Pediatrics
94:757–760, 1994.
ASTM, American Society for Testing and Materials; BCVA, best-corrected visual acuity; BP, blood pressure; HIV, human immunodeficiency virus.
*
National Heart, Lung, Blood Institute: Report of the 2nd task force on blood pressure control in children — 1987, Pediatrics 79:1-25, 1987.
†
16th Bethesda Conference: Cardiovascular abnormalities in the athlete: recommendations regarding eligibility for competition, J Am Coll
Cardiol 6:1189-1190, 1985. Continued
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 23
Table 2-3
Medical Conditions and Sports Participation—cont’d
Condition Explanation Participation
‡
HIV infection Because of the apparent minimal risk to others, all sports may be Yes
played, as allowed by the patient’s state of health. In all athletes,
skin lesions should be properly covered, and athletic personnel
should use universal precautions when handling blood or body
fluids with the presence of visible blood.
Kidney, absence of one The athlete with one kidney needs individual assessment for Qualified yes
contact/collision and limited contact sports.
Liver, enlarged If the liver is acutely enlarged, athletic participation should be Qualified yes
avoided because of a risk of rupture. If the liver is chronically
enlarged, individual assessment is needed before contact/collision
or limited contact sports are played.
Malignancy The athlete needs an individual assessment. Qualified yes
Musculoskeletal disorders The athlete needs an individual assessment. Qualified yes
History of serious head or spine The athlete needs an individual assessment for participation in Qualified yes
trauma, severe or repeated contact/collision or limited contact sports and also for
concussions, or craniotomy noncontact sports if deficits in judgment or cognitions are
present. Recent research supports a conservative approach to the
management of concussions.
Convulsive disorder, well controlled The risk of convulsions during sports participation is minimal. Yes
Convulsive disorder, poorly The athlete needs an individual assessment before participation in Qualified yes
controlled contact/collision or limited contact sports. Because a convulsion
may pose a risk to the athlete or to others, the following
noncontact sports should be avoided: archery, riflery, swimming,
weight lifting or power lifting, strength training, and sports
involving heights.
Obesity Because of the risk of heat illness, obese persons need careful accli- Qualified yes
matization and hydration.
Organ transplant recipient The athlete needs an individual assessment. Qualified yes
Ovary, absence of one The risk of severe injury to the remaining ovary is minimal. Yes
Pulmonary compromise, includ- The athlete needs an individual assessment, but generally all sports Qualified no
ing cystic fibrosis may be played if oxygenation remains satisfactory during a graded
exercise test. Patients with cystic fibrosis need acclimatization and
good hydration to reduce the risk of heat illness.
Asthma With proper medication and education, only athletes with the most Yes
severe asthma need to modify their participation.
Acute upper respiratory infection Upper respiratory obstruction may affect pulmonary function. Qualified yes
Athletes, with the exception of those with mild disease, need an
individual assessment. (See “Fever.”)
Sickle cell disease The athlete needs an individual assessment. In general, if the status Qualified yes
of the illness permits, the athlete may play all sports except high-
exertion, contact/collision sports. Overheating, dehydration, and
chilling must be avoided.
‡
American Academy of Pediatrics Committee on Sports Medicine Fitness: Human immunodeficiency virus (acquired immunodeficiency
syndrome [AIDS] virus) in the athletic setting, Pediatrics 88:640-641, 1991.
Note: This table is designed to be understood by medical and nonmedical personnel. In the Explanation column, a notation that the athlete
needs an evaluation means that a physician with appropriate knowledge and experience should determine whether an athlete with the listed
medical condition can safely participate in a given sport. Unless otherwise noted, these evaluations are generally recommended because of
variations in the severity of disease and in the risk of injury in specific sports. Continued
24 SECTION I • Preparation and Prevention in Sports Medicine
Table 2-3
Medical Conditions and Sports Participation—cont’d
Condition Explanation Participation
Sickle cell trait Individuals with the sickle cell trait (AS) are unlikely to have an increased Yes
risk of sudden death or other medical problems during athletic
participation in most conditions. Exceptions include the most extreme
conditions of heat; humidity; and, possibly, increased altitude. Like all
athletes, those with the sickle cell trait should be carefully conditioned,
acclimatized, and hydrated to reduce any possible risk.
Skin boils, herpes simplex, impe- During the periods in which the patient is contagious, participa- Qualified yes
tigo, scabies, molluscum conta- tion in gymnastics with mats, martial arts, wrestling, or other
giosum contact/collision or limited-contact sports is not allowed. Herpes
simplex virus is probably not transmitted via mats.
Spleen, enlarged Patients with an acutely enlarged spleen should avoid all sports be- Qualified yes
cause of the risk of rupture. Those with chronically enlarged
spleens need an individual assessment before playing contact/
collision or limited-contact sports.
Testicle, absent or undescended Athletes in certain sports may require a protective cup. Yes
competition. His or her specific academic training, historical information to identify common sites of injury,
professional experience, and certification (e.g., National and (4) searching the literature for information relevant to
Strength and Conditioning Association Certified Strength the sport. If no direct evidence exists, then the sports
and Conditioning Specialist) makes the strength and medicine staff should consider directly measuring physio-
conditioning coordinator unique from other members logical and mechanical demands of the sport and publishing
of the sports medicine staff. Therefore, the strength and this information. A thorough needs analysis addresses the
conditioning coordinator is extremely valuable in designing, following questions:
administering, and interpreting the PFP test battery. What are the physical and physiological needs of
the sport? Each sport requires different physical
attributes. The most common characteristics required by
Clinical Point a sport are strength, power, speed, acceleration, anaerobic
capacity, aerobic capacity, agility, and flexibility. Some
A physical fitness profile involves a battery of physical tests that are:
• Specific to an athlete’s sport and position sports (e.g., cross-country, shot put) require only one or
• Designed to determine whether the athlete has the necessary two physical attributes for success. However, most sports
physical and physiological attributes to compete at the desired (particularly team sports) require numerous physical
level attributes. For instance, soccer requires speed to out-run
• Designed to establish a baseline and screen for the athlete in opponents, anaerobic capacity to perform repeated sprints,
case of injury aerobic endurance to maintain performance throughout
• Designed to prevent and treat injury or correct poor mechanics the entire match, agility to out-maneuver and successfully
• Designed to predict performance defend opponents, strength to hold off opponents and
maintain position, and flexibility to kick at various angles
and trajectories. To complicate matters, some team sports
involve specialized position players whose physical
Needs Analysis attributes are unique from other team members.50,51
The initial step in designing the PFP is performing a needs For instance, soccer goalkeepers depend heavily on
analysis. As the name implies, the purpose of the needs explosive power and reaction time for success, yet require
analysis is to assess the physical requirements of the sport, relatively little aerobic endurance compared with their
and then use this information to design an appropriate PFP teammates. These factors require that the PFP use a
test battery. A successful needs analysis requires (1) study- battery of tests, as opposed to a single test, to adequately
ing the athlete’s games and practices (either live or via profile the athletes.
video) to identify the physical and physiological needs of Which specific movement patterns are most impor-
the sport, (2) consulting with the team coaching staff to tant for the sport? The PFP battery should consist of
identify the player’s or team’s strengths and weaknesses, tests that are specific to the movement patterns used in
(3) consulting with the sports medicine staff to obtain the sport. For instance, it has already been stated that a
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 25
soccer player needs strength and speed to be successful. In contrast, there are few eccentric contractions of the
This does not imply, however, that the test battery quadriceps in the sport of road cycling. Therefore, tests of
developed for soccer players should be the same as the eccentric strength in road cyclists would be unnecessary,
test battery used for football defensive linemen, who also and would provide irrelevant data.
require strength and speed. Defensive linemen require In addition to the muscle actions, the kinetics of
much more upper-body strength and their speed require- the sport should be considered to provide a sport-specific
ments are typically more intermittent and for shorter testing battery. Most sports are played on a field, court,
distances (approximately 5 to 10 yards [4.5-9.1 meters]) or track that requires an athlete to move his or her body
compared with soccer players. mass or opponent’s body mass against gravity. Some
What are the common sites of injury for the sport and sports require an athlete to move a projectile (e.g., discus,
population? Each sport (e.g., ice hockey, cross-country) and shot-put, softball) against gravity. In each of these
certain populations (e.g., older athletes, women) poses unique cases, mass is constant but force varies depending on the
injury predispositions. For instance, epidemiological evidence acceleration of the mass. The kinetics of these movements
indicates that poor hamstring-to-quadriceps strength ratio are closely simulated using dynamic constant external
may predict noncontact anterior cruciate ligament (ACL) resistance (DCER) testing (i.e., free weights). Swimming
injuries in female athletes.52 However, this relationship does is an example of a sport in which the kinetics are not
not necessarily exist in male athletes within similar sports. replicated using DCER testing. The resistance encoun-
Therefore, isokinetic testing of knee extension and flexion tered in the sport of swimming is predominantly fluid
strength is indicated in female athletes, but might be unneces- resistance. Therefore, a test more specific to the sport
sary in male athletes participating in similar sports. It is im- of swimming would incorporate hydraulic resistance
perative the sports medicine staff consistently read and inter- testing.
pret emerging literature to develop a PFP test battery (and
subsequent interventions) that will prevent future injury. The Importance of a Physical Fitness
Profile
Clinical Point The initial profiling session provides critical data that
benefits the athlete, sports medicine staff, and strength and
A physical fitness profile must take into account: conditioning coordinator (Box 2-2). PFP data can be used
• The physical attributes needed to perform the sport
to establish baseline measures useful in tracking changes in
• The level at which the sport will be played
• The attributes needed to play different positions
the physical performance of the athlete over time. Compar-
• The movement patterns necessary for the sport ing these data with results from subsequent tests allows
• The sport’s unique injury patterns for objective evaluation of the training program. If insuffi-
• Muscle actions required for the sport ciencies are identified, then the strength and conditioning
• The kinetics of the sport coordinator can adjust the training program accordingly.
The PFP also provides baseline data from which initial
training loads can be derived. For instance, one-repetition
maximum (1-RM) strength tests are commonly used in
What are the common muscle actions and kinetics PFP batteries. Strength and conditioning coaches can use
of the sport? Each sport requires a unique combination of this information to prescribe resistance training loads to a
muscle actions (i.e., concentric, eccentric, and isometric) induce specific physiological adaptations (e.g., by prescrib-
and kinetics. Downhill or mogul skiing, for example, are ing squats using loads that are a percentage of 1-RM).
sports that require high eccentric and isometric strength.53,54 Baseline PFP can also be used for comparative analysis
Therefore, it is important to incorporate tests that specifi- during rehabilitation from injury. An often-used method of
cally address the eccentric and isometric strength of these assessing an athlete’s ability to return to sport after injury
athletes to determine their physical readiness for sport. is to compare an injured limb with the uninjured limb.55
Box 2-2 Select Benefits of Physical Fitness Profiling to the Athlete, Sports Medicine Staff, and Strength
and Conditioning Coordinator
Athlete Sports Medicine Staff Strength and Conditioning Coordinator
Benchmark with which to set goals Identify and screen for injuries Screen for injurious technique during exercise
Data can be compared with team or Baseline data to describe general physical readiness Predict success in sport
national norms In case of future injury, data serves as bench- Baseline data for daily exercise prescription
Gauge of success in training mark to determine full recovery Monitor effectiveness of training program
26 SECTION I • Preparation and Prevention in Sports Medicine
Isokinetic knee extension and flexion strength is used by are made available to NFL scouts and they are used to
many physicians as a test to determine the physical readiness make draft decisions. Sierer and colleagues studied the NFL
of an athlete to return to activity after an ACL surgery. combine performance scores from 2004 and 2005, compar-
Typically, when the strength of the involved limb reaches ing the scores of drafted and undrafted players.69 Further-
75% to 85% of the uninvolved limb, then the athlete is more, they divided the players into skill (i.e., wide receivers,
declared ready to return to running activity.55 However, the running backs, strong safeties, and free safeties), big skill
inherent flaw in this methodology is that it is possible that players (i.e., full backs, tight ends, linebackers, and defensive
the involved limb was significantly stronger or weaker than ends), and lineman (i.e., offensive guards, offensive tackles,
the uninvolved limb prior to the injury. If baseline data are and defensive tackles). The investigators found that height,
collected on the athlete prior to injury, the sports medicine body mass, and broad jump did not predict draft status within
staff can quantitatively substantiate “full recovery” in any of the player categories. Time in the 40-yard sprint,
response to rehabilitation. vertical jump, pro-agility drill, and three-cone drill were
PFP testing can serve to reveal incompletely rehabilitated significantly different in drafted and undrafted skill players.
injuries that athletes may not have disclosed during the Drafted big skill players had faster 40-yard sprint times and
PPE.56,57 Initial profiling may illuminate muscular asymme- three-cone drills compared with undrafted players. Finally,
tries that increase the risk for injury. As mentioned previ- drafted linemen had faster three-cone drills and 40-yard sprint
ously, female athletes often have poor knee flexion strength times, and were able to bench press 225 pounds more times
relative to knee extension strength, which increases the risk than undrafted linemen. These data indicate that the predic-
for noncontact ACL injuries.52 As such, in sports with fe- tive ability of the combine tests differs across player groups
male participants in which there are high numbers of ACL and some of the tests have limited or no predictive ability of
injuries, it is sensible to perform isokinetic knee extension draft status. The data also suggest that not all PFP tests are
and flexion tests to identify at-risk athletes. Corrective exer- suitable for every athlete. When considering test inclusions
cise programs can then be implemented to reduce the asym- and exclusions, data such as these can be used to select
metries and subsequently reduce the risk of ACL injury. In appropriate tests for the individual athlete.
other sports, asymmetrical flexibility in joints may increase The ultimate goal of PFP testing is to actually predict
the risk for injury. In baseball pitchers, deficits in internal playing ability based on the score of a test. This is com-
rotation range of motion of the shoulder (i.e., glenohu- plicated given the difficulty of quantifying “playing ability”
meral internal rotational deficit) may indicate capsular of sports that are skill-intensive. Some investigators have
changes that predispose the throwing athlete to glenohu- assessed the predictive ability of a test by comparing starters
meral joint injuries.58,59 In such cases, specific programs and nonstarters within a given sport.70,71 Black and Roundy
could be implemented to correct range-of-motion imbal- compiled human performance data from 44 Division
ances and mitigate these risks. I collegiate football strength and conditioning programs.72
In addition to screening for asymmetrical muscle strength Using biserial correlation coefficients, they compared the
and flexibility, the initial testing session may be used to scores of starter versus nonstarter football players. Their
screen for injurious technique during key athletic move- analysis indicated that body mass, 1-RM back squat
ments. If foundational sport movements (e.g., running, and bench press, vertical jump, and 40-yard sprint speed
jumping) are performed with poor mechanics, the athlete significantly predicted playing status. However, the results
may be at risk for acute or chronic injuries. Female athletes differed greatly between positions, suggesting that there are
exhibit different biomechanics compared with males when dissimilar qualities needed to play different positions in
performing foundational sports skills such as running, football. Schmidt also compared the physiological charac-
jumping, landing, and cutting.60-67 These unique biome- teristics of starters and nonstarters in football. Using a
chanics increase valgus stress on the knee joint, contributing single Division III collegiate football team (78 players), he
to a greater number of noncontact ACL injuries in female demonstrated that the predictive ability of a test differed by
athletes. However, if the “at-risk” athletes are identified playing position.73 However, his data suggest that seated
and specific mechanical training is implemented, the risk of medicine ball throw and the 1-RM bench press and leg
ACL injuries is dramatically reduced.68 press were the best predictors of playing status. Finally,
Finally, the initial testing or profiling session may be used Fry and Kraemer compared the physical performance of
to predict performance. Normative data exist for many stan- 30 collegiate football programs.74 They surveyed 10 strength
dard tests. Therefore, the athlete’s scores can be compared and conditioning programs from Divisions I, II, and III
against national or international norms for an age group. (30 total programs) and compared performance scores
Perhaps the most renowned PFP session occurs at the between positions. It was determined that 1-RM power
National Football League (NFL) “combine” each April in clean and bench press, 40-yard sprint, and vertical jump
Indianapolis, Indiana. At the combine, athletes compete in a were good predictors of playing level. However, back squat
series of athletic tests specific to the game of football. The data was not a good predictor of playing level.
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 27
Clinical Point
Physical fitness profiling tests may be classed as:
Although PFP has predictive ability for many athletes • Clinical
• Laboratory
in various sports, there are always athletes who perform
• Field tests
poorly on tests yet are world-class performers in their
sport. Therefore, results should be interpreted with
caution. PFP testing results should be integrated with
other sources of information (e.g., on-field or court per- Laboratory tests are another category that may be
formance) to ultimately evaluate the potential success of used in the PFP. Generally, these tests are performed in
the athlete. laboratory settings under carefully controlled conditions.
The advantages of these tests are that they can precisely
Administering the Physical quantify the underlying constructs of human perfor-
mance. For example, aerobic capacity is quantified in
Fitness Profile the laboratory by measuring oxygen consumption in a
Unlike many of the screening tools used to assess the maximal exercise condition (VO2 max test). However, the
medical readiness of the athlete, the PFP has some inherent limitations associated with laboratory tests are that they
dangers. Because the sports medicine staff is interested in typically require highly trained professionals, expensive
testing the peak abilities of the athlete, it is possible that equipment, and substantial time, and in some cases
injury could occur with such testing. It may be necessary to do not necessarily translate to real-world competitive
develop and administer an activity questionnaire to deter- environments. These restrictions often make laboratory
mine the training experience of the athlete. For instance, an tests impractical if attempting to assess large groups of
athlete who is performing his or her first 1-RM test for an athletes (e.g., a football team). However, when working
exercise may score low simply because he or she lacks with a manageable number of athletes, the benefits of
familiarization with the test.76 In addition, he or she may laboratory testing might outweigh the costs.
be at greater risk for injury because of poor technique. Field tests are normally performed outside of the
Therefore, test familiarization is warranted for athletes who clinic. The primary advantages of these tests are cost- and
are performing a test for the first time. time-effectiveness, which makes them practical for testing
28 SECTION I • Preparation and Prevention in Sports Medicine
large groups of athletes. They can also be designed to minimum the strength and conditioning coordinator should
assess the specific needs of the sport (e.g., agility). evaluate mechanics during these movements. Particular
However, if field tests are not carefully designed, then the emphasis should be placed on the foot, knee, and hip bio-
tests will be plagued by poor reliability. The U.S. military mechanics. The strength and conditioning coordinator
provides an excellent example of effective field testing. should work together with other members of the sports
Because they test more than 1 million soldiers each medicine staff to effectively conduct movement screenings.
year, VO2 max testing is not a practical measure of aerobic The team athletic trainer or sport physical therapist can
capacity. Instead, they use 1.5 to 3 mile (2.4 to 4.8 km) provide helpful insight in the screening process.
run times to extrapolate maximal aerobic capacities
of their soldiers and to track fitness over time.77,78
Even though these tests do not provide precise measures Clinical Point
of oxygen consumption, they provide a valid and reliable
way to classify aerobic fitness within large groups of Movement screen tests should include:
• The fundamental movements of the sport
individuals.
• Movements that could result in injury
• Multiple joints at the same time
Profiling Athletic Performance
As stated earlier, the PFP should include tests that are spe-
cific to the physical needs of the sport (e.g., energy systems,
movement patterns). Generally, the following constructs are Muscular Strength
tested in athletic profiling: movement screening, muscle Most sports require athletes to exert force against an
strength, muscle endurance, power, speed and acceleration, opponent, a projectile, or the ground. Therefore, muscle
flexibility and ROM, aerobic capacity, and anaerobic capac- strength is an important component to sport. Muscle strength
ity. Many tests are available to evaluate these constructs so can be tested using isometric, isokinetic, or DCER (i.e., free
it is imperative to remember that the tests chosen should be weight) muscle contractions. Further, it can be tested using
specific to the demands of the sport. isolated, single-joint movements that determine the force-
generating capabilities of a small group of muscles, or it can
be tested using multi-joint movements that determine force
capabilities during complex movements. Single-joint muscle
Clinical Point strength tests are well controlled, safe, and reliable measures
Athletic profiling should include: of muscle strength. However, they are dissimilar to most sport
• Movement screen tests movements. Generally, functional sport movement requires
• Muscle strength tests the coordination of multiple joints and muscle groups to
• Muscle endurance tests generate strength and power against the ground or the
• Power opponent. Therefore, multi-joint testing is likely more appli-
• Velocity and acceleration cable to most sport movements.
• Agility and quickness The most often used field assessment of strength is
• Flexibility and range of motion 1-RM testing using free weights. Free weights are univer-
• Aerobic capacity
sally available and can be used to test a variety of functional
• Anaerobic capacity
movements. If performed correctly, 1-RM testing is
reliable, safe, and efficient.82-86 To administer a 1-RM test,
the athlete performs a general warm-up, dynamic stretch-
ing, and an exercise-specific warm-up. The weight in
Movement Screening the exercise is gradually increased until the athlete can no
Movement screening has little ability to predict human per- longer perform a single repetition. The highest amount of
formance but may be a valuable tool in identifying athletes weight lifted for one repetition through a full ROM using
with functional limitations, abnormal biomechanics, or correct technique is recorded as the athlete’s 1-RM.
poor ROM during specific sport movements.79,80 These Alternately, 1-RM maximum strength can be estimated
data could be used to identify athletes at risk for injury. using submaximal loads.87-89 After a general warm-up,
Therefore, movement screening should include the funda- dynamic stretching, and exercise-specific warm-up, the
mental movements of the sport or those movements that athlete performs a single set of the exercise with a submaxi-
are known to result in injury. Some standardized movement mal load to failure (multi-RM testing). The number of
screening tools are available for use.81 However, most repetitions performed is used to estimate the 1-RM.
ground-based sports involve some variation of the The accuracy of multi-RM strength testing differs depend-
squat, lunge, jump and land, and running movements; at a ing on the number of repetitions performed; it has been
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 29
suggested that no more than 10 repetitions should be equipment.103 The reaction force generated against the
performed to obtain accurate data.88 ground while pulling against a fixed barbell in the mid-thigh
The exercises used in 1-RM or multi-RM testing differ position of the clean exercise (power position for most
depending on the sport. Generally, the strength and condi- sports) may be an effective measure of performance in
tioning coordinator should choose multi-joint exercises some sport skills.104-106 This type of isometric testing may be
that are specific to the strength movements required in a indicated for sports that require ground reaction forces.
sport. It has been suggested that the essential movements in Furthermore, testing set-up is relatively easy and could be
most sports are pushing, pulling, and squatting;90 therefore, completed on a large number of athletes.
bench press, bench pull, and back squat are appropriate 1-RM
test for most sports. For sports that involve high-power move- Local Muscle Endurance
ments, it may be appropriate to test 1-RM in the weightlifting Local muscle endurance, or the ability to exert a submaxi-
exercises (e.g., clean and snatch) as well. mal force repeatedly, is an important aspect of sports that
Isokinetic muscle strength testing is a reliable laboratory require continuous activity (e.g., swimming).107,108 Typi-
assessment that determines the force-generating capabilities of cally, local muscle endurance is tested using body weight
a muscle at a fixed angular velocity.91,92 Because muscle force exercises (e.g., push-ups, pull-ups, sit-ups) performed to
is indirectly related to velocity of movement,93 isokinetic test- failure.77,78,109 It can also be tested by performing a maximal
ing is able to isolate velocity, eliminating momentum as a number of repetitions in a certain amount of time or the
factor in completing a movement. Testing typically involves highest number of repetitions performed using submaximal
single-joint movements and may involve concentric and loads (e.g., maximal number of squat repetitions using a
eccentric contractions depending on the capabilities of the load of 50% of 1-RM).
dynamometer.94 Data derived from an isokinetic test includes
maximum force production, average force production, me- Power
chanical work, and other kinetic variables. Each of these kinetic Newtonian physics defines power as the product of force and
variables (except mechanical work) can also be described at any velocity, or work per unit of time. In practical terms, power can
instantaneous joint angle. Isokinetic testing is useful in describ- be described as the rapid or explosive expression of muscle
ing muscle imbalances between opposing muscle groups95,96 strength (e.g., maximal jumping, throwing). Because most
and may be helpful in screening for certain injuries.52 It is also team sports (e.g., baseball, football, soccer) require fast,
correlated with performance in some sports.97-100 explosive movements rather than slow, high-force move-
Isokinetic testing is considered a laboratory test. There- ments, power is a key indicator of athletic potential.110-112
fore, it can be time consuming and is impractical for testing Vertical jump height is the most common field test
large groups. In addition to the calibration and athlete for muscle power. Vertical jump predicts performance in
set-up time, only a single joint is measured with each various sports (e.g., rugby, football)70,71,74 and is correlated
test. To fully assess the strength of an athlete’s lower with running speed (Figure 2-4). Vertical jump height is mea-
extremity, it is necessary to test strength at the ankle, knee, sured as the difference between standing reach height and
and hip. Each of these tests require different machine con- vertical jump reach height. Because body weight affects verti-
figurations. In addition, to fully test the capabilities of the cal jumping performance, methods have been developed to
muscle, it may be necessary to test at multiple speeds and to directly (via a force plate) or indirectly (via Sayers’s equation
perform separate tests of eccentric and concentric strength. for peak power and Harman’s equation for average power)
Because of these limitations, isokinetic testing is unrealistic measure muscle power during vertical jumps. This allows a
for most testing situations and should be used on a limited strength and conditioning coordinator to compare power
basis as a tool to screen athletes who are at risk of injury. output of athletes of different body weights.
Muscle strength can also be assessed by testing the force- Sayers’s equation for calculating peak power is:113
generating capabilities against a fixed or immovable object
P(W) ( 60.7 Jump Height [ cm] )
(isometric testing). The advantages of isometric tests are the
time requirements ( 5 sec), reliability, and safety of the ( 45.3 BM[K g] ) 2055.0
test.101 The disadvantage is that it requires force-measuring
hardware (i.e., load cell or force plate). Isometric tests can Harman’s equation for calculating average power is:114
assess single-joint movements or multi-joint movements.
P(W) = ( 21.2 Jump Height [cm] )
The force-generating capabilities of a joint at a given angle
are specific to only a 30-degree arc surrounding the joint
( 23.0 BM[K g] ) 1393.0
angle tested.102 Therefore, to adequately assess the strength For sports in which upper-body power is important,
of a single joint it is necessary to test at multiple angles, an appropriate field test is the medicine ball throw
making isometric, single-joint movements impractical. for distance. The throw distance can be measured seated,
Whole-body isometric movements are a viable testing standing, twisting, or overhead, depending on the me-
option if the sports medicine staff has access to the necessary chanics of the sport.115-118
30 SECTION I • Preparation and Prevention in Sports Medicine
A
Figure 2-4
Unpublished data from the Human Performance Laboratory at the
University of Houston-Clear Lake and Memorial Hermann Sports
Medicine Institute displaying the relationship between 40-yard sprint
time and vertical jump (r 0.80). Data were collected on 1250 high
school football players.
The following equation calculates velocity (V) using ments needed to perform the drill. For instance, a drill that
distance (d) in meters and time (t) in seconds: requires only forward running would appropriately test the
agility required for a football defensive lineman; however, a
(
V M
sec ) = dt basketball player would be better tested in a drill requiring
forward, lateral, and backward movements.
Some positions in sport rarely require an athlete to Flexibility and Range of Motion
achieve top speed. For example, a defensive or offensive line- Flexibility and ROM may be important measurements
man infrequently runs at top speed during a game. There- for predicting injuries and performance limitations in athletes.
fore, a more important physical profile test may be the The type of test and joints measured should be specific to the
measurement of acceleration. Acceleration is the rate of sport and associated injuries. Furthermore, it should be noted
change in velocity over time and is typically expressed as that certain sports require more or less flexibility and ROM
m/sec2. The following equation calculates acceleration (a) for success. Ballet dancers, for instance, may have extreme
using the second velocity (V2) in meters per second, initial ROM in the muscles that surround the hip. Their activity
velocity (V1) in meters per second, and time (t) in seconds: necessitates such ROM for performance of many dancing
maneuvers. In contrast, distance runners, football players, and
(
a m
sec2 ) (V2 t V1) baseball players may have far less hip flexibility.
Although there is no conclusive evidence, it is logical
Velocity and acceleration can be determined using the to believe that hypomobility could lead to injury.130-136
same test. In the 40-yard (36.5-m) sprint, time can be Therefore, it is important for strength coaches to deter-
measured using a stopwatch or timing light system at four mine the baseline flexibility in their athletes. Almost all
different time points (10, 20, 30, and 40 yards [9.1, 18.2, sports require some hip mobility; therefore, it is vital to
27.9, and 36.5 m]). Then the average and interval velocity document hip flexibility and ROM. The sit-and-reach test
and acceleration can be determined at each time point in is commonly used to measure the flexibility of the ham-
the run. These data can be valuable in comparing and strings and lower back musculature,109 but it does not
evaluating players playing different positions that may rely assess unilateral flexibility. Because athletes may have
on interval acceleration more than velocity (Table 2-4). asymmetries between hips, a more rigorous evaluator of
hamstring flexibility may be the lying straight leg raise test.
Agility and Quickness Lying supine with both legs straight, the athlete raises a
Agility is the ability to accelerate, decelerate, and change single leg keeping the knee straight. Using a goniometer,
directions in a controlled and rapid manner. Sports such as the sports medicine staff measures the peak hip angle just
basketball and soccer require many such movements. Agility before the opposite leg begins to rise from the floor.137
is typically measured in a timed drill that requires change of Using the straight leg raise test, hip flexibility can be
direction. The type of drill used depends on the nature of compared between legs.
the sport. Two commonly used tests are the pro-agility test In addition to testing the flexibility of the hip extensors
(Figure 2-6, A) and T-test (Figure 2-6, B) for the sports of (i.e., hamstrings), it is important to measure the ROM of
football69 and basketball,129 respectively. When choosing an the hip flexors. Tight hip flexor muscles (i.e., rectus femoris,
agility test, the strength and conditioning coordinator iliopsoas) may contribute to injuries and limit sport per-
should consider the length of the drill and types of move- formance138 by decreasing the hip extension ROM and
Table 2-4
Theoretical Example of Two Players with Different Velocities and Accelerations During a Timed 40-Yard Sprint
Player A Player B
Interval Interval
Average Velocity Acceleration Average Velocity Acceleration
Distance (yd) Time (sec) (m/sec) (m/sec2) Time (sec) (m/sec) (m/sec2)
10 1.64 6.10 3.72 1.55 6.45 0.65
20 2.80 7.14 0.10 2.80 7.14 0.07
30 3.70 8.11 0.10 3.90 7.69 0.05
40 4.60 8.70 0.06 5.00 8.00 0.03
Note that the acceleration of Player B is greater than Player A for the first interval, but the acceleration of Player A is greater in the last three
intervals. Ultimately, the final velocity of Player A is greater than Player B. Depending on the position, the initial acceleration profile of Player
B may be more advantageous than the final velocity of Player A.
32 SECTION I • Preparation and Prevention in Sports Medicine
Table 2-5
Goal Running Times by Position for the 110 Anaerobic
Running Test
Goal Time to Run
Position 110 Yards
Football Running Iso-pull; 1- X Vertical X 40-yard Sit and reach, X 110 Test Pro-agility
RM (squat, jump, sprint (10, Thomas test drill
bench press broad 20, 30, 40
and bench jump, yard times)
pull, power medicine
clean) ball throw
Multi- 3
Basketball Jump and Iso-pull; 1- Push-up Vertical ⁄4 Court Sit and reach, 1-mile Yo-yo Short
land RM (squat, and pull- jump, vertical sprint Thomas test run intermit- T-test
bench press up to fail- medicine jump tent test
and bench ure ball throw
pull, power
clean)
Soccer Jump and 1-RM (squat, Push-up Broad jump Multi- 40-Yard Sit and reach, 3-mile Yo-yo Long
land bench press, and pull- vertical sprint (10, Thomas test run intermit- T-test
bench pull) up to fail- jump 20, 30, 40 tent test
ure yard times)
Baseball Running 1-RM (squat, X Vertical X 60-Yard Sit and reach, X X X
bench press, jump, sprint (10, Thomas
bench pull) broad 20, 30, 60 test, shoul-
jump, yard times) der internal
medicine and external
ball throw rotation
Track and Running 1-RM (squat, Push-up X X X Sit and reach, Tread- X X
field bench press, and pull- Thomas test mill
(distance) bench pull) up to fail- VO2
ure max
Track and Running Iso-pull; 1- X Vertical X Distance Sit and reach, X X X
field RM (squat, jump, specific Thomas test
(sprint) bench press broad speed and
and bench jump acceleration
pull, power
clean)
Cycling X Iso-pull; 1- X Broad jump Multi- X Sit and reach, Cycling Wingate X
(track) RM (squat, vertical Thomas VO2 cycle test
bench press jump test, shoul- max
and bench der internal
pull, power and external
clean) rotation
Cycling X 1-RM (squat, Push-up X X X Sit and reach, Cycling X X
(road) bench press, and pull- Thomas VO2
1-RM, One-repetition maximum; iso, isometric; ROM, range of motion; VO2 max, maximum oxygen consumption; X, test is not suggested.
35
36 SECTION I • Preparation and Prevention in Sports Medicine
Essential to any effective testing battery is a working knowl- 23. McKeag DB: Preseason physical examination for the prevention of
edge of the physical and physiological requirements of sport. sports injuries, Sports Med 2:413–431, 1985.
24. Carek PJ, Futrell M, Hueston WJ: The preparticipation physical
Therefore, the strength and conditioning coordinator, the
examination history: Who has the correct answers? Clin J Sports
entire sports medicine staff, the sport coaches, and the ath- Med 9:124–128, 1999.
letes should all contribute to the development, administra- 25. Kaplan NM, Deveraux RB, Miller HS: Systemic hyperextension,
tion, and interpretation of the PFP. Med Sci Sports Exerc 26:S268–S270, 1994.
26. Zabetakis PM: Profiling the hypertensive in sports, Clin Sports
Med 3:137–152, 1984.
References 27. Bonci CM, Ryan R: Preparticipation screening in intercollegiate
athletics. Postgraduate Advances in Sports Medicine, Philadelphia,
1. Superko HR, Bernauer E, Voss J: Effects of a mandatory health 1988, University of Pennsylvania Medical School and Forum
screening and physical maintenance program for law enforce- Medicum, Inc.
ment officers, Phys Sportsmed 16:99–109, 1988. 28. Halpern B, Blackburn T, Incremona B, et al: Preparticipation
2. Binda C: Precamp physical exams: Their value may be greater sports physicals. In Zachazewski JE, Magee DJ, Quillen WS,
than you think, Phys Sportsmed 17:167–169, 1989. editors: Athletic injuries and rehabilitation, Philadelphia, 1996,
3. Gurry M, Pappas A, Michaels J, et al: A comprehensive preseason WB Saunders Co.
fitness evaluation for professional baseball players, Phys Sportsmed 29. Dorsen PJ: Should athletes with one eye, kidney or testicle play
13:63–74, 1985. contact sports? Phys Sportsmed 14:130–138, 1986.
4. Metzel JD: The adolescent preparticipation physical examination— 30. Strong WB, Steed D: Cardiovascular evaluation of the young
Is it helpful? Clin Sports Med 19:577–592, 2000. athlete, Pediatr Clin North Am 29:1325–1339, 1982.
5. Kligman EW, Hewitt MJ, Crowell DL: Recommending exercise 31. Huston TP, Puffer JC, Rodney WM: The athletic heart syndrome,
to healthy older adults—The preparticipation evaluation and N Engl J Med 313:24–32, 1985.
exercise prescription, Phys Sportsmed 27(11):42–62, 1999. 32. McGrew CA: Clinical implications of the AHA preparticipation
6. Glover DW, Maron DJ, Matheson GO: The preparticipation cardiovascular screening guidelines, Athletic Ther Today 5:52–56,
physical examination—Steps toward consensus and uniformity, 2000.
Phys Sportsmed 27(8):29–34, 1999. 33. Fuller CM: Cost effectiveness analysis of screening of high school
7. Peltz JE, Haskell WL, Matheson GO: A comprehensive and cost- athletes for risk of sudden cardiac death, Med Sci Sports Exerc
effective preparticipation exam implemented on the world wide 32:887–890, 2000.
web, Med Sci Sports Exerc 31:1727–1740, 1999. 34. Maron BJ, Pollac DC, Kaplan JA, et al: Blunt impact to the chest
8. Tanji TL: The preparticipation exam: Special concerns for the leading to sudden death from cardiac arrest during sports activi-
Special Olympics, Phys Sportsmed 19:61–68, 1991. ties, N Engl J Med 333:337–342, 1995.
9. Hudson PB: Preparticipation screening of Special Olympics 35. Potera C: AHA Panel outlines sudden death screening standards,
athletes, Phys Sportsmed 16:97–104, 1988. Phys Sportsmed 24(10):27–28, 1996.
10. Hunter SC: Preparticipation physical examination. In Griffin LY, 36. Fuller CM, McNulty CM, Spring DA, et al: Prospective screen-
editor: Orthopedic knowledge update: Sports medicine, Rosemont, ing of 5,615 high school athletes for risk of sudden cardiac death,
IL, 1994, American Academy of Orthopaedic Surgeons. Med Sci Sports Exerc 29:1131–1138, 1997.
11. Committee on Sports Medicine: Recommendations for participa- 37. Salem DN, Isner JM: Cardiac screening in athletes, Orthop Clin
tion in competitive sports, Pediatrics 81:737–739, 1988. North Am 11:687–695, 1980.
12. Sanders B, Nemeth WC: Preparticipation physical examination, 38. Braden DS, Strong WB: Preparticipation screening for sudden
J Orthop Sports Phys Ther 23:144–163, 1996. cardiac death in high school and college athletes, Phys Sportsmed
13. American Academy of Orthopaedic Surgeons: Athletic training 16:128–144, 1988.
and sports medicine, Rosemont, IL, 1991, American Academy of 39. Mitchell JH, Hashell WL, Raven PB: Classification of sports,
Orthopaedic Surgeons. Med Sci Sports Exerc 26:S242–S245, 1994.
14. Harvey J: The preparticipation examination of the child athlete, 40. Belman MJ, King RR: Pulmonary profiling in exercise, Clin
Clin Sports Med 1:353–369, 1982. Sports Med 3:119–136, 1984.
15. DuRaaut RH, Seymore C, Linder CW, et al: The preparticipation 41. Ross RG: The prevalence of reversible airway obstruction in profes-
examination of athletes: Comparison of single and multiple sional football players, Med Sci Sports Exerc 32:1985–1989, 2000.
examiners, Am J Dis Child 139:657–666, 1985. 42. Rundell KW, Wilber RL, Szmedra L, et al: Exercise-induced
16. Sampler P: Preparticipation exams: Are they worth the time and asthma screening of elite athletes: Field versus laboratory exercise
troubles, Phys Sportsmed 14:180–187, 1986. challenge, Med Sci Sports Exerc 32:309–316, 2000.
17. St. Rauss RH, Johnson MD, Kibler WB , et al: Keys to successful 43. Khosla RK: Detecting sexually transmitted disease—A new role
preparticipation exams, Phys Sportsmed 21:109–123, 1993. for urinalysis in the preparticipation exam, Phys Sportsmed
18. Feinstein RA, Soileau EJ, Daniel WA: A national survey of pre- 23(1):77–80, 1995.
participation physical examination requirements, Phys Sportsmed 44. Lombardo JA: Preparticipation physical evaluation, Prim Care
16:51–59, 1988. 11:3–21, 1984.
19. McKeag DB: Preparticipation screening of the potential athlete, 45. Johnson MD: Tailoring the preparticipation exam to female
Clin Sports Med 8:373–397, 1989. athletes, Phys Sportsmed 20:61–72, 1992.
20. Stanley K: Preparticipation evaluation of the young athlete. In 46. Slavin JL: Assessing athletes’ nutritional status: Making it part of
Stanitski CL, DeLee JC, Drez D, editors: Pediatric and adolescent the sports medicine physical, Phys Sportsmed 19:79–94, 1991.
sports medicine, Philadelphia, 1994, WB Saunders Co. 47. Nelson MA: The child athlete with chronic disease. In Stanitski
21. Smilkstein G: Health evaluation of high school athletes, Phys CL, DeLee JC, Drez D, editors: Pediatric and adolescent sports
Sportsmed 9:73–80, 1981. medicine, Philadelphia, 1994, WB Saunders Co.
22. Heidt RS, Sweeterman LM, Carlonas RL, et al: Avoidance of 48. Magnes SA, Henderson JM, Hunter SC: What conditions limit
soccer injuries with preseason conditioning, Am J Sports Med sports participation: Experience with 10,540 athletes, Phys
28:659–662, 2000. Sportsmed 20:143–160, 1992.
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 37
49. American Academy of Pediatrics Committee on Sports Medicine players, with special reference to starters and non-starters, J Sci
and Fitness: Medical conditions affecting sports participation, Med Sport 12:215–222, 2009.
Pediatrics 94:757–760, 1994. 71. Young W, Newton R, Doyle T, et al: Physiological and anthropo-
50. Kraemer WJ, Torine JC, Silvestre R, et al: Body size and compo- metric characteristics of starters and non-starters and playing
sition of National Football League Players, J Strength Cond Res positions in elite Australian rules football: A case study, J Sci Med
19:485–489, 2005. Sport 8:333–345, 2005.
51. Kuzmits FE, Adams AJ: The NFL combine: Does it predict per- 72. Black W, Roundy E: Comparisons of size, strength, speed, and
formance in the National Football League, J Strength Cond Res power in NCAA Division 1-A football players, J Strength Cond
22:1721–1727, 2008. Res 8:80–85, 1994.
52. Myer GD, Ford KR, Barber Foss KD, et al: The relationship of 73. Schmidt WD: Strength and physiological characteristics of NCAA
hamstrings and quadriceps strength to anterior cruciate ligament Division III American football players, J Strength Cond Res
injury in female athletes, Clin J Sport Med 19:3–8, 2009. 13:210–213, 1999.
53. White AT, Johnson SC: Physiological aspects and injury in elite 74. Fry AC, Kraemer WJ: Physical performance characteristics of
Alpine skiers, Sports Med 15:170–178, 1993. American collegiate football players, J Appl Sport Sci Res 5:
54. Andersen RE, Montgomery DL: Physiology of Alpine skiing, 126–138, 1991.
Sports Med 6:210–221, 1988. 75. Noakes TD, Myburgh KH, Schall R: Peak treadmill running
55. Paulos L, Noyes FR, Grood E, et al: Knee rehabilitation after velocity during the VO2max test predicts running performance,
anterior cruciate ligament reconstruction and repair, J Orthop J Sports Sci 8:35–45, 1990.
Sports Phys Ther 13:60–70, 1991. 76. Ploutz-Snyder LL, Giamis EL: Orientation and familiarization in
56. Zazulak BT, Hewett TE, Reeves NP, et al: Deficits in neuromus- 1RM strength testing in old and young women, J Strength Cond
cular control of the trunk predict knee injury risk, Am J Sports Res 15:519–523, 2001.
Med 35:1123–1130, 2007. 77. MCO P6100.12: Marine Corps physical fitness test and body com-
57. Zazulak BT, Hewett TE, Reeves NP, et al: The effects of core position program manual, Washington, DC, 2002, Headquarters
proprioception on knee injury: A prospective biomechanical- Marine Corps.
epidemiological study, Am J Sports Med 35:368–373, 2007. 78. FM 21-20: Physical fitness training, Washington, DC, 1998,
58. Tehranzadeh AD, Fronek J, Resnick D: Posterior capsular fibrosis Headquarters Department of the Army.
in professional baseball pitchers: Case series of MR arthrographic 79. Hewett TE, Myer GD, Ford KR, et al: Biomechanical measures
findings in six patients with glenohumeral internal rotational of neuromuscular control and valgus loading of the knee predict
deficit, Clin Imaging 31:343–348, 2007. anterior cruciate ligament injury risk in female athletes a prospec-
59. Myers JB, Laudner KG, Pasquale MR, et al: Glenohumeral range tive study, Am J Sports Med 33:492–501, 2005.
of motion deficits and posterior shoulder tightness in throwers 80. Zazulak BT, Hewett TE, Reeves NP, et al: Deficits in neuromus-
with pathologic internal impingement, Am J Sports Med 34: cular control of the trunk predict knee injury risk: a prospective
385–391, 2006. biomechanical-epidemiologic study, Am J Sports Med 35:
60. Nagano Y, Ida H, Akai M, et al: Biomechanical characteristics of 1123–1130, 2007.
the knee joint in female athletes during tasks associated with 81. Murphy C: Functional movement screening of NCAA Division II
anterior cruciate ligament injury, Knee 16:153–158, 2009. male and female athletes, Eugene, OR, 2001, Microform Publi-
61. Pappas E, Hagins M, Sheikhzadeh A, et al: Biomechanical differ- cations, University of Oregon.
ences between unilateral and bilateral landings from a jump: 82. Tagesson SK, Kvist J: Intra- and interrater reliability of the
Gender differences, Clin J Sport Med 17:263–268, 2007. establishment of one repetition maximum on squat and seated
62. Cowley HR, Ford KR, Myer GD, et al: Differences in neuromus- knee extension, J Strength Cond Res 21:801–807, 2007.
cular strategies between landing and cutting tasks in female bas- 83. Faigenbaum AD, Milliken LA, Westcott WL: Maximal strength
ketball and soccer athletes, J Athl Train 41:67–73, 2006. testing in healthy children, J Strength Cond Res 17:162–166,
63. Chappell JD, Herman DC, Knight BS, et al: Effect of fatigue on 2003.
knee kinetics and kinematics in stop-jump tasks, Am J Sports Med 84. Rydwik E, Karlsson C, Frändin K, et al: Muscle strength testing
33:1022–1029, 2005. with one repetition maximum in the arm/shoulder for people
64. Urabe Y, Kobayashi R, Sumida S, et al: Electromyographic analy- aged 75: Test-retest reliability, Clin Rehabil 21:258–265, 2007.
sis of the knee during jump landing in male and female athletes, 85. Phillips WT, Batterham AM, Valenzuela JE, et al: Reliability of
Knee 12:129–134, 2005. maximal strength testing in older adults, Arch Phys Med Rehabil
65. Chappell JD, Creighton RA, Giuliani C, et al: Kinematics and 85:329–334, 2004.
electromyography of landing preparation in vertical stop-jump, 86. Levinger I, Goodman C, Hare DL, et al: The reliability of the
Am J Sports Med 35:235–241, 2007. 1RM strength test for untrained middle-aged individuals, J Sci
66. Joseph M, Tiberio D, Baird JL, et al: Knee valgus during drop Med Sport 12:310–316, 2009.
jumps in National Collegiate Athletic Association Division I 87. Kravitz L, Akalan C, Nowicki K, et al: Prediction of 1 repetition
female athletes, Am J Sports Med 36:285–289, 2008. maximum in high-school power lifters, J Strength Cond Res
67. Russell KA, Palmieri RM, Zinder SM, et al: Sex differences in 17:167–172, 2003.
valgus knee angle during a single-leg drop jump, J Athl Train 88. Reynolds JM, Gordon TJ, Robergs RA: Prediction of one repeti-
41:166–171, 2006. tion maximum strength from multiple repetition maximum testing
68. Hewett TE, Lindenfeld TN: The effect of neuromuscular train- and anthropometry, J Strength Cond Res 20:584–592, 2006.
ing on the incidence of knee injury in female athletes, Am J Sports 89. Horvat M, Franklin C, Born D: Predicting strength in high
Med 27:699–706, 1999. school women athletes, J Strength Cond Res 21:1018–1022,
69. Sierer SP, Battaglini CL, Mihalik JP, et al: The National Football 2007.
League combine: Performance differences between drafted and 90. Stone MH, O’Bryant H, Garhammer J: Hypothetical model for
nondrafted players entering the 2004 and 2005 drafts, J Strength strength training, J Sports Med Phys Fitness 21:342–351, 1981.
Cond Res 22:6–12, 2008. 91. Pincivero DM, Lephart SM, Karunakara RA: Reliability and pre-
70. Gabbett T, Kelly J, Ralph S, et al: Physiological and anthropo- cision of isokinetic strength and muscular endurance for the
metric characteristics of junior elite and sub-elite rugby league quadriceps and hamstrings, Int J Sports Med 18:113–117, 1997.
38 SECTION I • Preparation and Prevention in Sports Medicine
92. Moller M, Lind K, Styf J, et al: The reliability of isokinetic testing 113. Sayers SP, Harackiewicz DV, Harman EA, et al: Cross-validation
of the ankle joint and a heel-raise test for endurance, Knee Surg of three jump power equations, Med Sci Sports Exerc 31:
Sports Traumatol Arthrosc 13:60–71, 2005. 572–577, 1999.
93. Hill AV: The heat of shortening and the dynamic constants of 114. Harman EA, Posenstein MT, Frykman PN, et al: Estimation of
muscle, Proc R Soc Lond B Biol Sci 126:136–195, 1938. human power output from vertical jump, J Appl Sport Sci Res
94. Li RCT, Wu Y, Maffulli N, et al: Eccentric and concentric iso- 5:116–120, 1991.
kinetic knee flexion and extension: A reliability study using the 115. Mayhew JL, Bird M, Cole ML, et al: Comparison of the back-
Cybex 6000 dynamometer, Br J Sports Med 30:156–160, 1996. ward overhead medicine ball throw to power production in
95. Gerodimosa V, Manoua V, Stavropoulos N, et al: Agonist and college football players, J Strength Cond Res 19:514–518,
antagonist strength of ankle musculature in basketball players 2005.
aged 12 to 17 years, Isokinet Exerc Sci 14:81–89, 2006. 116. Duncan MJ, Al-Nakeeb Y, Nevill AM: Influence of familiariza-
96. Hill AM, Pramanik S, McGregor AH: Isokinetic dynamometry in tion on a backward, overhead medicine ball explosive power test,
assessment of external and internal axial rotation strength of Res Sports Med 13:345–352, 2005.
the shoulder: comparison of two positions, Isokinet Exerc Sci 13: 117. Ikeda Y, Kijima K, Kawabata K, et al: Relationship between side
187–195, 2005. medicine-ball throw performance and physical ability for male
97. Forthomme B, Crielaard JM, Forthomme L, et al: Field perfor- and female athletes, Eur J Appl Physiol 99:47–55, 2007.
mance of javelin throwers: Relationship with isokinetic findings, 118. Stockbrugger BA, Haennel RG: Validity and reliability of a
Isokinet Exerc Sci 15:195–202, 2007. medicine ball explosive power test, J Strength Cond Res 15:
98. Nunes T, Coetzee B: The contribution of isokinetic strength 431–438, 2001.
parameters to the performance of cricket batsmen, Isokinet Exerc 119. Dugan EL, Doyle TLA, Humphries B, et al: Determining
Sci 15:233–244, 2007. the optimal load for jump squats: A review of methods and
99. Tang WT, Shung HM: Relationship between isokinetic strength calculations, J Strength Cond Res 18:668–674, 2004.
and shooting accuracy at different shooting ranges in Taiwanese 120. Siegel JA, Gilders RM, Staron RS, et al: Human muscle power
elite high school basketball players, Isokinet Exerc Sci 13: output during upper- and lower-body exercises, J Strength Cond
169–174, 2005. Res 16:173–178, 2002.
100. Signorile JF, Sandler DJ, Smith WN, et al: Correlation analyses 121. Thomas GA, Kraemer WJ, Spiering BA, et al: Maximal power
and regression modeling between isokinetic testing and on-court at different percentages of one repetition maximum: Influence
performance in competitive adolescent tennis players, J Strength of resistance and gender, J Strength Cond Res 21:336–342,
Cond Res 19:519–526, 2005. 2007.
101. Malerba JL, Adam ML, Harris BA, et al: Reliability of dynamic 122. Hori N, Newton RU, Andrews WA, et al: Comparison of four
and isometric testing of shoulder external and internal rotators, different methods to measure power output during the hang
J Orthop Sports Phys Ther 18:543–552, 1993. power clean and the weighted squat jump, J Strength Cond Res
102. Kitai TA, Sale DG: Specificity of joint angle in isometric training, 21:314–320, 2007.
Eur J Appl Physiol Occup Physiol 58:744–748, 1989. 123. Drinkwater EJ, Galna B, McKenna MJ, et al: Validation of an
103. Kawamori N, Rossi SJ, Justice BD, et al: Peak force and rate of optical encoder during free weight resistance movements and
force development during isometric and dynamic mid-thigh analysis of bench press sticking point during fatigue, J Strength
clean pulls performed at various intensities, J Strength Cond Res Cond Res 21:510–517, 2007.
20:483–491, 2006. 124. McBride JM, Triplett-McBride T, Davie A, et al: The effect of
104. Stone MH, Sands WA, Carlock J, et al: The importance of heavy- vs. light–load jump squats on the development of
isometric maximum strength and peak rate-of-force development strength, power, and speed, J Strength Cond Res 16:75–82,
in sprint cycling, J Strength Cond Res 18:878–884, 2004. 2002.
105. Stone MH, Stone ME, Sands WA, et al: Maximum strength and 125. Wilson GJ, Newton RU, Murphy AJ, et al: The optimal training
strength training: A relationship to endurance? Strength Cond load for the development of dynamic athletic performance, Med
J 28:44–53, 2006. Sci Sports Exerc 25:1279–1286, 1993.
106. Haff GG, Carlock JM, Hartman MJ, et al: Force-time curve char- 126. Alemany JA, Pandorf CE, Montain SJ, et al: Reliability assess-
acteristics of dynamic and isometric muscle actions of elite women ment of ballistic jump squats and bench throws, J Strength Cond
Olympic weightlifters, J Strength Cond Res 19:741–748, 2005. Res 19:33–38, 2005.
107. Konstantaki M, Swaine IL: Lactate and cardiopulmonary responses 127. Coleman AE, Lasky LM: Assessing running speed and body
to simulated arm-pulling and leg-kicking in collegiate and composition in professional baseball players, J Appl Sport Sci Res
recreational swimmers, Int J Sports Med 20:118–121, 1999. 6:207–213, 1992.
108. Tesch PA, Wright JE, Vogel AJ, et al: The influence of muscle 128. Coleman E, Dupler TL: Changes in running speed in game situ-
metabolic characteristics on physical performance, Eur J Appl ations during a season of Major League Baseball, J Exerc Physiol
Physiol Occup Physiol 54:237–243, 1985. Online 7:89–93, 2004.
109. Whaley MH, Brubaker PH, Otto RM, editors: ACSM’s guide- 129. Delextrat A, Cohen D: Physiological testing of basketball players:
lines for exercise testing and prescription, ed 7, Baltimore, 2006, Toward a standard evaluation of anaerobic fitness, J Strength
Lippincott Williams & Wilkins. Cond Res 22:1066–1072, 2008.
110. Peterson MD, Alvar BA, Rhea MR: The contribution of maximal 130. Lawrence H: Effect of stretching on sport injury risk: A review.
force production to explosive movement among young collegiate Clin J Sport Med 15:113, 2005.
athletes, J Strength Cond Res 20:867–873, 2006. 131. Schwenk TL: Hamstring flexibility decreases overuse injuries,
111. Hori N, Newton RU, Andrews WA, et al: Does performance of Phys Sportsmed 27:26, 1999.
hang power clean differentiate performance of jumping, sprinting, 132. Hartig DE, Henderson JM: Increasing hamstring flexibility
and changing of direction? J Strength Cond Res 22:412–418, decreases lower extremity overuse injuries in military basic, Am
2008. J Sports Med 27:173, 1999.
112. Carlock JM, Smith SL, Hartman MJ, et al: The relationship 133. Jones BH, Knapik JJ: Physical training and exercise-related injuries:
between vertical jump power estimates and weightlifting ability: Surveillance, research and injury prevention in military populations,
A field-test approach, J Strength Cond Res 18:534–539, 2004. Sports Med 27:111–125, 1999.
Preparticipation Evaluation and Physical Fitness Profiling • CHAPTER 2 39
134. Gabbe BJ, Finch CF, Bennell KL, et al: Risk factors for hamstring 141. Peeler J, Anderson JE: Reliability of the Thomas test for assessing
injuries in community level Australian football, Br J Sports Med range of motion about the hip, Phys Ther Sport 8:14–21, 2007.
39:106–110, 2005. 142. Nakamizo H, Nakamura Y, Nobuhara K, et al: Loss of glenohu-
135. Witvrouw E, Mahieu N, Danneels L, et al: Stretching and injury meral internal rotation in little league pitchers: A biomechanical
prevention: An obscure relationship, Sports Med 34:443–449, study, J Should Elbow Surg 17:795–801, 2008.
2004. 143. Tomlin DL, Wenger HA: The relationship between aerobic
136. Weerapong P, Hume PA, Kolt GS: Stretching: Mechanisms and fitness and recovery from high intensity intermittent exercise,
benefits for sport performance and injury prevention, Phys Ther Sports Med 31:1–11, 2001.
Rev 9:189–206, 2004. 144. Sands WA, McNeal JR, Ochi MT, et al: Comparison of the
137. Stutchfield BM, Coleman S: The relationships between hamstring Wingate and Bosco anaerobic tests, J Strength Cond Res 18:
flexibility, lumbar flexion, and low back pain in rowers, Eur J Sport 810–815, 2004.
Sci 6:255–260, 2006. 145. Bangsbo J, Iaia FM, Krustrup P: The yo-yo intermittent recovery
138. Young W, Clothier P, Otago L, et al: Relationship between a test: A useful tool for evaluation of physical performance in inter-
modified Thomas test and leg range of motion in Australian-rules mittent sports, Sports Med 38:37–51, 2008.
football kicking, J Sport Rehabil 12:343–350, 2003. 146. Peter K: The yo-yo intermittent recovery test: Physiological
139. Harvey D: Assessment of the flexibility of elite athletes using response, reliability, and validity, Med Sci Sports Exerc 35:
the modified Thomas test, Br J Sports Med 32:68–70, 1998. 697–705, 2003.
140. Peeler JD, Anderson JE: Reliability limits of the modified 147. Thomas A, Dawson B, Goodman C: The yo-yo test: Reliability
Thomas test for assessing rectus femoris muscle flexibility about and association with a 20-m shuttle run and VO2 max, Int
the knee joint, J Athl Train 43:470–476, 2008. J Sports Physiol Perform 1:137–149, 2006.
3
CHAPTER
Considerations for Dealing with Today’s The more pervasive, less obvious problems are the
physical damage accompanying overuse injuries and
Young Athletes the emotional issues that are visited upon children and
Studies assessing the number of American youth playing adolescents in the name of competition and achievement.
organized sports between the ages of 6 and 18 vary from Physicians, physical therapists, and athletic trainers are
30 million to more than 45 million out of approximately often favorably situated at the nexus of youth, high school,
51 million children.1,2 The upper estimate comes from a and college sports and the physical and emotional
U.S. Department of Health and Human Services report problems that can be associated with the intense training
from the Surgeon General in 1996, Physical Activity and and competition that exists at increasingly younger ages.
Health, suggesting 87% of American youth participate in They can, and must be, key agents in the challenging
at least one organized sport by the of age 18.3 Although struggle to keep sports appropriately focused on what
the true measure of American participation is unclear should be the over-riding mission of youth, high school,
because many children may be involved in multiple sports and even collegiate sports: promoting healthy physical and
across multiple agencies (e.g., Little League baseball, Pop emotional development.
Warner football, Boys and Girls clubs, town or recreational Although the numbers clearly demonstrate the pervasive
activities, interscholastic teams, club sports), these figures appeal of organized youth sport, statistics also reveal
suggest that the great majority of American children are a troubling increase in overuse injuries. Brenner and
participating in organized sports sometime during their the American Academy of Pediatrics’ Council on Sports
lives. It may be said, then, that youth sports have become Medicine and Fitness2 state that the incidence of overuse
the most common ground on which we share a common injuries has more than kept pace with the increase in youth
experience. Sports have become one of the key defining sport participation, citing research that 50% of all injuries
experiences of an American child’s physical and emotional seen in pediatric sports medicine are from overuse.4
development.
As is the case with any powerful and pervasive phenom-
enon, there is a downside that accompanies the good.
Priorities that Physicians, Athletic Trainers,
Alongside the well-accepted rewards of an organized youth
sport program—the fun and friendships; the increased safety;
and Sports Physical Therapists Must Set in Caring
the opportunity for proper instruction and promotion for Young Athletes
of values such as teamwork, discipline, and fair play—there • Ensure the young athlete’s overall emotional and cognitive
is also risk. All too often, the pursuit of the spoils of compe- development, in addition to his or her physical development, are
tition (i.e., victories, championships, scholarships, and all crucial factors for the athlete’s well-being now and later in life.
the accolades of winning) completely overwhelm the more • Shield the young athlete from the increased pressures and
essential and healthier rewards of youth sport. The dramatic demands to perform and achieve at an earlier age than athletes
instances revealing the distorted priorities, loss of control, of the past. These pressures appear to leave young athletes more
and even violent episodes among adults in youth sport are vulnerable to injury and emotional burnout.
the observable tip of the iceberg.
40
Psychosocial Aspects of Youth Sports • CHAPTER 3 41
In addition to physical ailments and injuries associated they observed, “unrealistic parental expectations and/or
with overuse and overtraining, the number of young exploitation of young athletes for extrinsic gain can contrib-
athletes who burn out or drop out of sports has also ute to negative psychological consequences for elite young
dramatically increased. Control of children’s athletic play- athletes.” Tofler and his colleagues11 added that parents’
time has effectively become the domain of adults. Informal behavior in youth sports can become particularly problematic
athletic play has disappeared secondary to the proliferation if the parents fail to differentiate between their own needs
of organized sports at the earliest of ages and increasing for success and achievement and their child’s emotional
reluctance to leave even older children and young teenagers needs. The same could certainly be said for coaches and
“unsupervised.” The financial, logistical, physical, and managers of elite teams, whose jobs and livelihoods depend
psychological strain on the families of young athletes caught on the performance of a young athlete, as well as on the
in the crucible of increasingly fierce competition in satisfaction and financial backing of parents.
youth sports can be relentless and pervasively consuming. Injury and emotional overload are certainly not a given,
The fight for prep school placement, for college admission, and many young athletes and their parents manage to negoti-
for playing spots on elite travel teams, for finding “just the ate these issues to accrue great benefit from their sports
right coach” on “just the right team” so that “Johnny’s” or participation without serious consequence. However, athletic
“Mary’s” guaranteed athletic triumph can be secured can trainers, sport physical therapists, and physicians are crucial
be overwhelming for even the most level-headed and emo- to the health of young athletes and must serve as an early
tionally balanced of families. This pressurized, athletic life- warning system for injury and recognition of emotional
style appears to be starting earlier and earlier in the lives stress. A solid appreciation of what is at stake for the
of young athletes and includes an increasing demand for sports-oriented family can be critical for understanding
advanced specialized training as well as demanding expecta- the patient, building a good alliance and setting the stage
tions for a singular focus in one sport. for compliance with proper treatment, and facilitating a rea-
These pressures on the young athlete might not always sonable trajectory for the individual child’s athletic talents.
be for the greater good. Several studies suggest there is The cultural pressures for achievement and the high status
a growing split in children and adolescents with a small of the sports can affect everyone’s judgment concerning what
elite moving on to pursue intense athletic coaching and a is best for the young athlete. They are not mini-adults—they
worrisome majority quitting organized sport, particularly as are still developing cognitively and physically, and are actively
they enter adolescence. This trend has been reinforced by learning from adult behaviors and values. Parents may push
spending cuts that have limited elementary school, junior for inappropriate “age-specific” training such as intensive
high school, and after-school sports programs. As early weight training to develop increased muscle mass in a
as 1988, Gould and Petlichkoff reported that the rate prepubertal child. Parents can also be negative role models
for children who dropped out of their organized sport or for what might be considered unsportsman-like conduct or
dropped sport completely ranged up to 35%.5 According behavior. More positively, the young athlete still has many
to other studies, the statistics are even more troubling. developmental tasks such as peer relationships, down time,
Up to half of American youth do not engage in regular and, of course, academics (not just so that they are eligible but
vigorous exercise according to the Centers for Disease to learn how to learn for the rest of his or her career).
Control.6 Strikingly, the National Alliance of Youth Sports
states that by age 13, 70% of American youth will drop out
of sport.7 Despite the disparity of these findings, there is Clinical Point
agreement that one of the chief reasons children give
All health providers, regardless of their area of expertise or specialty,
for dropping a sport is simple: it is “no longer any fun.”8
need to focus on their patient, recognizing that the child and sometimes
As a result, teens are vulnerable to a sedate life of little the parent will lose perspective and consider the next game as “make
or no physical activity that substitutes video games and it or break it” the child’s career.
television for exercise.
The young athletes who completely drop out and quit are
reported to be more vulnerable to a slew of physical and
emotional problems, including the obvious reduction in What is the Healthy Focus for Youth
physical fitness, increased rates for depression, increased rates
for sexual promiscuity for girls, as well as increased vulnera-
Sports?
bility to drug use and obesity.9 Those who do not drop out The answer to this question has very much to do with
are at risk for premature pressure secondary to becoming the age, skills, and the developmental realities of the
mini-sports franchises whose parents act as business managers athlete. As Fraser-Thomas and Cote12 state in their review
for their young “free agents.” Pediatricians from the of recent findings in youth sport research, “youth sport
Committee on Sports Medicine and Fitness for the American should lead to physical health, psychosocial development
Academy of Pediatrics10 recognized this pressure when and lifelong recreational or elite sport participation.”
42 SECTION I • Preparation and Prevention in Sports Medicine
Balyi and Hamilton13 have done interesting and extensive Parents may be heavily influenced by recent studies by
writing (but no substantive research) on a model of Ericcson and colleagues,14 popularized by Malcolm Gladwell’s
long-term athletic development. They have proposed a best seller, Outliers: The Story of Success.15 Ericcson found that
model that has been promoted as the basis of the national 10 years or 10,000 hours of practice are required to reach an
framework for coaching healthy and successful sports expert or elite level of performance.14 These findings
participation and achievement in Canada and the United were originally based on expert chess players from Herbert
Kingdom.13 Briefly stated, Balyi and Hamilton stress the Simon’s original study in 1973 and virtuoso musicians.16
importance of recognizing the physical and emotional Although there may be growing evidence that this “10,000
capabilities and needs of the developing young athlete. hour practice rule” holds true in a wide range of athletic
Their model (Table 3-1) makes allowances for differences endeavors (e.g., Ericcson does cite data supportive of the
between early specialization sports (e.g., diving, figure hypothesis for swimmers and marathon runners), much
skating, gymnastics) and late specialization sports (most further study is required before the rule, “Earlier (age) is
team sports as well as cycling, rowing, and racquet better and more (practice) is better” can be viewed as a
sports).13 risk-free enterprise for young athletes between the ages of
The emphasis early on is for the young athlete to have 6 and 18.14
fun and learn overall motor skills (6 to 10 years of age Currently, the approach most consistently supported by
is the “FUNdamental” stage). As children enter ages 10 available research strongly suggests that adults involved in
to 12 (with some variation for gender differences), the youth sports and parents of athletes from ages 6 to 12 need
emphasis shifts to building the widest range of fundamental to encourage fun, friendship, and fitness as the true measures
sport skills (“Learning to Train” stage). The “Training to of their children’s sporting success. Children in this age range
Train” stage, which occurs at roughly 12 to 16 years of should sample many sport experiences in which the emphasis
age, should aim to build the athlete’s aerobic base and is on enjoyment and gradually improving fitness and overall
improve strength toward the end of the phase while further athletic skill. As children enter adolescence, they are generally
developing sport-specific skills. In the “Training to capable of being introduced to more intense competition as
Compete” stage (approximately 15 to 18 years of age and well as a more vigorous development of specific sport skill
beyond), athletes progress toward refining more special- and competencies. Still, it should be reiterated time and again
ized skills and tactics in their primary sport. This model that parents and coaches best serve their teen athletes by
allows for the gifted athlete who will go on to elite compe- promoting, in order of importance, character, camaraderie,
tition while also promoting lifelong fitness and athletic and athletic competence. A useful analogy is to think of the
participation for all throughout childhood, adolescence, young athlete as an automobile: Talent is the engine; the
and adult life.13 Although the scientific validity of this more the talent, the more the horsepower. Good coaching is
model as a high-performance template for national devel- like the transmission that transforms the power of the engine
opment of elite athletes is in dispute, its emphasis on to make the car move. Good coaching helps the athlete
a developmental approach for children and younger adoles- translate his or her talent into real action. But crucially, good
cent athletes is widely supported. The interested reader is character is akin to not only a proper steering mechanism but
encouraged to review Balyi and Hamilton’s work for a a well-trained, safe driver. Talent without good coaching will
more in-depth understanding of the goals of each sport necessarily underperform. Talent and good coaching without
developmental stage from preschool to retirement.13 proper character may not only underperform, but may
also lead the athlete to “recklessly drive into a tree” and
self-destruct. The promotion of good character is the
Table 3-1 ultimate insurance policy that an athlete will have a chance,
Bayli’s Long-Term Athletic Achievement Model barring injury, to get the most out of his or her talent.
Because the prevalent currents of “win-at-all-costs” and “do
Early Specialization Late Specialization
Model Model
everything you can do to play” are swift and powerful,
all adults and, most importantly, all health care providers
1. Training to train stage 1. FUNdamental stage involved in youth and scholastic sports must fully grasp the
2. Training to compete 2. Learning to train importance of this mission.
3. Training to win 3. Training to train
4. Retirement/retainment 4. Training to compete
5. Training to win
Adults Involved in Youth Sports and Parents
6. Retirement/retainment
Should Stress
From Balyi I, Hamilton A: Long-term athlete development: Trainability • Fun, friendship, and fitness in 6- to 12-year-olds
in childhood and adolescence. Windows of opportunity. Optimal
• Character, camaraderie, and athletic competence in teens
trainability, Victoria, 2004, National Coaching Institute British
Columbia & Advanced Training and Performance Ltd.
Psychosocial Aspects of Youth Sports • CHAPTER 3 43
Health care providers can point out to parents that, child is 21 years old, what kind of person do I want him
ironically, the very best sport psychologists seeking to or her to be, and how will sports help us as parents get our
enhance excellent performances in their athletes unani- child there?”
mously emphasize the goal of mastery and the joy of We advocate that parents focus on three to five virtues
the sport as key components of success. Parents need to that they cherish and make sure that sports always serve to
be reminded that overspecialization and an overemphasis promote and build those virtues. This is effectively done by
on outcome may actually decrease the player’s confidence following the following three steps.
and enjoyment and can increase the likelihood that their
children will join the ranks of the sporting dropouts, Know Your Child
burnouts, and injured. One would not ask 8-year-olds to baby sit, nor would
one expect 12-year-olds to drive a car. Adults easily seem to
understand that children need to grow and mature before
Key Psychosocial Components to Success in Sport they are capable of mastering certain skills and responsibilities.
• Joy of taking part in sport However, in sports, parents and coaches often expect con-
• Mastery of the sport sistent, adult-like performances from their young athletes.
Adult expectations for young athletes need to be in tune with
physical, cognitive, and psychological developmental realities.
In addition, children are unique, with different tempera-
ments; idiosyncrasies; rich and varied ethnic, cultural, and
What Makes Winning so Special? family backgrounds; and their own histories. A sports
There are many factors that make the thrill of “winning” program that fits the needs of the child necessarily takes this
intoxicating and powerful. Biologically, a child or teenager important knowledge into account.
engages the deeply wired “fight or flight” response in many
of the competitive sports activities. The experience of
the fear, passion, and stress of competition also helps to fuel Key Tools for Parents for Performance Enhancement
the sense of pleasure and release that comes with winning. in Children
Competition biologically stimulates the physiological state
of parents and coaches, as well as young players. All of this • Set goals
biology is embedded in a family that may be under consider- • Have a sports mission
• Know your child and his or her stage of physiological and
able pressure (e.g., time, finances, competing priorities).
emotional development
When the combination of individual parents, who have both • Know yourself and your own personal “baggage”
high hopes for their children and possibly unfulfilled hopes • Know the child’s sport environment
from their own childhoods, is added to all of the potential • Know the sport’s culture
cultural rewards of athletic success, there is a powerful effect • Know how to deal with over-involved parents
on the child. Health care providers are frequently at the
front lines trying to balance the pressures to win with the
realities of what is in the best interests of the child. Winning
can be considered so special that it overwhelms other values, Know Yourself
priorities, and even sportsmanship. Evidence of undesirable Adults, whether acting in the role of parent, coach, or
behavior can be seen in steroid use, undue pressure on or by caregiver, each have their own histories of success and
the injured athlete to return prematurely, undue privileges failure in the athletic domain. With increasing frequency
for the gifted star athlete, and the not-so-subtle promotion during the past decades since organized sport participa-
of a “win-at-all-costs” attitude. tion has blossomed, many adults involved in youth and
high school sports carry their own complex narratives
Performance Enhancement about competition with strongly held notions and even
scripts of how things should be. Sometimes parents
The Essential Questions and Three Steps for Parents (and even entire communities such as that profiled in the
of Athletes compelling book about Texas high school football by
One of the key tools of effective sports psychology for per- H.G. Bissinger, Friday Night Lights17) can hope to right
formance enhancement is goal setting. Goal setting allows the wrongs of their own lives and erase the sting of past
for the mapping and measuring of sports success. But goals or present failures through their children’s athletic
must be guided by a broader statement of purpose and success. This unresolved psychological baggage makes it
ultimate intent, a mission statement. The very first challenge extremely difficult for some parents and coaches to truly
for the parents of young athletes is to answer the following see what is best for the young athlete. Trainers, physical
questions to establish their family’s sports mission: “When my therapists, and physicians need to be aware of these
44 SECTION I • Preparation and Prevention in Sports Medicine
subtle, unseen issues that cloud what should be a clear excellence, which is (allegedly) 10,000 hours of practice at
history and picture of what the young athlete needs. increasingly elite levels.
Sometimes these parental hopes go beyond sports to Much research attention has focused on the role of
include college entry, scholarships, and then developing a parents in youth sports. When parents are attentive, posi-
profile allegedly attractive for a business career. tive, and supportive, their children have more fun, have
more positive beliefs about their abilities, and are likelier
Know Your Child’s Sports Environment and Culture to continue sports participation over time.19-22 Problems
Our culture places an enormous premium on winning as occur when parent involvement becomes distracting or
the ultimate justification and sign of success. Often success preoccupying to their children. Such involvement can take
in youth and high school sports is seen as the ticket to a both overt and subtle forms. In their most recognizable
good prep school or college placement. forms, overzealous and over-involved parents may cheer too
In fact, less than 1% of all high school athletes receive any loudly at athletic contests; be harsh critics of other coaches
form of athletic scholarship at the National Collegiate Athletic or referees; offer overly critical feedback to their child
Association (NCAA) Division 1 level.18 And only 5.5% of all before, during, or after practices and games; or burden
high school athletes progress to play intercollegiate sports at their children’s coaches with comments and suggestions.
4-year institutions.18 Parents guiding their college-bound Their thoughts and behaviors are often well intentioned,
athletes need to learn about playing time, the coach’s level of but translate into various expressions of pressure to their
training for the sport in question, familiarity with safety children. Researchers have found that children experience
procedures and proper injury protocol, as well as background increased anxiety, greater risk of burnout, and less enjoy-
screening for adults in the program. The health care provider ment when their parents burden them with pressure and
associating himself or herself with high school and college unrealistic expectations.23,24 The child might feel he or
programs should be aware of the level of expertise, the she is not “good enough” to meet the parent’s expectations
common practices, and program philosophy. and thus, despite considerable accomplishment, have an
By keeping the focus of youth and high school sports underlying sense of low self-esteem. Children and especially
on fitness and healthy physical development as well as on teenagers may see quitting a sport as a solution to the
the development of specific virtues associated with a good pressure.
character, such as courage, compassion, perseverance, a sense
of justice and fair play, respect for others, dedication, effort,
and teamwork, parents ensure that their children will get the Parents Should be
most out of their athletic talent over an entire lifespan.
• Attentive
• Positive
Dealing with the Over-Involved Parent • Supportive
• Have realistic expectations
Parents of young children are often unprepared for an
onslaught of unprecedented pressure to enroll their kids
in competitive youth sports at a young age. YMCA and
community-based programs start at age 4 or 5 and, for the More commonly, over-involved parenting evolves subtly
ambitious parent, serve as a path to club soccer, Amateur over time. An occasional disappointed facial expression
Athletic Union (AAU) basketball, and elite swimming or a seemingly benign comment about the child’s play
programs. Summer camps and tournaments throughout the contributes to this slowly building pressure. The child
year are “show cases,” necessary next steps to ensure talent is unable to articulate what is bothering him or her and
development and a future college scholarship. The recent the parent’s behavior is too insignificant in an isolated
financial recession has probably increased these pressures. moment for others to take notice. What starts out as mild
Some parents fear that failure to start sports participation irritation becomes a deeper burden for the child, gradually
early and intensely will deprive their children of future undermining the enjoyment of play and the quality of
happiness and success. As their anxiety mounts, some parents per formance. As the child’s performance worsens, the
may become zealous about their children’s sport activities, parent becomes increasingly concerned and involved, often
which often takes the form of intense over-involvement. exacerbating the situation.25
As previously mentioned, Outliers, by Malcolm Gladwell, has Clinicians may detect these subtler forms of pressure by
both added and changed the focus of these pressures.15 asking key questions of both the child and parent. Observing
Gladwell debunks the myth of unique talent and yet may add differences in the child’s and parent’s responses to these
to the pressure by pointing out the importance of age and questions can often provide a clearer picture of the child–
date-of-birth cut off policies in various leagues, the role of parent dynamic and reveal how the pressure is being
opportunity and chance, and the critical effect of culture.15 expressed. In the best circumstances, these discussions can
All of these influences facilitate the final common pathway to lead to greater awareness and prompt healthier adjustments.
Psychosocial Aspects of Youth Sports • CHAPTER 3 45
It is often helpful to ask parents about their short- and injuries such as broken bones or torn ligaments, can be-
long-term goals for their child’s athletics: For example, what come gut-wrenching and sickening terror. This is especially
are their goals for their child’s health, discipline, friendships, true for the young athlete, who may have no history of
pleasure, scholarships, professional career, or self-esteem? overcoming real adversity beyond the playing field.
What are their goals if the child does not hold up under the Accompanying the fear can be a sense of captivity, the
pressure of regional, state, or national pyramids? Do they sense that one is trapped by the injury. Often injury results
appreciate that their child has ultimate control by giving up in a physical inability to move, and in a literal sense
the sport or even unconsciously over-reacting to an injury, the athlete is trapped in a prone or immobilized position.
developing disabling psychosomatic illness, or becoming For athletes whose preferred mode of self-expression is the
overwhelmed at the next level of competition? A sophisticated ability to move their body at will with grace and power, this
discussion about these issues and pathways may help, or can be psychologically overwhelming. Outbursts of angry
nature may have to take its course with a less than optimal frustration, tears, and reckless attempts to over-ride the
outcome. Lastly, it is always helpful to remind families that an injury through sheer force of will are not uncommon.
enjoyable connection to physical activity is perhaps the most There is often a brief, cognitive disconnectedness
important goal to enhance the long-term health of their from the reality of the trauma, a sense that the injury isn’t
children as they progress into adulthood and beyond. real—“This can’t be happening to me. I never get hurt.
I’m bulletproof!” There can also be a powerful urge to
Considerations for Dealing engage in protective denial—“It’s not that bad. It’s only a
sprain. I can play.” This expectation to “play in pain” is
with the Injured Athlete often aided and abetted by coaches, parents, teammates,
Insights from research on the psychological responses to and fans, who also can be caught up in the heat of com-
physical and emotional trauma as experienced by victims petition. We have witnessed an overzealous father who
of violence or combat veterans can be useful in assisting engaged in a heated exchange that threatened to become
the injured athlete. Table 3-2 offers a useful schema violent because an athletic trainer refused to clear a high
for understanding where the injured athlete might be emo- school football player back to the playing field following
tionally in the course of injury and recovery. a concussion. The father only relented when his son
plaintively exclaimed, “Dad, it’s only a stupid game!”
Caregivers in these situations might be the only voice
The Initial Psychological Response to Physical Injury of caution, reason, and firm reassurance that the injured
In the initial shock of an injury, there can be a cluster of athlete can and will be properly treated.
overwhelming emotions that flood the injured athlete.
This initial cognitive and emotional reaction to the shock
of injury and trauma often involves fear, a sense of discon- Psychological Features of the Injured Athlete
nectedness or sense of things not being real, and a sense of Following Injury
captivity or feelings of being trapped. In the days and weeks directly following a serious injury
Certainly, the injured athlete often experiences a that results in lost practice and playing time, athletes are
high level of anxiety and fear, which, in the case of serious likely to experience a characteristic cluster of emotions and
behaviors. These include hyperaroused responses, intrusive
Table 3-2 effects, and emotional withdrawal or avoidance.
Psychological Response to Injury and Recovery Hyperarousal can frequently be understood as an “All
hands on deck! Battle Stations!” response, which can be both
Event Recovery
(Initial Response Symptoms (Recovery
adaptive yet counterproductive to the healing process. Ath-
to Injury) (Following Injury) from Injury) letes recovering from the initial shock of their injury might
often manifest an intense zeal “to do whatever it takes to get
Terror Hyperarousal Safety back on the field.” This desire can make them amenable to a
(Fear in mid- (Forced healing) (Predictable disciplined approach and a zealous compliance to treatment
or post-trauma) outcome) that the non-athlete might not bring to the doctor’s, thera-
Captivity Intrusion Adjustment pist’s, or trainer’s office. Such an athlete initially can really be
(No quick fix) (Preoccupied (Dealing with a “super” patient. However, this intense feeling can easily
with injury) limits)
morph into something less than helpful or healthy if frustra-
Disconnection Emotional withdrawal Reconnection
tion arises because the pace of healing isn’t what the injured
(Protective (Depression/despair) (Restoration
denial) of health) athlete expected. There can be a grandiose self-perception
that if the normal healing time is 8 weeks, the athlete will
Data from Herman, JL: Trauma & Recovery, New York, 1994, Basic make it in half the time—“I said I’d be back in 4 weeks max!
Books. It’s been 4 weeks. I’m ready to PLAY NOW!”
Psychosocial Aspects of Youth Sports • CHAPTER 3 47
The injured athlete might also be susceptible to intrusive and emotional support from knowledgeable health care
effects that hinder the healing process and undermine his providers. In addition, trainers, physicians, and sport
or her overall health. Intrusive effects can manifest as an physical therapists must be able to set firm limits based on
inability to sleep, a preoccupation with the injury and recov- sound clinical judgment for the often unrealistic expecta-
ery, an inability to concentrate on school work or other inter- tions and subtle pressures exerted by parents, coaches, and
ests, and even an obsessive replaying of the injury with an teammates on their young athletes.
“if only X had been different, I wouldn’t have been hurt”
scenario. At its most severe, these intrusive effects can include
a startle reflex or a hypersensitivity to any movement involving Psychological Features of Recovery
the injury or even external movement in the vicinity of the for the Injured Athlete
injury. For example, a young injured athlete might irritably A relative sense of emotional safety is a crucial psychological
explode at a sibling or friend who accidentally nudges the element in the recovery from trauma. This may take
crutches or at a parent who doesn’t respond quickly enough the form of the athlete’s recognition that those charged
to a request that is seen as vital in the injured athlete’s eyes. with assisting the healing process are knowledgeable and
In addition to the intrusive effects of his or her own understand how crucial a return to play is for the injured
thoughts, fears, and worries, the injured athlete must also athlete. The desired outcome of the initial encounter with
fend off what can feel like an incessant and monotonous litany any health care provider is that sense of recognition of the
of inquiries from caring family, friends, and fans. In some nature of the injury and course of treatment, but also a
professional sports, players are zealously protected from the sense of reassurance and even relief. “Okay, I am really
constant focus and emotionally draining effects of never- injured but these guys have helped other athletes with this
ending questions: “How are you feeling? Is your injury get- type of injury so maybe they do know how to help me.”
ting better? When do you expect to return to play?” Although This sense of relief and trust in an injured athlete is a
well intentioned, the constant attention paid to an injury function of good “trainer’s table” or “bedside” interpersonal
often serves to emotionally exhaust the injured athlete and act skills, as well as effective communication of predictable
as a trigger for negative thoughts about the healing process. outcome. The younger the athlete, the more concrete,
Health care professionals serve their athletes well by reviewing simple, and repetitive the instructions regarding the course of
this phenomenon with their athletes and strategizing about treatment should be. For example, the health care provider
acceptable ways to diplomatically cocoon them from the who bluntly orders “Rest!” to the young athletic patient
intrusive and tiresome questioning they may encounter. without a more careful step-by-step explanation that outlines
In short, parents, coaches, and health care providers the course of recovery, or at least improved functioning,
can greatly help the injured athlete by monitoring the will run the risk of losing the young athlete to a dismissive,
fundamentals of good health. Adequate physical and noncompliant, and even defiant approach to treatment.
emotional rest; proper hydration and diet; appropriate As the injured athlete gradually begins to trust the
exercise that does not exacerbate the injury; avoidance of healing process and builds a sense of trust with his or her
an obsessive focus on the injury; and a balanced approach doctor, sport physical therapist, and athletic trainer, his
to home life, academics, and friendships are important or her feelings, comments, and behaviors should begin to
factors in the healing process for young athletes. reflect a sense that he or she is adapting and adjusting
Finally, it is not unusual for the injured athlete to go to the process of recovery. This adjustment phase may
through a period of emotional withdrawal or avoidance and include some behaviors that are similar to grieving.
possible mini-depression. Just as naval crewmen at battle Comments or behaviors that reflect mourning for the
stations eventually need to stand down lest fatigue and lost playing time or season are not uncommon. For some
exhaustion overtake them, so too the injured athlete can athletes, there may be a lingering emotional avoidance
rarely sustain the gung-ho, hyperaroused “I will force myself and withdrawal from all contact with their sport. Other
to heal sooner” approach to recovery. Eventually, the injured athletes prefer to remain on the sidelines as an observer.
athlete hits the wall of realization that his or her body is The rule of thumb is that people are entitled to grieve in
well and truly damaged. There will be no magical overnight many ways. There is no preferred way to emotionally
recovery. Playing time will be lost. This can often hit the recover from the losses inflicted by a serious injury. Some
young athlete extremely hard. behaviors are certainly better than others. Provided the
It is important to remember that young athletes do not patient is complying with treatment, maintaining healthy
have the experience of an adult to fall back on. They have relationships, and meeting his or her academic require-
not yet had a life that includes successfully dealing with ments, then the issue of whether an injured young athlete
painful loss, suffering, and adversity and overcoming these seeks to withdraw from a high level of interaction with the
trials and tribulations with a fully operational adult brain. sport should be left to the athlete. For some, an injury
These patients are in need of clear information on what they can actually provide a surprising window into how life
can expect, along with ample doses of accurate reassurance outside the sport can be interesting and fulfilling.
48 SECTION I • Preparation and Prevention in Sports Medicine
If the recovery process has been successful, then the athlete Burnout seems to more frequently occur in quiet,
will enter a phase of reconnection to his or her previous perfectionistic, highly coachable athletes who work too
athletic endeavors. This return to the playing field and hard and too intensely for too long in unrewarding
presumably to the previous level of participation can be as situations.31,32 Coakley24 notes that the external con-
challenging as the earlier stages of injury. This can especially straints and social limitations placed on athletes hampers
be true for physicians, sport physical therapists, or athletic the development of a well-balanced, healthy identity
trainers who must deal with the athlete, parent, and coach and lifestyle and increases the risk of burnout in many
who may have a distorted and overly optimistic view of what collegiate athletic programs. Tofler and colleagues11 state,
“recovery” means. The coach who attempts to motivate the “Children should feel that parental love or a relationship
recovered athlete by saying, “The doc said you’re all better! with critical adults is not contingent on winning or
So you should be good to go!” might not recognize the excelling in any one educational, sporting, career or social
depth of the athlete’s hesitancy and shaky confidence that he goal.” Young athletes who are trapped in a situation in
or she is fully recovered. The young athlete is also frequently which they must live up to the unrealistic expectations of
unable to articulate what he or she is feeling and sensing parents, coaches, and the community are at greater risk
emotionally as well as physically. Therefore, he or she may for burnout and arrested emotional development.
be unable to express the anxiety being experienced. Further- More recent research based on the self-determination
more, the athlete may not even be aware that he or she is theory of Deci and Ryan33 suggests that burnout occurs
anxious! For example, the athlete who has recovered from when three basic psychological needs—autonomy, com-
anterior cruciate ligament surgery and the long rehabilitation petence, and relatedness—have been chronically frus-
process still faces a significant hurdle in psychologically trated. There can be multiple factors that contribute to
trusting his or her repaired knee in the heat of competition. staleness or burnout. These factors include the length
The seasoned coach and caregiver can often detect the hesi- of the season, the monotony of training, lack of positive
tancy and tentativeness in the athlete returning from injury. reinforcement, abusive coaches, overly stringent rules,
player boredom, a perception of low achievement and
failure, high levels of competitive stress, a sense of being
Clinical Point overloaded and helpless to effect constructive change in
Caregivers who can predict, clearly state and normalize some of the the sporting environment, and a sense of being trapped in
difficulties that the returning athlete may experience, can go a long an untenable situation.
way toward reassuring and calming the jittery, newly healed athlete. Whatever the theoretical underpinning of this phe-
nomenon, health care providers must be well versed in the
symptoms of burnout so as to help the struggling athlete
and accurately determine when physical complaint is
Burnout, Staleness, or Just a Slump? masking a deeper, potentially debilitating emotional and
Burnout has been defined as “state of mental, emotional physical exhaustion.
and physical exhaustion brought on by persistent devotion
to a goal whose achievement is dramatically opposed to
reality.”28-30 Burnout differs from the idea of staleness,
which has been defined as an early warning sign of possible
Signs of Burnout in Athletes
burnout characterized by diminishing physical and
emotional capabilities. The term slump usually refers to a • Increased fatigue or prolonged weariness
diminished performance that may or may not be a function • Increased irritability or apathy
of staleness or burnout. A baseball batter in a slump may • Increased somatic complaints or injuries with no apparent
in fact be hitting the ball well and not be suffering pathological cause
• Consistent feelings of intense ambivalence toward practice
from staleness or imminent burnout, but in fact may
or competition, including an expressed desire to quit
be well-energized and just hitting the ball right at
• Frequent missed practices or skipped games
well-positioned fielders. Burnout, staleness, and slump fall • Inexplicable pattern of poor athletic performance
under umbrella term of maladaptive fatigue syndrome. • Decreased confidence
• Behaviors that sabotage further athletic participation
• Narrowing of appropriate developmental opportunities in the
Maladaptive Fatigue Syndrome service of sport commitment (especially for teens)
• Parents who engage in a pattern of risky sacrifice to aid child’s
• Burnout athletic career (serious life choices or family decisions seem
• Staleness rashly and overly based on the parents’ view of a child’s athletic
• A slump potential)
Psychosocial Aspects of Youth Sports • CHAPTER 3 49
Dealing with Athletes with Attention the community in general. These individuals may be more
likely to get depressed in response to a persistent pattern
Deficit Disorder of relative failure and subsequent interpersonal difficulties
Attention deficit disorder and attention deficit hyperactivity with teachers, parents, coaches, and even peers.
disorder (ADD/ADHD) are psychological conditions It is recommended that caregivers take careful histories
that exist in approximately 3% to 5% of the population,36 when dealing with their athletes to determine whether
but some experts cite higher incidence rates.37 The preva- their patients are currently being treated for ADD/
lence is higher for boys than girls. ADD/ADHD can be ADHD. Often athletes avoid taking prescribed medica-
diagnosed by the presence of a cluster of symptoms tion when training or competing as they may identify
that include significantly elevated levels of distractibility, their problems as being solely a school-based phenome-
inattentiveness, and cognitive or behavioral impulsivity.36 non. Parents concerned about unnecessarily medicating
These weaknesses often undermine academic performance children may at times put pressure on their child
and can affect athletic performance as well as compliance to athlete to forego the use of their prescribed medicine.
medical treatment. This practice of not medicating during athletics or
Often, there are secondary psychological features of recreational activities may or may not be appropriate.
ADD or ADHD, including difficulty with organizational The student-athlete with ADD/ADHD may need and
and executive tasks such as fluidly handling transitions or benefit from medication for endeavors outside of the
following through on multistep tasks.36 It is important academic domain. The issues regarding athletes’ use
to note that often individuals with ADD/ADHD may of medication for treatment of ADD/ADHD need to
be more prone to engage in high-risk or thrill-seeking be addressed on a case-by-case basis in consultation
behaviors. This may be especially true for boys. Untreated with the athlete’s primary care physician or treatment
ADD/ADHD may place the individual at risk for addic- specialist.
tive, self-medicating behaviors such as substance abuse, Athletes with undiagnosed ADD/ADHD can pose a
sexual acting out, fighting, and gambling. Anecdotally, coaching, parenting, and treatment problem that may
there is some evidence to suggest that athletes as a group present in several ways. These patients may appear as the
may manifest a much higher incidence rate of ADD/ athlete whose inattentiveness or impulsivity leads to danger-
ADHD and the behaviors that have come to be associated ous, high-risk play in practice and competition and therefore
with the condition. frequent injury or physical complaint. In noncontact sports,
It is easy to understand how the constellation of these this risky behavior may present as overtraining to the point of
symptoms in an athlete might pose both a threat to physical burnout or overuse injury.
the maintenance of consistent good health and training Sometimes the inattentiveness and problems with
practices as well as an impediment to the successful following multitask instruction might give the athlete
implementation of therapeutic treatment and preventative a reputation for being “spacey” or unintelligent. Female
or rehabilitative work. The ADD/ADHD pattern of athletes with undiagnosed ADD/ADHD can be misla-
inattentiveness, impulsivity, risk-taking, and stubbornly beled in such a manner because, perhaps for cultural
rigid thinking or hyperfocus leaves these athletes more reasons, they may not display the higher risk behaviors
vulnerable to accident and injury. They may miss impor- or impulsive outbursts of anger that can typify the ADHD
tant information from coaches and health care providers, presentation in the male athlete. Finally, the stubborn,
which in turn may decrease consistent compliance with noncompliant athlete who routinely presents as being
preventative conditioning practices as well as proper play- unable to contain his or her irritability at the treatment
ing technique. Ironically, the athlete with ADD/ADHD regimen and fails to follow medical advice may also be
might be more likely to both over-do it and under-do exhibiting signs of ADD/ADHD. For example, although
it because they may manifest both a stubborn, single- many injured athletes wearing a cast for a fractured limb
mindedness and a reckless, haphazard style as they follow express deep dissatisfaction and threaten to forcibly
the beat of their own drummer. remove the cast, it stands to reason that the ADD/ADHD
In general, the pressures that exist for the injured athlete athlete is more likely to act on that irritability and
as outlined earlier in the chapter can be presumed to exist impulsively remove the protective cast against all medical
to a greater degree in the athlete with ADD or ADHD. advice. There are multiple anecdotes of athletes who
The impatience, impulsivity, inattention, and possible poor cut off their casts so they could play. These stories
judgment that so often exists with ADD/ADHD increases unfortunately can serve to glorify the physical and
the likelihood of ignoring treatment protocols, recklessly mental toughness of the athlete and can be passively
forcing “a rush to health,” and seeking alternative and condoned by coaches, teammates, parents, and support-
possibly contraindicated therapies. ers. These athletes, as well as their extended network
Untreated ADD/ADHD can result in underperfor- of relationships, need vigilant follow-up supervision
mance and behavioral problems in school, home, and in with ongoing reassurance regarding the efficacy of the
Psychosocial Aspects of Youth Sports • CHAPTER 3 51
treatment plan. Frequent reminders that such impulsive of loss of playing time or loss of status with his or her
acts expose the athlete to chronic injury or possible peers or coach.
career-ending debilitation may be necessary. The competitive pressure to continue to compete even
In conclusion, athletes with a history of inexplicable in the presence of a concussion that includes a loss of
academic difficulty, as well as problems associated with consciousness is a very powerful phenomenon. Recently,
inattentiveness, distractibility, impulsive behaviors, and a in an international rugby match between Scotland and
pattern of reckless or thrill-seeking acts should be referred Wales in 2009, a player was seriously concussed while
to their primary care physician or a mental health specialist making a tackle. It was clear on video, replayed on the
for appropriate evaluation and possible treatment. stadium screen, that the player in question had knocked
himself unconscious as his head hit an opposing player in
a violent tackle. The player’s body went limp upon impact
Possible Risks Associated with ADD/ADHD but, fortunately, he was cushioned from an unprotected,
in Athletes Recovering from Injury face-first fall by the body of his opponent. Six to seven
medical staff attended the injured rugby player for several
• Pattern of thrill-seeking or risk-taking behaviors minutes, during which time it was obvious to the
• Noncompliance or impatience with recovery (may seek alternative television commentators and spectators that the player
therapies)
had been rocked in the tackle and that, at least initially,
• Increased substance use
the player was dazed and unsteady on his feet. Despite
• Increased irritability, oppositional defiance, or fighting
• Increased addictive behaviors (e.g., sex, gambling, video games) his symptoms, including a brief loss of consciousness,
• Increased depressive symptoms the player was allowed to continue play for another
• Decreased academic performance 10 minutes. During this time, he was involved in
• Recurring injury, accident, or other trauma further physical contact on at least five occasions while
ADD, Attention deficit disorder; ADHD, attention deficit hyperactivity disorder. both tackling and running with the ball. It was left to
the match referee to order the player off the pitch after he
witnessed the player on his knees vomiting. The referee
was distinctly heard to say, “He still hasn’t recovered from
Dealing with the Concussion: the tackle. I’m not happy with that at all. I want him off!”
Hence, it was left to a neutral, nonmedical official to
Psychological Considerations accurately recognize the danger the injured player was in
Sports-related concussions that include a loss of and act in his best interest. This unfortunate but perhaps
consciousness are estimated to occur in 300,000 athletes not uncommon example of trained medical personnel
in the United States each year.38 Because, by definition, allowing a concussed athlete back in a highly competitive,
concussions can occur without a loss of consciousness, passionately contested contact sport sends a bad message
many researchers view these numbers as a gross underes- to athletes at all age levels, coaches, parents, and fans.
timate of the problem by as much as 50%.39 All sports- “Do no harm” is the mission, and concussed athletes
related concussions should be viewed as serious because placed back in the fray will necessarily be in harm’s
they pose a threat to the young athlete that only in recent way; the younger the athlete, the greater the short- and
years is being fully realized. Young athletes appear more long-term risk, a risk that can be fatal.
susceptible to second-impact syndrome, a condition that
results from a second head injury before full recovery
from an initial concussion. This phenomenon can lead to
acute and long-term neurological and neuropsychological Clinical Caution
problems that in rare cases have been fatal in athletes, Young athletes are more susceptible to second-impact syndrome
especially athletes 18 and younger. Because of the hidden following concussions.
nature of head injury, many concussions are unseen,
unrecognized, unreported, and therefore undiagnosed
and untreated. Because a blow to the head might result
in a dazed or confused state, many athletes might not Significant damage and risk can be present for the young
remember or understand the importance of their symp- athlete who has sustained a concussion even without a loss
toms. Athletes are trained and conditioned to ignore of consciousness. Headache and dizziness are the most
pain and physical adversity. Even the language of athletes commonly reported symptoms of concussion. Because there
serves to downplay potentially serious head injury: “I’m may be other reasons that young athletes might experience
okay, I just got a ding.” At times, the nature of com- headache or dizziness such as dehydration, fatigue, or inad-
petitive sports is such that the athlete may intentionally equate nutrition, the accurate diagnosis of a sports-related
hide the injury from the training and medical staff for fear concussion requires keen and ongoing observation.
52 SECTION I • Preparation and Prevention in Sports Medicine
to have a chance to make the high school football team in may develop feminine-appearing breasts, perhaps through
the fall may take cycles of steroids to accomplish this unrea- shock value, can trigger some change in their behavior.
sonable physical goal. If this boy is also socially isolated Young steroid users need to understand that there are
and has low self-esteem, then he may place even greater value healthy ways to build strength. Sport nutritionists can advise
on making the school team, as it represents a form of identity youth and their families about healthy eating and nutrition.
and validation. Driven to feel better about himself, he may Connecting young athletes with well-educated sport
be willing to experiment with steroids despite the risks to physical therapists and athletic trainers can help expose them
his physical and psychological well-being. In particular, to proper weight training regimens, supervised by caring
the mindset of an adolescent male—namely, the belief that adults. Redirecting youth away from gyms where there is
“I am bulletproof ”—makes health risks feel remote and the unsupervised interaction with unqualified adults (who are
potential benefits of getting stronger and faster much more possibly using steroids) is also advisable. And in certain
compelling. The fact that some athletes use steroids, lie about cases, when the self-esteem of the adolescent is considerably
it, and then face minimum consequences while maintaining low or his or her investment in athletics is imbalanced, a
multi-million dollar contracts only makes steroid use among referral to a sports or clinical counselor may be appropriate.
our youth more compelling and worth the risk. Further feel- Of course, steroid use, much like eating disorders, can
ing of being “bullet-proof ” might encourage risk taking in take place in the context of a culture and team. Assessing the
other areas of life beyond sports such as driving or drinking. team’s values, including pressure relating to performance,
Unfortunately, desperation to get immediate results may appearance, interpersonal dynamics, and quality of coaching,
lead to dangerous and unregulated experimentation with are all relevant to assessing the individual athlete and are
steroid use, including ordering steroids through the Internet critical if the clinician has an ongoing role with the team.
or acquiring the drugs through other steroid users at
local gyms. Intravenous steroid users have obvious risks of
infection, including human immunodeficiency virus (HIV)
Conclusion
and hepatitis.48 Because the drugs are obtained and used in The benefits of athletics—physical, emotional, psychologi-
secrecy, adequate education is not provided, much like the cal, and developmental—are clear. Parents and health
case of many professional athletes, leaving the adolescent professionals want the health benefits, the self-esteem,
similarly isolated in his dangerous experimentation. friendships, mentoring, and opportunities that come with
Detection of steroid use may occur through joint obser- every level of participation. As we strive for these worthy
vations by parents, coaches, sport physical therapists, athletic goals, we must always keep in sight the individuality, abili-
trainers, and physicians. Parents may notice changes in ties, aspirations, and needs of the child and adolescent.
mood, increased secrecy about weight training and in Lastly, we must be aware of the risks that are intrinsically
particular time spent at the gym. However, much like the linked with the benefits and recognize psychological and
difficulty parents with eating-disordered daughters may have medical issues that may interfere with the very worthy goals
in noticing significant weight loss, parents of steroid-using of athletic competition.
boys may not be able to detect the rapid weight gain and
muscle mass while living with their son every day. A sport
physical therapist, athletic trainer, or coach who may see the
athlete less frequently over the course of the summer may be References
better able to recognize unexpected and troubling changes. 1. Smoll F, Smith J: Children and youth in sport, ed 2, Dubuque,
A physician may also track significant changes in weight as 2002, Kendall Hunt Publishing.
well as increased acne. 2. Brenner J, Council on Sports Medicine and Fitness: Overuse inju-
ries, overtraining, and burnout in child and adolescent athletes,
Much like addressing concerns around eating and body
Pediatrics 119:1242–1245, 2007.
image, a collaborative approach between parents and 3. U.S. Department of Health and Human Services: Physical activity
clinicians is likely to be most effective in treating steroid and health: A report of the surgeon general (S/N 0-7-023-00196-5),
abuse. Adolescents using steroids may experience a tremen- Atlanta, 1996, Superintendent of Documents.
dous amount of shame and fear. Therefore, clinicians will 4. Dalton SE: Overuse injuries in adolescent athletes, Sports Med
13:58–70, 1992.
be most effective when being tactful about how they raise
5. Gould D, Petlichkoff L: Participation motivation and attrition in
their concerns. In particular, it is crucial that they recognize young athletes. In Smoll FL, Magill RA, Ash MJ, editors: Children
the importance of sports in these young athletes’ lives and in sport, ed 3, Champaign, IL, 1988, Human Kinetics.
the intoxicating power of the immense improvements in 6. Centers for Disease Control and Prevention: Adolescents and
strength and speed caused by steroid use, even while express- young adults. Retrieved on October 10, 2004, from http://www.
cdc.gov/nccdphp/sgr/adoles.htm.
ing strong concern about their health. Making specific
7. National Alliance for Youth Sports: http://www.nays.org, 2009.
references to immediate health risks may be a potentially 8. Seefeldt V, Ewing M, Walk S: Overview of youth sports programs in
effective deterrent. For young males, mentioning the fact the United States, Washington, DC, 1992, Carnegie Council on
that their testicles may shrink to the size of raisins or that they Adolescent Development.
Psychosocial Aspects of Youth Sports • CHAPTER 3 57
9. Pate RR, Trost SG, Levin S, Dowda M: Sports participation and 28. Freudenberger HJ, Richelson G: Burnout: how to beat the high cost
health-related behaviors among US youth, Arch Pediatr Med of success, New York, 1981, Bantam Books.
154(9):904–911, 2000. 29. Maslach C: Understanding burnout: definitional issues in analyz-
10. Committee on Sports Medicine and Fitness: Intensive training and ing a complex phenomenon. In Paine WS, editor: Job stress and
sports specialization in young athletes, Pediatrics 106(1):154–157, burnout: Research, theory and intervention perspectives, Beverly
2000. Hills, 1982, Sage.
11. Toffler IR, Knapp R, Penelop K, Dell MJ: The achievement 30. Pines A, Aronson E: Career burnout, New York, 1988, Free
by proxy spectrum in sports: Historical perspective and clinical Press.
approach to pressured and high-achieving children and 31. Fender LK: Athlete burnout: Potential for research and interven-
adolescents, Child Adolesc Psychiatr Clin North Am 7(4): tion strategies, Sport Psychol 3:63–71, 1989.
725–744, 1998. 32. Maslach C, Pines A: The burnout syndrome, Child Care Q 6:100–
12. Fraser-Thomas J, Cote J: Youth sports: Implementing findings 114, 1977.
and moving forward with research, Athletic Insight 8(3):12–27, 33. Deci EL, Ryan RM: Self-determination theory: A macrotheory
2006. of human motivation, development and health, Can Psychol
13. Balyi I, Hamilton A: Long-term athlete development: Trainability 49(3):182–185, 2008.
in childhood and adolescence. Windows of opportunity. Optimal 34. Henschen K: Maladaptive fatigue syndrome and emotions in
trainability, Victoria, 2004, National Coaching Institute British sport. In Harris YL, editor: Emotions in sport, Champaign, IL,
Columbia & Advanced Training and Performance Ltd. 1999, Human Kinetics.
14. Ericcson KA, Krampe RT, Tesch-Rommer C: The role of deliber- 35. Committee on Sports Medicine and Fitness, Committee on
ate practice in the acquisition of expert performance, Psychol Rev School Health: Intensive training and sport specialization in
100(3):363–406, 1993. young athletes, Pediatrics 106(1):154–157, 2000.
15. Gladwell M: Outliers: The story of success. New York, 2008, Little 36. American Psychiatric Association: Diagnostic and statistical man-
& Brown. ual of mental disorders-IV, Washington, DC, 1994, American
16. Simon HA, Chase WG: Skill in chess, Am Sci 61:394–403, 1973. Psychiatric Association.
17. Bissinger HK: Friday Night Lights: A town, a team and a dream, 37. Hallowell E, Ratey J: Driven to distraction, New York, 1994,
Cambridge, 1990, DaCapo Press. Pantheon Books.
18. NCAA Data: Estimated Probability of competing in athletics beyond 38. Martineau C, Kingma JJ, Bank L, McLeod TCV: Guidelines for
the high school interscholastic level, 2007. Retrieved November 1, treatment of sport-related concussions, J Am Acad Physician Assist
2008, from http://www.ncaa.org/wps/ncaa?ContentID⫽279. 20(5):123–132, 2007.
19. Anderson J: Parental support and pressure: Relationships with chil- 39. Meehan WP, Bachur RG: Sport-related concussion, Pediatrics
dren’s experience of extracurricular activities, Dissertation Abstracts 123:114–123, 2009.
International, Section B, The Sciences and Engineering 65:3696, 40. McCory P, Johnson K, Meeuwise W: Summary and agreement
2005. statement of the 2nd International Conference on Concussion in
20. Babkes ML, Weiss MR: Parental influence on cognitive and affec- Sport, Prague, 2004, Br J Sport Med 39(4):196–204, 2005.
tive responses in children’s competitive soccer participation, 41. Centers for Disease Control: National Center for Health Statistics
Pediatr Exerc Sci 11:44–62, 1999. Health, United States, 2007: With Chartbook on Trends in the
21. Hayashi SW: Understanding youth sport participation through Health of Americans, Hyattsville, 2007, CDC.
perceived coaching behaviors, social support, anxiety and coping, 42. Knight JR, Sherritt L, Shrier LA et al: Validity of the CRAFFT
Dissertation Abstracts International 59(7-A):2418, 1999. substance abuse screening test among adolescent clinic patients,
22. Hoyle RH, Leff SS: The role of parental involvement in youth Arch Pediatr Adolesc Med 156(6):607–614, 2002.
sport participation and performance, Adolescence 32(125): 43. Hobart JA, Smucker DR: The female athlete triad, Am Fam
233–243, 1997. Physician 61:3357–3367, 2000.
23. Stein GL, Raedeke TD, Glenn SD: Children’s perceptions of 44. Luder E, Schebendach J: Nutrition management of eating disor-
parental sport involvement: It’s not how much but to what degree ders, Top Clin Nutr 8:48–63, 1993.
that’s important, J Sport Behav 22:591–601, 1999. 45. Rock CL, Yager J: Nutrition and eating disorders: A primer for
24. Coakley J: Burnout among adolescent athletes: A personal failure clinicians, Int J Eat Disord 6:267–280, 1987.
or social problem? Sociol Sport J 9:271–285, 1992. 46. Reiff DW, Reiff KKL: Eating disorders: Nutrition therapy in the
25. Ginsburg RD, Durant S, Baltzell A: Whose game is it, anyway? recovery process, Gaithersberg, MD, 1992, Aspen.
A guide to helping your child get the most from sports, organized by 47. National Institute on Drug Abuse: Monitoring the future study,
age and stage, Boston, 2006, Houghton Mifflin Company. 2003. Retrieved June 1, 2007 from http://www.nida.nih.gov/In-
26. Smith RE, Smoll FL, Curtis B: Coaching behaviors in Little fofax/HSYouthtrends.html.
League baseball. In Smoll FL, Smith RW, editors: Psychological 48. Volkow N, The National Institute on Drug Abuse: Consequences
perspectives in youth sports, Washington, DC, 1978, Hemisphere of the abuse of anabolic steroids, 2005. Retrieved November 15,
Publishing. 2008, from http://www.drugabuse.gov/about/welcome/
27. Herman JL: Trauma & recovery, New York, 1994, Basic Books. MessageSteroids305.html.
4
CHAPTER
58
Nutrition Counseling and Athletes • CHAPTER 4 59
individual or population for which the assessment is being use is that it is fairly time-consuming. Another disadvantage
conducted. Valid, reliable dietary assessment tools appropri- is that the accuracy depends on either a trained person
ate for the individual or population for which the assessment sitting with the individual to define portion sizes and quan-
is being conducted will help achieve the most accurate tities, or the individual’s understanding of the questionnaire
results possible. Other factors to consider when choosing and how accurately he or she self-assesses portions and
the appropriate dietary assessment tool include objectives of frequency.
the assessment, dietary information of interest (i.e., energy, One may also use an abbreviated version of the food
specific nutrients, food groups, and dietary patterns), the frequency questionnaire by going through the food
timeframe involved, cost, and the interviewer’s qualifications groups in the food guide pyramid (i.e., grains, fruits, veg-
and experience.1 etables, dairy, meat and beans, and fats) (Figure 4-1) and
question how often and in what quantity the athlete
eats these foods, including what foods and beverages
Clinical Point the athlete consumed prior to and just after exercise,
training, and an event; what typical snack foods are
The primary goal of a dietary assessment is to determine the most eaten; and what, if any nutritional supplements the athlete
accurate and typical nutrient and foot intake of an individual. takes.
Table 4-1
Caloric Expenditure for Various Physical Activities
Body Weight (kcal · min1 · kg1)
Kg 45 48 50 52 55 57 59 61 64 66
Pounds 100 105 110 115 120 125 130 135 140 145
Sedentary Activities
Lying quietly .99 1.0 1.1 1.1 1.2 1.3 1.3 1.4 1.4 1.5
Sitting and writing, card playing, etc. 1.2 1.3 1.4 1.5 1.5 1.6 1.7 1.7 1.8 1.8
Standing with light work, cleaning, etc. 2.7 2.9 3.0 3.1 3.3 3.4 3.5 3.7 3.8 3.9
Physical Activities
Archery 3.1 3.3 3.5 3.6 3.8 4.0 4.1 4.3 4.5 4.6
Badminton
Recreational singles 3.6 3.8 4.0 4.2 4.4 4.6 4.7 4.9 5.1 5.3
Social doubles 2.7 2.9 3.0 3.1 3.3 3.4 3.5 3.7 3.8 3.9
Competitive 5.9 6.1 6.4 6.7 7.0 7.3 7.6 7.9 8.2 8.5
Baseball
Player 3.1 3.3 3.4 3.6 3.8 4.0 4.1 4.3 4.4 4.5
Pitcher 3.9 4.1 4.3 4.5 4.7 4.9 5.1 5.3 5.5 5.7
Basketball
Half court 3.0 3.1 3.3 3.5 3.6 3.8 3.9 4.1 4.2 4.4
Recreational 4.9 5.2 5.5 5.7 6.0 6.2 6.5 6.7 7.0 7.2
Vigorous competition 6.5 6.8 7.2 7.5 7.8 8.2 8.5 8.8 9.2 9.5
Bicycling, level
(mph) (min/mile)
5 12:00 1.9 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8
6 10:00 2.7 2.8 3.0 3.1 3.2 3.4 3.5 3.6 3.8 3.9
8 7:30 3.4 3.6 3.8 4.0 4.1 4.3 4.5 4.7 4.8 5.0
10 6:00 4.2 4.4 4.6 4.8 5.1 5.3 5.5 5.7 5.9 6.1
11 5:28 5.0 5.2 5.5 5.7 6.0 6.2 6.5 6.7 7.0 7.2
12 5:00 5.7 6.0 6.3 6.6 6.9 7.2 7.5 7.8 8.1 8.4
13 4:37 6.8 7.1 7.5 7.8 8.2 8.5 8.8 9.2 9.5 9.9
Bowling 2.7 2.8 3.0 3.1 3.3 3.4 3.5 3.7 3.8 3.9
Calisthenics
Light type 3.4 3.6 3.8 4.0 4.1 4.3 4.5 4.7 4.8 5.0
Timed vigorous 9.7 10.1 10.6 11.1 11.6 12.1 12.6 13.1 13.6 14.1
Canoeing
(mph) (min/mile)
2.5 24 1.9 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8
4.0 15 4.4 4.6 4.9 5.1 5.3 5.5 5.8 6.0 6.2 6.4
5.0 12 5.7 6.0 6.3 6.6 6.9 7.2 7.5 7.8 8.1 8.4
Dancing
Moderate (waltz) 3.1 3.3 3.5 3.6 3.8 4.0 4.1 4.3 4.5 4.6
Active (square, disco) 4.5 4.7 5.0 5.2 5.4 5.6 5.9 6.1 6.3 6.6
Aerobic (vigorous) 6.0 6.3 6.7 7.0 7.3 7.6 7.9 8.2 8.5 8.8
Fencing
Moderate 3.3 3.5 3.6 3.8 4.0 4.1 4.3 4.5 4.6 4.8
Vigorous 6.6 7.0 7.3 7.7 8.0 8.3 8.7 9.0 9.4 9.7
Field hockey 5.0 6.3 6.7 7.0 7.3 7.6 7.9 8.2 8.5 8.8
Football
Moderate 3.3 3.5 3.6 3.8 4.0 4.1 4.3 4.5 4.6 4.8
Touch, vigorous 5.5 5.8 6.1 6.4 6.6 6.9 7.2 7.5 7.8 8.0
Golf
Twosome (carry clubs) 3.6 3.8 4.0 4.2 4.4 4.6 4.7 4.9 5.1 5.3
Foursome (carry clubs) 2.7 2.9 3.0 3.1 3.3 3.4 3.5 3.7 3.8 3.9
Power cart 1.9 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8
Nutrition Counseling and Athletes • CHAPTER 4 61
68 70 73 75 77 80 82 84 86 89 91 93 95 98 100
150 155 160 165 170 175 180 185 190 195 200 205 210 215 220
1.5 1.5 1.6 1.6 1.7 1.7 1.8 1.8 1.9 1.9 2.0 2.0 2.1 2.1 2.2
1.9 2.0 2.0 2.1 2.2 2.2 2.3 2.4 2.4 2.5 2.5 2.6 2.7 2.7 2.8
4.1 4.2 4.4 4.5 4.6 4.8 4.9 5.0 5.2 5.3 5.4 5.6 5.7 5.9 6.0
4.8 4.9 5.1 5.3 5.4 5.6 5.7 5.9 6.0 6.2 6.4 6.5 6.7 6.9 7.0
5.4 5.6 5.8 6.0 6.2 6.4 6.6 6.7 6.9 7.1 7.3 7.4 7.6 7.8 8.0
4.1 4.2 4.4 4.5 4.6 4.8 4.9 5.0 5.2 5.3 5.4 5.6 5.7 5.9 6.0
8.8 9.1 9.4 9.7 10.0 10.3 10.6 10.9 11.2 11.5 11.8 12.1 12.4 12.7 13.0
4.7 4.8 5.0 5.2 5.3 5.5 5.6 5.8 5.9 6.1 6.3 6.4 6.6 6.8 6.9
5.9 6.0 6.3 6.5 6.7 6.9 7.1 7.3 7.4 7.7 7.9 8.0 8.2 8.5 8.6
4.5 4.7 4.8 5.0 5.1 5.3 5.4 5.6 5.7 5.9 6.0 6.2 6.4 6.5 6.7
7.5 7.7 8.0 8.2 8.5 8.7 9.0 9.2 9.5 9.7 10.0 10.2 10.5 10.7 11.0
9.9 10.2 10.5 10.9 11.2 11.5 11.9 12.2 12.5 12.9 13.2 13.5 13.8 14.2 14.5
2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3
4.0 4.2 4.3 4.4 4.6 4.7 4.9 5.0 5.1 5.3 5.4 5.5 5.7 5.8 6.0
5.2 5.4 5.5 5.7 5.9 6.1 6.3 6.4 6.6 6.8 6.9 7.1 7.3 7.5 7.7
6.4 6.6 6.8 7.0 7.2 7.4 7.6 7.9 8.1 8.3 8.5 8.7 8.9 9.1 9.4
7.5 7.8 8.0 8.3 8.5 8.8 9.0 9.3 9.5 9.8 10.0 10.3 10.6 10.8 11.1
8.7 9.0 9.3 9.5 9.8 10.1 10.4 10.7 11.0 11.3 11.6 11.9 12.2 12.5 12.8
10.2 10.6 10.9 11.3 11.6 12.0 12.3 12.6 13.0 13.3 13.7 14.0 14.4 14.7 15.0
4.1 4.2 4.4 4.5 4.6 4.8 4.9 5.0 5.2 5.3 5.5 5.6 5.7 5.9 6.0
5.2 5.4 5.5 5.7 5.9 6.1 6.3 6.4 6.6 6.8 7.0 7.1 7.3 7.5 7.7
14.6 15.1 15.6 16.1 16.6 17.1 17.6 18.1 18.6 19.1 19.6 20.0 20.5 21.0 21.5
2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3
6.7 6.9 7.1 7.4 7.6 7.8 8.0 8.2 8.5 8.7 8.9 9.1 9.4 9.6 9.8
8.7 9.0 9.3 9.5 9.8 10.1 10.4 10.7 11.0 11.3 11.6 11.9 12.2 12.5 12.8
4.8 4.9 5.1 5.3 5.4 5.6 5.7 5.9 6.0 6.2 6.4 6.5 6.7 6.9 7.0
6.8 7.0 7.3 7.5 7.7 7.9 8.2 8.4 8.6 8.9 9.1 9.3 9.5 9.8 10.0
9.1 9.4 9.7 10.0 10.3 10.6 10.9 11.2 11.5 11.8 12.1 12.4 12.7 13.0 13.3
5.0 5.2 5.3 5.5 5.7 5.8 6.0 6.2 6.3 6.5 6.7 6.8 7.0 7.1 7.3
10.0 10.4 10.7 11.0 11.4 11.7 12.1 12.4 12.7 13.1 13.4 13.8 14.1 14.4 14.8
9.1 9.4 9.7 10.0 10.3 10.6 10.9 11.2 11.5 11.8 12.1 12.4 12.7 13.0 13.3
5.0 5.2 5.3 5.5 5.7 5.8 6.0 6.2 6.3 6.5 6.7 6.8 7.0 7.1 7.3
8.3 8.6 8.9 9.2 9.4 9.7 10.0 10.3 10.6 10.8 11.1 11.4 11.7 12.0 12.2
5.4 5.6 5.8 6.0 6.2 6.4 6.6 6.7 6.9 7.1 7.3 7.4 7.6 7.8 8.0
4.1 4.2 4.4 4.5 4.6 4.8 4.9 5.0 5.2 5.3 5.4 5.6 5.7 5.9 6.0
2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3
Continued
62 SECTION I • Preparation and Prevention in Sports Medicine
Table 4-1
Caloric Expenditure for Various Physical Activities—cont’d
Body Weight (kcal · min1 · kg1)
Kg 45 48 50 52 55 57 59 61 64 66
Pounds 100 105 110 115 120 125 130 135 140 145
Handball
Moderate 6.5 6.8 7.2 7.5 7.8 8.2 8.5 8.8 9.2 9.5
Competitive 7.7 8.0 8.4 8.8 9.2 9.6 10.1 10.4 10.8 11.1
Hiking, pack (3 mph) 4.5 4.7 5.0 5.2 5.4 5.6 5.9 6.1 6.3 6.6
Hockey, ice 6.6 7.0 7.3 7.7 8.0 8.3 8.7 9.0 9.4 9.7
Horseback riding
Walk 1.9 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8
Sitting to trot 2.7 2.9 3.0 3.1 3.3 3.4 3.5 3.7 3.8 3.9
Posting to trot 4.2 4.4 4.6 4.8 5.1 5.3 5.5 5.7 5.9 6.1
Gallop 5.7 6.0 6.3 6.6 6.9 7.2 7.5 7.8 8.1 8.4
Horseshoes 2.5 2.6 2.8 2.9 3.0 3.1 3.3 3.4 3.5 3.7
Jogging (see running)
Judo 8.5 8.9 9.3 9.8 10.2 10.6 11.0 11.5 11.9 12.3
Karate 8.5 8.9 9.3 9.8 10.2 10.6 11.0 11.5 11.9 12.3
Mountain climbing 6.5 6.8 7.2 7.5 7.8 8.2 8.5 8.8 9.2 9.5
Paddle ball 5.7 6.0 6.3 6.6 6.9 7.2 7.5 7.8 8.1 8.4
Pool (billiards) 1.5 1.6 1.6 1.7 1.8 1.9 1.9 2.0 2.1 2.2
Racquetball 6.5 6.8 7.1 7.5 7.8 8.1 8.4 8.8 9.1 9.4
Roller skating (9 mph) 4.2 4.4 4.6 4.8 5.1 5.3 5.5 5.7 5.9 6.1
Running (steady state)
(mph) (min/mile)
5.0 12:00 6.0 6.3 6.6 7.0 7.3 7.6 7.9 8.2 8.5 8.8
5.5 10:55 6.7 7.0 7.3 7.7 8.0 8.4 8.7 9.0 9.4 9.7
6.0 10:00 7.2 7.6 8.0 8.4 8.7 9.1 9.5 9.8 10.2 10.6
7.0 8:35 8.5 8.9 9.3 9.0 10.2 10.6 11.0 11.5 11.9 12.3
8.0 7:30 9.7 10.2 10.7 11.2 11.6 12.1 12.6 13.1 13.6 14.1
9.0 6:40 10.8 11.3 11.9 12.4 12.9 13.5 14.0 14.6 15.1 15.7
10.0 6:00 12.1 12.7 13.3 13.9 14.5 15.1 15.7 16.4 17.0 17.6
11.0 5:28 13.3 14.0 14.6 15.3 16.0 16.7 17.3 18.0 18.7 19.4
12.0 5:00 14.5 15.2 16.0 16.7 17.4 18.2 18.9 19.7 20.4 21.1
Sailing, small boat 2.7 2.9 3.0 3.1 3.3 3.4 3.5 3.7 3.8 3.9
Skating, ice (9 mph) 4.2 4.4 4.6 4.8 5.1 5.2 5.5 5.7 5.9 6.1
Skiing, cross-country
(mph) (min/mile)
2.5 24:00 5.0 5.2 5.5 5.7 6.0 6.2 6.5 6.7 7.0 7.2
4.0 15:00 6.5 6.8 7.2 7.5 7.8 8.2 8.5 8.8 9.2 9.5
5.0 12:00 7.7 8.0 8.4 8.8 9.2 9.6 10.0 10.4 10.8 11.1
Skiing, downhill 6.5 6.8 7.2 7.5 7.8 8.2 8.5 8.8 9.2 9.5
Soccer 5.9 6.2 6.6 6.9 7.2 7.5 7.8 8.1 8.4 8.7
Squash
Normal 6.7 7.0 7.3 7.7 8.0 8.4 8.7 9.1 9.5 9.8
Competition 7.7 8.0 8.4 8.8 9.2 9.6 10.0 10.4 10.8 11.1
Swimming (yards/min)
Backstroke
25 2.5 2.6 2.8 2.9 3.0 3.1 3.3 3.4 3.5 3.7
30 3.5 3.7 3.9 4.1 4.2 4.4 4.6 4.8 4.9 5.1
35 4.5 4.7 5.0 5.2 5.4 5.6 5.9 6.1 6.3 6.6
40 5.5 5.8 6.1 6.4 6.6 6.9 7.2 7.5 7.8 8.0
Breaststroke
20 3.1 3.3 3.5 3.6 3.8 4.0 4.1 4.3 4.5 4.6
30 4.7 5.0 5.2 5.4 5.7 5.9 6.2 6.4 6.7 6.9
40 6.3 6.7 7.0 7.3 7.6 8.0 8.3 8.6 8.9 9.3
Nutrition Counseling and Athletes • CHAPTER 4 63
68 70 73 75 77 80 82 84 86 89 91 93 95 98 100
150 155 160 165 170 175 180 185 190 195 200 205 210 215 220
9.9 10.2 10.5 10.9 11.2 11.5 11.9 12.2 12.5 12.9 13.2 13.5 13.8 14.2 14.5
11.5 11.9 12.3 12.7 13.1 13.5 13.9 14.3 14.7 15.0 15.4 15.8 16.2 16.6 17.0
6.8 7.0 7.3 7.5 7.7 7.9 8.2 8.4 8.6 8.9 9.1 9.3 9.5 9.8 10.0
10.0 10.4 10.7 11.0 11.4 11.7 12.1 12.4 12.7 13.1 13.4 13.8 14.1 14.4 14.8
2.9 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 3.9 4.0 4.1 4.2 4.3
4.1 4.2 4.4 4.5 4.6 4.8 4.9 5.0 5.2 5.3 5.4 5.6 5.7 5.9 6.0
6.4 6.6 6.8 7.0 7.2 7.4 7.6 7.9 8.1 8.3 8.5 8.7 8.9 9.1 9.4
8.7 9.0 9.3 9.5 9.8 10.1 10.4 10.7 11.0 11.3 11.6 11.9 12.2 12.5 12.8
3.8 3.9 4.0 4.2 4.3 4.4 4.5 4.7 4.8 4.9 5.2 5.2 5.3 5.4 5.6
12.8 13.2 13.6 14.1 14.5 14.9 15.4 15.8 16.2 16.6 17.1 17.5 17.9 18.4 18.8
12.8 13.2 13.6 14.1 14.5 14.9 15.4 15.8 16.2 16.6 17.1 17.5 17.9 18.4 18.8
9.8 10.2 10.5 10.8 11.2 11.5 11.8 12.1 12.5 12.8 13.1 13.5 13.8 14.1 14.5
8.7 9.0 9.3 9.5 9.8 10.1 10.4 10.7 11.0 11.2 11.6 11.9 12.2 12.5 12.8
2.2 2.3 2.4 2.5 2.6 2.6 2.7 2.8 2.9 2.9 3.0 3.1 3.2 3.2 3.3
9.8 10.1 10.4 10.7 11.1 11.4 11.7 12.0 12.4 12.7 13.0 13.4 13.7 14.0 14.4
6.4 6.6 6.8 7.0 7.2 7.4 7.6 7.9 8.1 8.3 8.5 8.7 8.9 9.1 9.4
9.1 9.4 9.7 10.0 10.3 10.6 10.9 11.2 11.6 11.9 12.2 12.5 12.8 13.1 13.4
10.0 10.4 10.7 11.1 11.4 11.7 12.1 12.4 12.8 13.1 13.4 13.8 14.1 14.5 14.8
10.9 11.3 11.7 12.0 12.4 12.8 13.1 13.5 13.8 14.3 14.6 15.0 15.4 15.7 16.1
12.8 13.2 13.6 14.1 14.5 14.9 15.4 15.8 16.2 16.6 17.1 17.5 17.9 18.4 18.8
14.6 15.1 15.6 16.1 16.6 17.1 17.6 18.1 18.5 19.0 18.5 20.0 20.5 21.0 21.5
16.2 16.8 17.3 17.9 18.4 19.0 19.5 20.1 20.6 21.2 21.7 22.2 22.8 23.3 23.9
18.2 18.8 19.4 20.0 20.7 21.3 21.9 22.5 23.1 23.7 24.2 24.8 25.4 26.0 26.7
20.0 20.7 21.4 22.1 22.7 23.4 24.1 24.8 25.4 26.1 26.8 27.5 28.1 28.8 29.5
21.9 22.6 23.3 24.1 24.8 25.6 26.3 27.0 27.8 28.5 29.2 30.0 30.7 31.5 32.2
4.1 4.2 4.4 4.5 4.6 4.8 4.9 5.0 5.2 5.3 5.4 5.6 5.7 5.9 6.0
6.4 6.6 6.8 7.0 7.2 7.4 7.6 7.9 8.1 8.3 8.5 8.7 8.9 9.1 9.4
7.5 7.8 8.0 8.3 8.5 8.8 9.0 9.3 9.5 9.8 10.0 10.3 10.6 10.8 11.1
9.9 10.2 10.5 10.9 11.2 11.5 11.9 12.2 12.5 12.9 13.2 13.5 13.8 14.2 14.5
11.5 11.9 12.3 12.7 13.1 13.5 13.9 14.3 13.7 15.0 15.4 15.8 16.2 16.6 17.0
9.9 10.2 10.5 10.9 11.2 11.5 11.9 12.2 12.5 12.9 13.2 13.5 13.8 14.2 14.5
9.0 9.3 9.6 9.9 10.2 10.5 10.8 11.1 11.4 11.7 12.0 12.3 12.6 12.9 13.2
10.1 10.5 10.8 11.2 11.5 11.8 12.2 12.5 12.9 13.2 13.5 13.9 14.2 14.6 14.9
11.5 11.9 12.3 12.7 13.1 13.5 13.9 14.3 14.7 15.0 15.4 15.8 16.2 16.6 17.0
3.8 3.9 4.0 4.2 4.3 4.4 4.5 4.7 4.8 4.9 5.1 5.2 5.3 5.4 5.6
5.3 5.5 5.6 5.8 6.0 6.2 6.4 6.5 6.7 6.9 7.1 7.2 7.4 7.6 7.8
6.8 7.0 7.3 7.5 7.7 7.9 8.2 8.4 8.6 8.9 9.1 9.3 9.5 9.8 10.0
8.3 8.6 8.9 9.2 9.4 9.7 10.0 10.3 10.6 10.8 11.1 11.4 11.7 12.0 12.2
4.8 4.9 5.1 5.3 5.4 5.6 5.7 5.9 6.0 6.2 6.4 6.5 6.7 6.9 7.0
7.1 7.4 7.6 7.9 8.1 8.3 8.6 8.8 9.1 9.3 9.5 9.8 10.0 10.3 10.5
9.6 9.9 10.2 10.5 10.9 11.2 11.5 11.9 12.2 12.5 12.8 13.1 13.5 13.8 14.1
Continued
64 SECTION I • Preparation and Prevention in Sports Medicine
Table 4-1
Caloric Expenditure for Various Physical Activities—cont’d
Body Weight (kcal · min1 · kg1)
Kg 45 48 50 52 55 57 59 61 64 66
Pounds 100 105 110 115 120 125 130 135 140 145
Front crawl
20 3.1 3.3 3.5 3.6 3.8 4.0 4.1 4.3 4.5 4.6
25 4.0 4.2 4.4 4.6 4.8 5.0 5.2 5.4 5.6 5.8
35 4.8 5.1 5.4 5.6 5.9 6.1 6.4 6.6 6.8 7.0
45 5.7 6.0 6.3 6.6 6.9 7.2 7.5 7.8 8.1 8.4
50 7.0 7.4 7.7 8.1 8.5 8.8 9.2 9.5 9.9 10.3
Table tennis 3.4 3.6 3.8 4.0 4.1 4.3 4.5 4.7 4.8 5.0
Tennis
Singles, recreational 5.0 5.2 5.5 5.7 6.0 6.2 6.5 6.7 7.0 7.2
Doubles, recreational 3.4 3.6 3.8 4.0 4.1 4.3 4.5 4.7 4.8 5.0
Competition 6.4 6.7 7.1 7.4 7.7 8.1 8.4 8.7 9.1 9.4
Volleyball
Moderate, recreational 2.9 3.0 3.2 3.3 3.5 3.6 3.8 3.9 4.1 4.2
Vigorous, competition 6.5 6.8 7.1 7.5 7.8 8.1 8.4 8.8 9.1 9.4
Walking
(mph) (min/mile)
1.0 60:00 1.5 1.6 1.7 1.8 1.8 1.9 2.0 2.1 2.2 2.3
2.0 30:00 2.1 2.2 2.3 2.4 2.5 2.6 2.8 2.9 3.0 3.1
2.3 26:00 2.3 2.4 2.5 2.7 2.8 2.9 3.0 3.1 3.2 3.4
3.0 20:00 2.7 2.9 3.0 3.1 3.3 3.4 3.5 3.7 3.8 3.9
3.2 18:45 3.1 3.3 3.4 3.6 3.8 4.0 4.1 4.3 4.4 4.5
3.5 17:10 3.3 3.5 3.7 3.9 4.0 4.2 4.4 4.6 4.7 4.9
4.0 15:00 4.2 4.4 4.6 4.8 5.1 5.3 5.5 5.7 5.9 6.1
4.5 13:20 4.7 5.0 5.2 5.4 5.7 5.9 6.2 6.4 6.7 6.9
5.0 12:00 5.4 5.7 6.0 6.3 6.5 6.8 7.1 7.4 7.7 7.9
5.4 11:10 6.2 6.6 6.9 7.2 7.5 7.9 8.2 8.5 8.8 9.2
5.8 10:20 7.7 8.0 8.4 8.8 9.2 9.6 10.0 10.4 10.8 11.1
Water skiing 5.0 5.2 5.5 5.7 6.0 6.2 6.5 6.7 7.0 7.2
Weight training 5.2 5.4 5.7 6.0 6.2 6.5 6.8 7.0 7.3 7.6
Wrestling 8.5 8.9 9.3 9.8 10.2 10.6 11.0 11.5 11.9 12.3
From Williams MH: Nutrition for Fitness and Sport, 2nd ed. Copyright 1988 Davenport, IA, William C. Brown Communication, Inc. 1988.
Copyright 2004 by the National Academy of Sciences. All rights reserved.
Nutrition Counseling and Athletes • CHAPTER 4 65
68 70 73 75 77 80 82 84 86 89 91 93 95 98 100
150 155 160 165 170 175 180 185 190 195 200 205 210 215 220
4.8 4.9 5.1 5.3 5.4 5.6 5.7 5.9 6.0 6.2 6.4 6.5 6.7 6.9 7.0
6.0 6.2 6.4 6.6 6.8 7.0 7.2 7.4 7.6 7.8 8.0 8.2 8.4 8.6 8.8
7.3 7.5 7.8 8.0 8.3 8.5 8.8 9.0 9.2 9.4 9.7 9.9 10.2 10.4 10.7
8.7 9.0 9.3 9.5 9.8 10.1 10.4 10.7 11.0 11.3 11.6 11.9 12.2 12.5 12.8
10.6 11.0 11.3 11.7 12.0 12.4 12.8 13.1 13.5 13.8 14.2 14.5 14.9 15.2 15.6
5.2 5.4 5.5 5.7 5.9 6.1 6.3 6.4 6.6 6.8 7.0 7.1 7.3 7.5 7.7
7.5 7.8 8.0 8.3 8.5 8.8 9.0 9.3 9.5 9.8 10.0 10.3 10.6 10.8 11.1
5.2 5.4 5.5 5.7 5.9 6.1 6.3 6.4 6.6 6.8 7.0 7.1 7.3 7.5 7.7
9.8 10.1 10.4 10.8 11.1 11.4 11.8 12.1 12.4 12.8 13.1 13.4 13.7 14.1 14.4
4.4 4.5 4.7 4.8 5.0 5.1 5.3 5.4 5.6 5.7 5.9 6.0 6.1 6.3 6.4
9.8 10.1 10.4 10.7 11.1 11.4 11.7 12.0 12.4 12.7 13.0 13.4 13.7 14.0 14.4
2.3 2.4 2.4 2.5 2.6 2.7 2.8 2.9 2.9 3.0 3.1 3.2 3.2 3.3 3.4
3.2 3.3 3.4 3.5 3.6 3.7 3.9 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7
3.5 3.6 3.7 3.8 4.0 4.1 4.2 4.3 4.4 4.5 4.7 4.8 4.9 5.0 5.1
4.1 4.2 4.4 4.5 4.6 4.8 4.9 5.0 5.2 5.3 5.4 5.6 5.7 5.9 6.0
4.7 4.8 5.0 5.2 5.3 5.5 5.6 5.8 5.9 6.1 6.3 6.4 6.6 6.8 6.9
5.1 5.3 5.4 5.6 5.8 6.0 6.2 6.3 6.5 6.7 6.9 7.0 7.2 7.4 7.6
6.4 6.6 6.8 7.0 7.2 7.4 7.6 7.9 8.1 8.3 8.5 8.7 8.9 9.1 9.4
7.1 7.4 7.6 7.9 8.1 8.3 8.6 8.8 9.1 9.3 9.5 9.8 10.0 10.3 10.5
8.2 8.4 8.7 9.0 9.2 9.5 9.8 10.1 10.4 10.6 10.9 11.2 11.5 11.8 12.0
9.5 9.8 10.1 10.4 10.8 11.1 11.4 11.8 12.1 12.4 12.7 13.0 13.4 13.7 14.0
11.5 11.9 12.3 12.7 13.1 13.5 13.9 14.3 14.7 15.0 15.4 15.8 16.2 16.6 17.0
7.5 7.8 8.0 8.3 8.5 8.8 9.0 9.3 9.5 9.8 10.0 10.3 10.6 10.8 11.1
7.8 8.1 8.3 8.6 8.9 9.1 9.4 9.7 9.9 10.2 10.5 10.7 11.0 11.2 11.5
12.8 13.2 13.6 14.1 14.5 14.9 15.4 15.8 16.2 16.6 17.1 17.5 17.9 18.4 18.8
66 SECTION I • Preparation and Prevention in Sports Medicine
guidelines for professional intervention.7 The stages of change glycogen (300 to 400 kcal or 75 to 100 g), and, lastly, blood
are shown in Table 4-11. During the assessment, it is useful glucose (100 kcal or 25 g).8 The liver’s glycogen storage is
to determine the athlete’s stage to determine an appropriate used to maintain blood glucose levels, whereas muscle gly-
intervention strategy. An example is the athlete who has no cogen is used by the muscles for energy. An athlete’s perfor-
idea that his or her diet is nutritionally inadequate and there- mance (i.e., greater endurance and delayed fatigue) can be
fore may not be ready to take action and start goal setting. maximized by ensuring greater energy reserve in the form of
Information regarding nutrition and exercise is first muscle glycogen for endurance and strength activities. Dur-
needed to move the athlete to the next stage: contempla- ing endurance activities requiring 65% maximum oxygen
tion. Once the athlete has contemplated making the dietary consumption (VO2 max), our bodies prefer carbohydrate as
changes, it is time to clarify any preconceived notions and the primary fuel source.8-10
to provide additional information regarding the benefits of High-intensity, short-duration exercise (sprinting) relies
the change. The athlete may then be ready to move to the on the anaerobic pathway for the production of energy. Only
preparation stage. During this stage, the athlete is able to glucose derived primarily from the breakdown of muscle
identify a motivation for taking action and begins to inves- glycogen can be used as fuel. Muscle glycogen is used about
tigate strategies for change. A list of action strategies for the 18 times faster when glucose is broken down anaerobically
athlete ready to implement changes is shown in Box 4-1. than when glucose is broken down aerobically. During high-
Learning whether the individual is ready to make changes intensity exercise (i.e., more than 70% of aerobic capacity) and
requires good listening skills on the part of the interviewer. in extended mixed anaerobic and aerobic sports (such as soc-
The interviewer can learn what motivates the athlete and cer, basketball, football drills, and interval running or swim-
where to start in the process of making behavior changes. ming) the aerobic pathway is also used. A more rapid rate of
muscle glycogen breakdown occurs in these events.
Exercise of low-to-moderate intensity is fueled almost
Nutrient Recommendations entirely aerobically. Increased epinephrine, norepinephrine,
The body requires at least 40 nutrients, which are classified growth hormone, and decreased insulin promote the release
into six groups: macronutrients (carbohydrates, fat, and of fatty acids from the adipose tissue into the bloodstream.
protein), micronutrients (vitamins and minerals), and water. Half of the energy is supplied by these fatty acids, whereas
These nutrients are classified as essential because they muscle glycogen and blood glucose supply the rest for this
cannot be made in the body; therefore, they must be type of event. However, muscle glycogen is the predominant
supplied from the diet. There are three categories of fuel for most types of exercise.
macronutrients: carbohydrates, fat, and protein; and two It is extremely important that endurance athletes (e.g.,
categories of micronutrients: vitamins and minerals. The cyclists, long-distance runners, triathletes) consume a high-
macronutrients, in addition to alcohol, provide energy in the carbohydrate diet because one of the limiting factors
form of calories (Table 4-12). Vitamins, minerals, and water in prolonged performance is glycogen depletion. Recent
have no calories and therefore are not a source of energy. debate has been focused around the two primary fuel
sources of the body (carbohydrates and fat) during the
recovery phase. Burke and colleagues conducted a literature
Groups of Nutrients review that focused on successful day-to-day refueling meth-
• Carbohydrates ods and recovery between daily sessions or multiple work-
• Fat Macronutrients outs.11 Although fat consumption remains an important part
• Protein of an athlete’s overall diet, Burke and colleagues concluded
• Vitamins Micronutrients that foods rich in carbohydrate with a moderate-to-high
• Minerals glycemic index value provided a readily available source of
carbohydrate for muscle glycogen synthesis, and should be
• Water
the major carbohydrate choice in recovery meals.11 They
also concluded that even though new interest revolves
around the recovery of intramuscular triglyceride stores, at
the present time, no evidence supports advantages of high-
Macronutrients fat, restricted carbohydrate diets to enhance training.11
Carbohydrates Recommended carbohydrate intakes for athletes varies,
Carbohydrates are the body’s preferred source of energy, depending on current training needs and other factors such
used to spare protein for body growth and repair. However, as current body mass and nutrition goals. Generally speak-
storage space for carbohydrates is limited within the body. ing, most athletes require 6 to 10 g/kg/day.8 For example,
The predominant method of storage is in the form of a 65-kg marathon runner would require 455 to 650 g of
glycogen and intracellular polysaccharide. Muscle glycogen carbohydrate per day (using 7- to 10-g carbohydrate/day),
represents the major source of carbohydrate in the body whereas a 65-kg basketball player may only require 390 to
(1200 to 1600 kcal or 300 to 400 g), followed by liver 455 g of carbohydrate per day.
text cont’d on page 77
68 SECTION I • Preparation and Prevention in Sports Medicine
Table 4-2
Dietary Reference Intakes (DRIs): Recommended Intakes for Individuals, Vitamins (Food and Nutrition Board, Institute
of Medicine, National Academies)
Life Stage Vit A Vit C Vit D Vit E Vit K Thiamin
Group (g/day)a (mg/day) (g/day)b,c (mg/day)d (g/day) (mg/day)
Infants
0–6 mo 400* 40* 5* 4* 2.0* 0.2*
7–12 mo 500* 50* 5* 5* 2.5* 0.3*
Children
1–3 y 300 15 5* 6 30* 0.5
4–8 y 400 25 5* 7 55* 0.6
Males
9–13 y 600 45 5* 11 60* 0.9
14–18 y 900 75 5* 15 75* 1.2
19–30 y 900 90 5* 15 120* 1.2
31–50 y 900 90 5* 15 120* 1.2
51–70 y 900 90 10* 15 120* 1.2
70 y 900 90 15* 15 120* 1.2
Females
9–13 y 600 45 5* 11 60* 0.9
14–18 y 700 65 5* 15 75* 1.0
19–30 y 700 75 5* 15 90* 1.1
31–50 y 700 75 5* 15 90* 1.1
51–70 y 700 75 10* 15 90* 1.1
70 y 700 75 15* 15 90* 1.1
Pregnancy
14–18 y 750 80 5* 15 75* 1.4
19–30 y 770 85 5* 15 90* 1.4
31–50 y 770 85 5* 15 90* 1.4
Lactation
14–18 y 1,200 115 5* 19 75* 1.4
19–30 y 1,300 120 5* 19 90* 1.4
31–50 y 1,300 120 5* 19 90* 1.4
NOTE: This table (taken from the DRI reports, see www.nap.edu) presents Recommended Dietary Allowances (RDAs) in bold type and
Adequate Intakes (AIs) in ordinary type followed by an asterisk (*). RDAs and AIs may both be used as goals for Individual intake. RDAs are set
to meet the needs of almost all (97 to 98 percent) individuals in a group. For healthy breastfed infants, the AI is the mean intake. The AI for
other life stage and gender groups is believed to cover needs of all individuals in the group, but lack of data or uncertainty in the data prevent
being able to specify with confidence the percentage of individuals covered by this intake.
a
As retinol activity equivalents (RAEs). 1 RAE 1 g retinol, 12 g -carotene, 24 g -carotene, or 24 g -cryptoxanthin. The RAE for
dietary provitamin A carotenoids is twofold greater than retinol equivalents (RE), whereas the RAE for preformed vitamin A is the same as RE.
b
As cholecalciferol. 1 g cholecalciferol 40 IU vitamin D.
c
In the absence of adequate exposure to sunlight.
d
As -tocopherol. -Tocopherol includes RRR--tocopherol, the only form of -tocopherol that occurs naturally in foods, and the 2R-
stereoisomeric forms of -tocopherol (RRR-, RSR-, RRS-, and RSS--tocopherol) that occur in fortified foods and supplements. It does not
include the 2S-stereoisomeric forms of -tocopherol (SRR-, SSR-, SRS-, and SSS--tocopherol), also found in fortified foods and supplements.
e
As niacin equivalents (NE). 1 mg of niacin 60 mg of tryptophan; 0–6 months preformed niacin (not NE).
f
As dietary folate equivalents (DFE). 1 DFE 1 g food folate 0.6 g of folic acid from fortified food or as a supplement consumed with
food 0.5 g of a supplement taken on an empty stomach.
g
Although AIs have been set for choline, there are few data to assess whether a dietary supply of choline is needed at all stages of the life cycle,
and it may be that the choline requirement can be met by endogenous synthesis at some of these stages.
h
Because 10 to 30 percent of older people may malabsorb food-bound B12, it is advisable for those older than 50 years to meet their RDA
mainly by consuming foods fortified with B12 or a supplement containing B12.
i
In view of evidence linking folate intake with neural tube defects in the fetus, it is recommended that all women capable of becoming pregnant
consume 400 g from supplements or fortified foods in addition to intake of food folate from a varied diet.
j
It is assumed that women will continue consuming 400 g from supplements or fortified food until their pregnancy is confirmed and they enter
prenatal care, which ordinarily occurs after the end of the periconceptional period—the critical time for formation of the neural tube.
Copyright 2004 by the National Academy of Sciences. All rights reserved.
Nutrition Counseling and Athletes • CHAPTER 4 69
Table 4-3
Dietary Reference Intakes (DRIs): Recommended Intakes for Individuals, Elements (Food and Nutrition Board, Institute
of Medicine, National Academies)
Life Stage Calcium Chromium Copper Fluoride Iodine Iron Magnesium
Group (mg/day) (g/day) (g/day) (mg/day) (g/day) (mg/day) (mg/day)
Infants
0-6 mo 210* 0.2* 200* 0.01* 110* 0.27* 30*
7-12 mo 270* 5.5* 220* 0.5* 130* 11 75*
Children
1-3 y 500* 11* 340 0.7* 90 7 80
4-8 y 800* 15* 440 1* 90 10 130
Males
9-13 y 1300* 25* 700 2* 120 8 240
14-18 y 1300* 35* 890 3* 150 11 410
19-30 y 1000* 35* 900 4* 150 8 400
31-50 y 1000* 35* 900 4* 150 8 420
51-70 y 1200* 30* 900 4* 150 8 420
70 y 1200* 30* 900 4* 150 8 420
Females
9-13 y 1300* 21* 700 2* 120 8 240
14-18 y 1300* 24* 890 3* 150 15 360
19-30 y 1000* 25* 900 3* 150 18 310
31-50 y 1000* 25* 900 3* 150 18 320
51-70 y 1200* 20* 900 3* 150 8 320
70 y 1200* 20* 900 3* 150 8 320
Pregnancy
14-18 y 1300* 29* 1000 3* 220 27 400
19-30 y 1000* 30* 1000 3* 220 27 350
31-50 y 1000* 30* 1000 3* 220 27 360
Lactation
14-18 y 1300* 44* 1300 3* 290 10 360
19-30 y 1000* 45* 1300 3* 290 9 310
31-50 y 1000* 45* 1300 3* 290 9 320
NOTE: This table presents Recommended Dietary Allowances (RDAs) in bold type and Adequate Intakes (AIs) in ordinary type followed by
an asterisk (*). RDAs and AIs may both be used as goals for individual intake. RDAs are set to meet the needs of almost all (97% to 98%)
individuals in a group. For healthy breastfed infants, the AI is the mean intake. The AI for other life stage and gender groups is believed to cover
needs of all individuals in the group, but lack of data or uncertainty in the data prevent being able to specify with confidence the percentage of
individuals covered by this intake.
SOURCES: Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride (1997); Dietary Reference Intakes for
Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (1998); Dietary Reference Intakes for
Vitamin C, Vitamin E, Selenium, and Carotenoids (2000); Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium,
Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2001); and Dietary Reference Intakes for Water, Potassium,
Sodium, Chloride, and Sulfate (2004). These reports may be accessed via http:www.nap.edu. Copyright 2004 by the National Academy of
Sciences. All rights reserved.
Nutrition Counseling and Athletes • CHAPTER 4 71
Table 4-4
Dietary Reference Intakes (DRIs): Tolerable Upper Intake Levels (ULa), Vitamins (Food and Nutrition Board, Institute
of Medicine, National Academies)
Life Stage Vitamin A Vitamin C Vitamin D Vitamin E
Group (mg/day)b (mg/day) (g/day) (mg/day)c,d Vitamin K Thiamin Riboflavin
Infants
0-6 mo 600 NDf 25 ND ND ND ND
7-12 mo 600 ND 25 ND ND ND ND
Children
1-3 y 600 400 50 200 ND ND ND
4-8 y 900 650 50 300 ND ND ND
Males,
Females
9-13 y 1700 1200 50 600 ND ND ND
14-18 y 2800 1800 50 800 ND ND ND
19-70 y 3000 2000 50 1000 ND ND ND
70 y 3000 2000 50 1000 ND ND ND
Pregnancy
14-18 y 2800 1800 50 800 ND ND ND
19-50 y 3000 2000 50 1000 ND ND ND
Lactation
14-18 y 2800 1800 50 800 ND ND ND
19-50 y 3000 2000 50 1000 ND ND ND
a
UL The maximum level of daily nutrient intake that is likely to pose no risk of adverse effects. Unless otherwise specified, the UL represents
total intake from food, water, and supplements. Due to lack of suitable data, ULs could not be established for vitamin K, thiamin, riboflavin,
vitamin B12, pantothenic acid, biotin, carotenoids. In the absence of ULs, extra caution may be warranted in consuming levels above
recommended intakes.
b
As preformed vitamin A only.
c
As -tocopherol; applies to any form of supplemental -tocopherol.
d
The ULs for vitamin E, niacin, and folate apply to synthetic forms obtained from supplements, fortified foods, or a combination of the two.
e
-Carotene supplements are advised only to serve as a provitamin A source for individuals at risk of vitamin A deficiency.
f
ND Not determinable due to lack of data of adverse effects in this age group and concern with regard to lack of ability to handle excess
amounts. Source of intake should be from food only to prevent high levels of intake.
SOURCES: Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride (1997); Dietary Reference Intakes for
Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (1998); Dietary Reference Intakes for
Vitamin C, Vitamin E, Selenium, and Carotenoids (2000); and Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium,
Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2001). These reports may be accessed via. http://www.nap.edu.
Copyright 2004 by the National Academy of Sciences. All rights reserved.
Nutrition Counseling and Athletes • CHAPTER 4 73
ND ND ND ND ND ND ND ND
ND ND ND ND ND ND ND ND
10 30 300 ND ND ND 1.0 ND
15 40 400 ND ND ND 1.0 ND
20 60 600 ND ND ND 2.0 ND
30 80 800 ND ND ND 3.0 ND
35 100 1000 ND ND ND 3.5 ND
35 100 1000 ND ND ND 3.5 ND
30 80 800 ND ND ND 3.0 ND
35 100 1000 ND ND ND 3.5 ND
30 80 800 ND ND ND 3.0 ND
35 100 1000 ND ND ND 3.5 ND
74 SECTION I • Preparation and Prevention in Sports Medicine
Table 4-5
Dietary Reference Intakes (DRIs): Tolerable Upper Intake Levels (ULa), Elements (Food and Nutrition Board, Institute of Medicine,
National Academies)
Boron Copper Fluoride Iodine Iron
Life Stage (mg/ Calcium (g/ (mg/ (g/ (mg/ Magnesium Manganese
Group Arsenicb day) (g/day) Chromium day) day) day) day) (mg/day)c (mg/day)
Infants
0-6 mo NDf ND ND ND ND 0.7 ND 40 ND ND
7-12 mo ND ND ND ND ND 0.9 ND 40 ND ND
Children
1-3 y ND 3 2.5 ND 1000 1.3 200 40 65 2
4-8 y ND 6 2.5 ND 3000 2.2 300 40 110 3
Males,
Females
9-13 y ND 11 2.5 ND 5000 10 600 40 350 6
14-18 y ND 17 2.5 ND 8000 10 900 45 350 9
19-70 y ND 20 2.5 ND 10000 10 1100 45 350 11
70 y ND 20 2.5 ND 10000 10 1100 45 350 11
Pregnancy
14-18 y ND 17 2.5 ND 8000 10 900 45 350 9
19-50 y ND 20 2.5 ND 10000 10 1100 45 350 11
Lactation
14-18 y ND 17 2.5 ND 8000 10 900 45 350 9
19-50 y ND 20 2.5 ND 10000 10 1100 45 350 11
a
UL The maximum level of daily nutrient intake that is likely to pose no risk of adverse effects. Unless otherwise specified, the UL represents
total intake from food, water, and supplements. Due to lack of suitable data, ULs could not be established for arsenic, chromium, silicon,
potassium, and sulfate. In the absence of ULs, extra caution may be warranted in consuming levels above recommended intakes.
b
Although the UL was not determined for arsenic, there is no justification for adding arsenic to food or supplements.
c
The ULs for magnesium represent intake from a pharmacological agent only and do not include intake from food and water.
d
Although silicon has not been shown to cause adverse effects in humans, there is no justification for adding silicon to supplements.
e
Although vanadium in food has not been shown to cause adverse effects in humans, there is no justification for adding vanadium to food and
vanadium supplements should be used with caution. The UL is based on adverse effects in laboratory animals and this data could be used to set
a UL for adults but not children and adolescents.
f
ND Not determinate due to lack of data of adverse effects in this age group and concern with regard to lack of ability to handle excess
amounts. Source of intake should be from food only to prevent high levels of intake.
SOURCES: Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride (1997); Dietary Reference Intakes for
Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (1998); Dietary Reference Intakes for
Vitamin C, Vitamin E, Selenium, and Carotenoids (2000); Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium,
Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2001); and Dietary Reference Intakes for Water, Potassium,
Sodium, Chloride, and Sulfate (2004). These reports may be accessed via.http:www.nap.edu. Copyright 2004 by the National Academy
of Sciences. All rights reserved.
Nutrition Counseling and Athletes • CHAPTER 4 75
ND ND ND ND 45 ND ND ND 4 ND ND
ND ND ND ND 60 ND ND ND 5 ND ND
1.50 (59) Sedentary 41.6 (92) 56.2 (124) 1848 2080 1625 1762
Low active 2009 2267 1803 1956
Active 2215 2506 2025 2198
Very active 2554 2898 2291 2489
1.65 (65) Sedentary 50.4 (111) 68.0 (150) 2068 2349 1816 1982
Low active 2254 2566 2016 2202
Active 2490 2842 2267 2477
Very active 2880 3296 2567 2807
1.80 (71) Sedentary 59.9 (132) 81.0 (178) 2301 2635 2015 2211
Low active 2513 2884 2239 2459
Active 2782 3200 2519 2769
Very active 3225 3720 2855 3141
a
For each year below 30, add 7 kcal/day for women and 10 kcal/day for men. For each year above 30, subtract 7 kcal/day for women and 10 kcal/day for men.
b
PAL physical activity level.
c
BMI body mass index.
*Derived from the following regression equations based on doubly labeled water data:
Adult man: EER 662 9.53 age (y) PA (15.91 wt [kg] 539.6 ht [m])
Adult woman: EER 354 6.91 age (y) PA (9.36 wt [kg] 726 ht [m])
Where PA refers to coefficient for PAL
PAL total energy expenditure √ basal energy expenditure
PA 1.0 if PAL
1.0 1.4 (sedentary)
PA 1.12 if PAL
1.4 1.6 (low active)
PA 1.27 if PAL
1.6 1.9 (active)
PA 1.45 if PAL
1.9 2.5 (very active)
Copyright 2004 by the National Academy of Sciences. All rights reserved.
Nutrition Counseling and Athletes • CHAPTER 4 77
Table 4-7
Dietary Reference Intakes (DRIs): Acceptable Macronutrient Distribution Ranges (Food and Nutrition Board, Institute
of Medicine, National Academies)
Range (percent of energy)
Macronutrient Children, 1-3 year Children, 4-18 year Adults
a
Approximately 10% of the total can come from longer-chain n-3 or n-6 fatty acids.
SOURCE: Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (2002).
Copyright 2004 by the National Academy of Sciences. All rights reserved.
Daily Recommendations for Carbohydrate Intake8 diet, but does not train to develop muscle strength and
endurance, there will be a limited capacity to store glycogen.
• 4 to 5 g/kg/day for general population with physical activity However, reducing exercise 2 days before the event and rest-
of low-intensity ing the day before allows the muscles the opportunity to
• 6 to 7 g/kg/day for general training needs replace depleted glycogen stores. Rest is an essential part of
• 7 to 10 g/day for endurance athletes
carbohydrate loading to promote muscle glycogen storage
• 10 g/day for ultra endurance athletes
for optimal endurance performance.13
Protein
To maximize overall performance during and after an Requirements for protein are actually requirements for amino
event, athletes who engage in continuous, intense endurance acids, the building blocks of protein. Protein can be compared
training (i.e., 90 minutes or more) may combine a specific with a chain-link fence, the links representing amino acids.
training schedule and dietary regimen termed carbohydrate There are 20 amino acids in which our bodies require and are
loading or glycogen super compensation. Normally, each 100 g involved in multiple tasks such as protein turnover, membrane
of muscle contains about 1.7 g of glycogen; carbohydrate transport, immune function, acid-base regulation, and inter-
loading packs up to 5 g of glycogen per 100 g of skeletal mediary metabolism. Amino acids are divided into two cate-
muscle.12 Because of the extreme demands of the classic carbo- gories, nonessential and essential. Essential amino acids are
hydrate loading method, most athletes resort to a modified ones the body cannot synthesize and that therefore must be
carbohydrate loading method, which has been an accepted ingested into the body through diets. The term nonessential
carbohydrate loading method since the early 1980s. Using this does not mean they are unimportant; rather, they must be
method, athletes taper their training, following a more realistic synthesized from other compounds already in the body at a
exercise preparation during the week before an important rate to meet demands for normal growth and tissue repair.15
event.13 As depicted in Figure 4-2, during the first 3 days of Protein, the component of many hormones, is a constituent
the week, exercise duration is longer, carbohydrates are limited of antibodies for the body’s immune system and is part of every
to approximately 50% of overall caloric intake for the day (or enzyme in the body. Approximately 45% of the human body is
about 5 g/kg/day), and fat and protein make up the other protein; second only to water, it makes up the largest percent-
50%. As exercise decreases on days 4 and 5, carbohydrates are age of material in the human body. Although carbohydrate is
increased to 70% or more of overall daily caloric intake (7 to the body’s most-used source of energy, in aerobic sports amino
10 g/kg/day), and fat and protein are decreased. Day 6 results acids may supply up to 15% of the total energy used.16
in a complete rest day from exercise and maximal carbohydrate Evaluation of protein needs should consider the energy
uptake, stimulating muscle glycogen storage. The modified content of the diet. Although protein requirements are
carbohydrate loading method results in nearly as much of a based on degree and intensity of training, energy intake is
gain in muscle glycogen synthesis when compared with the the most important factor affecting protein requirements.
classic method, without all of the struggles of exhaustive exer- When energy intake is less than that required by the body,
cise and a rigorous carbohydrate diet regimen. protein breakdown occurs to provide the energy needed.
This dietary protocol maintains high glycogen stores and Therefore, sports that require specific body weight such as
may be followed numerous times throughout the year with- wrestling, dancing, and gymnastics may lead to insufficient
out health risk.14 If an athlete adheres to a high-carbohydrate energy intake, and protein needs may exceed the RDA.
78 SECTION I • Preparation and Prevention in Sports Medicine
Table 4-8
Dietary Reference Intakes (DRIs): Recommended Intakes for Individuals, Macronutrients (Food and Nutrition Board,
Institute of Medicine, National Academies)
Life Stage Total Watera Carbohydrate Total Fiber Fat Linoleic Acid -Linolenic Proteinb
Group (L/day) (g/day) (g/day) (g/day) (g/day) Acid (g/day) (g/day)
Infants
0-6 mo 0.7* 60* ND 31* 4.4* 0.5* 9.1*
7-12 mo 0.8* 95* ND 30* 4.6* 0.5* 11.0c
Children
1-3 y 1.3* 130 19* ND 7* 0.7* 13
4-8 y 1.7* 130 25* ND 10* 0.9* 19
Males
9-13 y 2.4* 130 31* ND 12* 1.2* 34
14-18 y 3.3* 130 38* ND 16* 1.6* 52
19-30 y 3.7* 130 38* ND 17* 1.6* 56
31-50 y 3.7* 130 38* ND 17* 1.6* 56
51-70 y 3.7* 130 30* ND 14* 1.6* 56
70 y 3.7* 130 30* ND 14* 1.6* 56
Females
9-13 y 2.1* 130 26* ND 10* 1.0* 34
14-18 y 2.3* 130 26* ND 11* 1.1* 46
19-30 y 2.7* 130 25* ND 12* 1.1* 46
31-50 y 2.7* 130 25* ND 12* 1.1* 46
51-70 y 2.7* 130 21* ND 11* 1.1* 46
70 y 2.7* 130 21* ND 11* 1.1* 46
Pregnancy
14-18 y 3.0* 175 28* ND 13* 1.4* 71
19-30 y 3.0* 175 28* ND 13* 1.4* 71
31-50 y 3.0* 175 28* ND 13* 1.4* 71
Lactation
14-18 y 3.8* 210 29* ND 13* 1.3* 71
19-30 y 3.8* 210 29* ND 13* 1.3* 71
31-50 y 3.8* 210 29* ND 13* 1.3* 71
NOTE: This table presents Recommended Dietary Allowances (RDAs) in bold type and Adequate Intakes (AIs) in ordinary type followed by
an asterisk (*). RDAs and AIs may both be used as goals for individual intake. RDAs are set to meet the needs of almost all (97% to 98%)
individuals in a group. For healthy infants fed human milk, the AI is the mean intake. The AI for other life stage and gender groups is believed
to cover the needs of all individuals in the group, but lack of data or uncertainty in the data prevent being able to specify with confidence the
percentage of individuals covered by this intake.
a
Total water includes all water contained in food, beverages, and drinking water.
b
Based on 0.8 g/kg body weight for the reference body weight.
c
Change from 13.5 in prepublication copy due to calculation error.
Copyright 2004 by the National Academy of Sciences. All rights reserved.
Nutrition Counseling and Athletes • CHAPTER 4 79
Table 4-9
Dietary Reference Intakes (DRIs): Additional Macronutrient Recommendations
(Food and Nutrition Board, Institute of Medicine, National Academies)
Macronutrient Recommendation
SOURCE: Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol,
Protein, and Amino Acids (2002). Copyright 2004 by the National Academy of Sciences. All rights
reserved.
For years, health professionals have agreed that the RDA excessive. When energy intake is low, as may be observed
for protein “represents a margin of safety to account for for many young women or in low–body weight athletes,
amino acids catabolized during exercise and amino acids protein needs calculated as a percentage of energy may be
required for protein synthesis following exercise.”12 inadequate. In both of these cases, 1.0 to 1.5 g protein
Protein’s limited capacity for use as a fuel source has been per–kilogram body weight may be a more appropriate guide
thought to result from its primary role of tissue synthesis, for intake than protein as a percentage of total energy.14
minimal protein breakdown during endurance exercise,17 Table 4-13 lists dietary sources of proteins. To add
and resistance training demands for muscle tissue synthesis. 1 pound of muscle per week, an additional 100 g of protein
According to recent research, however, protein may have an is needed in the diet.21 One hundred grams of protein in a
increased role as a source of fuel for energy. Following en- week is 14 g of protein per day, which is obtained in 2 oz
durance or resistance exercise, muscle protein synthesis is of high-biological-value protein such as lean red meat,
increased. Thus, two factors justify re-examining protein poultry, fish, cheese, or two servings of milk or yogurt.
intake recommendations for those involved in exercise Extra protein is not preferentially laid down as muscle mass.
training: (1) increased protein breakdown during long-term Rather, extra protein is used as an energy source if calories
exercise and heavy training and (2) increased protein and carbohydrates are inadequate, stored as fat if the pro-
synthesis in recovery from exercise.12 tein is in excess of calorie needs, or used for its primary and
Branched-Chain Amino Acids. Three amino acids, structural roles (i.e., formation of tissues, hormones, and
leucine, valine, and isoleucine, are branched-chain amino antibodies; maintenance of water and acid-based balance;
acids. These amino acids are predominantly oxidized during and control of blood-clotting processes).
exercise and are essential amino acids. Increased use of Special Considerations Regarding Protein Intake.
branched-chain amino acids and increased breakdown of In women, research has shown one potential problem with
protein are two factors contributing to the increased protein consuming excessive protein—increasing dietary protein
requirement in endurance athletes.18 Protein intakes range leads to elevated calcium excretion.22,23 A high-protein diet
from 1.2 to 1.4 g/kg/day for endurance athletes and from combined with a low intake of calcium can over time lead to
1.6 to 1.7 g/kg/day for resistance-training athletes.3 osteoporosis. Most studies have been done on sedentary
It is unlikely that amino acid oxidation plays an impor- women, and more research is needed on athletes to deter-
tant role in providing energy for strength training because, mine the role of exercise, dietary protein, and calcium in the
although it may be intense, each bout is brief. Also, weight development and prevention of osteoporosis in athletes.
training may actually improve the efficiency of protein Another special consideration is that the metabolism of
use.19 Carbohydrate in the form of glycogen is the major protein requires more water than carbohydrate or fat me-
fuel for strength activities. tabolism. As dietary protein increases, increased water in-
Most research on the actual protein intake of athletes in take is recommended to minimize dehydration.
developed countries reveals that the average athlete con- Vegetarian Diets and Protein. Vegetarian diets are
sumes protein in the highest recommended range.20 Those divided into six categories: In the semi category, dairy
at highest risk of consuming inadequate protein are indi- products, eggs, poultry, and fish are allowed, but red
viduals who already have elevated protein requirements for meat (i.e., beef and pork) is not. In the pesco category,
reasons other than sports, those who consume inadequate no beef pork or poultry is allowed. In the lacto-ovo cate-
calories, and those who participate in multiple daily training gory, dairy products and eggs are allowed. In the lacto
sessions. Protein needs can be calculated both as a percent- category, plant and dairy products are allowed. In the ovo
age of the total energy and on a per–kilogram body weight category, only eggs are allowed as a protein source. In
basis. For athletes with exceptionally high energy intakes, the vegan category, no animal products or derivatives are
providing 12% to 15% of total energy from protein may be allowed.
80 SECTION I • Preparation and Prevention in Sports Medicine
Table 4-10
Dietary Reference Intakes (DRIs): Estimated Average Requirements for Groups (Food and Nutrition Board, Institute
of Medicine, National Academies)
CHO Vit A Vit C Vit E Niacin
Life Stage (g/ Protein (g/ (mg/ (mg/ Thiamin Riboflavin (mg/ Vit B6
Group day) (g/day)a day)b day) day)c (mg/day) (mg/day) day)d (mg/day)
Infants
7-12 mo 9*
Children
1-3 y 100 11 210 13 5 0.4 0.4 5 0.4
4-8 y 100 15 275 22 6 0.5 0.5 6 0.5
Males
9-13 y 100 27 445 39 9 0.7 0.8 9 0.8
14-18 y 100 44 630 63 12 1.0 1.1 12 1.1
19-30 y 100 46 625 75 11 1.0 1.1 12 1.1
31-50 y 100 46 625 75 12 1.0 1.1 12 1.1
51-70 y 100 46 625 75 12 1.0 1.1 12 1.4
70 y 100 46 625 75 12 1.0 1.1 12 1.4
Females
9-13 y 100 28 420 39 9 0.7 0.8 9 0.8
14-18 y 100 38 485 56 12 0.9 0.9 11 1.0
19-30 y 100 38 500 60 12 0.9 0.9 11 1.1
31-50 y 100 38 500 60 12 0.9 0.9 11 1.1
51-70 y 100 38 500 60 12 0.9 0.9 11 1.3
70 y 100 38 500 60 12 0.9 0.9 11 1.3
Pregnancy
14-18 y 135 50 530 66 12 1.2 1.2 14 1.6
19-30 y 135 50 550 70 12 1.2 1.2 14 1.6
31-50 y 135 50 550 70 12 1.2 1.2 14 1.6
Lactation
14-18 y 160 60 885 96 16 1.2 1.3 13 1.7
19-30 y 160 60 900 100 16 1.2 1.3 13 1.7
31-50 y 160 60 900 100 16 1.2 1.3 13 1.7
NOTE: This table presents Estimated Average Requirements (EARs), which serve two purposes: for assessing adequacy of population intakes,
and as the basis for calculating Recommended Dietary Allowances (RDAs) for individuals for those nutrients. EARs have not been established
for vitamin D, vitamin K, pantothenic acid, biotin, choline, calcium, chromium, fluoride, manganese, or other nutrients not yet evaluated via the
DRI process.
a
For individual at reference weight (Table 1-1). *Indicates change from prepublication copy due to calculation error.
b
As retinol activity equivalents (RAEs). 1 RAE 1 g retinol, 12 g -carotene, 24 g -carotene, or 24 g -cryptoxanthin. The RAE for
dietary provitamin A carotenoids is two-fold greater than retinol equivalents (RE), whereas the RAE for preformed vitamin A is the same as RE.
c
As -tocopherol. -Tocopherol includes RRR--tocopherol, the only form of -tocopherol that occurs naturally in foods, and the
2R-stereoisomeric forms of -tocopherol (RRR-, RSR-, RRS-, and RSS--tocopherol) that occur in fortified foods and supplements. It does not
include the 2S-stereoisomeric forms of -tocopherol (SRR-, SSR-, SRS-, and SSS--tocopherol), also found in fortified foods and supplements.
d
As niacin equivalents (NE). 1 mg of niacin 60 mg of tryptophan.
e
As dietary folate equivalents (DFE). 1 DFE 1 g food folate 0.6 g of folic acid from fortified food or as a supplement consumed with
food 0.5 g of a supplement taken on an empty stomach.
SOURCES: Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D, and Fluoride (1997); Dietary Reference Intakes for
Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (1998); Dietary Reference Intakes for
Vitamin C, Vitamin E, Selenium, and Carotenoids (2000); Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium,
Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2001), and Dietary Reference Intakes for Energy,
Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids (2002). These reports may be accessed via.www.nap.edu.
Copyright 2002 by the National Academy of Sciences. All rights reserved.
Nutrition Counseling and Athletes • CHAPTER 4 81
6.9 2.5
Table 4-11
Stages of Change
Stage Description Intervention at this Stage
Precontemplation Athlete unaware of, denies, or Provide personalized information, allow athlete to
minimizes the problem or need express emotions or feelings
to make a change
Contemplation Aware of the problem but Encourage support networks; give positive feedback
weighing costs/benefits of about athlete’s abilities to make the change; clarify
change notions, misconceptions (e.g., carbohydrates are
not fattening); emphasize expected benefits
Preparation/motivation Has made decision to make Encourage athlete to set specific, achievable goals;
change, plans to do so within the reinforce small changes that athlete may have
next month already achieved
Action Plan is in progress, attitudinal and Refer to an education program for behavioral skill
behavioral changes have begun training and to learn tools and techniques to imple-
ment goals; set, implement, and evaluate goals
Maintenance/relapse Action plan maintained for Encourage athlete to anticipate and plan for potential
6 consecutive months; high rate difficulties; if a lapse or relapse occurs, go back to
of relapse before 6 months previous stages; do not assume that initial action
means permanent change; do not be discouraged
or judgmental about a lapse or relapse
Nutrients to Focus on for Vegetarians Plant sources of protein alone can provide adequate
amounts of essential amino acids. Whole grains, legumes,
• Protein has many important functions in the body and is essential vegetables, seeds, and nuts all contain essential amino
for growth and maintenance. Protein needs can easily be met by acids. It was once thought that vegetarian sources of pro-
eating a variety of plant-based foods. Combining different protein tein needed to be consciously combined for the vegetarian
sources in the same meal is not necessary. Sources of protein for
to meet his or her protein needs; for example, legumes are
vegetarians include beans, nuts, nut butters, peas, and soy prod-
low in the amino acid methionine but are also low in
ucts (tofu, tempeh, veggie burgers). Milk products and eggs are
also good protein sources for lacto-ovo vegetarians. lysine. But most vegetarian diets provide adequate protein
• Iron functions primarily as a carrier of oxygen in the blood. Iron without conscious food combining.24 Athletes who are
sources for vegetarians include iron-fortified breakfast cereals, striving for a high carbohydrate (60% to 70%), low fat, and
spinach, kidney beans, black-eyed peas, lentils, turnip greens, moderate protein diet can benefit from a well-planned
molasses, whole wheat breads, peas, and some dried fruits (dried vegetarian diet. Figure 4-3 provides a daily food guide for
apricots, prunes, raisins). planning a vegetarian diet, and Figure 4-4 is a sample
• Calcium is used for building bones and teeth and in maintaining lacto-vegetarian menu.
bone strength. Sources of calcium for vegetarians include fortified
breakfast cereals, soy products (tofu, soy-based beverages), Fat
calcium-fortified orange juice, and some dark green leafy vegeta-
Dietary fat provides essential fatty acids and is necessary for
bles (collard greens, turnip greens, bok choy, mustard greens).
absorption of fat-soluble vitamins. It is an energy source
Milk products are excellent calcium sources for lacto vegetarians.
• Zinc is necessary for many biochemical reactions and also helps the that provides flavor and meal satiety (feeling satisfyingly
immune system function properly. Sources of zinc for vegetarians full), and converts more efficiently to body fat than other
include many types of beans (white beans, kidney beans, and chick- macronutrients.
peas), zinc-fortified breakfast cereals, wheat germ, and pumpkin The degree to which fats are used as fuel during exercise
seeds. Milk products are a zinc source for lacto vegetarians. is determined by exercise intensity and duration, diet, en-
• Vitamin B12 is found in animal products and some fortified foods. durance training history, and altered metabolic state.25 Fatty
Sources of vitamin B12 for vegetarians include milk products, eggs, and acid metabolism requires more oxygen than carbohydrate
foods that have been fortified with vitamin B12. These include breakfast metabolism. Low-intensity exercise ( 50% VO2 max) may
cereals, soy-based beverages, veggie burgers, and nutritional yeast. rely extensively on free fatty acids for fuel. As exercise inten-
From the United States Department of Agriculture: Tips and Resources— sity increases, there is a greater requirement for glucose as
Vegetarian Diets, U.S. Department of Agriculture Center for Nutrition Policy
and Promotion. Available at http://www.mypyramid.gov/tips_resources/ fuel. Blood glucose, muscle, and liver glycogen are the
vegetarian_diets_print.html. primary fuels when rapid energy is needed.
Nutrition Counseling and Athletes • CHAPTER 4 83
Table 4-12
Balancing the Sports Diet*
Nutrient Calories† Sports Diet (%)
40 Min
Run
Run
Min
decline in total amount of fat intake.6 Although no RDA
Min
20
20
Rest
exists for total fat intake, the American Heart Association
Figure 4-2 suggests total fat intake as a percentage of total energy
Modified carbohydrate loading. (From Doyle JA, Papadopoulos C, should be 30% or less. The National Cholesterol Education
Green MS: Utilization of carbohydrates in energy production. In
Wolinsky I, Driskell JA, editors: Sports nutrition, energy, metabolism
Program also suggests total energy from fat intake should
and exercise, p 34, Boca Raton, 2008, CRC Press, Taylor and Frances be 30% or less, and recommends that 10% come from poly-
Group. Adapted from Sherman WM, Costill DL, Fink WJ, Miller JM: unsaturated, 10% from monounsaturated, and a range of
Effect of exercise-diet manipulation on muscle glycogen and its 7% to 10% from saturated fats per day.
subsequent utilization during performance, Int J Sports Med 2: When discussing fat intake for athletes, these guidelines
114–118, 1981.)
may not be appropriate unless the athlete suffers from high
cholesterol or other implications that require a more strict
Aerobic training increases the cell’s number of mito- dietary fat intake. In general, fat intake among athletes var-
chondria and enzymes involved in fatty acid oxidation, ies depending on the sport in which they participate. For
thereby enhancing the athlete’s ability to burn fat as fuel instance, long-distance runners tend to consume lower fat
efficiently. This increased ability is demonstrated in four diets than short-distance runners and sprinters. Regardless,
distinct ways:25 (1) a more efficient use of oxygen; (2) more the position of the American Dietetic Association states that
oxygen can be used at a given work load; (3) less glycogen athletes should not restrict their dietary fat intake because
and more fat used to meet energy needs; and (4) lower there is no performance benefit of very low fat diets (15%
lactate production, representing more complete oxidation total energy intake) when compared with moderate fat diets
Table 4-13
Protein Sources
Type Nutritional Breakdown Food Sources
Lean sources, serving size 1 oz 55 cal, 0 g CHO, 7 g protein, 3 g fat Lean beef and pork
Fish
Poultry without skin
Medium-fat sources, serving 75 cal, 0 g CHO, 7 g protein, 5 g fat Ground beef
size 1 oz (or otherwise noted) Skim/part skim mozzarella, ricotta
4 oz tofu
1 egg
High-fat sources, serving size 100 cal, 0 g CHO, 7 g protein, 8 g fat Corned beef, spare ribs, cheese
1 oz (or otherwise noted) (cheddar, Swiss), cold cuts
1 hot dog
1 tbsp peanut butter
Dairy, nonfat 90-150 cal, 12 g CHO, 8 g protein, 0 g fat 8 oz skim milk
Nonfat yogurt
Dairy, low fat, 1%-2% 90-150 cal, 12 g CHO, 8 g protein, 3-5 g fat 8 oz 1%-2% milk
Plain low fat yogurt, 1%-2%
Dairy, high fat 90-150 cal, 12 g CHO, 8 g protein, 8 g fat 8 oz whole milk
1
Vegetables 25 cal, 5 g CHO, 2 g protein, 0 g fat ⁄2 c cooked or 1 c raw
Fruit and fat contain no protein
Cal, Calories; CHO, carbohydrate; c, cup; g, gram; oz, ounce; tbsp, tablespoon.
Data from: American Diabetic Association.
Nutrition Counseling and Athletes • CHAPTER 4 85
Breakfast Breakfast
4 oz. orange juice
1 cup hot cereal
1 piece fresh fruit
1 tsp. margarine
4 oz. low-fat milk
Lunch Lunch
4 oz. apple juice
1 cup vegetarian chili
1 cup tossed salad
1 tbsp. Italian dressing
1 slice whole-grain bread
1 tsp. margarine
Snack Snack
Figure 4-3 1 piece fresh fruit
Vegetarian food pyramid. (Adapted from the U.S. Department of
Agriculture and U.S. Department of Health and Human Services: Nu- Dinner Dinner
trition and your health: Dietary guidelines for Americans, Washington,
DC, 2005, U.S. Government Printing Office; www.mypyramid.gov; 1 cup pasta entree with
and General Conference [of Seventh-day Adventists] Nutrition Coun- vegetables (with 1 tbsp. oil)
cil: My vegetarian food pyramid, Silver Spring, MD, 2006.) 4 oz. sauteed tofu
or
1 cup bean soup
1 slice whole-grain bread
(20% to 25% total energy intake).3 Athletes should be 8 oz. low-fat milk
encouraged to consume a diet that consists of 20% to 35%
Snack Snack
of total energy from fat and limit saturated fat intake to 10%
or less, but discouraged from very low fat diets (15% or less 1 sesame roll
of total energy), given the importance of fat within the 1 tbsp. peanut butter
4 oz. low-fat milk
body and fat energy use during exercise.
Dietary sources of fat include added fats and hidden fat Figure 4-4
sources (Table 4-14). Examples of added fats are butter, Sample lactovegetarian menu. (From the Massachusetts General
margarine, oils, mayonnaise, and salad dressings. Fat found Hospital Department of Dietetics.)
in meat, the skin of poultry, nuts, seeds, and baked products
are examples of hidden fats. Because fat consumed in
amounts in excess of body needs is most likely to be stored
in the form of adipose tissue, reducing total fat intake is one Table 4-14
way to reduce total calories. Alcohol promotes fat storage;26 Dietary Sources of Fats
therefore, it may be beneficial to count alcohol calories
Type* Source
as part of the athlete’s total fat allowance if the athlete
consumes alcohol regularly. Saturated Animal fats
Butter fat
Alcohol Cocoa butter
Although alcohol has a high caloric content (7 kcal/g), it Palm and coconut oils
has limited food value. Alcohol acts on the brain Hydrogenated oils
by depressing its ability to reason and make judgments. Polyunsaturated Most vegetable oils (corn,
Information-related processes are slowed; fine-motor skills safflower, sunflower, etc.)
are decreased; reaction time is reduced; coordination, Soybean oil
Fish oils
balance, and visual perception are altered; and muscular
Monounsaturated Canola oil
reflexes are impaired.
Olive oil
Alcohol can weaken myocardial contractility and dimin-
ish sprinting, middle distance,27 and endurance perfor-
*All fats contain 9 kcal per gram.
mance.28 One of the most harmful effects of alcohol in an
athletic event is evident in prolonged endurance contests.
The liver is the primary organ for the detoxification of alco-
hol. Once alcohol is present in the blood, the metabolism
86 SECTION I • Preparation and Prevention in Sports Medicine
of alcohol takes priority over other liver functions. An ele- performance improvement with vitamin and mineral sup-
vated level of blood alcohol may block the biochemical plementation in either aerobic or anaerobic exercise within
pathway that supplies extra glucose to the body. A drop in nutritionally adequate healthy people. However, because
blood glucose during an endurance event could lead to there have been reports of toxic effects of pyridoxine
early fatigue. (vitamin B6) and niacin, supplementation in large doses is
Peak concentration of alcohol in the blood occurs within not recommended. Table 4-15 lists food sources for these
1 hour of consumption, depending on whether or not food vitamins.
is in the stomach. Because the absorbed alcohol is distrib- Vitamin C, also known as ascorbic acid, is used in the
uted within the water compartments of cells, it can disturb synthesis of collagen, oxidation of fatty acids, epinephrine,
the water balance in muscle cells and consequently alter the and anti-inflammatory corticoids of the adrenal gland. It
cellular enzymatic activity producing adenosine triphos- also aids in healing, facilitates iron absorption, and is con-
phate, the substrate that provides fuel for muscle contrac- sidered an antioxidant. Vitamin C also serves as a protector
tion, active transport, and biosynthesis within the body.29 against oxidative stress within endurance athletes, including
Body size and composition alters dose response; a small, upper respiratory infections. Supplementing vitamin C is
lean athlete is likely to experience fatigue sooner than a popular among athletes, possibly as a result of its role in the
larger person with more body fat. healing process and the expectation that high doses of vita-
min C will improve physical performance, which appears to
be unfounded.31 Well-controlled studies have reported
Micronutrients no benefits of vitamin C supplementation on strength,
Micronutrients are vitamins (Table 4-15) and minerals. maximum oxygen consumption, or aerobic capacity.32-36
Vitamins are complex organic compounds and exist in very Athletes should be encouraged not to exceed the UL for
small quantities in foods. The role of vitamins is in the vitamin C—adequate diet will supply enough vitamin C
action of several hundred enzymes that serve as catalysts to without supplementation.
body function such as muscle contraction, digestion, ab-
sorption, and metabolism. The findings of studies evaluat- Fat-Soluble Vitamins
ing the effectiveness of high-level vitamin or mineral supple- The fat-soluble vitamins are A, D, E, and K (see Table 4-15),
mentation on athletic performance lead to the conclusion which are stored in the body in fat. Because these vitamins
that large therapeutic doses of vitamins and minerals are not are stored in the body, excess intake can lead to toxicity.
useful in improving athletic performance.30 However, There are few studies on the relation of vitamins A, D, and
focusing on the quality of the athlete’s caloric intake to K regarding physical performance. Vitamin E, an antioxi-
ensure that the vitamins and minerals necessary for optimal dant, is well known for its role within immune function and
functioning of energy metabolic process are present is of prevention of cell membrane free radical damage.13 As with
primary importance. Physical activity increases the need for vitamins A, D, and K, no reports have shown improved ex-
some vitamins and minerals; however, the increased need ercise performance with supplemental vitamin E. Table 4-15
can be met by a diet that provides a variety of foods and is lists food sources of fat-soluble vitamins.
high in complex carbohydrates, moderate in protein, and
low in fat. Individuals who consume a low-calorie diet are Minerals
at risk for low vitamin and mineral intake. When it comes to exercise metabolism, minerals are equally
as important as vitamins. Minerals serve multiple roles
Water-Soluble Vitamins within the body. More specifically, minerals help regulate
The classification of vitamins is based on their solubility metabolism; provide structure for bone formation, and play
within the body. Water-soluble vitamins are those that do functional roles within the cardiac and neural systems.12 As
not require fat for their absorption. Vitamins within this with vitamins, minerals can be classified into two categories:
category include vitamin C and the B complex vitamins. trace or major.
These vitamins act as co-enzymes or co-factors in metabolic Trace Minerals. Trace minerals include iron, zinc,
reactions involved in the oxidation of food and the produc- copper, selenium, iodide, fluoride, chromium, manganese,
tion of energy. Water soluble vitamins are not stored, and molybdenum, boron, and vanadium. They are called trace
therefore need to be consumed on a daily basis. minerals simply because they are found in smaller amounts
The B complex vitamins thiamin, riboflavin, niacin, pyri- within the body. Of all of the trace minerals, iron is the only
doxine, cyanocobalamin (B12), pantothenic acid, folacin, one for which exercise may increase an athlete’s required
and biotin, work together to ensure proper digestion, intake, especially if they suffer from iron-deficiency anemia
muscle contraction, and energy release. or become iron depleted.
Through the years, there has been speculation as to Iron. Iron is a component of hemoglobin and myoglo-
whether or not supplementations of the B complex bin, and plays a key role in making oxidative metabolism
vitamins enhance energy release, thus enhancing overall possible. Problematic factors related to iron associated with
performance. The latest research fails to show significant exercise are hemolysis of erythrocytes, alterations in iron
Nutrition Counseling and Athletes • CHAPTER 4 87
metabolism, hematuria, increase in erythrocyte osmotic is warranted, the DRI should be taken into consideration
fragility resulting in decreased red blood cell survival time, before supplementing.
and a possible shift in the oxygen dissociation curve.37 Calcium. Many athletes who have low body weight do
Athletes, especially endurance athletes, tend to have not consume enough calories or choose low-nutritional-
lower hemoglobin concentrations than nonathletes, placing quality foods and, therefore, do not consume adequate
them at greater risk for iron-deficiency anemia. Sports ane- calcium. Calcium is necessary for the contractile ability of
mia, a condition in which hemoglobin levels tend to be at muscles, the maintenance of healthy bones and teeth, blood
the low end of the normal range when all other blood clotting, and nerve transmission. Because bone formation
parameters remain normal, is not a true anemia. This can and dissolution is a continuous process, calcium must be
occur in all athletes initiating a period of intense exercise, as supplied to the cells on demand. When dietary calcium is
well as the general public just starting an exercise program, low, the body draws from its own reserves in bone, which
and is caused by the quick increase in blood volume. Blood reduces bone density and can lead to stress fractures.
concentration becomes diluted as a result of this rapid Women are at higher risk because, overall, they have thinner
change, and causes hemoglobin to show up relatively low bones (bones that are not as dense) and as they mature,
during a blood test. After 1 to 2 months of consistent train- they lose bone density at a faster rate. Amenorrhea, found
ing, blood concentration returns to normal and the sports in many female athletes, is also associated with decreased
anemia is remedied.38 spinal bone mass.39
The most common cause of true anemia in athletes is iron Osteoporosis is a major health concern for women.
deficiency anemia. Research suggests that female athletes, Calcium intake; estrogen level; alcohol, caffeine, and pro-
distance runners, and vegetarian athletes are at greatest risk tein intake; family history; and the type and amount of
to become iron-deficient. However, they are not the only physical activity are all related to the development of osteo-
athletes at risk of iron-deficiency anemia. Factors that lead to porosis. Ninety-nine percent of dietary calcium is deposited
increased risk of iron deficiency anemia include (1) decreased in the bone. Increased physical activity improves the effi-
dietary intake of foods rich in iron; (2) high demand for ciency of calcium use and is important for the maintenance
myoglobin, hemoglobin, and energy-producing enzymes; of optimal bone mass and strength.
(3) demands of the sport; and (4) loss of iron through The DRIs for calcium are listed in Tables 4-3 and 4-5.
sweat.38 Supplemental iron should only be advised for those Athletes at risk for early osteoporosis, amenorrhea, or have
athletes in whom true iron deficiency has been diagnosed. disordered eating may require up to 1500 mg/day of ele-
Normalizing iron levels improves endurance and perfor- mental calcium and a recommended 400 to 800 IU per day
mance in the iron-deficient athlete. On the flip side, supple- of Vitamin D.3 Table 4-17 lists dietary and supplemental
mentation of iron by athletes whose iron stores are normal sources of calcium.
and dietary intake of iron (Table 4-16) is adequate will prob- Sodium. Sodium is an essential mineral needed to regu-
ably not see any increase in performance and the supplemen- late water balance in the cells and to maintain blood volume
tation may be harmful to the athletes. If an athlete is supple- and normal nerve and muscle activity. Sodium increases the
menting iron based on a physician’s recommendation, is absorption of fluids in the small intestine and helps to main-
taking a daily multiple vitamin with iron to meet the RDA tain the osmotic drive for drinking and reduces water clear-
for iron, or is consuming dietary sources of iron, the follow- ance associated with reduced serum electrolyte concentration
ing are recommendations to enhance absorption: (1) include that results from electrolyte losses during exercise. In athletes
a source of vitamin C at the same time and (2) do not con- who train daily at high intensity or in high temperatures, a
sume iron within 1 hour of having coffee or tea, because prolonged state of hypohydration can occur. Rehydration
these interfere with iron absorption. occurs when a dilute solution of sodium rather than plain
water is consumed under these conditions.40
Clinical Note Sodium makes up as much as 40% of common table salt
(chloride constitutes the remaining approximately 60%).
Sports anemia is a condition in which hemoglobin levels tend to be Requirements for sodium vary with age, environmental
at the lower end of normal range and all other blood parameters are conditions, and level of activity. However, it is recom-
normal. mended that a healthy, sedentary adult consume 1500 to
2400 mg per day, which can be achieved by consuming a
typical American diet. During prolonged exercise in
Major Minerals. Calcium, phosphorus, magnesium, hot weather, sodium losses in sweat and urine may exceed
sulfur, potassium, sodium, and chloride are classified as 10 g per day. The sodium concentration of sweat is
major minerals, or minerals that are essential to life.12,13 approximately 50 mEq/L; the average daily urine sodium
Like trace minerals, most major minerals occur naturally loss is 120 mEq/L.41 Therefore, an athlete working out
within our environment. As with vitamins, if an adequate 4 hours per day and losing sweat at a moderate rate of
diet is maintained, no supplementation is required. How- 1.5 L per hour may benefit from an electrolyte replacement
ever, if medical evaluation determines that supplementation drink containing 0.5 to 0.7 g/L of sodium or a slightly
88
SECTION I • Preparation and Prevention in Sports Medicine
Table 4-15
Vitamins: Food Sources and Recommended Amounts
Adult DRI*
Vitamin (AI if no DRI) Major Food Sources What it Does Potential Benefits Supplementation
A Males: 900 mcg/day Carrots, broccoli, tomatoes Promotes good vision; helps May inhibit the development Not recommended because
Females: 700 mcg/day form and maintain skin, of certain tumors; may in- it is toxic in high doses
teeth, bones, and mucous crease resistance to infection
membranes in children
Deficiency can increase suscep-
tibility to infectious disease
C Males: 90 mg/day Citrus fruits and juices, Helps promote healthy gums May reduce the risk of certain 250-500 mg a day for
Females: 75 mg/day strawberries, tomatoes, and teeth; aids in iron absorp- cancers, as well as coronary anyone not consuming
peppers (especially red), tion; maintains normal con- artery disease; may prevent several fruits or vegetables
broccoli, potatoes, kale, nective tissue; helps in healing or delay cataracts rich in C daily and for
cauliflower, cantaloupe, of wounds smokers
brussel sprouts As an antioxidant, it combats Larger doses may cause
the adverse effects of free diarrhea
radicals
D Males and females: Milk, fish oil, fortified Promotes strong bones and May reduce the risk of 400 IU for people who do
5 mcg/day (AI) margarine; also produced teeth by aiding the absorption osteoporosis not drink milk or get sun
by the body in response to of calcium exposure, especially strict
sunlight Helps maintain blood levels of vegetarians and elderly
calcium and phosphorus Toxic in high doses
E Males and females: Vegetable oil, nuts, margarine, Helps in the formation of red May reduce the risk of certain 200 to 800 IU advised for
15 mg/day wheat germ, leafy greens, blood cells and the use of cancers, as well as coronary everybody; you cannot get
seeds, almonds, olives, vitamin K artery disease; may prevent that much from food,
asparagus As an antioxidant, it combats or delay cataracts; may especially on a low-fat diet
the adverse effects of free improve immune function in No serious side effects at
radicals the elderly that level, although
diarrhea and headaches
have been reported
K Males: 120 mcg (AI) Intestinal bacteria produce Essential for normal blood May help maintain strong Not necessary, not
Females: 90 mcg (AI) most of the K needed by the clotting bones in the elderly recommended
body
The rest is supplied by leafy
greens, cauliflower, broccoli,
cabbage, milk, soybeans,
and eggs
Thiamin Males: 1.2 mcg/day Whole grains, enriched grain Helps cells convert Unknown Not necessary, not
Females: 1-1.1 mcg/ products, beef liver, oysters, carbohydrate into energy recommended
day peanuts, green peas, raisins, Necessary for healthy brain,
collard greens, brewer’s yeast nerve cells, and heart
function
Riboflavin Males: 1.3 mg/day Dairy products, liver, meat, Helps cells convert Unknown Not necessary, not
Females: 1-1.1 mg/ chicken, fish, enriched grain carbohydrate into energy recommended
day products, leafy greens, beans, Essential for growth, produc-
nuts, eggs, almonds tion of red blood cells, and
health of skin and eyes
Niacin Males: 16 mg/day Nuts, meat, fish, chicken, liver, Aids in the release of energy Large doses lower elevated Megadoses may be
(B3) Females: 14 mg/day enriched grain products, from foods blood cholesterol prescribed by doctor to
dairy products, peanut Helps maintain healthy skin, lower blood cholesterol
butter, brewer’s yeast nerves, and digestive system May cause flushing, liver
damage, and irregular
heartbeat
B6 Males: 1.3-1.7 mg/ Whole grains, bananas, meat, Vital in chemical reactions of May boost immunity in the Megadoses can cause
day beans, nuts, wheat germ, proteins and amino acids elderly numbness and other
Females: 1.2-1.5 mg/ brewer’s yeast, chicken, fish, Helps maintain brain function neurological disorders
day liver and form red blood cells
B12 Males and females: Liver, beef, pork, poultry, Necessary for development of Unknown Strict vegetarians may need
2.4 mcg eggs, milk, cheese, yogurt, red blood cells. Maintains supplements
Continued
89
90
SECTION I • Preparation and Prevention in Sports Medicine
Table 4-15
Vitamins: Food Sources and Recommended Amounts—cont’d
Adult DRI*
Vitamin (AI if no DRI) Major Food Sources What it Does Potential Benefits Supplementation
Panto- Males and females: Whole grains, beans, milk, Vital for metabolism of food Unknown Not necessary, not
thenic 5 mg (AI) eggs, liver and production of essential recommended
body chemicals May cause diarrhea
AI, Adequate intake; DNA, deoxyribonucleic acid; DRI: dietary reference intake.
*DRI values adopted from the National Academy of Science.
Among the achievements for which this century will surely be remembered is the discovery of vitamins, a scientific advance truly beneficial to humanity. For hundreds of years, of course,
people had noticed that certain foods seemed to prevent diseases—most famously, the limes and lemons that British sailors ate to ward off scurvy—but the first vitamin was isolated in the
laboratory only in 1911. That was thiamin, a B vitamin. Now 13 vitamins are known. In the past, vitamins were discussed in terms of preventing deficiency diseases (beriberi, caused by a lack
of thiamin, for instance; or scurvy, caused by a lack of vitamin C). The recommended dietary allowances, devised by scientists in the United States and revised and updated over the years,
were designed partly to prevent such deficiency diseases and partly to meet the needs, as they were understood, of healthy people.
But we still have much to learn about the functions of these powerful chemicals. Indeed, in the last decade alone, hundreds of scientific studies have found that vitamins play a much larger
role in health than was dreamed of even 20 years ago.
What Is a Vitamin?
Vitamins are organic substances required to regulate the functioning of cells. They are essential to life. They take part in myriad biological processes, among them promoting good vision,
forming normal blood cells, creating strong bones and teeth, and ensuring the proper function of the heart and nervous system. Although vitamins supply no energy, they do aid in the
conversion of foods into energy. The 13 vitamins fall into two categories: fat-soluble (A and its precursor betacarotene, D, E, and K) and water-soluble (the B vitamins and C). This
distinction is important because the body stores fat-soluble vitamins in the liver and fatty tissue for relatively long periods (many months), but it stores the water-soluble vitamins for only a
short time (up to a few weeks). In general, you have to consume vitamins: the body cannot manufacture them (though it does synthesize some vitamin K, D, and B12 and convert
betacarotene into vitamin A). For a description of the specific functions of each vitamin, consult the chart.
Who Needs Supplements?
If you follow the government’s dietary recommendations, you may not need supplements to meet the DRIs. Still, we think it’s wise for adults to consume extra amounts of antioxidants
(vitamin E and C and betacarotene), and for premenopausal women to eat a folacin-rich diet or take supplements (see chart for recommended amounts). Most people do not need a daily
multivitamin and mineral supplement, although millions of Americans take one. It can’t be said too often that a pill a day won’t turn poor diet into a healthy one. However, elderly people,
especially those who may have reduced their food intake for any reason, may benefit from a daily multivitamin. So may frequent aspirin takers, heavy drinkers, smokers, and those with
impaired immune systems. Pregnant women have special needs and should follow professional advice. Taking huge doses of most vitamins is not wise. Some vitamins—A and D,
specifically—are toxic in large doses. Others, like niacin, have serious side effects in the large doses described on the chart.
Modified from the University of California at Berkeley Wellness Letter. Health Letter Associates, 1994.
Nutrition Counseling and Athletes • CHAPTER 4 91
Table 4-16
Dietary Sources of Iron
Fluids
Nonvegetarian When it comes to optimal performance, adequate hydration
Sources of Iron Vegetarian Sources of Iron plays a leading role. To prevent dehydration, athletes should
be encouraged to hydrate before, during, and after exercise.3
5 mg/Serving 4-9 mg/Serving Dehydration adversely affects muscle strength, endurance,
Liver (high in choles- Fortified cooked cereal, and coordination. It also increases the risk of cramps, heat
3
terol), 3 oz ⁄4 cup exhaustion, and life-threatening heat stroke.43,44 During
Oysters 1⁄2 cup Fortified dry cereal, 1 oz exercise, heat produced within working skeletal muscle is
3-5 mg/Serving 6-7 mg/Serving carried by the convective flow of blood to the body core,
1
Most beef, lean ⁄2 cup tofu
elevating its temperature and stimulating warm receptors
1-3 mg/Serving 3-4 mg/Serving
located in the anterior hypothalamus. In response to the rise
Fish, chicken Soybeans, 1⁄2 cup
Lentils, 1⁄2 cup in temperature, sweating is initiated. Sweat loss means the
Pumpkin/squash seeds, 1 oz loss of vital body fluids, which can result in circulatory and
thermal impairments if these fluids are not replaced. Fluid,
electrolyte, and energy supplementation are desirable during
exercise to support circulatory, metabolic, and thermoregu-
Table 4-17 latory functions and to maintain plasma volume.
Dietary Sources of Calcium To monitor fluid lost during training and exercise
Food Calcium (mg) sessions, the athlete should weigh before and after each ses-
sion. For each pound (0.45 kg) lost, 16 to 24 oz of fluid
Calcium-enriched bread, 2 slices 580 should be consumed.3 Sufficient fluids should ideally be
8 oz lactose-free, calcium-fortified 500
consumed during exercise so that weight remains constant
nonfat milk
before and after activity. It is important to drink fluids be-
8 oz yogurt, plain, nonfat 452
8 oz yogurt, low fat 415 fore becoming thirsty. Work capacity can be reduced by 10%
8 oz milk, skim 352 to 15% due to body fluid loss.
8 oz yogurt, fruit 314
Calcium-enriched orange juice, 8 oz 293
Swiss cheese, 1 oz 272
Clinical Note
Dry cereal, 3⁄4 cup (variable amount) 250
Cheddar cheese, 1 oz 204 To monitor fluid loss during activity, the athlete should be weighed
Sardines, canned in water with bones, 185* before and after each session. For each pound lost, 16 to 24 oz of
2 oz fluid should be consumed.
Mozzarella, 1 oz 183
Tofu with calcium sulfate, 3 oz 150†
Almonds, 1⁄4 cup 94
Broccoli, turnip greens, 1⁄2 cup 36
The process of rehydration depends on both gastric
*Average of major brands.
emptying and intestinal absorption. For exercise longer
†
Estimates of brands. than 60 to 90 minutes, using a 6% to 8% carbohydrate solu-
Supplements: calcium carbonate (e.g., Tums) is better absorbed with tion (e.g., diluted fruit juice, Gatorade) during the event
meals; calcium citrate (e.g., enriched orange juice, tablets) is better optimizes stamina and endurance, because the carbohydrate
absorbed on an empty stomach. helps to maintain normal blood glucose levels and to
provide energy for muscle.45 Highly concentrated sweets
(i.e., greater than 8%) tend to empty more slowly from the
more liberal use of sodium with meals. Concentrated salt stomach than diluted fluids and impair fluid absorption.
tablets are generally not recommended and may actually be Therefore, it is not recommended that high-concentrate
harmful. Acclimatization to heat or exercise can compen- sweets be taken during the event.46 Cold fluids help cool
sate for some, but not all, sodium loss.42 Heat-acclimated core body temperature and leave the stomach more rapidly
subjects lose considerably less salt at a given sweat rate than than warm fluids.
their unacclimated counterparts. The amount of sodium Once the gastric contents empty into the small intestine,
lost increases as sweat rate increases. During exercise bouts this solution must be absorbed before any benefit of hydration
lasting more than 3 hours, sodium losses can result in is realized. Absorption from the small intestine is accelerated
hyponatremia, a plasma sodium content of less than by the combination of glucose and sodium.47 It has been
130 mEq sodium/L, a potentially fatal condition that can reported that the most effective glucose-to-sodium ratio
be prevented.40 promoting water absorption is 2:1.40,48
92 SECTION I • Preparation and Prevention in Sports Medicine
Table 4-18
Carbohydrate Content of Food and Beverages
CHO CHO
Food (grams) Beverages (grams/8 oz)
Apple 21 Gatorade 14
Banana, large 40 Apple juice 30
Baked potato, large 51 Powerade 19
Yogurt, fruited (1 cup) 40 Orange juice 26
Bread, whole wheat (2 slices) 22 Cranapple juice 43
Bagel, medium 50 G2 18
Raisins (2⁄3 cup) 79 Low-fat chocolate milk (1 cup) 26
Rice (1 cup) 50 All Sport 20
Spaghetti with sauce (1 cup) 37 Propel 3
Tortilla, flour (6”) 15 Endurox R4 35
Waffles, buttermilk (2 waffles) 29
CHO, Carbohydrates.
Nutrition Counseling and Athletes • CHAPTER 4 93
athlete’s performance. Because it truly is a science of interest 18. Tarnopolsky M, MacDougall D, Atkinson S: Influence of protein
to our population, the popular press will continue to sensa- intake and training status on nitrogen balance and lean body mass,
J Appl Physiol 64:187–193, 1988.
tionalize information regarding nutrition. Because of the lack
19. Marable NL, Hickson JF, Korslund M, et al: Urinary nitrogen
of governance over the diet and supplement industry, athletes, excretion as influenced by a muscle-building exercise program
health care providers, and the general public are encouraged and protein intake variation, Nutr Rep Int 19:795–805,
to seek out registered dietitians (the nutrition experts) for ac- 1979.
curate nutrition information, as well as to develop optimal 20. Burke L, Read R: Diet Patterns of elite Australian male triathletes,
Phys Sports Med 15:140–145, 1987.
nutrition plans for individualized performance enhancement.
21. Williams MH: The role of protein in physical activity. In William
MH, editor: Nutritional aspects of human physical and athletic
performance, Springfield, IL, 1985, Charles C Thomas.
22. Heaney RP: Protein intake and the calcium economy, J Am Diet
References Assoc 93:1261–1262, 1993.
23. Nordin BEC, Need AG, Morris HA, et al: Sodium, calcium and
1. Manore MM: Health screening and dietary assessment. In Dunford osteoporosis. In Burckhardt P, Heane RP, editors: Nutritional
M, editor: Sports nutrition—A practice manual for professionals, aspects of osteoporosis, New York, 1991, Raven Press.
ed 4, Chicago, 2006, American Dietetic Association. 24. Position of the American Dietetic Association: Vegetarian diets,
2. McArdle WD, Katch FI, Katch UL: Exercise physiology: Energy, J Am Diet Assoc 93(11):1317–1319, 1993.
nutrition and human performance, ed 2, Philadelphia, 1986, 25. Wright ED, Paige DM: Lipid metabolism and exercise, J Clin
Lea & Febiger. Nutr 7:28–32, 1988.
3. American College of Sports Medicine, American Dietetic Associa- 26. Berg FM: Alcohol promotes fat storage. Obesity Health Nov/Dec
tion, Dietitians of Canada: Nutrition and athletic performance, 107–108, 1993.
Med Sci Sport Exer 41(3):709–731, 2009. 27. McNaughton L, Preece D: Alcohol and its effects on sprint and
4. Brown J: Nutrition through the life cycle, Belmont, 2002, middle distance running, Br J Sports Med 20:56–59, 1986.
Wadsworth/Thomas Learning. 28. Houmard JA, Langenfeld ME, Wiley RL, et al: Effects of the acute
5. Pennington JAT, Spungen DB: Bowe’s and Church food values of ingestion of small amounts of alcohol on 5-mile run times,
portions commonly used, ed 18, Baltimore, 2005, Lippincott J Sports Med 27:253–257, 1987.
Williams & Wilkins. 29. Berning J, McKibben G, Benardot D, et al: Fuel supplies for exer-
6. Jonnalagadda SS: Dietary fat and exercise. In Dunford M, editor: cise in sports nutrition. In Benardot D, editor: Sports nutrition:
Sports nutrition—A practice manual for professionals, ed 4, A guide for the professional working with active people, ed 2, Chi-
Chicago, 2006, American Dietetic Association. cago, 1992, American Dietetic Association.
7. Prochaskas J, DiClemente C, Morcross J: In search of how people 30. Keith RE: Vitamins in sports and exercise. In Wolinsky I, Hickson
change: Applications to addictive behaviors, Am Psychol 47(9): JF, editors: Nutrition, exercise and sport, Boca Raton, FL, 1989,
1102–1114, 1992. CRC Press.
8. Coleman EJ: Carbohydrate and exercise. In Dunford M, editor: 31. Gerster H: The role of vitamin C in athletic performance, J Am
Sports nutrition—A practice manual for professionals, ed 4, Coll Nutr 8:636–643, 1989.
Chicago, 2006, American Dietetic Association. 32. Baily D, Carron AV, Teece RD: Effect of vitamin C supplementa-
9. Sherman WM, Lamb DR: Nutrition and prolonged exercise. tion upon the physiological response to exercise in trained and
In Lamb DR, Murray R, editors: Perspectives in exercise science and untrained runners, Int Z Vitaminforsch 40:435–441, 1979.
sports medicine: Prolonged exercise, Indianapolis, 1988, Benchmark 33. Henschel A, Taylor H, Brozek J, et al: Vitamin C and ability to
Press. work in hot environments, Am J Trop Med Hyg 24:259–265,
10. Roberts KM, Noble EG, Hayden DB, et al: Simple and complex 1944.
carbohydrate-rich diets and muscle glycogen content of marathon 34. Howald H, Segesser B: Ascorbic acid and athletic performance,
runners, J Appl Physiol 57:70–74, 1988. Ann NY Acad Sci 258:458–464, 1975.
11. Burke LM, Kiens B, Ivy JL: Carbohydrates and fat for training and 35. Keren G: The effect of high dosage vitamin C intake on aerobic
recovery, J Sports Sciences 22:15–30, 2004. and anaerobic capacity, J Sports Med Phys Fitness 20:145–148,
12. McArdle WD, Katch FI, Katch VL: Sports and exercise nutrition, 1980.
ed 3, Baltimore, 2008, Lippincott Williams & Wilkins. 36. Rasch P, Arnheim D, Klafs C: Effects of vitamin C supplementa-
13. Doyle JA, Papadopoulos C, Green MS: Utilization of carbohy- tion on cross-country runners, Sportsartzliche Prax 5:10–13,
drates in energy production. In Wolinsky I, Driskell JA, editors: 1962.
Sports nutrition energy metabolism and exercise, Boca Raton, 2008, 37. Clement DB, Sawchuk LL: Iron status and sports performance,
CRC Press, Taylor and Francis Group. Sports Med 1:65, 1984.
14. Position of the American Dietetic Association and the Canadian 38. Fink HH, Burgoon LA, Mikesky AE: Practical applications in
Dietetic Association: Nutrition for physical fitness and athletic sports nutrition, Sudbury, MA, 2006, Jones and Bartlett.
performance for adults, J Am Diet Assoc 93(6):691–696, 1993. 39. Drinkwater BL, Nilson K, Chestnut CH, et al: Bone mineral content
15. Volpe SL: Vitamins, mineral, and exercise. In Dunford M, editor: of amenorrheic and eumenorrheic athletes, N Engl J Med 311:
Sports nutrition—A practice manual for professionals, ed 4, 277–281, 1984.
Chicago, 2006, American Dietetic Association. 40. Gisolfi CV, Duchman SM: Guidelines for optimal replacement
16. Berning J, McKibben G, Bernardot D, et al: Fuel supplies for beverages for different athletic events, Med Sci Sports Exerc
exercise. In Bernardoe D, editor: Sports nutrition: A guide for the 24(6):679–687, 1992.
professional working with active people, ed 2, Chicago, 1992, The 41. Hiller WDB: Dehydration and hyponatremia during triathlons,
American Dietetic Association, Chicago. Med Sci Sports Exerc 21:S219–S221, 1989.
17. Otten JJ, Hellwig JP, Meyers LD. Dietary reference intakes: 42. Morimoto T, Miki K, Nose H, et al: Changes in body fluid and its
The essential guide to nutrient requirements, Washington, 2006, composition during heavy sweating and effect of fluid electrolyte
National Academies Press. replacement, Jon J Biometeorol 18:31–39, 1981.
Nutrition Counseling and Athletes • CHAPTER 4 97
43. Nadel ER: Limits imposed on exercise in a hot environment, 50. World Anti-Doping Agency accessed at www.wada-ama.org.
Sports Sci Exchange 3:27, 1990. 51. Coyle EF: Carbohydrates and athletic performance, Sports Sci
44. Sawka MN, Pandolf KB: Effects of body water loss on physiologi- Exchange 1(7):October, 1988.
cal function and exercise performance. In Gisolfi CV, Lamb DR, 52. Cummings S: Obesity management. In Carlson KM, Eisenstat S,
editors: Perspectives in exercise science and sports medicine, Vol 3: editors: Primary care of women, Chicago, 1995, Mosby Year
Fluid homeostatis during exercise, Indianapolis, 1990, Benchmark Book.
Press. 53. Luder E, Schebendach J: Nutrition management of eating
45. Coggan AR, Coyle EF: Carbohydrate ingestion during prolonged disorders, Top Clin Nutr 8:48–63, 1993.
exercise: Effects on metabolism and performance, Exerc Sports Sci 54. Rock CL, Yager J: Nutrition and eating disorders: A primer for
Rev 19:1–40, 1991. clinicians, Int J Eat Disord 6:267–280, 1987.
46. Coyle EF, Montain SJ: Benefits of fluid replacement with carbohy- 55. Reiff DW, Reiff KKL: Eating disorders: Nutrition therapy in the
drate during exercise, Med Sci Sports Exerc 24(Supplement 9): recovery process, Gaithersburg, MD, 1992, Aspen.
S324–S330, 1992. 56. American Psychiatric Association: Diagnostic and statistical man-
47. Leiper JB, Maughan RJ: Comparison of absorption rates from two ual of mental disorders, ed 4, Washington, DC, 1994, American
hypotonic and two isotonic rehydration solutions in the intact Psychiatric Association.
human jejunum, Clin Sci 75(Supplement 19):22P, 1988. 57. Foreyt JP, Goodrick GK: Factors common to successful therapy
48. Lifshitz F, Wapnir RA: Oral hydration solutions: Experimental for the obese patient, Med Sci Sports Exerc 23:292–297, 1991.
optimization of water and sodium absorption, J Pediatr 106: 58. Wilmore JH: Body weight standards and athletic performance.
383–389, 1984. In Brownell KD, Rodin J, Wilmore JH, editors: Eating, body
49. US Olympic Committee: Drug Control Program, Committee on weight and performance in athletes: Disorders of modern society,
Substance Abuse Research and Education, 1986. Philadelphia, 1992, Lea & Febiger.
5
CHAPTER
ENVIRONMENTAL CONSIDERATIONS
FOR SPORTS
Travis L. Francis and Rich Bomgardner
98
Environmental Considerations for Sports • CHAPTER 5 99
Heat Exposure
Core Temperature Responses
to Exercise-Heat Stress
During physical exercise in ambient conditions that allow
steady-state heat balance, core temperature initially increases
rapidly and then increases more slowly until heat loss equals
heat production (Figure 5-2). The initial increase in core
temperature is due to a lag in the activation of the heat dis-
sipation mechanisms (i.e., sweating, cutaneous vasodilata-
tion). The magnitude of increase in core temperature is
proportional to the metabolic rate (e.g., the exercise inten-
sity) and is nearly independent of environmental conditions
within a range of climatic conditions termed the prescriptive
zone (Figure 5-3).2-6 The prescriptive zone refers to a range Figure 5-3
of ambient air conditions in which there is little or no differ- Relationship of steady-state core temperature responses and the “old”
effective air temperature at three metabolic rates. Effective air temper-
ence in steady-state exercise core temperature despite vary- ature derived from dry and wet bulb temperature, and wind speed.
ing ambient air conditions. During exercise in climatic con- (Modified from Lind AR: A physiological criterion for setting thermal
ditions above the prescriptive zone, the steady-state core environmental limits for everyday work, J Appl Physiol 18:51, 1963.)
temperature is elevated in proportion to the climatic condi-
tions. Therefore, steady-state body core temperature will
be similar during exercise in a temperate (20°C to 28°C/ the core temperature increase widens the temperature gra-
68°F to 82.5°F) environment, but will be elevated when dient between the body core and the skin, preserving heat
performing the same exercise in hot environments. Equally transport to the peripheral circulation despite lower skin
important, Figure 5-3 illustrates that the upper end of the blood flow.
prescriptive zone is shifted to a lower ambient temperature
condition with increasing exercise intensity. This means
that core temperature will begin to be affected by environ- Clinical Point
mental conditions at a lower ambient temperature when
performing high-intensity exercise than during moderate- or During exercise, the core temperature increase is the result of inte-
low-intensity exercise. grated physiological responses that optimize skeletal muscle perfusion
and heat transport without compromising arterial blood pressure.
The core temperature increase during endurance exer-
cise does not reflect a failure of the temperature control
system. On the contrary, core temperature is finely regu-
lated even under extremes of exercise and environmental
temperature. Under conditions in which skin blood flow is There are climatic conditions, however, in which steady-
compromised (e.g., dehydration, high exercise intensity), state core temperature values cannot be attained. Whenever
heat production exceeds the environment’s capacity to accept
heat, core temperature progressively increases, and individu-
als are at increased risk for heat exhaustion and heatstroke.
Athletes, race organizers, and trainers must evaluate the am-
bient weather conditions prior to beginning exercise and
modify the exercise intensity and duration, as well as fluid
requirements, to reduce the risk of heat injury.
Clinical Point
The American College of Sports Medicine has recommended that
Figure 5-2 endurance athletic events be rescheduled when the ambient wet
Esophageal and rectal temperature responses to rest and exercise during bulb globe temperature exceeds 28°C (82.4°F) (WBGT 0.7 Twb
compensable heat stress. (From Sawka MN, Wenger CB: Physiological 0.2 Tg 0.1 Tdb).
responses to acute exercise-heat stress. In Pandolf KB, Sawka MN,
Tdb, Dry bulb temperature; Tg, black globe temperature; Twb, wet bulb
Gonzalez RR, editors: Human performance physiology and environmen-
temperature.7
tal medicine at terrestrial extremes, p 110, Indianapolis, 1988,
Benchmark Press.)
Environmental Considerations for Sports • CHAPTER 5 101
L
ERATURE
L
L
Figure 5-4
Summary of cardiovascular responses to graded upright exercise in neutral (25.6°C, solid circles) and hot
(43.3°C, open triangles) environments. Heat stress–reduced cardiac output at the two higher workloads
and depressed stroke volume and central blood volume at all levels of exercise. Each data point is the
average of multiple measurements during each 15-minute exercise period from six men. The data points
in parentheses show where data from one subject are missing. (From Rowell LB: Human circulation:
Regulation during physical stress, p 379, New York, 1986, Oxford University Press.)
may be accompanied by a feeling of lassitude and increased or evening and spends the rest of the day in an air-
fatigue. Fortunately, repeated exposure to hot environ- conditioned room.
ments produces adaptations that improve an individual’s
work capacity during subsequent heat exposures. The
Clinical Point
physiological adjustments that improve work capacity in
the heat are collectively termed heat acclimatization. Heat acclimatization occurs in first week of heat exposure, is com-
As depicted in Figure 5-5, most heat acclimatization plete after 10 days of exposure, and occurs best when heat stress
occurs during the first week of heat exposure, and acclimatiza- and exercise are combined.
tion to a given environmental condition is virtually complete
after 10 days of exposure. Heat acclimatization leads to marked
reductions in exercise heart rate, core temperature, skin tem- Regular exercise in a cool environment has been shown to
perature, and the core temperature at which cutaneous vasodi- improve one’s ability to thermoregulate during exercise-heat
latation and sweating begin.32 There appears to be little change stress.34,35 The exercise-induced “internal” heat stress (e.g.,
in cardiac output, mean arterial pressure, pulse pressure, or increased core temperature) stimulates adaptation of the pe-
total vascular conductance with acclimatization.32 ripheral circulation and evaporative capacity, similar to what
occurs with heat exposure. As a result, aerobically trained
persons store less body heat during exercise than untrained
Heat Acclimatization Leads to a Decrease in: persons. However, regular exercise in a cool environment
• Exercise heart rate does not fully acclimatize an individual to exercise in a hot
• Core temperature environment, as regular training in a hot environment can
• Skin temperature further reduce the thermal and cardiovascular strain associ-
• Core temperature at which sweating and cutaneous vasodilation ated with exercise in a hot environment.36-39 Therefore, if
begins exercise is to be performed in hot weather, it is optimal to
acclimatize to that climate.
Figure 5-5
Rectal temperature, sweating rate, and heart rate responses over 9 consecutive days of exercise-heat
stress. Each data point is the average response of three men after 100 minutes of exercise in a desert
climate (49°Cdb, 17% rh). (Modified from Lind AR, Bass DE: Optimal exposure time for development
of acclimatization to heat, Fed Proc 22:704, 1963.)
104 SECTION I • Preparation and Prevention in Sports Medicine
Aging
Studies have documented that older populations have a
greater incidence of heat intolerance compared with younger
Figure 5-6 adults.51 The elderly also exhibit a larger-than-normal basal
Influence of dehydration on esophageal and rectal temperature dur- body temperature fluctuation compared with younger adults.52
ing 2 hours of moderately intense exercise. (From Montain SM, This latter liability appears to be largely due to a reduced cir-
Coyle EF: Influence of graded dehydration on hyperthermia and culatory effectiveness in controlling heat transport between
cardiovascular drift during exercise, J Appl Physiol 73:1340, 1992.)
the body core and the cutaneous circulation. Research sug-
gests, however, that aging per se is not responsible for the
negates the thermoregulatory advantage of heat acclimati- greater incidence of heat intolerance in the elderly.53,54 When
zation and aerobic training.43,44 Dehydration also increases matched for activity and aerobic fitness, and when exercise is
the perception of effort41 and reduces endurance exercise performed at the same relative percentage of maximal aerobic
performance.35,40,45 In addition, a recent study showed that capacity, older and younger adults have similar increases in
dehydrated subjects incurred exhaustion from heat strain at core temperature. In addition, aging per se does not impair
lower core temperatures than did normally hydrated sub- the ability to acclimatize to hot environments.53,54 The greater
jects during uncompensable heat stress, suggesting that incidence of heat intolerance observed in the elderly is now
dehydrated persons have a reduced tolerance to exercise- thought to result from functional changes accompanying a
heat strain.46 more sedentary lifestyle, obesity, a reduced sweating response,
To minimize dehydration, fluids should be ingested during cardiovascular insufficiency, and the effects of medication.51
prolonged exercise. The increase in core temperature during
Gender
Both men and women have similar thermoregulatory
Dehydration Leads to: responses during exercise and moderate heat stress when
• Elevated core body temperature matched for fitness and training.55-57 Yet differences between
• Elevated heart rate genders do exist. Women appear to sweat more efficiently
• Increases perception of effort than men in humid climates, because more of their secreted
• Negates heat acclimatization sweat is evaporated and less sweat drips from the body prior
• Reduces endurance to evaporation.57,58 The menstrual cycle produces regular
• Reduced tolerance to exercise heat strain fluctuations in basal body temperature. During the luteal
phase of the menstrual cycle, basal body temperature is
Environmental Considerations for Sports • CHAPTER 5 105
roughly 0.4°C (0.72°F) higher than during the follicular Populations Susceptible to Heat Intolerance
phase.59 Whether the phase of the menstrual cycle alters the Although the causal factors of heat intolerance are poorly
ability to regulate body temperature remains unresolved. Al- understood, there are a number of congenital and acquired
though several investigations reported that the luteal phase risk factors that have been associated with reduced heat
simply produces a graded increase in steady-state core tem- tolerance (Box 5-1). The identification of susceptible per-
perature during exercise, compared with exercise during the sons is important for reducing the risk of heat injury during
follicular phase,59,60 a separate investigation found that women work in hot weather.
were unable to achieve a steady-state core temperature during Congenital anomalies underlying heat intolerance usually
the luteal phase.61 The ability of women to effectively train impair the ability to produce and secrete sweat onto the skin
and compete throughout the menstrual cycle, however, sug- surface. Ectodermal dysplasia is the most common form of
gests that body temperature is adequately regulated during congenital anhidrosis (inadequate perspiration). It is attrib-
the luteal phase, albeit at a higher core temperature. uted to an autosomal-dominant or X-linked recessive trait
and therefore affects only males.64 The sweat glands of those
afflicted are either absent, functionally impaired, or histo-
To Reduce Heat Stress
logically present but not innervated. Patients with cystic
• Drink fluids before and during exercise (check body weight before fibrosis and Parkinson disease have altered neural sweat gland
and after exercise).
• Wear proper clothing.
• Modify exercise intensity (check heart rate).
Box 5-1 Factors Associated with Heat Intolerance
Functional-Physiological Factors
• Dehydration
Clothing • Low physical fitness/activity
Clothing impairs the ability to dissipate heat during exercise- • Lack of acclimatization
heat stress, because it creates a barrier for the transfer of heat • Surface area/mass ratio
between the skin and the environment. The properties of • Age
the clothing, such as its insulation properties and air and • Fatigue
vapor permeability, as well as the proportion of the body
Concurrent Disease
surface covered, determine the effect of clothing on
• Central nervous system lesions
body temperature regulation and exercise-heat tolerance. • Cardiovascular disease
Warm-weather clothing should be loose-fitting to permit • Sweat gland dysfunction
free circulation of air between the skin and the environment. • Infectious diseases
Furthermore, it should be light colored to reflect radiant • Psychiatric illness
light and minimize radiant heat gain in sunny weather. The • Diabetes mellitus
protective clothing worn by fire-fighters and soldiers on • Extensive skin burns
the chemical-biological battlefield greatly increases the • Hyperthyroidism
thermal and cardiovascular strain of exercise and reduces • Parkinsonism
physiological tolerance to heat strain.62,63 • Pheochromocytoma (vascular tumor of adrenal medulla or sympa-
thetic paraganglia characterized by hypersecretion of epinephrine
and norepinephrine causing hypertension)
Exercise Training in Hot Environments
Exercise training can be conducted safely in hot environ- Congenital Abnormalities
ments if precautions are taken to minimize the risk of heat • Ectodermal dysplasia
illness. Persons exercising in hot environments should • Linear skin dystrophy
attempt to attenuate dehydration by drinking fluids before • Idiopathic anhidrosis
and during exercise. Individual fluid requirements can be • Cystic fibrosis
• Scleroderma
estimated from body weight lost during exercise. Proper
clothing should be worn to minimize added heat stress dur- Drugs
ing the exercise bout. Finally, persons exercising in the heat • Drug abuse
should adjust the exercise intensity to accommodate circula- • Medications
tory strain accompanying exercise in hot environments. • Alcohol
Heart rate remains a reliable indicator of cardiovascular Other
strain during exercise-heat stress. Using the exercise heart • Clothing
rate to set the exercise intensity is a good method for reduc- • Previous heatstroke
ing thermal strain in hot climates. However, it should be Data from Epstein Y: Heat intolerance: predisposing factor or residual injury?
realized that this method reduces the training stimulus Med Sci Sports Exerc 22:29, 1990.
placed on skeletal muscle.
106 SECTION I • Preparation and Prevention in Sports Medicine
regulation, which may predispose them to heat intolerance thermoregulatory skin blood flow and skeletal muscle and
during environmental heat stress.65-67 vital organ blood flow. Individuals become fatigued, with
Several skin disorders, such as miliaria rubra (heat rash), orthostatic dizziness and ataxia. Common features include
impede heat transfer, increase heat storage, and impair dyspnea and tingling in hands and feet. Persons may be
performance.68-70 Psoriatic patients have been shown to disconsolate, uncoordinated, and mentally dull. Acute
have reduced sweating and elevated core temperatures dur- management should be focused on reducing cardiovascular
ing heat stress.70 Burn victims have an impaired ability to demand and reversing water and salt deficits.
sweat, and heat tolerance is negatively correlated with the
burnt skin area.51 Conversely, mild sunburn does not seem Heatstroke
to increase the thermal strain accompanying exercise in hot Heatstroke is an inherent risk during any outdoor physical
climates.71 activity and becomes prominent when the ambient tempera-
Obese individuals appear to be less tolerant to heat ture and humidity elevates. Heatstroke is the most severe
stress.72,73 The lower heat tolerance in this population form of the heat-related illnesses and can be associated with
may be due to their lower cardiovascular fitness compared neurological dysfunction. There have been two types of
with lean individuals (as evidenced by a higher heart rate heatstroke identified: classic heatstroke (CHS) and exer-
at rest and during exercise) as well as their lower surface tional heatstroke (EHS).81 CHS more commonly affects
area/body mass ratio.51 sedentary elderly individuals, persons who are chronically ill,
Spinal cord–injured persons cannot dissipate body heat and very young persons. It also occurs during environmental
as effectively as able-bodied persons during exercise-heat heat waves and is more common in areas that have not ex-
stress. They cannot redistribute blood flow as effectively as perienced a heat wave in many years. The main factor of
able-bodied persons, and their maximal whole-body sweat CHS is the inability of the body to dissipate heat in the hot
rate is impaired because of insensate skin. The magnitude of environment. EHS generally occurs in young individuals
this impairment depends on the level of the spinal lesion. who engage in strenuous physical activity for a prolonged
Patients with multiple sclerosis typically demonstrate period in a hot environment.81 EHS is one of the most seri-
adverse reactions to heat exposure. External heat, in the ous conditions that occur when excess heat, generated by
form of either climatic conditions or therapeutic modalities, muscular exercise, exceeds the body’s heat-dissipation rate.
may exacerbate clinical symptoms and induce fatigue.74 The consequent elevated body core temperature causes
Various pharmaceutical agents impair heat transfer to the damage to the body’s tissues, resulting in a characteristic
environment.75-77 For example, anticholinergic drugs, such multiorgan failure syndrome, which is occasionally fatal.
as atropine, increase core temperature and reduce exercise EHS is defined by core temperature of more than 40°C
tolerance time when working in hot environments.78 Acute (104°F).81-83 EHS is a potentially lethal outcome for any
amphetamine poisoning commonly leads to hyperpyrexia athlete, laborer, soldier, or other individual who participates
and fatal heat stroke.51 Neuroleptic drugs such as chlor- in physical activity in warm or hot conditions. The incidence
promazine can also impair heat transfer.75 of EHS varies depending on the event and increases with
rising ambient temperature and humidity.
Although heatstroke is relatively rare, its incidence rate
Heat Illness is as high as 1 in 1000 at some athletic endurance events
There are several illnesses that may occur during exercise- because these events often include 10,000 or more partici-
heat stress (Table 5-1). The clinical features and treatment of pants.84 Early recognition is critical to the survival of athletes
these illnesses have been discussed in detail elsewhere.79,80
Table 5-1
Diagnosis and Treatment of Heat Disorders
Cause/Predisposing Clinical Features
Disorder Factor and Diagnosis Treatment Prevention
Heat cramps Heavy and prolonged Low serum and Severe cramps: Adminis- Ensure
sweating chloride ter intravenous saline acclimatization.
Inadequate salt intake Muscle twitching, infusion. Provide extra salt
cramps, and spasms Mild cramps: Orally at meals and with
in arms, legs, and administer 0.1% salt fluids.
abdomen solution.
Rest in cool
environment.
Eat salty foods.
Heat Inability of the cardiovas- Fatigue, orthostatic Rest supine in cool Provide adequate
exhaustion cular system to meet dizziness, ataxia, environment. fluids.
demands of thermoregu- hypotension Provide intravenous Ensure
latory, muscular and Syncope saline infusion. acclimatization.
visceral blood flow Nausea and Sponge with cool water. Provide opportunity
Water or salt depletion vomiting Provide small quantities for intermittent
caused by heavy, Tingling in hands and of semiliquid food. cooling and
prolonged sweating feet Keep record of body adequate rest.
Inadequate fluid or salt Wrist or ankle spasm weight, water and salt Reduce work rate
intake Dyspnea intake, and body when exercising in
Polyuria or diarrhea Elevated skin and core temperature. hot temperatures
Vomiting temperatures Avoid exercise-heat and high-humidity
Inadequate High hematocrit, stress for 24 to climates.
acclimatization serous protein, and 48 hours.
Heat production exceeds sodium
environmental heat-loss Dry tongue and
capacity mouth
Excessive thirst
Weak, disconsolate,
uncoordinated, and
mentally dull
Heat stroke Distinguished from heat Collapse Provide active cooling. Provide adequate
exhaustion by presence Severe encephalopathy Administer IV fluids.
of tissue injury and hyperthermia dextrose-saline Ensure acclimatiza-
Two types: Dehydration infusion. tion.
Classic heatstroke Rhabdomyolysis Administer isoprotere- Provide opportunity
Exertional heatstroke Myoglobinuria nol, dopamine, or for intermittent
Diarrhea and vomiting dobutamine as needed. cooling and ade-
Maintain airway. quate rest.
Monitor and treat Reduce work rate
hyperkalemia. when exercising in
Monitor and treat acute hot temperatures
renal injury. and high-humidity
Keep record of core climates.
temperature.
Treat secondary
disorders.
Avoid exercise-heat
stress until clinical
recovery is complete.
Continued
108 SECTION I • Preparation and Prevention in Sports Medicine
Table 5-1
Diagnosis and Treatment of Heat Disorders—cont’d
Cause/Predisposing Clinical Features
Disorder Factor and Diagnosis Treatment Prevention
Heat syncope Inability to maintain Weakness and fatigue Place supine and elevate Ensure
blood pressure Hypotension legs. acclimatization.
Peripheral vasodilatation Increased venous Rest in cool Avoid sustained
and pooling of blood compliance environment. upright static work.
Circulatory instability and Blurred vision Provide oral saline if
loss of vasomotor tone Pallor conscious and resting.
Hyperventilation Syncope Keep record of blood
Inadequate Elevated skin and core pressure and body
acclimatization temperatures temperature.
Infection
Miliaria rubra, Local inflammation Pruritic, inflamed Cool and dry affected Wear loose-fitting
miliaria caused by occlusion of papulovesicular skin skin clothing.
profunda the sweat gland eruptions Avoid re-exposure until Practice good
High ambient lesions have healed. hygiene.
humidity Control for infection.
Hyponatremia Too low concentration of Nausea, vomiting, Administer IV sodium if Watch water intake
sodium in bloodstream headache, fatigue, severe. and only drink
causes cells to swell lethargy, loss of Prescribe medications. as much as you
Swelling in brain appetite, restlessness Prescribe hormone lose because of
especially dangerous and irritability, therapy if cause is sweating.
muscle weakness, adrenal insufficiency. Consider using
muscle cramps and sports beverage
spasm, seizures that contains
electrolytes.
IV, Intravenous.
with EHS. Signs and symptoms are often disorientation, be total body cooling, which is usually necessary to
confusion, dizziness, unusual behavior, headache, loss of achieve a positive outcome. The quickest rates of cooling
balance, inability to walk, vomiting, diarrhea, seizures, have been reported in therapy using cold-water and
syncope, and possible coma. A body core temperature is ice-water immersion. Secondarily, simultaneously using
essential to establish for an accurate diagnosis. Rectal tem- ice-water towels over the head, trunk, and extremities
perature is the most reliable method and is preferred over and ice packs over the axillary, groin, and neck has been
other standard measurements. Although oral, tympanic, and demonstrated to be effective in reducing body core tem-
axillary methods are often used, these methods are affected perature.83 Advanced preparation is critical to minimize
by swallowing of cold liquids, hypoventilation, or facilities delays in reduction of core temperature. Athletes should
with air conditioning.81,83 be placed in a cooling tub so that as much surface area is
submerged as possible. Constant supervision and reassess-
ment of blood pressure, heart rate, and rectal temperature
Clinical Point are monitored every 5 to 10 minutes. The athlete can be
Rectal temperature is the most accurate method of determining core
removed from the cooling tub when the rectal tempera-
body temperature. ture reaches 38°C to 39°C (100.4°F to 102°F).85 How-
ever, it is extremely important in event management that
personnel are trained and equipped to handle these emer-
gencies.
EHS requires immediate attention as a life-threatening Recommendations for returning to competition after
medical emergency. The first hour after the athlete an EHS episode are undefined; however, the following
collapses has proven to be the most challenging and criti- protocol has been recommended85: (1) no activity for
cal to survival. The best management protocol appears to 7 days after hospital dismissal, (2) physician consultation
Environmental Considerations for Sports • CHAPTER 5 109
after dismissal and a heat tolerance test to be administered pressure, which can progress to pulmonary edema through
within 3 to 4 weeks, (3) gradual acclimation to exercise either increased alveolar and interstitial fluid or through
and heat for 7 to 14 days at the beginning of training with pulmonary vasoconstriction with increase capillary hydro-
particular attention being paid to intensity and duration, static pressure.88 At the same time, central nervous system
and (4) physician clearance to full participation after the alterations can begin to appear. In hyponatremia, the imbal-
7- to 14-day trial period of exercise. Medical staff should ance of water to salt is caused by one of three conditions:85
be trained and prepared to handle EHS conditions, par- 1. Hypervolemic hyponatremia: Both sodium and water
ticularly when the event has large groups of athletes com- content in the body increase, but water gain is
peting. greater
2. Euvolemic hyponatremia: Excess of total body water
Miliaria Rubra and Miliaria Profunda with either normal or slightly reduced whole-body
Miliaria rubra (heat rash or prickly heat) is a papulovesicu- sodium
lar skin eruption that can arise when active eccrine sweat 3. Hypovolemic hyponatremia: Water and sodium are
glands become occluded by organic debris. It generally both lost from the body, but the sodium loss is
occurs in humid climates or to skin that is sufficiently encap- greater
sulated by clothing to produce high-humidity conditions. Reports indicate most hyponatremia events take place
It is treated by cooling and drying the skin, treating itching during military training, long hikes, marathons, and Iron-
symptoms, and controlling for infection. Exercise-heat man or other triathlons.86,87 Generally, events lasting
exposure should be avoided until the rash has disappeared. longer than 7 to 17 hours are more likely to cause hypo-
Miliaria that becomes generalized and prolonged is natremia. However, depending on the health of the
termed miliaria profunda. It can lead to anhidrotic heat individual, climate, ambient temperature, or humidity, a
exhaustion, because the occluded sweat glands no longer hyponatremia episode could occur in as little as 4 hours.
produce sweat for evaporation. The lesions are truncal, non- Besides event duration, individuals who drink water
inflamed, and papular. They are also asymptomatic. Persons excessively and slower runners are predisposed to hypona-
with miliaria profunda are less heat tolerant compared with tremia. In addition, other common physical predisposing
the general population. factors include being female, having small or thin stature,
sweating excessively, and having a low body mass index of
Hyponatremia 20 or less.
Hyponatremia is an abnormally low concentration of The severity of hyponatremia depends on how much
sodium in the blood. Normal ranges of sodium range are sodium levels are decreased to produce typical signs and
from 135 to 55 mEq/L.86 Too little sodium can cause cells symptoms. These results range from:87
to malfunction and extremely low sodium can be fatal. 1. Mild (sodium 131-134 mEq/L): Generally no
Hyponatremia occurs over time if the hypertonic sweat symptoms
is being replaced by hypotonic fluid (water) leading to a 2. Moderate (sodium 126-130 mEq/L): Nausea,
decrease in serum sodium.87 In other words, as the athlete vomiting, headache, disorientation, confusion, ab-
sweats out water and sodium, water is being replaced, but normal behavior, loss of coordination, and muscle
the sodium is not. Drinking appropriate electrolyte solu- weakness
tions can allow replacement of water and sodium as well as 3. Severe (sodium 126 mEq/L): Altered mental
other needed electrolytes. When significant amounts of capacity, coma and potential death
fluid are lost through high-intensity exercise, replacement There is some variability in the signs and symptoms; there-
with water alone can lead to a chemical imbalance in the fore, it is critical for medical personnel to be aware of event
body and deficiencies in electrolytes, which are nutrients participation, predisposing factors, and identification of
critical for organ functioning. Sodium circulates in the body lowered sodium levels.
fluids outside the cells. It is very important for maintaining
blood pressure. Sodium is also needed for nerves and mus- Cold Exposure
cles to function properly. Adequate sodium balance is neces-
sary for transmitting nerve impulses and proper muscle Thermoregulation in Cold Climates
function, and even a slight depletion of this concentration Cold weather need not be a deterrent for outdoor exercise.
can cause problems. Physical exercise can be performed safely in extremely cold
When sodium levels drop in the fluids outside the cells, conditions if sufficient clothing is worn to maintain body
water seeps into the cells to balance the salt levels. The cells core temperature and protect the skin from cold injury.
swell as a result of the excess water. Although most cells can It does require special consideration for the exercise par-
handle this swelling, brain cells cannot because the skull con- ticipant, however, as inadequate clothing can lead to rapid
fines them. Brain swelling causes most of the symptoms of reductions in body temperature and commensurate impair-
hyponatremia. Cerebral edema causes elevated intracranial ment of exercise performance.
110 SECTION I • Preparation and Prevention in Sports Medicine
heat loss. The addition of air motion accelerates body development of hypothermia, as physical movement in-
cooling, as the movement of air past the skin surface creases conductive heat transfer from the active limb mus-
replaces the warmer insulating air surrounding the cles to the water, with little metabolic heat left to warm the
body with colder air. As a consequence of air movement, body core.118 However, moderate-intensity exercise (heat
body cooling can occur rapidly in relatively mild ambient production approximately 400 watts) can retard or prevent
air temperatures. The wind-chill index (Table 5-2) the reduction in core temperature that occurs when resting
provides a useful index for the combined effects of ambi- in 20°C to 26°C (68°F to 78.8°F) water.119
ent temperature and air velocity on subjective comfort
and the potential for peripheral cold injury. Skin wetness Clothing
increases the effective wind-chill and the rate of body Clothing is an effective method for attenuating body heat
heat loss. loss during cold exposure. By choosing clothing with high
insulation, humans can remain comfortably warm even in
extreme cold conditions. For optimal effectiveness, the
The Magnitude of Environmental Cold Stress insulative value of the clothing should be balanced with
is Determined by: metabolic heat production. It is important not to wear too
much clothing during cold exposure, as this can lead to
• Ambient temperature increases in core body temperature and the stimulation of
• Wind velocity sweating. Profuse sweating is not advisable in cold climates,
• Wetness as many clothing materials lose their insulative properties
when wet, and peripheral cold injury is more likely when
skin is wet. Similarly, if too little clothing is worn, hypother-
mia and its consequences can occur. It is generally recom-
Water immersion increases the rate of body cooling mended that individuals wear several layers of clothing
compared with ambient air exposure. Water has a 25-fold during cold exposure. This method of dressing enables the
greater heat transfer coefficient compared with air. As a individual to add or remove clothing as exercise intensity
consequence, body cooling occurs much more quickly and and weather conditions dictate.
begins at a higher absolute temperature in water than in As discussed, the energy cost of exercise can be 10% to
air. Low-intensity exercise in water can actually speed the 20% higher when wearing cold-weather clothing. The
Table 5-2
Windchill Chart*
Actual Temperature (ºF)
* To determine the windchill temperature, enter the chart at the row corresponding to the wind speed and read right until reaching the column
corresponding to the actual air temperature.
Environmental Considerations for Sports • CHAPTER 5 113
greater energy cost means that exercise at the same work during cold exposure. There is evidence that endurance-
rate requires a greater percentage of an individual’s maximal trained individuals have a reduced sensitivity to cold
oxygen uptake. The greater relative exercise stress may stress, as suggested by a delayed onset of shivering during
shorten time to fatigue. body cooling.125 However, Bittel and colleagues126 found
that aerobically fit individuals had greater metabolic
Body Morphology heat production during cold exposure as well as an
Both body morphology (e.g., mass, surface area) and increased shivering sensitivity; that is, the onset of shiver-
composition affect the body cooling rate during cold stress. ing began at warmer skin temperatures. Similarly, skin
Individuals with small body mass or high surface area/mass temperatures during cold exposure have been reported to
ratios cool faster than larger persons with similar body both increase118,127 and decrease128 after physical training.
morphology.119,120 Similarly, persons with thicker layers of Young and colleagues129 recently showed that aerobic
subcutaneous fat, and therefore greater peripheral insulation, training improves the vasoconstrictor response to cold
cool more slowly than those with less fat.93,94,121,122 A thick exposure. Obviously, more study is needed to clarify the
subcutaneous fat layer also enables individuals to tolerate role of fitness and training on the physiological responses
lower ambient temperatures before initiating shivering.123 to cold exposure.
Differences in body size and composition are considered to
be largely responsible for much of the interindividual Aging
variability in physiological responses to cold exposure. The risk of hypothermia is widely considered to be greater
in older compared with younger adults, and hypothermia is
Gender thought to contribute to the increased winter mortality rate
Whether gender alters the ability to defend body tempera- in the elderly.130-132 Studies have found that older persons
ture during cold stress remains unresolved. Although there are less able than younger adults to defend body tempera-
are well-documented differences between men and women ture during cold stress.133 This has been attributed to a
during cold stress, these differences may not be due to dif- reduced ability to vasoconstrict peripheral arterioles during
ferences between the genders per se but rather due to cold exposure134,135 and a smaller rise in heat production
differences in body mass, body composition, surface area, during cold stress.136 Older persons have also been reported
and aerobic power. To date, no study examining the physi- to have less CIVD response than younger persons.137 The
ological responses to cold exposure has matched men and difference between the older and younger adults in these
women for weight, fitness, body surface area, and fatness. studies may not have been the result of aging per se, but to
During cold-water immersion, women generally lose other factors such as differences in body morphology, fit-
heat at a faster rate than men.94 This can be explained, in ness, and health. When these confounding variables are
part, because women have a smaller body mass and a greater experimentally controlled, the rate of body cooling appears
surface area/body mass ratio. However, women show less to be similar between old and young adults in some138,139
increase in metabolic rate for the same magnitude of body but not all studies.140
cooling,124 suggesting that they have a blunted response to
reductions in core temperature. Nutritional Status
During cold-air exposure, women generally maintain Persons who become hypoglycemic during cold exposure
body core temperature as effectively as men.124 They have a reduced tolerance to cold stress and are more suscep-
accomplish this by maintaining a lower skin temperature tible to cold injury.141-143 Those with hypoglycemia exhibit
compared with men during cold stress.124 The lower skin either attenuated shivering or no shivering during cold
temperature not only reduces heat transfer to the periphery stress,142-144 and they therefore have lower rates of heat
but also serves to increase the insulative barrier between the production. Interestingly, Gale and colleagues144 demon-
body core and the environment. strated that intravenous glucose infusion restored shivering
within seconds after euglycemia (i.e., normal sugar in
Aerobic Fitness and Training blood) was restored in persons rendered hypoglycemic dur-
The physiological adaptations that occur with regular phys- ing cold stress. The restoration of shivering occurred even
ical activity can improve tolerance to cold environments. in a limb removed from circulation by arterial occlusion.
Because endurance exercise training increases maximal aer- These findings suggest that hypoglycemia affects tempera-
obic power and endurance performance, trained individuals ture regulation through a central rather than peripheral
can sustain relatively high exercise intensities for prolonged mechanism. Regardless of the mechanism, hypoglycemia
periods. This ability is of great value when high rates of heat can have traumatic consequences for persons working
production are necessary to prevent hypothermia during in cold environments and should be prevented whenever
cold exposure. possible.
It is controversial whether exercise training produces Both carbohydrate and fat are oxidized to meet the meta-
adaptations that improve thermoregulatory responses bolic cost of shivering. The increase in plasma catecholamine
114 SECTION I • Preparation and Prevention in Sports Medicine
Table 5-3
Hypothermia Core Temperature, Signs and Symptoms
Stage Core Temperature Signs and Symptoms
Modified from Curtis R: Outdoor action guide to hypothermia and cold weather injuries. Rick Curtis, Outdoor Action Program, The Trustees of
Princeton University. Retrieved November 18, 2008 from http://www.princeton.edu/⬃oa/safety/hypocold.shtml.
circulation or disorders.161 Clinical signs and symptoms the skin by such methods as friction massage over the
of hypothermia often begin before an individual is skin, placing the individual in a warm bath or covering
aware that he or she needs help. The first sign or symp- him or her with an electric blanket. With severe hypother-
tom is shivering. Shivering is the body’s first attempt to mia and some advanced cases of moderate hypothermia,
produce more heat by muscle activity.160,162 Often, the internal rewarming is indicated. Cardiopulmonary bypass,
next sign or symptom is altered motor coordination and in which the patient’s blood is circulated through a re-
changes in consciousness noted when the individual warming device and then returned to the body, is consid-
mumbles and stumbles and has slurred speech, an abnor- ered the best, and can raise body temperature by 0.5°C to
mally slow rate of breathing, cold pale skin, and fatigue.162 1°C (1°F to 2°F) every 3 to 5 minutes. However, many
To treat an individual with hypothermia, one must hospitals are not equipped to offer this treatment. The
rewarm the individual, but this process depends on the alternative is to introduce warm oxygen or fluids into the
stage of hypothermia the individual is experiencing. Indi- body.163
viduals with mild hypothermia are often rewarmed
passively. Passive rewarming relies of the individual’s Frostbite (Freezing Injury)
own body metabolism.163 All wet clothing must be re- Frostbite occurs when skin tissue freezes and is defined as a
moved and the skin dried. All other predisposing factors medical condition in which damage is caused to the skin
must be remedied, such as removal from an outdoor and other tissues as a result of extreme cold.164 It primarily
environment into a shelter and covering the individual in affects the digits, ears, and exposed facial tissue. Initially, the
blankets to aid his or her own body to increase core body frozen tissue is cold, hard, and bloodless. The severity of
temperature. The goal is to increase core temperature by frostbite is classified by the depth of the injury. First-degree
0.5°C to 2°C (0.9°F to 3.6°F) per hour.163 Moderate frostbite affects the epidermal tissue. After thawing, the skin
hypothermia is best treated with active external rewarm- may become wheal-like, red, and painful, and it may be-
ing techniques followed by passive techniques. Active come edematous but does not blister. Second-degree frostbite
external rewarming techniques involve applying heat to affects the superficial dermis and is characterized by blister
116 SECTION I • Preparation and Prevention in Sports Medicine
formation. Third-degree frostbite extends to the reticular anesthetic, pulseless, and immobile. The skin is frequently
layer. It is characterized by edema with hemorrhagic bullae. macerated and slightly edematous. After warming, there is
Permanent tissue loss is possible. Fourth-degree frostbite in- marked hyperemia, pain, and blister formation. Immersion foot
volves the full thickness of skin. Thawing does not restore can occur after prolonged immersion in cold water. The clini-
muscle function, and the affected area shows early necrotic cal features are similar to trench foot. Acute treatment for both
change. There will be permanent tissue and functional loss. trench foot and immersion foot is directed at passively warm-
The affected area should be warmed gradually (tempera- ing the affected feet, protecting the area from physical injury,
tures greater than 39°C [102.2°F] can aggravate injury). controlling for infection, and treating concomitant hypother-
During initial treatment, affected areas should be protected mia and dehydration. Nonfreezing injuries can be reduced by
from physical injury and excessive cold or heat exposure. frequent hand and foot inspection and by regularly warming
The tissue should be elevated to reduce swelling. The risk and drying exposed limbs. Table 5-4 summarizes the diagnosis
of frostbite can be minimized by wearing proper clothing, and treatment of cold disorders.
ensuring adequate diet and hydration, and avoiding unduly
prolonged cold exposure.
High Terrestrial Altitude
Nonfreezing Injuries Improved access to mountainous areas has increased the
Sustained exposure to cold and wet conditions can induce skin number of people visiting and living at high altitude. It is
injury. Chilblain is a skin condition that primarily now possible for travelers to fly to a major airport and
affects the hands and feet. Patients present with red, swollen, quickly drive to a high-altitude destination. In the moun-
tender areas on the dorsum of the extremities between the tain states of Utah, Colorado, Wyoming, and New Mexico,
joints. The affected area should be warmed and carefully dried. for example, major roads reach 12,000 feet (3650 meters),
Persons should be treated for infection, and re-exposure some towns are located above 10,000 feet (3050 meters),
should be avoided until the affected region is healed. Trench and lodges are at 9000 feet (2750 meters) and higher. In
foot can occur with prolonged exposure to wet, cold condi- these states, approximately 7 million people ascend to alti-
tions when circulation is restricted. The tissue becomes pale, tudes above 8500 feet (2590 meters) each year.165
Table 5-4
Diagnosis and Treatment of Cold Disorders
Cause/Predisposing Clinical Features
Disorder Factor and Diagnosis Treatment Prevention
Accidental Body heat loss ex- Mild hypothermia (core Measure core Wear proper
hypothermia ceeds body heat temperature 32°C to 35°C): temperature. clothing for
production ability to spontaneously re- Warm afflicted indi- weather
Insufficient clothing warm; no cardiac arrhythmias vidual; remove wet conditions.
Inadequate nutrition Severe hypothermia (core clothing. Ensure adequate
and fluid intake temperature 28°C): active Mild hypothermia: nutritional and
Alcohol and drug use rewarming required, high risk warm, sweet oral hydration state.
Infection of ventricular fibrillation fluids. Seek warm shelter
In conscious victim: Moderate to severe at the earliest
Persistent shivering hypothermia: IV suspicion of
Cool, pale skin fluid for hypothermia.
Withdrawal and irritability dehydration and
Confusion, lethargy, and hypovolemia.
obtundation Maintain airway.
Bradycardia and hypotension Medical management
Weak peripheral pulse if hypoglycemia is
Hypopnea suspected, alcohol
or opiate intoxica-
tion.
Manage secondary
complications
(e.g., pneumonia,
pancreatis, rhabdo-
myolysis, and renal
failure).
Environmental Considerations for Sports • CHAPTER 5 117
Table 5-4
Diagnosis and Treatment of Cold Disorders—cont’d
Cause/Predisposing Clinical Features
Disorder Factor and Diagnosis Treatment Prevention
Freezing injury Freezing of skin Frozen tissue is cold, hard, and Warm affected areas; Wear proper
(frostbite) tissue bloodless temperatures 39°C clothing.
Predominantly afflicts Classified by depth of injury will aggravate injury. Ensure adequate
digits, ears, and (see below) Protect affected areas diet and hydration.
exposed facial skin from physical injury Avoid unduly
and excessive cold prolonged cold
First-degree Epidermal injury
or heat exposure. exposure.
frostbite Post-thawing is wheal-like, red, and painful
Treat coincident
Affected area may become edematous but has no blister
medical problems—
formation
hypothermia,
Second-degree Affects superficial dermis dehydration.
frostbite Some initial limits on range of motion Elevate tissue to
Edema with blister formation reduce swelling.
Prescribe prophylactic
Third-degree Affects dermis to reticular layer
antibiotics for
frostbite Edema with hemorrhagic bullae
postinjury infection.
Swelling restricts range of motion
Whirlpool debridement
Permanent tissue and functional loss
for second-
Fourth-degree Involves full thickness of skin to fourth-degree
frostbite Thawing does not restore muscle function, and skin injuries.
reperfusion is poor
Affected area shows early necrotic change
Permanent tissue and functional loss
Nonfreezing Initially, afflicted area is pale, Warm (passively) and Perform frequent
injuries anesthetic, pulseless, and dry feet. foot inspection.
immobile Protect affected area Perform regular
Trench foot Prolonged exposure Skin is frequently macerated from physical injury. warming and
of extremities to and lightly edematous Treat for infection drying of feet
wet, cold conditions After warming, marked hyper- and pain. during exposure.
Restricted circulation emia, proximal burning pain, Treat concomitant Boots and socks
Immersion Prolonged immersion and blister formation appear hypothermia and should not be
foot in cold water Classified by degree of severity dehydration. replaced until feet
Avoid weight-bearing are warm, with
activity until healing normal feeling.
is complete.
Chilblain Sustained exposure Red, swollen, tender areas on Warm and dry Perform frequent
to cold, wet condi- dorsum of extremities between afflicted skin areas. foot and hand
tions joints Treat for infection. inspection.
Primarily afflicts Itching Avoid re-exposure Take frequent
hands and feet Chronic lesions may be turgid, until affected region breaks to warm
with blister formation is healed. and dry feet and
hands.
Boots, socks, and
gloves should not
be replaced until
limbs are warm,
with normal
feeling.
IV, Intravenous.
118 SECTION I • Preparation and Prevention in Sports Medicine
Table 5-5
Typical Acute Reduction in Arterial Oxygen Partial Pressure and Saturation with Increasing Altitude for Unacclimatized Men
Elevation PB PIO2 PAO2 PaO2 PACO2 SaO2
m ft (torr) (torr) (torr) (torr) (torr) (%)
PAO2, Alveolar oxygen partial pressure; PaO2, arterial oxygen partial pressure; PACO2, alveolar carbon dioxide partial pressure; PB, barometric
pressure; PIO2, inspired oxygen partial pressure; SaO2, arterial oxygen saturation.
Modified from Fulco CS, Cymerman A: Human performance and acute hypoxia. In Pandolf KB, Sawka MN, Gonzalez RR, editors: Human
performance physiology and environmental medicine at terrestrial extremes, p 471, Indianapolis, 1988, Benchmark Press.
Environmental Considerations for Sports • CHAPTER 5 119
because training time and intensity are reduced as a result well as athletic performance during sporting events.187 For
of acute mountain sickness and hypoxia. It may also be due example, Maher and colleagues195 reported a 45% increase in
to a lower maximal cardiac output, as maximal heart rate is time to exhaustion during cycle exercise between the second
reduced following acclimatization to high altitude,190,191 and twelfth day at 4300 meters (14,108 feet), and Horstman
and this is not completely reversed either by breathing nor- and colleagues174 found a 60% increase in treadmill running
moxic air or with atropine infusion.190 time between the second and sixteenth day of acclimatization
The reduced oxygen-carrying capacity at high altitude at the same altitude.
also affects the physiological responses during submaximal The improved endurance performance appears to be due,
exercise. At high altitude, the same absolute power output at least in part, to altered substrate use and less disturbance
elicits a greater percentage of maximal oxygen uptake than of cellular homeostasis. Following high-altitude acclimatiza-
at sea level (Figure 5-9). As a consequence of the lower tion, there is less reliance on anaerobic energy metabolism,
maximal oxygen uptake at altitude, heart rate, ventilation, as evidenced by lower plasma ammonia and lactate concen-
and lactate concentration are higher during hypoxia than at trations,195,197,198 less glycogen use,197 and reduced lactate
sea level at the same power output.183,184 During exercise at production.198 There is also less disturbance of cellular
the same percentage of environment-specific maximal oxy- homeostasis, because the adenosine triphosphate/adenosine
gen uptake, however, heart rate, ventilation, and lactate diphosphate ratio is higher and the inorganic phosphate
concentration are similar under hypoxia and sea-level concentration lower after high-altitude acclimatization.199
conditions.192-195 Because intracellular acidosis (which accompanies lactic acid
formation) and elevations in inorganic phosphate concentra-
tion have been shown to induce fatigue in skeletal muscle,200
Exercise Performance at High Altitude less reliance on anaerobic metabolism should enhance en-
Acute exposure to hypoxia impairs endurance performance. durance performance.
Hypoxia reduces the time to exhaustion during exercise An improved intracellular buffering capacity may
at a given absolute power output, with the magnitude of be another possible mechanism for the improved endur-
decrement proportional to the magnitude of hypoxia. ance performance following high-altitude acclimatization.
Reducing the workload to elicit the same percentage of Mizuno and colleagues196 reported that 2 weeks of exercise
environment-specific maximal oxygen uptake results in training at altitude (8850 feet; 2700 meters) produced a
similar time to exhaustion during high-altitude and sea-level 6% increase in in-vitro skeletal muscle buffer capacity. In
exercise.174,195 addition, they reported a strong relationship (r 0.83)
Acclimatization to high altitude can dramatically improve between improved skeletal muscle buffer capacity and
time to exhaustion during submaximal exercise174,195,196 as short-duration (range 240 to 380 seconds) running endur-
ance time (average improvement of 17%) after high-
altitude acclimatization.
Ascent to high altitude does not impair skeletal muscle
strength, but does increase fatigability of skeletal muscle
during small muscle mass activity.181,201 Acclimatization to
high altitude, however, improves skeletal muscle endurance
capacity,201 presumably as a result of improved oxygen
delivery and less disturbance of intracellular homeostasis.
Perception of effort during exercise at a given percentage of with coronary artery disease have decreased exercise toler-
maximal oxygen uptake is lower following acclimatization to ance and earlier onset of angina and ST-segment changes
altitude. However, it has been suggested that the improve- during exercise at altitude.206-208 Those who can achieve
ments may be related to recovering from mountain sickness 9 minutes on the Bruce protocol without anginal symp-
rather than acclimatization per se.170 toms will probably be safe at altitude.166 Those with severe
angina and limitation of effort at sea level should not go
to altitude, as hypoxia will increase cardiac energy demand
Special Considerations at High Altitude and precipitate anginal episodes. Those afflicted should
Exercise Training choose an itinerary with access to easy descent and medical
Because high altitude reduces maximal oxygen uptake and help. A good suggestion is to simulate the activity at mod-
results in elevated heart rate at a given oxygen uptake, exer- erate altitudes before attempting a specific activity at
cise prescriptions based on tests at sea level need modifica- higher altitudes.
tion. Heart rate remains a reliable indicator of cardiovascu- Individuals with mild to moderate lung disease may
lar stress during exercise, but exercise at a given heart rate tolerate modest altitudes but have a higher incidence of
provides less absolute stress to skeletal muscle. Therefore, acute mountain sickness.209 Patients with primary pulmo-
to provide the same overload to skeletal muscle, exercise nary hypertension do not do well at altitude. Diabetics
must be performed at a greater absolute heart rate. may experience problems regulating their insulin doses
Optimal training for improving athletic performance at because of varying energy expenditure and food intake.
altitude depends on the altitude of residence and the ath- More frequent insulin dosing may be needed, as well
letic event. For aerobic activities (events lasting longer than as more frequent blood glucose determinations. The
3 to 4 minutes) at altitudes above 2000 meters (6562 feet) presence of sickle cell disease is a contraindication for as-
acclimatization for 10 to 20 days is necessary for maximal cent to altitude, as ascent to altitudes as low as 6320 feet
performance.165 Highly anaerobic activities at intermediate (1925 meters) is associated with an increased incidence of
altitudes require only arrival at the time of the event.165 clinical symptoms.166
The effects of high-altitude training on sea-level athletic
performance remain controversial.203 Studies have sug-
gested that sea-level performance can be improved by living High-Altitude Illness
and training at altitude.185,189,196,204 These studies, however, Acute Mountain Sickness
often lacked a control group performing similar training at Acute mountain sickness is a common illness that arises
sea level. Studies containing the proper control groups have after rapid ascent ( 24 hours) to altitudes above 8200
not found altitude training to be superior to sea-level train- feet (2500 meters), with symptoms beginning within
ing with regard to sea-level performance.186,188,205 Regard- hours to days after exposure. Individuals often present
less, any benefit appears to depend on choosing an altitude with headache, anorexia (loss of appetite), insomnia, nau-
that maximizes physiological stress but minimizes the de- sea, and malaise.165,166,210 In moderate forms, there may
training that is inevitable when maximal oxygen uptake is be vomiting, unrelieved headache, and decreased urine
limited (altitudes greater than 4900 to 6550 feet [1500 to production. Severe mountain sickness produces altered
2000 meters]). Levine and Stray-Gundersen203 reported consciousness, localized rales (abnormal respiratory
that athletes train faster and at greater oxygen uptakes at sound), cyanosis, and ataxia (uncoordinated movement).
low altitude (3900 feet; 1200 meters) than at higher alti- It is most common among those who ascend quickly
tude (9150 feet; 2800 meters), suggesting that altitude and those who have a past history of acute mountain
exposure may compromise training overload. They also sickness. Vigorous physical activity during ascent or within
found that athletes who lived at altitude but trained near 24 hours of ascent increases the incidence and severity of
sea level had improved maximal aerobic power (5%) and symptoms. Whether physical fitness attenuates the symp-
5000-meter running time (30 seconds) compared with a toms remains questionable. Mountain sickness is most
control group who lived and trained near sea level. Levine likely to occur in those who retain fluid at altitude and
and Stray-Gundersen203 suggested that living at altitude have a blunted ventilatory response.176,211 The symptoms
stimulates beneficial changes for athletic performance, and typically improve over a few days if hypobaric stress is not
training near sea level provides optimal exercise training. increased.
Table 5-6
Diagnosis and Treatment of High-Altitude Illnesses
Cause/Predisposing Clinical Features
Disorder Factor and Diagnosis Treatment Prevention
Acute mountain Hypoxia-induced Symptoms typically begin Descend to lower Ascend in stages or
sickness subclinical cerebral 3 to 24 hr after ascent elevation graded manner
edema Headache and nausea Supplemental Acetazolamide
Lack of acclimatiza- Anorexia, vomiting, and oxygen prophylaxis
tion to high altitude general malaise Acetazolamide High-carbohydrate
Rapid ascent ( 24 hr) Dizziness and oliguria therapy diet ( 70% of
to altitudes greater Analgesic for head- total Kcal)
than 6000 ft ache symptoms
Condition self-
limited
High-altitude Combination of Symptoms typically begin Immediate passive Ascend in stages or
pulmonary hypoxia-induced within 2 to 4 days after descent graded manner
edema hypertension and ascent Supplemental Nifedipine
increased Early: nonproductive cough oxygen prophylaxis
permeability of and a few rales; as edema Nifedipine Acetazolamide
pulmonary capillaries progresses, cough becomes Transport to prophylaxis
Lack of acclimatiza- productive and rales medical facility
tion to high altitude become numerous
Rapid ascent ( 24 hr) Dyspnea on exertion; fatigue
to high altitude and weakness
Resting tachycardia and
tachypnea
Cyanosis
Environmental Considerations for Sports • CHAPTER 5 123
Table 5-6
Diagnosis and Treatment of High-Altitude Illnesses—cont’d
Cause/Predisposing Clinical Features
Disorder Factor and Diagnosis Treatment Prevention
High-altitude Edema of the brain Time of symptom onset is Immediate passive Staged or graded
cerebral edema associated with high highly variable; generally descent ascent
altitude several days after ascent Supplemental High-carbohydrate
Increased permeability Severe headache, nausea, oxygen diet
of the blood-brain vomiting, and lassitude Portable hyperbaric Acetazolamide
barrier or alteration Truncal ataxia chamber prophylaxis
of cell fluid regulation Ataxic gait Dexamethasone
Lack of acclimatiza- Mental confusion, Transport to
tion to high altitude disorientation, drowsiness medical facility
Rapid ascent ( 24 hr) Social withdrawal
to altitudes greater Cyanosis
than 12,000 ft
Acute mountain
sickness
Prior history
High-altitude Hypoxia-induced Primarily afflicts hands and Descent to lower Salt prophylaxis
peripheral retention of sodium periorbital areas of the face altitudes Acetazolamide
edema and water Associated with decreased Diuretic therapy prophylaxis
More frequent in urine output and weight gain
females More evident upon
awakening
Chronic Disease and Air Pollutants inland against the mountain ranges that surround the city.
Additional factors that determine whether air pollutants
Air Pollution will affect our health are whether breathing is done nasally
There are several chemical compounds present in the atmo- or orally and the quantity of air inspired. Oral ventilation
sphere that can directly affect our health. These compounds, removes fewer air pollutants than nasal breathing, resulting
collectively termed air pollutants, have been classified as ei- in greater exposure to air pollutants per unit time.
ther primary or secondary pollutants. Primary pollutants are Because physical exercise increases the rate and depth of
those emitted directly into the environment. They are pro- inspiration, more air pollutants are inspired during exercise
duced primarily from the combustion of petroleum-based than at rest.
fuels and include carbon monoxide, sulfur oxides, nitrogen Certain individuals are more susceptible to the adverse
oxides, hydrocarbons, and particulates. Secondary pollutants effects of air pollutants. It is well documented that sub-
are those that develop from the interaction of the primary threshold concentrations of air pollutants for healthy adults
pollutants with the environment and include ozone, peroxy- can compromise respiratory and cardiovascular function in
acetyl nitrate, sulfuric acid, aldehydes, and sulfates. The smog children and the elderly, persons with respiratory disorders
or brown cloud associated with large metropolitan areas usu- (e.g., those with asthma or chronic obstructive pulmonary
ally contains both primary and secondary pollutants. disease), and persons with ischemic heart disease.212-215
The quantity of air pollution inhaled during exercise is In many regions of the country, the air quality meets the
determined by several factors. The concentration of both national air quality standards (Table 5-7). However, in
primary and secondary air pollutants is influenced by the many areas of southern California, the concentration of
season, the ambient weather conditions, and the topogra- air pollutants often exceeds national air quality standards.
phy of the region. Ozone typically reaches peak concentra- For example, in Los Angeles County, California, each of the
tion in the late morning and early afternoon in summer and 16 Environmental Protection Agency testing stations ex-
is lowest at night during the winter months. The highest ceeded the national standard for ozone (0.12 ppm for
carbon monoxide concentrations are typically during peak 1 hour) on one or more occasions during a 2-year period
traffic periods. The geography of the region also affects the spanning 1991 through 1993, with several locations ex-
dispersion of air pollutants. The relatively high ozone con- ceeding the national standard 50 days or more during the
centrations in the inland valleys of Los Angeles, for example, calendar year. Similar results have been reported for the
are the result of prevailing sea breezes pushing the pollutants other counties along the coast of southern California.
124 SECTION I • Preparation and Prevention in Sports Medicine
Table 5-7
National Ambient Air Quality Standards
Primary Standards Secondary Standards
Averaging
Pollutant Level Averaging Time Level Time
From United States Environmental Protection Agency: National ambient air quality standards. Retrieved September 1, 2009 from http://www.
epa.gov/air/criteria.html.
EPA, Environmental protection agency; PM, particulate matter; STD, standard.
a
Not to be exceeded more than once per year.
b
Final rule signed October 15, 2008.
c
Not to be exceeded more than once per year on average over 3 years.
d
To attain this standard, the 3-year average of the weighted annual mean PM2.5 concentrations from single or multiple community-oriented
monitors must not exceed 15.0 µg/m3.
e
To attain this standard, the 3-year average of the 98th percentile of 24-hour concentrations at each population-oriented monitor within an area
must not exceed 35 g/m3 (effective December 17, 2006).
f
To attain this standard, the 3-year average of the fourth-highest daily maximum 8-hour average ozone concentrations measured at each monitor
within an area over each year must not exceed 0.075 ppm (effective May 27, 2008).
g
(1) To attain this standard, the 3-year average of the fourth-highest daily maximum 8-hour average ozone concentrations measured at each
monitor within an area over each year must not exceed 0.08 ppm.
(2) The 1997 standard—and the implementation rules for that standard—will remain in place for implementation purposes as EPA undertakes
rule-making to address the transition from the 1997 ozone standard to the 2008 ozone standard.
h
(1) The standard is attained when the expected number of days per calendar year with maximum hourly average concentrations greater than
0.12 ppm is
1.
(2) As of June 15, 2005, the EPA has revoked the 1-hour ozone standard in all areas except the 14 8-hour ozone nonattainment early action
compact (EAC) areas. For one of the 14 EAC areas (Denver, CO), the 1-hour standard was revoked on November 20, 2008. For the other
13 EAC areas, the 1-hour standard was revoked on April 15, 2009.
Unfortunately, although there has been a great deal of resulting in recurrent episodes of reversible airway narrowing,
research on the effect of individual air pollutants on pulmo- separated by periods of relative normal ventilations.216 Attacks
nary function and the ability to tolerate the stress of exer- vary greatly from occasional periods of wheezing and slight
cise, relatively few studies have investigated the interaction dyspnea to severe attacks that almost cause suffocation.217
of these pollutants with exercise performance. There is even Asthma is commonly divided into two types: allergic (extrin-
less information addressing the effect of air pollutants and sic) asthma and nonallergic (intrinsic) asthma.218 Asthma can
other environmental stressors (e.g., heat, cold, altitude) on be triggered by both internal and external factors and stimuli.
pulmonary function and exercise performance. The goal of In general, once the asthma has been triggered by one or
this section is to discuss the physiological effect of several more internal or external factors, the airway begins to swell
major air pollutants, both alone and in combination. and fill with mucus, causing the individual to wheeze or have
a dyspneic attack. Furthermore, the muscles within the airway
contract causing further narrowing and restriction of the air-
Asthma way. This process decreases the ability of the individual to
Asthma is a disease that affects the respiratory system exhale from the lungs effectively. This decreased ability to
of individuals of all ages, both sedentary and active, and exhale causes the typical symptoms of an asthma attack.
can be affected by many intrinsic as well as extrinsic environ- Asthma is categorized depending on the body systems
mental factors (Table 5-8). This disease is caused by hyper- affected, or by the stimuli or “trigger” that causes the dys-
responsiveness of the trachea and bronchi to various stimuli pnea, or even by the time of day.219
Environmental Considerations for Sports • CHAPTER 5 125
Table 5-9
Medications Used to Treat Asthma
Medication Type
Data from Mayo Clinic: Asthma—Treatments and Drugs, 2008. Retrieved November 6, 2008, from http://www.mayoclinic.com/health/
asthma/DS00021/DSECTIONtreatments-and-drugs.
IgE, Immunoglobulin E.
A methacholine challenge is a test in which the indi- symptoms is by doing skin and blood tests or by eliminat-
vidual “challenges” his or her bronchial airways with one ing foods in the diet.224 Chest x-ray examinations are
of the following: methacholine, histamine, cold air, or typically not useful in diagnosing asthma, but they are use-
exercise.223 The test is used to determine if the bronchial ful in determining if other conditions of the lungs, chest,
airways are hyper-responsive to a particular stimuli. If the and heart are present.223
bronchial airways are hyper-responsive, then they will nar- An estimated 20 million Americans suffer from asthma
row in response to the specific stimuli. If the methacholine (1 in 15 Americans), and 50% of asthma cases are “allergic
challenge does not reproduce hyper-responsiveness, then asthma.”218 Asthma is the most common chronic condition
asthma is unlikely. Generally, the methacholine challenge in children and it affects 1 in 20 children, with a higher
test is only used if a spirometry test is inconclusive, but incidence in male children than female children (3:2 ratio),
asthma is still considered a possibility.223 Allergy testing but it is more common in older women than older men.225
may be used for people who have been diagnosed with Ethnic differences in asthma prevalence, morbidity, and
asthma because certain allergies may play a significant role mortality are highly correlated with poverty, urban air qual-
in exacerbating asthma symptoms. The most common and ity, indoor allergens, and lack of patient education and
effective way to determine if allergies play a role in asthma inadequate medical care (Table 5-10).226
Environmental Considerations for Sports • CHAPTER 5 127
Table 5-10
Estimated Average Annual Prevalence Percents for Self-Reported Current Asthma, by Age, Sex, Race, Ethnicity, Region
and Poverty Level—National Health Interview Survey, United States, 2001-2003
Age (yrs)
Characteristic Total 18 18 0-4 5-14 15-34 15-19 20-24 25-34 35-64 65
Sex
Male 6.2 9.6 4.9 6.8 11.1 6.3 8.9 6.4 4.7 4.5 4.6
Female 8.1 7.4 8.4 5.0 7.8 8.9 10.0 9.4 8.0 8.7 6.8
Race*
White 6.9 7.7 6.7 4.4 8.8 7.5 9.2 8.0 6.3 6.6 5.8
Male 5.8 8.6 4.8 5.2 10.1 6.1 8.5 6.6 4.5 4.5 4.6
Female 8.0 6.8 8.4 3.6 7.5 8.9 9.8 9.4 8.1 8.7 6.7
Black 9.2 12.5 7.6 12.4 12.8 9.0 11.2 9.7 7.2 7.4 6.1
Male 8.2 14.0 5.2 12.8 15.4 7.3 10.5 6.9 5.2 4.6 3.8
Female 10.0 11.0 9.5 12.0 10.2 10.4 12.0 11.8 8.8 9.7 7.6
Other races 6.8 8.9 5.7 7.1 9.5 6.6 9.4 5.5 5.8 5.4 6.7
NTA
Male 6.9 11.2 4.7 9.1 12.1 6.2 10.0 — 5.1 4.1 6.4†
Female 6.7 6.5 6.7 5.0 6.9 7.0 8.7 6.2 6.6 6.7 7.0
Ethnicity‡
Hispanic or 5.4 7.0 4.6 5.2 7.7 4.9 7.3 4.2 4.0 4.8 5.2
Latino
Male 4.8 7.6 3.2 5.7 8.4 3.9 7.2 3.0 2.8 3.1 4.5
Female 6.1 6.3 6.0 4.7 6.9 5.9 7.4 5.4 5.4 6.5 5.7
Puerto Rican 14.5 18.7 12.4 10.7 21.5 14.4 21.0 13.2 11.6 12.1 13.0
Male 12.4 18.7 8.8 10.2 23.1 10.1 16.1 11.5† 5.7 9.3 —
Female 16.6 18.7 15.7 11.2† 19.8 18.9 26.6 14.9 17.2 14.6 15.8
Mexican 3.9 4.8 3.3 3.8 5.4 3.3 4.6 2.9 2.9 3.5 3.9
Male 3.4 5.4 2.2 4.3 5.8 2.8 4.5 2.7 2.0† 2.2 3.0†
Female 4.4 4.2 4.5 3.3 4.9 3.9 4.8 3.2 3.9 4.8 4.7
Not Hispanic 7.4 8.9 7.0 6.1 9.9 8.1 9.9 8.7 6.8 6.8 5.9
or Latino
Male 6.4 10.1 5.1 7.0 11.7 6.7 9.3 7.2 5.1 4.6 4.6
Female 8.4 7.6 8.7 5.0 8.0 9.4 10.5 10.2 8.5 8.9 6.9
Region
Northeast 8.1 10.2 7.4 7.1 11.3 8.4 10.8 9.3 6.6 7.6 6.0
Midwest 7.5 8.7 7.1 6.7 9.5 8.3 9.8 9.0 7.0 6.7 6.3
South 6.7 8.3 6.2 6.0 9.4 7.0 8.9 7.0 6.0 6.1 5.4
West 6.8 7.3 6.6 3.9 8.3 7.1 9.0 7.1 6.1 6.6 6.2
Ratio of family
income to pov-
erty threshold§
0-.99 10.3 11.1 9.8 10.2 11.1 9.5 11.6 9.5 7.8 11.2 8.8
1.00-2.49 7.9 8.5 7.6 6.9 9.1 7.9 9.0 8.2 7.1 7.9 7.1
2.50-4.49 6.8 7.7 6.5 3.9 9.2 7.4 8.9 8.0 6.4 6.3 5.2
4.50 6.4 8.0 6.0 3.8 9.5 6.9 9.1 7.4 5.9 6.1 4.3
Total 7.2 8.5 6.7 5.9 9.5 7.6 9.5 8.0 6.4 6.6 5.9
*Race categorized according to the 1997 revision of Statistical Policy Directive No. 15. Race Ethnic Standards for Federal Statistics and
Administrative Reporting. Race categories “white” and “black” are comprised persons who indicated only a single race group. “Other races
NTA (not tabulated above)* Includes Asian, American Indian and Alaskan Native, Native Hawaiian and Other Pacific Islander, persons
reporting more than one race, and persons reporting their race as something other than those listed here or above.
†
The estimate is unreliable because the relative standard error of the estimate is 30%-50%. For missing estimate, the relative standard error of the
estimate exceeded 50% and the estimate was suppressed. All other relative standard errors are < 30%.
‡
The 1997 revision of Statistical Policy Directive No. 15. Race and Ethnic Standards for Federal Statistics and Administrative Reporting changed
the ethnicity category name for “Hispanic or Latino,” but the definition of persons in that category remained the same. “Puerto Rican” and
“Mexican” are a subset of “Hispanic or Latino”; Mexican includes responses of Mexican and Mexican American.
§
Missing income responses were not imputed or included.
From Moorman JE, Rudd RA, Johnson CA et al: National Surveillance for Asthma—United States, 1980-2004, Morb Mortal Wkly Rep
56(S S08);1-14, 18-54, 2007. Retrieved November 7, 2008, from http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5608a1.htm#tab1.
128 SECTION I • Preparation and Prevention in Sports Medicine Environ-
suggests that VCD may occur in approximately 3% of ath- Persons with cardiovascular or pulmonary disease have a
letes who have a history of exercise-induced asthma. If VCD reduced ability to perform exercise when COHb is acutely
is the only diagnosis with no asthma involvement, then elevated. Several investigators have reported that patients
speech language therapy is beneficial.229 Speech language with angina have a decreased exercise time to angina onset;
therapy encompasses exercises to increase the patient’s systolic blood pressure and heart rate are lower at the onset
awareness of abdominal breathing and relaxing of the throat of angina, suggesting that angina occurs at a lower myocar-
muscles. This allows the patient to have more control of the dial oxygen uptake.214,215,238-240 Carbon monoxide expo-
vocal cords and throat.228 Also, learning cough suppression sure has also been shown to reduce the exercise tolerance
and throat clearing techniques can also be extremely benefi- of persons with chronic bronchitis, emphysema,241 and
cial. Practicing these techniques while asymptomatic is the anemia.242
key to overcoming abnormal vocal cord spasms and control-
ling the vocal cords to allow for proper airflow.228
Sulfur Oxides
Sulfur oxides are products of fossil fuel combustion and are
Carbon Monoxide upper respiratory tract irritants that can cause reversible
Carbon monoxide is the most frequently occurring air bronchoconstriction and increased airway resistance. The
pollutant in urban environments. It is released primarily dominant forms of sulfur oxides are sulfur dioxide, sulfuric
from auto emissions, but is also a byproduct of industrial acid, and sulfate, with 98% of the sulfur released into the
combustion and cigarette smoke. Carbon monoxide affects atmosphere in the form of sulfur dioxide.212
our health and physiological function by reducing the In healthy adults, sulfur dioxide does not impair pulmo-
oxygen-carrying capacity of the blood, as hemoglobin has a nary function until the concentration exceeds 1 to 3 ppm.243
200-times greater affinity for carbon monoxide than for However, in asthmatics and others with pulmonary hyperac-
oxygen. Thus, when the carboxyhemoglobin (COHb) con- tivity, the threshold for airway restriction is less than
centration is elevated, there is less hemoglobin available to 1 ppm,244-247 with one study reporting progressive broncho-
transport oxygen for cell respiration. constriction with exposure to 0.1 to 0.5 ppm sulfur diox-
Normal resting COHb concentration is approximately ide.246 To these authors’ knowledge, no study has evaluated
1%, but many behaviors can significantly increase COHb whether sulfur dioxide exposure impairs either endurance
concentration. Driving with an open window during exercise performance or maximal oxygen uptake.
peak traffic hours, for example, can raise the COHb con- Repeated exposure to sulfur dioxide does induce adapta-
centration to 5%.214 Aerobic exercise under similar condi- tion. Industrial workers routinely exposed to 10 ppm sulfur
tions can further increase COHb, as the greater minute dioxide retain normal pulmonary function when exposed to
ventilation increases the amount of carbon monoxide 5 ppm sulfur dioxide.248 Andersen and colleagues249 con-
inhaled per unit time. Nicholson and Case230 reported ducted studies investigating the physiological responses that
that 30 minutes of running in New York City resulted occur when subjects breathe 1, 5, or 25 ppm sulfur dioxide
in COHb concentrations of 4% to 5%. Smoking three for 6 hours. They reported that the subjects tolerated each
cigarettes over a short time can increase COHb to concentration of sulfur dioxide “very well,” but investiga-
approximately 5%.39 tors who occasionally entered the climatic chamber reported
During light- to moderate-intensity aerobic exercise (30% that the 25-ppm sulfur dioxide concentrations were “almost
to 75% maximal oxygen uptake), healthy individuals can tol- intolerable.” These adaptations to sulfur dioxide occur in
erate COHb concentrations of up to 20% with no reduction both healthy and asthmatic individuals.250
in physical performance.231-233 However, during exercise at
70% to 75% maximal oxygen uptake, individuals with elevated
COHb have increased heart rates, greater respiratory distress, Nitrogen Oxides
and higher blood lactate concentrations compared with con- Nitrogen oxides develop from high-temperature combus-
trol conditions.231,234 In addition, there is evidence that high tive processes involving nitrogen and oxygen. The concen-
COHb (25% to 35%) concentrations may result in higher tration of nitrogen oxides is elevated during peak traffic
core temperatures during prolonged exercise.235 periods, at airports, and in the smoke accompanying ciga-
Carbon monoxide exposure appears to have little effect rette smoking and fire fighting. There are several forms
on maximal oxygen uptake up to 4% COHb.236 Beyond this of nitrogen oxides, including nitrous oxide, nitric oxide,
apparent threshold, however, maximal oxygen uptake nitrogen dioxide, dinitrogen dioxide, dinitrogen pentox-
declines approximately 0.9% with every 1% increase in ide, and nitrate ions. Nitrogen dioxide is known to be
COHb up to 35% COHb.237 Carbon monoxide appears to harmful to health; acute exposure to high nitrogen dioxide
reduce maximal oxygen uptake by reducing blood oxygen levels (200 to 4000 ppm) can cause severe pulmonary
transport capacity. Maximal cardiac output is unaffected by edema and death.251 At lower concentrations (2 to
carbon monoxide exposure.236 5 ppm), nitrogen dioxide increases airway resistance and
130 SECTION I • Preparation and Prevention in Sports Medicine
reduces pulmonary diffusion capacity.252,253 Fortunately, Ozone is a potent airway irritant, causing reflex broncho-
the ambient air concentration of nitrogen dioxide is gener- constriction in upper airways. The most common subjective
ally less than 1 ppm. symptoms are a cough, substernal soreness, and dryness of
For healthy persons, nitrogen dioxide concentrations of the upper respiratory passages. These symptoms can occur
less than 0.7 ppm appear to have no adverse affects on pul- after brief exposures to low concentrations of ozone (0.05 to
monary function or exercise performance.243,254 Aging does 0.10 ppm) and can persist for several hours after exposure.212
not appear to reduce tolerance to nitrogen dioxide.255 Furthermore, there may be heightened sensitivity to ozone
However, people with chronic obstructive pulmonary dis- during the initial hours following ozone exposure.260
ease and, presumably, other respiratory diseases have re- During light- to moderate-intensity exercise, exposure to
duced pulmonary function when exposed for 4 hours to ozone in the range of 0.2 to 0.4 ppm reduces pulmonary
0.3 ppm nitrogen dioxide.255 function and enhances subjective discomfort,261 but does not
appear to impair exercise performance. These ozone concen-
trations can produce cough, substernal pain, wheezing, and
Primary Particulates malaise during exercise,262 with the incidence of symptoms
Primary particulates include dust, soot, and smoke.212,256 increasing in proportion to the ozone concentration.263,264
These pollutants are of physiological importance because During high-intensity aerobic exercise (75% to 85% maxi-
they can impair pulmonary function after they are inhaled mal oxygen uptake), ozone inhalation can impair endurance
into the lungs. The fine dust from charcoal257 and cigarette exercise performance. Schelegle and Adams265 evaluated the
smoke258 has been shown to increase airway resistance and effect of 0, 0.12, 0.18, or 0.24 ppm ozone exposure on the
reduce forced expiratory volume. The lung depth reached endurance performance of 10 highly trained athletes during
by the dust is determined by the particle size. The disper- 60 minutes of simulated competition (the last 30 minutes
sion of dust within the lung is influenced by the tidal vol- were at 86% of maximal oxygen uptake). All subjects com-
ume, frequency of breathing, and whether the particle was pleted the protocol when breathing 0 ppm ozone, whereas
inhaled nasally or orally.243 Because aerobic exercise in- one, five, and seven subjects did not complete the exercise
creases ventilation and oral inhalation, it is likely that exer- when exposed to 0.12, 0.18, and 0.24 ppm ozone, respec-
cise increases the effective dose of this pollutant. tively. Folinsbee and colleagues266 reported that inhalation of
Unfortunately, there is little information on the physio- 0.21 ppm ozone during 60 minutes of exercise at 75% of
logical consequences of particulate inhalation during exer- maximal oxygen uptake induced significant reductions in
cise. Klausen and colleagues259 suggested that inhalation of pulmonary function, and six of seven subjects developed
particulates may reduce endurance exercise time. In their subjective distress (symptoms included tracheal irritation,
study, subjects performed a maximal exercise test under substernal soreness, chest tightness, and shortness of breath).
control conditions after inhalation of the smoke of three Adams and Schelegle267 also documented decrements in pul-
cigarettes and after sufficient carbon monoxide inhalation monary function and subjective discomfort. In addition,
to raise their COHb concentration to the same magnitude they reported that 4 of 10 subjects could not complete the
as when they smoked three cigarettes. Interestingly, Klausen exercise trials when breathing 0.35 ppm ozone. Similarly,
and colleagues found that raising the COHb concentration Gibbons and Adams268 reported that 3 of 10 subjects discon-
produced a 7% reduction in maximal oxygen uptake in both tinued exercise prematurely when exposed to 0.3 ppm ozone
treatment groups, but endurance time during the maximal during 60 minutes of moderate-intensity (66% maximal oxy-
oxygen uptake test was reduced 20% after smoking and only gen uptake) exercise in a 35°C (95°F) environment.
10% after carbon monoxide inhalation. They interpreted Ozone inhalation can reduce maximal oxygen uptake.
the results to suggest that the decrease in maximal oxygen Folinsbee and colleagues269 reported a 10% reduction in
uptake after smoking or carbon monoxide inhalation was maximal oxygen uptake in those exposed to 0.75 ppm ozone.
due to reduced oxygen carrying capacity of the blood, Similarly, Gong and colleagues264 reported that 0.20 ppm
whereas the decrease in endurance time was a combined ozone reduced maximal oxygen uptake (16%), maximal
effect of the carbon monoxide concentration and the in- ventilation (18%), and exercise tolerance time (30%) dur-
creased cost of breathing caused by the smoke particulates. ing a graded exercise test following 1 hour of exercise. Not
all investigators have reported reductions in maximal oxygen
uptake after ozone exposure.270,271 One explanation for these
Ozone divergent findings may be the duration of ozone exposure
Ozone is produced in oxygen-containing atmospheres pri- prior to initiating the maximal exercise test, as the studies
marily from the interaction of hydrocarbons and nitrogen reporting no change in maximal oxygen uptake exposed the
dioxide in the presence of solar ultraviolet (UV) radiation. subjects to ozone only during the exercise test.
As a consequence, ozone is most prevalent in urban areas There is evidence that repeated ozone exposure produces
and reaches its highest concentration during the midday adaptations that attenuate ozone-induced reductions in pul-
hours. monary function261,272-280 and decrements in maximal oxygen
Environmental Considerations for Sports • CHAPTER 5 131
uptake and exercise time to exhaustion.281 This adaptation exercise performance and health. Because temperature typi-
generally occurs within 2 to 5 days of repeated exposure261,275- cally falls approximately 10°C with every 1500-meter (4921
280,282
and persists for 7 to 20 days upon discontinuation of feet) rise in elevation, even moderate increases in elevation can
exposure,280,282 with the least persistent adaptation occurring significantly magnify the degree of cold stress.293 Therefore,
in persons sensitive to ozone. However, acclimatization to individuals traveling to high altitudes should bring adequate
ozone does not attenuate decrements in pulmonary function clothing to protect themselves against environmental cold
when subjects are exposed to higher ozone concentrations.278 stress.
The time course of adaptation is similar between genders.261 The combined effects of cold and hypoxia on injury and
exercise performance remain poorly understood because of
a lack of experimental information. However, it is likely
Interactions Between Various Air Pollutants that the combined stress of cold and altitude exposure pre-
Because polluted atmospheres contain many contaminants, it disposes individuals to injury and premature fatigue be-
is important to investigate whether combinations of various cause (1) both body cooling and hypoxia impair mental
pollutants interact to affect pulmonary function and exercise function and decision-making ability; (2) the lower maxi-
performance in an additive, synergistic, or subtractive man- mal oxygen uptake at altitude reduces an individual’s abil-
ner. The majority of research has focused on the interaction ity to increase heat production and defend core tempera-
of various air pollutants with ozone. Although the early work ture; (3) both cold and hypoxic stress are associated with
of Hazucha and Bates283 suggested that exposure to 0.37 hemoconcentration and peripheral vasoconstriction, which
ppm ozone and 0.37 ppm sulfur dioxide resulted in synergis- may contribute to peripheral cold injury; and (4) because
tic reductions in pulmonary function, subsequent investiga- both cold and hypoxia increase blood lactic acid concentra-
tions found only additive effects.272,284-286 Koenig and col- tion at a given exercise intensity, premature fatigue may
leagues287 reported that asthmatic patients who received occur during exercise.
prior exposure to ozone had a greater decrement in pulmo-
nary function during subsequent exposure to sulfur dioxide
at dosages that were subthreshold for normal subjects. They Air Pollution and Heat
concluded that ozone exposure made the asthmatic subjects Because elevated concentrations of air pollutants are often
more susceptible to low concentrations of sulfur dioxide. associated with excessive heat and humidity,294 which are
Experiments that have evaluated the interaction of nitro- known to impair exercise performance, it is likely that the
gen dioxide and ozone suggest that there is no interaction combined stresses of excessive heat, humidity, and poor air
between the two compounds; the effects of the combina- quality further impair exercise performance. Gibbons and
tion produced no greater effects than exposure to ozone Adams268 found that subjective symptoms increased when
alone.262,263,288 The combination of nitrogen dioxide and ambient temperature was 35°C (95°F) rather than 25°C
sulfur dioxide appears to produce only additive effects. Pul- (77°F) and subjects were exposed to either 0.15 or 0.30
monary resistance is increased abruptly after sulfur dioxide ppm ozone during 60 minutes of moderately intense exer-
exposure, with no persistent effects; nitrogen dioxide has a cise. Furthermore, they reported that 3 of 10 subjects were
more delayed and persistent effect.289 Combining sub- unable to complete the 1-hour exercise bout (66% maximal
threshold doses of nitrogen dioxide (0.5 ppm) and sulfur oxygen uptake) when heat or ozone was present. Similarly,
dioxide (0.3 to 0.5 ppm) during 2 hours of light-intensity Folinsbee and colleagues295 reported greater reductions in
exercise does not induce deficits in pulmonary function in pulmonary function when subjects were exposed to 0.5 ppm
either healthy or asthmatic subjects.245 ozone during exercise in a hot climate compared with a cool
Particulates interact with carbon monoxide to produce climate. However, the same primary investigator subse-
greater reductions in endurance time than carbon monox- quently found no temperature interaction when subjects
ide alone.39 However, particulates do not appear to accen- were exposed to 0.5 ppm ozone and 0.5 ppm nitrogen
tuate the effects of ozone on pulmonary function in either dioxide.288
normal subjects or asthmatics.290-292 Rather surprisingly, there is no evidence that hot ambi-
ent temperatures and carbon monoxide produce either
additive or synergistic effects on maximal oxygen uptake
Interactions Between Environmental or performance. Because both hot ambient conditions and
Stressors increased COHb have individually been shown to reduce
maximal oxygen uptake, it would be expected that the
Cold and Altitude combination would produce additive reductions on maxi-
Ascent to high altitude is typically accompanied by reductions mal oxygen uptake and performance. The only studies to
in ambient temperature and humidity and increased wind date, however, reported no additive effect on maximal
velocity. These added environmental stressors exacerbate oxygen uptake when heat and carbon monoxide were
the physiological stress of hypoxia, potentially compromising combined.296-298
132 SECTION I • Preparation and Prevention in Sports Medicine
Athletes participating in outdoor activities should be 18. Consolazio CF, Matoush LO, Nelson RA, et al: Environmental
mindful of UV light and the negative effects on the skin temperature and energy expenditure, J Appl Physiol 18:65–68,
1963.
(also see Chapter 19, “Dermatologic Considerations in
19. Consolazio CF, Shapiro R, Masterson JE, et al: Energy require-
Athletics”). Athletes should train during times of low UV ments of men in extreme heat, J Nutr 73:126–134, 1961.
light exposure; wear appropriate clothing to adequately 20. Dimri GP, Malhotra MS, Sen Gupta J, et al: Alterations in
cover the skin, especially those areas identified as areas of aerobic-anaerobic proportions of metabolism during work in
high risk (neck, legs, arms); and use a sunscreen for areas heat, Eur J Appl Physiol 45:43–50, 1980.
21. Fink WJ, Costill DL, Van Handel WJ: Leg muscle metabolism
of the skin that cannot effectively be covered by clothing.
during exercise in the heat and cold, Eur J Appl Physiol 34:
A recent study noted high rates of sunburn and low rates of 183–190, 1975.
sun-protective behavior in high school and collegiate 22. Nielsen B, Savard G, Richter EA, et al: Muscle blood flow and
athletes despite their knowledge of the risks of excessive, muscle metabolism during exercise and heat stress, J Appl Physiol
unprotected sun exposure.317 Constant education from the 69:1040–1046, 1990.
23. Brouha L, Smith PE Jr, De Lanne R, et al: Physiological reactions
health care team and coaches on appropriate UV light pro-
of men and women during muscular activity and recovery in
tection from the sun is a critical component to ensure safe various environments, J Appl Physiol 16:133–140, 1960.
and healthy training during outdoor activities. 24. Petersen ES, Vejby-Christensen H: Effect of body temperature
on steady-state ventilation and metabolism in exercise, Acta
References Physiol Scand 89:342–351, 1973.
25. Williams CG, Bredell GAG, Wyndham CH, et al: Circulatory
1. Hardy JD: Physiology of temperature regulation, Physiol Rev and metabolic reactions to work in heat, J Appl Physiol 17:
41:521–606, 1961. 625–638, 1962.
2. Gonzalez RR, Berglund LG, Gagge AP: Indices of thermoregu- 26. Young AJ, Sawka MN, Levine L, et al: Skeletal muscle metabo-
latory strain for moderate exercise in the heat, J Appl Physiol lism during exercise is influenced by heat acclimation, J Appl
44:889–899, 1978. Physiol 59:1929–1935, 1985.
3. Lind AR: A physiological criterion for setting thermal environ- 27. Savard G, Nielsen B, Laszczynska I, et al: Muscle blood flow is
mental limits for everyday work, J Appl Physiol 18:51–56, 1963. not reduced in humans during moderate exercise and heat stress,
4. Nielsen M: Die Regulation der Körpertemperatur bei Muskelarbeit, J Appl Physiol 64:649–657, 1988.
Skand Arch Physiol 79:193–230, 1938. 28. Yaspelkis BB III, Scroop GC, Wilmore KM, et al: Carbohydrate
5. Nielsen M: Heat production and body temperature during rest metabolism during exercise in hot and thermoneutral environ-
and work. In Hardy JD, Gagge AP, Stolwijk JAJ, editors: Physi- ments, Int J Sports Med 14:13–19, 1993.
ological and behavioral temperature regulation, Springfield, IL, 29. Bean WB, Eichna LW: Performance in relation to environmental
1970, Charles C. Thomas. temperature: Reactions of normal young men to simulated desert
6. Stolwijk JAJ, Saltin B, Gagge AP: Physiological factors associated environment, Fed Proc 2:144–158, 1993.
with sweating during exercise, Aerospace Med 1968; 39:1101. 30. Eichna LW, Bean WB, Ashe WF, et al: Performance in relation to
7. American College of Sports Medicine: The prevention of thermal environmental temperature: Reactions of normal young men to
injuries during distance running, Med Sci Sports Exerc 19: hot, humid (simulated jungle) environment, Bull Johns Hopkins
529–533, 1987. Hosp 76:25–58, 1945.
8. Rowell LB: Human circulation: Regulation during physical stress, 31. Machle W, Hatch TF: Heat: Man’s exchanges and physiological
New York, 1986, Oxford University Press. responses, Physiol Rev 27:200–227, 1947.
9. Bevegård BS, Shepherd JT: Reaction in man of resistance and 32. Wenger CB: Human heat acclimatization. In Pandolf KB, Sawka
capacity vessels in forearm and hand to leg exercise, J Appl Physiol MN, Gonzalez RR, editors: Human performance physiology and
21:123–132, 1966. environmental medicine at terrestrial extremes, Indianapolis,
10. Hanke D, Schlepper M, Westermann K, et al: Venentonus, hut- 1988, Benchmark Press.
und mskeldurchblutung an uterarm und hand bei beinarbeit, 33. Armstrong LE, Maresh CM: The induction and decay of heat
Pflugers Arch 309:115–127, 1969. acclimatization in trained athletes, Sports Med 12:302–312,
11. Klausen K, Dill DB, Phillips EE Jr, et al: Metabolic reactions to 1991.
work in the desert, J Appl Physiol 22:292–296, 1967. 34. Gisolfi CV, Wilson NC, Claxton B: Work-heat tolerance of dis-
12. Rowell LB, Murray JA, Brengelmann GL, et al: Human cardio- tance runners. In Milvy P, editor: The marathon: Physiological,
vascular adjustments to rapid changes in skin temperature during medical, epidemiological, and psychological studies, New York,
exercise, Circ Res 24:711–724, 1969. 1977, New York Academy of Sciences.
13. Saltin B, Gagge AP, Stolwijk JAJ: Body temperatures and sweat- 35. Armstrong LE, Pandolf KB: Physical training, cardiorespiratory
ing during thermal transients caused by exercise, J Appl Physiol physical fitness and exercise-heat tolerance. In Pandolf KB, Sawka
28:318–327, 1970. MN, Gonzalez RR, editors: Human performance physiology and
14. Sawka MN, Young AJ, Cadarette BS, et al: Influence of heat environmental medicine at terrestrial extremes, Indianapolis,
stress and acclimation on maximal aerobic power, Eur J Appl 1988, Benchmark Press.
Physiol 53:294–298, 1985. 36. Avellini BA, Shapiro Y, Fortney SM, et al: Effects on heat toler-
15. Saltin B, Gagge AP, Bergh U, et al: Body temperatures and ance of physical training in water and on land, J Appl Physiol
sweating during exhaustive exercise, J Appl Physiol 32:635–643, 53:1291–1298, 1982.
1972. 37. Adams WC, Fox RH, Fry AJ, et al: Thermoregulation during
16. Nybo L: Exercise and heat stress: Cerebral challenges and conse- marathon running in cool, moderate, and hot environments,
quences, Prog Brain Res 162:29–43, 2007. J Appl Physiol 38:1030–1037, 1975.
17. Nielsen B, Nybo L: Cerebral changes during exercise in the heat, 38. Piwonka RW, Robinson S, Gay VL, et al: Preacclimatization of
Sports Med 33(1):1–11, 2003. men to heat by training, J Appl Physiol 20:379–384, 1965.
134 SECTION I • Preparation and Prevention in Sports Medicine
39. Piwonka RW, Robinson S: Acclimatization of highly trained men 62. Montain SJ, Sawka MN, Quigley MD, et al: Physiological tolerance
to work in severe heat, J Appl Physiol 22:9–12, 1967. to uncompensable heat stress: Effect of exercise intensity, protective
40. Ladell WSS: The effects of water and salt intake upon the perfor- clothing and climate, J Appl Physiol 77:216–222, 1994.
mance of men working in hot and humid environments, J Physiol 63. Speckman KL, Allan AE, Sawka MN, et al: Perspectives in micro-
127:11–46, 1955. climate cooling involving protective clothing in hot environ-
41. Montain SJ, Coyle EF: Influence of graded dehydration on ments, Int J Ind Ergonomics 3:121–147, 1988.
hyperthermia and cardiovascular drift during exercise, J Appl 64. Cage GW, Sato K, Schwachman N: Eccrine glands. In Fitzpatrick
Physiol 73:1340–1350, 1992. TB, Eisen AZ, Wolff K, et al, editors: Dermatology in general
42. Sawka MN, Young AJ, Francesconi RP, et al: Thermoregulatory medicine, New York, 1987, McGraw–Hill.
and blood responses during exercise at graded hypohydration 65. Davis PB, di Sant’Agnese PA: Diagnosis and treatment of cystic
levels, J Appl Physiol 59:1394–1401, 1985. fibrosis: An update, Chest 85:802–809, 1984.
43. Buskirk ER, Iampietro PF, Bass DE: Work performance after 66. Matthews LW, Drotar D: Cystic fibrosis—A challenging long-term
dehydration: Effects of physical conditioning and heat acclimati- chronic disease, Pediatr Clin North Am 31:133–151, 1984.
zation, J Appl Physiol 12:189–194, 1958. 67. De Marinis M, Stocchi F, Testa SR, et al: Alterations in thermo-
44. Sawka MN, Toner MM, Francesconi RP, et al: Hypohydration and regulation in Parkinson’s disease, Funct Neurol 6:279–283,
exercise: Effects of heat acclimation, gender, and environment, 1991.
J Appl Physiol 55:1147–1153, 1983. 68. Pandolf KB, Griffin TB, Munro EH, et al: Persistence of
45. Below PR, Coyle EF: Fluid and carbohydrate ingestion individu- impaired heat tolerance from artificially induced miliaria rubra,
ally benefit intense exercise lasting one-hour, Med Sci Sports Exerc Am J Physiol 239:R226–R232, 1980.
27:200–210, 1995. 69. Pandolf KB, Griffin TB, Munro EH, et al: Heat intolerance as a
46. Sawka MN, Young AJ, Latzka WA, et al: Human tolerance to function of percent of body surface involved with miliaria rubra,
heat strain during exercise: Influence of hydration, J Appl Physiol Am J Physiol 239:R233–R240, 1980.
73:368–375, 1992. 70. Leibowitz E, Seidman DS, Laor A, et al: Are psoriatic patients at
47. Rothstein A, Towbin EJ: Blood circulation and temperature of risk of heat intolerance? Br J Dermatol 124:439–442, 1991.
men dehydrating in the heat. In Adolph EF, editor: Physiology of 71. Pandolf KB, Gange RW, Latzka WA, et al: Human thermoregula-
man in the desert, New York, 1947, Interscience. tory responses during heat exposure after artificially induced
48. Montain SJ, Coyle EF: Influence of the timing of fluid ingestion sunburn, Am J Physiol 262:R610–R616, 1992.
on temperature regulation during exercise, J Appl Physiol 75: 72. Bar-Or O, Lundegren H, Buskirk ER: Heat tolerance of exercis-
688–695, 1993. ing obese and lean women, J Appl Physiol 26:403–409, 1969.
49. Coyle EF, Montain SJ: Carbohydrate and fluid ingestion during 73. Buskirk ER, Lundegren H, Magnusson L: Heat acclimation
exercise: Are there tradeoffs? Med Sci Sports Exerc 24:671–678, patterns in obese and lean individuals, Ann N Y Acad Sci 131:
1992. 637–653, 1965.
50. Mitchell JB, Voss KW: The influence of volume on gastric empty- 74. O’Sullivan SB, Schmitz TJ: Physical rehabilitation: Assessment
ing and fluid balance during prolonged exercise, Med Sci Sports and treatment, Philadelphia, 1988, FA Davis.
Exerc 23:314–319, 1991. 75. Clark WG, Lipton JM: Drug-related heatstroke. In Schönbaum E,
51. Epstein Y: Heat intolerance: Predisposing factor or residual Lomax P, editors: Thermoregulation: Pathology, pharmacology, and
injury? Med Sci Sports Exerc 22:29–35, 1990. therapy, New York, 1991, Pergamon Press.
52. Exton-Smith AN: Accidental hypothermia, Br Med J 4:727–729, 76. Lomax P: Drug induced changes in the thermoregulatory system.
1973. In Khogali M, Hales JRS, editors: Heat stroke and temperature
53. Pandolf KB, Cadarette BS, Sawka MN, et al: Thermoregulatory regulation, New York, 1983, Academic Press.
responses of matched middle-aged and young men during 77. Lomax P: Drug abuse and heatstroke. In Lomax P, Schönbaum E,
dry-heat acclimation, J Appl Physiol 65:65–71, 1988. editors: Thermoregulation: Research and clinical applications,
54. Seals DR: Influence of aging on autonomic-circulatory control at Basel, 1988, Karger.
rest and during exercise in humans. In Gisolfi CV, Lamb DR, Nadel 78. Levine L, Cadarette BS, Gonzalez RR, et al: Atropine and ther-
ER, editors: Perspectives in exercise science and sports medicine, Vol 6: moregulation in man (a report of three studies), Technical Report
Exercise, heat, and thermoregulation, Dubuque, 1993, Wm. C. T12/85, Natick, MA, 1985, US Army Research Institute of
Brown. Environmental Medicine.
55. Kolka MA, Stephenson LA, Gonzalez RR: Depressed sweating 79. Burr RE: Heat illness: A handbook for medical officers, Technical
during exercise at altitude, J Thermal Biol 14:167–170, 1989. Report 91–3, Natick, MA, 1991, US Army Research Institute of
56. Kolka MA, Stephenson LA, Rock PB, et al: Local sweating and Environmental Medicine.
cutaneous blood flow during exercise in hypoxic environments, 80. Haymes EM, Wells CL: Environment and human performance,
J Appl Physiol 62:2224–2229, 1987. Champaign, IL, 1986, Human Kinetics.
57. Frye AJ, Kamon E: Responses to dry heat of men and women 81. Howe AS, Boden BP: Heat-related illness in athletes, Am J Sports
with similar aerobic capacities, J Appl Physiol 50:65–70, 1981. Med 35(8):1384–1395, 2007.
58. Avellini BA, Kamon E, Krajewski JT: Physiological responses 82. Binkley HM, Beckett J, Casa DJ, et al: National Athletic Trainers’
of physically fit men and women to acclimation to humid heat, Association position statement: Exertional heat illnesses, J Athl
J Appl Physiol 49:254–261, 1980. Training 37(3):329–343, 2002.
59. Stephenson LA, Kolka MA: Thermoregulation in women, Exerc 83. Armstrong LE, Casa DJ, Millard-Stafford M, et al: Exertional
Sport Sci Rev 21:231–262, 1992. heat illness during training and competition, Med Sci Sports Exerc
60. Carpenter AJ, Nunneley SA: Endogenous hormones subtly alter 39(3):556–572, 2007.
women’s response to heat stress, J Appl Physiol 65:2313–2317, 84. Roberts WO: A 12-yr profile of medical injury and illness for the
1988. Twin Cities Marathon, Med Sci Sports Exerc 32:1549–1555, 2000.
61. Pivarnik JM, Marichal CJ, Spillman T, et al: Menstrual cycle 85. Casa DJ, Armstrong LE: Exertional heatstroke: A medical
phase affects temperature regulation during endurance exercise, emergency. In Armstrong LE, editor: Exertional heat illnesses,
J Appl Physiol 72:543–548, 1992. Champaign, 2003, Human Kinetics.
Environmental Considerations for Sports • CHAPTER 5 135
86. Armstrong LE, Casa DJ, Watson G: Exertional hyponatremia, 111. Bigland-Ritchie B, Thomas CK, Rice CL, et al: Muscle tempera-
Curr Sports Med Rep 5(5):221–222, 2006. ture, contractile speed, and motoneuron firing rates during
87. Salis RE: Fluid balance and dysnatremias in athletes, Curr Sports human voluntary contractions, J Appl Physiol 73:2457–2461,
Med Rep 7(4):S14–S19, 2008. 1992.
88. Mortiz ML, Ayus JC: Exercise-associated hyponatremia: Why are 112. Marshall HC: The effects of cold exposure and exercise upon
athletes still dying? Clin J Sports Med 18(5):379–381, 2008. peripheral function, Arch Environ Health 24:325–330, 1972.
89. Pendergast DR: The effect of body cooling on oxygen transport 113. Vanggaard L: Physiological reactions to wet-cold, Aviat Space
during exercise, Med Sci Sports Exerc 20:S171–S176, 1988. Environ Med 46:33–36, 1975.
90. Hong SI, Nadel ER: Thermogenic control during exercise in a 114. Johnson DJ, Leider FE: Influence of cold bath on maximum
cold environment, J Appl Physiol 47:1084–1089, 1979. handgrip strength, Percept Mot Skills 44:323–326, 1977.
91. Nielsen B: Metabolic reactions to changes in core and skin 115. Oliver RA, Johnson DJ, Wheelhouse WW, et al: Isometric muscle
temperature in man, Acta Physiol Scand 97:129–138, 1976. contraction response during recovery from reduced intramuscu-
92. Young AJ: Human adaptation to cold. In Pandolf KB, Sawka MN, lar temperature, Arch Phys Med Rehabil 60:126–129, 1979.
Gonzalez RR, editors: Human performance physiology and 116. Michalski WJ, Séguin JJ: The effects of muscle cooling and
environmental medicine at terrestrial extremes, Indianapolis, 1988, stretch on muscle spindle secondary endings in the cat, J Physiol
Benchmark Press. 253:341–356, 1975.
93. McArdle WD, Magel JR, Lesmes GR, et al: Metabolic and car- 117. Eldred E, Lindsley DF, Buchwald JS: The effect of cooling on
diovascular adjustments to work in air and water at 18, 25 and mammalian muscle spindles, Exp Neurol 2:144–157, 1960.
33ºC, J Appl Physiol 40:85–90, 1976. 118. Keatinge WR: The effect of work and clothing on the
94. McArdle WD, Magel JR, Gergley TJ, et al: Thermal adjustment maintenance of body temperature, Q J Exp Physiol 46:69–82,
to cold water exposure in exercising men and women, J Appl 1961.
Physiol 56:1572–1577, 1984. 119. Toner MM, McArdle WD: Physiological adjustments of man to
95. Nadel ER, Homer I, Bergh U, et al: Energy exchanges of swim- the cold. In Pandolf KB, Sawka MN, Gonzalez RR, editors:
ming man, J Appl Physiol 36:465–471, 1974. Human performance physiology and environmental medicine at
96. Amor AF, Vogel JA, Worsley DE: The energy cost of wearing mul- terrestrial extremes, Indianapolis, 1988, Benchmark Press.
tilayer clothing, Technical Report 18/73, Farnborough, England, 120. Toner MM, Sawka MN, Pandolf KB: Thermal responses during
1973, Royal Aircraft Establishment. arm and leg and combined arm-leg exercise in water, J Appl
97. Teitlebaum A, Goldman RF: Increased energy cost with multiple Physiol 56:1355–1360, 1984.
clothing layers, J Appl Physiol 32:743–744, 1972. 121. Park VS, Pendergast DR, Rennie DW: Decreases in body insula-
98. Pandolf KB, Givoni B, Goldman RF: Predicting energy expendi- tion with exercise in cold water, Undersea Biomed Res 11:
ture with loads while standing or walking very slowly, J Appl 159–168, 1984.
Physiol 43:577–581, 1977. 122. Veicsteinas A, Ferretti GT, Rennie DW: Superficial shell insula-
99. Bergh U, Ekblom B: Physical performance and peak aerobic power tion in resting and exercising man in cold, J Appl Physiol
at different body temperatures, J Appl Physiol 46:885–889, 1979. 52:1557–1564, 1982.
100. Davies M, Ekblom B, Bergh U, et al: The effects of hypothermia 123. Smith RM, Hanna JM: Skinfolds and resting heat loss in cold air and
on submaximal and maximal work performance, Acta Physiol water: Temperature equivalence, J Appl Physiol 39:93–102, 1975.
Scand 95:201–202, 1975. 124. Graham TE: Thermal, metabolic, and cardiovascular changes in
101. Dressendorfer RH, Morlock JF, Baker DG, et al: Effect of head- men and women during cold stress, Med Sci Sports Exerc 20:
out water immersion on cardiorespiratory responses to maximal S185–S192, 1988.
cycling exercise, Undersea Biomed Res 3:177–187, 1976. 125. Baum E, Bruck K, Schwennicke HP: Adaptive modifications in
102. Holmér I, Bergh U: Metabolic and thermal response to the thermoregulatory system of long-distance runners, J Appl
swimming in water at varying temperatures, J Appl Physiol Physiol 40:404–410, 1976.
37:702–705, 1974. 126. Bittel JHM, Nonotte-Varly C, Livecchi-Gonnot GH, et al:
103. Patton JF, Vogel JA: Effects of acute cold exposure on submaxi- Physical fitness and thermoregulatory reactions in a cold environ-
mal endurance performance, Med Sci Sports Exerc 16:494–497, ment in men, J Appl Physiol 65:1984–1989, 1988.
1984. 127. Kollias J, Boileau R, Buskirk ER: Effects of physical conditioning
104. Faulkner JA, White TP, Markley JM: The 1979 Canadian ski in man on thermal responses to cold air, Int J Biometeorol
marathon: A natural experiment in hypothermia. In Nagle FJ, 16:389–402, 1994.
Montoye HJ, editors: Exercise in health and disease—Balke 128. Adams T, Heberling EJ: Human physiological responses to a
Symposium, Springfield, IL, 1981, Charles C. Thomas. standardized cold stress as modified by physical fitness, J Appl
105. Adolph EF, Molnar GW: Exchanges of heat and tolerances Physiol 13:226–230, 1958.
to cold in men exposed to outdoor weather, Am J Physiol 129. Young AJ, Sawka MN, Latzka WA, et al: Effect of aerobic fitness
146:507–537, 1946. on thermoregulation, Med Sci Sports Exerc 25:S62, 1993.
106. Doubt TJ: Physiology of exercise in the cold, Sports Med 11: 130. Vaisrub S: Accidental hypothermia in the elderly, J Am Med Soc
367–381, 1991. 239:1888, 1978.
107. Bergh U, Ekblom B: Influence of muscle temperature on 131. Taylor G: The problem of hypothermia in the elderly, Practitioner
maximal muscle strength and power output in human skeletal 193:761–767, 1964.
muscles, Acta Physiol Scand 107:33–37, 1979. 132. Horvath SM, Rochelle RD: Hypothermia in the aged, Environ
108. Asmussen E, Bonde-Peterson F, Jorgensen K: Mechano-elastic Health Perspect 20:127–130, 1977.
properties of human muscles at different temperatures, Acta 133. Young AJ: Effects of aging on human cold tolerance, Exp Aging
Physiol Scand 96:83–93, 1976. Res 17:205–213, 1991.
109. Petrofsky JS: Isometric exercise and its clinical implications, 134. Collins KJ, Dore C, Exton-Smith AN, et al: Accidental hypother-
Springfield, IL, 1982, Charles C Thomas. mia and impaired temperature control homeostasis in the elderly,
110. Edwards RHT, Harris RC, Hultman E, et al: Effect of temperature Br Med J 1:353–356, 1977.
on muscle energy metabolism and endurance during successive 135. Collins KJ, Easton JC, Exton-Smith AN: Shivering thermogen-
isometric contractions, sustained to fatigue, of the quadriceps esis and vasomotor responses with convective cooling in the
muscle in man, J Physiol 220:335–352, 1972. elderly, J Physiol 320:76, 1981.
136 SECTION I • Preparation and Prevention in Sports Medicine
136. Horvath SM, Radcliffe CE, Hutt BK, et al: Metabolic responses 159. Paton BC: Accidental hypothermia. In Schönbaum E, Lomax P,
of old people to a cold environment, J Appl Physiol 8:145–148, editors: Thermoregulation: Pathology, pharmacology and therapy,
1955. New York, 1991, Pergamon Press.
137. Spurr GB, Hutt BK, Horvath SM: The effects of age on finger 160. Curtis R: Outdoor action guide to hypothermia and cold weather
temperature responses to local cooling, Am Heart J 50:551–555, injuries, Outdoor Action Program, The Trustees of Princeton
1955. University. Accessed November 18, 2008.from http://www.
138. Mathew L, Purkayastha SS, Singh R, et al: Influence of aging in princeton.edu/⬃oa/safety/hypocold.shtml.
the thermoregulatory efficiency of man, Int J Biometeorol 161. Wilkerson JA, editor: Medicine for mountaineering and other
30:137–145, 1986. wilderness activities, Seattle, WA, 1992, The Mountaineers
139. Wagner JA, Robinson S, Marino RP: Age and temperature regu- Books.
lation of humans in neutral and cold environments, J Appl Physiol 162. Mayo Clinic: Hypothermia, Mayo Foundation for Medical Edu-
37:562–565, 1974. cation and Research (MFMER), 2008. Accessed November 18,
140. Falk B, Bar-Or O, Smolander J, et al: Response to rest and exer- 2008 from www.MayoClinic.com.
cise in the cold: Effects of age and aerobic fitness, J Appl Physiol 163. Health A to Z: Hypothermia, August 2006. Accessed November
76:72–78, 1994. 18, 2008 from www.healthatoz.com/healthatoz/Atoz/common/
141. Freund BJ, O’Brien C, Young AJ: Alcohol ingestion and tem- standard/transform.jsp?requestURI5/healthatoz/Atoz/ency/
perature regulation during cold exposure, Wildern Med 5:88–98, hypothermia.jsp.
1994. 164. Wikipedia The Free Encyclopedia: Frostbite, Wikimedia Founda-
142. Haight JSJ, Keatinge WR: Failure of thermoregulation in the tion Inc, 2008. Accessed November 18, 2008 from http://
cold during hypoglycemia induced by exercise and ethanol, en.wikipedia.org/wiki/Frostbite.
J Physiol 229:87–97, 1973. 165. Hackett PH, Roach RC, Sutton JR: High altitude medicine. In
143. Graham T, Dalton J: Effect of alcohol on man’s response to mild Auerbach PS, Geehr EC, editors: Management of wilderness and
physical activity in a cold environment, Aviat Space Environ Med environmental emergencies, St Louis, 1989, Mosby.
51:793–796, 1980. 166. Bezruchka S: High altitude medicine, Med Clin North Am
144. Gale EAM, Bennett T, Green JH, et al: Hypoglycaemia, hypo- 76:1481–1497, 1992.
thermia and shivering in man, Clin Sci 61:463–469, 1981. 167. Dempsey JA, Forester HV: Mediation of ventilatory adaptations,
145. Wagner JA, Horvath SM: Influences of age and gender on Physiol Rev 62:262–346, 1982.
human thermoregulatory responses to cold exposure, J Appl 168. Laciga P, Koller EA: Respiratory, circulatory, and ECG changes
Physiol 58:180–186, 1985. during acute exposure to high altitude, J Appl Physiol 41:
146. Jacobs I, Tiit T, Kerrigan-Brown D: Muscle glycogen depletion 159–167, 1976.
during exercise at 9ºC and 21ºC, Eur J Appl Physiol 54:35–39, 169. Huang SY, Alexander JK, Grover RF, et al: Hypocapnia and
1985. sustained hypoxia blunt ventilation on arrival at high altitude,
147. Martineau L, Jacobs I: Muscle glycogen utilization during shiver- J Appl Physiol 56:602–606, 1984.
ing thermogenesis in humans, J Appl Physiol 65:2046–2050, 170. Young AJ, Young PM: Human acclimatization to high terrestrial
1988. altitude. In Pandolf KB, Sawka MN, Gonzalez RR, editors:
148. Blomstrand E, Essén-Gustavsson B: Influence of reduced muscle Human performance physiology and environmental medicine at
temperature on metabolism in type I and type II human muscle terrestrial extremes, Indianapolis, 1988, Benchmark Press.
fibres during intensive exercise, Acta Physiol Scand 131:569–574, 171. Alexander JK, Hartley LH, Modelski M, et al: Reduction of
1987. stroke volume in man following ascent to 3,100 m altitude,
149. Young AJ, Sawka MN, Neufer PD, et al: Thermoregulation dur- J Appl Physiol 23:849–858, 1967.
ing cold water immersion is unimpaired by low muscle glycogen 172. Vogel JA, Hansen JE, Harris CW: Cardiovascular responses in
levels, J Appl Physiol 66:1809–1816, 1989. man during exhaustive work at sea level and high altitude, J Appl
150. Hong SK, Rennie DW, Park YS: Cold acclimatization and deac- Physiol 23:531–539, 1967.
climatization of Korean woman divers, Exerc Sport Sci Rev 14: 173. Vogel JA, Hartley LH, Cruz JC, et al: Cardiac output during
231–268, 1986. exercise in sea level residents at sea level and high altitude, J Appl
151. LeBlanc J: Man in the cold, Springfield, IL, 1975, Charles C. Physiol 36:169–172, 1974.
Thomas. 174. Horstman D, Weiskopf R, Jackson RE: Work capacity during
152. Nelms JD, Soper DJG: Cold vasodilation and cold acclimatiza- 3-week sojourn at 4300 m: Effects of relative polycythemia,
tion in the hands of British fish filleters, J Appl Physiol 17: J Appl Physiol 49:311–318, 1980.
444–448, 1962. 175. Lockhart A, Saiag B: Altitude and the human pulmonary circula-
153. LeBlanc J: Local adaptation to cold of the Gaspé fishermen, tion, Clin Sci 60:599–605, 1981.
J Appl Physiol 17:950–952, 1962. 176. Milledge JS: Salt and water control at altitude, Int J Sports Med
154. Claus-Walker J, Halstead LS, Carter RE, et al: Physiological 13(suppl 1):S61–S63, 1992.
responses to cold stress in healthy subjects and in subjects with 177. Fortney SM, Nadel ER, Wenger CB, et al: Effect of blood vol-
cervical cord injuries, Arch Phys Med Rehabil 55:485–490, ume on sweating rate and body fluids in exercising humans,
1974. J Appl Physiol 51:1594–1600, 1981.
155. Teng HC, Heyer HE: The relationship between sudden changes 178. Hannon JP: Comparative altitude adaptability in young men and
in weather and the occurrence of acute myocardial infarction, women. In Folinsbee LJ, Wagner JA, et al, editors: Environmen-
Am Heart J 49:9–20, 1955. tal stress, New York, 1978, Academic Press.
156. Anderson SD: Issues in exercise-induced asthma, J Allergy Clin 179. Buskirk ER: Decrease in physical work capacity at high altitude.
Immunol 76:763–772, 1985. In Hegnauer AH, editor: Biomedicine of high terrestrial
157. Kalant H, Le AD: Effects of ethanol on thermoregulation, elevations, Natick, MA, 1969, US Army Research Institute of
Pharmacol Ther 23:313–364, 1984. Environmental Medicine.
158. Kortelainen MJ: Drugs and alcohol in hypothermia and hyper- 180. Young AJ, Cymerman A, Burse RL: The influence of cardiorespi-
thermia related deaths: A retrospective study, J Forensic Sci ratory fitness on the decrement in maximal aerobic power at high
32:1704–1712, 1987. altitude, Eur J Appl Physiol 54:12–15, 1985.
Environmental Considerations for Sports • CHAPTER 5 137
181. Fulco CS, Cymerman A: Human performance and acute 203. Levine BD, Stray-Gundersen J: A practical approach to altitude
hypoxia. In Pandolf KB, Sawka MN, Gonzalez RR, editors: training: Where to live and train for optimal performance
Human performance physiology and environmental medicine at enhancement, Int J Sports Med 13(suppl 1):S209–S212, 1992.
terrestrial extremes, Indianapolis, 1988, Benchmark Press. 204. Daniels J, Oldridge N: The effects of alternated exposure to alti-
182. Gleser MA: Effects of hypoxia and physical training on hemody- tude and sea level on world-class middle-distance runners, Med
namic adjustments to one-legged cycling, J Appl Physiol 34: Sci Sports Exerc 2:107–112, 1970.
655–659, 1973. 205. Levine BD, Engfred K, Friedman DB, et al: High altitude endur-
183. Grover RF, Weil JV, Reeves JT: Cardiovascular adaptation to exer- ance training: Effect on aerobic capacity and work performance,
cise at high altitude, Exerc Sport Sci Rev 14:269–302, 1986. Med Sci Sports Exerc 22:S35, 1990.
184. Stenberg J, Ekblom B, Messin R: Hemodynamic response 206. Brammell H, Morgan B, Niccoli S, et al: Exercise tolerance is
to work at simulated altitude, 4000m, J Appl Physiol 21: reduced at high altitude in patients with coronary artery disease,
1589–1594, 1966. Circulation 55(suppl 2):371, 1988.
185. Faulkner JA, Daniels JT, Balke B: Effects of training at moderate 207. Neill W, Hallenhauer M: Impairment of myocardial O2 supply
altitude on physical performance capacity, J Appl Physiol 23: due to hyperventilation, Circulation 52:854–858, 1975.
85–89, 1967. 208. Ziolkowski L, Wojcik-Ziolkowska E: Ischemic alterations in elec-
186. Hansen JR, Vogel JA, Stelter GP, et al: Oxygen uptake in man trocardiogram and hemodynamic insufficiency during physical
during exhaustive work at sea level and high altitude, J Appl exercise in the mountain environment in patients after myocar-
Physiol 26:511–522, 1967. dial infarction, Przegl Lek 44:400–406, 1987.
187. Buskirk ER, Kollias J, Akers RF, et al: Maximal performance at 209. Graham WG, Houston CS: Short-term adaptation to moderate
altitude and on return from altitude in conditioned runners, altitude—Patients with chronic obstructive pulmonary disease,
J Appl Physiol 23:259–266, 1967. JAMA 240:1491–1494, 1978.
188. Adams WC, Bernauer EM, Dill DB, et al: Effects of equivalent 210. Cymerman A, Rock PB: Medical problems in high mountain envi-
sea level and altitude training on VO2 max and running perfor- ronments: A handbook for medical officers, Technical Report TN
mance, J Appl Physiol 39:262–266, 1975. 94-2, Natick, MA, 1994, US Army Research Institute of
189. Dill DB, Adams WC: Maximal O2 uptake at sea level and at Environmental Medicine.
3,090 m altitude in high school champion runners, J Appl Physiol 211. Rathat C, Richalet JP, Herry JP, et al: Detection of high-risk
30:854–859, 1971. subjects for high altitude diseases, Int J Sports Med 13(suppl 1):
190. Saltin B: Limitations to performance at altitude. In Sutton JR, S76–S78, 1992.
Houston CS, Coates G, editors: Hypoxia: The tolerable limits, 212. McCafferty WB: Air pollution and athletic performance, Spring-
Indianapolis, 1988, Benchmark Press. field, IL, 1981, Charles C. Thomas.
191. Reeves JT, Groves BM, Sutton JR, et al: Cardiac function with 213. Raven PB: Heat and air pollution: The cardiac patient. In Pollock
prolonged hypoxia. In Sutton JR, Houston CS, Coates G, ML, Schmidt DH, editors: Heart disease and rehabilitation,
editors: Hypoxia: The tolerable limits, Indianapolis, 1988, Boston, 1979, Houghton Mifflin.
Benchmark Press. 214. Aronow WS, Harris CN, Isbell MW, et al: Effect of freeway travel
192. Bouissou P, Peronnet F, Brisson G, et al: Metabolic and endo- on angina pectoris, Ann Intern Med 77:669–676, 1972.
crine responses to graded exercise under acute hypoxia, Eur 215. Aronow WS, Isbell MW: Carbon monoxide effect on exercise-
J Appl Physiol 55:290–294, 1986. induced angina pectoris, Ann Intern Med 79:392–395, 1973.
193. Escourrou P, Johnson DG, Rowell LB: Hypoxemia increases 216. Turcotte H, Langdeau JB, Thibault G, et al: Prevalence of respira-
plasma catecholamine concentrations in exercising humans, tory symptoms in an athlete, Respir Med 97(8):955–963, 2003.
J Appl Physiol 57:1507–1511, 1984. 217. Dorland’s Illustrated Medical Dictionary, ed 31, Philadelphia,
194. Knuttgen HG, Saltin B: Oxygen uptake, muscle high-energy 2007, Saunders.
phosphates, and lactate in exercise under acute hypoxic condi- 218. Allergy and Asthma Foundation of America: Asthma Overview,
tions in man, Acta Physiol Scand 87:368–376, 1973. 2008. Accessed November 7, 2008 from http://www.aafa.org/
195. Maher JT, Jones LG, Hartley LH: Effects of high altitude expo- display.cfm?id8.
sure on submaximal endurance capacity of man, J Appl Physiol 219. About.com: Asthma triggers—Causes of asthma, 2006. Accessed
37:895–898, 1974. November 6, 2008 from http://lungdiseases.about.com/od/
196. Mizuno M, Juel C, Bro-Rasmussen T, et al: Limb skeletal muscle asthma/a/asthma_causes.htm.
adaptation in athletes after training at altitude, J Appl Physiol 220. Mayo Clinic: Asthma—Treatments and drugs, 2008. Accessed
68:496–502, 1990. November 6, 2008 from http://www.mayoclinic.com/health/
197. Young AJ, Evans WJ, Cymerman A, et al: Sparing effect of asthma/DS00021/DSECTIONtreatments-and-drugs.
chronic high-altitude exposure on muscle glycogen utilization, 221. Discovery Health: Allergies and asthma—Diagnosing allergy and
J Appl Physiol 52:857–862, 1982. asthma, 2007. Accessed November 7, 2008 from http://health.
198. Brooks GA, Butterfield GE, Wolfe RR, et al: Decreased reliance discovery.com/centers/allergyasthma/treatment/testing.html.
on lactate during exercise after acclimatization to 4,300 m, 222. Health A to Z: Spirometry, June 2007. Accessed November 7,
J Appl Physiol 71:333–341, 1991. 2008 from http://www.myoptumhealth.com/portal/Informa-
199. Green HJ, Sutton JR, Wolfel EE, et al: Altitude acclimatization tion/item/Spirometry?archiveChannelHome%2FArticle&
and energy metabolic adaptations in skeletal muscle during exer- clickedtrue.
cise, J Appl Physiol 73:2701–2708, 1992. 223. About.com: Methacholine challenge for asthma testing—
200. Cooke R, Pate E: The effects of ADP and phosphate on the Bronchoprovation, May 2008. Accessed November 7, 2008 from
contraction of muscle fibers, Biophys J 48:789–798, 1985. http://asthma.about.com/od/asthmatesting/p/methchallenge.
201. Fulco CS, Cymerman A, Muza SR, et al: Adductor pollicis mus- htm.
cle fatigue during acute and chronic altitude exposure and return 224. About.com: Allergy testing for asthma. Diagnosing asthma,
to sea level, J Appl Physiol 77:179–183, 1994. December 2007. Accessed November 7, 2008 from http://asthma.
202. Crow TJ, Kelman GR: Psychological effects of mild acute about.com/lw/Health-Medicine/Conditions-and-diseases/
hypoxia, Br J Anaesth 45:335–337, 1973. Allergy-Testing-and-Asthma.htm.
138 SECTION I • Preparation and Prevention in Sports Medicine
225. Morton AR, Fitch KD: Asthma. In Skinner JS: Exercise testing 246. Sheppard D, Saisho A, Nadel JA, et al: Exercise increases sulfur
and exercise prescription for special cases, ed 3, Baltimore, 2005, dioxide–induced bronchoconstriction in asthmatic subjects, Am
Lippincott Williams & Wilkins. Rev Respir Dis 123:486–491, 1981.
226. Moorman JE, Rudd RA, Johnson CA, et al: National Surveillance 247. Sheppard D, Wong WS, Uehara CF, et al: Lower threshold
for Asthma –United States, 1980-2009, Morb Mortal Wkly Rep and greater bronchomotor responsiveness of asthmatic sub-
56(s508):1–4, 18–54, 2007. Accessed 11/7/2008 from http:// jects to sulfur dioxide, Am Rev Respir Dis 122:873–878,
www.cdc.gov/ mmwr/preview/mmwrhtml/ss5608/al.htm 1980.
227. Sidofsky C: Can’t breathe? Suspect vocal cord dysfunction! 2001. 248. Amdur MO, Melvin WW Jr, Drinker P: Effects of inhalation of
Accessed at http://www.cantbreathesuspectvcd.com/. sulfur dioxide in man, Lancet 265:758–759, 1953.
228. National Jewish Health: Management and treatment of vocal cord 249. Andersen I, Lundqvist GR, Jensen PL, et al: Human response
dysfunction, July 2006. Accessed November 7, 2008 from to controlled levels of sulfur dioxide, Arch Environ Health
http://www.nationaljewish.org/disease-info/diseases/vcd/ 28:31–39, 1974.
management.aspx. 250. Sheppard D, Epstein J, Bethel RA, et al: Tolerance to sulfur
229. Brugman SM, Simons MD, Stephen M: Vocal cord dysfunction: dioxide–induced bronchoconstriction in subjects with asthma,
Don’t mistake it for asthma, Phys Sportsmed 26(5):63–85, Environ Res 30:412–419, 1983.
1998. 251. Lowry T, Schuman LM: “Silo-filler’s disease”—A syndrome
230. Nicholson JP, Case DB: Carboxyhemoglobin levels in New York caused by nitrogen dioxide, JAMA 162:153–160, 1956.
City runners, Phys Sportsmed 11:135–138, 1983. 252. Von Nieding G, Krekeler G, Fuchs H, et al: Studies of the acute
231. Ekblom B, Huot R: Response to submaximal and maximal exer- effects of NO2 on lung function: Influence of diffusion, perfu-
cise at different levels of carboxyhemoglobin, Acta Physiol Scand sion, and ventilation in the lungs, Int Arch Arbeitsmed 31:
86:474–482, 1972. 61–72, 1973.
232. Gliner JA, Raven PB, Horvath SM, et al: Man’s physiological 253. Von Nieding G, Wagner M, Krekeler G, et al: Minimum concentra-
response to long-term work during thermal and pollutant stress, tions of NO2 causing acute effects on the respiratory gas exchange
J Appl Physiol 39:628–632, 1975. and airway resistance in patients with chronic bronchitis, Int Arch
233. Pirnay F, Dujardin J, Deroanne R, et al: Muscular exercise during Arbeitsmed 27:338–348, 1971.
intoxication by carbon monoxide, J Appl Physiol 31:573–575, 254. Horvath SM, Folinsbee LJ: The effect of nitrogen dioxide on lung
1971. function in normal subjects, Research Triangle Park, NC, 1978,
234. Vogel JA, Gleser MA: Effect of carbon monoxide on oxygen US Environmental Protection Agency.
transport during exercise, J Appl Physiol 32:234–239, 1972. 255. Morrow PE, Utell MJ, Bauer MA, et al: Pulmonary performance
235. Nielsen B: Exercise temperature plateau shifted by a moderate of elderly normal subjects and subjects with chronic obstructive
carbon monoxide poisoning, J Physiol (Paris) 63:362–365, 1971. pulmonary disease exposed to 0.3 ppm nitrogen dioxide, Am
236. Horvath SM, Raven PB, Dahms TE, et al: Maximal aerobic Rev Respir Dis 145:291–300, 1992.
capacity at different levels of carboxyhemoglobin, J Appl Physiol 256. Pierson WE, Covert DS, Koenig JQ: Air pollutants, bronchial
38:300–303, 1975. hyperreactivity, and exercise, J Allergy Clin Immunol 73:
237. Horvath SM: Impact of air quality in exercise performance, Exerc 717–721, 1984.
Sport Sci Rev 9:265–296, 1981. 257. Widdicombe JG, Kent DC, Nadel JA: Mechanism of broncho-
238. Anderson EW, Andelman RJ, Strauch JM, et al: Effect of low- constriction during inhalation of dust, J Appl Physiol 17:
level carbon monoxide exposure on onset and duration of angina 613–616, 1962.
pectoris: A study in ten patients with ischemic heart disease, Ann 258. Nadel JA, Comroe JH Jr: Acute effects of inhalation of
Intern Med 79:46–50, 1973. cigarette smoke on airway conductance, J Appl Physiol 16:713–716,
239. Allred EN, Bleecker ER, Chaitman BR, et al: Short-term effects 1961.
of carbon monoxide exposure on the exercise performance 259. Klausen K, Andersen C, Nandrop S: Acute effects of cigarette
of subjects with coronary artery disease, N Engl J Med 321: smoking and inhalation of carbon monoxide during maximal
1426–1432, 1989. exercise, Eur J Appl Physiol 51:371–379, 1983.
240. Adams KF, Koch G, Chatterjee B, et al: Acute elevation of blood 260. Schonfeld BR, Adams WC, Schelegle ES: Duration of enhanced
carboxyhemoglobin to 6% impairs exercise performance and responsiveness upon re-exposure to ozone, Arch Environ Health
aggravates symptoms in patients with ischemic heart disease, 44:229–236, 1989.
J Am Coll Cardiol 12:900–909, 1988. 261. Dimeo MJ, Glenn MG, Holtzman MJ, et al: Threshold concen-
241. Calverley PM, Leggett RJ, Flenley DC: Carbon monoxide and tration of ozone causing an increase in bronchial reactivity in
exercise tolerance in chronic bronchitis and emphysema, Br Med J humans and adaptation with repeated exposures, Am Rev Respir
283:878–880, 1981. Dis 124:245–248, 1981.
242. Aronow WS, Schlueter WJ, Williams MA, et al: Aggravation of 262. Hackney JD, Linn WS, Mohler JG, et al: Experimental studies on
exercise performance in patients with anemia by 3% carboxyhe- human health effects of air pollutants II: Four-hour exposure to
moglobin, Environ Res 35:394–398, 1984. ozone alone and in combination with other pollutant gases, Arch
243. Pandolf KB: Air quality and human performance. In Pandolf KB, Environ Health 30:379–384, 1975.
Sawka MN, Gonzalez RR, editors: Human performance 263. Hackney JD, Linn WS, Law DC, et al: Experimental studies on
physiology and environmental medicine at terrestrial extremes, human health effects of air pollutants III: Two-hour exposure to
Indianapolis, 1988, Benchmark Press. ozone alone and in combination with other pollutant gases, Arch
244. Kirkpatrick MB, Sheppard D, Nadel JA, et al: Effect of the oro- Environ Health 30:385–390, 1975.
nasal breathing route on sulfur-dioxide-induced bronchocon- 264. Gong H, Brandley PW, Simmons MS, et al: Impaired exercise
striction in exercising asthmatic subjects, Am Rev Respir Dis performance and pulmonary function in elite cyclists during low-
125:627–631, 1982. level ozone exposure in a hot environment, Am Rev Respir Dis
245. Linn WS, Jones MP, Bailey RM, et al: Respiratory effects of 134:726–733, 1986.
mixed nitrogen dioxide and sulfur dioxide in human volunteers 265. Schelegle ES, Adams WC: Reduced exercise time in competitive
under simulated ambient exposure conditions, Environ Res simulations consequent to low level ozone exposure, Med Sci
22:431–438, 1980. Sports Exerc 18:408–414, 1986.
Environmental Considerations for Sports • CHAPTER 5 139
266. Folinsbee LJ, Bedi JF, Horvath SM: Pulmonary function changes 288. Folinsbee LJ, Bedi JF, Gliner JA, et al: Combined effects of
after 1 h continuous heavy exercise in 0.21 ppm ozone, J Appl ozone and nitrogen dioxide on respiratory function in man, Am
Physiol 57:984–988, 1984. Ind Hyg Assoc J 42:534–541, 1981.
267. Adams WC, Schelegle ES: Ozone and high ventilation effects on 289. Abe M: Effects of mixed NO2–SO2 gas on human pulmonary
pulmonary function and endurance performance, J Appl Physiol functions, Bull Tokyo Med Dent Univ 14:415–433, 1967.
55:805–812, 1983. 290. Avol EL, Linn WS, Shamoo DA, et al: Acute respiratory effects
268. Gibbons SI, Adams WC: Combined effects of ozone exposure of Los Angeles smog in continuously exercising adults, J Air
and ambient heat on exercising females, J Appl Physiol 57: Pollut Control Assoc 33:1055–1060, 1983.
450–456, 1984. 291. Avol EL, Linn WS, Venet TG, et al: Comparative respiratory
269. Folinsbee LJ, Silverman F, Shephard RJ: Decrease of maximum effects of ozone and ambient oxidant pollution exposure during
work performance following ozone exposure, J Appl Physiol heavy exercise, J Air Pollut Control Assoc 34:804–809, 1984.
42:531–536, 1977. 292. Linn WS, Jones MP, Bachmayer EA, et al: Short-term respiratory
270. Savin WM, Adams WC: Effects of ozone inhalation on work effects of polluted ambient air: A laboratory study of volunteers
performance and VO2 max, J Appl Physiol 46:309–314, 1979. in a high-oxidant community, Am Rev Respir Dis 121:243–252,
271. Horvath SM, Gliner JA, Matsen-Twisdale JA: Pulmonary func- 1980.
tion and maximum exercise responses following acute ozone 293. Ward M: Mountain medicine: A clinical study of cold and high
exposure, Aviat Space Environ Med 50:901–905, 1979. altitude, London, 1975, Crosby Lockwood Staples.
272. Bell KA, Linn WS, Hazucha M, et al: Respiratory effects of 294. Ellis FP: Mortality from heat illness and heat-aggravated illness in
exposure to ozone plus sulfur dioxide in southern Californians the United States, Environ Res 5:1–58, 1972.
and eastern Canadians, Am Ind Hyg Assoc J 38:696–706, 1977. 295. Folinsbee LJ, Horvath SM, Raven PB, et al: Influence of exercise
273. Hackney JD, Linn WS, Karuza SK, et al: Effects of ozone expo- and heat stress on pulmonary function during ozone exposure,
sure in Canadians and southern Californians: Evidence for adap- J Appl Physiol 43:409–413, 1977.
tation? Arch Environ Health 32:110–116, 1977. 296. Raven PB, Drinkwater BL, Horvath SM, et al: Age, smoking
274. Hackney JD, Linn WS, Mohler JG, et al: Adaptation to short- habits, heat stress, and their interactive effects with carbon mon-
term respiratory effects of ozone in men exposed repeatedly, oxide and peroxyacetylnitrate on man’s aerobic power, Int
J Appl Physiol 43:82–85, 1977. J Biometeorol 18:222–232, 1974.
275. Folinsbee LJ: Effects of ozone exposure on lung function in man: 297. Drinkwater BL, Raven PB, Horvath SM, et al: Air pollution,
A review, Rev Environ Health 3:211–240, 1981. exercise and heat stress, Arch Environ Health 28:177–181,
276. Folinsbee LJ, Bedi JF, Gliner JA, et al: Concentration depen- 1974.
dence of pulmonary function adaptation to ozone. In Mehlman 298. Raven PB, Drinkwater BL, Ruhling RO, et al: Effect of carbon
MA, Lee SD, Mustafa MG, editors: The biomedical effects of ozone monoxide and peroxyacetyl nitrate on man’s maximal aerobic
and related photochemical oxidants, Princeton Junction, NJ, capacity, J Appl Physiol 36:288–293, 1974.
1983, Princeton Scientific Publishers. 299. Katz RM: Prevention with and without the use of medications
277. Folinsbee LJ, Bedi JF, Horvath SM: Respiratory responses in for exercise-induced asthma, Med Sci Sports Exerc 18:331–333,
humans repeatedly exposed to low concentrations of ozone, Am 1986.
Rev Respir Dis 121:431–439, 1980. 300. Strauss RH, McFadden ER, Ingram RH Jr, et al: Enhancement
278. Gliner JA, Horvath SM, Folinsbee LJ: Preexposure to low ozone of exercise-induced asthma by cold air, N Engl J Med 297:
concentrations does not diminish the pulmonary function re- 743–747, 1977.
sponse on exposure to higher ozone concentrations, Am Rev 301. Wagner JA, Horvath SM, Andrew GM, et al: Hypoxia, smoking
Respir Dis 127:51–55, 1983. history, and exercise, Aviat Space Environ Med 49:785–791,
279. Horvath SM, Gliner JA, Folinsbee LJ: Adaptation to ozone: 1978.
Duration of effect, Am Rev Respir Dis 123:496–499, 1981. 302. Weiser PC, Morrill CG, Dickey DW, et al: Effects of low-level
280. Farrell BP, Kerr HD, Kulle TJ, et al: Adaptation in human sub- carbon monoxide exposure on the adaptation of healthy young
jects to the effects of inhaled ozone after repeated exposure, Am men to aerobic work at an altitude of 1,610 meters. In Folinsbee
Rev Respir Dis 119:725–730, 1979. LJ, Wagner JA, Borgia JF, et al, editors: Environmental stress:
281. Foxcroft WJ, Adams WC: Effects of ozone exposure on four Individual human adaptations, New York, 1978, Academic
consecutive days on work performance and VO2 max, J Appl Press.
Physiol 61:960–966, 1986. 303. National Weather Service: http://www.lightningsafety.noaa.
282. Linn WS, Medway DA, Anzar UT, et al: Persistence of adapta- gov/overview.htm. Accessed April 10, 2009.
tion to ozone in volunteers exposed repeatedly for six weeks, Am 304. DeFranco MJ, Baker CL, DaSilva JJ, et al: Environmental issues
Rev Respir Dis 125:491–495, 1982. for team physicians, Am J Sports Med 36(11):2226–2237, 2008.
283. Hazucha M, Bates DV: Combined effect of ozone and sulphur 305. Fish R: Lightning injuries. In Tintinalli JE, Kelen GD,
dioxide on human pulmonary function, Nature 257:50–51, 1975. Stapczynski JS, editors: Emergency medicine: A comprehensive
284. Bedi JF, Folinsbee LJ, Horvath SM, et al: Human exposure to study guide, New York, 2004, McGraw Hill.
sulfur dioxide and ozone: Absence of a synergistic effect, Arch 306. Walsh KM, Bennett B, Cooper MA, et al: National Athletic
Environ Health 34:233–239, 1979. Trainers’ Association position statement: Lightning safety for
285. Bedi JF, Horvath SM, Folinsbee LJ: Human exposure to sulfur athletics and recreation, J Athl Training 35(4):471–477,
dioxide and ozone in a high temperature-humidity environment, 2000.
Am Ind Hyg Assoc J 43:26–30, 1982. 307. National Severe Storms Laboratory: Accessed April 19, 2009 from
286. Folinsbee LJ, Bedi JF, Horvath SM: Pulmonary response http://www.nssl.noaa.gov/primer/lightning/ltg_damage.html.
to threshold levels of sulfur dioxide (1.0 ppm) and ozone 308. Moehrle M: Ultraviolet exposure in the Ironman triathalon, Med
(0.3 ppm), J Appl Physiol 58:1783–1787, 1985. Sci Sports Exerc 33:1385–1386, 2001.
287. Koenig JQ, Covert DS, Hanley QS, et al: Prior exposure to 309. Moehrle M, Heinrich L, Schmid A, et al: Extreme UV exposure
ozone potentiates subsequent response to sulfur dioxide in ado- of professional cyclists, Dermatology 201:44–45, 2000.
lescent asthmatic subjects, Am Rev Respir Dis 141:377–380, 310. DeFranco MJ, Baker CL III, DaSilva JJ, et al: Environmental issues
1990. for team physicians, Am J Sports Med 36:2226–2237, 2008.
140 SECTION I • Preparation and Prevention in Sports Medicine
311. Cho E, Rosner BA, Feskanich D, et al: Risk factors and individual 315. Han A, Maibach HI: Management of acute sunburn, Am J Clin
probabilities of melanoma for whites, J Clin Oncol 23: Dermatol 5:39–47, 2004.
2669–2675, 2005. 316. Katiyar SK, Matsui MS, Mukhtar H: Kinetics of UV light-
312. Elwood JM, Jopson J: Melanoma and sun exposure: An overview induced cyclobutane pyrimidine dimers in human skin in vivo:
of published studies, Int J Cancer 73:198–203, 1997. An immunohistochemical analysis of both epidermis and dermis,
313. Gallagher RP, Hill GB, Bajdik CD, et al: Sunlight exposure, Photochem Photobiol 72:788–793, 2000.
pigmentary factors, and risk of nonmelanocytic skin cancer. 317. Cohen PH, Tsai H, Puffer JC: Sun-protective behavior among
I Basal cell carcinoma, Arch Dermatol 131:157–163, 1995. high school and collegiate athletes in Los Angeles, CA, Clin
314. Kricker A, Armstrong BK, English DR, et al: Does intermittent J Sport Med 16:253–260, 2006.
sun exposure cause basal cell carcinoma? A case-control study in
Western Australia, Int J Cancer 60:489–494, 1995.
6
CHAPTER
USE OF ERGOGENIC
AIDS IN SPORT*
Jeffrey J. Zachwieja, Elizabeth A. Mooradian, and Kimberly M. White
141
142 SECTION I • Preparation and Prevention in Sports Medicine
muscle glycogen (glycogenolysis) or uptake of blood glu- capacity (i.e., maximum oxygen consumption [VO2 max]),
cose, which for a time remains relatively constant because but, more importantly, also improve an athlete’s ability to
liver glucose output is able to keep pace with muscle glu- tolerate a higher percentage of aerobic capacity during pro-
cose extraction. Likewise, fatty acids liberated from periph- longed exercise. This equates to a faster pace and hence a
eral adipose tissue or intramuscular triglyceride stores can reduced time to cover a competitive distance.
provide substrate for the citric acid cycle and subsequent Left ventricular hypertrophy accounts for a substantial
ATP production by the electron transport chain. This portion of the increase in heart size that results from endur-
so-called fatty acid oxidation is fundamentally important, ance exercise training. Left ventricular hypertrophy contrib-
especially during endurance activity, because it lessens the utes to an increased stroke volume and greater maximal
demand on the limited supply of glucose for ATP produc- cardiac output in trained individuals. Submaximal heart rate
tion. Lastly, amino acids generated from protein breakdown is decreased during exercise because of a greater stroke vol-
can provide carbon backbone for citric acid cycle intermedi- ume and expanded plasma volume allowing for a greater
ates and thereby contribute to reducing equivalent genera- venous return in the trained state. Together with an
tion during exercise. Furthermore, amino acids such as ala- increased hemoglobin concentration and greater capillariza-
nine and glutamine are gluconeogenic precursors in the tion of skeletal muscle, these cardiovascular adaptations
liver and thus support liver glucose output. allow for a greater oxygen delivery to skeletal muscle during
The cardiovascular system is also an integral part of the maximal exercise.
response to endurance exercise. Heart rate, stroke volume,
and blood pressure increase to provide effective delivery of
Cardiovascular Endurance Adaptations
blood throughout the vascular system. Vasodilation and
vasoconstrictive processes direct blood flow to and permit
with Training
adequate perfusion of contracting skeletal muscle, and tis- • Hypertrophy of left ventricle
sues that are less metabolically active such as the gut, spleen, • Increased stroke volume
and kidney are perfused to a smaller extent. Adequate blood • Submaximal heart rate decreases
perfusion of contracting skeletal muscle is necessary to meet • Expanded plasma volume
the need for augmented oxygen and nutrient (i.e., glucose, • Greater venous return
fatty acids, and amino acids) uptake as well as removal of • Increased hemoglobin concentration
• Increased capillarization of skeletal muscle
metabolic wastes such as carbon dioxide (CO2), lactate,
and amino nitrogen from amino acid transamination and
deamination processes. Metabolic processes within skeletal
muscle are not 100% efficient. Therefore, heat is generated Regular endurance training also stimulates adaptations
and this too must be removed to ensure effective operating within skeletal muscle. The most prominent is an increase in
temperatures within skeletal muscle. The dissipation of mitochondrial biogenesis, which leads to more mitochondria
metabolic heat is achieved primarily by vascular adjustments and an expanded reticulum of mitochondria that resides amid
that redirect a portion of the blood flow to the skin. Vaso- the muscle cell architecture. This allows for more efficient
dilatation of blood vessels in the skin allow for heat loss oxygen use during submaximal exercise and the ability to
through conductive and convective processes. However, the consume more of the oxygen delivered to muscle during
largest portion of heat loss comes from evaporative cooling. maximal exercise. The activity of each mitochondria is also
Heat-activated sweat glands secrete large quantities of water enhanced in the trained state, exemplified by elevations in
and salts (sweat). When this sweat comes in contact with key enzymes responsible for the Krebs cycle and electron-
and evaporates from the skin surface, a cooling effect transport activity (i.e., citrate synthase and cytochrome C
occurs. The cooled skin reduces the temperature of blood oxidase, respectively). In the trained state, skeletal muscle has
that is shunted to it and in turn mitigates an excessive rise an increased capacity to oxidize fatty acids as a fuel and this
in core temperature. Although effective for cooling, sweat helps to conserve carbohydrate during prolonged exercise.
evaporation during prolonged exercise can significantly Paradoxically, endurance exercise training results in increased
reduce the body’s water and electrolyte reserves and induce intramuscular stores of triglycerides. Muscle glycogen content
a state of hypohydration. This can compromise cardiovascu- is also increased, most likely because of greater insulin sensitiv-
lar function and impede further heat dissipation. ity. Lactate production during submaximal exercise is de-
creased in endurance-trained muscle in addition to a greater
capacity for lactate clearance and oxidation. This is exempli-
Adaptation of Physiological Systems fied by lower blood lactate levels for any given level of sub-
to Chronic Endurance Training maximal exercise in the trained state. Lastly, endurance exer-
Cardiovascular and metabolic adaptations in skeletal muscle cise training up-regulates key endogenous antioxidant enzymes
occur in response to chronic endurance exercise training. and systems most likely to deal with elevated production of
These adaptations allow for an increase in maximum aerobic reactive oxygen species (ROS) (i.e., free radicals).
Use of Ergogenic Aids in Sport • CHAPTER 6 143
The brain is indeed a metabolically active organ and its temperature regulation, sleep, lethargy, drowsiness, and loss
metabolism is in response to heightened neurological activ- of motivation. The latter behavioral effects of serotonin
ity and helps to drive such activity. For example, when the have been used to form the basis of an exercise central
brain is activated in response to a mental task, global blood fatigue hypothesis.7 The amino acid tryptophan is the pre-
flow to the brain is increased to supply oxygen and nutri- cursor for serotonin synthesis. During exercise, free trypto-
ents. However, during exercise, global blood flow to the phan levels in the blood increase because an elevation in free
brain is similar to blood flow to the brain at rest because it fatty acids (FFAs) displaces albumin-bound tryptophan.
seems to be under the influence of arterial CO2 tension This, in combination with a reduction in circulating
rather than changes in the metabolic state related to motor branched amino acid concentration, increases the transport
activation.4 With increasing exercise intensity, arterial CO2 of tryptophan across the blood-brain barrier, resulting in an
tension is reduced (as a result of hyperventilation) and this elevated rate of serotonin synthesis and the resultant behav-
results in a constriction of cerebral arterioles leading to re- ioral effects of lethargy and loss of motivation, leading to a
duced blood flow even though brain metabolic activity is decline in physical effort. Indeed, exercise in humans ele-
elevated. Fortunately, increased oxygen extraction can vates free tryptophan levels in blood as well as prolactin
compensate for lower perfusion under these circumstances. levels, a hormone secreted from the pituitary gland and
Regional blood flow in the brain may be the more impor- under the influence of serotonin stimulation. Thus, an ele-
tant dynamic at the onset and with continued exercise.5,6 vation in blood prolactin concentration has been used as a
During exercise, blood flow to cortical motor areas in the “biomarker” of central serotonergic activity. However, sero-
brain increase, as does flow to sensorimotor cortex areas tonin is one of many neurotransmitters in the brain and it
presumably for adjustment of central command or fatigue- seems extremely unlikely that it could be the sole source of
related feedback. In addition, exercise increases flow to fatigue induction during exercise. For example, dopamine is
areas of the brain related to cardiovascular, respiratory, and known to play an important role in motor activation and its
thermoregulatory control. metabolism is enhanced during exercise. An emerging
Increases in regional blood flow in the brain are important variation on the central fatigue hypothesis states the ratio of
not only for oxygen delivery but also for glucose delivery. serotonin-to-dopamine may be an important determinant
Glucose is the main energy source for brain cells and a con- of fatigue development rather than either one alone.8
tinuous systemic supply is necessary because there is very
little glycogen storage in neuronal tissue. Under conditions of
demanding exercise, glucose metabolism in the brain can Clinical Point
limit performance in two main ways. First, if neuronal activity
Neurotransmitters and its production play a major role in autonomic
exceeds the capacity for aerobic and anaerobic metabolism of
and behavioral functions.
glucose, brain cell function will deteriorate, lessening the
effectiveness of central command and homeostatic regulation.
Second, the energy generated as the result of oxidation of
glucose in brain cells will end up entirely as heat because no
mechanical work is performed in these cells. Although under Causes of Fatigue During Endurance Activity
normal circumstances this heat is adequately removed by the There are likely two contributing factors to the onset of
cerebral circulation, during exercise, especially under condi- fatigue during prolonged exercise, one that is centrally medi-
tions of environmental heat stress, heat removal from the ated and another that is peripherally mediated. Environmen-
brain is impaired and heat storage can occur. tal conditions (e.g., hot, humid, cold, altitude) and the level
of physical training can have an influence on how and when
these site-specific fatigue mechanisms are expressed. Classic
Clinical Point literature reduction tells us that peripheral fatigue likely re-
sults from substrate depletion (i.e., low muscle glycogen and
Elevation of brain temperature above a critical level can reduce blood glucose) or accumulation of metabolic byproducts,
activity of motor neurons and thus central drive.
including the possibility of free-radical mediated oxidative
damage to contractile proteins and those proteins responsible
for initiating and maintaining calcium fluxes important for
The most popular and well-studied brain biochemical contractile activity. Hypohydration and hyperthermia are
pathway as it relates to exercise is the serotonergic system. common during prolonged exercise and can influence cen-
Serotonergic neurotransmission depends on the synthesis, trally mediated mechanisms (e.g., CNS and cardiovascular)
storage, release, and re-uptake of serotonin from neuronal that precipitate fatigue. In what seems to be the ultimate
projections. Serotonergic neurons play a key role in various central fatigue hypothesis, Noakes and colleagues9 have pro-
autonomic and behavioral functions; elevations in brain posed the central governor model. Essentially, this model
serotonin levels have been linked to feeding behavior, proposes that the brain regulates motor unit recruitment
Use of Ergogenic Aids in Sport • CHAPTER 6 145
during exercise with a modus operandi of preventing com- That said, there are some emerging data for protein, various
plete physiological failure. Nonetheless, exercise-induced fa- amino acids, antioxidants, and carnitine that make these
tigue and fatigue processes remain a very controversial topic. ingredients increasingly attractive as ergogenic aids. Scien-
The exact mechanism or combinations of mechanisms have tific support and practical application principals for these
not been completely defined and to add to the complexity, ingredients are reviewed in the next section.
no one definition for fatigue during exercise can be agreed
upon. For example, does fatigue occur at a specific point in
time or are there small, incremental reductions in muscle Ergogenic Aids for Endurance that Have Little
force production that begin with the onset of exercise that Scientific Support, Lack Investigation or Are Illegal
are not detectable (mentally or physiologically) until later? • Aspartate
• Asparagine
• Bee Pollen
Clinical Point • Calcium
• Choline
Fatigue during endurance exercise may be centrally or peripherally • Coenzyme Q10
mediated. • Dimethylglycine (B15)
• Folic acid
• Ginseng
• Inosine
What does seem to be clear is that fatigue during pro-
• Citrulline-malate
longed exercise is simply not the result of substrate deple- • Medium chain triglycerides
tion (i.e., muscle and liver glycogen). Results of research • Niacin
conducted by Coggan and Coyle10 eloquently support this • Phosphates
point. They had cyclists pedal a stationary bicycle to a point • Rhodiola rosea
of volitional fatigue. Thereafter, three randomized, double- • Riboflavin (B2)
blind treatments were administered in a repeated measures • Ribose
design: (1) placebo, (2) oral glucose, and (3) glucose infu- • Taurine
sion. During the placebo and oral glucose trials, saline infu- • Thiamine
sions were conducted to achieve complete blinding, as was
oral ingestion of a placebo during glucose infusion. Time to
volitional fatigue during a second stationary cycling bout Although scientific support is often used as a guiding light
was longer during both glucose trials relative to placebo and for effectiveness, the statistical methodologies used to deter-
longest during glucose infusion. Glucose was infused at a mine if an experimental result is “significant” may be too
rate to match carbohydrate oxidation during exercise and to stringent for practical use. For example, most exercise and
maintain blood glucose. Thus, glucose substrate supply was nutrition science research uses hypothesis-testing approaches
not limiting, yet the subjects still became fatigued approxi- that deem results significant when there is a probability of
mately 40 minutes after initiating the second bout of exer- 1 out of 20 responses showing a false-positive effect. Most
cise. This indicates that factors in addition to substrate athletes would be far more lenient in their evaluation of the
supply contribute to fatigue during prolonged exercise. chance to receiving a positive benefit from a nutritional ergo-
genic aid. Furthermore, such objective measures as power
output and time are used as dependent variables in ergogenic
Sorting Out the Pros and Cons aid research. But consideration must be given to mood, sen-
for Nutritional Ergogenic Aids sation, and emotional domains, because they may be more
The basic tenet of a nutritional ergogenic aid for endurance powerful indicators of a positive effect and future success.
exercise is that consumption of a particular ingredient or Ultimately it comes down to calculating a favorable risk/
combination of ingredients will enhance performance, pre- benefit ratio when athletes and their advisors are deciding
sumably by delaying the onset of fatigue. Often, such aids whether to use an ergogenic aid. They should develop
derive from a focus on single metabolic pathways thought to ergogenic routines rooted in scientific support but also
be integral for muscle energy metabolism or central medi- proven within the realm of personal experience.
ated processes. Given the complexity of the underlying
physiological mechanisms contributing to the onset of fa-
tigue, it is not surprising that there is a long list of so-called
Clinical Point
ergogenic aids that have proven to be ineffective for prevent- If an athlete has a preconceived notion or believes something will
ing fatigue during prolonged exercise. In fact, nutritional work, there is a good chance that a positive performance outcome
approaches beyond simple hydration and carbohydrate feed- will be derived from the ergogenic tactic he or she believes in.
ing paradigms often fall short on relative effectiveness scales.
146 SECTION I • Preparation and Prevention in Sports Medicine
Most exercise scientists and practitioners recommend of exercise, he or she should try to drink an additional
water and electrolyte intake for hydration purposes during 24 ounces for a total of 36 ounces (12 24) to keep pace
prolonged exercise. Sodium is the major electrolyte lost in with sweat loss during that hour of exercise. It is important
sweat and its replacement seems to be the most critical for to note, however, the goal is to replace what has been lost
performance and health. Consuming pure water during without drinking too much. A weight gain after exercise
prolonged exercise at a rate that completely replaces sweat indicates that too much fluid has been consumed. Other
loss results in a progressive decline in plasma sodium, practical tips include drinking small volumes of fluid more
whereas consumption of an equal volume of water with frequently rather than a large bolus once feeling parched
sodium added maintained plasma sodium concentration.23 and drinking fluids that are lightly flavored, slightly salty,
Maintenance of plasma sodium during prolonged exercise and somewhat sweet as this will help encourage drinking
keeps cells and the vasculature in proper fluid balance for behavior that better offsets sweat loss, and, whenever pos-
optimal functioning. In addition, consumption of sodium sible, drink fluids that are cool (i.e., refrigerator tempera-
in water appears to increase voluntary drinking through an ture) rather than room temperature or warmer.
osmotic stimulus24 and can result in better replacement of
the fluid lost through sweat.25 In general, the causes of
muscle cramping are complex, but there appears to be a Clinical Point
subset of muscle cramps that are brought on by large fluid
and electrolyte losses during intense exercise in the heat. Monitoring body weight before and after exercise is a good way to
For example, there is a high incidence of exercise-induced monitor sweat loss and fluid needs.
muscle cramping in tennis players,26 American football
players,27 and military personnel deployed to hot environ-
ments.28 In particular, it has been shown that those football
players with a history of muscle cramping exhibit higher Adverse Effects. The only adverse effect associated
sweat rates and sweat sodium concentrations than those with hydration practices during prolonged exercise is
who do not.27 Likewise, Bergeron26 described a tennis the development of hyponatremia. Hyponatremia is a com-
player who suffered from frequent muscle cramping as hav- plication caused by low plasma sodium levels. A strict
ing a sweat rate of 2.5 L/hr and a sweat sodium concentra- definition of hyponatremia is a plasma sodium level less than
tion of 1.9 g/L (a normal value is approximately 0.9 g/L). 130 mEq/L, but symptoms and serious complications
Thus, it appears prudent to supplement these players with generally occur when plasma sodium decreases to less than
extra sodium, which is often the recommendation, but to 125 mEq/L. The cause of hyponatremia is likely associated
date there is no empirical data to support this approach for with multiple factors, but overdrinking fluid has been iden-
preventing or reversing muscle cramps. tified as the greatest risk factor for developing hyponatre-
On the surface, prevention of hypohydration seems to be mia, particularly when overdrinking pure water. This is
as simple as water in versus water out, as can be surmised because the excess water has the potential to dilute the
from the previous discussion; however, there are numerous plasma-sodium concentration. Therefore, as indicated pre-
scientific-, practical-, performance-, and health-related con- viously, one should ingest fluid during prolonged exercise at
siderations when assessing the effect of exercise-induced a rate that closely matches fluid loss and does not result in
water and electrolyte loss and rehydration practices and weight gain after the training or competitive session
principles. Many of these topics have been discussed and has ended. Consuming fluids with electrolytes, particularly
debated at scientific conferences, in the literature, and in the sodium, has the potential to maintain plasma sodium levels
media. A complete recounting of these topics is not possible throughout the course of prolonged exercise. Some have
within this brief review. Thus, if readers are keen to learn suggested that allowing hypohydration would guard against
more, the authors point them to several review articles,29-32 hyponatremia because of a contraction of the extracellular
position stands,33,34 and a recent debate35 for greater depth fluid space and consequent rise in plasma sodium. However,
and breadth of information. the increased risk of heat illness associated with hypohydra-
Application. Because athletes differ in body size, sweat tion does not warrant this approach.
rates, and training regimens, it is difficult to recommend
one hydration approach that suits all athletes. Therefore, Glycerol
individual athletes (or those working with the athlete) need Action. Ingestion of glycerol in a water-based solution
to know how much they sweat during prolonged exercise so prior to exercise promotes fluid retention and increases total
they can best understand how much fluid they need to body water. This so-called hyperhydration effect could ef-
replace. Monitoring the change in body weight before fectively delay the amount of time it takes to reach a level of
and after exercise is a good way to gauge sweat loss and hypohydration that increases cardiovascular strain, disrupts
thus fluid needs. For example, if an athlete loses 1.5 pounds thermoregulation, and leads to a decrement in exercise
(0.7 kg) while consuming 12 ounces of fluid during 1 hour performance.
148 SECTION I • Preparation and Prevention in Sports Medicine
Research. Rapid clearance of excess fluid intake makes exhaustion following glycerol ingestion.48,49 Despite this,
it difficult to hyperhydrate with common water-based results from Coutts and colleagues47 are rather intriguing.
drinks. However, it has been reported that solutions with a They had well-trained triathletes ingest a placebo or a glyc-
very high sodium and citrate concentration can increase erol-containing solution 2 hours prior to competing in an
fluid retention and expand plasma volume.36 The problem Olympic distance triathlon in a high-temperature environ-
is that the palatability of such drinks is quite low. Orally ment. Times during the final leg of the triathlon, a 10-km
ingested glycerol can also create an osmotic stimulus for run, were significantly faster after having ingested glycerol.
hyperhydration, especially when subsequent water intake Furthermore, reduced urine output and increased fluid re-
approaches 20 mL/kg/body weight (bw).37 The usefulness tention suggested that a hyperhydration state had been
of this approach to delay the point at which an athlete be- achieved after glycerol ingestion. This data set offers high
comes hypohydrated during exercise has been debated for ecological value and indicates that more work needs to be
more than 20 years. Although generally it is agreed that done to elucidate the environmental and exercise condi-
hyperhydration likely provides no clear physiological or tions in which glycerol-induced hyperhydration may impart
performance advantage over normal hydration, involuntary physiological or performance benefits.
dehydration during exercise is more common than not,38 Application. Despite significant knowledge and educa-
even in the presence of readily accessible fluid. Further- tion on the importance of consuming fluid during exercise
more, there are often logistical issues that preclude accessi- evoking a high rate of sweat loss, most athletes and active
bility to fluid intake during certain endurance events or people still voluntarily dehydrate because they consciously
team sport competitions. For these reasons, hyperhydration or subconsciously choose not to drink sufficient quantities
methodologies should not be discounted as means to pre- of fluid. Pre-exercise hyperhydration has the potential to
vent or delay hypohydration during prolonged exercise. delay the onset of significant hypohydration, especially
Glycerol-induced hyperhydration has the potential to when combined with a minimal amount of fluid intake dur-
increase total body water and expand plasma volume, and ing exercise. Furthermore, there are certain athletic situa-
thereby improve or maintain cardiovascular function, ther- tions in which it is extremely difficult to ingest fluid during
moregulation, and performance during prolonged exercise. competition, and those athletes may benefit from a modest
There is some evidence to support an increase in plasma vol- level of hyperhydration prior to competition. To this end,
ume following glycerol-induced hyperhydration,39 but the Siegler and colleagues50 have recently shown that consum-
significance of these data should be judged in light of the fact ing a glycerol-containing drink 30 minutes before and at
that the changes have been small (75-100 mL) and mostly half-time of a soccer simulation resulted in better overall
determined from a commonly used calculation method based hydration status than when consuming a beverage without
on changes in hematocrit and hemoglobin concentration40 glycerol. It is important to note that the hydrating effects
that only predicts percent change in plasma volume. None- of glycerol can wear off after 4 or more hours, so the use
theless, if plasma volume is truly expanded by hyperhydra- of glycerol needs to be properly timed such that the
tion, then venous return will be improved and this will kidneys will not begin excreting excess water just prior to
increase stroke volume and lower heart rate compared with or during a competitive or training session. If a modest level
control conditions. Although some studies do report a re- of hyperhydration prior to competition or training is desir-
duction in heart rate with glycerol-induced hyperhydration,41 able, glycerol (approximately 1 g/kg/bw) in a sufficient
others report no change.39 The effect on stroke volume and quantity of water (20-25 mL/kg/bw) appears to be reason-
cardiac output has been equally inconsistent.42,43 Such equiv- ably effective.
ocal results may derive from a reduction in plasma glycerol Adverse Effects. Glycerol appears fairly safe, especially
concentration during exercise caused by metabolism and when consumed orally at doses less than 5 g/kg/bw. Some
discontinued glycerol intake. Consequently, a pre-exercise investigators have reported side effects such as nausea, vom-
expansion of plasma volume will not be maintained during iting, and headache46,49 that others have not observed.48
exercise. Some have found that glycerol-induced hyperhydra- Incidence of side effects may be particularly related to the
tion attenuates the rise in rectal temperature during ingestion of highly concentrated (i.e., 10% or greater) glyc-
exercise,44 and in some cases this was related to an increased erol solutions. One potential side effect that has not been
sweat rate44,45 and skin blood flow41 relative to control. Con- studied is reduction in plasma sodium (hyponatremia;
versely, other studies have found that glycerol intake does not discussed previously) caused by excess fluid retention,
improve thermoregulation.46,47 especially when a glycerol solution without sodium is
Glycerol-induced hyperhydration has also been investi- consumed.
gated for its effects on exercise performance. Endurance
times during constant load cycle ergometry exercise have Carbohydrate
been found to be increased relative to control, but, as with Action. Carbohydrate intake before and during exer-
cardiovascular and thermoregulatory variables, other stud- cise prolongs time to exhaustion and improves exercise
ies have not found improvement in endurance time to performance (e.g., time to complete a set distance or work
Use of Ergogenic Aids in Sport • CHAPTER 6 149
accumulation for a set amount of time) by preventing hypo- study, subjects exercised on a stationary bicycle ergometer
glycemia, sparing liver glycogen, maintaining a high level of at an exercise intensity of approximately 74% of VO2 max.
carbohydrate oxidation, or through neuromuscular effects. During one test, subjects consumed a glucose polymer solu-
Research. A high-carbohydrate diet during periods of tion, and in another test, they received an artificially sweet-
intensified training or coupled with reduced training (i.e., ened placebo. Ingesting the glucose polymer delayed
taper) helps to maintain or elevate muscle glycogen to fatigue by approximately 23 minutes. This set off a flurry of
higher-than-normal levels.51,52 This is important because research activity and now it is generally accepted that carbo-
studies dating back to the late 1960s and early 1970s docu- hydrate intake during exercise can improve endurance
mented a strong correlation between pre-exercise muscle capacity (i.e., time to exhaustion) and performance (time
glycogen levels and endurance performance.53-55 Carbohy- trial) that is prolonged in nature.67 Furthermore, more re-
drate intake during the 3 to 5 hours prior to training or cent studies have shown that appropriate mixtures of simple
competition may also elevate muscle glycogen levels56 and sugars (glucose, polymers of glucose, fructose, sucrose) at
thereby improve performance,57 but more likely will help to an osmolality of less than 400 mOsm results in gastric emp-
restore liver glycogen levels, especially if the athlete has tying and intestinal water absorption rates similar to that of
fasted overnight, and this should lead to better maintenance water.68-70 The use of stable (13C) and radioactive (14C)
of blood glucose during subsequent exercise. It has been isotopes of glucose and fructose along with advanced math-
debated whether carbohydrate should be consumed within ematical modeling techniques has also yielded strong data
the hour that precedes training or completion because early to show mixtures of simple sugars ingested during exercise
studies showed that the combined stimulatory effects of can account for a rather large percentage of the total carbo-
hyperinsulinemia and contractile activity on glucose uptake hydrate oxidized, especially late in exercise when endoge-
resulted in a rapid decline in blood glucose, a reduction in nous carbohydrate stores are low.71-73 Taken together, it
fat use, and an accelerated muscle glycogen use, all of which is indeed possible to strike a balance between fluid avail-
could predispose to poor performance.58,59 However, sub- ability and carbohydrate delivery during exercise and the
sequent research has shown that performance is either benefits of such are well recognized, as reflected in the latest
unchanged or improved when consuming carbohydrate in American College of Sports Medicine (ACSM) position
the hour before exercise.60-62 Nonetheless, there are some stand on exercise and fluid replacement.34
individuals who seem to be particularly sensitive to the Carbohydrate ingestion also seems to be ergogenic dur-
“hypoglycemic” effects of pre-exercise carbohydrate feed- ing repeated bouts of intermittent shuttle running meant to
ing, so the usefulness of this practice may have to be based mimic the physical demands of team sports such as football,
on individual experiences. That said, what seems to be clear basketball, and soccer.74,75 In addition to a physical perfor-
is that when carbohydrate is consumed before exercise, it mance benefit in this scenario, better maintenance of motor
has little or no negative effect on metabolism and perfor- skill ability and improved mood state, including feelings
mance when ingestion of carbohydrate is continued during of less fatigue in the later stages of the protocol, were
exercise.63 observed.76,77 This is in line with field research that has
shown carbohydrate ingestion during activity is associated
with improved stroke quality during the latter part of pro-
Clinical Point longed tennis play78 and a trend for reduced ratings of
perceived exertion during the final 4 km of a marathon
Carbohydrate intake improves exercise performance, delays fatigue,
run.79 Regarding the marathon research, a more substantial
and improves motor skill ability and mood state.
finding was that when ingesting carbohydrate relative to
placebo, the subjects ran at a higher intensity (i.e., higher
heart rate) despite statistically similar overall ratings of per-
Early research indicated that the addition of glucose to ceived exertion. These observations suggest that carbohy-
water slowed the gastric emptying rate.64 These authors drate ingestion affects CNS function and processing, likely
concluded that their data demonstrated the importance of by preventing hypoglycemia. Direct evidence of this comes
“minimizing the glucose content of solutions ingested in from Nybo.80 He tested CNS activation of skeletal muscle
order to obtain an optimal rate of fluid replacement.” This, before and after 3 hours of cycling during two randomized
in combination with other research at the time suggesting trials, one with and another without (placebo) glucose in-
that ingested glucose contributed very little to total energy gestion. During the placebo trial blood glucose declined to
expenditure during exercise,65 underpinned the thinking hypoglycemic levels and the level of CNS activation was
that the physiological benefits of fluid replacement during reduced compared with baseline. Glucose ingestion main-
exercise were far greater than energy replacement and there tained both blood glucose and CNS activation relative to
was little need to strike a balance between the two. That baseline. An alternative explanation is that glucose ingestion
consensus began to change in the early 1980s with the pub- could activate receptors in the mouth or gastrointestinal
lication of a classic article by Coyle and co-workers.66 In this (GI) track that leads to central activation to improve motor
150 SECTION I • Preparation and Prevention in Sports Medicine
consumed carbohydrate and protein the prior day, and at observations by Williams and colleagues85 and Saunders and
the onset of this additional exercise blood levels of colleagues87 has guided these efforts, emanating especially
creatine phosphokinase (a marker for muscle damage) were from the observation that protein ingestion reduced circu-
significantly reduced. There are several concerns that lating markers of muscle damage.87,89 Nonetheless, this
should be noted about this research. First, the experiment research92-97 has been equivocal at best and there are no
was not placebo-controlled and the amount of carbohydrate additional studies that have confirmed or denied the obser-
consumed (approximately 37 g/hr) during both treatments vation that carbohydrate-protein ingestion during an initial
was less than what is normally considered as optimal prolonged exercise bout improves (or maintains) perfor-
for enhancing exercise endurance. Second, total energy mance in a subsequent bout 12 or more hours later.
intake was not matched between the carbohydrate and Additional research on these topics would be useful.
carbohydrate-protein conditions. Thus, it is difficult to Application. Existing literature could be interpreted to
know whether protein intake was driving the response or suggest that consuming a combination of carbohydrate and
whether total calorie intake was primarily responsible for protein during prolonged exercise may be effective for
the endurance benefit. Indeed, this latter point seems to improving performance under certain circumstances. First,
bear significance because subsequent research by the when consuming carbohydrate at a low rate ( 60 g/hr)
Saunders group that has controlled for total calorie intake during prolonged exercise, a small amount of protein intake
has not provided evidence for a specific carbohydrate- (15–20 g/hr) may be ergogenic, although data to date sug-
protein benefit.88,89 gest this is no more effective than consuming carbohydrate
Another issue that has been debated is the significance of at a higher rate.89 Second, protein may be ergogenic in situ-
a time-to-exhaustion benefit when consuming carbohydrate- ations in which training or competition requires prolonged
protein for endurance athletes. Most competitions require extension of activity or play versus completing a certain
covering a certain distance in the shortest time possible amount of work or covering a set distance in the quickest
(e.g., cycling time-trial, 10-km running race). To this end, time possible. Examples are “overtime” in team sports or
Van Essen and Gibala90 have reported that ingesting a car- extra sets in a tennis match. As with carbohydrate intake
bohydrate drink during a simulated 80-km cycling time- prior to or during exercise, there may be certain individuals
trial in a laboratory setting improved performance relative who are particularly sensitive to positive or negative effects
to placebo, but consuming a carbohydrate-protein bever- of consuming protein during exercise. Because protein
age provided no additional benefit. Osterberg and col- intake during prolonged exercise has gone through less
leagues recently published data91 that supports the work of extensive experimentation, it is advisable when working
Van Essen and Gibala. Her results indicated that relative to with athletes to use systematic trial and error to identify
placebo, carbohydrate and carbohydrate-protein intake whether protein ingestion during prolonged exercise works
during 2 hours of stationary laboratory cycling improved for them, given their particular training or competitive
subsequent time-trial performance to a similar extent. scenarios. Lastly, protein intake (again, in small amounts—
Thus, it appears carbohydrate-protein ingestion during 15-20 g) during or shortly after prolonged training or
prolonged exercise may improve time to exhaustion, espe- competition may be an effective recovery nutrition
cially when carbohydrate intake is less than optimal, but approach, particularly from the standpoint of protein bal-
when performance is tested in a manner in which endur- ance and especially when multiple training or competitive
ance athletes normally compete, a protein benefit is not events are held within a 24-hour period.
observed. It is also important to note that the Van Essen Adverse Effects. When adding protein to the fluids
and Osterberg studies delivered carbohydrate at a rate consumed or nutritional strategy employed during pro-
believed to elicit a significant exogenous carbohydrate oxi- longed exercise, the biggest risk is a slowed gastric empty-
dation, endogenous carbohydrate sparing, and therefore ing rate resulting from increased energy density.98 Further-
improvement in performance (i.e., ⬃ 60g/hr). Thus, an more, gram for gram, protein in solution may impart a
alternative explanation is that when carbohydrate is con- slower gastric emptying rate than a simple carbohydrate.99
sumed in sufficient amounts during exercise, protein does A slowed gastric emptying rate during exercise could lead to
not provide any additional performance or endurance ad- feelings of stomach fullness, nausea, and cramping, as well
vantage. Finally, a limitation to the studies indicating that as a delayed water absorption rate from the small intestine
protein ingestion provides an endurance capacity advan- and thus a less effective offset of sweating-induced dehydra-
tage has been that there is little to no evidence for a bio- tion. Gastric emptying rates vary widely among individuals.
logical mechanism through which the benefit is derived. Thus, an athlete with a high sweat rate and a low gastric
There is a developing literature on the effect of emptying rate may not be a good candidate for consuming
carbohydrate-protein ingestion after prolonged exercise a carbohydrate-protein mixture during exercise. Another
with the intent to maximize performance during additional potential concern for protein consumption during exercise
exercise 4 to 6 hours later (e.g., two-a-day practices, multi- is a reduction in fat metabolism. Maintenance of a high rate
game and multievent tournaments). In part, the initial of fat metabolism during prolonged exercise is beneficial in
152 SECTION I • Preparation and Prevention in Sports Medicine
that it slows carbohydrate use and, indeed, is a hallmark of time-trial performance. Despite an elevation in blood BCAA
a very effectively and highly trained endurance athlete (refer levels (and a reduced tryptophan/BCAA ratio) by the end
back to “Adaptation of Physiological Systems”). In some of exercise, there was no difference in time to complete the
studies, protein along with carbohydrate consumption dur- time-trial among the three treatments. Curiously, glucose
ing exercise elevates plasma insulin to a greater extent than ingestion alone did not improve performance relative to the
when consuming carbohydrate alone. An elevated insulin placebo. Still, if central fatigue was truly a manipulatable
level acts to depress fat metabolism. More studies are factor as a result of BCAA ingestion, it is likely this would
needed to better understand the effect of protein intake have occurred independent of a glucose effect on perfor-
during exercise on the interplay of carbohydrate and fat mance. That said, other experiments have shown improve-
metabolism. ments in exercise performance with carbohydrate intake but
no further benefit from the addition of BCAA.104 All of the
Branched-Chain Amino Acids experiments mentioned to this point were conducted in
Action. Branched-chain amino acid (BCAA) ingestion a reasonably temperate environment. There is reason to
during prolonged exercise may enhance endurance perfor- believe that heat stress may heighten susceptibility to central
mance by providing fuel in addition to carbohydrate and fatigue. In this regard, Mittleman and colleagues105
fat, reducing net protein breakdown in muscle and by reported that BCAA supplementation extended exercise
delaying the onset of central fatigue. The efficacy for BCAA time to exhaustion in a hot environment. Watson and
to prevent central fatigue has been the most frequently colleagues106 also determined the effect of BCAA ingestion
studied topic because it is well known that BCAA competes during exercise in a hot environment. Although they re-
with tryptophan for transport across the blood-brain ported no significant difference in time to exhaustion for
barrier. Tryptophan, the direct precursor for serotonin syn- BCAA and placebo, five out of nine subjects had at least a
thesis, is the linchpin of the central fatigue hypothesis as 5% improvement in endurance when consuming BCAA.
mentioned previously. However, other data seems to indicate that under condi-
Research. As indicated earlier, prolonged exercise low- tions of greater thermal strain (i.e., higher rectal tempera-
ers muscle glycogen. This sets up a scenario by which ture than that achieved in the Mittleman and Watson
BCCA could be taken up and oxidized by muscle to main- studies) and hypohydration, BCAA ingestion does not
tain a high rate of energy production late in exercise.100 improve performance.107
Unfortunately, the activities of enzymes involved in the Much like consumption of protein during exercise, there
oxidation of BCAA in muscle are too low to allow for a are reports on how BCAA ingestion before and during pro-
major contribution of BCAA to total energy expenditure longed exercise suppresses muscle protein breakdown,108
during exercise.101 Thus, consumption of BCCA during attenuates markers of muscle damage,109,110 and reduces the
exercise does not make sense from the standpoint of energy amount of delayed onset muscle soreness.110 To some
provision and this is why it has been so surprising that a extent, the applicability of these findings should be inter-
combination of low carbohydrate-protein intake during preted with caution because only one of the three studies
exercise has been shown to extend exercise time to exhaus- experimented on reasonably trained subjects. It might be
tion (see previous discussion on protein). However, ingest- that the effects are more likely to occur in untrained muscle.
ing BCCA during prolonged exercise prevents a decline in For example, it is well known that although a single bout of
its blood concentration. This reduces the ratio of total eccentric exercise in a novice exerciser can cause significant
tryptophan to BCCA, which favors a reduced-tryptophan muscle damage, a subsequent bout or bouts results in less
transport across the blood-brain barrier. Thus, this nutri- damage (i.e., the so-called repeated bout effect111). None-
tional intervention could potentially enhance prolonged theless, BCAA ingestion during exercise may have particular
exercise performance by reducing serotonin mediated merits for recovery after exercise. However, as was indicated
central fatigue. in the previous section on protein, much more work needs
Following an initial positive field study,102 the literature to be done to understand whether reduction in markers of
has been mixed on whether BCAA consumption during muscle damage lead to a preferred muscle performance
prolonged exercise delays fatigue or improves performance. outcome.
Blomstrand and colleagues102 reported that marathon run- Application. Fatigue during exercise likely results from
ning performance was improved in “slower” runners when a complex array biological and biochemical factors and
BCAAs were taken throughout the race. However, this there is little doubt that limitations in CNS functioning
study has been criticized for lack of a control group and plays a role. Attempts at nutritional manipulations of brain
a creative statistical analysis that included retrospectively neurotransmission have been equivocal in terms of their
dividing the subject population into “slower” and “faster” ability to offset central fatigue, at least when tested using
runners. In a well-designed and controlled laboratory study, prolonged exercise protocols characteristic of the demands
Madsen and colleagues103 compared the effects of placebo, of running and cycling. Other sports can be prolonged in
glucose, and glucose-BCAA ingestion on 100-km cycling nature and rely on successful execution of motor skills and
Use of Ergogenic Aids in Sport • CHAPTER 6 153
tactics that have a high level of dependability on cognitive resulting in a loss of ability to cope with stress-related
functioning. Although not tested in this regard, BCAA behaviors. Tyrosine depletion via short-term reduction in
ingestion during prolonged sports competitions may alter dietary tyrosine intake is possible and manifests as low brain
neurotransmission processes such that during the later levels of dopamine.113 It then follows that increasing tyro-
stages of a game, cognitive functioning for skill and tactical sine intake should elevate brain dopamine and norepineph-
outcomes is better maintained or enhanced despite limited rine levels. Although there is little direct evidence for this in
effects on endurance capacity. For this reason, BCAA still humans, some studies report the expected behavioral effects
should be considered as having ergogenic properties but associated with an elevation in central catecholamines.114
athletes will need to go through trial and error routines as Tyrosine also competes for the same transport mecha-
well as make assessments of personal tolerance in a dose nism across the blood-brain barrier as tryptophan. Thus, by
range of between 10 and 20 g per prolonged exercise bout elevating free tyrosine in blood through supplemental
until science catches up with the practical nature of sport. intake, it may be possible to not only reduce central sero-
Lastly, consideration should be given to obtaining BCAA toninergic actively but to decrease the ratio of serotonin to
through ingestion of small amounts of protein during train- dopamine, which has been proposed as key modulator of
ing or competition. This may result in a more balanced central fatigue, rather than serotoninergic activity alone.8 It
influence over the body’s amino acid systems as discussed is also important to note that carbohydrate intake has the
next in the section about “Adverse Effects.” potential to reduce central serotoninergic activity. Carbohy-
Adverse Effects. There are few, if any, reports on drate intake during exercise reduces FFA accumulation in
adverse effects associated with BCAA supplementation. blood, which results in more tryptophan (rather than FFA)
From a metabolic standpoint, however, what should be being bound to albumin. Thus the free tryptophan levels
considered is the potential for excess ammonia production remain low and less is transported into the brain for sero-
associated with high intakes of BCAA during prolonged tonin synthesis. Thus a potentially effective way to decrease
exercise. MacLean and colleagues108 showed that relative the serotonin/dopamine ratio during prolonged exercise is
to a placebo, contracting skeletal muscle produced much to ingest both carbohydrate and tyrosine before and during
more ammonia when BCAA were consumed before exer- exercise. Chinevere and colleagues115 compared the effects
cise. The amount of BCAA intake was approximately 5 g of placebo, tyrosine, carbohydrate, and combined carbohy-
and enough to double arterial levels of BCAA before and drate and tyrosine on cycling time-trial performance follow-
during exercise. Excess ammonia can cross the blood-brain ing a 90-minute preload ride at 70% of peak oxygen uptake.
barrier and enter the CNS, where it can have detrimental Drinks were consumed before (60 and 30 minutes) and
effects on cerebral function that could lead to the manifes- every 30 minutes during the 90-minute preload exercise
tation of central fatigue. In fact, it has been shown that period. Tyrosine was administered each time in an amount
with an increasing arterial concentration of ammonia dur- of 25 mg/kg/bw for a total intake of approximately 11 g
ing prolonged exercise, there is an increased cerebral am- up to the start of the time trial. Results indicated that
monia uptake.112 In part, this may be why it has been although carbohydrate intake improved performance, in-
difficult to demonstrate a robust effect of BCAA ingestion take of tyrosine did not provide any additional benefit.
on the mitigation of central fatigue during prolonged Likewise, the tyrosine alone and placebo trial were not sig-
exercise. Furthermore, it is interesting to note that protein nificantly different. It is interesting to note that numerically,
ingestion during prolonged exercise does not result in there was slightly more than a 1-minute improvement for
excess ammonia accumulation. One reason for this may be carbohydrate-tyrosine versus carbohydrate alone. Likewise,
that when ingesting protein, both ammonia-producing when consuming tyrosine, time to complete the time trial
and ammonia-reducing amino acids are consumed, pro- was almost 2 minutes faster than placebo and six of the nine
viding for a more balanced amino acid metabolism. There- subjects finished faster when on tyrosine than when on the
fore, consumption of protein during exercise may be a placebo. As can be the case in these types of experiments,
better way to derive a BCAA preventative effect on central the results can inspire a debate about the practical versus
fatigue. statistical benefits. The authors are aware of only one other
human study on tyrosine supplementation and prolonged
Tyrosine exercise performance. Strüder and colleagues116 reported
Action. Ingestion of tyrosine before or during pro- no benefit of tyrosine administration when subjects were
longed exercise increases central dopamine levels, decreases asked to exercise to exhaustion on a cycle ergometer at
the ratio of central serotonin to dopamine, and thereby an intensity that elicited a blood lactate concentration of
delays the onset of central fatigue. approximately 2 mM. However, the amount of tyrosine
Research. Tyrosine is a precursor to the synthesis administered in this experiment may have been too large
of norepinephrine and dopamine in the brain. During (20 g), and in fact may have had a negative effect as indi-
acute mental and physical stress, large amounts of these cated by hormonal measurements that suggested a decrease
neurotransmitters are released and a depletion can occur, rather than an increase in central dopamine levels.
154 SECTION I • Preparation and Prevention in Sports Medicine
The U.S. military has had a lot of interest in tyrosine improves performance. Desbrow and Leveritt125 recently
supplementation because of its potential to alter mood and reported that of 140 triathletes competing in the 2005
enhance cognitive performance under conditions of Ironman Triathlon World Championships, “73% believed
extreme stress (see reviews by Lieberman117,118). In brief, that caffeine is ergogenic” and “84% believe that it im-
their research has shown that tyrosine administration re- proves their concentration.” Caffeine intake during triath-
duces the psychological stress of military operations,119 cold lon competition was achieved primarily through “flat” cola
stress,120 combined cold and altitude stress,121 the negative drinks and caffeinated carbohydrate gels.
consequences of sleep deprivation,122 and stress associated Research on caffeine and human endurance exercise per-
with sustained operations.123 Although all of these are formance dates back to the late 1970s. Costill’s group at
highly stressful situations, there is some indication that Ball State University examined the effect of ingesting
tyrosine can improve cognitive performance under condi- 330 mg of caffeine 1 hour prior to cycling to exhaustion at
tions void of significant stress-related biological changes.124 80% of VO2 max.126 They found an improvement in time to
Application. It appears that if tyrosine is going to be exhaustion of 21 minutes compared with a placebo condi-
effective, the ingested dose should be no more than 10 g tion. In a subsequent study, 250 mg of caffeine was associ-
either as a bolus or spread out over multiple feedings in and ated with a 20% increase in the amount of work performed
around the training or competitive scenario. For possible during 2 hours of isokinetic cycling.127 These observations
influence over central fatigue, it makes sense to consume have held up over the years, especially experiments that have
tyrosine along with carbohydrate, but as was discussed pre- tested caffeine’s effect on exercise time to exhaustion. From
viously for BCAA, what still needs to be sorted out is a series of studies by Graham and Spriet, it was reported
whether effective doses of tyrosine could be ingested as part that a caffeine dose of 9 mg/kg/bw improved running
of protein consumption, especially because as little as 2 to and cycling time to exhaustion in elite runners and recre-
3 g of tyrosine may provide a benefit. Consideration should ational athletes.128,129 They also tested doses of 3, 6, and
be given to tyrosine supplementation under training and 9 mg/kg/bw and found equal improvements for the 3
competitive conditions at environmental extremes such and 6 mg/kg/bw doses, but no further benefit from the
as altitude and extreme cold and situations in which sleep 9 mg/kg/bw dose.130 This seems to indicate there is a
deprivation has the possibility of contributing to poor threshold of caffeine intake above which no further ergo-
performance. genic benefit is derived. Furthermore, they reported that on
Adverse Effects. Supplemental tyrosine is reasonably a habitual basis, “light” caffeine users were least likely to
safe, especially when consumed in the recommended dose benefit from the highest dose (9 mg/kg/bw), and may
range of 7 to 10 g/day. It should be noted, however, that even have a negative response. In the most recent time-
long-term safety studies in humans consuming supplemen- to-exhaustion research we could find, Hogervosrst and
tal doses have not been conducted. If consumed before colleagues131 had their subjects pedal a stationary bike for
bed time, it may result in insomnia. Use should be avoided 2.5 hours at 60% of VO2 max. Thereafter they were re-
by those consuming stimulant or antidepressant medica- quired to pedal to exhaustion at 75% of VO2 max. Immedi-
tions because tyrosine may increase sensitivity to those ately before exercise they consumed a carbohydrate sports
medications. bar, a carbohydrate sports bar with 100 mg of caffeine, or a
placebo beverage in a randomized, repeated measures de-
Caffeine sign. Carbohydrate intake improved time to exhaustion, but
Action. Caffeine is a CNS and metabolic stimulant that caffeine intake resulted in an even further increment versus
is known to improve both physical and mental performance. placebo. Thus caffeine appears to have ergogenic benefits in
The exact mechanisms behind these effects have not been addition to those of carbohydrate. Lastly, it is interesting to
completely worked out, but more than likely involve three note that a majority of caffeine studies have tested the
primary modes of action: (1) antagonism of adenosine recep- “pure” form of the drug, either in capsule form or incorpo-
tors in the CNS; (2) direct effects of caffeine metabolites on rated into a processed food or beverage. Ingestion of caf-
lipolysis, blood vessels, and smooth muscles; and (3) com- feine as coffee appears to be ineffective for performance as
petitive inhibition of cyclic adenosine monophosphate– compared with pure caffeine, possibly because there are
phosphodiesterase (cAMP). ingredient components in coffee that modulate caffeine’s
Research. Caffeine is probably one of the most popular effect on performance.132
ergogenic aids among endurance athletes, but it is also one As was discussed in the previous section about protein,
of the most controversial. For example, until recently, the significance of time-to-exhaustion protocols within the
caffeine was on the list of substances banned by the Inter- context of competitive performance has been debated
national Olympic Committee. Caffeine has no nutritive because most endurance competitions are designed to cover
value, yet it is widely available in our food supply. It occurs a set distance in the shortest time possible. Results from
naturally in coffee beans, tea leaves, kola nuts, and cocoa a recent meta-analysis on caffeine and laboratory exercise
beans. Endurance athletes have a strong belief that caffeine testing led to the conclusion that caffeine intake improves
Use of Ergogenic Aids in Sport • CHAPTER 6 155
exercise performance, but time-to-exhaustion protocols are improved exercise performance. Although there are data to
much more likely to reveal this benefit than a time-trial pro- support these various aspects of caffeine’s effects,126,129,141
tocol.133 Thus, if one believes that time to exhaustion is not low doses of caffeine (i.e., 250 mg) do not always stimu-
a relevant performance test for endurance athletes, it seems late epinephrine release and fat metabolism, yet perfor-
reasonable to downgrade expectations for a performance mance benefits have been observed.128,134 Another explana-
benefit from caffeine in “real-world” competitive scenarios. tion is that caffeine can have a direct effect on skeletal
Independent of this comparison, there is fairly robust scien- muscle.142 For example, caffeine is known to increase the
tific support for the addition of small amounts of caffeine to rate of release of calcium from the sarcoplasmic reticulum
carbohydrate-containing drinks to induce improvements in (SR) and increase the sensitivity of contractile proteins to
time-trial performance.134,135 It also appears that consuming calcium, both of which could improve excitability for mus-
a small amount of caffeine (⬃120 mg) late in exercise is as cle contraction. A third explanation relates to the stimula-
effective as consuming higher doses of caffeine prior to or tory effects of caffeine on the CNS. In this manner, percep-
during exercise.135 Regardless, ultimate support for caffeine tion of effort may be reduced and signal transduction from
ergogenicity should derive from field tests of exercise perfor- the brain to muscle could be improved. It is likely that
mance. Results from studies in this regard have indicated one or both effects could happen through adenosine
that consuming 3 and 5 mg/kg/bw of caffeine 1 hour metabolism in the brain. Adenosine is believed to be an
prior to 8- and 5-km running races, respectively, induced endogenous inhibitory neurotransmitter. When it binds to
small (1%-1.5%) but statistically significant improvements in functional adenosine receptors brain excitatory activity is
performance.136,137 In another controlled field study, reduced. Caffeine is an adenosine receptor antagonist; thus
caffeine consumption during an 18-km competitive running it can compete with adenosine for binding, reduce its
race did not improve performance relative to placebo; effects, and thereby stimulate brain neuronal activity. This is
however, total caffeine intake during the race was less than associated with behavioral changes that lead to improve-
100 mg.138 More research concerning the effects of caffeine ments in mental and physical endurance.143
on performance in ecologically valid race settings seems Caffeine is known to maintain brain performance, espe-
warranted. cially under conditions of sleep deprivation. Furthermore,
As mentioned earlier, exercise-to-exhaustion type tests military research has consistently shown maintenance or
may have applicability for individual or team sports in which improvements in attention, psychomotor skills, memory,
the game winner is decided in overtime or “sudden-death” concentration, and vigilance under conditions of severe
scenarios. Although in these sports the type of activity is operational stress.118 Such cognitive, or brain performance,
prolonged, the intensity is high and activity is intermittent benefits for caffeine have also been identified after pro-
in nature. Hence, response to caffeine in time to exhaustion longed cycling exercise that mimics the intensity and dura-
protocols may not necessarily predict performance in this tion of road racing.131 Such effects combined with the
type of physical effort. Thus, Schneiker and colleagues139 physical performance benefits of caffeine could lead to sig-
conducted an experiment to test the hypothesis that caf- nificant improvement in physically demanding sports that
feine consumption improves the performance of intermit- require concentration, quick thinking, and tactical deci-
tent sprints. They had team sport athletes consume caffeine sions. However, this hypothesis has not been tested in a
(6 mg/kg/bw) or placebo 1 hour prior to testing. The holistic fashion. Finally, although there are data to show
results revealed that after two bouts of 18 4-second sprints that caffeine consumption reduces perception of effort dur-
with 2 minutes of active recovery between each sprint, total ing exercise,135 Cole and colleagues144 used a unique
amount of sprint work accumulated was greater after con- approach to further make this point. They asked test sub-
suming caffeine. The same amount of caffeine was tested jects to pedal a stationary cycle ergometer at what they
for its ability to improve performance during tests of agility, perceived to be a rating of 9, 12, and 15 on a Borg scale for
which is an important component of the athletic skills sequential 10-minute bouts of exercise. This was done
needed for team sport competition. In this case, measures 1 hour after receiving placebo or caffeine at a dose of
of agility did not benefit from caffeine consumption.140 6 mg/kg/bw. Total work performed during the caffeine
Taken together, it seems caffeine has the potential to im- trial was greater than that of the placebo.
prove ability to withstand the high-intensity, intermittent-
type activity required in team sports, but a total perfor-
mance benefit requires a positive effect on skill and agility
(positive data lacking) as well as on cognitive function, Clinical Point
mental alertness, and concentration.118
The “classic” hypothesis for the ergogenic effects of Caffeine seems to alter neural perception of effort and this either
caffeine is that it stimulates epinephrine release, increases drives or contributes to the physical performance benefits derived
peripheral and intramuscular lipolysis, and increases fat after caffeine consumption.
oxidation, and thereby spares muscle glycogen use for
156 SECTION I • Preparation and Prevention in Sports Medicine
Application. The potential for an ergogenic effect from process, but for simplicity, the authors will limit this discus-
caffeine is impressive. Nevertheless, caffeine, although preva- sion to contractile activity per se. Fortunately, skeletal
lent in society, is a drug, and it has been questioned whether muscle is endowed with a system of antioxidant enzymes
athletes should use it for the benefits it can provide or avoid that can degrade or “neutralize” ROS. Other molecular
it because it could be considered doping. This ethical di- structures complement these enzymes and reside both in
lemma likely will not be solved any time soon. Effective doses the aqueous and lipid fractions of the muscle cell. Although
appear to be near 100 mg for the mental and cognitive ben- there are numerous antioxidant compounds and antioxi-
efits and more than 200 mg for physical performance benefits. dant vitamins (A, C, E) available, it is not clear to what
Most administration protocols call for pre-exercise dosing to extent supplementation complements (or hurts) the endog-
account for absorption and metabolism of caffeine, although enous antioxidant systems, especially for the preservation of
there are sufficient data to support benefits from intake during muscle performance. For example, although supplementa-
exercise as well as during the latter parts of prolonged exer- tion with antioxidant vitamins has been shown to reduce
cise. Although data for mental and physical performance markers of oxidative stress during exercise, they do little to
benefits derived from caffeine ingestion are largely positive, prevent fatigue.147 Furthermore, numerous phytochemicals
one must keep in mind that there can be big individual differ- (e.g., quercetin, resveratrol, epigallocatechin gallate
ences in response to caffeine. As with any ergogenic aid, [EGCG]) in the foods we eat offer antioxidant potential but
practical experience is as important as science-based decisions few have been tested within the context of human muscle
for its use. Some of the variability in response to caffeine may fatigue during exercise.148 To date, it appears that exercise-
be derived from habitual use. Those with a high habitual daily induced muscle fatigue is most consistently offset by anti-
intake of caffeine may have a blunted metabolic response to oxidants or antioxidant systems that target thiol (sulfhydryl
acute caffeine dosing, but it is debated whether this reduces groups; RSH) oxidation. Of these, glutathione and the
the performance benefit that can be derived from use. Like- glutathione system seem to be the most important. The
wise, it has been hypothesized that a person with a high thiol moiety of the amino acid cysteine can participate in
habitual intake of caffeine may require a larger-than-normal covalent interactions with muscle-derived ROS. Thiol oxi-
dose to derive a benefit, but there are no data the authors are dation is known to occur in important contractile proteins
aware of that supports this. Lastly, it seems unlikely that acute such as actin149 and myosin150 and could precipitate the
caffeine withdrawal will sensitize body systems for a greater development of fatigue. Glutathione and the glutathione
performance effect upon reintroduction of use. cycle can regulate thiol redox state in muscle and thereby
Adverse Effects. The use of caffeine is associated with guard against excessive thiol oxidation of important con-
side effects. First, habitual users who stop using caffeine of- tractile proteins. Glutathione is composed of three amino
ten experience symptoms of withdrawal such as lethargy and acids; cysteine, glutamate, and glycine. Availability of cyste-
headache. High intakes of caffeine (i.e., 400 mg) or acute ine seems to be rate-limiting for glutathione synthesis.
use of a high dose by those who normally avoid caffeine are Therefore, antioxidant strategies that support glutathione
associated with tachycardia, elevated blood pressure, rest- synthesis and the glutathione system have been tested
lessness, irritability, tremor, and premature ventricular con- within the context of contraction-induced (exercise) muscle
tractions. Caffeine is also considered a diuretic, but the fatigue. For example, N-acetylcysteine (NAC) has been
effect this can have on hydration status and performance has used to increase cysteine availability in humans. Administra-
recently been challenged.145 In support of this, it is known tion of NAC has been shown to reduce isolated muscle fa-
that during exercise, the diuretic effect of caffeine is coun- tigue in individual muscles151 or muscle groups152 subjected
teracted by an elevation in catecholamines.146 to contractile paradigms. Furthermore, NAC has been
shown to delay fatigue during prolonged cycling exercise in
Antioxidants endurance athletes.153 Interestingly, -lipoic acid, also a
Action. Oral antioxidant supplementation can assist or thiol donor, does not seem to be effective at guarding
enhance endogenous antioxidant systems in neutralizing against muscle fatigue, at least in an animal model.154 In
ROS and thereby prevent premature fatigue in contracting addition to NAC’s ability to stimulate glutathione synthesis,
skeletal muscle. its thiol moiety can interact directly with ROS and may in
Research. There is little doubt that contracting skeletal part explain the difference in effectiveness between NAC
muscles generate ROS and reactive nitrogen species (RNS). and -lipoic acid. However, muscle performance studies in
These so-called free radicals can interfere with biological humans with -lipoic acid supplementation are lacking.
structures and functions within a muscle cell and predispose Unfortunately, side effects of NAC administration have
to early onset fatigue. Although there is reasonably strong limited its experimental and practical use (see following sec-
evidence that ROS can modify key muscle components and tion about “Adverse Effects”). However, experimental evi-
proteins integral to the contractile process, evidence for dence from Lands and colleagues155 is encouraging in that
RNS is less strong. RNS may have particular influence over they reported 3 months of supplementation with a cysteine
vascular control, which could be part of the overall fatigue donor protein increased 30-second isokinetic cycling peak
Use of Ergogenic Aids in Sport • CHAPTER 6 157
power and total work in young, healthy men and women Research. Carnitine in the body is derived from dietary
relative to a casein (low cysteine content) control. intake (meat) as well as endogenous synthesis from the
amino acids methionine and lysine. Approximately 98% of
carnitine in the body is stored in skeletal muscle and heart.
Clinical Point Skeletal muscle takes up carnitine against a very large con-
centration gradient. For example, the concentration of
Exercise induced fatigue is offset by antioxidants and their systems.
carnitine inside muscle is roughly 100 times that in blood.
However, carnitine is actively transported into muscle by a
saturable, sodium-dependent, high-affinity, active transport
Application. Antioxidants and antioxidant systems are process. The transport protein for carnitine has been identi-
clearly involved in muscle function and therefore prolonged fied as the novel organic cation transporter OCTN2.156
exercise performance can benefit from their effects. As Understanding the regulation of this transport process is
noted earlier, regular exercise training up-regulates the key to an effective carnitine supplementation routine.
expression of various antioxidant enzymes and enzyme sys- Carnitine supplementation is effective at enhancing fat
tems. What remains strongly debated is whether supple- metabolism only if it stimulates an increase in muscle total
mentation with various antioxidant compounds is a neces- carnitine content. Early research suggested that this was
sary complement to these up-regulated systems. The most not possible. Barnett and colleagues157 and Wächter and
conservative and possibly best approach is to ensure ade- colleagues158 reported that both short-term (4 g/day for
quate daily fruit and vegetable intake not only for the anti- 2 weeks) and long-term (4 g/day for 3 months) carnitine
oxidant vitamins they provide, but for the various phyto- supplementation did not increase skeletal muscle carnitine
chemicals possessing antioxidant potential. There is likely a content. Furthermore, IV infusion of carnitine for 5 hours
particular effectiveness of nature’s balance and it guards did not increase net carnitine uptake across the leg159 or
against potential negative effects from over-providing a muscle carnitine content.160 The latter observation sug-
single antioxidant compound. The acute potential for cyste- gests that it is likely transport of carnitine that limits accu-
ine donors to up-regulate the glutathione system and mulation in muscle. Based on these observations, it is not
thereby improve exercise performance cannot be denied surprising to find that a majority of well-controlled carni-
and, although the standard approach to prove this has used tine supplementation studies have not found an effect on
a druglike intervention, emerging data suggests that pro- VO2 max,161 enhancement of whole-body or muscle-fat
teins particularly high in cysteine content may provide metabolism,159,162,163 muscle glycogen use,164 or exercise
effective (and safer) glutathione system support. performance.158 Accordingly, most reviews of ergogenic
Adverse Effects. NAC is sold as a nutritional supple- aids, even recently165 have concluded that carnitine supple-
ment, but strong consideration should be given to the po- mentation is not effective for augmenting muscle fat
tential for side effects. Dose-dependent side effects of NAC metabolism during prolonged exercise.
include anaphylactic reactions, hypotension, nausea, light- Recent experimentation from Paul Greenhaff’s lab at the
headedness, and dysphoria. It appears that only mild side University of Nottingham Medical School has begun to
effects occur after oral dosing of 150 mg/kg/bw (⬃10 g). change opinions on the usefulness of carnitine supplemen-
Nonetheless, the effectiveness and potential harmful effects tation for exercise fat metabolism and performance. Under-
of chronic low doses of NAC are not known. In this light, standing that insulin likely stimulates sodium-dependent
what must be considered is that on one hand ROS and RNS active transport of carnitine via OCTN2, they hypothesized
create oxidative stress, whereas on the other they can also act that simultaneous elevations in plasma insulin and carnitine
as signaling molecules within a cell for various transcription would stimulate uptake and accumulation of carnitine in
and translation processes leading to cell adaptation. It is pos- muscle. Indeed, Stephens and colleagues160 have shown
sible there is a fine line between complementing and stimu- that carnitine infusion during a hyperinsulinemic euglyce-
lating endogenous antioxidant systems with oral antioxidant mic clamp procedure resulted in approximately a 15% in-
compounds for exercise performance benefits and creating crease in muscle carnitine content after 5 hours. They have
potential for deleterious effects on cell messaging systems. also demonstrated that oral feedings of carnitine (3 g) and
carbohydrate, which substantially increased plasma insulin
Carnitine concentration, resulted in an increase in whole-body carni-
Action. Carnitine is an important molecule that assists tine retention (versus carnitine supplementation alone) cal-
in the transport of fatty acids from the cytosol into the culated from 24-hour urinary carnitine excretion.166 Lastly,
mitochondria for subsequent oxidation. Increasing the car- they have also shown that a combined hyperinsulinemia and
nitine content of skeletal muscle should enhance fatty acid hypercarnitinemia resulted in a reduced carbohydrate oxi-
uptake and oxidation by mitochondria during exercise and dation in a condition of surfeit carbohydrate availability,
potentially lead to reduced glycogen use and improved possibly resulting from enhanced fat oxidation in muscle.167
endurance capacity. These findings reinvigorate the possibility that carnitine can
158 SECTION I • Preparation and Prevention in Sports Medicine
be used as an effective ergogenic aid to enhance metabolism Power activities, such as shot put or weightlifting, rely
and possibly performance during prolonged exercise. heavily on immediate energy sources. There are three main
Application. The effective dose for elevating muscle sources for immediate energy production. They include
carnitine levels seems to be within the range of 2 to 4 g/day energy production from (1) ATP: hydrolysis (splitting) of
when taken with ample carbohydrate to raise circulating ATP yielding adenosine diphosphate (ADP) and an inorganic
insulin levels. Along this line, consuming supplemental car- phosphate, (2) creatine phosphate (CP): combining CP and
nitine with meals (as would be done with a vitamin pill) may ADP to produce ATP and creatine, and (3) myokinase: join-
be as effective at getting carnitine into muscle. It is unlikely ing two ADP molecules to form ATP and adenosine mono-
that acute carnitine ingestion along with carbohydrate will phosphate (AMP). All three sources are immediately available
have immediate effects. Thus, carnitine supplementation to fuel muscle contractions. However, these sources can only
should be pursued over weeks to months. Because of the sustain activities lasting no longer than 5 to 15 seconds.
potential for elevated fat metabolism when muscle carnitine
levels are increased, it is possible that over time, fat loss will
be observed. However, carnitine should not be used in the Sources of Immediate Energy for Power and Speed
context of a “magic” fat loss remedy. (Anaerobic Activity)
Adverse Effects. There are no known adverse effects
associated with carnitine supplementation. There are reports • Adenosine triphosphate
of poor bioavailability after ingestion, which may indicate • Creatine phospate
slow absorption. This could induce symptoms of GI distress • Myokinase reaction
in susceptible individuals; thus individual tolerance needs to
be worked out through systematic trial and error.
High-intensity exercise with a speed component, such as
a 200-meter run or a 50-meter swim, depends most heavily
Ergogenic Aids for High-Intensity on glycolysis for energy production. This process involves
Exercise and Physical Strength the breakdown of glucose and glycogen stored in the mus-
cle. The breakdown of one glucose molecule results in the
and Power production of two ATPs, with the net formation of lactic
Activities that Require Power and Speed acid. Anaerobic glycolysis is a rapid process that provides
The other two groups by which athletic activities are classified significantly more energy than immediate energy sources.
include power and speed. Because the two are often required However, even when combined, both sources provide only
simultaneously, they are referred to collectively as high-intensity a small fraction of the energy that can be produced through
exercise. High-intensity exercise is characterized by short- oxidative means. Therefore, intense exercise lasting more
duration, maximal-effort tasks. By definition, high-intensity than approximately 30 seconds is supplemented with oxida-
exercise lasts less than 2 minutes for a given bout. Sprinting, tive energy sources to help sustain the activity. However,
jumping, kicking, wrestling, weightlifting, and throwing are oxidative metabolism is much slower to produce energy
examples of high-intensity activities. Although all sports in- than nonoxidative energy systems, so it will not play a
clude some degree of high-intensity exercise, this section of the dominate role in energy production until the exercise ex-
chapter focuses on those sports or sporting activities that are ceeds approximately 2 minutes, which is outside the scope
dominated by intense exercise (i.e., power, speed, or both). of the activities being discussed in this section.
The metabolic requirements for high-intensity activities vary As mentioned, anaerobic or fast glycolysis forms lactate as
greatly from endurance activities and therefore require a differ- a byproduct of ATP production. As glucose is broken down,
ent strategy for achieving peak performance. pyruvate is formed. If pyruvate does not enter the mitochon-
dria immediately, it is reduced to lactate. In tissues and cells
where there is high glycolytic activity and low mitochondrial
Physiology and Physiological Consequences density, such as type IIb muscle fibers and red blood cells,
of Energy Generation for High-Intensity Activity lactate accumulation is likely. Therefore, lactate accumula-
Physical activities that primarily consist of high-intensity tion depends on the glycolytic and mitochondrial activity of
exercise are often called anaerobic. This is because the main the muscle, not the presence of oxygen.
energy systems involved do not require oxygen to produce
the energy. The ATP produced to fuel high-intensity exer-
cise is primarily generated by immediate energy sources Causes of Fatigue and Optimizing Performance
(power) and anaerobic, or fast, glycolysis (speed). Both of During High-Intensity Exercise
these categories of energy production have a much faster During high-intensity exercise, lactate accumulation occurs
rate of energy production than aerobic energy systems, but because the rate of lactic acid production exceeds the rate at
yield far less total energy. which it is removed. The lactic acid disassociates a hydrogen
Use of Ergogenic Aids in Sport • CHAPTER 6 159
ion (H), leading to a decline in pH. The accumulation of These adaptations lead to an improvement in performance.
these unbuffered H can have deleterious effects on athletic For example, strength training is important for high-
performance. The three main negative effects of H accu- intensity activities. It leads to increased strength and muscle
mulation (i.e., lower pH) include inhibition of phospho- hypertrophy through neural and muscle tissue adaptations.
fructokinase, which is the rate-limiting enzyme in glycolysis, Neural adaptations allow for improved force generation
causing a slower glycolysis rate; interference of muscular unrelated to muscle hypertrophy. Muscle hypertrophy oc-
contraction because calcium (Ca2) is displaced from tropo- curs mainly after the neural adaptations have developed and
nin; and possible stimulation of pain receptors. Therefore, is due to the muscle tissue adaptations that occur with
the ability to better buffer the accumulation of H during strength training. Other muscle tissue adaptations that re-
high-intensity exercise will help optimize performance. sult from strength training are increased cross-sectional area
Another means for optimizing high-intensity exercise of the muscle, increased myosin heavy chain IIx and IIb
performance is to increase or better maintain CP levels isoforms, increased muscle fiber area, decreased muscle fiber
in the muscle. The ability to sustain muscular contraction mitochondrial density, increased high-energy phosphate
depends on the balance between CP use and restoration. pool in the muscle, increased ATP-use rate, increased phos-
During exercise, as ATP levels begin to decline, CP works phokinase and myokinase, increased androgen receptor
to maintain them. Because of the relatively small amount of sites, and increased intracellular glycogen and lipids.
CP stored in the muscle, if there is even a slightly greater Beyond increasing the size and strength of the muscle, these
rate of CP use versus restoration (as is common during adaptations also improve the contractile and energy produc-
high-intensity exercise), the exercise will not be maintained ing capabilities of the muscle that are beneficial for
for long. The rate of CP depletion is directly related to the speed and power. Similar adaptations can result for sprints,
intensity of exercise (i.e., high intensity exercise leads to plyometrics, and interval exercise.
faster depletion). Depletion of CP results in muscle fatigue
and thereby impaired athletic performance.
Muscle fatigue during high-intensity exercise can also Neural Adaptations that Occur Early in a Strength
result from a decrease in Ca2 release and responsiveness. It Training Program
is believed that lactate accumulation plays a role in the
impairment in the ability of the ryanodine receptor to re- • Increased electrical activity of the muscle
lease Ca2 in the SR. The resulting lower levels of free Ca2 • Increased rate of motor unit recruitment
have been associated with fatigue. Similarly, the decrease in • Increased coordination of antagonist muscle groups
• Increased motor unit synchronization
muscle pH that is associated with lactate accumulation dur-
• Improved ability to recruit high-threshold motor units
ing high-intensity exercise, has been linked to a reduction
in Ca2 sensitivity. This impairment of Ca2 responsiveness
results in a decrement of muscle force. Therefore, prevent-
ing declines in Ca2 release and responsiveness is important Taking into account the physiological factors mentioned
in preventing fatigue. in this section that can increase high-intensity athletic per-
The last factor to consider for optimizing speed and formance, various ergogenic aids have been proposed to
power performance is enlargement of the muscle. Muscle improve high-intensity exercise performance. Others have
hypertrophy allows for an increase in muscular force gen- little scientific support for efficacy or are illegal. Those dis-
eration and results primarily from an increase in cellular cussed in the following section have been shown to possibly
cross sectional area, not from an increase in the number of aid performance, and are safe and legal. However, it should
muscle fibers (hyperplasia). As the muscle fibers increase in be noted that the best means for improving performance is
size, there will be an increase in the number of sarcomeres training. These substances are not meant to be a substitute
arranged in parallel leading to an increase in force produc- for a well-designed training program.
tion. Power is also enhanced with muscle hypertrophy
because the muscle can move at a faster velocity for a given
submaximal workload. Ergogenic Aids for Power and Speed
That Have Little Scientific Support, Lack
Adaptation of Physiological Systems Investigation or Are Illegal
to High-Intensity Exercise • Amphetamines
Physical training is the most effective way to enhance the • Dehydroepiandrosterone
factors mentioned to improve athletic performance. Using • Human growth hormone
the principle of specificity of training to stress the body • Anabolic steroids
systems necessary for the activity, the body will make physi- • Carnosine
ological adaptations to overcome the stress placed on it.
160 SECTION I • Preparation and Prevention in Sports Medicine
contractility and causes peripheral vasodilation. Studies have mass (FM) and groups bone, water, and muscle together as
also shown caffeine to increase muscle motor unit recruit- the fat-free mass (FFM). Common techniques to measure
ment and enhance calcium transport through increases in these two components of body composition, FM and FFM,
calcium permeability in the SR. include skinfold measurements, bioelectrical impedance,
Research. The research on the use of caffeine for im- underwater weighing, air displacement plethysmography
proving high-intensity performance is mixed. There does (using the Bod Pod), and dual x-ray absorptiometry (DXA).
not appear to be a conclusive benefit of caffeine in speed and DXA also has the ability to separate out bone mass, resulting
power activities. The differences in study results might be in the measurement of lean body mass rather than FFM, an
explained by dosage differences or performance outcome. indication of the composition of only water and muscle.
For example, in a study by Anselme and colleagues,174 no
effect was found with a 200-mg dose of caffeine on con-
secutive Wingate tests. Yet, with a much higher dose of caf- Improving Body Composition Through Nutrition
feine (6 mg/kg/bw), Schneiker and colleagues139 found and Exercise
enhanced intermittent sprint cycle performance with the use Optimal body composition, achieved via both diet and ex-
of caffeine. The effect of caffeine on strength is also incon- ercise, is important for both athletic performance and
clusive. Beck and colleagues175 studied resistance-trained health. Thus, methods to improve body composition, spe-
men and found an improved one-repetition maximum cifically decreasing FM while also increasing FFM, are
(1-RM) performance on the bench press with caffeine sup- attractive to athletes.178 Resistance training is one such
plementation versus no improvement in the placebo group. method to achieve these alterations in body composition, as
Conversely, Astorino and colleagues176 found no difference well as to increase strength.178 Various methodologies are
in bench press 1-RM performance with caffeine supplemen- used, all involving variations of the types of exercises,
tation (6 g/kg/bw) in resistance-trained males. In addition, amount of resistance, number of repetitions, and number of
in a subsequent study, Beck and colleagues177 were unable to sets. In addition, athletes often use nutrition and ergogenic
replicate their earlier findings in nonresistance-trained males. aids to maximize the changes in body composition with
This suggests that trained athletes are more likely to display strength training.
a benefit from caffeine ingestion on strength performance Increased FFM is most often related to an increase in
than their untrained counterparts. muscle mass. Increased muscle mass with chronic resis-
Application. Because of the inconsistency in findings, tance training results from repeated acute positive incre-
there does not appear to be a recommended efficacious ments in net muscle protein balance, which is achieved
dose for high-intensity exercise. Research studies that have from either an increase in muscle protein synthesis or a
found a beneficial effect of caffeine on high-intensity exer- decrease in muscle protein breakdown.179 Muscle protein
cise have used 200 mg—6 mg/kg/bw. The caffeine was synthesis is influenced by increases in the hormones
ingested 45 to 60 minutes prior to exercise. insulin, growth hormone, insulin-like growth factor-1,
Adverse Effects. Caffeine ingestion can cause increased and testosterone, whereas muscle protein breakdown is
heart rate and blood pressure. It can also lead to insomnia, stimulated by increases in cortisol.180 These hormones are
nervousness, and cardiac arrhythmias. Chronic use can be altered by resistance exercise and nutrition, specifically
addictive. carbohydrate and protein.180
Resistance exercise training is an effective method to
Protein increase muscle protein synthesis, and nutrition can influ-
Action. The timing, type, and amount of protein con- ence both muscle protein synthesis (protein and amino ac-
sumption can enhance high-intensity exercise performance ids) and decrease muscle protein breakdown (carbohy-
through aiding the development of muscle. The benefits of drates).179 For maximal gains in muscle mass with strength
proper protein intake for muscle development during train- training, adequate dietary protein is necessary, in amounts
ing are described next. of at least the recommended daily allowance (RDA) of
0.8 g/kg/bw, although slightly more might be necessary
for strength athletes (1.2-1.6 g/kg/bw).181 Dietary protein
Ergogenic Aids to Improve Body provides the building blocks for muscle protein synthesis
Composition and, particularly when combined with carbohydrate, sup-
ports the appropriate balance of hormones. Specifics around
Measurement of Body Composition supplemental protein, including the timing of ingestion and
The composition of an individual’s body can be divided into combination with carbohydrate, is discussed in the follow-
the four compartments of bone, water, muscle, and fat, and ing text. Beyond nutrition, a few ergogenic aids, also dis-
analytical techniques have been developed to quantify each. cussed in the following text, may promote gains in FFM
These techniques are expensive and complex. Therefore, when combined with strength training by stimulating
measurement of body composition usually quantifies fat the muscle to contract more forcefully, initiating signaling
162 SECTION I • Preparation and Prevention in Sports Medicine
pathways to stimulate muscle protein synthesis, or decrease training programs of 10 to 12 weeks.187,188 However, the
muscle protein breakdown. combination of macronutrients appears to be more effective
The most effective method to decrease FM is to expend than either alone. During a 6-week resistance training pro-
greater calories than are consumed, which is usually best gram, consumption of whey or soy protein with sucrose was
achieved through a combination of both exercise and calorie more effective in increasing lean tissue mass than consump-
restriction. When energy balance is negative, lipolysis (the tion of the calorie-matched, carbohydrate-only supplement
breakdown of triglycerides stored in adipose tissue) is in- in men and women (n 27).189 For each group, the sup-
creased and FFAs are liberated to be used for energy produc- plement was divided into three equal doses and consumed
tion. Lipolysis is primarily stimulated by the catecholamines immediately before and after each training session, as well
(i.e., epinephrine and norepinephrine),182 which are acutely as before going to bed. No differences were observed be-
increased during resistance exercise.183 Ergogenic aids to tween the whey and soy protein groups. Likewise, using
alter FM could theoretically work to increase the hormones fat-free milk as the protein source, Hartman and col-
that signal lipolysis, increase resting metabolic rate and the leagues190 observed greater increases in type II muscle fiber
oxidation of fatty acids for energy, or to decrease fat storage area and FFM when compared with calorie-matched carbo-
in adipose tissue. To illustrate the relationship between com- hydrate or soy protein beverages when consumed immedi-
partments of body composition, increased metabolic rate ately following each exercise bout and again 1 hour later.
may be related to the amount of FFM184; therefore, one In summary, consumption of a supplement containing both
method to decrease FM may be to increase FFM. carbohydrate and protein during a strength training pro-
gram appears to be more effective at increasing muscle mass
than providing nutrition to the exercised muscle as carbo-
Ergogenic Aids to Increase Muscle Mass hydrate or protein alone.
Carbohydrate and Protein Supplements
Action. Consumption of protein or amino acids in
close proximity to a bout of resistance exercise augments Clinical Point
the anabolic response to exercise, resulting in increased Protein and carbohydrate supplementation together are more effec-
muscle mass over the course of a strength training program. tive at increasing muscle mass during strength training if consumed
The addition of carbohydrate further improves the result, immediately or within 1 hour of training.
presumably because of the higher insulin response, which
helps amino acid uptake into the muscle. The type and tim-
ing of protein and carbohydrate supplement consumption Application. The type, timing, and amount of carbohy-
are important factors related to the extent of increased drate plus protein supplementation are all important consid-
muscle hypertrophy. erations for maximal gains in muscle mass with resistance
Research. Acute responses to exercise can be enhanced training. A high-quality protein that provides all of the es-
through appropriate nutrition, which then should translate sential amino acids is the best choice, such as whey, casein, or
into chronic adaptations, in this case increased muscle soy. The benefit of soy protein is equivocal,189,190 and some
mass.179 Much of the research conducted on protein and concern exists over the relationship between soy protein and
carbohydrate focuses on acute ingestion before or after a testosterone levels. However, Kalman and colleagues191
bout of resistance exercise to increase muscle protein syn- found that 12 weeks of supplementation during resistance
thesis and the acute anabolic response.185 However, the training with soy protein concentrate or isolate, as compared
research discussed in this section focuses on the benefit of with a soy isolate and whey blend or whey alone, did not
chronic use of protein and carbohydrate supplements with decrease testosterone levels and resulted in similar increases
training to increase muscle mass. in muscle mass in male subjects (n 20). Whey and casein
Nutrition in combination with resistance training is have been found to be equally effective in promoting net
more effective than training alone to increase muscle mass. muscle protein synthesis,192 as has their combination as
Holm and colleagues186 conducted a 24-week training pro- found naturally in milk.190 In general, a high-quality protein
gram in postmenopausal women who consumed either a supplement, such as whey, casein, or milk-based protein
supplement containing protein, carbohydrate, calcium, and should be the choice as a supplement to resistance training.
vitamin D (730 kJ) or a placebo containing minimal energy Any simple carbohydrate source is an effective way to stimu-
from carbohydrate (102 kJ) immediately after each training late insulin and maximize the benefit of protein.
session. Lean body mass was significantly increased in the Timing of nutrient ingestion in relation to each training
group provided with nutrition as compared with minimal session is also an important consideration. Consumption of
calories. When comparing the types of nutritional supple- a carbohydrate and protein supplement either immediately
ment, consumption of a protein supplement around the prior or immediately following exercise results in the same
time of the exercise bout is more effective than a carbohy- effect on net muscle protein synthesis,193 whereas in elderly
drate supplement to increase muscle mass with resistance subjects a carbohydrate-protein supplement consumed
Use of Ergogenic Aids in Sport • CHAPTER 6 163
immediately after each session of 12 weeks of resistance reviewed 22 studies of creatine supplementation during
training resulted in greater increases in lean body mass as resistance training, and found 17 to result in an ergogenic
compared with consumption 2 hours following each train- benefit. On average, an 8% gain in strength was found with
ing bout.194 In general, carbohydrate with high-quality creatine supplementation versus placebo.200 Although cre-
protein should be consumed immediately or within 1 hour atine supplementation overall appears to be effective in in-
following resistance exercise.181 creasing muscle mass with strength training, individuals may
Although most athletes consume adequate protein in a respond differently. Syrotuik and Bell201 suggest that individu-
day to support muscle hypertrophy, the timing of a certain als who respond to creatine supplementation typically begin
amount of protein and carbohydrate in relation to a strength with a low amount of muscle creatine, have a high percentage
training session may be more important than total daily pro- of type II muscle fibers, and have the greatest muscle fiber
tein consumption.181 To stimulate acute net muscle protein cross-sectional areas and FFM.
synthesis with resistance training, 6 g of essential amino acids Application. Several different protocols are suggested for
plus 35 g of sucrose is sufficient.195 In terms of whole pro- creatine use; most involve a loading phase followed by a main-
tein, Tang and colleagues196 found that 10 g of whey protein tenance phase. For example, an effective method is loading
with 21 g of fructose was sufficient to significantly increase with 20 g/day for 5 days, followed by 2 g/day for 30 days.202
the rate of muscle protein synthesis in resistance-trained However, loading may not be necessary because supplemen-
young men when consumed immediately after leg extension tation with 3 g/day of creatine for 28 days has been found
exercise, as compared with calorie-matched carbohydrate. to result in similar muscle creatine concentrations as the
The upper limits to the doses of carbohydrate and high- 5-day loading protocol.202 Addition of carbohydrate alone203
quality protein needed are 35 g and 20 to 25 g, respec- or with protein204 may enhance the benefit of creatine
tively.181 Protein intake of more than this amount provides supplementation. For example, when combined with a
no additional stimulation of muscle protein synthesis.181 carbohydrate-protein supplement during a 10-week strength
Carbohydrate and protein in the amounts described pre- training program, creatine supplementation (0.1 g/kg/day)
viously can easily be obtained from whole foods. However, resulted in greater muscle hypertrophy than the carbohydrate-
for athletes who need a quick and easy solution, protein and protein supplement alone.204 A loading phase was not used in
carbohydrate supplements are sold as powders, shakes, and this protocol. The use of a carbohydrate-protein-creatine
bars. Individuals should check the nutrition labels to make supplement appears to be most effective when consumed
sure the supplement contains a high-quality protein source, immediately before and after the exercise bout.205
does not contain high amounts of fat or other unwanted Adverse Effects. Acute ingestion of creatine does not
substances, and the amounts of carbohydrate and protein appear to result in adverse effects in the general population,
are reasonable and fit the previously listed guidelines. with clinical studies not reporting significant changes in
Adverse Effects. For individuals with normal renal renal, hepatic, cardiac, or muscle function.206 Less is known
function, there does not appear to be any adverse effects to about the long-term side effects of creatine supplementa-
consumption of protein plus carbohydrate supplements.181 tion, but chronic intake of up to 5 g/day for up to 1 year
appears to be safe.207,208
Creatine
Action. CP is the first source of energy the muscle uses Beta-Hydroxy-Beta-Methylbutyrate
for contraction. The creatine found in muscle used to gen- Action. Beta-hydroxy-methylbutyrate (HMB) supple-
erate CP is synthesized from amino acids (arginine, glycine, mentation may increase muscle mass when consumed
and methionine), or consumed in the diet, primarily from during resistance training. It is hypothesized that the mecha-
meat. Consumption of creatine supplements can add to nism for this benefit occurs though an inhibition of muscle
this creatine pool in the muscle. Although the exact mech- protein breakdown or by promoting repair of damaged
anism is not known, creatine supplementation appears to muscle cells.209 For a detailed description of the mechanism
prevent fatigue. Ingestion of creatine itself will not increase of action, refer to the comprehensive review by Wilson and
muscle mass; however, creatine supplementation in combi- colleagues.209
nation with resistance training is effective in increasing Research. In individuals without a history of strength
muscle mass and strength as compared with training training, HMB supplementation during a training program
alone. has been found to increase muscle mass210 and decrease
Research. A large number of studies examining the ergo- muscle damage,210,211 although increases in muscle mass have
genic benefit of creatine supplementation have been pub- not always been observed even with significant decreases in
lished, the majority of which find a benefit of increased muscle markers of muscle damage.212 Regardless of training history
mass and strength.197 Branch198 and Nissen and Sharp199 have or gender, Panton and colleagues213 found a trend (p
both conducted meta-analyses of the creatine literature, and 0.08) to increased muscle mass with HMB supplementation
concluded that creatine supplementation does increase lean versus placebo (1.4
0.2 versus 0.9
0.2 kg, respectively)
body mass and strength. In addition, Rawson and Volek200 during a 4-week strength training study (39 men and
164 SECTION I • Preparation and Prevention in Sports Medicine
36 women participated in the study). Perhaps a significant for 28 days (6 g/day) did not significantly change FFM, FM,
difference would have been observed with a longer training or bone mass.219 However, statistical trends to greater altera-
program. When examining highly trained athletes, a random- tions in FFM and FM with moderate to large effect sizes were
ized, double-blind crossover study of collegiate football play- found. The 28-day study is a very short period to be able to
ers (n 35) did not find a benefit of HMB supplementation detect any significant changes in body composition associated
on muscle mass or strength versus placebo.214 More research with training, especially in a highly-trained population; there-
is needed in trained individuals with training programs fore, a longer training period may have resulted in a statistical
designed to induce a greater state of catabolism than needed benefit of CLA.
to see a benefit in untrained individuals. Overall, a meta- Application. CLA is sold as a supplement in a 50:50
analysis conducted by Nissen and Sharp,199 which included isomer mixture. The effective dose appears to be approxi-
nine studies of HMB supplementation in both trained and mately 3.2 g/day. More research needs to be conducted to
untrained individuals, found supplementation with 3 g/day find an ideal effective dose in combination with strength
resulted in a 0.28% gain in lean mass and 1.5% increase in training.
strength per week. Adverse Effects. In some studies, supplementation with
Application. HMB is sold as a supplement primarily in CLA has been found to induce insulin resistance.220,221
the form of calcium HMB monohydrate. The effective dose However, this observation has been made in overweight and
appears to be 3 g/day, consumed in separate 1-g doses obese humans, not with exercise training. The majority of
throughout the day, or 38 mg/kg.209,215 More research is studies do not report adverse events with supplementation.
needed to investigate higher doses and define an optimal The Food and Drug Administration (FDA) has declared CLA
amount for supplementation. to be generally recognized as safe in recommended doses.
Adverse Effects. HMB supplementation appears to be The focus of this section is nutritional ergogenic aids
safe, with no adverse or side effects reported in the current that may improve the potential of strength training to
literature.209 Eight weeks of supplementation with 0, 38, or increase FFM and decrease FM. There are a few supple-
76 mg HMB/kg during resistance training did not alter ments that have limited research relating them to increased
liver enzyme or renal function, lipid profile, or the immune FFM (vitamin D in older adults222-224) and decreased FM
system.216 (calcium225 and alpha-hydroxycitric acid, a plant extract
from Garcinia cambogia226); however, the ability of these
supplements to further augment the outcomes of exercise
Ergogenic Aids to Decrease Fat Mass have not been researched. Furthermore, there are various
and Increase Fat-Free Mass other ergogenic aids that have been proposed to improve
Conjugated Linoleic Acid body composition but are not discussed in this section
Action. Conjugated linoleic acid (CLA) is an unsatu- because they are illegal or lack scientific support.
rated fatty acid, small amounts of which are found naturally
in milk and meat. Although there are several isomers of
this fatty acid, the most common are c9, t11-CLA and t10, Ergogenic Aids for Body Composition that Have
c12-CLA. The supplemental form found to be efficacious Little Scientific Support, Lack Investigation
contains a 50:50 mixture of these two isomers. The stron- or Are Illegal
gest benefit of CLA supplementation appears to be reduc-
• Chromium picolinate
tion in FM, although some evidence suggests the ability to
• Pyruvate
increase FFM as well when consumed during strength train-
• Leucine
ing. The exact mechanism of action is currently unknown. • Carnitine
Research. The ability of CLA to alter body composition • Anabolic steroids
has been studied primarily in overweight and obese individu- • Human growth hormone
als during routine activities of daily living. Although not • Androstenedione
all studies have a shown a benefit, a recent meta-analysis indi-
cates consistent-but-modest decreases in FM (average loss of
0.05 kg/wk with 3.2 g CLA/day for 6 months).217 Applied
to an exercising population, it seems CLA may augment the A Note on Anabolic Steroids
effects of exercise training on body composition. In normal- Although the focus of this chapter is legal, nutritional ergo-
weight males and females with a moderate strength training genic aids, the media attention and prevalence of anabolic
history (at least two times per week, n 85), supplementa- steroid use to increase muscle mass and improve perfor-
tion with 5 g/day CLA during 7 weeks of resistance training mance warrants a brief discussion. Much of the information
was found to significantly increase lean tissue mass and for this section was adapted from Chapter 15, “The Use
decrease FM as compared with placebo.218 When studying of Ergogenic Aids in Athletics,” in Athletic Injuries and
resistance-trained athletes (n 28), CLA supplementation Rehabilitation.227
Use of Ergogenic Aids in Sport • CHAPTER 6 165
vitamins A, C, and K, magnesium, zinc, copper, iron, fluo- Although omega-3 fatty acids, collagen hydrolysate
ride, as well as adequate protein.256 proteins, and glucosamine-chondroitin supplements have
Mechanical loading of the bone via weight-bearing exer- not been studied as ergogenic aids to exercise for
cise is also essential for healthy bone mass both during the additive benefits, it can be argued that improved joint
formative years and for maintenance.257-259 Running, walk- functioning or reduced joint pain can lead to better exer-
ing, strength training, and jumping are all modes of exercise cise performance.
that have positive influence on the bone. When bone is
overloaded by exercise, formation is favored over resorption
of the bone.259 Theories as to the mechanism by which the
Conclusion
mechanical stimulus from impact exercise enhances bone The information presented in this chapter has focused on
formation may include prostaglandin release, changes in nutritional ergogenic aids that are safe, legal, and to date
electrical stimulation, increased bone blood flow, micro- have been shown to be reasonably effective. However, new
damage that leads to the formation of new bone, and al- information on this topic will continue to emerge. The fol-
terations in hormones such as testosterone and calcitriol.259 lowing web resources provide some of the most up-to-date
Exercise appears to enhance the effect of nutrition, particu- information related to nutritional ergogenic aids: the U.S.
larly calcium, on bone mass.257,260,261 Additional ergogenic Department of Agriculture’s website for nutritional supple-
aids beyond the nutrition discussed previously have not ments and ergogenic aids (fnic.nal.usda.gov), www.ncaa.org
been identified to help augment the effect of exercise on (search “nutritional supplements”), www.supplementwatch.
bone. However, limited information exists in humans that com, and www.drugfreesport.com.
omega-3 fatty acid consumption may be related to higher
bone mass.262,263
Joint function and health, particularly the collagen struc-
tures linking joints to bone, may also be influenced by References
supplementation with omega-3 fatty acids. A meta-analysis 1. Rowell LB: Human circulation regulation during human stress,
of 17 randomized, controlled trials conducted by Goldberg New York, 1986, Oxford University.
2. Borg G: Simple rating for estimation of perceived exertion.
and Katz264 found disease-related joint pain, stiffness, and
In Borg G, editor: Physical work and effort, New York, 1975,
nonsteroidal anti-inflammatory drug use to be reduced by Pergamon Press.
consumption of omega-3 fatty acids. Greater improvements 3. Friedman R, Elliot AJ: Exploring the influence of sports drink
were observed when the dose was greater than 2.7 g/day. exposure on physical endurance, Psychol Sport Exerc 9:749–759,
Research has not been conducted on omega-3 fatty acids 2008.
4. Nybo L, Nielsen B: Middle cerebral artery blood flow velocity is
with athletes suffering from joint pain; however, supple-
reduced with hyperthermia during prolonged exercise in hu-
mentation with collagen hydrolysate protein (10 g/day for mans, J Physiol 534:279–286, 2001.
24 weeks) has been found to decrease joint pain in colle- 5. Johannsen P, Christensen L, Sinkjaer T, et al: Cerebral functional
giate athletes suffering from activity- or injury-related pain, anatomy of voluntary contractions in ankle muscles in man,
but not disease-related joint pain.265 J Physiol 535:397–406, 2001.
6. Liu JZ, Shan ZY, Zhang LD, et al: Human brain activation dur-
A combination of glucosamine and chondroitin is
ing sustained and intermittent submaximal fatigue muscle con-
probably the most well-known supplement related to tractions: An fMRI study, J Neurophysiol 90:300–312, 2003.
joint health. The evidence for efficacy of these supple- 7. Newsholme EA, Acworth IN, Blomstrand E: Amino acids, brain
ments is primarily related to lessening of the symptoms of neurotransmitters and a functional link between muscle and brain
knee and hip osteoarthritis.266,267 Osteoarthritis is com- that is important in sustained exercise. In Benzi G, editor: Advances
in myochemistry, London, UK, 1987, John Libby Eurotext.
mon several years after joint injuries, particularly injuries
8. Meeusen R, Watson P, Hasegawa H, et al: Central fatigue: the
to the anterior cruciate ligament;268 therefore, prevalence serotonin hypothesis and beyond, Sports Med 36:881–909,
in athletes may be high. Also, alleviating symptoms of 2006.
osteoarthritis may help people stay active. Little informa- 9. Noakes TD, St. Clair Gibson A, Lambert EV: From catastrophe
tion is available on the efficacy of glucosamine and chon- to complexity: A novel model of integrative central neural regula-
tion of effort and fatigue during exercise in humans, Br J Sports
droitin for athletes suffering from nonosteoarthritis joint
Med 38:511–514, 2004.
pain or for maintenance of joint health to prevent injury. 10. Coggan AR, Coyle EF: Reversal of fatigue during prolonged
One published study in athletes investigated glucosamine exercise by carbohydrate infusion or ingestion, J Appl Physiol 63:
(1500 mg/day, without chondroitin) use for 4 weeks 2388–2395, 1987.
following knee injury. Significant differences between the 11. Cheuvront SN, Carter R, Castellani JW, et al: Fluid balance
and endurance exercise performance, Curr Sports Med Rep 2:
glucosamine and placebo groups were not found for
202–208, 2003.
swelling or pain during rest or walking. However, at 12. Maughan RJ: Physiological responses to fluid intake during exer-
the end of 4 weeks, the glucosamine group had better cise. In Maughan RJ, Murray R, editors: Sports drinks: Basic science
knee flexion and extension compared with placebo.269 and practical aspects, Boca Raton, FL, 2001, CRC Press.
Use of Ergogenic Aids in Sport • CHAPTER 6 167
13. Binkley HM, Beckett J, Casa DJ, et al: National Athletic Train- 34. Sawka MN, Burke LM, Eichner ER, et al: American College of
ers’ position statement: Exertional heat illness, J Athl Train 37: Sports Medicine position stand. Exercise and fluid replacement,
329–343, 2002. Med Sci Sports Exerc 39:377–390, 2007.
14. Gonzalez-Alonso J: Separate and combined influences of dehy- 35. Sawka MN, Noakes TD: Does dehydration impair exercise per-
dration and hyperthermia on cardiovascular responses to exer- formance? Med Sci Sports Exerc 39:1209–1217, 2007.
cise, Int J Sports Med 19:S111–S114, 1998. 36. Greenleaf JE, Looft-Wilson R, Wisherd JL, et al: Pre-exercise
15. Lieberman HR: Hydration and cognition: A critical review hypervolemia and cycle ergometer endurance in men, Biol Sport
and recommendations for future research, J Am Coll Nutr 14:103–114, 1997.
26:555S–561S, 2007. 37. Riedesel ML, Allen DY, Peake GT, et al: Hyperhydration with
16. Baker LB, Dougherty KA, Chow M, et al: Progressive dehydra- glycerol solutions, J Appl Physiol 63:2262–2268, 1987.
tion causes a progressive decline in basketball skill performance, 38. Greenleaf JE: Problem: Thirst, drinking behavior, and involun-
Med Sci Sports Exerc 39:1114–1123, 2007. tary dehydration, Med Sci Sports Exerc 24:645–656, 1992.
17. Montain SJ, Coyle EF: Influence of the timing of fluid ingestion 39. Freund BJ, Montain SJ, Young AJ, et al: Glycerol hyperhydra-
on temperature regulation during exercise, J Appl Physiol 75: tion: Hormonal, renal, and vascular fluid responses, J Appl Physiol
688–695, 1993. 79:2069–2077, 1995.
18. Stover EA, Zachwieja J, Stofan J, et al: Consistently high urine 40. Dill DB, Costill DL: Calculation of percentage changes in vol-
specific gravity in adolescent American football players and the umes of blood, plasma, and red cells in dehydration, J Appl
impact of an acute drinking strategy, Int J Sports Med 27: Physiol 37:247–248, 1974.
330–335, 2006. 41. Anderson MJ, Cotter JD, Garnham AP, et al: Effect of glycerol-
19. Godek SF, Godek JJ, Bartolozzi AR: Hydration status in college induced hyperhydration on thermoregulation and metabolism
football players during consecutive days of twice-a-day preseason during exercise in the heat, Int J Sports Nutr 11:315–333,
practices, Am J Sports Med 33:843–851, 2005. 2001.
20. Bergeron MF, Waller JL, Marinik EL: Voluntary fluid intake 42. Montner P, Zou Y, Robergs RA, et al: Glycerol hyperhydration
and core temperature responses in adolescent tennis players: alters cardiovascular and renal function, J Exerc Physiol Online
Sports beverage versus water, Br J Sports Med 40:406–410, 2:1–10, 1999.
2006. 43. Latzka WA, Sawka MN, Montain SJ, et al: Hyperhydration: Tol-
21. Castellani JW, Maresh CM, Armstrong LE, et al: Intravenous vs. erance and cardiovascular effects during uncompensable exercise-
oral rehydration: Effects on subsequent exercise-heat stress, J heat stress, J Appl Physiol 84:1858–1864, 1998.
Appl Physiol 82:799–806, 1997. 44. Lyons TP, Riedesel ML, Meuli LE, et al: Effects of glycerol-
22. Casa DJ, Maresh CM, Armstrong LE, et al: Intravenous versus oral induced hyperhydration prior to exercise in the heat on sweat-
rehydration during a brief period: Responses to subsequent exercise ing and core temperature, Med Sci Sports Exerc 22:477–483,
in the heat, Med Sci Sports Exerc 32:124–133, 2000. 1990.
23. Vrijens DMJ, Rehrer NJ: Sodium-free fluid ingestion decreases 45. Marino FE, Day D, Cannon J: Glycerol hyperhydration fails to im-
plasma sodium during exercise in the heat, J Appl Physiol prove endurance performance and thermoregulation in humans in a
86:1847–1851, 1999. warm humid environment, Pflugers Arch 446:455–462, 2003.
24. Nose H, Mack GW, Shi XR, Nadel ER: Role of osmolality and 46. Murray R, Eddy DE, Paul GL, et al: Physiological responses to
plasma volume during rehydration in humans, J Appl Physiol glycerol ingestion during exercise, J Appl Physiol 71:144–149,
65:325–331, 1988. 1991.
25. Wilk B, Bar-Or O: Effect of drink flavor and NaCl on voluntary 47. Coutts A, Reaburn P, Mummery K, et al: The effect of glycerol
drinking and hydration in boys exercising in the heat, J Appl hyperhydration on Olympic distance triathlon performance in high
Physiol 80:1112–1117, 1996. ambient temperatures, Int J Sports Nutr 12:105–119, 2002.
26. Bergeron MF: Heat cramps during tennis: A case report, Int J 48. Montner P, Stark DM, Riedesel ML, et al: Pre-exercise glycerol
Sports Nutr 6:62–68, 1996. hydration improves cycling endurance time, Int J Sports Med
27. Stofan JR, Zachwieja JJ, Horswill CA, et al: Sweat and sodium 17:27–33, 1996.
losses in NCAA football players: A precursor to heat cramps? Int 49. Latzka WA, Sawka MN, Montain SJ, et al: Hyperhydration:
J Sports Nutr 15:641–652, 2005. Thermoregulatory effects during compensable exercise-heat
28. Armstrong LE: Considerations for replacement beverages: Fluid stress, J Appl Physiol 83:860–866, 1997.
–electrolyte balance and heat illness. Marriott BM, editor: In 50. Siegler JC, Mermier CM, Amorim FT, et al: Hydration, thermo-
Fluid replacement and heat stress, National Academy Press, regulation, and performance effects of two sports drinks during
Washington, DC, 1994. soccer training sessions, J Strength Cond Res 22:1394–1401,
29. Murray B: Hydration and physical performance, J Am Coll Nutr 2008.
26:542s–548s, 2007. 51. Sherman WM, Costill DL, Fink WJ, et al: The effect of exercise
30. Coyle EF: Fluid and fuel intake during exercise, J Sports Sci and diet manipulation on muscle glycogen and its subsequent
22:39–55, 2004. utilization during performance, Int J Sports Med 2:114–118,
31. Maughan RJ, Shirreffs SM, Leiper JB: Errors in the estimation 1981.
of hydration status from changes in body mass, J Sports Sci 25: 52. Fairchild TJ, Fletcher S, Steele P, et al: Rapid carbohydrate load-
797–804, 2007. ing after short bout of near maximal intensity exercise, Med Sci
32. King RFGJ, Cooke C, Carroll S, O’Hara J: Estimating changes Sports Exerc 34:980–986, 2002.
in hydration status from changes in body mass: Considerations 53. Bergstrom J, Hultman E: A study of the glycogen metabolism
regarding metabolic water and glycogen storage, J Sports Sci during exercise in man, Scan J Clin Lab Invest 19:218–228,
26(12):1361–1363, 2008. 1967.
33. Casa DJ, Armstrong LE, Hillman SK, et al: National Athletic 54. Hultman E: Studies on muscle metabolism of glycogen and ac-
Trainers’ Association position statement: Fluid replacement for tive phosphate in man with special reference to exercise and diet,
athletes, J Athl Train 35:212–224, 2000. Scan J Clin Lab Invest 19:94, 1967.
168 SECTION I • Preparation and Prevention in Sports Medicine
55. Karlsson J, Saltin B: Diet, muscle glycogen and endurance per- 77. Winnick JJ, Davis JM, Welsh RS, et al: Carbohydrate feedings
formance, J Appl Physiol 31:203–206, 1971. during team sport exercise preserve physical and CNS function,
56. Coyle EF, Coggan AR, Hemmert MK, et al: Substrate usage dur- Med Sci Sports Exerc 37:306–315, 2005.
ing prolonged exercise following a pre-exercise meal, J Appl 78. Vergauwen L, Brouns F, Hespel P: Carbohydrate supplementa-
Physiol 59:429–433, 1985. tion improves stroke performance in tennis, Med Sci Sports Exerc
57. Sherman WM, Brodowicz G, Wright DA, et al: Effects of 4 h 30:1289–1295, 1998.
preexercise carbohydrate feedings on cycling performance, Med 79. Utter AC, Kang J, Robertson RJ, et al: Effect of carbohydrate
Sci Sports Exerc 21:598–604, 1989. ingestion on ratings of perceived exertion during a marathon,
58. Costill DL, Coyle E, Dalsky G, et al: Effects of elevated FFA and Med Sci Sports Exerc 34:1779–1784, 2002.
insulin on muscle glycogen usage during exercise, J Appl Physiol 80. Nybo L: CNS fatigue and prolonged exercise: effects of glucose
43:695–699, 1977. supplementation, Med Sci Sports Exerc 35:589–594, 2003.
59. Foster C, Costill DL, Fink WJ: Effects of pre-exercise feedings on 81. Carter JM, Jeukendrup AE, Jones DA: The effect of carbohy-
endurance performance, Med Sci Sports Exerc 11:1–5, 1979. drate mouth rinse in 1-h cycle time trial performance, Med Sci
60. Goodpaster BH, Costill DL, Fink WJ, et al.: The effects of pre- Sports Exerc 36:2107–2111, 2004.
exercise starch ingestion on endurance performance, Int J Sports 82. Clark VR, Hopkins WG, Hawley JA, et al: Placebo effect of car-
Med 17:366–372, 1996. bohydrate feedings during a 40-km cycling time trial, Med Sci
61. Sherman WM, Peden MC, Wright DA: Carbohydrate feedings 1 Sports Exerc 32:1642–1647, 2000.
h before exercise improves cycling performance, Am J Clin Nutr 83. Colombani PC, Kovacs E, Frey-Rindova P, et al: Metabolic
54:866–870, 1991. effects of protein-supplemented carbohydrate drink in marathon
62. Moseley L, Lancaster GI, Jeukendrup AE: Effects of timing of pre- runners, Int J Sports Med 9:181–201, 1999.
exercise ingestion of carbohydrate on subsequent metabolism and 84. Koopman R, Pannemans DLE, Jeukendrup AE, et al: Combined
cycling performance, Eur J Appl Physiol 88:453–458, 2003. ingestion of protein and carbohydrate improves protein balance
63. Burke LM, Claassen A, Hawley JA, et al: Carbohydrate intake during ultra-endurance exercise, Am J Physiol 287:E712–E720,
during prolonged cycling minimizes the effect of glycemic index 2004.
of pre-exercise meal, J Appl Physiol 85:2220–2226, 1998. 85. Williams MB, Raven PB, Fogt DL, et al: Effects of recovery
64. Costill DL, Saltin B: Factors limiting gastric emptying during rest beverages on glycogen restoration and endurance exercise
and exercise, J Appl Physiol 37:679–683, 1974. performance, J Strength Cond Res 17:12–19, 2003.
65. Costill DL, Bennett A, Branam G, et al: Glucose ingestion at rest 86. Ivy JL, Res PT, Sprague RC, Widzer MO: Effect of carbohydrate-
and during prolonged exercise, J Appl Physiol 34:764–769, protein supplement on endurance performance during exercise of
1973. varying intensity, Int J Sports Nutr 13:382–395, 2003.
66. Coyle EF, Hagberg JM, Hurley BF, et al: Carbohydrate feeding 87. Saunders MJ, Kane MD, Todd MK: Effects of carbohydrate-
during prolonged exercise can delay fatigue, J Appl Physiol protein beverage on cycling endurance and muscle damage, Med
55:230–235, 1983. Sci Sports Exerc 36:1233–1238, 2004.
67. Jeukendrup AE: Carbohydrate intake during exercise and perfor- 88. Romano-Ely BC, Todd MK, Saunders MJ, et al: Effect of an
mance, Nutrition 20:669–677, 2004. isocaloric carbohydrate-protein-antioxidant drink on cycling
68. Murray R, Bartoli W, Stofan J, et al: A comparison of the gastric performance, Med Sci Sports Exerc 38:1608–1616, 2006.
emptying characteristics of selected sports drinks, Int J Sports 89. Valentine RJ, Saunders MJ, Todd MK, et al: Influence of
Nutr 9:263–274, 1999. carbohydrate-protein beverage on cycling endurance and indices
69. Shi X, Summers RW, Schedl HP, et al: Effects of carbohydrate of muscle disruption, Int J Sports Nutr 18:363–378, 2008.
type and concentration and solution osmolality on water absorp- 90. Van Essen M, Gibala MJ: Failure of protein to improve time trial
tion, Med Sci Sports Exerc 27:1607–1615, 1995. performance when added to a sports drink, Med Sci Sports Exerc
70. Ryan AJ, Lambert GP, Shi X, et al: Effect of hypohydration on 38:1476–1483, 2006.
gastric emptying and intestinal absorption during exercise, J Appl 91. Osterberg KL, Zachwieja JJ, Smith JW: Carbohydrate and carbo-
Physiol 84:1581–1588, 1998. hydrate protein for cycling time trial performance, J Sports Sci
71. Jentjens RLPG, Moseley L, Waring RH, et al: Oxidation of com- 26:227–233, 2008.
bined ingestion of glucose and fructose during exercise, J Appl 92. Betts JA, Stevenson E, Williams C, et al: Recovery of endurance
Physiol 96:1277–1284, 2004. running capacity: Effect of carbohydrate-protein mixtures, Int J
72. Jentjens RLPG, Venables MC, Jeukendrup AE: Oxidation of Sports Nutr 15:590–609, 2005.
exogenous glucose, sucrose and maltose during prolonged cy- 93. Betts J, Williams C, Duffy K, et al: The influence of carbohydrate and
cling exercise, J Appl Physiol 96:1285–1291, 2004. protein ingestion during recovery from prolonged exercise on subse-
73. Rowlands DS, Thorburn MS, Thorp RM, et al: Effect of graded quent endurance performance, J Sports Sci 25:1449–1460, 2007.
fructose coingestion with maltodextrin on exogenous 14C-fruc- 94. Millard-Stafford M, Warren GL, Thomas LM, et al: Recovery
tose and 13C-glucose oxidation efficiency and high-intensity cy- from run training: Efficacy of a carbohydrate-protein beverage?
cling performance, J Appl Physiol 104:1709–1719, 2008. Int J Sports Nutr 15:610–624, 2005.
74. Nicholas C, Williams C, Lakomy H, et al: Influence of ingesting 95. Karp JR, Johnston JD, Tecklenburg S, et al: Chocolate milk as a
carbohydrate-electrolyte solution on endurance capacity during post-exercise recovery aid, Int J Sports Nutr 16:78–91, 2006.
intermittent, high-intensity shuttle running, J Sport Sci 13: 96. Rowlands DS, Rossler K, Thorp RM, et al: Effect of dietary pro-
283–290, 1995. tein content during recovery from high-intensity cycling on
75. Davis JM, Welsh R, Alderson N: Effects of carbohydrate and subsequent performance and markers of stress, inflammation,
chromium ingestion during intermittent high-intensity exercise and muscle damage in well-trained men, Appl Physiol Nutr Metab
to fatigue, Int J Sports Nutr 10:476–485, 2000. 33:39–51, 2008.
76. Welsh RS, Davis JM, Burke JR, et al: Carbohydrates and physi- 97. Rowlands DS, Thorp RM, Rossler K, et al: Effect of protein-rich
cal/mental performance during intermittent exercise to fatigue, feeding on recovery after intense exercise, Int J Sports Nutr
Med Sci Sports Exerc 34:723–731, 2002. 17:521–543, 2007.
Use of Ergogenic Aids in Sport • CHAPTER 6 169
98. Hunt JN, Stubbs DF: The volume and energy content of meals 117. Lieberman HR: Amino acid and protein requirements: Cognitive
as determinants of gastric emptying, J Physiol 245:209–225, performance, stress, and brain function. In The Committee of
1975. Military Nutrition, editor: The role of protein and amino acids in
99. Maughan RJ, Leiper JB, Vist GE: Gastric emptying and fluid sustaining and enhancing performance, Washington, DC, 1999,
availability after ingestion of glucose and soy protein hydrolysate National Academy Press.
solutions in man, Exp Physiol 89:101–108, 2004. 118. Lieberman HR: Nutrition, brain function and cognitive perfor-
100. Blomstrand E, Celsing F, Newsholme EA: Changes in plasma mance, Appetite 40:245–254, 2003.
concentrations of aromatic and branched-chain amino acids dur- 119. Deijen JB, Wientjes CJE, Vullinghs HFM, et al: Tyrosine
ing sustained exercise in man and their possible role in fatigue, improves cognitive performance and reduces blood pressure in
Acta Physiol Scand 133:115–121, 1988. cadets after one week of a combat training course, Brain Res Bull
101. Wagenmakers AJM, Beckers EJ, Brouns F, et al: Carbohydrate 48:203–209, 1999.
supplementation, glycogen depletion and amino acid metabolism 120. Shurtleff D, Thomas JR, Schrot J, et al: Tyrosine reverses a cold-
during exercise, Am J Physiol 260:E883–E890, 1991. induced working memory deficit in humans, Pharmacol Biochem
102. Blomstrand E, Hassmen P, Ekblom B, et al: Administration of Behav 47:935–941, 1994.
branched chain amino acids during sustained exercise—Effects 121. Banderet LE, Lieberman HR: Treatment with tyrosine, a neu-
on performance and on plasma concentration of some amino rotransmitter precursor, reduces environmental stress in humans,
acids, Eur J Appl Physiol 63:83–88, 1991. Brain Res Bull 22:759–762, 1989.
103. Madsen K, MacLean DA, Kiens B, et al: Effects of glucose, 122. Magill RA, Walters WF, Bray GA, et al: Effects of tyrosine, phen-
glucose plus branched-chain amino acids, or placebo on bike termine, caffeine, D-amphetamine, and placebo on cognitive and
performance over 100 km, J Appl Physiol 81:2644–2650, motor performance deficits during sleep deprivation, Nutr Neu-
1996. rosci 6:237–246, 2003.
104. Davis JM, Welsh RS, De Volve KL, et al: Effects of branched-chain 123. Neri DF, Wiegmann D, Stanny RR, et al: The effects of tyrosine
amino acids and carbohydrate on fatigue during intermittent, on cognitive performance during extended wakefulness, Aviat
high-intensity running, Int J Sport Med 20:309–314, 1999. Space Environ Med 66:313–319, 1995.
105. Mittleman KD, Ricci MR, Bailey SP: Branched-chain amino acids 124. Thomas JR, Lockwood PA, Singh A, et al: Tyrosine improves
prolong exercise during heat stress in men and women, Med Sci working memory in a multitasking environment, Pharmacol
Sports Exerc 30:83–91, 1998. Biochem Behav 64:495–500, 1999.
106. Watson P, Shirreffs SM, Maughan RJ: The effect of acute 125. Desbrow B, Leveritt M: Well-trained endurance athletes’ knowl-
branched-chain amino acid supplementation on prolonged exer- edge, insight and experience of caffeine use, Int J Sports Nutr
cise capacity in a warm environment, Eur J Appl Physiol 93: 17:328–339, 2007.
306–314, 2004. 126. Costill DL, Dalsky G, Fink W: Effects of caffeine ingestion on
107. Cheuvront SN, Carter R, Kolka MA, et al: Branched-chain metabolism and exercise performance, Med Sci Sports Exerc
amino acid supplementation and human performance when 10:155–158, 1978.
hypohydrated in the heat, J Appl Physiol 97:1275–1282, 2004. 127. Ivy JL, Costill DL, Fink WJ, et al: Influence of caffeine and car-
108. MacLean DA, Graham TE, Saltin B: Branched-chain amino bohydrate feedings on endurance performance, Med Sci Sports
acids augment ammonia metabolism while attenuating protein Exerc 11:6–11, 1979.
breakdown during exercise, Am J Physiol 267:E1010–E1022, 128. Graham TE, Spriet LL: Performance and metabolic responses to
1994. a high caffeine dose during prolonged exercise, J Appl Physiol
109. Koba T, Hamada K, Sakurai M, et al: Branched-chain amino 71:2292–2298, 1991.
acids supplementation attenuates the accumulation of blood lac- 129. Spriet LL, MacLean DA, Dyck DJ, et al: Caffeine ingestion and
tate dehydrogenase during distance running, J Sports Med Phys muscle metabolism during prolonged exercise in humans, Am J
Fitness 47:316–322, 2007. Physiol 262:E891–E898, 1992.
110. Greer BK, Woodard JL, White JP, et al: Branched-chain amino 130. Graham TE, Spriet LL: Metabolic, catecholamine, and exercise
acid supplementation and indicators of muscle damage after performance responses to various doses of caffeine, J Appl Physiol
endurance exercise, Int J Sport Nutr 17:595–607, 2007. 78:867–874, 1995.
111. Clarkson PM, Hubal MJ: Exercise-induced muscle damage in 131. Hogervorst E, Bandelow S, Schmitt J, et al: Caffeine improves
humans, Am J Phys Med Rehabil 81:S52–69, 2002. physical and cognitive performance during exhaustive exercise,
112. Nybo L, Dalsgaard MK, Steensberg A, et al: Cerebral ammonia Med Sci Sports Exerc 40:1841–1851, 2008.
uptake and accumulation during prolonged exercise in humans, 132. Graham TE, Hibbert E, Sathasivam P: Metabolic and exercise
J Physiol 563:285–290, 2005. endurance effects of coffee and caffeine ingestion, J Appl Physiol
113. Montgomery AJ, McTavish SFB, Cowen PJ, et al: Reduction of 85:883–889, 1998.
brain dopamine concentration with dietary tyrosine plus phenyl- 133. Doherty M, Smith PM: Effects of caffeine ingestion on exercise
alanine depletion: An [11C]raclopride PET study, Am J Psychiatry testing: A meta-analysis, Int J Sports Nutr 14:626–646, 2004.
160:1887–1889, 2003. 134. Kovacs EMR, Stegen JHCH, Brouns F: Effect of caffeinated
114. Young SN: Behavioral effects of dietary neurotransmitter precur- drinks on substrate metabolism, caffeine excretion, and perfor-
sors: Basic and clinical aspects, Neurosci Biobehav Rev 20: mance, J Appl Physiol 85:709–715, 1998.
313–323, 1996. 135. Cox GR, Desbrow B, Montgomery PG, et al: Effect of different
115. Chinevere TD, Sawyer RD, Creer AR, et al: Effects of L-tyrosine protocols of caffeine intake on metabolism and endurance per-
and carbohydrate ingestion on endurance exercise performance, formance, J Appl Physiol 93:990–999, 2002.
J Appl Physiol 93:1590–1597, 2002. 136. Bridge CA, Jones MA: The effect of caffeine ingestion on 8 km run
116. Strüder HK, Hollmann W, Platen P, et al: Influence of parox- performance in a field setting, J Sports Sci 24:433–439, 2006.
etine, branched-chain amino acids and tyrosine on neuroendo- 137. O’Rourke MP, O’Brien BJ, Knez WL, et al: Caffeine has a
crine system responses and fatigue in humans, Horm Metab Res small effect on 5-km running performance of well-trained and
30:188–194, 1998. recreational runners, J Sci Med Sport 11:231–233, 2008.
170 SECTION I • Preparation and Prevention in Sports Medicine
138. Van Nieuwenhoven MA, Brouns F, Kovacs EMR: The effect of 160. Stephens FB, Constantin-Teodosiu D, Laithwaite D, et al: Insu-
two sports drinks and water on GI complaints and performance lin stimulates L-carnitine accumulation in human skeletal muscle,
during an 18-km run, Int J Sports Med 26:281–285, 2005. FASEB J 20:377–379, 2006.
139. Schneiker KT, Bishop D, Dawson B, et al: Effects of caffeine on 161. Greig C, Finch KM, Jones DA, et al: The effect of oral supple-
prolonged intermittent-sprint ability in team-sport athletes, Med mentation with L-carnitine on maximum and submaximum exer-
Sci Sports Exerc 38:578–585, 2006. cise capacity, Eur J Appl Physiol 56:457–460, 1987.
140. Lorino AJ, Lloyd LK, Crixell SH, et al: The effects of caffeine on 162. Oyono-Enguelle S, Freund H, Ott C, et al: Prolonged submaxi-
athletic agility, J Strength Cond Res 20:851–854, 2006. mal exercise and L-carnitine in humans, Eur J Appl Physiol
141. Essig D, Costill DL, van Handel PJ: Effects of caffeine ingestion 58:53–61, 1988.
on utilization of muscle glycogen and lipid during leg ergometer 163. Decombaz J, Deriaz O, Acheson K, et al: Effect of L-carnitine
cycling, Int J Sports Med 1:86–90, 1980. on submaximal exercise metabolism after depletion of muscle
142. Tarnopolsky M, Cupido C: Caffeine potentiates low frequency glycogen, Med Sci Sports Exerc 25:733–740, 1993.
skeletal muscle force in habitual and nonhabitual caffeine con- 164. Vukovich MD, Costill DL, Fink WJ: Carnitine supplementation:
sumers, J Appl Phsyiol 89:1719–1724, 2000. Effect of muscle carnitine and glycogen content during exercise,
143. Davis JM, Zhao Z, Stock HS, et al: Central nervous system Med Sci Sports Exerc 26:1122–1129, 1994.
effects of caffeine and adenosine on fatigue, Am J Physiol 284: 165. Spriet LL, Perry CG, Talanian JL: Legal pre-event nutritional
R399–R404, 2002. supplements to assist energy metabolism, Essays Biochem 44:
144. Cole KJ, Costill DL, Starling RD, et al: Effect of caffeine inges- 27–43, 2008.
tion on perception of effort and subsequent work production, 166. Stephens FB, Evans CE, Constantin-Teodosiu D, et al: Carbohy-
Int J Sports Nutr 6:14–23, 1996. drate ingestion augments L-carnitine retention in humans, J Appl
145. Ganio MS, Casa DJ, Armstrong LE, et al: Evidence-based Physiol 102:1065–1070, 2006.
approach to lingering hydration questions, Clin Sports Med 167. Stephens FB, Constantin-Teodosiu D, Laithwaite D, et al:
26:1–16, 2007. Skeletal muscle carnitine accumulation alters fuel metabolism
146. Wemple RD, Lamb DR, McKeever KH: Caffeine vs. caffeine-free in resting human skeletal muscle, J Clin Endocrinol Metab
sports drinks: Effects on urine production at rest and during 91:5013–5018, 2006.
prolonged exercise, Int J Sports Med 18:40–46, 1997. 168. Requena B, Zabala M, Padial P, et al: Sodium bicarbonate and
147. Powers SK, Deruisseau KC, Quindry J, et al: Dietary antioxi- sodium citrate: Ergogenic aids? J Strength Cond Res 19:
dants and exercise, J Sports Sci 22(1):81–94, 2004. 213–224, 2005.
148. Bischoff AC: Quercetin: Potentials in the prevention and therapy 169. McNaughton LR, Backx K, Palmer G, et al: Effects of chronic
of disease, Curr Opp Clin Nutr Metab Care 11:733–740, 2008. bicarbonate ingestion on the performance of high-intensity
149. DalleDonne I, Milzani A, Colombo R: H2O2-treated actin: Assem- work, Eur J Appl Physiol 80:333–336, 1999.
bly and polymer interactions with cross-linking proteins, Biophys J 170. Harris RC, Soderlund K, Hultman E: Elevation of creatine in
69:2710–2719, 1995. resting and exercised muscle of normal subjects by creatine sup-
150. Ajtai K, Burghardt TP: Fluorescent modification and orientation plementation, Clin Sci 83:367–374, 1992.
of myosin sulfhydryl 2 in skeletal muscle fibers, Biochemistry 171. Bemben MG, Lamont HS: Creatine supplementation and exer-
28:2204–2210, 1989. cise performance: Recent findings, Sports Med 35:107–125,
151. Matuszczak Y, Farid M, Jones J, et al: Effects of N-acetylcysteine 2005.
on glutathione oxidation and fatigue during handgrip exercise, 172. Terjung RL, Clarkson P, Eichner ER, et al: American College
Muscle Nerve 32:633–638, 2005. of Sports Medicine Roundtable. The physiological and health
152. Reid MB, Stokic DS, Koch SM, et al: N-acetylcysteine inhibits effects of oral creatine supplementation, Med Sci Sport Exerc
muscle fatigue in humans, J Clin Invest 94:2468–2474, 1994. 32:706–717, 2000.
153. McKenna MJ, Medved I, Goodman CA, et al: N-acetylcysteine 173. Pritchard NR, Kalra PA: Renal dysfunction accompanying oral
attenuates the decline in muscle Na, K-pump activity and de- creatine supplementation, Lancet 351:1252–1253, 1998.
lays fatigue during prolonged exercise in humans, J Physiol 174. Anselme F, Collomp K, Mercier B, et al: Caffeine increases
576:279–288, 2006. maximal anaerobic power and blood lactate concentration, Eur J
154. Coombes JS, Powers SK, Rowell B, et al: Effects of vitamin E Appl Physiol 65:188–191, 1992.
-lipoic acid on skeletal muscle contractile properties, J Appl 175. Beck TW, Housh TJ, Schmidt RJ, et al: The acute effects of a
Physiol 90:1424–1430, 2001. caffeine-containing supplement on strength, muscular endur-
155. Lands LC, Grey VL, Smountas AA: Effect of supplementation ance, and anaerobic capabilities, J Strength Cond Res 20:
with a cysteine donor on muscle performance, J Appl Physiol 506–510, 2006.
87:1381–1385, 1999. 176. Astorino TA, Rohmann RL, Firth K: Effect of caffeine ingestion
156. Tamai I, Ohashi R, Nezu J, et al: Molecular and functional iden- on one-repetition maximum muscular strength, Eur J Appl
tification of sodium ion-dependent, high affinity human carnitine Physiol 102:127–132, 2008.
transporter OCTN2, J Biol Chem 273:20378–20382, 1998. 177. Beck TW, Housh TJ, Malek MH, et al: The acute effects of a
157. Barnett C, Costill DL, Vukovich MD, et al: Effect of L-carnitine caffeine-containing supplement on bench press strength and time
supplementation on muscle and blood carnitine content and to running exhaustion, J Strength Cond Res 22:1645–1658,
lactate accumulation during high-intensity sprint cycling, Int J 2008.
Sports Nutr 4:280–288, 1994. 178. Winett R, Carpinelli R: Potential health-related benefits of resis-
158. Wächter S, Vogt M, Kreis R, et al: Long-term administration of tance training, Preventive Medicine 33:503–513, 2001.
L-carnitine to humans: Effect on skeletal muscle carnitine content 179. Tipton K, Ferrando A: Improving muscle mass: Response of
and physical performance, Clin Chim Acta 318:51–61, 2002. muscle metabolism to exercise, nutrition and anabolic agents,
159. Soop M, Björkman O, Cederblad G, et al: Influence of carnitine Essays Biochem 44:85–98, 2008.
supplementation on muscle substrate and carnitine metabolism 180. Volek J: Influence of nutrition on responses to resistance training,
during exercise, J Appl Physiol 64:2394–2399, 1988. Med Sci Sports Exerc 36:689–696, 2004.
Use of Ergogenic Aids in Sport • CHAPTER 6 171
181. Phillips S, Moore D, Tang J: A critical examination of dietary 200. Rawson E, Volek J: The effects of creatine supplementation and
protein requirements, benefits, and excesses in athletes, Int J resistance training on muscle strength and weightlifting perfor-
Sport Nutr Exerc Metab 17:S58–S76, 2007. mance, J Strength Cond Res 17:822–831, 2003.
182. Jaworski K, Sarkadi-Nagy S, Duncan R, et al: Regulation of 201. Syrotuik D, Bell G: Acute creatine monohydrate supplementation:
triglyceride metabolism IV. Hormonal regulation of lipolysis A descriptive physiological profile of responders and nonre-
in adipose tissue, Am J Physiol Gastroinest Liver Physiol 293: sponders, J Strength Cond Res 18:610–617, 2004.
G1–G4, 2007. 202. Hultman E, Soderlund K, Timmons J, et al: Muscle creatine
183. Kraemer W, Ratamess N: Hormonal responses and adaptations loading in men, J Appl Physiol 81:232–237, 1996.
to resistance exercise and training, Sports Med 35:339–361, 203. Green A, Hultman E, Macdonald I, et al: Carbohydrate ingestion
2005. augments skeletal muscle creatine accumulation during creatine
184. La Forgia J, van der Ploeg G, Withers R, et al: Impact of indexing supplementation in humans, Am J Physiol 271:E821–E826,
resting metabolic rate against fat-free mass determined by differ- 1996.
ent body composition models, Eur J Clin Nutr 58:1132–1141, 204. Cribb P, Williams A, Hayes A: A creatine-protein-carbohydrate
2004. supplement enhances responses to resistance training, Med Sci
185. Tipton K, Rasmussen B, Miller S, et al: Timing of amino acid- Sports Exerc 39:1960–1968, 2007.
carbohydrate ingestion alters anabolic response of muscle to 205. Cribb P, Hayes A: Effects of supplement timing and resistance
resistance exercise, Am J Physiol Endocrinol Metab 281:E197–206, exercise on skeletal muscle hypertrophy, Med Sci Sports Exerc
2001. 38:1918–1925, 2006.
186. Holm L, Olesen J, Matsumoto K, et al: Protein-containing nutri- 206. Persky A, Rawson E: Safety of creatine supplementation, Subcell
ent supplementation following strength training enhances the Biochem 46:275–289, 2007.
effect on muscle mass, strength, and bone formation in post- 207. Kreider R, Melton C, Rasmussen C, et al: Long-term creatine
menopausal women, J Appl Physiol 105:274–281, 2008. supplementation does not significantly affect clinical markers of
187. Willoughby D, Stout J, Wilborn C: Effects of resistance training health in athletes, Mol Cell Biochem 244:95–104, 2003.
and protein plus amino acid supplementation on muscle anabo- 208. Shao A, Hathcock J: Risk assessment for creatine monohydrate,
lism, mass, and strength, Amino Acids 32:467–477, 2007. Regul Toxicol Pharmacol 45:242–251, 2006.
188. Kerksick C, Rasmussen C, Lancaster S, et al: The effects of protein 209. Wilson G, Wilson J, Manninen A: Effects of beta-hydroxy-
and amino acid supplementation on performance and training beta-methylbutyrate (HMB) on exercise performance and body
adaptations during ten weeks of resistance training, J Strength composition across varying levels of age, sex, and training experi-
Cond Res 20:643–653, 2006. ence: A review, Nutr Metab 5:1, 2008.
189. Candow D, Burke N, Smith-Palmer T, et al: Effect of whey and 210. Nissen S, Sharp M, Ray J, et al: Effect of leucine metabolite
soy protein supplementation combined with resistance training beta-hydroxy-beta-methylbutyrate on muscle metabolism during
in young adults, Int J Sport Nutr Exerc Metab 16:233–244, resistance-exercise training, J Appl Physiol 81:2095–2104, 1996.
2006. 211. Van Someren K, Edwards A, Howatson G: Supplementation
190. Hartman J, Tang J, Wilkinson S, et al: Consumption of fat-free with beta-hydroxy-beta-methylbutyrate (HMB) and alpha-
fluid milk after resistance exercise promotes greater lean mass ac- ketoisocaproic acid (KIC) reduces signs and symptoms of
cretion than does consumption of soy or carbohydrate in young, exercise-induced muscle damage in man, Int J Sport Nutr Exerc
novice, male weightlifters, Am J Clin Nutr 86:373–381, 2007. Metab 15:413–424, 2005.
191. Kalman D, Feldman S, Martinez M, et al: Effect of protein 212. Gallagher P, Carrithers J, Godard M, et al: Beta-hydroxy-
source and resistance training on body composition and sex beta-methylbutyrate ingestion, part I: Effects on strength and fat
hormones, J Int Soc Sports Nutr 4:4, 2007. free mass, Med Sci Sports Exerc 32:2109–2115, 2000.
192. Tipton K, Elliott T, Cree M, et al: Ingestion of casein and whey 213. Panton L, Rathmacher J, Baier S, et al: Nutritional supplementa-
proteins result in muscle anabolism after resistance exercise, Med tion of the leucine metabolite beta-hydroxy-beta-methylbutyrate
Sci Sports Exerc 36:2073–2081, 2004. (HMB) during resistance training, Nutrition 16:743–749,
193. Tipton K, Elliott T, Cree M, et al: Stimulation of net muscle 2000.
protein synthesis by whey protein ingestion before and after 214. Ransone J, Neighbors K, Lefavi R, et al: The effect of beta-
exercise, Am J Physiol Endocrinol Metab 292:E71–E76, 2007. hydroxy-beta-methylbutyrate on muscular strength and body
194. Esmark B, Anderson S, Olsen E, et al: Timing of post-exercise composition in collegiate football players, J Strength Cond Res
protein intake is important for muscle hypertrophy with resis- 17:34–39, 2003.
tance training in elderly humans, J Physiol 535:301–311, 2001. 215. Crowe M, O’Connor D, Lukins J: The effects of beta-hydroxy-
195. Rasmussen B, Tipton K, Miller S, et al: An oral essential amino beta-methylbutyrate (HMB) and HMB/creatine supplementa-
acid-carbohydrate supplement enhances muscle protein anabo- tion on indices of health in highly trained athletes, Int J Sport
lism after resistance exercise, J Appl Physiol 88:386–392, 2000. Nutr Exerc Metab 13:184–197, 2003.
196. Tang J, Manolakos J, Kujbida G, et al: Minimal whey protein with 216. Gallagher P, Carrithers J, Godard M, et al: Beta-hydroxy-beta-
carbohydrate stimulates muscle protein synthesis following resis- methylbutyrate ingestion, part II: Effects on hematology, hepatic
tance exercise in trained young men, Appl Physiol Nutr Metab and renal function, Med Sci Sports Exerc 32(12):2116–2119,
32:1132–1138, 2007. 2000.
197. Volek J, Rawson E: Scientific basis and practical aspects of creatine 217. Whigham L, Watras A, Schoeller D: Efficacy of conjugated
supplementation for athletes, Nutrition 20:609–617, 2004. linoleic acid for reducing fat mass: A meta-analysis in humans,
198. Branch JD: Effect of creatine supplementation on body composi- Am J Clin Nutr 85:1203–1211, 2007.
tion and performance: A meta-analysis, Int J Sport Nutr Exerc 218. Pinkoski C, Chilibeck P, Candow D, et al: The effects of conju-
Metab 13:198–226, 2003. gated linoleic acid supplementation during resistance training,
199. Nissen SL, Sharp RL: Effect of dietary supplements on lean mass Med Sci Sports Exerc 38:339–348, 2006.
and strength gains with resistance exercise: A meta-analysis, 219. Kreider R, Ferreira M, Greenwood M, et al: Effects of conju-
J Appl Physiol 94:651–659, 2003. gated linoleic acid supplementation during resistance training on
172 SECTION I • Preparation and Prevention in Sports Medicine
body composition, bone density, strength, and selected hemato- 241. Hartgens F, Kuipers H: Effects of androgenic-anabolic steroids
logical markers, J Strength Cond Res 16:325–334, 2002. in athletes, Sports Med 34:513–554, 2004.
220. Thrush A, Chabowski A, Heigenhauser G, et al: Conjugated 242. Baume N, Schumacher Y, Sottas P, et al: Effect of multiple oral
linoleic acid increases skeletal muscle ceramide content and de- doses of androgenic anabolic steroids on endurance performance
creases insulin sensitivity in overweight, non-diabetic humans, and serum indices of physical stress in healthy male subjects, Eur
Appl Physiol Nutr Metab 32:372–382, 2007. J Appl Physiol 98:329–340, 2006.
221. Riserus U, Vessby B, Arnlov J, et al: Effects of cis-9, trans-11 243. Trenton A, Currier G: Behavioural manifestations of anabolic
conjugated linoleic acid supplementation on insulin sensitivity, steroid use, CNS Drugs 19:571–595, 2005.
lipid peroxidation and proinflammatory markers in obese men, 244. Graham M, Davies B, Grace F, et al: Anabolic steroid use: Patterns
Am J Clin Nutr 80:279–283, 2004. of use and detection of doping, Sports Med 38:505–525, 2008.
222. Roth S, Zmuda J, Cauley J, et al: Vitamin D receptor phenotype 245. Nieminen M, Ramo M, Viitasalo M, et al: Serious cardiovascular
is associated with fat-free mass and sarcopenia in elderly men, side effects of large doses of anabolic steroids in weight lifters,
J Geronotol Biol Sci Med Sci 59:10–15, 2004. Eur Heart 17:1576–1583, 1996.
223. Bischoff-Ferrari H, Stahelin H, Dick W, et al: Effects of vitamin D 246. Bahrke M, Yesalis C, Wright J: Psychological and behavioural
and calcium supplementation on falls: A randomized controlled effects of endogenous testosterone and anabolic-androgenic
trial, J Bone Miner Res 18:343–351, 2003. steroids. An update, Sports Med 22:367–390, 1996.
224. Sato Y, Iwamoto J, Kanoko T, et al: Low-dose vitamin D pre- 247. Beaver K, Vaughn M, Delisi M, et al: Anabolic-androgenic
vents muscular atrophy and reduces falls and hip fractures in steroid use and involvement in violent behavior in a nationally
women after stroke: A randomized controlled trial, Cerebrovasc representative sample of young adult males in the United States,
Dis 20:187–192, 2005. Am J Public Health 98:2185–2187, 2008.
225. Teegarden D: Calcium intake and reduction in weight or fat 248. Ebenbichler C, Sturm W, Ganzer H, et al: Flow-mediated,
mass, J Nutr 133:249S–251S, 2003. endothelium-dependent vasodilatation is impaired in male body
226. Downs B, Bagchi M, Subbaraju G, et al: Bioefficacy of a novel builders taking anabolic-androgenic steroids, Atherosclerosis
calcium-potassium salt of ()-hydroxycitric acid, Mutat Res 158:483–490, 2001.
579:149–162, 2005. 249. Hartgens F, Rietjens G, Keizer H, et al: Effects of androgenic-
227. Bell AT: The use of ergogenic aids in athletics. In Zachazewski anabolic steroids on apolipoproteins and lipoprotein (a), Br J
JE, Magee DJ, Quillen WS: Athletic injuries and rehabilitation, Sports Med 38:253–259, 2004.
Philadelphia, 1996, WB Saunders. 250. Laseter J, Russell J: Anabolic steroid-induced tendon pathology:
228. Gregg D: Anabolic steroids: The debate builds up, Clin Update A review of the literature, Med Sci Sports Exerc 23:1–3, 1991.
Sports Med 1:3, 1984. 251. Martin N, Abu Dayyeh B, Chung R: Anabolic steroid abuse
229. Shahidi N: A review of the chemistry, biological action, and causing recurrent hepatic adenomas and hemorrhage, World J
clinical applications of anabolic-androgenic steroids, Clin Ther Gastroenterol 14:4573–4575, 2008.
23:1355–1390, 2001. 252. Modlinski R, Fields K: The effect of anabolic steroids on the
230. Prentice B: Pharmacologic considerations for sports medicine. In gastrointestinal system, kidneys, and adrenal glands, Curr Sports
Malone T, editor: Physical and occupational therapy: Drug impli- Med Rep 5:104–109, 2006.
cations for practice, Philadelphia, 1989, JB Lippincott. 253. Nottin S, Nguyen L, Terbah M, et al: Cardiovascular effects of
231. Celotti F, Negri Cesi P: Anabolic steroids: A review of their androgenic anabolic steroids in male bodybuilders determined by
effects on the muscles, of their possible mechanisms of action and tissue Doppler imaging, Am J Cardiol 97:912–915, 2006.
of their use in athletics, J Steroid Biochem Mol Biol 43:469–477, 254. Pope H, Katz D: Psychiatric and medical effects of anabolic-
1994. androgenic steroid use. A controlled study of 160 athletes, Arch
232. Kadi F, Eriksson A, Holmner S, et al: Effects of anabolic steroids Gen Psychiatry 51(5)375–382, 1994.
on the muscle cells of strength-trained athletes, Med Sci Sports 255. Jenkinson D, Harbert A: Supplements and sports, Am Fam
Exerc 31:1528–1534, 1999. Physician 78:1039–1046, 2008.
233. Rogozkin V: Metabolic effects of anabolic steroids on skeletal 256. Illich J, Kerstetter J: Nutrition in bone health revisited: A story
muscle, Med Sci Sports Exerc 11:160–163, 1979. beyond calcium, J Am Coll Nutr 19:715–737, 2000.
234. Stamford B, Moffat R: Anabolic steroid: Effectiveness as an 257. Weaver C: The role of nutrition on optimizing peak bone mass,
ergogenic aid to experienced weight trainers, J Sports Med Phys Asia Pac J Clin Nutr 17:135–137, 2008.
Fitness 14:191–197, 1974. 258. Bailey C, Brooke-Wavell K: Exercise for optimizing peak bone
235. Ward P: The effect of anabolic steroids on strength and lean body mass in women, Proc Nutr Soc 67:9–18, 2008.
mass, Med Sci Sports 5:277–282, 1973. 259. Chilibeck P, Sale D, Webber C: Exercise and bone mineral
236. Johnson L, Fisher G, Sylvester L, Hofheins CC: Anabolic steroid: density, Sports Med 19:103–122, 1995.
Effects on strength, body weight, oxygen uptake, and spermato- 260. Vicente-Rodriguez G, Ezquerra J, Mesana M, et al: Independent
genesis upon mature males, Med Sci Sports 4:43–45, 1972. and combined effect of nutrition and exercise on bone mass
237. Bowers RW, Reardon JP: Effects of Dianabol on strength devel- development, J Bone Miner Metab 26:416–424, 2008.
opment and aerobic capacity, Med Sci Sports 4:54, 1972. 261. Borer K: Physical activity in the prevention and amelioration of
238. Golding LJ, Freydinger J, Fishel S: Weight, size, and strength— osteoporosis in women: Interaction of mechanical, hormonal and
Unchanged with steroids, Phys Sports Med 2:39–45, 1974. dietary factors, Sports Med 35:779–830, 2005.
239. Fahey TD, Brown CH: The effects of anabolic steroids on 262. Griel A, Kris-Etherton P, Hilpert K, et al: An increase in dietary
strength, body composition, and endurance of college males n-3 fatty acids decreases a marker of bone resorption in humans,
when accompanied by a weight training program, Med Sci Sports Nutr J 6:2, 2007.
5:272–276, 1973. 263. Hogstrom M, Nordstrom P, Nordstrom A: n-3 Fatty acids are
240. Elashoff J, Jacknow A, Shain S, et al: Effects of anabolic- positively associated with peak bone mineral density and bone
androgenic steroids on muscular strength, Ann Intern Med accrual in healthy men: The NO2 study, Am J Clin Nutr
115:387–393, 1991. 85:803–807, 2007.
Use of Ergogenic Aids in Sport • CHAPTER 6 173
264. Goldberg R, Katz J: A meta-analysis of the analgesic effects of 267. Poolsup N, Suthisisang C, Channark P, et al: Glucosamine
omega-3 polyunsaturated fatty acid supplementation for inflam- long-term treatment and the progression of knee osteoarthritis:
matory joint pain, Pain 129:210–223, 2007. Systematic review of randomized controlled trials, Ann Pharma-
265. Clark K, Sebastianelli W, Flechsenhar K, et al: 24-Week study on cother 39:1080–1087, 2005.
the use of collagen hydrolysate as a dietary supplement in athletes 268. Lohmander L, Englund P, Dahl L, et al: The long-term
with activity-related joint pain, Curr Med Res Opin 24: consequence of anterior cruciate ligament and meniscus injuries:
1485–1496, 2008. Osteoarthritis, Am J Sports Med 35:1756–1769, 2007.
266. McAlindon T, LaValley M, Gulin J, et al: Glucosamine and chon- 269. Ostojic S, Arsic M, Prodanovic S, et al: Glucosamine administra-
droitin for treatment of osteoarthritis: A systematic quality assess- tion in athletes: Effects on recovery of acute knee injury, Res
ment and meta-analysis, JAMA 283:1469–1475, 2000. Sports Med 15:113–124, 2007.
7
CHAPTER
174
Sports Drug Testing • CHAPTER 7 175
taken to treat an underlying condition or disease. Although biggest proponents of comprehensive and evenly applied
some of these drugs are banned by sports organizations, drug testing programs. The author’s personal experience, as
therapeutic use exemptions (TUEs) are generally allowed well as NCAA surveys, confirms that the majority of athletes
if there are no nonprohibited alternatives. An explanation of support drug testing programs.
the TUE process can be found at the end of the chapter. An
example of this is an asthmatic athlete that needs to use a
beta-2 agonist (e.g., albuterol) inhaler to treat his or her
Collection and Chain of Custody Issues
disease while competing. Drug testing begins with an overlooked, but vitally impor-
Under this system, a single drug can be classified in mul- tant, first step in the process: sample collection. A drug test-
tiple categories depending on usage pattern. One example ing program can have the most comprehensive prohibited
is a stimulant such as amphetamines. These are sometimes list and use the most thorough and expensive laboratory, but
used ergogenically by athletes to ward off fatigue and to unless the process starts with an accurate collection process,
achieve a perceived increase in energy. Amphetamine, in the it is of limited value. A substandard collection process can
form of a drug like methamphetamine, can also be used render the results worthless and can embolden drug-using
recreationally and has a high risk for addiction. Finally, am- athletes and dismay clean athletes. In the author’s opinion,
phetamines can be prescribed as therapy for the treatment a drug testing program that does not employ a stringent
of conditions such as attention deficient hyperactivity disor- collection process is worse than no program at all. Sports
der (ADHD). Although the same drug can be used in three drug testing is much different from basic biomedical drug
different situations, an understanding of why the athlete testing or even workplace drug testing, and it is imperative
used it is imperative to deter its unauthorized use. It is very to understand the distinction.
clear that each of these scenarios need to be addressed quite
differently.
Although the abuse of recreational, and to a lesser extent Urine Testing
therapeutic, drugs can be a significant issue in sports, this Most athletic drug testing begins with witnessed urine col-
chapter focuses on drug testing for ergogenic drugs. There lection according to a rigorous set of standards that must be
are several reasons for this approach. The first is that, as men- adhered to in order to have a valid sample. It is not unusual
tioned previously, recreational drugs tend to have ergolytic for athletes to resort to very creative methods of substituting
(performance-reducing) effects. Educational and behavioral a urine sample. The collection process is the first step in a
programs designed to inform athletes about the negative con- strict chain of custody. In sports drug testing, chain of cus-
sequences of these drugs on performance can often be very tody usually describes any written procedures to ensure that
effective at reducing their use. Athletes are goal-oriented by the collection, transportation, and laboratory analysis of
nature and can respond very favorably to these types of edu- urine, blood, or other specimens remain secure from outside
cational programs. If an athlete does develop an abuse prob- tampering, review, or disclosure. Sports drug testing pro-
lem with a recreational drug, then interventions, treatment, grams publish chain-of-custody protocols to provide athletes
and counseling are required to treat serious addiction. In with assurance that their specimens’ location, possession,
these circumstances, drug testing may become part of the and security are known at all times. These procedures should
treatment plan, but is rarely used alone. Second, it is unusual be available for athletes to review before they consent to be
to develop significant problems with therapeutic drugs and tested. Chain of custody usually includes three facets of the
these situations are typically handled by the TUE process. testing process: collection, transportation, and laboratory
Drug testing for ergogenic drugs is the main focus of this analysis.3 Any material deviation from the chain of custody
chapter. The actual effects of these drugs are addressed in procedure typically invalidates the test.
other chapters. Educational programs have had mixed results
deterring this type of drug use because the substances often
have short-term positive results on athletic performance. Chain of Custody in Testing Process
Athletes focus on their performance and are often willing to
try drugs to improve performance even if they are prohibited • Collection
by the sport, illegal, or have significant adverse effects. An • Transportation
• Laboratory analysis
example of this is an Internet study of 500 AAS users in
which 100% of the respondents reported experiencing at least
one adverse effect from the drugs, yet continued to use them.
The fact that so many would continue to use AAS even in the The collection of urine specimens in sports drug testing is
face of negative health consequences is testimony to both a sequential process with many steps. Such steps include but
their perceived “positive” effects and addictive potential.2 For are not limited to identification of the athlete to be tested,
this reason, drug testing is often needed to ensure a fair play- selection of a collection container by the athlete, completion
ing field for all athletes. Indeed, athletes are amongst the of the voiding process under the direct observation of a
176 SECTION I • Preparation and Prevention in Sports Medicine
same-sex validator, completion of specimen integrity checks Blood testing requires the same strict chain of custody
(e.g., specific gravity, pH), completion of specimen number- protocol as urine collection; however, there are several
ing and packaging by the athlete or by the collector under unique aspects of blood collection that require special con-
the athlete’s watch, and the certification by all parties that the sideration. The first is the personnel required to perform
published collection process was followed. Once completed, the testing. Blood testing requires a trained phlebotomist
the typical protocol is for the athlete’s sample to be divided who is in compliance with all of the local regulations re-
into “A” and “B” bottles that are both securely sealed. These garding blood collection. These requirements vary from
steps are essential because when athletes challenge the valid- state to state and also by country. Next is a proper setting
ity of positive drug test results, the integrity of the collection for the blood collection. Although urine testing is typically
process is often called into question.4 The increased legal performed in a bathroom facility, blood collection requires
scrutiny of the process has led to the formation of indepen- a hygienic environment to reduce the risk of infection.
dent companies that serve as “third party administrators” for Typically, blood sampling requires 6 to 10 mL of blood
the drug testing process. from an athlete for the currently available testing, which
Once the sample has been sealed, it is securely transported should not affect an athlete’s performance. The present
to an accredited laboratory. Although there are a variety of WADA guidelines allow for up to three attempts at veni-
commercial laboratories in the United States that perform puncture before terminating the collection.5 Finally, all
workplace drug testing and are certified by organizations such blood samples must be handled and stored according to
as Substance Abuse and Mental Health Services Administra- established safety guidelines.
tion, the World Anti-Doping Agency (WADA) has a rigorous
certification process for those laboratories that are qualified to
perform Olympic-caliber testing. As of this writing, there are Clinical Point
only three WADA-certified laboratories in North American in At the present time, the majority of drug testing is conducted via
Los Angeles, Montreal, and Salt Lake City. urine tests, but the proliferation of bioengineered substances and the
Once received by the laboratory, the samples are immedi- potential for genetic doping may increase the need for blood testing
ately examined to ensure there has been no break in the chain in sport. Blood testing is currently limited to the Olympics and there
of custody and the samples are intact. An internal chain of are serious practical, legal, and ethical issues that need to be ad-
custody is generated to allow tracking of the sample through- dressed prior to blood testing becoming commonplace in American
out the analytical process and to account for each individual professional and collegiate sports.
who has access to that particular sample. Initially, only the
“A” bottle is unsealed and undergoes screening analysis. If the
screening is negative, no further testing takes place and even-
tually both the “A” and “B” samples are discarded. However,
Drug Testing Methodology
in the event the “A” screening is positive, a confirmation test The next several sections discuss various specific methods
is performed on a new aliquot from the “A” bottle. Only if that are frequently used to interpret drug test results. Al-
the second “A” confirmation test is positive are the results though not inclusive of all testing, these represent some
reported to the sports organization. At this point, the athlete of the more common performance-enhancing drugs that
is generally entitled to have the “B” sample analyzed and is offer challenges in interpretation. The 2010 WADA list of
allowed to either witness the analysis or have a representative prohibited substances can be found in Box 7-1.
present. The “B” sample bottle is then unsealed for the first
time and analyzed. If the “B” result does not match the “A”
result, it is considered a negative test. In summary, by the time Anabolic-Androgenic Steroids (AASs)
a positive result is reported by a WADA laboratory, there have AASs represent an area of great concern because of their
been at least two and usually three separate analyses per- ability to enhance strength and threaten the integrity of
formed on the athlete’s sample that all yield the same result. sports, and because of their widespread availability. There are
two types of AASs that are identified by drug testing: exog-
enous (xenobiotic) and endogenous compounds. Some of
Blood Testing the more common AASs are listed in Table 7-1. The relative
Although urine testing has typically been the mainstay of popularity of these types of AAS depends to a large degree
sports drug testing, athlete abuse of drugs such as EPO and on the detectability of various drugs, and testing for AASs
human growth hormone (hGH) have exposed some of the has been an integral part of doping control since the 1970s.
limitations of urine testing. Owing to this, blood testing on a The introduction of gas chromatography–mass spectrometry
limited basis has been conducted in Olympic sports. This rep- (GC-MS) to doping control in the 1980s heralded a new era
resents a major change in sports drug testing, and guidelines and continued improvement and refinement of technique
have been developed for blood testing in sports. The specific has allowed for the identification of several designer AASs in
tests for these drugs are discussed later in this chapter. the past several years, including tetrahydrogestrinone (THG),
Sports Drug Testing • CHAPTER 7 177
Table 7-1
Box 7-1 World Anti-Doping Association 2010
List of Common Anabolic Steroids
Prohibited List
Generic Name Trade Name
Substances and Methods Prohibited at All Times (In and Out
of Competition) Testosterone Depo-testosterone
S1. Anabolic Agents Nandrolone Deca-durabolin
1. Anabolic-androgenic steroids Methandienone Dianabol
a. Exogenous AAS Oxandrolone Oxandrin/Anavar
b. Endogenous AAS Oxymetholone Anadrol
2. Other anabolic agents (e.g., clenbuterol, zeranol, zilpaterol), Stanozolol Winstrol
selective androgen receptor modulators (SARMs) Trenbolone* Finaplix
Boldenone* Equipoise
S2. Hormones and Related Substances
1. Erythropoiesis-Stimulating Agents [e.g. EPO, darbepoetin, methoxy
From Green G: Doping control for the team physician, Am J Sports
glycol-epoetin beta (CERA)] Med 34(10):1-9, 2006.
2. Chorionic gonadotropins, luteinizing hormones in males *
Veterinary products.
3. Insulins
4. Corticotrophins
5. Growth hormone, insulin-like growth factor (IGF-1), mechano norbolethone, and desoxymethyltestosterone (Madol),
growth factors, Platelet-derived growth factor, fibroblast growth
which were developed as part of the Bay Area Laboratory
factors, vascular-endothelial growth factor and hepatocyte growth
factor
Cooperative (BALCO) scandal.6-8
6. Platelet-derived preparations (e.g., Platelet Rich Plasma-PRP) by GC-MS testing involves separating the components of a
intramuscular route mixture based on chromatographic retention time and frag-
menting each component to its characteristic ions. The re-
S3. Beta-2 Agonists tention time and fragmentation pattern is then matched
S4. Hormone Antagonists and Modulators against those of reference standards. This allows for a spe-
1. Aromatase inhibitors cific “fingerprint” of a compound. Identification is achieved
2. Selective estrogen receptor modulators by matching the relative retention times and mass spectra of
3. Other antiestrogenic substances the parent drug or metabolites with those of known refer-
4. Agents modifying myostatin function ence standards. The finding of metabolites confirms that
S5. Diuretics and Other Masking Agents the individual had in fact ingested the AAS in question.9
GC-MS results have been accepted in both the formal legal
Prohibited Methods
system as well as sports arbitration.
M1. Enhancement of Oxygen Transfer
M2. Chemical and Physical Manipulation
The assay process involves enzymatic hydrolysis and
M3. Gene Doping solid-phase extraction from the urine to prepare the steroids
for the analysis. The extract is then derivatized using a tri-
Substances and Methods Prohibited In Competition methylsilyl ether forming reagent before being analyzed by
S6. Stimulants GC-MS. Derivatization protects the more polar groups and
1. Nonspecified stimulants
increases the molecular weight. This has the effect of assist-
2. Specified stimulants
ing the fragmentation process and augmenting the amena-
S7. Narcotics bility to GC-MS. A GC-MS can be operated in either the full
S8. Cannabinoids scan or the more sensitive selective ion monitoring (SIM)
S9. Glucocorticosteroids mode. Typically, steroid screening tests are conducted in the
Substances Prohibited in Particular Sports SIM mode. If a banned drug is detected, a confirmation test
P1. Alcohol must be employed for definitive identification. The more
P2. Beta-blockers specific full-scan mode is used for confirmation when the
Data from The World Anti-Doping Agency 2010 Prohibited List International concentration of an AAS is high.10 The introduction of
Standard. http://www.wada-ama.org/Documents/World_Anti-Doping_ high-resolution mass spectrometry in doping control has
Program/WADP-Prohibited-list/WADA_Prohibited_List_2010_EN.pdf.
Accessed February 2010 extended the period of detectability of exogenous AAS as a
AAS, Anabolic-androgenic steroid. result of the instrument’s greater sensitivity. For example,
nandrolone decanoate may be detectable for more than a full
year after an intramuscular injection.
The AAS nandrolone, or 19-nortestosterone, deserves
special mention as it is one of the most commonly de-
tected exogenous AASs and there is a great deal of confu-
sion regarding positive test results. Some of the reasons for
178 SECTION I • Preparation and Prevention in Sports Medicine
this are the long period of detection following injection suspension and others do not make any exception for mul-
of nandrolone decanoate and the relative availability tiple positives from a single use. The opinion justifying this
of 19-norandrostenedione, which was previously sold as latter case is based on several reasons: that parenteral use is a
a dietary supplement. The first clarification is that a more serious offense, that the athlete receives a continued
“nandrolone”-positive result does not indicate that the advantage with a long-acting AAS, and that there is no
AAS nandrolone was found in the urine. In actuality, the definitive method for determining whether a subsequent
laboratory measures two metabolites of nandrolone, positive test represents a residual positive or continued use.
19-norandrosterone (19NA), and 19-noretiocholanolone As testing for xenobiotic AAS improved, athletes predict-
(19NE) with the former more commonly reported. ably turned to endogenous compounds (e.g., testosterone)
Further confusing the situation is that 19NA and as an ergogenic aid. Testosterone is problematic because
19NE can result from the use of either nandrolone, pharmaceutical and endogenous testosterone both have
19-norandrostenedione, or 19-norandrostenediol.11 Until identical patterns on mass spectrometry. Since 1983, the
the passage of the 2004 Anabolic Steroid Control Act, accepted approach has been to monitor the testosterone/
these latter two were available as dietary supplements, epitestosterone (T/E) ratio that normally exists in approxi-
creating more uncertainty. Although the Act reclassified mately a 1:1 ratio.17 The use of testosterone, or compounds
19-norandrostenedione and 19-norandrostenediol as AAS that increase testosterone (e.g., dehydroepiandrosterone
and banned them from being sold as dietary supplements, [DHEA], androstenedione, androstenediol), will raise uri-
enforcement of the Act is lax and these substances can still nary testosterone proportionally much more than epitestos-
be found in dietary supplements. It was also discovered terone. Historically, a level greater than 6:1 was considered
that microgram amounts of 19-norandrostenedione, which an indication of testosterone use. Athletes, however,
could occur from microcontamination, could result in a attempted to subvert the test by taking epitestosterone
positive test.12 Although it is difficult to determine which (a biologically inactive compound) in conjunction with tes-
of the three substances resulted in a positive test, it is tosterone to maintain a normal T/E. To prevent this, epi-
typically a moot point in that all three compounds are testosterone is quantified in a urine test and concentrations
banned by most sports organizations of more than 200 ng/mL result in a positive test.
The second area of clarification is that whereas the mere Owing to these factors, WADA lowered the threshold in
presence in the urine of all other exogenous AASs is re- 2005 and decreed that a T/E ratio of greater than 4 requires
ported as a positive result, nandrolone (or more properly further investigation. Other organizations, such as the
19NA) is the only one reported with a specific concentra- National Football League, quickly followed suit.
tion level. This is because small amounts of 19NA can occur An elevated T/E ratio is a common reason for an athlete
without ingesting a prohibited substance and WADA has to be required to undergo additional testing. The main
therefore set cut-off levels for 19NA of 2 ng/mL. Pregnant limitation of the T/E ratio is that there are a small percent-
women excrete small amounts of 19NA and consumption age of individuals who are naturally in the 4 to 10:1 range,
of oral contraceptives containing norethisterone may result despite not using testosterone or related compounds. Sev-
in the excretion of small amounts of 19NA. The latter case eral options exist in these individuals to determine whether
can be resolved by locating specific norethisterone metabo- they are misusing testosterone or have a “naturally occur-
lites.13 It has also been found that some males may naturally ring” elevated T/E ratio. The most common method is to
produce miniscule amounts of 19NA in the urine, and thus perform serial, unannounced drug tests and compare the
a cut-off level has been established at 2 ng/mL. results. The T/E ratio should be relatively stable and a
Nandrolone-positive results have been involved in addi- marked drop in T/E ratio is suggestive of previous use.
tional controversy because of dietary interference or exer- WADA recommends three unannounced tests in a 3-month
cise effects. Athletes have claimed that consuming large period.18 The T/E test has the disadvantage of requiring a
quantities of uncastrated boar organs resulted in a positive great deal of time and expense and still can be subverted by
test for nandrolone metabolites.14 Although highly improb- an athlete carefully monitoring his or her T/E ratio. Media
able, a positive test could technically result from consuming coverage from the United States BALCO affair revealed
more than a half-pound of uncastrated boar testicles, liver, that athletes were given a cream containing both testoster-
and kidney within 24 hours of a test. Intense exercise was one and epitestosterone to maintain their T/E ratio. An
also mentioned as a potential cause of elevated 19NA levels, alternative to serial testing is the ketoconazole challenge in
but studies have refuted this claim.15,16 which the drug ketoconazole is orally administered and the
Lastly, the use of injectable nandrolone decanoate has T/E ratio measured. Normal males react to ketoconazole
been detected for many months and in some cases more by suppressing testosterone and a reducing the T/E ratio,
than a year after injection. This creates a quandary for sports whereas T/E ratio increases in the face of exogenous testos-
authorities to determine if a repeat positive test represents terone administration. In fact, this test is rarely employed.
continued use. Many sports organizations require a clean The most reasonable solution is likely to be carbon isotope
“exit” urine test before allowing an athlete to return from ratio testing (also called isotope ratio MS [IRMS]), which
Sports Drug Testing • CHAPTER 7 179
can differentiate exogenous testosterone and epitestoster- with precursors provides strong indication of the use testos-
one from that which is naturally occurring.9 terone or its precursors such as androstenedione, andro-
stenediol, or possibly DHEA. The test is frequently used to
obtain additional information to consider whether an ele-
Isotope Ratio Mass Spectrometry vated T/E ratio is consistent with the misuse of male hor-
One of the WADA-acceptable methods to determine mones.19 IRMS has also been used to resolve cases of
whether an elevated T/E ratio is the result of exogenous low levels of 19NA and 19NE in the setting of potentially
testosterone is a new tool called gas chromatography– “unstable” urine samples.20
combustion–IRMS. This can detect small differences in the
isotopic composition of organic compounds relative to an
international conventional reference standard. IRMS is Testing for Erythropoiesis-Stimulating Agents
based on the finding that 98.9% of the carbon atoms in such as Erythropoietin and Darbepoetin
nature are 12C, with 1.1% being 13C, an isotope of carbon The synthesis of a recombinant human EPO (r-HuEPO) in
that contains an additional neutron. The ratio of 13C/12C 1987 dramatically changed the landscape of endurance
can be measured with high accuracy and precision by an sports events. Although it had been well known that increas-
IRMS scan. Accordingly, very small differences in the abun- ing the red cell mass would improve maximum oxygen
dance of 13C can be detected to allow differentiation of consumption, prior to 1987 rapid increases in hemoglobin
carbon sources. IRMS values for steroids are expressed as could only be accomplished through the inconvenient, com-
delta values: ␦ 13C ‰. The more negative a delta value, the plicated, and potentially dangerous process of packed red
less 13C the compound contains. blood cell transfusions. The advent of r-HuEPO meant that
The basis for IRMS is that plants fix atmospheric CO2 at a simple subcutaneous injection could increase hematocrit to
varying rates and most plants fall into one of two main the desired level. Even more advantageous, r-HuEPO and
photosynthetic processes, C3 or C4, each of which yields its long-acting cousin darbepoetin (introduced in 2001), is
different amounts of 13C content. C3 plants, such as soy- nearly identical to naturally produced EPO, making detec-
beans, are considered isotopically “light” because they fix tion by conventional means impossible. The only difference
relatively less 13C. On the other hand, C4 plants (e.g., corn) is the presence of additional sugar chains on the synthetic
incorporate more 13C and are thus “heavy” with respect to compounds. Although banned by the International Olympic
their carbon. Most humans eat both plants and animals Committee in 1990, the lack of an effective test led to re-
containing various amounts of 13C and studies have deter- ports of rampant use in sports such as long-distance running
mined ethnic differences in the IRMS of different popula- and cycling. Despite a previous report in the literature, nei-
tions, depending on their respective diets. IRMS has also ther GC-MS nor high-performance liquid chromatography
been shown to be sensitive to changes in diet and the total can be used to detect r-HuEPO.21
amount of 13C consumed. As applied to the detection of The detection of r-HuEPO was attempted through both
anabolic steroids, IRMS has the ability to distinguish exog- blood and urine testing. The blood test relies on an index
enous from endogenous testosterone. Pharmaceutical tes- of various markers, such as hematocrit, reticulocytes, and
tosterone is manufactured from stigmasterol (a soy com- iron parameters, which are known to change following the
pound) that contains relatively less 13C content as compared administration of nonphysiological r-HuEPO.22 This test is
with endogenously produced testosterone thus yielding considered “indirect” or “pharmacodynamic” because it
significantly different results on IRMS analysis. measures the effect of the drug, rather than the actual drug
IRMS testing can determine much more than the amount or metabolite as in GC-MS testing for AAS. The urine test
of 13C in urinary testosterone and can provide more defini- takes advantage of the additional charges associated with
tive information as to the source. Following pharmaceutical the extra sugar molecules on r-HuEPO and darbepoetin.
testosterone administration, the delta values of urinary tes- This glycosylation allows for separation of exogenous and
tosterone metabolites, such as androsterone and etiochola- endogenous EPO in an pH gradient electrical field and
nolone, will be more negative. In contrast, the delta values detection with a very sensitive and selective method. This
of testosterone precursors, or endogenous steroids not in- results in the so-called isoform patterns of EPO in urine23
volved in testosterone metabolism, will not change. These and the isoform pattern of rHuEPO is distinctively different
compounds can be used as endogenous references. A sig- from natural EPO. The isoelectric focusing urine test also
nificant difference in the delta value between testosterone yields a pattern for darbepoetin that is distinct from both
or its metabolites and an endogenous reference compound EPO and r-HuEPO.24
indicates an exogenous source of testosterone or of any ste- The urine method provides a direct test for r-HuEPO
roid in its metabolism. Looking for such gaps is a superior and has been upheld in court many times since three cross-
approach because the delta value of testosterone alone in a country skiers tested positive for darbepoetin at the 2002
nonuser might be affected by factors such as diet and is dif- Salt Lake City Olympics. Although it is unlikely that some-
ficult to interpret. Taking testosterone levels in comparison one outside a laboratory would be asked to interpret an
180 SECTION I • Preparation and Prevention in Sports Medicine
electropherogram, it is important to understand the pro- in 10% of normal samples but is suppressed when hGH is
cess when confronted with a positive finding for these given. This method has been shown to be capable of detect-
substances. ing hGH within 24 hours of the last dose; however, it
An example of how medical progress can be co-opted by requires a blood test and cannot detect cadaveric GH. An
the athletic community is demonstrated by the new drug alternative method has been explored as well that relies on
methoxy glycol-epoetin beta (CERA). By surrounding the pharmacodynamics and measures evidence of supraphysio-
EPO molecule with a very large polyethylene glycol moiety, logical use of hGH. Studies have revealed that of the many
the EPO is minimally excreted in the urine and thus has an markers of hGH use, IGF-1, and procollagen type III can
extremely long therapeutic half-life. While this is advanta- consistently discriminate hGH users from nonusers.26,27 It
geous for patients, the lack of urinary excretion makes it remains to be seen whether this approach to drug testing
very difficult to detect by urinary isoelectric focusing. In would survive forensic challenges to a system that has tradi-
order to detect it, a modified form of isoelectric focusing tionally relied on a “fingerprint” identification of the
can be used on blood samples. Several high-profile athletes banned substance. Although testing for growth hormone
have tested positive for this drug and been sanctioned as a continues to make strides, hGH remains a significant
result. challenge for doping control at all levels.28
Interpretation of Drug Testing Levels From Green G: Doping control for the team physician, Am J Sports
Med 34(10):1-9, 2006.
There are two types of results that are encountered in drug *
Caffeine is monitored by WADA, but not subject to sanctions,
testing: (1) the presence of substances for which any amount NCAA sanctions at this level.
†
represents a positive test, and (2) tests that have quantitated WADA and NCAA threshold is 10 micrograms/mL; NFL threshold
is 1.5 micrograms/mL.
detection limits or thresholds of reporting. The former are ‡
WADA and NFL threshold is 4:1; NCAA threshold is 6:1.
relatively easy to interpret in that the test is either positive or NCAA, National Collegiate Athletic Association; NFL, National
negative; the reporting laboratory performs semiquantitative Football League; WADA, World Anti-Doping Agency.
tests and exact levels are not necessary. In the latter category,
we have discussed examples such as 19NA and testosterone
and epitestosterone in conjunction with the T/E ratio. nontherapeutic use of genes, genetic elements, or cells that
Other substances are not reported as a positive test result have the capacity to enhance athletic performance.18
unless they exceed certain levels. Examples of this include Gene transfer technology has focused on inserting
the stimulants cathine, caffeine, and ephedrine. In addition, genetic sequences to induce synthesis of various substances.
many sports organizations set a threshold for tetrahydrocan- It has the potential to correct genetic diseases, such as im-
nabinol (THC), the active ingredient in the recreational munodeficiency states, in a manner that will revolutionize
drug marijuana. A level of 15 ng/mL is high enough to the treatment of many diseases. Once a genetic abnormality
distinguish between passive inhalation of marijuana smoke is identified, inserting a correct genetic sequence can poten-
and actual use. Owing to its half-life of 2 weeks and its tially reverse the disease. However, just as in sports pharma-
popularity, a positive test for THC is frequently encountered cology, a distinction must be drawn between therapeutic
in the athletic population. When evaluating an athlete with and ergogenic use. An example is of therapeutic use is using
a positive drug test for THC, it is incumbent on the profes- gene transfer to treat a child with absolute growth hormone
sional to thoroughly review the athlete’s drug history and deficiency. An example of ergogenic use is using it to help a
not merely focus on marijuana use. In the author’s experi- child with normal levels achieve a basketball scholarship.
ence, athletes with a positive test for THC are more likely to Gene therapy is a difficult issue for a variety of reasons.
have a problem with drugs other than THC, such as alcohol First, it challenges the notion of a “level playing field” because
or cocaine.29 Substances with reporting thresholds are it offers the opportunity for everyone to have similar genetic
summarized in Table 7-2. endowments with respect to sports (e.g., testosterone, growth
hormone, hemoglobin, muscle fiber type). It also speaks to
Genetic Alteration for Performance the dichotomy of traditional enjoyment of sports encompass-
ing both the adoration of an ideal, super athlete and the
Enhancement (Gene Doping) appreciation for the underdog triumphing over adversity.
Genetic manipulation for the expressed purpose of enhanc- Second, genetic manipulation would render current test-
ing athletic performance once seemed like science fiction, ing methods essentially obsolete. The transferred genetic
but may soon become a reality for sports. Whether this in- material would turn on the body’s own machinery to pro-
volves the manipulation of genetic material in a person or duce ergogenic substances. This has already been achieved
embryonic alterations, it has the capacity to redefine drug with the experimental drug Repoxygen that induces EPO
testing, performance enhancement, and the definition of production in response to lowered oxygen tension. It was
sports. Although it is still mainly theoretical, WADA spe- developed for patients with anemia and designed to turn
cifically banned gene doping in its 2004 Prohibited List off EPO production when normal oxygen tension returns.
in its prohibited methods section. It is defined as the Although it would be unlikely to be helpful in healthy
182 SECTION I • Preparation and Prevention in Sports Medicine
of subnormal testosterone levels. This TUE criterion performed, how much advance notice is given to athletes,
makes it clear that an athlete could not receive a benefit who is informed of the positive tests, counseling options,
after such use. and penalty structure. Each one of these is an important
The WADA criteria may not be appropriate for every component of a comprehensive drug testing program and
sports organization and is not an exact science, but it does failure to adequately consider them can reduce a program
provide a framework for developing a program. It offers to little more than window dressing.
guidelines for ensuring that all athletes adhere to similar
principles with respect to using prohibited substances for
legitimate therapeutic indications. Physicians and other Clinical Point
medical personnel play key roles in reporting accurate infor- Effective drug testing programs for athletes are complex, expensive
mation in the TUE application and applying sound medical processes involving many steps and procedures to ensure they are
judgment to their evaluation. effective and successful.
Clinical Point
Third-party administrators should be used to collect samples, not
existing medical or paramedical personnel.
Ethical Considerations
Any discussion of sports drug testing is incomplete without
mentioning its ethical implications. Drug testing is often
described as expensive, time-consuming, and ineffective,
Institutional drug testing programs also tend to be more and it is argued that athletes should be allowed to do what
successful if as many “stakeholders” support it as possible. they wish to improve themselves. There have been several
These include administrators, coaches, athletes, certified rationales proposed as to why sports drug testing is unethi-
athletic trainers, sports physical therapists, and physicians. cal. These include rebuttals of paternalism, protecting the
Interestingly, most studies of athletes31 reveal that athletes athlete, and violating the spirit of sport. The most cogent
are in favor of drug testing programs. In addition to these argument in favor of sports drug testing is to consider the
personnel, it is imperative that legal counsel be involved alternative sports world where any type of drug use is
early in the planning stages. Decisions need to be made allowed. Under this scenario, the athlete who wants to
concerning which drugs are tested for, how often testing is compete drug-free faces three obvious choices: (1) compete
184 SECTION I • Preparation and Prevention in Sports Medicine
at a competitive disadvantage, (2) quit the sport, or (3) go upon completion of the urine sample stating that all proce-
against his or her principles and take the drug. This is not dures were followed.
a theoretical ethical dilemma. Indeed, an excellent example Many appeals focus on the actual analysis of the sample.
of the quandary that athletes experience was succinctly In these cases, the laboratory must produce appropriate
stated by the disgraced British sprinter Dwain Chambers. documentation to support the result. This usually includes
Mr. Chambers tested positive for THG in the BALCO scan- the laboratory standard operating procedure for the test in
dal in 2003. In an interview in 2009 explaining why question, the laboratory accreditation, quality controls, and
he chose to use banned performance-enhancing drugs, sample analysis. The athlete, his or her representatives, and
Chambers stated, “I had to make a decision: If I wasn’t experts all have the option to review the laboratory analysis.
going to beat them [by not using drugs], I had to join Any significant breaches are grounds for concern and may
them. The decision ended up ruining me.”34 lead to a successful appeal.
This author would argue that all three are poor ethical Although all of the above reasons are legitimate grounds
choices. Some also argue that drug testing is arbitrary and for an appeal, the collection process, chain of custody, and
the banned drug list is also arbitrary. In fact, all sports follow sample analysis are almost always correct during an appeal.
arbitrary rules, but it is those rules that define a sport and The reasons for this are that if these steps have not been
provides a common framework that allows fair competition. conducted properly, the athlete is usually exonerated well
For example, is there any rational reason why a baseball team before any appeal process. For example, the United States
fields 9 players on defense? It would clearly be unfair if some Anti-Doping Agency convenes a review board at the ath-
teams were allowed to use 10 players in the field. lete’s request that reviews all written documentation. The
review board has the ability to set aside a positive result on
the basis of a significant discrepancy or protocol violation.
Clinical Point By the time an appeal is filed, there have been multiple
Ergogenic drug use has the potential to change a sport so dramati- reviews of the test result.
cally that it renders competition meaningless. What our society has Many appeals for a positive drug test then typically
come to value in sports are the expression of natural talents and the involve an acceptance of the analytical result and a request to
virtuous perfection of those talents.35 There may be legitimate scien- have the result overturned because of extenuating circum-
tific debate as to which drugs violate these principles and should be stances. These may include failure to be notified that a sub-
prohibited, but there is good agreement that there should be a stance was on the prohibited list, lack of awareness of the
banned drug list in sports. drug testing program, or inadvertent ingestion of a banned
substance. These are mentioned because it is important
when designing a drug testing program to be aware of any
potential gaps in the program. For example, it is important
Legal Challenges to Sports Drug Testing to educate athletes with respect to the details of the drug
One of the key components of any sports drug testing pro- testing program. Athletes need to be fully educated about
gram is the ability of the athlete to appeal the results of the prohibited list in their sport and the penalties for use.
a positive drug test. This can take many forms, including Inadvertent ingestion of a banned substance is a com-
institutional appeals, arbitration, or a formal legal process. mon reason given for having a positive test. This has been
Although legal challenges occur, courts in the United States exacerbated by the wildly unregulated nature of the dietary
have consistently upheld the right of sports organizations to supplement industry in the United States and elsewhere.
conduct athletic drug tests. Although it is beyond the scope Many banned substances can be found, either labeled or
of this chapter to provide an in-depth report of the legal unlabeled, in easily available dietary supplements and can
process, it is worth noting some of the more common obfuscate drug test results. Owing to the fact that it can be
challenges to a positive drug test. very difficult or impossible to sort this out, many sports
The usual first step in an appeal of a positive result to an organizations have adopted a strict liability policy with re-
“A” sample is to have the “B” bottle tested. The athlete, or spect to drug test results. This means that if an athlete has
his or her representative, is allowed to witness the entire consented to participate in a drug testing program and a
analytical process to ensure that it is correct. As mentioned drug test confirms the presence of a banned substance,
previously, if the “A” and “B” samples are not identical, the the athlete is guilty regardless of how it entered the body.
test result is considered negative. Once that is confirmed, Under this type of a program, the only legitimate appeals
the next focus is on the collection process and chain of cus- are for challenges to the collection, chain of custody, or
tody. In most appeals, the laboratory produces a documen- analytical process. This creates a situation in which the test-
tation pack that provides a full chain of custody for the ing authority is responsible for the quality of the program
sample. The athlete can review this and ensure that there and the athlete is responsible for what he or she puts
are no discrepancies. Regarding the collection process, most into his or her body. Although draconian, it does make the
drug testing programs include a form that the athlete signs program very clear to all involved.
Sports Drug Testing • CHAPTER 7 185
21. Tokish JM, Kocher MS, Hawkins RJ: Ergogenic aids: A review of 30. WADA international standard for therapeutic use exemptions.
basic science, performance, side effects, and status in sports, Am J Accessed February 2010 from http://www.wada-ama.org/
Sports Med 32(6):1543–1553, 2004. Documents/World_Anti-Doping_Program/WADP-IS-TUE/
22. Parisotto R, Wu M, Ashenden MJ, et al: Detection of recombinant WADA_ISTUE_2010_EN.pdf.
human erythropoietin abuse in athletes utilizing markers of altered 31. National Collegiate Athletic Association: NCAA 2005 study of
erythropoiesis, Haematologica 86:128–137, 2001. substance use habits of collegiate student athletes, Indianapolis, IN,
23. Lasne F, De Ceaurriz J: Recombinant erythropoietin in urine, 2006, NCAA.
Nature 405:635, 2000. 32. Goldberg L, Elliot DL, Clarke GN, et al: Effects of a multidimen-
24. Breidbach A: Erythropoietin (EPO)/darbepoetin. In Bartlett R, sional anabolic steroid prevention intervention. The Adolescents
Gratton C, Rolf CR, editors: Encyclopedia of international sports Training and Learning to Avoid Steroids (ATLAS) Program,
studies, New York, 2006, Routledge. JAMA 276(19):1555–1562, 1996.
25. Green GA: HGH/somatomedins. In Bartlett R, Gratton C, 33. Elliot DL, Goldberg L, Moe EL, et al: Preventing substance use
Rolf CR, editors: Encyclopedia of international sports studies, New and disordered eating: Initial outcomes of the ATHENA (athletes
York, 2006, Routledge. targeting healthy exercise and nutrition alternatives) program,
26. Zida W, Bidlingmaier M, Dall R, Strasburger CJ: Detection of Arch Pediatr Adolesc Med 158(11):1043–1049, 2004.
doping with human growth hormone, Lancet 353:895, 1999. 34. Los Angeles Times, “Boxer Shane Mosley, sprinter Dwain Cham-
27. Erotokritou-Mulligan I, Bassett EE, Kniess A, et al: Validation of bers take different paths after BALCO allegations.” January 22,
the growth hormone (GH)-dependent marker method of detect- 2009, p D8.
ing GH abuse in sport through the use of independent data sets, 35. Murray T: Ethical considerations. In Bartlett R, Gratton C,
Growth Horm IGF Res 17(5):416–423, 2007. Rolf CR, editors: Encyclopedia of international sports studies, New
28. Green GA: Doping control for the team physician: A review York, 2006, Routledge.
of drug testing procedures in sport, Am J Sports Med 34(10): 36. Genel M: Gender verification no more? Medscape Women’s Health
1690–1698, 2006. 5(3), 2000. Accessed February 5, 2009 from http://womenshealth.
29. Green GA: Cannabinoids. In Bartlett R, Gratton C, Rolf CR, medscape.com/Medscape/WomensHealth/journal/2000/v05.
editors: Encyclopedia of international sports studies, New York, n03/wh7218.gene/wh7218.gene.html.
2006, Routledge.
8
CHAPTER
187
188 SECTION II • Applied Biomechanics of Selected Sport Activities
Muscles are major force producers as well as sensors that total excursion of 45° for the thigh, 75° for the knee,
provide both length and force input to the nervous system and 20° for the ankle. These values were measured at a
during movement. Finally, common cycling injuries and seat height chosen for comfort by the cyclist. Using an
cycling used by more challenged populations for rehabilita- angle convention similar to the one employed by Faria and
tion, exercise, and elite competition (e.g., amputee athletes) Cavanagh2 (Figure 8-1), Rugg and Gregor3 (Figure 8-2)
are presented. demonstrate the effect of seat height changes on hip and
knee ROM as seat height varied from 100% to 115% of
pubic symphysis height (i.e., height measured from the
Cycling Domains pubic symphysis, or crotch, to the floor). This range of seat
heights is considered somewhat extreme however, because
• High-level competition the comfortable range chosen by most competitive riders
• Recreational activity
usually varies from 106% to 109% of pubic symphysis
• Aerobic and anaerobic conditioning
• Rehabilitation of disease and injury
height.
• Enhancing quality of life A striking feature of the hip and knee patterns is the
increase in peak knee extension (approximately 30°)
coupled with smaller increases in peak hip extension (less than
10°) as seat height increases,. The general shape and timing
of each joint’s kinematic profile, however, remained fairly
Cycling Kinematics
Most reports on cycling kinematics have been limited to
sagittal plane motion: hip and knee flexion and extension
and ankle dorsiflexion and plantar flexion. Displacements,
velocities, and accelerations of the thigh, shank (tibia), and
foot are most affected by cadence and bicycle geometry
(e.g., seat height or crank length). Seat height is defined as
the distance from the top of the pedal to the top of the
saddle when the crank is down and in line with the seat
tube. The complex interactions between bicycle geometry
and rider kinematics and attempts at “optimizing” the
bicycle-rider interface have been the subject of many studies
that systematically varied rider kinematics by changing
bicycle configuration, pedaling cadence, or both.1 Peak
flexion and extension of the lower extremity joints varies
depending on the seat height and fore-aft seat adjustments.
However, once the rider position is established, the con-
strained cyclic movement of the lower extremity remains
quite consistent.
Kinematic, kinetic, and muscle activity patterns during
cycling are most often described relative to the angle of the
crank, with 0° or 360° representing top dead center (TDC)
and 180° representing bottom dead center (BDC) in up-
right cycling. The power, or propulsive, phase takes place
between TDC and BDC. During this time, the contralateral
limb is in the recovery phase between BDC and TDC.
A point to remember is that during recumbent cycling
the power phase rotates back approximately 90° making
the power phase between 270° and 90°. This point is
raised again in the “Muscle Mechanics” section later in this
chapter.
Kinematic data, for example the ROM at each joint, vary
according to bicycle set-up. Although linear and angular
displacements, velocities, and accelerations change with Figure 8-1
Sketch of the right lower extremity showing reference angles for the hip,
bike fit changes, it is useful to present some examples re- knee, and ankle. An angle of 0° at the hip is the vertical reference, with a
garding steady-state seated cycling performance. Faria and positive angle representing hip flexion; 0° at the knee is full extension,
Cavanagh2 studied sagittal plane kinematics and reported a and 0° at the ankle is the anatomic position.
Applied Biomechanics of Cycling • CHAPTER 8 189
Cycling Kinetics
Reaction Forces Between the Rider and the Bicycle
A kinetic analysis of lower extremity function requires
knowledge of the interactive forces between the rider and
the bicycle. Newton’s third law of motion states that forces
act in pairs that are equal in magnitude and opposite in
direction. Therefore, when the foot applies a force to the
pedal, it will be met with a reaction force acting on the foot
that is equal in magnitude and opposite in direction. These
forces, called pedal reaction forces, act on the foot during B
cycling and have been quantified in many laboratories using
specially instrumented pedals.1 All pedal designs are basically
similar to the force platforms widely used to measure ground
reaction forces during gait. Force components perpendicular
to the pedal surface (Fz) and shear forces tangential to the
pedal surface, both mediolateral (Fx) and anteroposterior
(Fy) (Figure 8-4, A) have been widely reported. From these
components a center of pressure (Figure 8-4 C, Ay and Ax),
or point-of-force application, can be calculated. In addition,
a rotational moment about an axis perpendicular to the sur-
face of the pedal (Figure 8–4 B, Mz) and positioned at the
center of pressure can be calculated and has been used
to monitor cycling performance related to injury.23 Al-
though pedal reaction forces have been reported for more C
than 100 years, the complexity of the instrumentation used Crank Angle
to make the measurements has had little effect on the overall (deg)
pedal reaction force profiles in standard seated.1 The effects Figure 8-4
of load, cadence, and position on the bicycle on both the Mean patterns for five pedal revolutions for the pedal reaction force
(A), applied moment (B), and center of pressure patterns (C) during
magnitude and direction of these force components are dis- one pedaling cycle (top dead center [TDC] at 0 degrees to TDC
cussed later in this section. at 360 degrees). A, Fz is the component orthogonal to the pedal
In addition to the magnitude of the pedal reaction force, surface, Fy is anteroposterior (AP) shear, and Fx is the medial-lateral
the orientation of the resultant vector (Fr) with respect to shear. B, The applied moment (Mz) about an axis orthogonal to
the lower extremity is an important factor that will markedly the pedal surface when this axis is through the center of pressure
(Mz-var) or through the center of the pedal (Mz-fixed). C, Coordi-
influence how the leg musculature responds to various pedal nates of the applied load in the x (Ax) and y (Ay) directions. (From
loading demands. An exemplar pattern of the resultant pedal Broker JP, Gregor RJ: A dual piezoelectric element force pedal for
reaction force measured in the sagittal plane at six intervals kinetic analysis of cycling, Int J Sport Biomech 6:394–403, 1990.
during the pedaling cycle is presented in Figure 8-5, Copyright 1990 by Human Kinetics Publishers, Inc.)
together with the relationship between the resultant vector
192 SECTION II • Applied Biomechanics of Selected Sport Activities
Figure 8-5
Resultant pedal reaction force with respect to the right lower extremity for six separate locations during
the pedaling cycle. The length of the arrow indicates increases and decreases in magnitude.
and reaction force components must be calculated using (see section later in this chapter on joint moments) and
either inverse dynamics or forward dynamics simulations25 one- and two-joint muscle coordination (see section later in
to more completely evaluate the effect of these loads on this chapter on muscle and EMG patterns during cycling).
muscle and bone. This latter example may be very useful in the rehabilitation
Translation of pedal force components to “effective” of neurologically impaired patients as well as elite athletes
force patterns designed to “optimize” crank rotation is of recovering from injury to a single joint in which interven-
great interest to cyclists, engineers, movement scientists, tion strategies warrant a redistribution of joint moments to
and physical therapists, and can be calculated using pedal “off-load” an injured joint during the early rehabilitation
reaction forces and knowledge of pedal and crank position. period.
LaFortune and Cavanagh26 first presented the concept of Although the legs receive the largest loads (i.e., pedal re-
pedaling effectiveness by calculating the “effective” force action forces), interactive forces also exist at the handlebar–
on the crank, that is, the force component perpendicular to rider and seat–rider interfaces. One of the first reports
the crank doing work to rotate the crank (Figure 8-7). In documenting these loads was presented by Bolourchi and
addition, a component parallel to the crank was calculated Hull.31 Varying cadence from 63 to 100 rpm, a fully instru-
and considered to be the “ineffective force,” that contributes mented bicycle was used to measure reactive and propulsive
minimally to crank rotation. An index of effectiveness has forces continuously during each successive pedaling cycle.
also been presented as the ratio between the effective and Results suggest seat load profiles were independent of
ineffective force components. rider and cadence and at all conditions, seat load profiles
These calculations can be used to enhance training and went through two complete periods for each crank cycle
rehabilitation. Broker and colleagues27,28 examined the ef- (Figure 8-8).
fect of visual feedback, both summary and concurrent, on Although very few reports have emerged since these
the ability to produce a more effective pattern of force studies, it is important to realize that there are five points
application during cycling. Additionally, Perell29 reported of contact in seated cycling (i.e., two pedals, one seat, and
the use of an effective force pattern as feedback for stroke two sides of the handlebar). At each interface, loads vary
patients to enhance lower limb symmetry with carry-over to (e.g., hill climbing in a standing position involves substan-
gait symmetry. More recently, Hasson and colleagues30 used tial forces at each pedal and the handlebars) and if a
a force-directing task during cycling to study how the complete description of the task is warranted, all loads
nervous system coordinates one- and two-joint muscles in must be considered. This is also true of course, in the
directing force at the pedal. Using real-time feedback of the recumbent cycling position in a rehabilitation environment
force component orthogonal to the crank during constant (see “Muscle Mechanics” section on the effect of body
cadence cycling, their results suggest the subjects were able position on muscle activity patterns). Anything the body
to learn a complex task by changing the direction of their comes in contact with produces reactive loads on the indi-
applied pedal forces through reorganization of joint torques vidual that should be considered in any program designed
for rehabilitation or training.
Specific to recumbent cycling, one must keep in mind
the change in the power and recovery phases in the
pedaling cycle (i.e., a rotation of the power phase from
vertical TDC to vertical BDC as used often in upright
cycling) to a power phase that in some cases ranges from
deepest flexion of the lower extremity to full extension
and in some cases from the 270° point to the 90° point
in the normal upright cycle orientation. It is important
to consider the power phase relative to the pedaling
cycle convention when interpreting joint reaction
forces,8,32,33 muscle activity patterns,6,34,35 and unique
clinical applications.36-41
63 RPM
180.000 80 RPM
100 RPM
172.000
164.000
156.000
F
Z 148.000
N
140.000
132.000
124.000
116.000
108.000
100.000
0.00 72.00 144.00 216.00 288.00 360.00
CRANK ANGLE DEGREE
63 RPM
105.000 80 RPM
100 RPM
63 RPM 100.000
5.000 80 RPM
100 RPM 95.000
8.000
F 90.000
11.000
M Z
85.000
Y 14.000
N 80.000
N 17.000
20.000 75.000
S
23.000 70.000
M
26.000 65.000
29.000 60.000
32.000 55.000
0.00 72.00 144.00 216.00 288.00 360.00
35.000
0.00 72.00 144.00 216.00 288.00 360.00 CRANK ANGLE DEGREE
CRANK ANGLE DEGREE
63 RPM
63 RPM 80.000 80 RPM
7.500 80 RPM 100 RPM
100 RPM 75.000
6.000
70.000
4.500
M F 65.000
X 3.000 X
60.000
N 1.500
N 55.000
0.000
S
50.000
1.500
M
45.000
3.000
4.500
40.000
6.000 35.000
7.500 30.000
0.00 72.00 144.00 216.00 288.00 360.00 0.00 72.00 144.00 216.00 288.00 360.00
CRANK ANGLE DEGREE CRANK ANGLE DEGREE
in Figure 8-11 (i.e., the magnitude of Mz was reduced anterior cruciate ligament (ACL)–deficient individuals are
when using a “float” design pedal). It seems when using this reviewed.
pedal force analysis system the peak internally applied mo- Vector components in the sagittal plane specific to the
ment (Mz) increased significantly with load whereas knee joint are schematically presented in Figure 8-12, with
the “clipless” float system decreased both the internally and a positive tensile-compressive component (Fyk) and positive
externally applied moments. Knee pain subjects exhibited anteroposterior component (Fxk); the mediolateral compo-
distinctly different moment patterns, whereas cyclists with nent is orthogonal to this vector, described with respect to
chronic anterior knee pain—the most common type re- the tibial plateau. These three vector components, both
ported by cyclists—demonstrated exaggerated peak inter- magnitude and direction, are affected by load, cadence,
nally applied moments, increased rates of loading (dMz/dt), rider position relative to the bike (e.g., bike set-up), the
and a longer duration of the applied internal moment during type of bicycle, (e.g., recumbent versus upright), and type
the power phase (0° to 180°). of shoe–pedal interface.
Although this information seems to be important to In a recent investigation,50 four separate instrumented
function and injury, little is known about what amount of pedal platforms were used to test the effect of foot position
rotation is desirable for the foot at the pedal surface or the on intersegmental knee loads in three dimension. The mul-
shank and thigh during the pedaling cycle. A review of the tidegree of freedom pedal interface allowed both inversion
literature49 regarding clipless pedal designs concluded that and eversion and adduction and abduction separately or
permitting the foot to rotate at the pedal surface markedly in combination. There was a general reduction in both
attenuates the loads experienced by the joints in the lower coupled knee moments and in the valgus knee moment
extremity, especially the knee joint. when using the dual-rotation platform. Consistent with
Figure 8-11
The applied moment (Mz) pattern during the pedal cycle averaged
across 27 subjects using three separate shoe–pedal interface designs: a
standard toe-strap and cleat, a clipless fixed design, and a clipless float
design. A positive moment indicates an inwardly applied moment
against the pedal surface (heel out). (From Wheeler JB, Gregor RJ, Figure 8-12
Broker JP: The effect of clipless float design on shoe/pedal interface Isometric view of the proximal tibia showing orientation and direction
kinetics: Implications for overuse injuries during cycling, J Appl of forces with respect to the long axis of the tibia. Fy is the tensile-
Biomech 11:119–141, 1995. Copyright 1995 by Human Kinetics compressive component, Fx is the anteroposterior component, and Fz
Publishers, Inc.) is the mediolateral knee reaction force component.
Applied Biomechanics of Cycling • CHAPTER 8 197
Muscle Moments
Muscle moments may be calculated for the cycling
A task using a linked segment model and equations of
motion with kinematic, pedal reaction force, center of
pressure, and anthropometry (i.e., mass and moment
of inertia of each of the segments) data used as input.
Zajac25 used forward dynamics simulations in analyzing
the cycling task and for the most part he and his col-
leagues focused their efforts on rehabilitation and neural
control.
The vast majority of data reported in the literature has
focused on moments calculated in the sagittal plane, in
particular, the large hip and knee extensor moments, as
B the primary source of energy used to rotate the crank dur-
ing propulsion. During recovery, flexor moments may act to
unload the pedal (e.g., unload the pedal by pulling up
on the pedal during the recovery phase), potentially
minimizing resistance to the contralateral propulsive limb.
Investigations using a force pedal system to evaluate lower
extremity kinetics during cycling have produced a great deal
of information on moment patterns during normal, steady-
state cycling and recently on cycling mechanics during
standing, climbing, and crank acceleration. These data have
C demonstrated, as first reported by Gregor55 (Figure 8-16),
that the moments at the hip, knee, and ankle have fairly
repeatable patterns, despite changes in loading conditions,
Figure 8-14 subject population, and bike setup. Magnitudes appear to
Anteroposterior knee joint reaction force profiles for three anterior
cruciate ligament (ACL)–deficient patients. The solid line represents
increase in response to increased load, and timing features
the ACL-deficient limb, and the dashed line represents the contralateral seem to be affected by cadence as well as during accelera-
limb. (From Furumizo SH: A biomechanical analysis of anterior/ tion cycling. However, in almost all cases, the general
posterior shear joint reaction forces in the ACL-deficient knee during patterns remain essentially the same.
stationary cycling, unpublished master’s thesis, UCLA Department As presented in Figure 8-16, the hip and knee perform
of Kinesiology, 1991.)
very different actions during the propulsive phase of cycling
(i.e., the hip consistently produces an extensor moment,
while the knee produces an extensor and then flexor moment
during the power phase). These observations are well docu-
orientation of the pedal reaction force) that are transfer- mented in the literature.56-60 Gregor and colleagues56 for
able to patient population to be used during the rehabili- example, discussed the moment reversal at the knee during
tation plan. propulsion with reference to the paradoxical behavior of
Information concerning calculated knee joint reaction biarticular muscles, in that a two-joint muscle may act as an
force components, when combined with kinematic and extensor of the joint of which it is a flexor.61 Andrews57 rede-
electromyographic (EMG) data, indicates that cycling is an fined “paradoxical” muscle action in that any explanation of
excellent form of rehabilitation for patients after ACL injury two-joint muscle function in a kinetic analysis of the lower
and surgical repair. Changing seat height, for example, extremity may depend on the method of classification
changes the ROM in individual joints; changing shoe– employed in the study. Van Ingen Schenau62 concluded that
pedal interface mechanics changes the orientation of joint the uniarticular muscles were “power producers” and the
reaction force vectors (i.e., changes ACL loading patterns); biarticular muscles were “power distributors” in the coordi-
changing load modifies loads experienced by the different nated action of the lower extremity segments during the
tissues (e.g., the ACL); and changing cadence modifies cycling task. More recently, Kuo63 argued that any classifica-
loading rates on muscle, ligaments, tendons, and bone. tion of muscles according to the joints they span could be
Applied Biomechanics of Cycling • CHAPTER 8 199
100
90
70
60
50
40
30
20
10
0
75W 125W 175W 75W 125W 175W
60 rpm 90 rpm
Figure 8-15
Mean percentage of power output (± standard deviation) that each limb contributed to the total power
output during cycling at two cadences and three power outputs. Patterns indicate left leg control (dots),
right leg control (diagonal lines), anterior cruciate ligament (ACL)–intact limbs (black), and ACL-
deficient limbs (open). The horizontal line represents 50% contribution from each limb. (From Hunt MA,
Sanderson DJ, Moffet H, Inglis JJ: Interlimb asymmetry in persons with and without an anterior cruciate
ligament deficiency during stationary cycling, Arch Phys Med Rehabil 85:1475–1478, 2004.)
misleading. The manner and degree to which a muscle con- with respect to the bike, cadence, and load. Because large
tributes to a task such as cycling ultimately depends on the frontal plane knee moments may result in injury and the bike
redundant nature of the musculoskeletal system and the syn- is commonly employed in the rehabilitation of medial
ergism of the muscles involved in responding to the specific collateral ligament injuries, the greatest amount of data
task. Hence, in cycling, the integrated response of the reported has focused on the knee.
entire lower extremity needs to be considered when meeting For example, McCoy and Gregor51 reported frontal
the imposed challenges (e.g., increased load) and not just plane moments at the knee beginning as a valgus
the output of individual muscles and joints (see “Muscle moment at TDC, with initial values between 6 and 7 Nm
Mechanics” section later in this chapter). (Newton-meters) across different seat height conditions
Moment patterns can be influenced to a limited degree and pedaling at a modest load51 (Figure 8-17). Magnitudes
by bike configuration. For example, Browning and col- increased and peaked near 90° of crank rotation at
leagues58 reported that the ankle muscle moment, although each seat height condition.51 Ruby and colleagues64 sug-
almost entirely plantar flexor throughout the pedaling gested that because external loads are applied to the foot
cycle, increased in peak magnitude as seat height decreased. during pedaling, variations in foot inversion and eversion
Seat height also affected the magnitude of peak knee may contribute to the loads transmitted to the knee, the
moment (i.e., higher peak extensor magnitudes at lower potential orientation of these loads and, subsequently, to
seat heights and higher peak flexor magnitudes at higher the potential for knee joint injury. A valgus moment is
seat heights), a finding also supported by McCoy16 and calculated at the knee during the power phase in response
McCoy and Gregor.51 to a medially directed pedal reaction force whereas a varus
Hip moments, although extensor for almost the entire moment is calculated during recovery in response to a lat-
cycle, can also be affected to some degree by changes in seat erally directed pedal reaction force (see Figure 8-6). Col-
height. Greater variability was observed at the hip as lectively, data from these two studies51,64 suggest that if
opposed to the knee and ankle, and the magnitude of the knee injuries result from varus and valgus loads, then lateral
hip moment tended to increase as seat height increased.58 knee structures may be more vulnerable during the power
Moments in the frontal plane have also been reported phase, whereas medial knee structures may be more vulner-
and appear to be affected as well by bike setup, rider position able during the recovery phase.
200 SECTION II • Applied Biomechanics of Selected Sport Activities
Figure 8-17
Knee moment patterns in the frontal plane averaged for 150 pedal
revolutions (10 subjects in five trials) at 200 W and 80 rpm for three
seat height conditions: 94%, 100%, and 106% of leg length. (From
McCoy RW: The effect of varying seat position on knee loads during
cycling, unpublished doctoral dissertation, University of Southern
California Department of Exercise Science, 1989.)
Lower Extremity Muscle Mechanics recruited just prior to the gastrocnemius with peak activity
occurring before 90° in the pedaling cycle. Peak gastrocne-
Muscle Activity Patterns in the Lower Extremity mius activity occurred at an average of 107° into the pedal
To rehabilitate a patient following injury or appropriately cycle, declining gradually during recovery, and ending at
condition an athlete, knowledge of muscle activation pat- approximately 270° of crank rotation. This phase shift in the
terns (considering intensity, duration, and timing in the gastrocnemius relative to soleus onset may be related to two
pedaling cycle) is paramount. Activation intensity in muscles factors. First, peak stretch occurs later in the gastrocnemius
used to energize the bicycle should be optimized at the than in the soleus and in both muscles peak EMG activity
proper time during the pedaling cycle with intensity mini- occurs just prior to peak stretch. Second, a delay in peak
mized in muscles whose action may be counterproductive gastrocnemius activation would support its contribution to
to propulsion or may stress healing tissue. Muscle recruit- the knee flexor moment consistently observed after 90° in
ment patterns during cycling have been reported for major the pedal cycle (see previous section on “Kinetics”). Force
lower extremity muscles using both surface and fine-wire enhancement may occur as a result of the presence of active
EMG.10,67-70 Activity patterns are most commonly described stretch prior to muscle shortening in both the gastrocnemius
relative to the angle of the crank and, in general, the great- and the soleus muscles.71 In addition, the anterior tibial
est activity occurs in the leg that is in the propulsive phase muscle is active during the propulsive phase in many indi-
between 0° (TDC) and 180° (BDC) of crank rotation, viduals, is coactive with the ankle extensors, and may be used
when almost all of the energy needed to drive the bicycle to enhance ankle stability during propulsion and force trans-
is imparted from the rider to the bicycle. During this mission to the crank.
time, the opposite-side limb is in the recovery phase between The hamstring muscles are also active during the power
BDC and TDC. During this recovery phase, however, phase of cycling and most likely function to extend the hip
observable muscle activity in the flexors (e.g., hamstring during simultaneous knee extension. The semimembrano-
muscles) has been shown to assist net forward propulsion sus and semitendinosus muscles are recruited after TDC,
of the crank and observable activity in the extensors with peak activity occurring at or slightly after 90°, when
(e.g., gluteus maximus) could act to oppose net forward activity in the gluteal and vasti muscles is rapidly declining.
propulsion of the bicycle. Peak activity in the semitendinous muscle occurs slightly
Several reports published over the past twenty years have after that of the semimembranous. Biceps femoris activity is
shown a generally repeatable pattern of muscle activation the most variable of the hamstring group. In some individu-
among the major flexors and extensors in the lower extrem- als, timing of the biceps femoris is similar to that in the
ity during the pedaling cycle. Representative data published semimembranous and semitendinous muscles, while in
from 18 experienced cyclists riding at 90 rpm and 250 W others, the biceps femoris is already maximally active at
on their own bicycles are shown in Figure 8-19.10 During TDC and declines throughout propulsion.10 Finally, contin-
the propulsive phase, power is imparted to the bicycle via ued activation of the hamstrings for the remainder of
forceful hip and knee extension, with the gluteal (e.g., glu- the power phase contributes to the knee flexor moment,
teus maximus) and quadriceps muscles heavily recruited especially in the absence of any quadriceps activity after
during this time. For example, onset of activity for the 90° of crank rotation.54
gluteus maximus occurs just before TDC, with peak activity While the power phase is of primary interest because of
observed at approximately 55° of crank rotation. Both high loads and energy transfer to the bicycle, the recovery
medial and lateral vasti muscles exhibit a rapid onset and phase has been given greater attention in recent years for
cessation with relatively constant activity in between, while essentially the same reason (i.e., effective transmission of
the rectus femoris demonstrates a more gradual rise and energy to the bicycle). The fundamental question regarding
decline. Rectus femoris activity onset occurs before the vasti the recovery phase is, “Does the recovery leg assist or
and declines earlier in the power phase, a pattern generally impede effective energy transmission to the bicycle?” For-
attributed to its biarticular function at the knee and mulating an answer to this question usually requires an
hip. EMG activity ceases shortly after 90° in all three of understanding of the activation patterns of major lower ex-
these quadricep muscles, essentially ending their role as tremity muscles during this period in the pedaling cycle.
significant contributors to the work necessary to drive the Ideally, net flexion of the lower extremity during recovery
bicycle. would require just enough energy to match the acceleration
Major ankle extensors are also active during the propul- of the crank between 180° and 360° of the cycle. If this were
sive phase and, although not considered major power pro- the case, no counter-torques would be present to resist crank
ducers, these muscles are important in providing a stable link rotation or the efforts of the propulsive limb, and the recov-
between the pedal, the foot, and the more proximal joints ery limb would not be “pulling up” on the crank, actively
enabling the energy produced in lower extremity muscula- adding to crank rotation. In short, there should be a fine bal-
ture to be transmitted to the pedal. Both the soleus ance of active muscles during recovery to provide just enough
and gastrocnemius are active before TDC. The soleus is energy to lift the limb. More energy would actively lift the
Applied Biomechanics of Cycling • CHAPTER 8 203
Figure 8-19
Mean patterns of muscle activation during the pedaling cycle for 10 muscles in the lower extremity. The
dark lower curve is the average pattern from 15 pedaling cycles across 18 subjects (270 cycles), and the
lighter upper curve is one standard deviation above the mean. Magnitudes are normalized to maximal
activation. (From Ryan MM, Gregor RJ: EMG profiles of lower extremity muscles during cycling at
constant workload and cadence, J Electromyogr Kinesiol 2:69–80, 1992.)
204 SECTION II • Applied Biomechanics of Selected Sport Activities
crank and possibly be an efficient contribution to crank rota- by, for example, changes in body position with respect to the
tion, while less energy (i.e., lower magnitude EMG) would bicycle (i.e., “bike fit,” cadence, load, and cycling ability).
be counterproductive and force the propulsive limb to pro- These variables are somewhat interdependent, and the fol-
vide excess energy to lift the recovery limb and drive the lowing text is devoted to recent work describing how and
bicycle forward. In reviewing EMG patterns in the “recovery under what conditions these patterns may change.
leg,” the representative data in Figure 8-19 show that Data from Chapman and colleagues74 suggest EMG
between 180° and 235° of the pedal cycle, the hamstrings patterns may differ between novice and highly skilled
and gastrocnemius, already active, provide a major compo- cyclists, and that changes in cadence can affect certain
nent to flex the knee. Later in the recovery phase, between aspects of muscle activation. Fine-wire electrodes were
235° and 360°, the tibialis anterior muscle acts to dorsiflex placed in the tibialis anterior, tibialis posterior, peroneus
the ankle, and the rectus femoris (also a knee extensor) acts longus, lateral gastrocnemius, and soleus muscles. Using
to flex the hip. their own bicycles on a magnetically loaded trainer, four
Although reports on single-joint hip flexor activity are ranges of cadence were employed: 55 to 60 rpm, 75 to
few, Juker and colleagues72 presented data on the activity 80 rpm, 90 to 95 rpm, and each cyclist’s own preferred
patterns of the lumbar psoas, erector spinae, and three cadence. Novice riders displayed greater variability in their
different layers of the abdominal wall muscles during five EMG, greater co-activation, and greater EMG magnitudes
different styles of cycling. These data are difficult to obtain between the primary bursts of activity within each pedaling
but valuable to an understanding of hip and low-back func- cycle. Peak EMG increased with cadence, but lower EMG
tion during cycling, and an understanding of lower limb magnitude was observed at the preferred cadence in all
function during the “recovery” phase of the pedaling cycle. 19 subjects. EMG timing was affected by cadence in novice
The five different stationary cycling positions presented by riders, but not in the elite riders, suggesting some level
Juker and colleagues72 included normal posture (slightly of neuromuscular adaptation resulting from repeated
flexed), upright posture, a racing flexed posture, standing, performance in the elite riders.
and standing while sprinting. The general conclusion from Pursuing the effects of cadence on the performance of
this novel investigation was that position on the bike influ- specific muscles, Sanderson and colleagues12 reported inter-
enced the timing and magnitude of the muscles under esting differences in the way the gastrocnemius and soleus
study. During normal posture the psoas was active, at muscles responded to changes in cadence from 50 rpm to
approximately 14% of maximum voluntary contraction 110 rpm. It seems the soleus peak EMG is not affected by
(MVC), and was most active during recovery near TDC. cadence, but at the highest cadence of 110 rpm a second
Activity then increased to approximately 30% of MVC smaller peak appeared during early recovery. In contrast, the
during a flexed posture and 60% of MVC during sprinting. gastrocnemius muscle increased dramatically as cadence
Activity in the abdominal wall was very low, with almost no increased and, although there was a second smaller peak in
activity during standing and sprinting. early recovery at lower cadences, this was not observed at
When discussing activity patterns in hip and pelvic mus- the higher cadences. The authors attributed these differ-
cles during cycling, it should be remembered that cyclists ences in part to the higher shortening velocities experienced
are known to be vulnerable to low back pain. Because of by the gastrocnemius relative to the soleus as cadence
this, interest in the abdominal muscles, internal and external increased. This hypothesis was supported by the findings of
obliques, and in particular the erector spinae function Wakeling and colleagues75 showing higher muscle fascicle
during cycling has recently increased. Data presented by strains in the gastrocnemius as pedaling cadence increased.
Juker and colleagues72 show very low erector spinae activity In short, although muscles seem to modify their activation
except for the standing and sprinting postures when it was patterns in response to changes in cadence, these changes
much higher. Burnett and colleagues73 further suggested seem to be specific to the muscles themselves with regard to
one of the possible causative factors in low back pain in articulation, fiber type, and location in the limb.
cyclists was an overactive erector spinae during prolonged Finally, a series of papers have been published using
forward flexion and mechanical creep under high mechani- forward dynamic simulation with two major goals being a
cal loads. Evaluating key stabilizers of the lumbar spine, better understanding of the role played by different muscles
they reported loss of co-contraction of the lower lumbar in energizing the bicycle and understanding the fundamen-
multifidus as lower lumbar flexion and rotation increased, tal muscle coordination principles associated with delivering
suggesting that alterations in motor control patterns in the energy to the crank. Raasch and colleagues,76 studied the
lower lumbar spine might be associated with the develop- effect of maximum speed pedaling on muscle coordination
ment of low back pain in cyclists. during cycling and suggested that certain functional muscle
Although most of the evidence on muscle activity pat- groups exhibited alternating patterns representing a cen-
terns during cycling suggests the muscles act in a very trally generated motor program. The value of reducing the
repeatable manner, data presented by Juker and colleagues72 many different muscles in the lower extremity to apparently
suggest these patterns, although generally robust under functional groups lies in their possible relationships to
steady-state conditions, are changeable and can be affected central commands from the nervous system. Maximum
Applied Biomechanics of Cycling • CHAPTER 8 205
speed pedaling was a clearly defined goal, but the theory (both active and passive) the rehabilitation program
behind the study is applicable to a variety of circumstances imposes. Following acute injuries, rehabilitation should
and populations using cycling for exercise and rehabilita- begin with exercises that minimize muscle length changes,
tion. It seems the uniarticular extensors are important in the especially in active muscle, because muscle length changes
down-stroke or power phase and uniarticular flexors in the may increase tension on healing structures. Cycling can be
upstroke or recovery phase. It was reported that dorsiflexors an especially gentle exercise following injuries that might
and the rectus femoris were important in the transition occur to two-joint muscles of the lower extremity (e.g.,
through TDC and that the plantar flexors and hamstrings hamstrings, gastrocnemius, and rectus femoris). Angular
were important in the transition through BDC. Cadence changes in adjacent joints have an opposing effect on
dictates the role certain muscles play in controlling the muscle length, for example (increasing versus decreasing),
lower extremities during the cycling task. And although resulting in minimal length change in these two-joint
patterns, in general, are fairly robust, timing of muscle acti- muscles. During cycling, hip extension acts to decrease
vation, even at a constant resistance, appears to be affected hamstring length, while knee extension acts to increase it
by cadence. during the propulsive phase. During the recovery phase, hip
Body position is an important consideration that is flexion acts to increase hamstring length, while flexion at
related to the type of bicycle used (e.g., upright versus the knee acts to decrease it.
recumbent) and the position the rider assumes on the bike. Using hip, knee, and ankle joint angular kinematics and
Controlled studies conducted in the laboratory use a range lower-extremity anatomy, estimates of length changes for
of cycling positions (e.g., upright to an advanced aerody- all major lower-extremity MTUs have been developed.18
namic position), similar to the ones used by elite competi- Results indicate that changes in seat height have a marked
tors during road and track races. Addressing the issue of effect on muscle-length patterns and further imply that as
upper body position and its potential effect on the rider’s seat height increases, MTU shortening and lengthening
performance, Savelberg and colleagues77 manipulated trunk velocities increase. In addition, for all cases, cyclic patterns
angle during ergometer cycling and, directing their atten- of lengthening and subsequent shortening appear in each
tion to recumbent cycling, found a dramatic effect of muscle group during a complete pedaling cycle.
trunk inclination on muscle activity patterns. In a position Rugg and Gregor3 reported that changes in seat height
extended 20° back from an upright trunk position, peak appear to affect the soleus more than the gastrocnemius
EMG increased in seven of the eight muscles studied. Peak MTUs. These data were obtained at a constant cadence using
activity only decreased in the gluteus maximus. Gluteus seat height conditions of 96% to 108% of pubic symphysis
maximus activity, however, did increase in a position 20° height.3 The gastrocnemius displays essentially the same pat-
forward, more flexed, of the neutral upright trunk position. tern at each seat height condition, lengthening markedly dur-
In opposition to these general findings Chapman and ing the first 90° of crank rotation (approximately 1.5 cm),
colleagues78 suggested that upper body position had no then shortening approximately 2 cm, only to lengthen again
substantial effect on muscle recruitment (i.e., the main prior to TDC. In contrast, the soleus MTU displays very dif-
bursts of muscle activity) during cycling but did report ferent patterns at the separate seat height conditions, length-
greater co-activation and poor EMG modulation (i.e., ening slightly during the early stages of propulsion and then
greater magnitude of EMG) between the primary bursts of markedly shortening as the crank approaches BDC. The
EMG in an aerodynamic riding position among novice and MTU then lengthens again during the second half of the
elite triathletes. This finding was not present in elite cyclists pedaling cycle (180° to 360°). Although the magnitude of
and supports their contention that elite cyclists have better initial lengthening is approximately the same for each seat
control over muscle recruitment as a consequence of re- height, the magnitude of shortening dramatically increases
peated training performances. from less than 1 cm at the 96% condition to approximately
2.5 cm at the 108% condition. Shortening velocities of the
MTU increased as well.
Muscle-Tendon Unit Length and Velocity Sanderson and colleagues12 focused on the effects of
Measurements cadence on MTU lengths, velocities, and EMG in the
Changes in limb kinematics will naturally affect the length- gastrocnemius and soleus muscles. These data showed a dif-
tension and force-velocity relationship of separate muscle- ferential response to changes in cadence between the gas-
tendon units (MTUs), as well as the performance of muscle trocnemius and soleus and supported the data of Gregor
groups (e.g., quadriceps and hamstrings). Therefore, knowl- and colleagues71,79 and Marsh and Martin.80 EMG, MTU
edge of muscle length, velocity, previous history (e.g., length, and MTU velocity patterns are different between the
muscle stretch), muscle architecture, and activation—all two muscles in response to changes in cadence, suggesting
variables that affect the muscle’s ability to produce force—is the soleus muscle was more involved in generating initial
important. ROM information is also significant when propulsive forces, while the gastrocnemius shifted in phase
applied to a situation in which the MTU sustains an injury, to peak later in the cycle and made a more prolonged con-
because it is important to know what type of length changes tribution to the ankle extensors in delivering force to the
206 SECTION II • Applied Biomechanics of Selected Sport Activities
SOLEUS GASTROCNEMIUS
6
50 rpm
Lengthening 1 65 rpm
80 rpm Lengthening 1
4 95 rpm
Length (% Seg. Len.)
110 rpm
2
A D
50 rpm
30 65 rpm
80 rpm
95 rpm
Velocity (% Seg. Len/sec)
110 rpm
15
15
30
0.8
0.4
0
09 0 180 270 360 09 0 180 270 360
C Crank Angle (Degrees) F Crank Angle (Degrees)
Figure 8-20
Mean length, velocity, and electromyogram (EMG) for the soleus muscle (left panel) and the gastrocne-
mius muscle (right panel). Panels A and D are length change, B and E are muscle velocity, and C and F
are the normalized EMG data. In panels B and E the shaded portion indicates lengthening velocity. (From
Sanderson DJ, Martin PE, Honeyman G, Keefer J: Gastrocnemius and soleus muscle length, velocity, and
EMG responses to changes in pedaling cadence, J Electromyogr Kinesiol 16:642–649, 2006.)
208 SECTION II • Applied Biomechanics of Selected Sport Activities
120
100
80
nEMG (%) 60
40
20
0
0
90 110
Cra
nk 95
A 180
ng 80
le )
(D
eg 270 (rpm
nce
ree
s)
65 Cade
360 50
80
60
nEMG (%)
40
20
0
0
90 110
Cra
nk 95
A 180
ng 80
le
(D pm)
eg 270 n ce (r
ree
s)
65 Cade
360 50
Figure 8-21
Mean normalized electromyographic data plotted in a three-dimensional format to illustrate the appearance
of a second bump in soleus (bottom panel) and the simultaneous disappearance of the second bump in the
gastrocnemius (top panel). (From Sanderson DJ, Martin PE, Honeyman G, Keefer J: Gastrocnemius and
soleus muscle length, velocity, and EMG responses to changes in pedaling cadence, J Electromyogr Kinesiol
16:642–649, 2006.)
Overuse injuries caused by cycling may affect the foot The knee is the most common site for sports-related
and ankle, knee, hip, back, or neck. The incidence of over- injuries, and cycling is no exception. A recent prospective
use injuries to the ankle–foot complex is usually related to study examined the number of knee injuries per 1000 hours
the interface between the foot and pedal. Factors such as of exposure across a spectrum of physical activities for a
shoe design, pedal design, and seat height should be exam- randomly selected cohort (n 3633).82 The number of
ined if discomfort occurs. Shoe design is an important knee injuries caused by cycling as a commuting activity was
factor and must incorporate foot support and comfort as quite low (0.1), but increased considerably when performed
well as effective transmission of force.47 Shoes should be as a recreation or competitive sport activity (0.43). This
sufficiently stiff to distribute pressure, but flexible enough incidence was similar to the average found for all other
to permit natural foot motion. recreation or competitive sport activities (0.44), but was
Applied Biomechanics of Cycling • CHAPTER 8 209
sound limb was compensating for the amputated limb not be the best solution. During cycling, lower limb mus-
enough to maintain the same output so that, despite the cles generate much of the energy necessary to turn the
asymmetry, metabolic efficiency was maintained. cranks.98 A lot of this energy is produced during the power
The cycling task provides an excellent method to study phase and then declines during the bottom of the pedal
asymmetries between limbs because the cranks provide a stroke (see Figure 8-18). When a flexible prosthetic foot is
mechanical coupling between limbs. This coupling holds used for cycling, some of the energy produced during the
each limb 180° out of phase while allowing energy from power phase is absorbed and stored in the prosthetic foot,
one limb to transfer to the other (presumably deficient) only to be returned ineffectively at the bottom of the pedal
limb. When one limb compensates for the other, an asym- stroke. This removes energy from the cyclist–pedal system
metry develops between the two limbs. Asymmetry and requires input of additional energy from the sound limb
between the limbs can be quantified from a force or work to compensate. The result is a larger dependence on the
perspective and each of these measures tell a slightly differ- sound limb and increases in work asymmetries compared
ent story. Asymmetry in the magnitude of force production with a rigid prosthetic foot.90 However, the vertical forces
is related to geometric (i.e., leg length), inertial, and in cycling increase with power output87 and commercially
strength differences between limbs.92 Work asymmetry available prosthetic feet are generally stiff enough at lower
combines not just the force magnitude (and thus force outputs seen by recreational cyclists. Dynamic response–
asymmetries) but also the direction of those forces to turn type prosthetic feet designed for walking are acceptable
the cranks and produce work.92 Therefore, it is affected by for low-power outputs used in recreational cycling, but
everything related to force production but also everything do not have sufficient stiffness for higher outputs used by
related to how the body may manipulate the direction of competitive cyclists.99
that force. One goal of the neuromuscular system is to gen- Muscle coordination is also altered within the CTAs’
erate and direct forces appropriately to turn the crank. If gastrocnemius.100 An amputation through the tibia results in
one limb has not only lost the ability to generate forces but the alteration of the gastrocnemius from a two-joint knee
also direct those forces, a change within the motor control flexor/ankle extensor to a single-joint knee flexor. The other,
strategy should occur to compensate for this. Factors that more proximal muscles have not been surgically affected by
can account for a change in motor control strategy are dif- the amputation and retain their original bony attachment
ferences in muscle properties, difficulty in sensorimotor points. Questions about neuromuscular adaptation following
integration, and poor coordination between limbs. Work a change in muscle function were investigated in a group of
asymmetries have been well documented in the intact popu- six CTAs. Measurements were taken using surface EMG over
lation and are generally low (i.e., less than 10%),92-94 the gastrocnemius, rectus femoris, biceps femoris, and vastus
whereas pedaling asymmetries within CTAs have been medialis bilaterally. The results indicated a shift in muscle
documented as higher than the intact population (i.e., ap- activation within three of the six CTAs to a later period of the
proximately 30%).90,95 Within these cyclists, the sound limb crank cycle (Figure 8-22) when a knee flexion moment is
becomes dominant and work asymmetries are three times present. This new activation pattern is more appropriate for
greater than force asymmetries. These results indicate that a single-joint knee flexor and reflects neuromuscular adapta-
strength imbalances documented with unilateral transtibial tion of the gastrocnemius to its new functional role following
amputees do not fully explain the work asymmetries be- amputation.100 However, data could only be obtained in
tween limbs, thus indicating a change in the motor control three of the six CTAs studied. Problems with signal artifact
strategy.96 More research is necessary to fully understand from the electrodes hitting the prosthetic socket caused
the underlying causes of the increase in work asymmetries problems in one subject, and no signal could be gathered in
so that better rehabilitation strategies may be developed. the other two subjects. It is not clear why no signal was col-
Asymmetries are quantified by comparing forces developed lected from these CTAs, but it could be related to excessive
at the foot–pedal interface of each limb.92 Some commercial scarring of the residual limb and presumably the muscle
power measuring devices claim to quantify asymmetries by underneath the skin or possible detachment of the muscle’s
measuring the total power output of both limbs. These sys- distal end following surgery. More research needs to be done
tems are measuring the sum of both limbs and not each limb to determine what factors affect this neuromuscular adapta-
individually as is done by placing load cells within each tion and if this also occurs with transfemoral amputees.
pedal.97 The clinician should use caution interpreting asym-
metry or power fraction data gathered using these commer-
cially available power measuring system.97 Cycling Interventions for Individuals
CTA cycling performance is also influenced by the stiff- with Cerebral Palsy
ness of the prosthetic foot. Flexible or dynamic response– The importance of strength and cardiorespiratory exercise to
type prosthetic feet are designed for walking to deflect and improve and maintain general health in the general popula-
store energy at initial contact, and then decompress and tion is well known. Individuals with cerebral palsy (CP) have
release that energy at toe-off. The demands of cycling are difficulty performing fitness programs because of balance,
different than walking and use of these feet in cycling may strength, and motor control deficits. In addition, there are
212 SECTION II • Applied Biomechanics of Selected Sport Activities
Figure 8-22
Onset, offset, and peak muscle activity for five muscles in the lower limb for intact cyclists (white), the sound
limb (black), and amputated limb (grey) of cyclist with unilateral transtibial amputation. Peak activation is
indicated by a vertical line within the bar. Note the shift in activation of the amputated gastrocnemius muscle.
barriers to accessing equipment and facilities. The promotion Less information is available about responses to training
of fitness interventions for this population has been a recent protocols. Children with CP exhibiting a wide range of dis-
focus of the Pediatric Section of the American Physical ability were able to improve oxygen uptake, at a given heart
Therapy Association.101 Cycling is an excellent exercise mode rate HR, following an intervention regimen emphasizing sta-
because there are minimal requirements for balance and tionary cycling.107,108 In addition, six adolescents with mild
coordination. With modifications, both overground and sta- CP improved their physical endurance during cycling, as evi-
tionary cycles are options. In addition to physiological ben- denced by VO2 at the anaerobic threshold, following the first
efits, road cycling using adapted bicycles or tricycles is a form 3 months of a stationary cycling intervention.109 Benefits also
of mobility and provides opportunities for participation in have been reported for children with more severe physical
community recreation and sports programs. Cycling has disability. Following a 6-week intervention using an adapted
been recommended as an appropriate exercise for individuals stationary bicycle, eleven nonambulatory adolescents with CP
with CP;102 however, therapeutic evidence is limited. improved their gross motor function (p .01).110 A random-
Available evidence indicates that children with CP can ized control trial investigating a cycling intervention for
successfully pedal a stationary bicycle, although physical children with spastic diplegia was recently completed.111
assistance may be required.103 Assistance may be required Sixty-four children were randomized to either Cycling or
initially for forward pedal progression at TDC, prevention of Control (no-cycling) groups. This 12-week, 30 session cy-
knee hyperextension during recumbent cycling and to pre- cling intervention focused on both lower extremity strength-
vent excessive hip motion.104 Recumbent stationary cycling ening and cardiorespiratory training. While many children
kinematics, EMG, and pedal forces were described for required physical assistance to cycle at the beginning of the
10 adolescents with CP at 30 and 60 rpm.105 The foot was program, all became independent with practice. While a signifi-
positioned on the pedal to accommodate limb deformities cant difference in outcome measures was not found between
and minimize hip and knee movement out of the sagittal the two groups, significant baseline to post-intervention
plane. Despite this modification, excessive joint excursions improvements were found within the cycling group for
were observed in children with CP in the frontal and trans- gross motor function, walking and running endurance
verse planes. Greater peak hip flexion, knee extension, and and a subset of isokinetic knee extensor and flexor moments
dorsiflexion were found. As previously outlined in this chap- (p 0.05). Considerable intra-subject variability in perfor-
ter, these anatomic deviations are predisposing factors that mance was observed contributing to this result. Following
contribute to chronic overuse injuries; particularly at the the intervention, participants were provided with an adapted
knee joint. Differences in muscle activation patterns were bicycle and their level of participation and enjoyment is cur-
observed. Compared with adolescents without disability, rently being assessed. In summary, cycling is a safe and effec-
excessive co-activation was found, which was greater at tive exercise for individuals with CP that promotes muscular
60 rpm (Figure 8-23). Additional research revealed an strength and cardiorespiratory endurance. More research is
increased duration of negative (pulling up) as opposed to needed to examine the potential for long-term health benefits
positive pedal forces for adolescents with CP.106 and the prevention of secondary conditions in this population.
Applied Biomechanics of Cycling • CHAPTER 8 213
Percentage of Co-contraction
TD60
60
CP60
40
20
0
rectus/biceps rectus/mham viat/biceps viat/mham TA/gastroc TA/sol
Figure 8-23
Percentage (mean and standard deviation) of the cycling revolution in which co-contraction occurred
for each agonist and antagonist pairing around the left knee and ankle for each subject. Subjects with
cerebral palsy had increased co-contraction compared with the subjects with typical development
(TD), and all subjects displayed increased co-contraction when cycling at 60 rpm compared with
30 rpm. Rectus, Rectus femoris muscle; biceps, biceps femoris muscle; vlat, vastus lateralis muscle;
mham, medial hamstring muscle; TA, anterior tibialis muscle; gastroc, gastrocnemius muscle; sol,
soleus muscle. a, Significant main effect of group. b, Significant main effect of cadence. c, Interaction
of group and cadence. Significance defined as p .004 caused by 12 agonist and antagonist
pairings being studied (6 per side). TD30, Subjects typically developing TD at cadence of 30 rpm;
CP30, subjects with cerebral palsy (CP) at cadence of 30 rpm, TD60, subjects TD at cadence of
60 rpm; CP60, subjects with CP at cadence of 60 rpm. (From Johnston TE, Barr AE, Lee SCK:
Biomechanics of submaximal recumbent cycling in adolescents with and without cerebral palsy,
Phys Ther 87:572–585, 2007.)
Conclusion References
The cycling task is widely used in the fields of exercise and 1. Gregor RJ, Broker JP, Ryan MM: The biomechanics of cycling,
rehabilitation science primarily because it offers an interven- Exerc Sport Sci Rev 19:127–169, 1991.
2. Faria E, Cavanagh PR: The physiology and biomechanics of cycling,
tion that can be controlled by the user. Just as elite competi-
ACSM Series, New York, 1978, John Wiley & Sons.
tive cyclists match the bicycle to their specific morphological 3. Rugg SG, Gregor RJ: The effect of seat height on muscle
needs and strengths, the clinician, exercise specialist, and lengths, velocities and moment arm lengths during cycling,
physical therapist must “match” the bicycle to the rider or J Biomech 20:899, 1987.
patient to meet the specific objectives of each selected inter- 4. Price D, Donne B: Effect of variation in seat tube angle at differ-
ence seat heights on submaximal cycling performance in man,
vention. The rider’s physical interface with the bicycle (e.g.,
J Sports Sci 15:395–402, 1997.
“bike fit”), as well as the resistance (i.e., load) can be regu- 5. Too D: The effect of hip position/configuration on anaerobic
lated by the clinician or exercise specialist to selectively meet power and capacity in cycling, Int J Sport Biomech 7:359–370,
needs related to, for example, cardiorespiratory exercise, 1991.
strength training, rehabilitation of the knee post ACL repair 6. Brown DA, Kautz SA, Dairaghi CA: Muscle activity patterns al-
tered during pedaling at different body orientations, J Biomech
or proprioceptive input resulting from the cyclic nature of the
29:1349–1356, 1996.
task. The objective of this chapter is to convey the idea that 7. Heil DP, Derrick TR, Whittlesey S: The relationship between
cycling is a very useful task with wide-ranging applications in preferred and optimal positioning during submaximal cycle er-
exercise and rehabilitation. The kinematics and kinetics of the gometry, Eur J Appl Physiol 75:160–165, 1997.
task from the level of the muscle fiber to the whole lower 8. Reiser RF, Peterson ML, Broker JP: Anaerobic cycling power
output with variations in recumbent body configuration, J Appl
extremity have been presented and applications to individuals
Biomech 17:204–216, 2001.
with special needs discussed. The clinician and exercise spe- 9. Broker JP, Gregor RJ: Mechanical energy management in cy-
cialist can use this information to continue to develop unique cling: Source relations and energy expenditure, Med Sci Sport
applications of this task to improve human performance. Exerc 26:64–74, 1994.
214 SECTION II • Applied Biomechanics of Selected Sport Activities
10. Ryan MM, Gregor RJ: EMG profiles of lower extremity muscles 33. Reiser RF, Broker JP, Peterson ML: Knee loads in the standard
during cycling at constant workload and cadence, J Electromyogr and recumbent cycling positions, Biomed Sci Instrum 40:36–42,
Kinesiol 2:69–80, 1992. 2004.
11. Pierson-Carey CD, Brown DA, Dairaghi CA: Changes in resul- 34. Brown DA, Kautz SA: Speed-dependent reductions of force
tant pedal reaction forces due to ankle immobilization during output in people with post-stroke hemiparesis, Phys Ther 79:
pedaling, J Appl Biomech 13:334–346, 1997. 919–930, 1999.
12. Sanderson DJ, Martin PE, Honeyman G, Keefer J: Gastrocnemius 35. Hakansson NA, Hull ML: Functional roles of the leg muscles
and soleus muscle length, velocity, and EMG responses to changes when pedaling in the recumbent versus the upright position,
in pedaling cadence, J Electromyogr Kinesiol 16:642–649, 2006. J Biomech Eng 127:301–310, 2005.
13. Sanderson DJ, Black A: The effect of prolonged cycling on pedal 36. Gregor SM, Perell KL, Rushatakankovit S, et al: Lower extremity
forces, J Sports Sci 21:191–199, 2003. general muscle moment patterns in healthy individuals during
14. Dingwell JB, Joubert JE, Diefenthaeler F, Trinity JD: Changes recumbent cycling, Clin Biomech 17:123–129, 2002.
in muscle activity and kinematics of highly trained cyclists during 37. Johnston TE: Biomechanical considerations for cycling interven-
fatigue, IEEE Trans Biomed Eng 55:2666–2673, 2008. tions in rehabilitation, Phys Ther 87:1243–1252, 2007.
15. Hannaford DR, Moran GT, Hlavac HF: Video analysis and treat- 38. Perell KL, Gregor RJ, Scremin AME: Lower extremity cycling
ment of overuse knee injury in cycling: A limited clinical study, mechanics in subjects with unilateral CVAs, J Appl Biomech
Clin Podiatr Med Surg 3:671–678, 1986. 14:158–179, 1998.
16. McCoy RW: The effect of varying seat position on knee loads dur- 39. Perell KL, Gregor RJ, Kim G: Comparison of cycling kinetics
ing cycling, unpublished doctoral dissertation, University of during recumbent bicycling in subjects with and without diabe-
Southern California, Department of Exercise Science, 1989. tes, J Rehabil Res Dev 39:13–20, 2002.
17. Ruby P, Hull ML, Hawkins D: Three-dimensional knee loading 40. Kautz SA, Patton C: Interlimb influences on paretic leg function
during seated cycling, J Biomech 25:41–53, 1992. in post-stroke hemiparesis, J Neurophysiol 93:2460–2473, 2005.
18. Boutin RD, Rab GT, Hassan IAG: Three dimensional kinematics 41. Kerr A, Rafferty D, Moffat F, Morlan G: Specificity of
and muscle length changes in bicyclists, Proceedings 13th Annual recumbent cycling as a training modality for the functional
Meeting ASB, Burlington, VT, UVM Conferences, 1989. movements: Sit-to-stand and step-up, Clin Biomech 22:
19. Bailey MP, Maillardet FJ, Messenger N: Kinematics of cycling in 1104–1111, 2007.
relation to anterior knee pain and patellar tendonitis, J Sports Sci 42. Sanderson DJ, Cavanagh PR: An investigation of the in-shoe
21:649–657, 2003. pressure distribution during cycling in conventional cycling shoes
20. Francis PR: Injury prevention for cyclists: A biomechanical or running shoes. In B Jonsson, editor: Biomechanics X-B,
approach. In Burke ER, editor: Science of cycling, Champaign, IL, Champaign, IL, 1987, Human Kinetics.
1986, Human Kinetics. 43. Sanderson DJ, Hennig EM: In-shoe pressure distribution in
21. Gregersen CS, Hull ML, Hakansson NA: How changing the cycling and running shoes during steady-rate cycling, Proceedings
inversion/eversion foot angle affects the nondriving interseg- of the Second North American Congress on Biomechanics,
mental knee moments and the relative activation of the Vastii Chicago, August 24–28, 1992.
muscles in cycling, J Biomed Eng 128:391–398, 2006. 44. Amoroso AT, Hennig EM, Sanderson DJ: In-shoe pressure distri-
22. Ruby P, Hull ML, Kirby KA, Jenkins DW: The effect of lower- bution for cycling at different cadences, Proceedings of the Second
limb anatomy on knee loads during seated cycling, J Biomech North American Congress on Biomechanics, Chicago, August
25:1195–1207, 1992. 24–28, 1992.
23. Wheeler JB, Gregor RJ, Broker JP: A dual piezoelectric bicycle 45. Hennig EM, Sanderson DJ: In-shoe pressure distribution for
pedal with multiple shoe/pedal interface compatibility, Int J cycling at different power outputs, Proceedings of the Second
Sports Biomech 8:251–258, 1992. North American Congress on Biomechanics, Chicago, August
24. Ericson MO, Nisell R, Ekholm J: Varus and valgus loads on the 24–28, 1992.
knee joint during ergometer cycling, Scand J Sports Sci 6:39–45, 46. Francis PR: Pathomechanics of the lower extremity in cycling.
1984. In Burke E, Newsom B, editors: Medical and scientific aspects of
25. Zajac FE: Understanding muscle coordination of the human leg cycling, Champaign, IL, 1988, Human Kinetics.
with dynamical simulations, J Biomech 35:1011–1018, 2002. 47. Sanderson DJ: The biomechanics of cycling shoes, Cycling Sci
26. LaFortune MA, Cavanagh PR: Effectiveness and efficiency dur- Sept: 27–30, 1990.
ing bicycle riding. In Matsui H, Kobayashi K, editors: Biome- 48. Gregor RJ, Wheeler JB: Knee pain: Biomechanical factors associ-
chanics VIII-B, Champaign, IL, 1983, Human Kinetics. ated with shoe/pedal interfaces: Implications for injury, Sports
27. Broker JP, Browning RC, Gregor RJ, Whiting WC: Effect of seat Med 17:117–131, 1994.
height on force effectiveness in cycling, Med Sci Sports Exerc 49. Wheeler JB, Gregor RJ, Broker JP: The effect of clipless float
20:S83, 1988. design on shoe/pedal interface kinetics: Implications for overuse
28. Broker JP, Gregor RJ, Schmidt RA: Extrinsic feedback and the injuries during cycling, J Appl Biomech 11:119–141, 1995.
learning of kinetic patterns in cycling, J Appl Biomech 9:111–123, 50. Boyd TF, Neptune RR, Hull ML: Pedal and knee loads using a
1993. multi-degree-of-freedom pedal platform in cycling, J Biomech
29. Perell KA: Force summary feedback training on the bicycle in 30:505–511, 1977.
patients with unilateral cerebrovascular accidents, unpublished 51. McCoy RW, Gregor RJ: The effect of varying seat position on
doctoral dissertation, UCLA, 1994. knee loads during cycling, Med Sci Sports Exerc 21:S79, 1989.
30. Hasson CJ, Caldwell GE, van Emmerik REA: Changes in muscle 52. Furumizo SH: A biomechanical analysis of anterior/posterior
and joint coordination in learning to direct forces, Hum Mov Sci shear joint reaction forces in the ACL-deficient knee during sta-
27:590–609, 2008. tionary cycling, unpublished Masters thesis, UCLA Department of
31. Bolourchi F, Hull ML: Measurement of rider-induced loads dur- Kinesiology, 1991.
ing simulated bicycling, Int J Sports Biomech 1:308–329, 1985. 53. Hunt MA, Sanderson DJ, Moffet H, Inglis JJ: Interlimb asym-
32. Reiser RF, Peterson ML, Broker JP: Understanding recumbent metry in persons with and without an anterior cruciate ligament
cycling: Instrumentation design and biomechanical analysis, deficiency during stationary cycling, Arch Phys Med Rehabil
Biomed Sci Instrum 38:209–214, 2002. 85:1475–1478, 2004.
Applied Biomechanics of Cycling • CHAPTER 8 215
54. Hunt MA, Sanderson DJ, Moffet H, Inglis JJ: Biomechanical 76. Raasch CC, Zajac FE, Ma B, Levine WS: Muscle coordination in
changes elicited by an anterior cruciate ligament deficiency maximum speed pedaling, J Biomech 30:595–602, 1997.
during steady state cycling, Clin Biomech 18:393–400, 2003. 77. Savelberg H, Van de Port I, Willems P: Body configuration
55. Gregor RJ: A biomechanical analysis of lower limb action during in cycling affects muscle recruitment and movement patterns,
cycling at four different loads, unpublished doctoral dissertation, J Appl Biomech 19:310–324, 2003.
The Pennsylvania State University, 1976. 78. Chapman AR, Vincenzino B, Blanch P, et al: Influence of body
56. Gregor RJ, Cavanagh PR, LaFortune M: Knee flexor moments position on leg kinematics and muscle recruitment during
during propulsion in cycling—A creative solution to Lombard’s cycling, J Sci Med Sport 11:519–526, 2008.
paradox, J Biomech 18:307–316, 1985. 79. Gregor RJ, Komi PV, Jarvinen M: Achilles tendon forces during
57. Andrews JG: The functional roles of the hamstrings and quadri- cycling, Int J Sports Med 8:9–14, 1987.
ceps during cycling: Lombard’s paradox revisited, J Biomech 80. Marsh AP, Martin PE: The relationship between cadence and
20:565–575, 1987. lower extremity EMG in cyclists and non-cyclists, Med Sci Sport
58. Browning RC, Gregor RJ, Broker JP, Whiting WC: Effects of Exerc 27(2):217–225, 1995.
seat height changes on joint force and moment patterns in expe- 81. Pruitt AL, Matheny F: Andy Pruitt’s complete medical guide for
rienced cyclists, J Biomech 21:871, 1988. cyclists, Boulder, CO, 2006, Velo Press.
59. Jorge M, Hull ML: Biomechanics of bicycle pedaling. In Terauds 82. Haapasalo H, Parkkari J, Kannus P, et al: Knee injuries in
T, Barthels K, Kreighbaum E, et al, editors: Sports biomechanics, leisure-time physical activities: A prospective one-year follow-
Del Mar, CA, 1984, Research Center for Sports. up of a Finnish population cohort, Int J Sports Med 28:72–77,
60. Redfield R, Hull ML: On the relation between joint moments 2007.
and pedaling rates at constant power in bicycling, J Biomech 83. Holmes JC, Pruitt AL, Whalen NJ: Cycling knee injuries,
19:317–329, 1986. Cycling Sci June:11–14, 1991.
61. Lombard WP: The action of two-joint muscles, Am Phys Ed Rev 84. Mellion MB: Common cycling injuries: Management and
8:141–145, 1903. prevention, Sports Med 11:52–70, 1991.
62. Van Ingen Schenau GJ: From rotation to translation: Constraints 85. Wanich T, Hodgkins C, Columbier J, et al: Cycling injuries of
on multi-joint movements and the unique action of bi-articular the lower extremity, J Am Acad Orthop Surg 15:748–756,
muscles, Hum Mov Sci 8:301–337, 1989. 2007.
63. Kuo AD: The action of two-joint muscles: Legacy of WP 86. Chin T, Sawamura S, Fujita H, et al: Effect of endurance training
Lombard. In Latash ML, Zatsiorsky VM, editors: Classics in program based on anaerobic threshold (AT) for lower limb
movement science, Champaign, IL, 2001, Human Kinetics. amputees, J Rehab Res Dev 38:7–11, 2001.
64. Ruby P, Hull ML, Kirby KA, Jenkins DW: The effect of lower- 87. Childers WL, Perell-Gerson KL, Kistenberg R, Gregor RJ:
limb anatomy on knee loads during seated cycling, J Biomech Pedaling forces normalized to body weight in intact and uni-
25:1195–1207, 1992. lateral transtibial amputees during cycling, Proceedings of the
65. Zatsiorsky V, Gregor R: Mechanical power and work in human 4th International State-of-the-Art Congress “Rehabilitation:
movement. In Sparrow WA, editor: Metabolic energy expenditure Mobility, Exercise & Sports”, Amsterdam, NL, April 7–9, 2009.
and the learning and control of movement, Champaign, IL, 2000, (in press).
Human Kinetics. 88. Walther V: MTB Amputee. Retrieved 2002 from http://www.
66. Ericson MO, Bratt A, Nisell R: Load moments about the hip and mtb-amputee.com/.
knee joints during ergometer cycling, Scand J Rehabil Med 89. Dillingham TR, Pezzin LE, Mackenzie EJ: Limb amputation and
18:165–172, 1986. limb deficiency epidemiology and recent trends in the United
67. Desipres M: An electromyographic study of competitive road States, South Med J 95:875–883, 2002.
cycling conditions simulated on a treadmill. In Nelson RC, 90. Childers WL, Kistenberg R, Gregor RJ: Pedaling asymmetry in
Morehouse CA, editors: Biomechanics IV, Champaign, IL, 1974, cyclists with uni-lateral transtibial amputation and the effect of
Human Kinetics. prosthetic foot stiffness, Proceeds of the AAOP 35th Annual Meet-
68. Ericson MO, Nisell R, Arborelius UP: Muscular activity during ing and Scientific Symposium, Atlanta, GA, March 4–7, 2009
ergometer cycling, Scand J Rehabil Med 17:53–61, 1985. (in press).
69. Houtz SJ, Fischer FJ: An analysis of muscle action and joint ex- 91. Murray JB: Efficiency of simulated amputee cycling, unpublished
cursion during exercise on a stationary bicycle, J Bone Joint Surg Master’s thesis, UC Boulder, Department of Integrative
Am 41:123–131, 1959. Physiology, 2003.
70. Jorge M, Hull ML: Analysis of EMG measurement during bicy- 92. Sanderson DJ: The influence of cadence and power output
cle pedaling, J Biomech 19:683–694, 1986. on asymmetry of force application during steady-rate cycling,
71. Gregor RJ, Komi PV, Browning RC, Jarvinen M: Comparison J Hum Mov Stud 19:1–9, 1990.
between the triceps surae and residual muscle moments at the 93. Daly DJ, Cavanagh PR: Asymmetry in bicycle ergometer pedaling,
ankle during cycling, J Biomech 24:287–297, 1991. Med Sci Sport 8:204–208, 1976.
72. Juker D, McGill S, Kropf P: Quantitative intramuscular myoelec- 94. Smak W, Neptune RR, Hull ML: The influence of pedaling rate
tric activity of lumbar portions of the psoas and abdominal wall on bilateral asymmetry in cycling, J Biomech 32:899–906,
during cycling, J Appl Biomech 14:428–438, 1998. 1999.
73. Burnett AF, Cornelius MW, Dankaerts W, O’Sullivan PB: Spinal 95. Broker JP, Gregor RJ: Cycling biomechanics. In Burke ER,
kinematics and trunk muscle activity in cyclists: A comparison editor: High-tech cycling, ed 1, Champaign, IL, 1996, Human
between healthy controls and non-specific chronic low back pain Kinetics.
subjects—A pilot investigation, Man Ther 9:211–219, 2004. 96. Isakov E, Burger H, Gregoric M, Marincek C: Isokinetic and
74. Chapman AR, Vincenzino B, Blanch P, Hodges PW: Patterns of isometric strength of the thigh muscles in below-knee amputees,
leg muscle recruitment vary between novice and highly trained Clin Biomech 11:233–235, 1996.
cyclists, J Electromyogr Kinesiol 18:359–371, 2008. 97. Broker JP: Cycling biomechanics. In Burke ER, editor: High-tech
75. Wakeling JM, Vehli K, Rozitis AI: Muscle fiber recruitment can cycling, ed 2, Champaign, IL, 2003, Human Kinetics.
respond to the mechanics of the muscle contraction, J Royal Soc 98. Kautz SA, Hull ML: A theoretical basis for interpreting the force
Interface 3:533–544, 2006. applied to the pedal in cycling, J Biomech 26:155–165, 1993.
216 SECTION II • Applied Biomechanics of Selected Sport Activities
99. Childers WL, Kistenberg R, Gregor RJ: Clinical guidelines 105. Johnston TE, Barr AE, Lee SCK: Biomechanics of submaximal
for adapting the bicycle to recreational cyclists with transtibial recumbent cycling in adolescents with and without cerebral palsy,
amputation, Proceeds of the AAOP 35th Annual Meeting Phys Ther 87:572–585, 2007.
and Scientific Symposium, Atlanta, GA, March 4–7, 2009 (in 106. Johnston TE, Prosser LA, Lee SCK: Differences in pedal forces
press). during recumbent cycling in adolescents with and without
100. Childers WL, Hudson-Toole EF, Gregor RJ: Activation changes cerebral palsy, Clin Biomech 23:248–251, 2008.
in the gastrocnemius muscle: Adaptation to a new functional role 107. Berg K: Effect of physical training of school children with
following amputation, Proceeds of the ACSM 56th Annual cerebral palsy, Acta Paediatr Scand 204:27–33, 1970.
Meeting, Seattle, WA, May 27–30, 2009 (in press). 108. Berg K, Bjure J: Methods for evaluation of the physical working
101. Fowler EG, Kolobe TH, Damiano DL, et al: Promotion capacity of school children with cerebral palsy, Acta Paediatr
of physical fitness and prevention of secondary conditions Scand 204:15–26, 1970.
for children with cerebral palsy, Section on Pediatrics 109. Shinohara TA, Suzuki N, Oba M, et al: Effect of exercise at the
Research Summit Proceedings, Phys Ther 87:1495–1510, AT point for children with cerebral palsy, Bull Hosp Joint Dis
2007. 61:63–67, 2002.
102. Rimmer JH: Physical fitness levels of persons with cerebral palsy, 110. Williams H, Pountney T: Effects of a static bicycling programme
Dev Med Child Neurol 43:208–212, 2001. on the functional ability of young people with cerebral palsy who
103. Kaplan SL: Cycling patterns in children with cerebral palsy, Dev are non-ambulant, Dev Med Child Neurol 49:522–527, 2007.
Med Child Neurol 37:620–630, 1995. 111. Fowler EG, Knutson LM, DeMuth SK, et al: Pediatric endurance
104. Siebert K, DeMuth SK, Knutson LM, Fowler EG: A stationary and limb strengthening (PEDALS) for children with cerebral
cycling intervention for children with cerebral palsy: A report on palsy using stationary cycling: a randomized controlled trial, Phys
two children, Phys Occup Ther Pediatr (in press). Ther (in press).
9
CHAPTER
217
218 SECTION II • Applied Biomechanics of Selected Sport Activities
reasonable to expect that if a golfer returns in a timely accuracy requirements of the planned shot. Furthermore,
fashion with the same swing as before, and if there were the large momentum developed by the various body seg-
components of that swing that contributed to the injury, ments during the downswing must be effectively deceler-
then it is only a matter of time before the player will suffer ated during the postimpact phase while still maintaining
a relapse. In other words, as a health care provider, “the postural stability and balance. Although the preceding de-
best treatment we can give is to study the biomechanics of scription explains the general elements of an ideal swing, it
a patient’s golf swing and try and spot any mechanical flaws appears that there is considerable variation in how this is
that may be causing injury.”15 accomplished, even among elite players.17 This suggests
there may not necessarily be one ideal swing for all players.
The reader is encouraged to keep this in mind as the general
General Swing Mechanics mechanics of the full golf swing are discussed in the follow-
The ultimate goal of the full golf swing is to consistently ing sections. The following descriptions are gathered from
and predictably hit the golf ball in the desired direction for a number of scientific sources5,6,18-21 and refer to a full swing
the proper distance. Although the goal of the golf swing for a right-handed player. The general swing phases, which
may be consistent across different skill levels, the methods consist of set-up, backswing, downswing, and follow-
used to execute the swing obviously vary. The following through, are illustrated schematically in Figure 9-1.
section describes the typical swing mechanics that occur
during a full golf swing from predominantly a kinematic
and muscle activity perspective. Detailed biomechanical
descriptions of key segments of the body during the swing, Phases of Golf Swing
particularly as they relate to injury susceptibility and reha- • Setup
bilitation, are discussed later in this chapter. The terms lead • Backswing
and trail are used to identify the different sides of the body, • Downswing (forward swing, impact)
although left and right designations are occasionally added • Follow-through
for clarity and refer to a right-handed player. The lead side
is the side closest to the target, which for a right-handed
player is the left side.
There are few more contentious issues in the sport of Set-Up
golf than what constitutes the ideal swing. One of the more The set-up position, sometimes referred to as ball address
respected scientific texts dealing with the golf swing was (see Figure 9-1, A), is the starting position for executing
written in 1968 by Alastair Cochran and John Stobbs and the golf swing in proper alignment with an established tar-
titled The Search for the Perfect Swing.16 In their book, they get. The role of the set-up is to provide an initial stable
describe the swing as a sequence of body rotations involving platform to allow the swing to proceed in a balanced and
the legs, hips, torso, shoulders, arms, and wrists that works biomechanically efficient manner. The set-up is influenced
together to create movement of the clubhead toward the by a number of factors, including the club being used and
ball in such a manner that a desirable and efficient transfer the nature of the intended shot. The following description
of energy is imparted to the ball at impact. These various of the set-up position is based on a typical full shot in which
body parts are essentially like springs that are “wound up” maximal distance is desired.5 The set-up incorporates a rela-
on the backswing until maximum stretch is achieved. tively symmetrical weight distribution with the feet
The greatest speed of the clubhead on the downswing is approximately shoulder width apart. Both hips are exter-
created only if the spring tension in each of the various body nally rotated approximately 25°, although this is often de-
segments is released in sequence starting from the ground scribed as turning the feet out rather than hip motion. It is
(i.e., legs) up: worth noting that some golf coaches teach a relatively neu-
tral position of the trail hip. The knees are flexed approxi-
[E]very part of the rotating and swinging system must
mately 25°, which positions the patellae vertically above the
be pulled around by the part nearer the ground, until that
balls of the feet. This knee flexion helps maintain the body’s
part can no longer apply useful effort. That is, in terms of
a human golfer, the legs pull around the hips, the hips the
center of gravity under the mid-portion of the feet by allow-
trunk, the trunk the upper chest and shoulders, the shoulders ing the weight of the hip and buttock region to offset the
the arms, the arms the hands, the hands the shaft, and the shaft weight of the upper body as the trunk leans forward. The
the clubhead.16 forward lean or flexion of the trunk is needed to bring the
clubhead down behind the ball. However, this lean should
In essence, the ideal swing pattern allows the golfer to be produced by hip flexion rather than spinal flexion (i.e.,
rotate the club away from the start position in a large arc, the spine maintains a relatively straight or “neutral” posi-
and then return it to an impact position in such a way that tion). The spine does demonstrate a slight right side bend
optimal launch conditions are achieved for the distance and and left rotation to compensate for the lower position of the
Applied Biomechanics of Golf • CHAPTER 9 219
Downswing
The downswing portion of the golf swing is where the ve-
locity of the clubhead and the angle of contact between the
club face and the golf ball are determined. However, the
resultant forces produced during this phase also increases
injury susceptibility.30 The downswing includes two sub-
C D E phases; the forward swing (see Figure 9-1, C) and ball
Figure 9-1 impact (see Figure 9-1, D). As mentioned previously, the
Body positions at key moments during the full golf swing. A, Set-up. movement of the golf club away from the ball to the top of
B, Top of backswing. C, Forward swing. D, Impact. E, Finish. the backswing takes approximately 0.8 seconds to com-
(Reproduced with permission, Fit Fore Golf, Inc.) plete. However, the forward swing actually starts approxi-
mately 0.1 seconds before the arms and golf club finish the
backswing.23,24 In other words, there is an initial shift of
right hand on the grip of the club.21,22 Both upper limbs body weight as well as a rotation of the lower body and
hang in a somewhat vertical orientation with the glenohu- pelvis toward the target (i.e., left) just before the upper
meral joints in neutral rotation, the elbows extended, and body and golf club finish rotating to the right. This initia-
the wrists in slight ulnar deviation. tion of the downswing with the lower limbs results in the
hips and shoulders momentarily rotating in opposite direc-
tions, further increasing the amount of trunk rotation
Backswing stretch at the start of the downswing.24 This increase in
The backswing involves the drawing back of the club using spinal rotation at the initial phase of the downswing has
predominantly a rotary motion of the body while maintaining been referred to as the X-factor stretch.
a consistent amount of hip and trunk flexion, as well as a steady Cheetham and colleagues23 attempted to quantify the
position of the head. The rotary motion is initiated with the X-factor stretch between 10 highly skilled golfers and nine
legs and pelvis, followed by the trunk, shoulders, arms, and less skilled players (handicap ⬎ 14). Results showed that the
club. The typical backswing of an elite player takes approxi- more-skilled players increased the X-factor stretch (i.e., the
mately 0.8 seconds to complete.23 The backswing is usually amount of spinal rotation) by 19% during the early part of
regarded as complete when the club stops moving, which is the downswing. This compared with 13% for the less-skilled
typically when the club shaft is approximately parallel with the players. The authors went on to state that the extra stretch
ground. At the top of the backswing the pelvis has turned ap- on the muscle, along with the active resistance to that
proximately 40° away from the target while an imaginary line stretch, can increase muscular contraction forces, leading to
bisecting both shoulder joints has turned more than 100°.21,24 more force production on the downswing and a resultant
The difference between the pelvis and shoulder turn is the re- higher clubhead speed through impact.
sult of near maximal right rotation of the spine,25 as well as lead Approximately 0.08 seconds after the lower limbs (fol-
side scapular protraction and trail side retraction.26 The pelvic lowed by the trunk) commence the downswing, the shoul-
turn places the lead or left hip in external rotation, while the der joints start to powerfully rotate toward the left. These
220 SECTION II • Applied Biomechanics of Selected Sport Activities
shoulder movements occur immediately before the golf club external and internal oblique muscles. Other authors have
reaches the top of the backswing. The lead (left) shoulder found a higher relative contribution from the lead internal
abducts and externally rotates while the trail side internally oblique compared with the trail external oblique on the
rotates and adducts bringing the arms down and across the downswing,35,36 with both muscles contracting before the
torso towards the ball. club reached the top of the backswing. High levels of bilat-
The final critical element of the downswing is the eral erector spinae activity on the downswing are thought to
“uncocking” or “release” of both wrist joints, which occurs help stabilize the spine during the powerful trunk flexion
just before impact between the golf club and the ball. The and rotation forces produced by the abdominal muscles.34,37
wrist release has two motion components, frontal plane Muscle activation patterns throughout the entire swing are
(e.g., radial and ulnar deviation) and axial rotation (supina- summarized in Tables 9-1 and 9-2.38
tion and pronation)31 that allow the hands to “turn over” or
rotate through impact.18,21 It is interesting to note that the
peak movement of these two components occurs at different Impact
stages of the downswing. The peak timing of the frontal The position of the body at impact (see Figure 9-1, D)
plane portion of the wrist release (i.e., ulnar deviation) occurs results from a shift of the body’s center of mass toward the left
0.1 seconds before impact, whereas the axial rotation motion as well as the rotary motions and subsequent centrifugal
(supination of the left forearm, pronation of the right fore- forces generated by the powerful muscle contractions through-
arm) peaks less than 0.002 seconds before impact.31 out the lower limbs, trunk, and shoulders. At impact,
For the downswing to proceed with maximum efficiency, approximately 80% of the golfer’s weight is situated on the
the pelvic, spinal, shoulder, and wrist rotations must conform lead foot.27 The hips and trunk extend slightly from the flexed
to the segmental rotation pattern identified by Cochran and posture adopted during ball address and the spine side bends
Stobbs16 and subsequently described by Burden and col-
leagues24 as the summation of speed principle. This principle
states that to maximize the speed of the distal end of the Table 9-1
system (i.e., the clubhead), the swing must start with move- Summary of the Most Active Muscles in Lower Body/
ments at the more proximal segments (legs) and progress Trunk During the Different Phases of the Golf Swing
sequentially to faster movements of the more distal segments. (% of Maximal Manual Testing)
The increased velocity of the distal segment often occurs as
Left Lower Right Lower
the velocity of the more proximal segments starts to de-
Phase of Swing Body/Trunk Body/Trunk
crease.32 The summation of speed principle has also been
called the kinematic sequence and underlies the importance of Backswing Erector spinae Semimembra-
initiating the downswing by contraction of the large muscles (26%) nosus (28%)
of the lower limbs and pelvis. Abdominal Biceps femoris
oblique (24%) (27%)
Downswing—early Vastus lateralis Gluteus maxi-
Kinematic Sequence (88%) mus (100%)
Adductor magnus Biceps femoris
The swing must start in the legs and progress sequentially and
(63%) (78%)
progressively to the more distal segments and finally the club for
Downswing—late Biceps femoris Abdominal
maximum force and velocity to the ball.
(83%) oblique (59%)
Gluteus maximus Gluteus medius
(58%) (51%)
Vastus lateralis
Bechler and colleagues33 studied the activity patterns of (58%)
the thigh and hip muscles in competitive golfers and re- Follow-through— Biceps femoris Gluteus medius
ported that the hip extensors and abductors on the trail early (79%) (59%)
side, in conjunction with the lead adductor muscles, initiate Vastus lateralis Abdominal
pelvic rotation and weight shift toward the target at the (59%) oblique (51%)
beginning of the downswing. The lead vastus lateralis and Follow-through— Semimembranosus Vastus lateralis
late (42%) (40%)
the hamstrings acted to stabilize the knee joints during this
Vastus lateralis Gluteus medius
pelvic rotation. Contraction of the large trunk muscles, in
(42%) (22%)
particular the abdominal oblique, erector spinae, and latis- Adductor magnus
simus dorsi, follows closely behind the lower limb and (35%)
hip muscles. Watkins34 reported that the trail-side abdomi-
nal oblique muscles showed the highest relative activity Modified from McHardy A, Pollard H: Muscle activity during the
although the authors did not differentiate between the golf swing, Br J Sport Med 39:802, 2005.
Applied Biomechanics of Golf • CHAPTER 9 221
Table 9-2 the lead side with the hip in full internal rotation, while just
Summary of the Most Active Muscles in Upper Body/ the toes of the trail foot remain in contact with the ground
Trunk During the Different Phases of the Golf Swing and the hip is in neutral rotation. At the completion of the
(% of Maximal Manual Testing) follow-through, the torso is maximally rotated toward the
target (i.e., left). The finish position for the shoulder joints is
Left Upper Right Upper
noteworthy in that it is characterized by a reversal of the
Phase of Swing Body/Trunk Body/Trunk
shoulder positions seen at the top of the backswing. The lead
Backswing Subscapularis Upper trapezius shoulder finishes in complete external rotation, approximately
(33%) (52%) 70° of horizontal abduction and 60° of elevation. The trail
Upper serratus Middle trapezius shoulder at follow-through demonstrates approximately 30°
(30%) (37%) of horizontal adduction, 110° of elevation and full or near-full
Downswing—early Rhomboid Pectoralis major internal rotation.28 During the follow-through, the lead wrist
(68%) (64%) proceeds into extension and radial deviation while the trail
Middle trapezius Upper serratus wrist folds into flexion and radial deviation.
(51%) (58%)
According to McCarroll and colleagues,10 25% of all golf
Downswing—late Pectoralis major Pectoralis major
(93%) (93%)
injuries occur during the follow-though, with the back,
Levator scapulae Upper serratus shoulder, knees, and wrists most often affected. Also nota-
(62%) (69%) ble are the stresses on the neck and lead-side hip. The neck
Follow-through— Pectoralis major Pectoralis major is subjected to a relatively violent rotation to the right soon
early (74%) (74%) after impact because of the rapid rotation of the torso
Infraspinatus Subscapularis toward the target (left) while the head remains facing the
(61%) (64%) spot on the ground where the ball lay prior to impact.
Follow-through— Infraspinatus Subscapularis
late (40%) (56%)
Pectoralis major Upper and lower
(39%) serratus (40%)
Clinical Point
Modified from McHardy A, Pollard H: Muscle activity during the
golf swing, Br J Sport Med 39:801, 2005. Twenty-five percent of golf injuries occur to the back, shoulders,
knees, and wrist during follow-through.
the body toward the target is also being created at the same
Clinical Point time as the rotational motion. If the lateral component is
The front leg experiences two to three times more rotational torque exaggerated or occurs too early in the downswing, then
and compression load than the trail leg. significantly greater pressure is carried to the front foot early
in the acceleration phase. This results in an effective shear
force being produced only under the lead foot, thereby
reducing the efficiency of the rotational force couple
Lindsay and colleagues,17 in their review of golf biome- applied to the hip segments.
chanics, reported that the sole-to-ground interactions vary It appears from the previous description that a balance
considerably between groups of elite and less-skilled players. exists between the amounts of lateral and rotational forces
To summarize, less-skilled golfers were found to have that a golfer uses on the downswing to create optimal club-
greater lateral forces on the feet during the backswing and head speed. It is very possible that injuries around the lower
downswing, delayed weight shift on the downswing, more limbs and in particular the hips may also be affected by how
movement of weight onto the anterior or toe portion of the far a golfer’s weight shift characteristics vary from the
feet, and a delay in the timing of essential joint actions. “balance” alluded to previously. Excessive lateral movement
These differences likely correspond to reduced efficiency toward the target not only tends to diminish the rotary
and a reduction in clubhead speed at impact. Overall, highly force couple beneath the golfer’s feet but may also create
skilled golfers did a better job harnessing the rotational increased internal loading of the lead hip joint, which in
power from the body through an effective weight shift, bet- turn could lead to increased wear and tear on that side.
ter balance, and proper rotational kinematic sequencing. Many factors likely contribute to increased lateral move-
ment on the downswing, including poor trunk stability.42
It is interesting to note that Jack Nicklaus and Tom Watson,
Clinical Point two great players who in their primes employed a fairly
Stress to the body during the backswing and downswing can be aggressive lateral weight shift, required hip replacement
decreased by proper weight transfer, better balance, and proper surgery only on their lead (left) side. In contrast to the
rotational sequencing. previous description, maintaining excessive weight on the
trail foot in the latter part of the downswing and through
impact tends to increase the abduction and external rota-
As can be seen in the previous description, a key differ- tion forces occurring on the trail (right) hip. Forceful
ence between the swings of highly skilled and less-skilled abduction and external rotation has been linked with injury
players is the nature of the weight transfer and rotational to the hip acetabular labrum.43 Acetabular labral injuries
forces as the downswing progresses. The ground reaction have affected the right hip of many elite PGA players
forces created by the golfer on the downswing have three including Greg Norman.
important components; a medial-lateral component, an
anterior-posterior component, and a torque or rotational
component. These components correspond with the rela- Lower Limb Injuries in Golf
tive motions of the lower limbs and pelvis during the golf The lead hip and knee are affected more often than the trailing side
downswing. In their biomechanical study of baseball swings, in the golf swing.
Welch and colleagues41, in a baseball study, describe how
linear (i.e., lateral) and rotational motions, associated with
ground reaction forces, contribute to the generation of
maximum bat speed. In a similar way, the golf swing also The hip is not the only part of the lower limb susceptible
produces lateral and rotational motions. The interaction to injury from the golf swing. The knee issues affecting top
between these two components determines how the proxi- professional golfer Tiger Woods have received worldwide
mal segment of the kinetic sequence (i.e., the lower limbs) media attention. The magnitude of knee joint forces and
will be used and ultimately what must happen within the moments generated during the golf swing are not of suffi-
remaining segments, including the upper limbs to square cient magnitude to categorize golf as high-risk for acute
the club face through impact to produce an optimum knee trauma.44 This is supported by the epidemiological
swing. literature that shows that knee injuries are relatively uncom-
As the downswing commences, the lower body power- mon, making up approximately 3% to 6% of the total num-
fully rotates toward the target. This rotational motion is ber of golf injuries.8,13,45 Although knee injuries occur infre-
the result of the clockwise torque (22 Nm) provided by the quently from golf, they are common among active
trail (right) foot against the ground as well as the anterior individuals and as such many recreational golfers have knee
(186 N) and posterior (145 N) force couple produced by problems that do not originate from golf but are aggravated
the lead and trail feet respectively.40 Lateral movement of by golfing activities.8
Applied Biomechanics of Golf • CHAPTER 9 223
The lead or left knee is more often affected than the trail responsible for the apparent high incidence of lower back
side, especially among professional players.11 One of the injuries among golfers, including the forceful nature of the
first studies to quantify the various compressive loads, shear full golf swing, which clearly incorporates considerable spi-
forces, and joint moments affecting the knee joints during nal movement. In general terms, the golf swing involves a
the golf swing was performed by Gatt and colleagues.44 The slow deliberate rotation of the trunk away from the target
authors reported that the forces and moments produced in on the backswing followed by a very powerful rotation of
the knee joints were similar in magnitudes to the forces the trunk toward the left (right-handed golfer) on the
associated with activities such as a side-cutting maneuver downswing. Although it is clear that other spinal motions
while running. The authors cautioned that clinicians should besides rotation occur during a golf swing, aggressive axial
take into account the implication of these forces to the in- twisting has been identified as a significant risk factor for
ternal structures of the knee when setting return-to-golf low back disorders in occupational settings.47
activity guidelines after knee injury or surgery.
Lynn and colleagues46 investigated frontal plane mo-
ments affecting the lead knee during the full golf swing. Clinical Point
In particular, the authors were interested in how a straight
(i.e., neutral hip rotation) versus a turned out (externally Thirty percent of golf injuries primarily occur to the lumbar spine and
predominantly on the trail side with compressive leads up to eight
rotated) lead foot affected the knee varus (adduction) and
times the golfer’s body weight being applied.
valgus (abduction) moments. Results showed that turning
the lead foot out significantly decreased the varus moment
at impact resulting in less medial compartment stress. The
authors postulated that golfers with medial compartment Hosea and colleagues48 calculated the compressive, shear,
osteoarthritis would likely experience less cartilage wear and lateral-bending, and rotational loads on the L3-4 segment
pain from adopting a turned-out lead foot. Furthermore, of the lumbar spine during golf swings using a five iron.
the authors suggested that having the front foot turned out Kinetic, kinematic, and surface electromyography (EMG)
should allow golfers to more easily transfer their weight data were collected from four professional (mean age:
onto this foot during the downswing, resulting in a more 37 yr) and four amateur (mean age: 34 yr) golfers. The
efficient swing. Lynn and colleagues did caution that having authors concluded that, except for compressive load, pro-
the front foot turned out resulted in a nonsignificant fessional golfers produced less spinal loads than amateur
increase in the valgus moment, which could reflect an players. The average compressive load for amateurs and
increase in lateral compartment knee stress. professionals was 6100 N and 7584 N, respectively, which
represents forces equivalent to approximately 8 times the
golfer’s body weight. In comparison, running produces
Clinical Relevance Summary – Lower Limb spinal compression forces equal to approximately 3 times
the runner’s body weight.9 It is worth noting that cadaveric
• Excessive lateral movement of the lower limbs toward the target studies have shown disc prolapse to occur with compressive
increases internal loading of the lead hip joint, which in turn could
loads of approximately 5500 N.49 The complex, rapid, and
lead to increased wear and tear on that side. Poor trunk stability
intense nature of the spinal loads associated with the golf
may contribute to increased lateral movement.
• Maintaining excessive weight on the trail foot in the latter part of swing led Hosea and colleagues48 to conclude that prepar-
the downswing and through impact increases the abduction and ticipation conditioning, reasonable practice habits, and
external rotation forces on the trail (right) hip and may harm the proper warm-up were important for preventing low back
hip acetabular labrum. pain (LBP) from golf.
• Forces on the lead (left) knee from the golf swing are similar to It appears the golf swing produces sufficient force to
those produced during a side-cutting maneuver when running. potentially create traumatic injury to the lumbar spine. How-
• Turning the lead foot out at set-up results in less medial compart- ever, even when the back survives a well-struck golf shot
ment stress and an easier transfer of weight onto this foot, but without any apparent ill-effect, it is possible that undetected
may increase lateral compartment knee stress. microtearing of the lumbar structures may still occur. This is
referred to as the cumulative load theory.50 The cumulative
load theory takes into account the total stress placed on the
system over time. Kumar51 reported that workers who devel-
Spinal Biomechanics oped LBP were found to have consistently worked for more
hours over their lifetimes than their pain-free colleagues, sup-
and Injury Relationships porting the cumulative load theory. Because many golfers
Injuries to the spine account for approximately 30% of all (particularly elite players) identify overuse as the cause of
golf ailments, with the vast majority of these specifically their LBP,13 the high frequency of swing repetitions com-
affecting the lumbar spine.8,10,14,45 Several factors are likely bined with large-magnitude spinal forces likely results in
224 SECTION II • Applied Biomechanics of Selected Sport Activities
lower back injury through the cumulative load process. successfully eliminating golf-related LBP in a professional
Lindsay and Horton52 showed that players who consistently golfer by increasing the range of hip turn on the backswing
suffered LBP during golfing activities tended to have a higher to reduce the relative amount of spinal rotation or torsion.
frequency of swing repetitions (i.e., spent more time playing Other coaching changes included reducing the amount of
and practicing) than healthy golfers. trunk flexion and lateral flexion during the downswing.
The kinetic results of Hosea and colleagues’ study48 Bulbulian and colleagues58 also postulated that excessive
showed that the golf swing produces considerable (and rotation of the trunk during the golf swing could contribute
likely cumulative) stress on the lower back. Sugaya and to LBP. These authors investigated using a shortened
colleagues,53 in a survey of 283 Japanese professional golf- backswing on ball-contact accuracy, clubhead speed and
ers, reported that LBP predominantly occurred on the trail EMG activity of select trunk and shoulder muscles. Results
(i.e., right) side. Furthermore, radiological investigations of showed that restricting the backswing by almost 20% had
elite players revealed a significantly higher rate of trail-side no negative effect on swing performance (e.g., ball-contact
vertebral body and facet joint arthritic change than age- accuracy and clubhead speed). Furthermore, there was a
matched control subjects. The authors concluded that both significant decrease in EMG root-mean square activity of
the repetitive and asymmetric nature of the golf swing con- the right abdominal external oblique muscle on the down-
tributed to LBP and injury in elite golfers. Morgan and swing, which the authors suggested would decrease low
colleagues54 used the term crunch factor to describe the back stress. However the shorter swing tended to increase
instantaneous product of lumbar right side–bend angle and shoulder muscle activation, which could in turn increase
left axial rotation velocity that occurred during the golf shoulder injury susceptibility.
downswing. Both axial rotation velocity and side-bending It has been speculated that golfers with LBP may use key
angles reached peak values almost simultaneously and just trunk muscles such as the abdominals differently during the
after ball impact—which coincided when the majority of downswing phase than golfers without LBP.34 Horton and
players in their cohort reported experiencing LBP. They colleagues36 attempted to quantify abdominal muscle activ-
concluded a high crunch factor (i.e., during and after the ity during the golf swings of elite golfers with and without
impact phase) was damaging to the lumbar spine, resulting LBP. Results indicated that the magnitude of the muscle
in injury and pain particularly on the trail side. Maximum activity for the rectus abdominis, external oblique, and
right side–bend angles and left rotation velocities on internal oblique did not differ significantly between those
the downswing have been measured at approximately golfers with LBP and those without. However, the authors
30° and 200° per second respectively.22,25 found onset times of major bursts of activity from some of
Research on industrial workers by Marras and col- the abdominal muscles were delayed in the golfers suffering
leagues55 has also shown that only small amounts of side- LBP. In particular, the lead external oblique (left in right-
bending combined with rotation are classified as high-risk handed golfers) was activated significantly later during the
for back injury. The combination of side-bending with rota- backswing in the golfers with LBP when compared with the
tion creates a large amount of intervertebral lateral shear. asymptomatic controls. Furthermore, lead internal oblique
This shearing motion is potentially harmful because it is onset times on the downswing were also delayed in the
resisted primarily by disc strength rather than bony architec- chronic LBP golfers, although this difference did not reach
ture.55 Furthermore, Tall and DeVault56 found that the statistical significance. In a related study investigating spinal
most common cause of disc herniation in a healthy disc was kinematics, Lindsay and Horton52 reported that golfers
lateral bending combined with compression and torsion. without LBP demonstrated more than twice as much trunk
Based on these findings, it is not unexpected that the very flexion velocity on the downswing compared with the golf-
nature of the golf swing could lead to disc irritation and ers with LBP. They went on to suggest that golfers without
subsequent injury. LBP may use their anterior trunk muscles (i.e., abdominal
Lindsay and Horton,52 in their investigation of spinal muscles) to a greater degree on the downswing than golfers
kinematics, were unable to show any difference in the with LBP. However, results from a study by Cole and Grim-
“crunch factor” magnitudes between elite golfers with and shaw59 investigating the magnitude of trunk muscle activity
without LBP. The authors did show that golfers with LBP in a small number of golfers with and without LBP showed
tended to address the ball with more spinal flexion, used that, in general, the low-handicap LBP golfers demon-
more left side–bend during the backswing, and tended to use strated reduced erector spinae activity and increased exter-
considerably more rotation ROM during the follow-through nal oblique activity during the downswing compared with
than the maximum rotation ROM that these same players their asymptomatic counterparts.
were able to demonstrate in a clinical setting from a neutral The EMG findings of Horton and colleagues36 plus Cole
posture and controlled speed. The authors suggested that and Grimshaw59 do not appear to support the speculation
spinal irritation and pain could result from this relative over- that golfers with LBP do not activate their abdominal mus-
rotation of the spine while performing the golf swing. In a cles to the same magnitude as healthy golfers. However, it is
single case study design, Grimshaw and Burden57 reported interesting to note that several studies have demonstrated
Applied Biomechanics of Golf • CHAPTER 9 225
decreased abdominal muscle strength and endurance perfor- that there is a fairly similar distribution of upper limb inju-
mance in golfers suffering LBP.60-62 It is possible the ob- ries between the shoulder, elbow, and the wrist and hand.
served deficiencies in abdominal strength and endurance However, there appears to be some regional differences
could be a reflection of lower activity levels from these in injury susceptibility depending on the demographic pro-
muscles. Furthermore, Archambault and colleagues63 rec- file of the golfers being studied. For example, elite golfers
ommended the use of a stabilized-spine golf swing to facili- (i.e., tour professionals) appear more susceptible to wrist
tate the use of the abdominal and other large trunk muscles problems,8,13 whereas recreational golfers, particularly men,
to control LBP during the swing motion. This technique are more likely to suffer elbow injury.8,10 Meanwhile,
involves setting up with a “proper” spine angle and initiating McCarroll and Mallon64 reported that most shoulder inju-
the backswing with the hips and shoulders moving ries from golf occurred in older players.
together. Kinetic testing showed the stabilized-spine swing
significantly increased trunk rotation velocity on the down-
swing while reducing spinal lateral bending force, shear
Clinical Point
force, and compression force, as well as axial torsion force In golf, 50% of the injuries occur to the upper limb.
compared with a more traditional “modern” golf swing.
Clinical Relevance Summary – The Spine The following section examines some of the specific bio-
mechanical factors associated with the golf swing that may
• Average spinal compressive loads for the golf swing are equivalent contribute to injury problems in the various major joints
to approximately eight times the golfer’s body weight which, in
composing the upper limbs.
cadaveric studies, is sufficient to cause disc prolapse.
• The asymmetrical nature of the golf swing may cause increased
trail (right) side vertebral body and facet joint arthritic change, Shoulder
which may relate to increased right side–bend range of motion
during and just after impact. It has previously been mentioned that both shoulder joints
• Golfers with low back pain address the ball with more spinal undergo considerable ROM during a full golf swing. How-
flexion and tend to over-rotate their spines during the follow- ever, injury data suggests the lead shoulder is more suscep-
through based on the maximum rotation range of motion these tible to problems compared with the trail side. For example,
same players were able to demonstrate in a clinical setting. McCarroll and Gioe13 reported that injuries to the lead
• Golfers suffering low back pain demonstrate delayed abdominal shoulder occurred three times more often than to the trail
muscle recruitment. They also show abdominal muscle weakness, side among professional players. Other authors have esti-
which may reflect poor recruitment strategies during the swing.
mated that as many as 90% of all golf-related shoulder inju-
ries occur to the lead side.65 This suggests that there
is something inherent in the technique of the golf swing
Upper Limb Biomechanics contributing to increased lead shoulder stress.
McCarroll and Mallon64 reported that injury to the
and Injury Relationships lead shoulder typically occurred during the transition
Biomechanical investigation of the upper limbs in golf is between the backswing and downswing and often
limited to kinematic and muscle activation studies. Kinetics, involved the rotator cuff muscles. Injuries to the rotator
which describes the resultant joint forces and torques that cuff are especially prevalent among middle-aged and
occur during the golf swing, are typically measured via force senior golfers.66,67 Rotator cuff muscles serve to both
transducers or force plates, which is partly why this method rotate and stabilize the normally loose glenohumeral
of investigation has limited application for the upper limbs. joint. Several researchers have studied rotator cuff muscle
Also, in golf, it is very difficult to separate upper limb function during the golf swing.65,68,69 In all cases, these
moments because both hands grip the club, thus creating a researchers found relatively low but constant EMG activ-
closed kinetic chain linking the movements of the body to ity from the rotator cuff external rotator muscle groups
the forces ultimately imparted on the golf ball. As a result (i.e., infraspinatus and supraspinatus) during the down-
of the lack of quantifiable data on upper limb forces, the swing. However, high levels of EMG activity were noted
influence of swing technique on upper limb joint loads and from the lead side internal rotator subscapularis muscle
hence injury susceptibility is not as clear as it is for the spine during the initial downswing even though this shoulder
and lower body. joint was powerfully rotating in the opposite (i.e., exter-
Epidemiological data on golf injuries shows some varia- nal rotation) direction. The range of activity varied from
tion among studies, but from a general perspective the up- 41% maximum voluntary contraction (MVC) to almost
per limbs account for approximately 50% of the injury 60% MVC65,68 at the initiation of the downswing and
totals.2,8,10,12,45 Furthermore, it appears from these studies progressed to even higher levels at the midpoint of the
226 SECTION II • Applied Biomechanics of Selected Sport Activities
downswing. This level of activity from an antagonistic of the wrist, extensor digitorum, extensor digiti minimi,
muscle suggests a high stability or protection function for and the supinator). Valgus stress to the medial side of the
the lead-side subscapularis muscle.65 Shoulder injury trail elbow is resisted by contraction of the common flexor
could result from either a reduction in the stability func- origin muscles (i.e., radial and ulnar flexors of the wrist,
tion (e.g., weakness) of the rotator cuff or from excessive flexor digitorum and profundus, as well as pronator teres).
activity (and hence load) from other larger shoulder Weakness or premature fatigue of these muscles may dimin-
muscles. ish the ability of these muscles to control the varus and
valgus loads and result in injury to the underlying capsular
and ligamentous structures.72
Clinical Point
Most shoulder injuries in golf occur during the transition between the
backswing and downswing. Clinical Point
Weakness or premature fatigue of the forearm muscles may diminish
the ability of these muscles to control the varus and valgus loads on
One factor that could cause a detrimental increase in the elbow and result in injury.
shoulder load is an inappropriate kinematic sequence result-
ing in overcompensation from the shoulder muscles to
produce acceptable clubhead speed.17,70 It has also been
shown that a shortened backswing resulting from a reduc- Increases in varus and valgus elbow stress may also occur
tion in the amount of trunk rotation caused an increase in from an especially sudden deceleration of the clubhead such
EMG activity from the large pectoralis major shoulder as that encountered when hitting a buried object such as a
muscles.58 These researchers cautioned that this may lead to rock or tree root through impact.2 Another factor influenc-
increased shoulder injury susceptibility. It is interesting to ing elbow (and wrist) stress is how the hands are positioned
note that shoulder injuries appear more common among on the golf grip. The use of a neutral grip (see the next
older golfers,14 and that older golfers use less trunk rotation paragraph) is regarded as extremely important for reducing
on the backswing.71 the risk of suffering elbow pain from golf.21 Positioning the
lower (right) hand in a stronger, more supinated position on
the golf club tends to increase the valgus load to the trail
Elbow elbow. Likewise, positioning the upper (left) hand in a
Elbow injury among golfers is sufficiently recognized that weaker, more supinated position increases the varus load on
the term golfer’s elbow is an established medical condition the lead elbow. See Figure 9-2 for an illustration of lower
(medial epicondylitis). However, tennis elbow (lateral epi- hand placements.
condylitis) from golf reportedly occurs five times more The correct or neutral golf grip means both hands, at
often than golfer’s elbow.10 Although it appears that injury address, are placed on the club in such a manner that the
to the elbow from golf-related activities is common, little wrist, elbow, and shoulder joints are in relatively relaxed
research of any kind, let alone biomechanical study, has resting positions. This neutral position allows adequate and
been conducted in this area.
Golf-related lateral epicondylitis occurs most frequently
on the lead (left) elbow, whereas medial epicondylitis usu-
ally occurs on the trailing elbow.2 Both conditions may
result from a single traumatic incident or overuse creating
cumulative load and microtearing of the structures that
attach to the respective epicondyles.2,72 A well-executed full
golf shot always involves some form of sudden deceleration
at impact as the club makes contact with the ball, ground,
or both. These decelerations produce a varus and valgus
moment about the lead and trail elbows respectively. These
moments are resisted by traction to noncontractile soft-
tissue restraints (e.g., joint capsule, ligaments) particularly
on the lead side of each elbow and by the dynamic contrac- Strong Neutral Weak
bottom bottom bottom
tile structures overlying the lateral and medial joint surfaces. hand hand hand
Varus stress to the lateral aspect of the lead elbow is Figure 9-2
controlled by contraction of the muscles composing the Terminologies associated with variations in lower hand positions on
common extensor mechanism (i.e., radial and ulnar extensors the golf club. (Reproduced with permission. Fit Fore Golf Inc.)
Applied Biomechanics of Golf • CHAPTER 9 227
synchronous wrist ROM during the backswing and down- Another mechanism contributing to additional loading on
swing to properly position the club face at impact.21 the lead elbow pertains to the amount the left elbow remains
Because of individual anatomic variations, the neutral grip flexed at the top of the backswing. Biomechanical research by
does not look exactly the same on every golfer. As each Zheng and colleagues70 found that less-skilled (i.e., recre-
hand is placed on the club, the direction of the line formed ational) golfers demonstrated increased lead-side elbow flex-
between the thumb and proximal portion of the index fin- ion compared with elite players. As the downswing proceeds,
ger should be noted. This line (on both hands) should be muscular contraction forces as well as centrifugal forces tend
aimed somewhere between the trail-side eye and acromio- to straighten the elbows (and wrists) through impact. This
clavicular joint (Figure 9-3). relatively violent straightening of the lead elbow at impact
In addition to hand position, grip tension is thought to likely produces considerable joint compression stress and
be a very important risk factor for elbow and forearm pain.18 potential microtrauma (Figure 9-4).
Gripping the club with excessive tension in the fingers in-
creases the eccentric load on the wrist extensor (lead) and
flexor (trail) muscles as the clubhead makes contact with the Wrist and Hand
ball and ground at impact. This potentially excessive muscu- The wrist and hand represent the final (i.e., most distal)
lar loading may result in cumulative microtearing at the hinge in the chain of body segments composing the
common origin of the wrist extensor and flexor muscles golf swing kinematic sequence,16,23 and as such are associ-
(lateral and medial epicondyles respectively) and result in ated with the largest rotational velocities (approximately
subsequent pain. A preliminary investigation into grip pres- 1000 m/s).31,75 Furthermore, the wrist joints are subjected
sures by Broker and Ramey73 showed that less-skilled ama- to large-amplitude ROM during the downswing and follow-
teur golfers tended to grip the golf club with greater force through. For example, Cahalan and colleagues29 recorded
than highly skilled players. This may partially account for the wrist flexion and extension ROM in a population of healthy
almost sixfold increase in elbow injuries among recreational golfers of approximately 35 degrees and 103 degrees respec-
golfers compared with professional players.74 tively in the lead (left) and trail sides. Radial and ulnar
deviation ROM totals were 36 degrees and 31 degrees
respectively for the lead and trail wrist joints.
This combination of large amounts of wrist angle on the
downswing and the timing of the wrist release is critical for
Clinical Point producing a highly efficient swing. Robinson76 reported that
Lateral epicondylitis is more likely to be seen in the lead elbow, 60% of the variation in clubhead speed between recreational
whereas medical epicondylitis is more common in the trailing and elite golfers can be predicted by knowing the magnitude
elbow. of the angle between the left forearm and the club shaft at
the midpoint of the downswing (Figure 9-5). This angle is
the result of radial deviation of the wrists. In other words,
elite golfers tend to incorporate more radial deviation at the
top of the backswing and delay the release of this angle
much later in the downswing.17,21 Excessive repetition of
the high-velocity, large-amplitude wrist release likely pro-
duces considerable stress on the wrist structures and in-
creases injury susceptibility, particularly among professional
Neutral grip
Figure 9-3 Improper technique Proper technique
Lines formed between thumb and first finger aligned between eye Figure 9-4
and shoulder region on trail side. (Reproduced with permission. Excessive lead elbow flexing can cause tennis elbow. (Reproduced
Fit Fore Golf Inc.) with permission. Fit Fore Golf Inc.)
228 SECTION II • Applied Biomechanics of Selected Sport Activities
Golf clubs represent the critical link between the human driver. As the club is accelerated, the linear forces associ-
body and the golf ball. When golfers use clubs that are not ated with a more vertical or steeper swing plane tend to
well-suited to their particular physical dimensions or swing drive the hips and trunk laterally, resulting in an increase in
characteristics, the body is forced to compensate. As men- thoracolumbar side-bend motion. Side-bending of the
tioned, the spine is particularly susceptible to injury from golf spine during the golf swing has been postulated as a con-
and as such needs to be protected during the swing. Golfers tributing factor to low back injury.53,71
who suffer LBP tend to address the ball with more spinal These studies appear to show, from a general perspective,
flexion.52 Increased spinal flexion at set-up may result from that shorter clubs produce additional loading on the lower
not using the hip joints to tilt the trunk forward when spine, which may contribute to LBP. However this is the case
addressing the clubhead behind the ball or from using a only if the shorter and longer clubs were swung with similar
golf club that is too short. For men, the standard club length intensity. A matching set of golf clubs includes as many as
is reportedly designed for someone 70 inches (178 cm) 14 different clubs, all of which are a different length. The
in height, whereas for women this number is 64 inches reason is that each club has a unique purpose that varies be-
(163 cm). However, these industry standards appear to be tween how far the club can hit the ball and the desired accu-
based more on tradition than scientific testing. Also, it is racy of the shot. This is why certain clubs, such as wedges, are
interesting to note that most major equipment manufactur- referred to as scoring clubs if the intention is to be as accurate
ers only offer a range of approximately 2.7 to 3.1 inches as possible. In comparison, the driver club is expected to hit
(7-8 cm) in the length of the shafts when “fitting” golf clubs the ball the longest distance possible and as such is manufac-
to new customers. However, the range in overall vertical tured with a much longer shaft than the wedge. Results from
height of these customers would be more in the vicinity of Neal and colleagues78 and Lindsay and colleagues22 might
12 inches (30 cm). This variation suggests that a golfer who suggest that the shorter length clubs (i.e., wedge) produce
is quite tall will likely receive a proportionately shorter shaft more harmful stresses on the lower back. However, these
(resulting in increased flexion when setting up to the ball) shorter clubs are typically not swung as hard as a “distance
than a much shorter golfer even though in both instances club” such as a driver, which in turn would tend to reduce the
they were fitted with the shaft length that was “recom- magnitude of the spinal load. The important message for
mended” by the manufacturer for their respective sizes. health care providers is to at least question golfers suffering
There is biomechanical evidence that the length of from LBP on whether their clubs were measured for their
the club shaft can affect spinal biomechanics. Neal and particular body dimensions (called club fitting). More specifi-
colleagues78 reported on the effects of using an inappropri- cally, golfers with LBP should not use clubs that are shorter
ately matched golf club on spinal swing mechanics. The than the length recommended by the manufacturer for their
authors found that using a club with a shaft that was particular body dimensions. All golf clubs can relatively easily
2 inches (5 cm) shorter than the recommended length and inexpensively be adjusted for length by appropriately
resulted in approximately 4° less spinal rotation at the top trained staff at most golf courses or golf retail outlets.
of the backswing, and 8° more flexion at impact. However, It has been mentioned that repetitive practice is essential
these numbers were not part of a specific scientific investi- for consistent performance. Often such practice involves
gation and were based on a single golfer. Lindsay and col- hitting full golf shots off hard artificial surfaces such as driv-
leagues22 completed an investigation comparing spinal ing range mats. Contact between the golf club and the
mechanics among elite golfers using a driver and 7-iron. driving range mat before, during, or after ball impact is
The purpose was to investigate the changes in set-up pos- another possible contributing factor to upper limb stress
ture and spinal motion during the swing caused by the and potential injury from golf activity. Repetitive and exces-
different length clubs. The 7-iron is approximately 18 cm sive loading may contribute to injuries such as wrist tendi-
shorter than the driver. The address position flexion angles nopathy, elbow epicondylitis, and rotator cuff strain.9,67
recorded in this study using the 7-iron (35.1° ⫾ 12.8°) A number of manufacturers produce simulated turf mats,
were significantly higher than the driver results (28.9° ⫾ and there are typically two main types installed at practice
10.9°). During the actual swing, greater maximum flexion facilities. One type is a solid mat that incorporates a thin
and side-bend ROM were observed when using the 7-iron. layer of a durable synthetic turf that is implanted or glued
The explanation for increased side-bending when swinging onto a 30-mm thick base composed of dense foam. The
the 7-iron may relate to the effect of the shorter club on other common mat consists of a pliable brushlike surface
swing plane. Swing plane refers to the oblique plane the composed of closely packed vertical strands of nylon fibers
golf club is moved through during the swing. The shorter- (approximately 40 mm long) set into a hard polymer base
length 7-iron typically requires the ball to be positioned (Figure 9-6). Although there is a lack of kinetic data com-
closer to the body and the spine to be more flexed than paring upper limb impact forces using different artificial
when using the driver. This combination necessitates a mats, Lindsay and colleagues79 did compare the perceived
more vertical orientation of the 7-iron shaft during the set- impact forces, upper limb stress, quality of shots, and simi-
up as well as during the actual swing, compared with the larity to hitting from grass between the two most common
230 SECTION II • Applied Biomechanics of Selected Sport Activities
force moments about the ankle, knee, hip, and spine, which
in turn decreases the risk of injury to these areas (http://
www.united-golfers.de/). Further research is needed to
substantiate the proposed benefits from this unique shoe
design. However, based on this information, it is reasonable
for health care providers to caution golfers with lower limb
injuries from playing in shoes that excessively anchor their
feet to the ground.
Warmup Considerations
The powerful movements making up the typical full golf
swing are repeated 100 or more times per practice session
or game, resulting in considerable stress being generated
and dissipated during each of these sessions. Owing to these
Figure 9-6 stresses, it seems logical that an adequate warmup routine
Brush fiber mat. should be performed prior to playing or practicing. How-
ever, research suggests that most golfers do not perform an
types of hitting mats. Results from this study showed that adequate warmup, especially seniors who often contend
perceptual differences clearly exist in how different types of with both age-related changes in the musculoskeletal
practice mats affect upper limb stress and the quality of golf system and chronic conditions such as osteoarthritis.5,80
shots. A minimum of 80% of the study participants selected The purpose of the warmup is to physiologically and
the brush fiber mat over the solid mat in terms of the com- psychologically prepare the body for competition while at
fort and quality of the hitting experience. The largest per- the same time reducing the risk of injury. Palmer and col-
ceived difference between mats pertained to upper limb leagues81 examined the typical warmup habits of a conve-
stress, with almost 91% of subjects stating they felt the nience sample of Canadian golfers, both men and women,
brush fiber mat produced the least stress during impact. with an average age of 70 years. Less than 25% of
The ground reaction forces that occur under a golfer’s the 100 recreational players surveyed spent more than
feet are another source of potential stress from golf, par- 5 minutes stretching and warming up prior to playing.
ticularly to the lower limbs. These forces are influenced by Fradkin and colleagues,82 in a survey of 304 golfers in the
a number of factors, including the type of shoe being worn. United States, found that only 18% of the sample per-
Worsfold and colleagues39 reported that rotation torques formed an adequate warmup. The authors also reported
under the front (i.e., left) foot were typically approximately that golfers who did not adequately warm up were
2 to 3 times higher than those under the trail foot when 1.3 times more likely to have suffered a golf-related injury.
executing full shots. The peak magnitude of this torque Gosheger and colleagues8 also reported that only 19% of
coincides with a rapid shift of weight onto the lead side.79 golfers surveyed in their European study warmed up
This rotational force and weight shift occurs while the front appropriately, and that these golfers reported 60% fewer
foot remains firmly anchored to the ground, usually with injuries than the golfers who did not warm up.
specially designed “spikes” attached to the undersurface of An appropriate warmup should last a minimum of
the shoe. Recently, a golf shoe has been designed and mar- 10 minutes and can be broken down into four sections.80,82
keted in which the upper portion of the lead-side shoe can The first involves low-intensity activity that uses as many of
“release” or rotate farther toward the target than the sole- the large muscle groups as possible. Examples include brisk
plate portion of the same shoe. An interesting biomechani- walking, climbing a flight of stairs, or carefully rotating the
cal case study carried out at the Sports Science Institute of trunk from side to side with a golf club held behind the
the Eberhard Karls University in Tübingen, Germany, was back. One very good tip for golfers is to park at the far end
able to show that the shoe released after impact, and, as of the parking lot when they arrive at the golf course, thus
such, did not affect the kinematics of the back and down- using the walk to the clubhouse to assist with the warmup
swings. However, at the finish position, the free-release process. The next component of the warmup involves
mechanism allowed the left foot to turn approximately stretching the key muscles used in the golf swing
20° to 25° farther toward the target than when the foot was (i.e., muscles of the back, hip, neck, shoulders, and fore-
constrained within a standard golf shoe. This release of the arms). Pregame stretching exercises for golf can be found at
shoe decreased the amount of lead-hip internal rotation at www.fitforegolf.com. The third component involves dy-
the finish position by approximately 10° and decreased namic stretching and may be accomplished by initially
spinal rotation by approximately 5°. The manufacturer swinging a short iron back and forth and progressing by
claims that this results in a considerable decrease in the gently swinging two clubs at once. It is important, due to
Applied Biomechanics of Golf • CHAPTER 9 231
the asymmetrical nature of the full swing, for warmup often played in a group of four individuals, Figure 9-7
swings to be performed both left and right handed to opti- metaphorically represents the “foursome” of management
mize muscle balance and coordination. The final part of the strategies for injured golfers. The effective implementation
warmup involves practicing actual shots. This further helps of a combination of the various elements outlined in
warm up the golf muscles and facilitates timing and consis- Figure 9-7 will not only help the injured player get back on
tency. Players should be instructed to start with a short club the golf course in the shortest time possible but, just as
such as a wedge and begin by hitting only shots that travel importantly, will likely prevent the injury from recurring in
approximately 20 yards. The length of the shots should the future.
increase progressively, followed by using other clubs that
produce different trajectories and distance.
Appropriate
equipment
modifications and
correction of bio-
Clinical Relevance Summary - Equipment mechanical swing
flaws to minimize
• Golf equipment, in particular shaft length, should be matched to MSK stress
the size of the golfer using the equipment.
• Using a set of clubs that are too short causes an increase in spinal
flexion throughout the swing. This produces a steeper swing plane, Implementation Treatment of
resulting in increased thoracolumbar side-bend motion on the of flexibility, musculoskeletal
INJURY
downswing, which increases the risk of suffering an injury to the cardio and problems that
MANAGEMENT
muscular affect the
lower back. FOR
conditioning golfer’s
• Hitting golf balls off a brush fiber mat at the practice range GOLFERS
prior to start of performance
is perceived to be more like hitting from grass and produces season and enjoyment
less stress on the upper limbs compared with a more solid
hitting mat.
• Golf shoes that allow the front foot to release or rotate farther Education on
proper pre-game
toward the target after impact can potentially reduce the range of
warm-up as well
motion magnitude (and hence stress) on the spine and lead hip at as on-course
the completion of the swing. hydration and
• Most golfers do not perform an adequate warmup prior to playing. nutritional
A proper warmup should last at least 10 minutes and should supplementation
include a general body warmup, static stretching, dynamic stretch-
Figure 9-7
ing, and progressive practice shots. An effective warmup routine is The “foursome” of management strategies for injured golfers.
particularly important for the senior golfer, whose age-related (Reproduced with permission. D. Lindsay and A. Vandervoort.)
musculoskeletal changes result in increased stiffness and suscep-
tibility to soft-tissue injuries.
References
1. Farrally MR, Cochran AJ, Crews DJ, et al: Golf science research at
the beginning of the twenty-first century, J Sports Sci 21:753–765,
Conclusion 2003.
2. Thériault G, Lachance P: Golf injuries: An overview, Sports Med
Golf has both real health benefits as well as certain injury 26:43–57, 1998.
risks, particularly to the upper limbs and spine. Many of 3. Parkkari J, Natri A, Kannus P, et al: A controlled trial of the health
benefits of regular walking on a golf course, Am J Sport Med
these injuries occur as a result of overuse in combination 109:102–108, 2000.
with biomechanical swing flaws creating unnecessary stress 4. Sell TC, Abt JP, Lephart SM: Physical activity-related benefits of
on certain parts of the body. Therefore, it is important for walking during golf. In Crews DS, Lutz RS, editors: Science and
health care providers treating injured golfers to investigate golf V. Proceedings of the Fifth World Scientific Congress of Golf,
factors such as swing technique when determining appro- Mesa, AZ, 2008, Energy in Motion.
5. Versteegh TH, Vandervoort AA, Lindsay DM, Lynn SK: Fitness,
priate rehabilitation strategies. Correction of biomechanical performance and injury prevention strategies for the senior golfer,
deficiencies in a player’s swing does not rest exclusively on Ann Rev Golf Coach 2:199–214, 2008.
the health care provider, but often involves collaboration 6. Cann AP, Lindsay DM, Vandervoort AA: Optimizing the benefits
between the health care provider and a certified golf coach. versus risks of golf participation by older people, J Geriatr Phys
Although the recognition and correction of swing flaws Ther 28:85–92, 2005.
7. Nesbit SM, Serrano M: Work and power analysis of the golf swing,
causing excessive stress on a golfer’s body are very impor- J Sports Sci Med 4:520–533, 2005.
tant, it is also clear that other factors including equipment 8. Gosheger G, Liem D, Ludwig K, et al: Injuries and overuse
and appropriate warmup also play a role. Because golf is syndromes in golf, Am J Sports Med 31:438–443, 2003.
232 SECTION II • Applied Biomechanics of Selected Sport Activities
9. McHardy A, Pollard H, Luo K: Golf injuries: A review of the 32. Putnam CA: Sequential motions of body segments in striking and
literature, Sports Med 36:171–187, 2006. throwing skills, J Biomech 26:125–135, 1993.
10. McCarroll JR, Rettig AC, Shelbourne KD: Injuries in the amateur 33. Bechler JR, Jobe FW, Pink M, et al: Electromyographic analysis
golfer, Phys Sportsmed 18:122–126, 1990. of the hip and knee during the golf swing, Clin J Sport Med
11. McCarroll JR: The frequency of golf injuries, Clin Sport Med 5:162–166, 1995.
15:1–7, 1996. 34. Watkins RG: Dynamic electromyographic analysis of trunk muscu-
12. Fradkin AJ, Windley TC, Myers JB, et al: Describing the epidemiol- lature in professional golfers, Am J Sport Med 24:535–538,
ogy and associated age, gender and handicap comparisons among 1996.
golfing injuries, Int J Inj Contr Safety Prom 14:264–266, 2007. 35. Lim TY: Lower trunk muscle activities during the golf swing—
13. McCarroll JR, Gioe TJ: Professional golfers and the price they pay, Pilot study, Proceedings of the third North American Congress on
Phys Sportsmed 10:64–70, 1982. Biomechanics, Waterloo, August 14–18, 1998.
14. McNicholas MJ, Neilsen A, Knill-Jones RP: Golf injuries in 36. Horton JF, Lindsay DM, MacIntosh BR: Abdominal muscle char-
Scotland. In Farrally MR, Cochran AJ, editors: Science and acteristics of elite male golfers with and without chronic low back
golf III: Proceedings of the World Scientific Congress of Golf, pain, Med Sci Sports Exerc 33:1647–1654, 2001.
Champaign, IL, 1999, Human Kinetics. 37. Pink M, Perry J, Jobe FW: Electromyographic analysis of the trunk
15. Duda M: Golf injuries: They really do happen, Phys Sportsmed in golfers, Am J Sport Med 21:385–388, 1993.
15:191–196, 1987. 38. McHardy A, Pollard H: Muscle activity during the golf swing,
16. Cochran AJ, Stobbs J: The search for the perfect swing, Philadelphia, Br J Sport Med 39:799–804, 2005.
1968, Lippincott. 39. Worsfold P, Smith NA, Dyson RJ: Low handicap golfers generate
17. Lindsay DM, Mantrop S, Vandervoort AA: A review of biome- more torque at the shoe-natural grass interface when using a
chanical differences between golfers of varied skill levels, Ann Rev driver, J Sports Sci Med 7:408–414, 2008.
Golf Coaching 2:187–197, 2008. 40. Barrentine SW, Fleisig GS, Johnson H: Ground reaction forces
18. Adlington GS: Proper swing technique and biomechanics of golf, and torques of professional and amateur golfers. In Cochran AJ,
Clin Sport Med 15:9–26, 1996. Farrally MR, editors: Science and golf II: Proceedings of
19. Mann R, Griffin F, Locum G: Swing like a pro: The breakthrough the World Scientific Congress of Golf, London, 1994, E & FN
method of perfecting your golf swing, New York, 1998, Broadway SPON.
Books. 41. Welch CM, Banks SA, Cook FF, Draovich P: Hitting a baseball:
20. Okuda I, Armstrong CW: Biomechanical analysis of professional A biomechanical description, J Orthop Sports Phys Ther 22:
golfer’s swing. In Thain E, editor: Science and golf IV: Proceed- 93–201, 1995.
ings of the World Scientific Congress of Golf, London, 2002, 42. Hellstrom J, Tinmark F: The association between stability and
Routledge. swing kinematics of skilled high school golfers. In Crews DS,
21. Hume PA, Keogh J, Reid D: The role of biomechanics in maxi- Lutz RS, editors: Science and golf V: Proceedings of the Fifth
mizing distance and accuracy of golf shots, Sports Med 35: World Scientific Congress of Golf, Mesa, AZ, 2008, Energy in
429–449, 2005. Motion.
22. Lindsay DM, Horton JF, Paley RD: Trunk motion of male profes- 43. Fitzgerald RH: Acetabular labral tears: Diagnosis and treatment,
sional golfers using two different golf clubs, J Appl Biomech Clin Orthop 311:60–68, 1995.
18:366–373, 2002. 44. Gatt CJ, Pavol MJ, Parker RD, Grabiner MD: A kinetic analysis of
23. Cheetham PJ, Martin PE, Mottram RE, St Laurent BF: The the knees during a golf swing. In Farrally MR, Cochran AJ,
importance of stretching the X-factor in the downswing of golf. editors: Science and golf III: Proceedings of the World Scientific
In Thomas PR, editor: Optimizing performance in golf, Brisbane, Congress of Golf, Champaign, IL, 1999, Human Kinetics.
2001, Australian Academic Press. 45. Batt ME: A survey of golf injuries in amateur golfers, Br J Sport
24. Burden AM, Grimshaw PN, Wallace ES: Hip and shoulder rota- Med 26:63–65, 1992.
tions during the golf swing of sub-10 handicap players, J Sports Sci 46. Lynn SK, MacKenzie H, Vandervoort AA: Frontal plane knee
16:165–176, 1998. moments during the golf swing: Effect of target side foot position
25. McTeigue M, Lamb SR, Mottram R, Pirozzolo F: Spine and hip at address. In Crews DS, Lutz RS, editors: Science and golf V:
motion analysis during the golf swing. In Cochran AJ, Farrally MR, Proceedings of the World Scientific Congress of Golf, Mesa, AZ,
editors: Science and golf II: Proceedings of the World Scientific 2008, Energy in Motion.
Congress of Golf, London, 1994, E & FN SPON. 47. Marras WS, Granata KP: A biomechanical assessment and model
26. Wheat JS, Vernon T, Milner CE: The measurement of upper body of axial twisting in the thoracolumbar spine, Spine 20:1440–1451,
alignment during the golf drive, J Sports Sci 25:749–755, 2007. 1995.
27. Wallace ES, Graham D, Bleakley EW: Foot-to-ground pressure 48. Hosea TM, Gatt CJ, Galli KM, et al: Biomechanical analysis of the
patterns during the golf drive: A case study involving a low handi- golfer’s back. In Cochran AJ, editor: Science and golf: Proceedings
cap player and a high handicap player. In Cochran AJ, editor: of the First World Scientific Congress of Golf, London, 1990, E &
Science and golf: Proceedings of the First World Scientific FN SPON.
Congress of Golf, London, 1990, E & FN SPON. 49. Adams MA, Hutton WC: Mechanics of the intervertebral disc.
28. Mitchell K, Banks S, Morgan D, Sugaya H: Shoulder motions dur- In Ghosh P, editor: The biology of the intervertebral disc, Boca
ing the golf swing in male amateur golfers, J Orthop Sport Phys Raton, FL, 1988, CRC Press.
Ther 33:196–203, 2003. 50. Gluck GS, Bendo JA, Spivak JM: The lumbar spine and low back
29. Cahalan TD, Cooney WP, Tamai K, Chao EYS: Biomechanics of the pain in golf: A literature review of swing biomechanics and injury
golf swing in players with pathological conditions of the forearm, prevention, Spine J 8:778–788, 2008.
wrist and hand, Am J Sport Med 19:288–293, 1991. 51. Kumar S: Theories of musculoskeletal injury causation, Ergonomics
30. McCarroll JR: Overuse injuries of the upper extremity in golf, 44:17–47, 2001.
Clin Sports Med 20:469–479, 2001. 52. Lindsay DM, Horton JF: Comparison of spine motion in elite
31. Neal R, Lumsden R, Holland M, Mason M: Body segment se- golfers with and without low back pain, J Sports Sci 20:599–605,
quencing and timing in golf, Ann Rev Golf Coach 1:25–36, 2007. 2002.
Applied Biomechanics of Golf • CHAPTER 9 233
53. Sugaya H, Tsuchiya A, Moriya H, et al: Low back injury in elite 70. Zheng N, Barrentine SW, Fleisig GS, Andrews JR: Kinematic
and professional golfers: An epidemiologic and radiographic study. analysis of swing in pro and amateur golfers, Internat J Sports Med
In Farrally MR, Cochran AJ, editors: Science and golf III: 29:965–70, 2008.
Proceedings of the World Scientific Congress of Golf, Champaign, 71. Morgan D, Cook F, Banks S, et al: The influence of age
IL, 1999, Human Kinetics. on lumbar mechanics during the golf swing. In Farrally MR,
54. Morgan D, Sugaya H, Banks S, et al: A new twist on golf kinemat- Cochran AJ, editors: Science and golf III: Proceedings of the
ics and low back injuries, Proceedings of the 21st Annual Meeting World Scientific Congress of Golf, Champaign, IL, 1999,
of the American Society of Biomechanics, Sept 24–27, 1997. Human Kinetics.
55. Marras WS, Lavender SA, Leurgans SE, et al: Biomechanical risk 72. McHardy AJ, Pollard HP: Golf and upper limb injuries: A sum-
factors for occupationally related low back disorders, Ergon mary and review of the literature, Chiropr Osteopathy 13:1–7,
38:377–410, 1995. 2005.
56. Tall RL, DeVault W: Spinal injury in sport: Epidemiologic consid- 73. Broker JP, Ramey MR: Understanding golf club control through
erations, Clin Sports Med 12:441–448, 1993. grip pressure measurement. In Crews DS, Lutz RS, editors:
57. Grimshaw PN, Burden AM: Case report: Reduction of low back Science and golf V: Proceedings of the World Scientific Congress of
pain in a professional golfer, Med Sci Sports Exerc 32:1667–73, Golf, Mesa, AZ, 2008, Energy in Motion.
2000. 74. Kohn HS: Prevention and treatment of elbow injuries in golf, Clin
58. Bulbulian R, Ball K, Seaman D: The short golf backswing: Effects Sports Med 15:65–83, 1996.
on performance and spinal health implications, J Manipulative 75. Nago M, Sawada Y: A kinematic analysis of the golf swing by
Physiol Ther 24:569–575, 2001. means of fast motion picture in connection with wrist action,
59. Cole MH, Grimshaw PN: Electromyography of the trunk and J Sports Med 17:413–418, 1977.
abdominal muscles in golfers with and without low back pain, J Sci 76. Robinson RL: A study of the correlation between swing character-
Med Sport 11:174–81, 2008. istics and club head velocity. In Cochran AJ, Farrally MR, editors:
60. Evans C, Oldreive W: A study to investigate whether golfers with Science and golf II: Proceedings of the World Scientific Congress
a history of low back pain show a reduced endurance of transverse of Golf, London, 1994, E & FN SPON.
abdominis, J Man Manip Ther 8:162–174, 2000. 77. Dalgleish MJ, Vicenzino B, Neal RJ: Swing technique change and
61. Evans K, Refshauge KM, Adams R, Aliprandi L: Predictors of low adjunctive exercises in the treatment of wrist pain in a golfer:
back pain in young elite golfers: A preliminary study, Phys Ther A case report. In Thomas PR, editor: Optimizing performance in
Sport 6:122–130, 2005. golf, Brisbane, 2001, Australian Academic Press.
62. Lindsay DM, Horton JF: Trunk rotation strength and endurance 78. Neal RJ, Sprigings EJ, Dalgleish MJ: How has research influ-
in healthy normals and elite male golfers with and without low enced golf teaching and equipment. In Thomas PR, editor:
back pain, North Am J Sport Phys Ther 1:80–91, 2006. Optimizing performance in golf, Brisbane, 2001, Australian
63. Archambault ML, Ling W, Chen B, Gatt C: A kinematic and Academic Press.
kinetic analyses of the modern and stabilized-spine golf swings. In 79. Lindsay, DM, Hadi W, Wright I, Vandervoort AA: Comparison of
Crews DS, Lutz RS, editors: Science and golf V: Proceedings of the perceived golf shot performance, upper limb stress and ball flight
World Scientific Congress of Golf, Mesa, AZ, 2008, Energy in characteristics between solid and brush fiber hitting mats. In
Motion. Crews DS, Lutz RS, editors: Science and golf V: Proceedings of the
64. McCarroll JR, Mallon WJ: Epidemiology of golf injuries. In Stover World Scientific Congress of Golf, Mesa, AZ, 2008, Energy in
CN, McCarroll JR, Mallon WJ, editors: Feeling up to par: Motion.
Medicine from tee to green, Philadelphia, 1994, FA Davis. 80. Vandervoort AA: Aging of the human neuromuscular system,
65. Lindsay DM, Horton JF, Vandervoort AA: A review of injury Muscle Nerve 25:17–25, 2002.
characteristics, aging factors and prevention programs for the 81. Palmer JL, Young SD, Fox E, et al: Senior recreational golfers:
older golfer, Sports Med 30:89–103, 2000. A survey of musculoskeletal conditions, playing characteristics and
66. Kim DH, Millett PJ, Warner JJP, Jobe FW: Shoulder injuries in warm up patterns, Physio Can 55:79–86, 2003.
golf, Am J Sport Med 32:1324–1330, 2004. 82. Fradkin AJ, Windley TC, Myers JB, et al: Describing the warm-up
67. Jobe FW, Moynes DR, Antonelli DJ: Rotator cuff function during habits of recreational golfers and the associated injury risk. In
a golf swing, Am J Sport Med 14:388–392, 1986. Crews DS, Lutz RS, editors: Science and golf V: Proceedings of the
68. Jobe FW, Perry J, Pink M: Electromyographic shoulder activity in World Scientific Congress of Golf, Mesa, AZ, 2008, Energy in
men and women professional golfers, Am J Sport Med 17: Motion.
782–787, 1989.
69. Pink M: Electromyographic analysis of the shoulder during the
golf swing, Am J Sport Med 18:137–140, 1990.
10
CHAPTER
234
Applied Biomechanics of Jumping • CHAPTER 10 235
Countermovement Jump
Squat Jump
Figure 10-1
Shown are sagittal plane representations of an athlete executing countermovement (top) and squat
(bottom) vertical jumps with an arm swing. Also shown is the magnitude and direction of the ground
reaction force produced during each jump. Note that each image represents the position of the jumper
at a different point in time—the athlete is not jumping across the page. The image in the lower left is
what the jump would look like if the images were not spaced apart. (From Reiser R, Rocheford E,
Armstrong CJ: Building a better understanding of basic mechanical principles through analysis of the
vertical jump, Strength Cond J 28[4]:70-80, 2006.)
Biomechanics of Vertical Jumps to jump height will be mainly determined by the factors
contributing to the flight height, specifically the vertical
Factors Affecting Jump Performance velocity that can be achieved at takeoff. As such, much of
The vertical jump is probably the most common jump seen the biomechanical research has focused on identifying how
in sports, and the goal, in general, is to elevate the COM as flight height can be maximized.
high as possible. There are many factors that affect jump
performance and the interactions can be complex. Hay and
Reid introduced the concept of using a deterministic model
Deterministic Models of Performance
to establish the relationships between various factors and
how they affect athletic performance.2 Since that time, A deterministic model is one of the best ways to identify and
numerous authors have used this technique to describe the establish relationships between variables and factors that affect
relationships between the various biomechanical variables athletic performance.
contributing to vertical jump performance. An example of
a deterministic model for a two-footed vertical jump is
provided in Figure 10-2.
At the top level of the model, the ultimate goal is Variations of this model have been developed by other
identified—jump height. Jump height is directly influenced investigators for both 2-foot3 and 1-foot jumps.4 The
by the two factors identified in the next level of the model, model developed by Vint and Hinrichs3 (Figure 10-3)
takeoff height and flight height. The process of identifying introduces two additional factors that directly affect jump
“contributing factors” continues with each subsequent level height: reach height, which, like the takeoff height, is
until ultimately one reaches a “base” level of controllable largely determined by body size and anthropometric vari-
and uncontrollable factors that affect performance. As the ables; and loss height which is related to the timing and
takeoff height is influenced primarily by uncontrollable an- coordination necessary to achieve maximum reach at the
thropometric factors (see Figure 10-2), any improvements same time the COM reaches its peak height. This model
236 SECTION II • Applied Biomechanics of Selected Sport Activities
HEIGHT
TAKEOFF FLIGHT
HEIGHT HEIGHT
POSITION at VELOCITY at
PHYSIQUE GRAVITY
TAKEOFF TAKEOFF
VELOCITY at
FIRST MOVEMENT CHANGE in
(VV 0) VELOCITY
GROUND
TAKEOFF
REACTION MASS GRAVITY
TIME
FORCE
FORCE on FORCE on
FORCE FORCE FORCE
TRUNK TRUNK
HIPS KNEES ANKLES
by HEAD by ARMS
Figure 10-2
The deterministic model establishes relationships between various factors that contribute to vertical
jump performance. Variables at one level are “determined” by the variables on the next lower level.
Ultimately, one reaches “base factors” that the athlete can, or in some cases cannot, control. (From
Feltner ME, Fraschetti DJ, Crisp RJ: Upper extremity augmentation of lower extremity kinetics
during countermovement vertical jumps, J Sport Sci 17:449-466, 1999.)
has been used successfully to evaluate jump performance Full Body Kinematics and Kinetics
in activities such as volleyball in which the elevation of Numerous studies have recorded kinematic profiles of SJs
the hands, and not just the COM, is important. In and CMJs, tracking the position, velocity, and acceleration of
determining the contributions made by each of the four the COM (Figure 10-4). Vertical jump height is noticeably
“top-level” factors, it was found that takeoff height, flight larger when a jump is performed with a countermovement
height, and reach height accounted for 41%, 17%, and and this is due to the fact that the countermovement allows
42% of the total jump height, respectively.3 The loss the individual to produce a greater vertical velocity during
height was found to be negligible, accounting for only the propulsive phase of the jump. The propulsive phase is
0.2% of the overall jump height (see Figure 10-3). Again, defined as the time between the minimum position of the
although flight height contributes the lowest percentage COM (vertical velocity 0) and takeoff. Although the pro-
toward total height, it is the one variable that can be con- pulsive phase starts with the onset of movement in an SJ, it
trolled or altered to any degree via technique changes or occurs at approximately 67% to 72% of the total movement
training. time5-7 in a CMJ. In most cases, the COM height is slightly
higher at takeoff than what is seen in standing because of the
ankle extension that occurs late in the jump.
Factors Contributing to Jump Height
• Takeoff height 41%
• Flight height 17% Jumping is a Ballistic Activity
• Reach height 42% Jump height is determined entirely by what happens before the feet
• Loss height 0.2% leave the ground.
• Take-off velocity
Reach Height
CM
Takeoff Height
Figure 10-3
Deterministic model for athletic performances in which reach is critical. This deterministic model adds
two factors at the top level of the model that affect how high the hand can reach in a vertical jump,
compared with the previous model that only deals with the COM trajectory. (From Vint P: Vertical
jumping performance: One-foot vs two-foot takeoff techniques. In Performance and conditioning for
volleyball, vol 3, pp 4-7, Lincoln, NE, 1996, Conditioning Press.)
7% before the feet leave the ground.5 This is a consistent In which vvf and vvi are the final and initial vertical velocity
finding across individuals and has been attributed to the of the COM, respectively, and Fvavg and t are the sum of
mechanical “disadvantage” faced by many of the shortened the average vertical forces acting on the body and the time
extensor muscles as their force producing capabilities during which they act.
are compromised near full extension according to the Neglecting air resistance, the only forces acting on the
force-length relationship for muscle as well as the need for body in the vertical direction are body weight (BW) and the
the body to dial back activation to protect the joints from vertical ground reaction force (GRF). In addition, the verti-
hyperextension. cal velocity at the start of the propulsive phase is zero in
There are two ways of viewing how vertical velocity is both SJs and CMJs.
produced. The first is through the framework of impulse According to this relationship, jump height can be im-
and momentum and the second is by analyzing the work proved by increasing the magnitude of the vertical GRF or the
performed and energy changes in the body. According to length of time during which that force acts. However, research
the impulse-momentum theorem, the final takeoff velocity has shown that athletes have very little direct control over the
is determined by vertical impulse produced during the pro- amount of time they are in contact with the ground.
pulsive phase, or the average net vertical force multiplied by It is generally accepted that the best way to maximize
the length of the propulsive phase. jump height is to focus on developing a larger GRF. GRF
profiles typical to what is seen in SJs and CMJs are shown
Impulse-momentum theorem:
in Figure 10-5. The “shape” of the GRF tracing closely
m (v v ,f − v v ,i ) = ∑ Fv ,avg • t resembles that of the acceleration tracing in Figure 10-4,
as would be expected according to Newton’s second law
238 SECTION II • Applied Biomechanics of Selected Sport Activities
1.6 CMJ
SJ
Clinical Points
1.4
Position (m)
3500
CMJ
3000 SJ
2500
Force (N)
2000
1500
1000
W
500
0
1.2 0.9 0.6 0.3 0 0.3 0.6 0.9 1.2
Time (sec)
Figure 10-5
Representative vertical ground reaction forces are shown for an athlete performing squat (gray) and
countermovement (black) jumps. The traces are aligned to the point of takeoff (t 0). For reference,
a horizontal line indicating the athlete’s body weight (W) has been added to the force profile. The
ground reaction force is defined as positive acting upward. (From Reiser R, Rocheford E, Armstrong CJ:
Building a better understanding of basic mechanical principles through analysis of the vertical jump,
Strength Cond J 28[4]:70-80, 2006.)
the kinetic energy at takeoff. Researchers have reported the time essentially remains unchanged across jumps, increased
total work performed during a vertical jump as 5.118 and power indicates that an individual is able to produce more
8.26 J/kg of body mass for SJs and CMJs, respectively. work (resulting in greater energy, higher velocity) during
The total work performed during a jump is equal to the the propulsive phase. Figure 10-6 provides a typical profile
change in energy of the system (Esystem). In other words for the instantaneous power generated during SJs and
the combined change of the system’s kinetic and potential CMJs.1 From the graph, it is clear that peak power is
energy (KEsystem PEsystem). higher in CMJs and occurs just prior to takeoff. The
power output drop seen immediately before takeoff in
Work performed Esystem Esystem PEsystem
Figure 10-6 parallels the drop seen in vertical velocity and
Although most of the work done by the muscles is used is attributed to the inability of the legs to generate high
to impart potential and kinetic energy to the body’s COM as movements as they near full extension. Peak power values
it accelerates upward, some is used to move the COM hori- have been reported by Harman and colleagues for physi-
zontally and provide rotational energy to the body segments. cally active adults5 performing various jump types and are
This is frequently thought of as inefficient energy because it presented in Table 10-1. In addition, Cormie and col-
is essentially “lost” and does not contribute to jump height. leagues provide evidence that power production is related
An efficacy ratio has been computed to relate the effective to experience, finding that experienced jumpers produced
energy (i.e., energy associated with the vertical movement 28% more power compared with inexperienced jumpers
and position of the COM) to the total energy of the system (71.74 10.69 W/kg of body mass vs. 55.89 7.96
or work performed by the muscles. This ratio has been found W/kg).23 Although it is not immediately apparent from
to be approximately 0.86 to 0.87 for maximal vertical jumps Figure 10-6, average power is also higher in CMJs (see
(indicating approximately 13% to 14% of the work performed Table 10-1). Keep in mind when evaluating the work and
by the muscles was “lost” to horizontal movement or seg- power in a vertical jump that it is important to look at
ment rotation) but increases for lower-intensity jumps.19 normalized values (e.g., work and power expressed as J/
Vanrenterghem and colleagues found, in studying jumps of kg and W/kg) as well as absolute values. This allows for
increasing height, the amount of noneffective energy in- more effective comparisons to be made across subjects
creased from 3% in the lowest-intensity jumps (25% of maxi- who may have different body masses.
mum jump height) to 14% for maximal jumps.20
Power is a measure of how quickly work is performed
during the propulsive phase (in other words, power equals
Clinical Point
the work performed divided by the time it took to pro-
Experienced jumpers are able to jump higher than novice
duce the work, Power Work ), and peak lower-body power jumpers—as much as 28% higher—suggesting practice and
t
is frequently cited as the variable most tightly correlated training plays a role in how high an individual can jump.
with jump height.5,21,22 Again, considering that propulsion
240 SECTION II • Applied Biomechanics of Selected Sport Activities
4000
CMJ
SJ
2000
Power (W)
0
2000
4000
6000
1.2 0.9 0.6 0.3 0 0.3 0.6 0.9 1.2
Time (sec)
Figure 10-6
The time course of power production (and absorption) is shown for an athlete performing squat (gray)
and countermovement (black) jumps. Positive power indicates that power is being produced, whereas
negative power indicates power absorption during eccentric muscle contraction as the COM is decelerated
in the countermovement and on landing. The plots are aligned to the point of takeoff at which time
equals zero. (From Reiser R, Rocheford E, Armstrong CJ: Building a better understanding of basic
mechanical principles through analysis of the vertical jump, Strength Cond J 28[4]:70-80, 2006.)
Clinical Point
Clinical Point
The hip extensors provide 28% to 52% of the total work done
The inability of the muscles to effectively absorb the energy produced by the lower body in maximum effort vertical jumps. The
when landing from a jump is primary contributor to lower-limb knee extensors contribute 29% to 45% and ankle plantar flexors
injuries during jumping. 16% to 29%.
Applied Biomechanics of Jumping • CHAPTER 10 241
180
HIP HIP HIP HIP
15 300 1500
90
5 100 500
180
KNEE KNEE KNEE KNEE
15 300 1500
90
5 100 500
180
ANKLE ANKLE ANKLE ANKLE
15 300 1500
90
5 100 500
300 200 100 300 200 100 300 200 100 300 200 100
t (ms) t (ms) t (ms) t (ms)
Figure 10-7
Joint angles, angular velocities, joint moments, and instantaneous joint power are shown for the hip, knee,
and ankle during the execution of a one-foot (solid line) and two-foot (dashed line) countermovement
jump. The traces represent the average of 10 subjects, beginning with the initiation of the propulsive phase
and ending with takeoff (t 0). (From van Soest AJ, Roebroeck ME, Bobbert MF et al: A comparison of
one-legged and two-legged countermovement jumps, Med Science Sports Exerc 17[6]:635-639, 1985.)
The movement patterns have been shown to be fairly two-footed CMJs.13 The joint movements and power show a
consistent for a given athlete executing repeated maximal proximal-to-distal pattern that parallels the kinematic profile.
and moderate intensity vertical jumps. As an example, the The greatest movements are typically seen at the hip, whereas
coefficients of variation (standard deviation/mean) describ- the highest power is observed at the ankle. The hip moment
ing the variability in hip, knee, and ankle excursion during decreases during the duration of the propulsive phase,
vertical jumps achieving 50% or more of an individual’s whereas the knee and ankle movement increase during the
maximum height were 12.1%, 11%, and 20.5%, respectively. first part of the propulsive phase before decreasing during the
Variability was found to increase appreciably, however, final 150 ms of the jump. Table 10-2 summarizes the peak
for lower-intensity jumps representing only 25% of an joint movements, work, and peak power (normalized with
individual’s maximum.20 respect to body mass) reported for vertical jumps in the lit-
A number of studies have also examined the kinetics erature. Additional data for “un-normalized” peak joint
of individual joints and the contributions each of them movements13,15,24; work performed13,17; and peak power13 at
makes to jump performance, particularly the work and power the hip, knee, and ankle can also be found in the literature.
produced by the muscles acting at the hip, knee, and ankle The percentage of the total work performed by each
joints. Figure 10-7 shows the joint movements and power joint is presented in Table 10-3. These data are interesting
generated at the hip, knee, and ankle during typical one- and as they reflect how each joint affects the development of
242 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 10-2
Peak Movements, Total Work Performed, and Peak Power Are Reported for Various Jump Styles and Are Normalized
with Respect to Body Mass
Normalized Peak Movements (Nm/Kg) at the Hips, Knees, and Ankles During Maximal Vertical Jump Tasks
Movement Ankles Knees Hips Study
Normalized Peak Power (W/Kg) Performed During Maximal Vertical Jump Tasks
Movement Ankles Knees Hips Study
vertical velocity of the COM. Although there is some vari- provided a picture of how these muscles are activated in
ability, the hip extensors generally perform the majority of relation to the production of the vertical GRF (Figure
the work during maximal jumps (range 28% to 52% of the 10-8).25 The authors described a proximal-to-distal
total work). The knee and ankle extensors provide between activation pattern in the joint extensors with muscles
29% to 45% and 16% to 29% of the total work, respectively. being activated in the following order: semitendinosus,
Interestingly, Vanrenterghem and colleagues20 and Lees and biceps femoris–long head, gluteus maximus, vastus me-
colleagues12 both found that in submaximal jumps, the per- dialis, rectus femoris, soleus, and gastrocnemius. This
centage of work performed by the hips decreased, and work sequencing follows the proximal-to-distal movement pat-
output is dominated by the knees and ankles. tern seen in the kinematic data and lends additional
support to the idea that extension of the hips and back-
ward rotation of the trunk occurs prior to knee and ankle
Electromyography and Muscle Function extension.
Bobbert and van Ingen Schenau25 recorded the electro- Great interest, and much debate, has been centered on the
myographic (EMG) activity from selected lower limb function of the biarticular (two-joint) muscles in the lower
muscles of volleyball players while performing a CMJ and limb, specifically the rectus femoris and the gastrocnemius, as
Applied Biomechanics of Jumping • CHAPTER 10 243
Table 10-3
Percentage of Work Performed at the Hip, Knee, and Ankle During the Propulsive Phase of a Vertical Jump
Movement Ankles Knees Hips Study
Fy (N)
2000
1000
t (ms) 0
400 300 200 100 0
t (ms) 0
400 300 200 100 0
100
m. semitendinosus
50
t (ms) 0
400 300 200 100 0
100
m. gluteus
maximus 50
t (ms) 0
400 300 200 100 0
100
m. rectus
femoris 50
t (ms) 0
400 300 200 100 0
100
m vastus
mediaus 50
t (ms) 0
400 300 200 100 0
100
medial head of
m. gastrocnemus 50
t (ms) 0
400 300 200 100 0
100
m. soleus
50
t (ms) 0
400 300 200 100 0
Figure 10-8
Muscle activity recorded from the lower limb during a countermovement jump. The left trace shows the
vertical ground reaction force and lower-limb muscle activity for one subject performing a countermove-
ment vertical jump. The right trace shows averages for the same variables across 10 subjects. Electromy-
ography is expressed as a percentage of maximum activation. Trials have been synchronized at takeoff,
represented by time 0. Muscles studied include the biceps femoris long head, semitendinosus, gluteus
maximus, rectus femoris, vastus lateralis, gastrocnemius-medial head, and the soleus. (From Bobbert M,
van Ingen Schenau, GJ: Coordination in vertical jumping, J Biomech 21(3):249-262, 1988.)
when performing SJs (this was reduced to 50 ms in joint movements was not sufficient to “officially” classify
CMJs). Extension of the knee, similarly, began prior to them as using a sequential pattern.
extension of the ankle. An example of an athlete using the The proximal-to-distal pattern of activation has been
simultaneous strategy is shown in Figure 10-10. Note reported as the predominant, and optimal, movement
how the angular velocities, joint movements, joint pow- pattern for jumping vertically. This control scheme is
ers, and EMG for muscles at the hip, knee, and ankle all thought to (1) restrain the angular velocities of proximal
start at essentially the same time. Hudson, in a 1986 segments, allowing the athlete to stay in contact with the
study of twenty athletic individuals,14 found most subjects ground for as long as possible and the muscles to produce
used a simultaneous strategy when performing CMJs and work over their full shortening range; (2) optimally in-
SJs. However, the classification of a simultaneous strategy volve monoarticulate and biarticulate muscles and balance
was based on the criteria that adjacent joints provided the segmental contributions to the COM vertical velocity;
“positive contributions” more than 50% of the time. In and (3) maximize the efficacy of the work produced.21
actuality, although most subjects showed a sequential pat- With this pattern of activation, most of the energy is used
tern, the short time delay between the start of successive (productively) to propel the body vertically. Very little
Applied Biomechanics of Jumping • CHAPTER 10 245
300 300
Ankle joint Ankle joint
100 100
100 100
Nm 500 Angular vel.
Nm 500
Angular vel.
300 300
100
100
Net. moment
100
Net. moment 100
w 3000
w 3000
2000
2000
1000
1000
Power 0 Power
0
1000
1000
800
1500 uV m. glut. max.
uV m. glut. max.
0
0
500
800
m. add. magn.
m. add. magn.
0
0
2500
2500 m. rect. fem.
m. rect. fem.
0
0
1500
1500 m. vast. lat.
m. vast. lat.
0
0 800
2000 m. semit.
m. semit.
0
0 2000
2000 m. gastroc.
m. gastroc.
0
0 1500
1500 m. soleus
m. soleus
0 ms
0 ms
300 200 100 0 100
300 200 100 0 100
Figure 10-10
Figure 10-9
Kinematic (joint angular velocities), kinetic (joint movements, power)
Kinematic (joint angular velocities), kinetic (joint movements, power)
and muscle activity levels are presented for an athlete performing a
and muscle activity levels are presented for an athlete performing a
squat jump using a simultaneous movement pattern. Note how
squat jump using a sequential movement pattern. Note the proximal-
extension of the hip, knee, and ankle and development of joint
to-distal movement pattern, which is exemplified in the angular
movements occur in synchrony along with the mass activation of all
velocity, joint movement, and electromyography traces. (From
the muscles in the lower limb. (From Ravn S, Voigt M, Simonsen EB
Ravn S, Voigt M, Simonsen EB et al: Choice of jumping strategy
et al: Choice of jumping strategy in two standard jumps, squat and
in two standard jumps, squat and countermovement jump—effect of
countermovement jump—effect of training background or inherited
training background or inherited preference? Scand J Med Sci Sports
preference? Scand J Med Sci Sports 9:201-208, 1999.)
9:201-208, 1999.)
cost of executing the jump. Using submaximal jumping (Figure 10-12). Vanrenterghem and colleagues20 showed
protocols, Lees and colleagues6 and Vanrenterghem and that the peak hip extension movement increased systemati-
colleagues20 have been able to gain important insights into cally with jump height and intensity. The ankle movement
the way the body organizes movement. Figure 10-11 pro- was seen to peak during the 50% trials and the knee move-
files the average joint excursions for a group of 10 male ment reached its highest values in the 75% trials. Although
volleyball players executing vertical jumps representing the ankle movement did not change with increased jump
25%, 50%, 75%, and 100% of their maximums.20 Jump height, the knee movement was been found to decrease
height was found to correlate with the depth of the coun- significantly as an athlete jumped for maximal height.
termovement, but the greater depth for the high-intensity Similar findings have been provided by other researchers.6
jumps was achieved almost exclusively via an increased Qualitative analysis of the EMG shows this drop in knee
range of motion at the hip. The ankle joint excursion extensor movement to correspond with increased early ac-
remained consistent across all jump intensities, whereas the tivity of the biceps femoris, likely because of the increased
knee angle excursion did not change significantly for jumps forward lean in the maximum jumps and the increased hip
of 50% intensity and higher. extension movement, as well a decreased activity in the
Analysis of the joint movements yielded results that vastus lateralis and rectus femoris.
paralleled what was seen in the joint motion patterns In looking at the work and power performed during the
jumps, the total positive work performed increased with
each successive increase in jump intensity (Table 10-4).
Work output was low for all joints in the 25% condition
100% ankle
75% 4
ankle
angle (rad)
100%
50% 3
5
torque (N.m/kg)
75%
2 4
25%
50% 3
1 2
1.5 1 0.5 0 25% 1
Time (s) 0
1
0.3 0.2 0.1 0
Time (s)
100% knee
torque (N.m/kg)
50% 4 75%
angle (rad)
4
3 3
50%
25% 2 2
25% 1
1
1.5 1 0.5 0 0
1
Time (s) 0.3 0.2 0.1 0
Time (s)
100% hip
100% hip
75% 5 torque (N.m/kg)
75%
4
50% 4
angle (rad)
50% 3
3 2
25% 25% 1
2
0
1 1
1.5 1 0.5 0 0.3 0.2 0.1 0
Time (s) Time (s)
Figure 10-11 Figure 10-12
Averaged time curves for ankle (top), knee (middle), and hip (lower) Averaged time curves for ankle (top), knee (middle), and hip (lower)
joint angles recorded during maximal and sub maximal jumps are joint movements produced during the execution of maximal and sub-
shown for comparison. Note the progressive increase in hip range maximal jumps. Note the progressive increase in the hip extension move-
of motion with increased intensity while the motion at the ankle ment with jump intensity while the ankle and knee movements peak for
remains relatively constant for all jumps. All trials are aligned at lower-intensity jumps. Extension movements are denoted as positive and
takeoff (t 0). (From Vanrenterghem J, Lees A, Lenoir M, et al: all trials are aligned at takeoff (t 0). (From Vanrenterghem J, Lees A,
Performing the vertical jump: Movement adaptations for Lenoir M, et al: Performing the vertical jump: Movement adaptations
submaximal jumping, Human Mov Sci 22:713-727, 2004.) for submaximal jumping, Human Mov Sci 22:713-727, 2004.)
Applied Biomechanics of Jumping • CHAPTER 10 247
ankle AS - NAS
torque (N.m/kg)
4 1
torque (N.m/kg)
3
0.5
2
1 0
0 0 10 20 30 40 50 60 70 80 90
0 10 20 30 40 50 60 70 80 90 0.5
(a) % time % time
knee AS - NAS
torque (N.m/kg)
1
torque (N.m/kg)
4
3
0.5
2
1 0
a1 a2 a3 a4 a5 a6 0
0.5
0 10 20 30 40 50 60 70 80 90
1 0 10 20 30 40 50 60 70 80 90
0% 54% 68% 78% 90% 100% (b) % time % time
A descent ascent
hip AS - NAS
torque (N.m/kg)
1
torque (N.m/kg)
4
3
0.5
2
1 0
0 0 10 20 30 40 50 60 70 80 90
0.5
1 0 10 20 30 40 50 60 70 80 90
(c) % time % time
ankle AS - NAS
b1 b3 b6 20 4
B 0% 67% 100% 2
power (W/kg)
power (W/kg)
10
Figure 10-13 0
0 2 0 10 20 30 40 50 60 70 80 90
Positions of the body during the arm swing (A) and no-arm swing 0 10 20 30 40 50 60 70 80 90 4
(B) jumps. Position 1 start, 2 maximum arm hyperextension, 10 6
(a) % time % time
3 low point of countermovement, 4 arms in downward vertical
orientation, 5 arms reach horizontal orientation, 6 take-off. knee AS - NAS
Positions 2, 4, and 5 are omitted for the no-arms jump. (From power (W/kg)
20
2
power (W/kg)
Lees A, Vanrenterghem J, DeClerq D: Understanding how an 10
0
0 10 20 30 40 50 60 70 80 90
0 2
arm swing enhances performance in the vertical jump, J Biomech 10 0 10 20 30 40 50 60 70 80 90
4
37:1929-1940, 2004.) (b) % time % time
hip AS - NAS
ankle AS - NAS
20 4
power (W/kg)
power (W/kg)
15
angular velocity
angular velocity
15 2 10 2
10 1 5 0
(rad/s)
(rad/s)
0
5 0 5 0 2 0 10 20 30 40 50 60 70 80 90
10 20 30 40 50 60 70 80 90
10 4
0 1 0 10 20 30 40 50 60 70 80 90
(c) % time % time
5 0 10 20 30 40 50 60 70 80 90 2
% time % time
A ankle, knee and hip work done AS - NAS
6 0.6
work done (J/kg)
15 2 2
0.2
0
10 1
(rad/s)
2
(rad/s)
0 10 20 30 40 50 60 70 80 90 0
5 0 4 0.2 0 10 20 30 40 50 60 70 80 90
0 1 0 10 20 30 40 50 60 70 80 90 (d) % time % time
5 0 10 20 30 40 50 60 70 80 90 2
% time % time B
B
hip AS - NAS
Figure 10-15
angular velocity
15
1
10 and work (B) graphs for the ankles, knees, and hips for arm swing
(rad/s)
(rad/s)
5 0
0 1 0 10 20 30 40 50 60 70 80 90 (AS—thick line) and no-arm swing (NAS—thin line) swing vertical
5 0 10 20 30 40 50 60 70 80 90 2 jumps. The difference between the two jump styles (AS-NAS) is
% time % time
C shown to the right. (From Lees A, Vanrenterghem J, DeClerq D:
Understanding how an arm swing enhances performance in the
Figure 10-14 vertical jump, J Biomech 37:1929-1940, 2004.)
Averaged time-normalized angular velocities for the (A) ankle, (B) knee,
and (C) hip during the execution of countermovement jumps with an
arm swing (AS—thick line) and no-arm swing (NAS—thin line). The
difference between the AS and NAS jumps is shown at the right. (From
Lees A, Vanrenterghem J, DeClerq D: Understanding how an arm swing with 6.81 J/kg for jumps with no arm swing. This ob-
enhances performance in the vertical jump, J Biomech 37:1929–1940, served increase was largely attributable to the work per-
2004.) formed by the shoulder and elbow musculature, which
produced 0.63 0.26 g and 0.28 0.26 J/kg of work,
respectively (accounting for approximately 16% of the
Further evidence has been provided by Lees and col- total work performed during the arm-swing jumps). The
leagues12 who found that the arm swing induces greater arm swing also augmented the work done at the hip,
forward rotation of the trunk (which has been shown to which increased from 2.84 0.78 J/kg to 3.24 0.62
augment lower-body power) as well as an increase in the J/kg. Similar findings were made by Hara and col-
positive work done by the joints, 8.15 J/kg compared leagues,18 who found the arm swing increased the positive
Applied Biomechanics of Jumping • CHAPTER 10 249
Individual scores on temporal factor Box 10-1 Using Vertical Jumps as a Training Tool
-4 -2 0 2 4
4 Vertical jumps can also be used to build lower-body power and are
often used as a strength and conditioning exercises. The points listed
here should be considered when determining how to integrate
Individual scores on force factor
CMJ CMJ
CDJ CDJ
BDJ 30 15 BDJ
600 600
HIPS 20 HIPS
10 400 400
10 5 200 200
400300 600500400
0 0 0 0
600500400300200 100 600 500 100 600500400300200100 300 100
5 200 200
10 400 400
20 800 6000
30 15 600 3000
KNEES 20 10 KNEES 400 2000
10 5 200 1000
400300
0 0 0 0
600 500 400 300 200 100 600500 200100 600500400300200100 600500400300200100
5 200 1500
3000
15
600 2000
30 10
ANKLES ANKLES 400 1000
20 5 400300200
400 300 200 200 0
10 0 600 500 100
600 500 100 0 1500
0 5 600500400300200100
600500400300200100 2000
10
3000
15
A B 6000
Figure 10-19
Joint kinematics (A) and kinetics (B) for countermovement jumps (CMJ), countermovement depth
jumps (CDJ), and bounce depth jumps (BDJ). Arrows indicate the start of the propulsive phase for
each jump type. (From Bobbert MF, Huijing P, van Ingen Schenau GJ: Drop jumping I: The influence
of jumping technique on the biomechanics of jumping, Med Sci Sports Exerc 19[4]:332-338, 1987.)
OFFICIAL
DISTANCE
.12 –.05
.93*
TAKEOFF FLIGHT LANDING
DISTANCE DISTANCE DISTANCE
.45 .12
.83* –.05
.77* .40
Figure 10-20
The deterministic model of long jump performance correlates various factors to jump performance.
(From Hay J, Miller J, Canterna RW: The techniques of elite male long jumpers, J Biomech 19[10]:
855-866, 1986.)
Applied Biomechanics of Jumping • CHAPTER 10 255
4L 4L 4L
3L 3L 3L
2L 2L 2L
L L L
J J
Figure 10-21
Analysis of the stride characteristics in the final strides leading to takeoff in the long jump shows the
flight distance is shorter for the final stride, the plant foot is placed down further in front of the center
of mass (COM) on the last step, and the position of the COM relative to plant foot is shortened at
takeoff. (From Hay J: Citius, altius, fortius (Faster, higher, longer): The biomechanics of jumping for
distance, J Biomech 26(Suppl 1):7-21, 1993.)
256 SECTION II • Applied Biomechanics of Selected Sport Activities
TOLS TD MKF TO
11
10
9 VX
8
7
Velocity (m.s1)
6
5
4 VY
3
2
1
0
1 VZ
0.00 0.05 0.10 0.15 0.20 0.25 0.30 0.35
Time (s)
Figure 10-22
Center of mass (COM) velocity profile during the execution of a long jump. The mean velocity of the
COM was tracked in three dimensions during the final stride and takeoff during the long jump. Vx, Vy,
and Vz are the horizontal, vertical, and mediolateral velocities, respectively. MKF, Point of maximum
knee flexion; TD, touch down; TO, takeoff into the jump; TOLS, take off from the last stride. (From
Graham-Smith P and Lees A: A three-dimensional kinematic analysis of the long jump take-off, J Sport
Sci 23(9):891-903, 2005.)
Applied Biomechanics of Jumping • CHAPTER 10 257
approach and takeoff.58,59 Typically athletes leave the ground to six times an individual’s BW when landing from moderate
with a small amount of angular momentum that, if heights on one or two legs,70,71 and can exceed nine times an
unchecked, would cause the body to somersault forward in individual’s BW when landing from a jump height of a meter
the air. Skilled athletes use one of two techniques to control (3.3 feet) or more.72 The inability to dissipate the energy
this angular momentum. Some will raise their arms and associated with landing can lead to acute injuries, such as a
extend their legs to increase the body’s moment of inertia tear of the anterior cruciate ligament (ACL), or a chronic,
and slow the forward rotation. More commonly, athletes use overuse injury like patellar tendinopathy (i.e., jumper’s knee).
a modified running technique in the air, using the motions Muscles act as the primary shock absorbers when landing
of the arms and legs to check the forward angular momen- from a jump and the eccentric contractions that occur in
tum of the body and position the body for landing. many of the limb extensors are important for absorbing
much of the energy of the landing.73 However, other lower-
limb structures, including the ACL, bear some of the burden.
Broad Jump Kinematics and Kinetics Consequently, the techniques used when landing are critical
The broad jump is commonly used as a testing tool to assess to preventing overload to any one structure that could
lower-body power, but also has a place in many sporting lead to injury either acutely or in time with repetitive
activities. Although not studied as extensively as the vertical jumps.74,75
jump, several investigators have reported kinetic and kine-
matic data related to performance in the standing broad
jumps.65-67 One of the most comprehensive studies was Clinical Point
recently conducted by Hara and colleagues67 who looked at
broad jumping mechanics and specifically the contributions Of noncontact jumping injuries, 58% to 63% occur during landing
made by the arms. Figure 10-23 shows average joint angles, and 61% to 72% of those occur to the knee.
angular velocities, and joint movements during the perfor-
mance of three jump “types”67: (1) a forward jump with no
arm swing, (2) a forward jump with a forward arm swing,
and (3) a forward jump with a backward arm swing. Figure Clinical Point—Landing Forces Exert
10-24 shows the corresponding joint power and work data.
• Three to six times body weight from moderate heights
The main findings were that the velocity and jump distance
• More than nine times body weight from 1 meter (3.3 feet)
were increased with the addition of an arm swing65,67 and
or more
that the arm swing contributed positive work directly to the
jump while also augmenting the work performed by the
lower limbs (Table 10-6). The increase in lower-body work
was primarily attributable to increases in the hip extension Landing Kinetics
movement as the arm swing loaded the lower limb and Researchers have identified two primary landing “styles”76,77:
slowed the extension velocity of the hip. This mechanism is a toe-heel style and a flatfoot style (although toe-only, heel-
similar to what was found when an arm swing was added to only, and heel-toe variations may also be used with lower
a vertical jump. Although the peak movement was not frequencies). In landing with a toe-heel pattern, an individ-
higher with the inclusion of an arm swing, the movement ual typically produces a bimodal GRF profile (Figure 10-25)
was increased in the time surrounding the peak, leading to in which the first peak occurs with toe contact (F1) and
the observed increase in work and power at this joint. the second, larger peak, occurs with heel contact (F2).78,79
Valiant and Cavanaugh found the first and second peak aver-
Landing from a Jump age 1.3 and 4.1 times an individual’s BW, respectively, in
individuals landing from a simulated basketball rebound.77
Overview Flatfoot landings produce a unimodal GRF pattern with
Although the mechanics underlying a jump are important for peak reaching forces rising in excesses of six times BW.77 The
maximizing performance, the mechanics used in landing are demands placed on the structures of the leg are closely
more commonly associated with injury and injury preven- linked to the type of jump that is performed. Bisseling saw
tion. Gray and colleagues68 and Gerberich and colleagues69 marked differences in landing from a block jump compared
have found that between 58% and 63% of the noncontact with a spike jump in volleyball, for example; the vertical GRF
injuries seen in jumping sports are associated with the land- experienced after a spike jump was 64% higher than what
ing, and between 61% to 72% of those injuries occur at the was seen in landing from a block jump and 46.7% higher
knee. The high incidence of lower-limb injury is related to than the landing force experienced when landing from a
the high impact forces that occur with landing and the countermovement vertical jump.80 The peak joint move-
amount of energy that must be dissipated during a short time ments, powers, and loading rates all increased in parallel with
(see power curve in Figure 10-6). Peak forces can reach three the greater GRFs. Interestingly, individuals landing with a
258 SECTION II • Applied Biomechanics of Selected Sport Activities
FJ
FJF
FJB
150 1000
200
Elbow
100 500
50 0
0.8 0.6 0.4 0.2 0 0
0.8 0.6 0.4 0.2 0
0 500
0.8 0.6 0.4 0.2 0
50 1000 200
150 1000
Shoulder
200
100 500
50 0
0.8 0.6 0.4 0.2 0 0
0.8 0.6 0.4 0.2 0
0 500
0.8 0.6 0.4 0.2 0
50 1000 200
150 1000
200
100 500
Hip
50 0
0.8 0.6 0.4 0.2 0 0
0.8 0.6 0.4 0.2 0
0 500
0.8 0.6 0.4 0.2 0
50 1000 200
150 1000
200
100 500
Knee
50 0
0.8 0.6 0.4 0.2 0 0
0.8 0.6 0.4 0.2 0
0 500
0.8 0.6 0.4 0.2 0
50 1000 200
150 1000
200
100 500
Ankle
50 0
0.8 0.6 0.4 0.2 0 0
0.8 0.6 0.4 0.2 0
0 500
0.8 0.6 0.4 0.2 0
50 1000 200
Figure 10-23
Average joint angles, angular velocities, and torques and movements for the elbow, shoulder, hip, knee,
and ankle in the performance of forward jumps (FJ) (thin black line), forward jumps with a forward arm
swing (FJF) (thick black line), and forward jumps with a backward arm swing (FJB) (gray line). The
positive direction represents extension for all joints except the shoulder, which is positive for shoulder
flexion. (From Hara M, Shibayama A, Arakawa H et al: Effect of arm swing direction on forward and
backward jump performance, J Biomech 41:2806-2815, 2008.)
toe-only pattern, in which the heels never touch the ground, players have been found to perform and land from 219
have been shown to produce peak GRFs that are 22% lower 7.4 jumps in a typical match,81 whereas indoor volleyball
than in toe-heel jumps.76 players may perform between 300 and 500 blocks and
Looking at specific activities, it is possible to get an idea spikes during a 4-hour practice.82 Similarly, it is not uncom-
of how much jumping athletes do during practice and com- mon for dancers to land 100 jumps in a 90-minute practice
petition and why injuries are so common. Beach volleyball session. However, the demands placed on the lower body
Applied Biomechanics of Jumping • CHAPTER 10 259
FJ
Table 10-6
FJF
Kinematic and Kinetic Comparison of Standing Broad
Jumps with and without an Arm Swing
FJB Forward Jump Forward Jump
with No-Arm with a Forward
Power (W) Work (J)
Variable Swing Arm Swing
2500 500
1500
400
Jump distance (m) 2.08 0.29 2.39 0.32
300
COM velocity 3.34 0.59 3.60 0.44
Elbow
500 200
at takeoff (m/s)
0.8 0.6 0.4 0.2 0 100
500 Total work (J) 514 77 583 96
0
1500
0.8
100
0.6 0.4 0.2 0 Work performed 322 53 361 53
at hips (J)
2500 500
Work performed 47 37 44 31
1500 400
at knees (J)
300
132 15 140 18
Shoulder
500 200
Work performed
0.8 0.6 0.4 0.2 0 100
at ankles (J)
500
0
Work performed — 5 19
0.8 0.6 0.4 0.2 0
1500
100 at shoulders (J)
2500 500 Work performed — 17 12
400 at elbows (J)
1500
300
500 200 Modified from Hara M, Shibayama A, Arakawa H et al: Effect of
Hip
0.8 0.6 0.4 0.2 0 100 arm swing direction on forward and backward jump performance,
500
0 J Biomech 41:2806-2815, 2008.
1500 0.8 0.6 0.4 0.2 0
100 COM, Center of mass.
2500 500
1500 400
300
500
Knee
200 30
0.8 0.6 0.4 0.2 F2
Ground reaction force (N/kg)
0 100
500
0 25
1500 0.8 0.6 0.4 0.2 0
100
2500 500 20
400
1500
300 15
500
Ankle
200
0.8 0.6 0.4 0.2 0 100 10 F1
500
0
0.8 0.6 0.4 0.2 0
1500 100 5
Time (s) Time (s)
Figure 10-24 0
Average joint power and work produced during the performance of 0 20 40 60 80 100 120 140
forward jumps (FJ) (thin black line), forward jumps with a forward Time (msec)
arm swing (FJF) (thick black line), and forward jumps with a back- Figure 10-25
ward arm swing (FJB) (gray line). The positive direction represents Vertical ground reaction forces during a landing from a jump. F1 and
extension for all joints except the shoulder, which is positive for F2 represent the two ground reaction force peaks associated with a
shoulder flexion. (From Hara M, Shibayama A, Arakawa H et al: toe-heel landing from a jump. (From Dufek J, Bates B: Biomechanical
Effect of arm swing direction on forward and backward jump factors associated with injury during landing in jump sports, Sports Med
performance, J Biomech 41:2806-2815, 2008.) 12(5):326-337, 1991.)
Table 10-7
Kinematic and Kinetic Differences Between Three Types of Depth Jumps
Variable Joint DJ20 DJ40 DJ60
Modified from Bobbert MF, Huijing P, van Ingen Schenau GJ: Drop jumping II: The influence of drop jump height on the
biomechanics of drop jumping, Med Sci Sports Exerc 19:339-346, 1987.
DJ20, Drop jump from 20 cm height; DJ40, drop jump from 40 cm height; DJ60, drop jump from 60 cm height; Mmax,
maximum joint moment; Pmax, peak joint power; Wneg, negative work.
Data represents the average of six subjects.
Applied Biomechanics of Jumping • CHAPTER 10 261
One primary area of concern is the knee, specifically the 1.6 times increased risk of injury.95 When the quadriceps
varus and valgus movement and movements experienced as muscles contract near full knee extension, they produce
an athlete lands.87,92-94 Females have consistently been an anterior shear force at the knee, which can, in turn,
shown to experience greater maximum knee valgus as well increase ACL strain versus what it would experience from
as a greater valgus range of motion, and this is thought to the jump landing alone.96 Appropriately timed activation
be a significant risk factor.87,92 Kernozek and colleagues of hamstring muscles that are sufficiently strong could
found that recreationally active females experience maxi- reduce the magnitude of anterior shear and reduce the
mum knee valgus angles of 24.9° 8.5°, whereas the risk of injury.97 Large strength imbalances have been
males studied achieved varus angles of 0.7° 6.9° when noted in the upper leg of females, often in conjunction
landing from a 60-cm (24-inch) drop.87 Although the find- with increased quadriceps activity and decreased ham-
ing that females experience increased knee valgus has been strings activity on landing compared with males.98-100
well substantiated in the literature, the extent of the dis- Bennett and colleagues, however, caution against using
crepancy between males and females has been disputed. peak forces or movements to evaluate strength imbalances
Hughes and colleagues suggest the magnitude of valgus as they do not take into consideration the dynamics of an
may depend on experience,92 because a group of collegiate activity nor do they take into account where in the range
athletes landed with less knee valgus than the recreational of motion those peaks occur.101
athletes in the Kernozek study (Figure 10-26—female av-
erage angle 10.4° 7.7° of valgus). In addition, Kernozek
and colleagues87 has speculated that the ability to generate Clinical Point
an internal varus moment may be insufficient for control-
Individuals with weak hamstrings (relative to the quadriceps) are at
ling the valgus position of the knee, particularly at the
an increased risk for knee injury when landing from a jump.
point of peak valgus, suggesting weakness may be a con-
tributing factor to the motion experienced at the knee. It
is unknown whether the increased knee valgus seen in fe-
males is a performance effect or due to anatomic differ- Because of the factors affecting acute injury to the knee,
ences between males and females. Females tend to have a efforts to improve landing mechanics have historically focused
larger Q-angle, which is often associated with increased on improving the mechanics of the landing, which usually
valgus loads. Regardless, an increased valgus torque, espe- includes manipulating factors such as contact patterns, foot
cially when coupled with anterior shear at the knee, in- placement, and limb geometries to lower GRFs, and address-
creases the load on the ACL. ing strength imbalances in the leg to mechanically reduce the
Strength imbalances in the lower limb are also thought shear forces experienced at the knee.102-106 Several studies
to contribute to an increased injury risk in females. Of have, in fact, shown it is possible to affect changes in landing
particular interest is the ratio of hamstring-to-quadriceps mechanics through neuromuscular training programs. Hewett
strength as individuals with a hamstring to quadriceps and colleagues found a 6-week training program designed to
strength ratio less than 0.75 are thought to be at a improve jumping and landing technique was able to decrease
landing forces by 22%, reduce the knee varus and valgus
movements by 50%, and increase the hamstring-to-quadriceps
strength ratio by 13% and 26% in the dominant and non-
10 dominant legs in female athletes, respectively.102,103 But others
Knee valgus (–) / varus (+) (°)
Related to chronic and overuse injuries, patellar tendi- 4. Ham D, Knez W, Young, WB: A deterministic mode of the verti-
nopathy (i.e., jumper’s knee) occurs most frequently and is cal jump: Implications for training, J Strength Cond Res
21(3):967–972, 2007.
seen in approximately 20% of the athletes participating in
5. Harman EA, Rosenstein MT, Frykman PN, et al: The effects of
jumping sports. The highest rates of occurrence are seen in the arms and countermovement on vertical jumping, Med Sci
male volleyball, in which 34% to 40% of elite athletes have Sport Exerc 22:825–833, 1990.
reported experiencing this injury.109-111 Rates of occurrence 6. Lees A, Vanrenterghem J, DeClerq D: The energetics and ben-
are typically lower in females, affecting approximately 7% of efit of an arm swing in submaximal and maximal vertical jump
performance, J Sport Sci 24(1):51–57, 2006.
the elite female volleyball players.110 As with ACL injuries,
7. Vanezis A, Lees A: A biomechanical analysis of good and
it is believed that both biomechanical and muscular factors poor performers of the vertical jump, Ergonomics 48(11–14):
contribute to jumper’s knee. Bisseling found that athletes 1594–1603, 2005.
with a history of jumper’s knee employ a “stiffer” landing 8. Urgrinowitsch C, Tricoli V, Rodacki ALF, et al: Influence of
strategy and that GRFs can be reduced when landing with training background on jumping height, J Strength Cond Res
21(3):848–852, 2007.
greater knee flexion and ankle plantar flexion.80 This stiff-
9. Feltner ME, Fraschetti DJ, Crisp RJ: Upper extremity augmenta-
ness, although related to joint configuration, may also have tion of lower extremity kinetics during countermovement vertical
an age dependence as well; older individuals tend to exhibit jumps, J Sport Sci 17:449–466, 1999.
greater limb stiffness.112 Other proposed injury mechanisms 10. Feltner ME, Bishop EJ, Perez CM: Segmental and kinetic contri-
surrounding jumper’s knee have been related to anatomic butions in vertical jumps performed with and without an arm
swing, Res Q Exerc Sport 75(3):216–230, 2006.
and muscular factors (e.g., overall upper leg strength, with
11. Challis J: An investigation of the influence of bi-lateral deficit on
particular emphasis on the vastus medialis oblique, ham- human jumping, Human Mov Sci 17:307–325, 1988.
string and quadriceps flexibility, leg-length discrepancy, foot 12. Lees A, Vanrenterghem J, DeClerq D: Understanding how an
pronation) although the relative contributions to injury are arm swing enhances performance in the vertical jump, J Biomech
debated in the literature.113-115 One additional factor to 37:1929–1940, 2004.
13. Van Soest AJ, Roebroeck ME, Bobbert MF, et al: A comparison
consider is rest and recovery. As jumper’s knee typically
of one-legged and two-legged countermovement jumps, Med Sci
presents itself as an overuse injury, lack of recovery between Sports Exerc 17(6):635–639, 1985.
intense workouts is believed to contribute to the injury 14. Hudson J: Coordination of segments in the vertical jump, Med
mechanism as well.80 Sci Sports Exerc 18(2):242–251, 1986.
15. Bobbert MF, Gerritsen KGM, Litjens MCA, et al: Why is coun-
termovement jump height greater than squat jump height? Med
Conclusion Sci Sports Exerc 28(11):1402–1412, 1996.
16. Hubley C, Wells R: A work-energy approach to determine indi-
Jumping is a complex biomechanical task and myriad vari- vidual joint contributions to vertical jump performance, Eur J
ables can and do affect jump performance and injury risk. Appl Physiol 50:247–254, 1983.
In the vertical jump, performance ultimately boils down to 17. Stefanyshyn D, Nigg B: Contributions of the lower extremity
joints to mechanical energy in running vertical jumps and run-
producing a high vertical velocity at takeoff and this is, in
ning long jumps, J Sport Sci 16:177–186, 1998.
turn, affected by such variables as muscle strength, power, 18. Hara M, Shibayama A, Takeshita D, et al: The effect of arm
and rate of force development as well as the coordinated swing on lower extremities in vertical jumping, J Biomech
integration of a countermovement and arm swing. In addi- 39:2503–2511, 2006.
tion, sport-specific constraints affect the technique used and 19. Bobbert, M, van Soest AJ: Why do people jump the way they do?
Exerc Sport Sci Rev 29(3):95–102, 2001.
the height attained when executing a vertical jump. Similar
20. Vanrenterghem J, Lees A, Lenoir M, et al: Performing the verti-
factors also play a role in the standing broad jump. In the cal jump: Movement adaptations for submaximal jumping,
long jump, the approach mechanics and the kinetics of the Human Mov Sci 22:713–727, 2004.
takeoff are what largely determine jump distance. When 21. Aragon-Vargas L, Gross M: Kinesiological factors in vertical
considering injuries, most noncontact leg injuries occur on jump performance: Differences among individuals, J Appl
Biomech 13:24–22, 1997.
landing from a jump and an individual’s susceptibility to
22. Aragon-Vargas L, Gross M: Kinesiological factors in vertical jump
injury depends on the landing technique as well as on performance: Differences within individuals, J Appl Biomech
lower-limb strength. 13:46–65, 1997.
23. Cormie P, McBride JM, McCaulley GO: Power-time, force-
time, and velocity-time curve analysis of the countermovement
References jump: Impact of training, J Strength Cond Res 23(1):177–186,
2009.
1. Reiser R, Rocheford E, Armstrong CJ: Building a better under- 24. Fukashiro S, Komi PV: Joint moment and mechanical power flow
standing of basic mechanical principles through analysis of the of the lower limb during vertical jump, Int J Sports Med
vertical jump, Strength Cond J 28(4):70–80, 2006. 8(Suppl):15–21, 1987.
2. Hay J, Reid JR: Anatomy, mechanics and human motion, 25. Bobbert, M, van Ingen Schenau, GJ: Coordination in vertical
Englewood Cliffs, 1988, Prentice-Hall. jumping, J Biomech 21(3):249–262, 1988.
3. Vint P, Hinrichs R: Differences between one-foot and two-foot 26. Bobbert MF, van Soest AJ: Two-joint muscles offer the
vertical jump performances, J Appl Biomech 12:338–358, solution, but what was the problem? Motor Control 4:48–52,
1996. 2000.
Applied Biomechanics of Jumping • CHAPTER 10 263
27. Gregoire L, Veeger H, Huijing P, et al: Role of mono- and 50. Dapena J, McDonald J, Cappaert J: A regression analysis of high
biarticular muscles in explosive movements, Int J Sports Med jumping technique, Int J Sports Biomech 6:246–261, 1990.
5:301–305, 1984. 51. McEwen F: High jump: Teaching the Fosbury Flop, Modern
28. Prilutsky B: Coordination of two- and one-joint muscles: Func- Athlete & Coach 45(4):10–14, 2007.
tional consequences and implications for motor control, Motor 52. Laffaye G, Bardy B, Durey A: Principal component structure and
Control 4:1–44, 2000. sport-specific differences in the running on-leg vertical jump, Int
29. Prilutsky B: Muscle coordination: The discussion continues, J Sports Med 28:420–425, 2007.
Motor Control 4:97–116, 2000. 53. Holcomb W, Lander J, Rutland RM, et al: A biomechanical
30. Van Ingen Schenau GJ, Bobbert M, Rosendal RH: The unique analysis of the vertical jump and three modified plyometric depth
action of bi-articular muscles in complex movements, J Anat jumps, J Strength Cond Res 10(2):83–88, 1996.
155:1–5, 1987. 54. Bobbert MF, Huijing P, van Ingen Schenau GJ: Drop jumping I:
31. Van Soest AJ, Schwab A, Bobbert MF, et al: The influence of the The influence of jumping technique on the biomechanics of
biarticularity of the gastrocnemius muscle on vertical-jumping jumping, Med Sci Sports Exerc 19(4):332–338, 1987.
achievement, J Biomech 26(1):1–8, 1993. 55. Alexander R: Optimum take-off techniques for high and long
32. Anderson F, Pandy M: Storage and utilization of elastic strain jumps, Phil Trans R Soc Lond B329:3–10, 1990.
energy during jumping, J Biomech 26(12):1413–1427, 1993. 56. Graham-Smith P, Lees A: A three-dimensional kinematic
33. Pandy M, Zajac F: Optimal muscular coordination strategies for analysis of the long jump take-off, J Sport Sci 23(9):891–903,
jumping, J Biomech 24(1):1–10, 1991. 2005.
34. Ravn S, Voigt M, Simonsen EB, et al: Choice of jumping strategy 57. Hay J: Citius, altius, fortius (faster, higher, longer): The biome-
in two standard jumps, squat and countermovement jump— chanics of jumping for distance, J Biomech 26(Suppl 1):7–21,
Effect of training background or inherited preference? Scand 1993.
J Med Sci Sports 9:201–208, 1999. 58. Hay J, Miller J, Canterna RW: The techniques of elite male long
35. Khalid W, Armin M, Bober T: The influence of the upper jumpers, J Biomech 19(10):855–866, 1986.
extremities movement on take-off in vertical jump. In Tsarouchas 59. Hay J, Nohara H: Techniques used by elite long jumpers in
VL, Terauds J, Gowitzke B, Holt L, editors: Biomechanics in preparation for takeoff, J Biomech 23(2):229–239, 1990.
sport V, Athens, Greece, Hellenic Sports Research Institute, 60. Kyrolainen H, Avela J, Komi PV, et al: Function of the neuromus-
1989. cular system during the two last steps in the long jump. In
36. Luhtanen P, Komi PV: Segmental contributions to forces in deGroot H, Huijing PA, and van Ingen Schenau GJ: Biomechanics
vertical jumps, Eur J Appl Physiol Occup Ther 38:181–188, XI-B, Amsterdam, 1998, Free University Press.
1978. 61. Lees A, Fowler N, Derby D: A biomechanical analysis of the last
37. Shetty A, Entyre B: Contribution of arm movement to the force stride, touch-down and take-off characteristics of the women’s
components of a maximum vertical jump, J Orthop Sports Phys long jump, J Sport Sci 11:303–314, 1993.
Ther 11:198–201, 1989. 62. Lees A, Graham-Smith P, Fowler N: A biomechanical analysis of
38. Payne A, Slater W, Telford T: The use of a force platform in the the last stride, touchdown, and takeoff characteristics of the
study of athletic activities, Ergonomics 11:123–143, 1968. men’s long jump, J Appl Biomech 10:61–78, 1994.
39. Enoka R: Neuromechanical basis of kinesiology, Champaign, IL, 63. Muraki Y, Ae M, Yokozawa T, et al: Mechanical properties of the
1988, Human Kinetics. take-off leg as a support mechanism in the long jump, Sports
40. Bosco C, Komi PV: Influence of countermovement amplitude in Biomech 4(1):1–16, 2005.
potentiation of muscular performance. In Marek A, Fidelis K, 64. Seyfarth A, Friedrichs A, Wank V, et al: Dynamics of the long
Kedzies K, Wit A, editors: Biomechanics VII-A, Baltimore, M, jump, J Biomech 32:1259–1267, 1999.
University Park Press, 1981. 65. Ashby B, Heegaard J: Role of arm motion in the standing long
41. Cavagna G, Dusman B, Margaria R: Positive work done by the jump, J Biomech 35:1631–1637, 2002.
previously stretched muscle, J Appl Physiol 24:21–32, 1968. 66. Ashby B, Delp S: Optimal control simulations reveal mecha-
42. Bobbert MF, Casius LJ, Sijpkens IWT, et al: Humans adjust nisms by which arm movement improves standing long jump
control to initial squat depth in vertical squat jumping, J Appl performance, J Biomech 39:1726–1734, 2006.
Physiol 105(5):1428–1440, 2008. 67. Hara M, Shibayama A, Arakawa H, et al: Effect of arm swing
43. Saunders H: A cinematographical study of the relationship direction on forward and backward jump performance, J Biomech
between speed of movement and available force, Dissertation. 41:2806–2815, 2008.
College Station, Texas A&M University, 1980. 68. Gray J, Taunton J, Taunton DC, et al: A survey of injuries to
44. Dapena J, Chung: Vertical and radial motions of the body during the anterior cruciate ligament of the knee in female basketball
the takeoff phase of high jumping, Med Sci Sports Exerc 20: players, Int J Sports Med 6:314–316, 1985.
290–302, 1988. 69. Gerberich SG, Luhmann S, Finke C, et al: Analysis of severe
45. Dapena J: Basic and applied research in the biomechanics of high injuries associated with volleyball injuries, Phys Sports Med
jumping, Med Sport Sci 25:19–33, 1987. 15(8):75–79, 1987.
46. Bobbert MF, De Graaf WW, Jonk JN, et al: Explanation of the 70. Adrian M, Laughlin C: Magnitude of ground reaction forces
bilateral deficit in human vertical squat jumping, J Appl Physiol while performing volleyball skills. In Kobayashi MA, editor:
100(2):493–499, 2006. Biomechanics VIII-B, Champaign, 1983, Human Kinetics.
47. Bobbert MF, Casius LJR: Is the effect of a countermovement 71. Steele J, Milburn P: Ground reaction forces on landing in
on jump height due to active state development? Med Sci Sports netball, J Human Mov Studies 13:399–410, 1987.
Exerc 37(3):440–446, 2005. 72. McNitt-Gray J: The influence of impact speed on joint kinematics
48. Vanrenterghem J, Lees A, DeClerq D: Effect of forward trunk and impulse characteristics of drop landings, 12th International
inclination on joint power output in vertical jumping, J Strength Congress of Biomechanics, Los Angeles, 1989.
Cond Res 22(3):708–714, 2008. 73. Devita P, Skelly P: Effect of landing stiffness on joint kinetics and
49. Dapena J: How to design the shape of a high jump run-up, Track energetics in the lower extremity, Med Sci Sports Exerc 24(1):
Coach 131:4179–4181, 1995. 108–115, 1992.
264 SECTION II • Applied Biomechanics of Selected Sport Activities
74. Kovacs I, Tihanyi J, Devita P, et al: Foot placement modifies 96. Withrow TJ, Huston, Wojtys EM, et al: The relationship
kinematics and kinetics during drop jumping, Med Sci Sports between quadriceps muscle force, knee flexion, and anterior cru-
Exerc 31(5):708–716. ciate ligament strain in an in-vivo simulated jump landing, Am J
75. Murphy D, Connolly D, Beynnon BD: Risk factors for lower- Sports Med 34:269–274, 2006.
extremity injury: A review of the literature, Br J Sports Med 97. Withrow TJ, Huston LJ, Wojtys EM, et al: A lengthening ham-
37(1):13–29, 2003. string contraction condition reduces ACL strain in and in-vitro
76. Dufek J: The effect of landing on lower extremity function, jump landing model: An ACL protective mechanism, 52nd Annual
Dissertation from the University of Oregon, 1988. Meeting of the Orthopaedic Research Society, Chicago, 2006.
77. Valiant G, Cavanaugh P: A study of landing from a jump: Impli- 98. Colby S, Francisco A, Yu B, et al: Electromyographic and
cations for the design of a basketball shoe. In Winter DA, kinematic analysis of cutting maneuvers, Am J Sports Med
Norman RW, Wells RP, et al: Biomechanics IX-B, Champaign, 28:234–240, 2000.
1985, Human Kinetics. 99. Lephart SM, Ferris CM, Reimann BL, et al: Gender differences
78. Dufek J, Bates B: The relationship between ground reaction forces and in strength and lower extremity kinematics during landing, Clin
lower extremity extensor joint moments in landing, Proceedings of the Orthop Relat Res 401:162–169, 2002.
14th Annual American Society of Biomechanics, Miami, 1990. 100. Malinak RA, Colby SM, Kirkendall DT, et al: A comparison of
79. Dufek J, Bates B: Biomechanical factors associated with injury knee joint motion patterns between men and women in selected
during landing in jump sports, Sports Med 12(5):326–337, athletic tasks, Clin Biomech 16:438–445, 2001.
1991. 101. Bennett DR, Blackburn JT, Boling MC, et al: The relationship
80. Bisseling R: Biomechanical determinants of the jumper’s knee in between anterior tibial shear force during a jump landing and
volleyball, Doctoral dissertation, University of Groningen, 2008. quadriceps and hamstring strength, Clin Biomech 23:1165–1171,
81. Turpin JP, Cortell JM, Chinchilla JJ, et al: Analysis of jump 2008.
patterns in competition for elite male beach volleyball players, 102. Hewett TE, Stroupe AL, Nance TA, et al: Plyometric training in
Int J Performance Anal Sport 8(2):94–101, 2008. female athletes: Decreased impact force and increased hamstring
82. Coleman J, Adrian M, Yamamato H: The teaching of the mechanics torques, Am J Sports Med 24(6):765–773, 1996.
of jump landing, Second National Symposium on Teaching Kine- 103. Hewett TE, Lindenfeld TN, Riccobene JV, et al: The effect of
siology and Biomechanics in Sport, DeKalb, IL, 1984. neuromuscular training on the incidence of knee injury in female
83. Chappell J, Yu B, Kirkendall DT, et al: A comparison of knee athletes, Am J Sports Med 27:699–706, 1999.
kinetics between male and female recreational athletes in stop- 104. Hewett TE, Ford K, Myer GD: Anterior cruciate ligament inju-
jumping, Am J Sports Med 30:261–267, 2002. ries in female athletes: Part 2, a meta-analysis of neuromuscular
84. Bobbert MF, Huijing P, van Ingen Schenau GJ: Drop jumping interventions aimed at injury prevention, Am J Sports Med
II: The influence of drop jump height on the biomechanics of 34:490–498, 2006.
drop jumping, Med Sci Sports Exerc 19:339–346, 1987. 105. Irmischer BS, Harris C, Pfeiffer RP, et al: Effects of a knee
85. Zelisko J, Noble H, Porter MA: A comparison of men’s and ligament injury prevention exercise program on impact forces in
women’s professional basketball injuries, Am J Sports Med women, J Strength Cond Res 18(4):703–707, 2004.
10(5):297–299, 1982. 106. Padua D, Marshall S: Evidence supporting ACL-injury prevention
86. Chandy T, Grana W: Secondary school athletic injury in boys and exercise programs: A review of the literature, Athletic Therapy
girls: A three-year comparison, Phys Sportsmed 13:314–316, 1985. Today 11:11–23, 2006.
87. Kernozek TW, Torry MR, van Hoof H, et al: Gender differences 107. Cronin J, Bressel E, Finn L: Augmented feedback reduces
in frontal and sagittal plane biomechanics during drop landings, ground reaction forces in the landing phase of the volleyball spike
Med Sci Sports Exerc 37(6):1003–1012, 2005. jump, J Sports Rehabil 17:148–159, 2008.
88. Hewett TE, Meyer G, Gregory D, et al: Biomechanical measures 108. Prapavessis H, McNair PJ: Effects of instruction in jumping
of neuromuscular control and valgus loading of the knee predict technique and experience jumping on ground reaction forces,
anterior cruciate ligament injury risk in female athletes: A pro- J Orthop Sports Phys Ther 29(6):352–356, 1999.
spective study, Am J Sports Med 33:492–501, 2005. 109. Ferretti A, Papandrea P, Conteduca F: Knee injuries in volleyball,
89. Padua DA, Carcia CR, Arnold BL, et al: Gender differences in Sports Med 10:132–138, 1990.
leg stiffness and stiffness recruitment strategy during two-legged 110. Gisslen K, Gyulai C, Soderman K: High prevalence of jumper’s
hopping, J Motor Behav 37:111–115, 2005. knee and sonographic changes in Swedish elite junior volleyball
90. Decker MJ, Torry MR, Wyland DJ, et al: Gender differences players compared to matched controls, Br J Sports Med 39:
in lower extremity kinematics, kinetics, and energy absorption 298–301, 2005.
during landing, Clin Biomech 18:662–669, 2003. 111. Lian O, Engebresten K, Bahr R: Prevalence of jumper’s knee
91. Cortes N, Onate J, Abrantes J, et al: Effects of gender and among elite athletes from different sports: A cross-sectional
foot-landing technique on lower extremity kinematics during study, Am J Sports Med 33:561–567, 2005.
drop-jump landings, J Appl Biomech 23:289–299, 2007. 112. Wang L, Lin D, Huang C: Age effects on jumping techniques
92. Hughes G, Watkins J, Owen N: Gender difference in lower and lower limb stiffness during vertical jump, Res Sports Med
limb frontal plane kinematics during landing, Sports Biomech 12:209–219, 2004.
7(3):333–341, 2008. 113. Blazina ME, Kerlan RK, Jobe FW: Jumper’s knee, Orthop Clin
93. Russell KA, Palmieri RM, Zonder SM, et al: Sex differences in North Am 4:665–678, 1973.
valgus knee angle during a single-leg drop jump, J Athl Training 114. Cook J, Kiss ZS, Khan KM: Anthropometry, physical perfor-
41(2):166–171, 2006. mance, and ultrasound patellar tendon abnormality in elite junior
94. Noyes FR, Barber-Westin SD, Fleckerstein C, et al: The drop- basketball players: A cross-sectional study, Br J Sports Med
jump screening test, Am J Sports Med 33(2):197–207, 2005. 38:206–209, 2004.
95. Knapick JJ, Bauman CL, Jones BH, et al: Preseason strength and 115. Witvrouw E, Bellemans J, Lysens R: Intrinsic risk factors for the
flexibility imbalances associated with athletic injuries in female development of patellar tendinitis in an athletic population, Am
collegiate athletes, Am J Sports Med 19:76–81, 1991. J Sports Med 29:190–195, 2001.
11
CHAPTER
Introduction both the forehand and backhand. Similar stages are used to
The modern game of tennis is characterized by specific describe the volley and half-volley strokes, with the former
inherent movement patterns that use sequential segmental characterized with ball contact prior to the ball striking the
rotations that ultimately result in powerful ground strokes court surface on the player’s side of the court and the latter
and serves and precise, accurate volleys. These characteristic pertaining to ball contact nearly immediately following the
movement patterns use the body’s entire kinetic chain to bounce, typically from a mid-court location.
produce power and optimize functional performance. Anal- The serve is studied and analyzed in a similar fashion to
ysis of the patterns of play in elite players identifies that 75% the throwing motion in many studies.2-4 It contains a wind-
or more of the shots hit in tennis involve the serve and up or preparation phase, arm-cocking phase, acceleration
forehand ground stroke,1 which use extremely powerful phase, and follow-though phase (Figure 11-1). The separa-
concentric shoulder internal rotation muscular work that tion between the preparation and arm-cocking phases
can lead to traditional muscular imbalances and predispose includes the initiation of the ball toss with the contralateral
the player to overuse injury. Although the primary scope of extremity with the initiation of the acceleration phase
this chapter is tennis, these muscular imbalances and char- occurring following maximal external rotation of the gleno-
acteristic concentric internal shoulder rotation use do apply humeral (GH) joint. Ball contact again separates the accel-
to nearly all racquet sports and overhead activities involving eration and follow-through phases as opposed to ball release
spiking, serving, and throwing. The primary purpose of this separating the same phases in the throwing motion.
chapter is to provide a detailed review of the biomechanics
of tennis strokes and movement patterns to give the clini-
cian an appreciation of the demands of the game of tennis Phases of a Tennis Serve
on the human body. This information has particular rele-
vance for understanding injury patterns, and anatomical • Wind-up (preparation) phase
adaptations and maladaptations in the tennis player’s • Arm-cocking phase
• Acceleration phase
musculoskeletal system.
• Follow-through phase
265
266 SECTION II • Applied Biomechanics of Selected Sport Activities
2
1
3
5
A 6
1 3 4
B 6
Figure 11-1
A, Traditional tennis serve. 1. Preparation phase; 2. Preparation phase; 3. Cocking phase (max external
rotation); 4. Early acceleration phase; 5. Late acceleration phase near ball contact; 6. Follow-through
phase. B, Abbreviated tennis serve. 1. Preparation phase; 2. Preparation phase; 3. Cocking phase (max
external rotation); 4. Acceleration phase; 5. Early follow-through phase; 6. Late follow-though phase.
Applied Biomechanics of Tennis • CHAPTER 11 267
higher muscular activity levels during the serve, indicating After the electrical silence of the shoulder musculature
that it is the most strenuous stroke in tennis from an upper- during impact or collision,9,10 forceful eccentric muscular
extremity muscular standpoint. contraction is necessary to decelerate the humerus and
The serve is broken down into the four previously men- maintain GH joint congruity.
tioned phases. The windup phase is characterized by the A relatively consistent pattern of muscular activity is
initiation of the serving stance to the toss of the ball by the reported for skilled tennis players. The presence of in-
contralateral extremity. There is very low electromyographic creased, as well as overlapping, muscular activity patterns
(EMG) activity during this phase in the muscles surround- across the outlined stages in the tennis serve has been
ing the shoulder.2 The second phase of the serving motion reported by untrained5 and less skilled10 tennis players. This
is the cocking phase, which begins after the ball toss and increase in the muscular contribution during the serving
terminates at the point of maximal external rotation of the motion in less-skilled players is a perfect example of how
GH joint of the racquet arm. Muscular activity during this nonoptimal timing and a lack of whole-body contributions
phase is moderately high in the supraspinatus, infraspinatus, to force generation and deceleration subject an individual’s
subscapularis, biceps brachii, and serratus anterior. Muscular shoulder to overuse injury. The contribution of the larger
activity levels expressed as a percentage of the maximum muscle groups in the lower extremities and trunk via proper
voluntary isometric contraction (MVC) were 53%, 41%, biomechanical energy transfer during the tennis serve pro-
25%, 39%, and 70%, respectively.2 The stabilizing and tect the player from injury and optimize performance.11-14
approximating role of the rotator cuff identified by Inman
and colleagues6 is clearly shown in the cocking phase of the
tennis serve.7 The moderately high activity during this Inherent Demands of Tennis on the Shoulder
phase shows the importance of both anterior and posterior The shoulder faces high loads in those playing tennis. Elite
rotator cuff strength, as well as scapular stabilization for players reach rotational velocities of up to 1700 deg/sec, re-
proper execution of the required mechanics for the cocking sulting in arm velocities of up to 72 miles per hour (115.2 kph)
phase.8 on the serve.15 The one-hand backhand stroke generates rota-
tional velocities up to 900 deg/sec (arm velocities of 34 miles
per hour [54.4 kph]), and the open-stance forehand generates
280 deg/sec, which, with trunk rotation through the
Clinical Point kinetic chain, created arm velocities of up to 46 miles per hour
Anterior (subscapularis) and posterior (infraspinatus and teres minor) (73.6 kph).15 Ranges of motion were found to be correspond-
rotator cuff muscles and scapular stabilizers (primarily trapezius and ingly large. Total arc of rotational motion (internal ⫹ external
serratus anterior) play a key role in the cocking phase. rotation) was between 160° and 180°.15
Torques generated in the serve by these loads and mo-
tions were found to be high at two critical times—maximum
external rotation (MER) during cocking and acceleration to
The third phase of the tennis serve is acceleration. This ball impact (ABI). At MER, men recorded 65 Nm and
phase begins at maximal external rotation and terminates at women 46 Nm. At ABI, men recorded 70 Nm and women
ball impact. Consistent with EMG recordings during the 50 Nm. Torques greater than 50 Nm are considered a
acceleration phase of throwing,4 high muscular activity was significant and potentially injurious factor in loading of the
found in the pectoralis major, subscapularis, latissimus upper extremity, so those inherent loads have the potential
dorsi, and serratus anterior during the forceful concentric to create overload injury.16
internal rotation of the humerus.2 EMG research published The deceleration force between the trunk and the arm at
by VanGheluwe and Hebbelinck9 using intermediate tennis ball impact and follow-through can be as high as 300 Nm.
players and by Miyashita and colleagues10 using skilled and This is required to stabilize and support the shoulder
unskilled tennis players also found high activity levels of the against the distraction forces that equal 0.5 to 0.75 times
pectoralis major, as well as the deltoid, trapezius, and body weight.
triceps, during the acceleration phase. Both reports showed These loads are placed on the shoulder with every stroke.
a relative silence of electrical activity in the accelerating The numbers of strokes per match vary greatly, depending
musculature during impact with peak levels of muscular on the type of match, skill level, opponent, and playing
activity occurring just before impact. One exception is surface. The average elite tennis match involves at least
the stabilizing contribution of the infraspinatus, which 100 repetitions of “game” serves and 250 repetitions of
remained active during impact.9 “game” ground-strokes.17 In junior tennis tournaments in
The fourth and final phase occurs after impact and is scholastic or collegiate tennis, these numbers are larger,
termed the follow-through. This phase is characterized by because two to three matches may be played per day. These
moderately high activity of the posterior rotator cuff, ser- numbers do not include the number of “practice” strokes,
ratus anterior, biceps brachii, deltoid, and latissimus dorsi. which in most estimates is four to five times higher.
268 SECTION II • Applied Biomechanics of Selected Sport Activities
The functional result of this stable base is considered to acceleration and allows the hand to go up and through the
represent core stability.27 In addition to generating force ball in follow-through to create topspin.
in the trunk and leg segments, kinetic chain activation Because the kinetic chain is composed of multiple seg-
through the core also generates force in the distal segments ments, there are multiple (up to 244) degrees of freedom
through the creation of interactive movements, or forces within the system.34 Preprogrammed muscle activations can
generated at joints by the position and motion of adjacent temporarily stabilize several links of the kinetic chain in
segments.28 At the shoulder, the interactive movement “coordinative structures” that convert multiple degrees of
produced by trunk rotation around a vertical axis is the freedom into one or two degrees of freedom.34 The task-
most important factor in generating forward arm motion, specific linkages have the effect of decreasing the degrees of
and the interactive movement produced by trunk rotation freedom within a linked system, creating maximal torques
around a horizontal axis from front to back is the most with minimal force development throughout the kinetic
important factor in generating arm abduction.17 chain. The result of these linkages is to create “nodes”—
The remaining kinetic chain segments play smaller roles specific body segment positions and motions that are fun-
in intrinsic force generation, mainly because of their smaller damental for efficiency and maximal sequencing of multiple
cross-sectional area and the production of interactive segment activations within a linked kinetic chain.34 Because
movements. The shoulder produces only 13% of the total of the task specific requirements of the nodes, each sport or
kinetic energy for the entire service motion. The high activity within a sport can have a unique set of nodes for
velocities and forces seen at the shoulder are predominantly that activity. From data compiled from a variety of scientific
produced through sequential kinetic chain activation. studies16-18,25,35-38 and from discussions with tennis
The shoulder functions in the kinetic chain primarily as a coaches,37,39 it has been determined that five specific nodes
funnel, transferring the forces developed in the engine of appear to be required in the tennis serve. These nodes are
the core to the delivery mechanism of the hand.24 Efficient observable in the tennis serve. In sequential order from the
activation of the segments within the kinetic chain regulates ground up, they are (1) adequate knee flexion in cocking
the loads seen at distal joints.23 In addition, the kinetic progressing to knee extension at ball impact, (2) hip and
chain can modify loads at the shoulder by aligning the trunk counter-rotation away from the court in cocking,
bones of the GH articulation so that ball-and-socket kine- (3) coupled scapular retraction and arm rotation to achieve
matics that produce concavity compression and stabilize the cocking in the scapular plane, (4) back leg–to–front leg
joint may be maximized through the majority of the range motion to create a “shoulder over shoulder” motion at
of motion (ROM) of the shoulder. Coordinated coupled ball impact, and (5) long-axis rotation into ball impact and
motions of the humerus and the scapula (scapulohumeral follow-through (Figure 11-2).
rhythm) keep the GH angle within 30° of the plane of the
scapula. This angle minimizes muscle activations required
for joint stability,29 keeps the compression forces directed
into the concavity of the glenoid,30 and minimizes strain of
the GH ligaments.31 These actions maximize the shoulder’s
role as a funnel for transfer of forces and motion of the
adjacent segments. Studies using baseball players have dem-
onstrated that at the moment of ball release, which is
equivalent to ball contact in tennis, only four body seg-
ments are responsible for forward movement of the arm.
They are trunk forward flexion, shoulder internal rotation,
elbow extension, and wrist flexion. Half of the force pro-
duced at the shoulder, 70% of the force produced at the
elbow, and more than 80% of the force produced at the
wrist is generated through the interactive moments.32,33
Beginner Elite
VLB
VMB
GAB
VLF
VMF
GAF
EET EET
Fz
0.5 s T0
Acc
Ecc Con Sus Ecc Con Sus
Figure 11-3
Differences between beginner and elite tennis players in lower extremity muscle activation during the
tennis serve. VLB, back vastus lateralis; VMB, back vastus medialis; GAB, back gastrocnemius lateralis;
VLF, front vastus lateralis; VMF, front vastus medialis; GNF, front gastrocnemius lateralis; FZ, vertical
ground reaction force; Acc, accelerometer; Ecc, eccentric phase; Con, concentric phase; Sus, suspension
phase. (From Girard O, Micallef JP, Millet GP: Lower-limb activity during the power serve in tennis:
Effects of performance level, Med Sci Sports Exerc 37([6]):1021-1029, 2005.)
Clinical Point
Push-through kinetic chain patterns of serve produce more stroke
power than pull-through patterns.
Figure 11-5
Gluteus medius activation of dominant leg during tennis serve.
Figure 11-7
Nondominant external oblique activation during tennis serve.
Ground Strokes
The forehand and backhand ground strokes can be broken
down into three phases: preparation, acceleration, and
follow-through (Figures 11-10 to 11-13). EMG activity dur-
ing the preparation phases of both the forehand and back-
hand is relatively low. Acceleration during the forehand in-
volves very high activity in the subscapularis, biceps brachii,
pectoralis major, and serratus anterior with a percentage of
MVC of 102%, 86%, 85%, and 76%, respectively.2 Accelera-
tion during the backhand stroke consists of high muscular
activity levels in the middle deltoid, supraspinatus, and
infraspinatus with percentage of MVC of 118%, 73%, and
78%, respectively.2 Again, the serratus anterior and biceps
musculature was active during acceleration for both the
forehand and backhand strokes.
Figure 11-6
Observable characteristics of the “push-through” serve are scapular
retraction and large degrees of knee flexion during cocking.
Figure 11-9
Figure 11-8 The “hip-back” position during a pull-through serve.
Observable characteristic of the “pull-through” serve is the lack of
knee flexion during cocking.
The follow-through phase of the forehand ground stroke early rotation of the shoulders leads to arm lag and hyperan-
produced moderately high activity of the serratus anterior, gulation at the shoulder joint.19,20,47,48 This premature open-
subscapularis, infraspinatus, and biceps musculature.2 The ing, which is similar to that seen in baseball pitchers, can lead
continued activity of the infraspinatus was evident during to shoulder injury and requires biomechanical intervention
impact and continued into the follow-through phase of the to prevent more serious injury and optimize technique.
forehand ground stroke.9 Follow-through activity during the
backhand was moderately high in the biceps, middle deltoid,
supraspinatus, and infraspinatus, but this level of activity was Joint Kinematics
significantly lower than during the acceleration phase. To further understand the demands placed on the upper
One of the primary changes in the modern game of extremity, analysis of shoulder joint angular velocities and
tennis is the use of open stances with the lower extremities.19 ranges of motion incurred during tennis play are indicated.
An open stance forehand is depicted in Figure 11-10 and Angular velocities incurred during the serving motion
shows how it contrasts with more traditional closed or necessitate high-velocity muscular stabilization outlined
square stances in which the entire body is perpendicular or previously. Biomechanical study of the tennis serve has pro-
sideways to the net. The open stance is characterized by duced data measuring the speed of internal rotation of the
the feet being essentially parallel to the net or baseline.19,20 humerus during acceleration. Shapiro and Stine14 filmed 14
Despite the placement of the feet parallel to the baseline, the highly skilled male tennis players and reported a maximum
shoulders remain rotated such that the degree of separation internal rotation velocity of 1074 to 1514 deg/sec. Slightly
between the hips and shoulders is optimized. This position faster velocities were reported by Dillman49 in a pilot
enables the player to use greater levels of angular momen- study of professional tennis players with maximal internal
tum during the stroke and facilitates the rotation during the rotation velocities up to 2300 deg/sec. Comparable veloci-
execution of the stroke. This segmental rotation, however, ties of internal rotation during the acceleration phase of
can be a liability when premature opening of the pelvis and throwing have been reported to exceed 7000 deg/sec.50
274 SECTION II • Applied Biomechanics of Selected Sport Activities
4
1
2
6
5
3
Figure 11-10
Forehand ground stroke. 1-3. Preparation phase of the forehand. 4-5. Acceleration phase of the
forehand. 6. Follow-through phase of the forehand.
2 4
5
1 3 6
Figure 11-11
One-handed backhand ground stroke. 1-3. Preparation phase of the backhand. 4-5. Acceleration phase
of the backhand. 6. Follow-through phase of the backhand.
Applied Biomechanics of Tennis • CHAPTER 11 275
1
5
3
2 4 6
Figure 11-12
Two-handed backhand ground stroke. 1. Ready position. 2-4. Preparation phase of the two-handed
backhand. 5. Acceleration phase of the two-handed backhand ground stroke. 6. Follow-through phase of
the two-handed backhand ground stroke. Note, player is left-handed in this illustration.
2 3
1
5
4
Figure 11-13
Forehand volley. 1. Starting phase of the split step. 2. Initial lateral step of split step. 3. Preparation phase
of the forehand volley. 4. Acceleration phase (forward phase) of the volley. 5-6. Follow-through phase of
the forehand volley.
276 SECTION II • Applied Biomechanics of Selected Sport Activities
Demands placed on the dominant shoulder during the extremity injury, particularly tennis elbow, because of bilat-
tennis serve are also high with respect to ROM. Dillman49 eral upper extremity force generation and load sharing.57
reported maximal external rotation values of 154°. Abduc-
tion angles at the shoulder in elite Australian players were
reported to average 83° during the cocking phase at the Implications for Evaluation of Stroke Mechanics
time of 90° of elbow flexion.3 Review of the athlete’s stroke mechanics by video or direct
These ROM characteristics have definite implications for observation is very helpful to check on poor techniques. The
overuse shoulder injury. Repeated maximal external rotation “nodes” model gives a framework for the evaluation. Obser-
during the cocking phase of the tennis serve produces adap- vation of multiple repetitions of the motion and focusing on
tations of the GH joint ROM on the dominant arm.51-53 one node per serve repetition can demonstrate if any of the
Greater external rotation of the GH joint may come at the nodes are not being used. The most commonly deficient
expense of anterior capsular attenuation and is similar to the nodes are lack of knee flexion and hip counter-rotation,
ROM and anterior laxity patterns found in highly skilled which results in the “pull-through” service motion, and lack
baseball players.54 of cocking, which results in GH hyperangulation. The
The degree of GH joint abduction during cocking and observable characteristics include minimal knee flexion upon
acceleration is of prime importance in proper mechanical ball toss, limited hip counter rotation away from the court,
serve execution. Increases in GH joint abduction can lead prominence of the back hip as the player moves to ball
to the shoulder being placed in a position of subacromial impact (the “hip back” position) (see Figure 11-9), and arm
impingement. Initial observation of a highly skilled player’s position behind the scapular plane at cocking. The Sony
service motion shows an apparent vertical orientation of the Ericsson Women’s Tennis Association tour has started a
arm to contact the ball overhead. Closer observation reveals program of evaluation of the nodes in the serve in profes-
that highly skilled players have significant contributions sional players. Players are observed by both direct visualiza-
from contralateral trunk lateral flexion and scapular abduc- tion and by video for the presence or absence of progression
tion. These components allow for a midrange of GH joint through the nodes in multiple successful serves in actual
abduction throughout the four phases of the tennis serve. game play. The preliminary data shows that the predominant
Analysis of joint angular velocities during forehand ground nodes that are not consistently being used in this group of
strokes shows maximum internal rotation at the shoulder to players are hip counter-rotation and coordinated arm cock-
be between 364 and 746 deg/sec.14 This finding again has ing in the maximum back scratch position. Specific coaching
implications in determining appropriate exercises for preven- techniques can be developed to modify these positions once
tion and rehabilitation of shoulder injuries. Groppel,11,55 they are observed.37,39,40 Also, specific physical examination
outlined the rationale and methodology for generation of for musculoskeletal-limiting factors such as knee injury, hip
topspin to the forehand ground stroke. Topspin is a desired weakness or rotational inflexibility, trunk inflexibility, or
characteristic used to improve both velocity and control of a scapular dyskinesis should be performed.
shot and has been taught by coaches emphasizing a low back-
swing during preparation and a high follow-through. This
creates a low-to-high stroke path that requires proper timing Anatomical Adaptations of Elite Tennis
and body segment positioning and preparation.13 Many Players in Response to the Biomechanical
unskilled and intermediate players use a method of “rolling
over” the ball to achieve topspin. This effect increases the
Demands of Tennis
pronation influence of the distal upper extremity and also Range of Motion
increases internal rotation acceleration during the stroke.12 The kinematic analysis presented earlier in this chapter showed
The close association between pronation of the forearm and the large arcs of humeral rotation required for highly skilled
internal rotation of the shoulder has been reported during the tennis players’ stroke execution. Several clinical studies have
serve.56 Distal upper extremity acceleration of pronation and presented active ROM measures of the shoulder in elite tennis
internal rotation compensation to incorrectly produce topspin players. Chandler and colleagues51 measured active ROM of
increase the demand on the posterior rotator cuff musculature the shoulder internal and external rotators in 90° of abduction
during the follow-through as the external rotators contract to in 86 junior elite tennis players between the ages of 12 and
counteract the internally rotating humerus after impact. 21 years. They found significantly less mean internal rotation
Angular velocities of external rotation during the back- range in the dominant arm compared with the nondominant
hand stroke in highly skilled tennis players range between arm (65° versus 76°). The dominant shoulder had only
328 and 1640 deg/sec.14 Rotation of the shoulders into a slightly greater external rotation active ROM (100° versus
position perpendicular to the net is of vital importance to 103°). Similar findings were reported by Ellenbecker52 in an
optimize the contribution of torso rotation and lower- earlier study of 26 elite junior players aged 11 to 14 years
extremity input to force generation.55 Use of a two-handed measured at 90° of abduction with scapular stabilization.
backhand has been recommended for players with upper Significantly greater external rotation was found on the
Applied Biomechanics of Tennis • CHAPTER 11 277
dominant arm of male tennis players only, with both male and of the entire posterior capsule, that humeral head kinemat-
female players showing less internal rotation active ROM on ics were changed or altered. In the presence of posterior
the dominant arm in players as young as 11 years of age. capsular tightness, the humeral head will shift in an
Another study by Ellenbecker and colleagues53 measured anterior superior direction, as compared with a normal
humeral rotation with scapular stabilization in elite junior shoulder with normal capsular relationships.62 With more
tennis players and professional baseball pitchers. This study extensive amounts of posterior capsular tightness, the hu-
also compared humeral rotation using the total rotation meral head was found to shift posterosuperiorly. These
ROM concept. The total rotation ROM value is obtained effects of altered posterior capsular tensions experimen-
by summing the external and internal rotation measures tally representing in vivo posterior GH joint capsular
together to obtain a combined or composite total of tightness highlight the clinical importance of using a reli-
humeral rotation. The findings of this study showed the able and effective measurement methodology, to assess
professional baseball pitchers to have greater dominant arm internal rotation ROM during examination of the shoul-
external rotation and significantly less dominant arm inter- der. In addition, Burkhart and colleagues36 have clinically
nal rotation, when compared with the contralateral non- demonstrated the concept of posterior-superior humeral
dominant or nonthrowing side. The total rotation ROM, head shear in the GH joint, in which the inherent
however, was not significantly different between extremities abducted externally rotated position along with posterior
in the professional baseball pitchers (145° dominant arm, capsular tightness has been hypothesized to lead to supe-
146° nondominant arm). This research showed that despite rior labral and rotator cuff injury.
bilateral differences in the actual internal and external rota-
tion ROM in the GH joints of baseball pitchers, the total
arc of rotational motion remained the same.53 A Tight Posterior Capsule of the Shoulder Causes:
In contrast, Ellenbecker and colleagues53 tested 117 elite
male junior tennis players. In the elite junior tennis players, • Loss of internal rotation
significantly less internal rotation ROM was found in the • Anterosuperior translation of humeral head
dominant arm (45° versus 56°), as well as significantly less • Superior migration of humeral head during abduction
total rotation ROM in the dominant arm (149° versus
158°) The total rotation ROM did differ between extremi-
ties. Approximately 10° less total rotation ROM can be
expected in the dominant arm of the uninjured elite junior Muscular Strength
tennis player, as compared with the nondominant extremity; Objective measurement of shoulder strength has been
however, differences of greater than 10° should be cau- performed in elite and recreational tennis players.52,63-66
tiously monitored as healthy, uninjured elite players from Concomitant with ROM, specific relationships in shoulder
this study had total rotation ROM bilateral comparisons strength have been identified in the tennis player that has
within the 10° range of their contralateral side. Humeral implications for the development of preventative and reha-
rotation measured with scapular stabilization is an impor- bilitative exercise programs.
tant part of the evaluation of the elite tennis player both Ellenbecker64 used a Cybex II isokinetic dynamometer to
during rehabilitation as well as during preventative screen- measure both shoulder internal and external rotation and
ing evaluation.47,48 flexion and extension in 22 highly skilled men tennis players.
The loss of internal rotation ROM is significant for He found significantly greater dominant-arm internal rota-
several reasons. The relationship between internal rotation tion, extension, and flexion compared with the nondominant
ROM loss (i.e., tightness in the posterior capsule of the extremity. No difference between extremities was found in
shoulder) and increased anterior humeral head translation shoulder external rotation. Significantly lower external and
has been scientifically identified.58,59 The increase in internal rotation unilateral strength ratios were reported for
anterior humeral shear force reported by Harryman and the dominant arm, showing a relative external rotation
colleagues60 was manifested by a horizontal adduction strength deficit on the tennis playing shoulder. Similar re-
cross-body maneuver, similar to that incurred during the search by Ellenbecker,52,66 Chandler and colleagues,51 and
follow-through of the throwing motion or tennis serve. Koziris and colleagues65 found similar results of greater inter-
Tightness of the posterior capsule has also been linked to nal rotation muscular strength on the dominant extremity
increased superior migration of the humeral head during with no significant difference between extremities in external
shoulder elevation.61 Koffler and colleagues62 studied rotation strength. In addition, Ellenbecker and Roetert67
the effects of posterior capsular tightness in a functional identified significantly lower absolute and relative fatigue in-
position of 90° of abduction and 90° or more of external dexes in the external rotators when compared with the inter-
rotation in cadaveric specimens. They found, with imbri- nal rotators in the dominant arm of elite junior tennis players,
cation (building a surface of overlapping layers) of either highlighting the importance of endurance-based strengthen-
the inferior aspect of the posterior capsule or imbrication ing of the posterior rotator cuff to prevent shoulder injury.
278 SECTION II • Applied Biomechanics of Selected Sport Activities
Ellenbecker64 measured significantly greater wrist flexion determine the typical distances covered. It was found that 80%
and extension strength and forearm pronation strength on the of all strokes were played with less than 2.5 meters (8.2 feet)
dominant arm compared with the nondominant extremity and fewer than 5% of strokes were played requiring more than
using and isokinetic dynamometer in elite tennis players. 4.5 meters (14.8 feet) between strokes.75 Other similar studies
Ellenbecker and Roetert68 found similar patterns of distal have found movement distances on average to cover less than
strength in elite junior tennis players with greater wrist flexion 4 meters (13.1 feet) per change of direction.76 Ferrauti and
and extension and forearm pronation strength on the domi- Weber75 have revealed that approximately 80% of all strokes
nant extremity. One final upper-extremity study measured are played within less than 3 meters (9.8 feet) from the
elbow extension and flexion strength in elite junior tennis baseline ready position. Relatively short distances that a
player.69 Greater dominant arm elbow extension strength was player covers on each stroke is typically less than 2 meters
found compared with the nondominant extremity. These (6.6 feet), yet under higher time-pressure (increased running
strength adaptations closely reflect the sport-specific demands demand) athletes can run on average approximately 4 meters
identified in the earlier part of this chapter based on the bio- (13.1 feet) (maximum of between 8 to 12 meters [26.2 to
mechanics inherent in tennis and the repetitive activation elite 39.4 feet]).77 It is interesting to note that tennis players can
players endure during practice and competition. cover approximately 0.25 to 0.50 meters (0.8 to 1.6 feet)
more on their forehand side than their backhand side.77 This
piece of information is very helpful when devising movement
Biomechanics of Tennis Movement training programs for tennis, as slightly longer distances may
Tennis movement is highly situation-specific and is performed need to be trained to an athlete’s right side (i.e., right-handed
in a reactive environment.70 This irregularity of movement forehand) than the athlete’s left side. These are important
and the need to continually respond to situations requires a findings, as most speed and quickness programs for
fine understanding of the athlete’s game style, strategy, and other sports focus on distances that are longer in which a full
movement strengths and weakness. Movement biomechanics traditional acceleration position may be reached. In tennis, it
for tennis is a complex area both from a practical coaching is rare that distances are achieved in which a traditional
standpoint, but especially from a research environment. Ten- acceleration technique will be experienced by the athlete, and
nis stroke biomechanics has been a fertile area of study, yet a maximum velocity running stride is never experienced
little information has been researched on tennis-specific during the confines of a tennis match.
movement biomechanics. This limited research may be due to Furthermore, the majority of tennis movements are in
the nature of the sport and the inconsistency of movement a lateral direction. In a study of professional players’
patterns. Although tennis movement has some consistent movement, it was found that more than 70% of move-
traits among all athletes, it is highly specific to the athlete’s ments were side-to-side with less than 20% of movements
position on the court and the type of shot his or her opponent in forward linear direction and less than 8% of movements
has just made. The movement biomechanics of tennis play has in a backward linear direction.77 This is a vitally important
some movement mechanics that are similar to other sports, statistic, because the development of lateral acceleration
but many of tennis’s movements require a different move- and deceleration in the distances described previously are
ment pattern, motor unit requirement continuum, and over- the major determining factors in great tennis movement.
all muscular strength profile than is needed to be a successful It is known that linear acceleration, linear maximum ve-
track sprinter or football wide receiver. Therefore, the data locity, and agility are all separate and distinct motor skills
that is available in some other high-profile sports may not be that need to be trained separately,78 as training one motor
appropriate to use as a guide for tennis. To understand the skill will not directly affect the improvement of the other.
biomechanical requirement of tennis movement, an analysis Therefore, preferred training recommendations for tennis
of movement demands needs to first be discussed. should be to focus training time between 60% to 80%
on lateral movements, 10% to 30% on linear forward
movements, and only approximately 10% on linear back-
Typical Movement Demands ward movement.
In competitive tennis, the average point length is less than
10 seconds,71,72 with the recovery between points usually
between 20 to 25 seconds depending on certain rules. Tennis
players make an average of four directional changes per
point,73,74 but a given point can range from a single move- Preferred Training Recommendations for Tennis
ment to more than 15 directional changes during a long rally.
In a competitive match, it is common for players to have more • 60% to 80% lateral movements
than 1000 direction changes. At the French Open (one of the • 10% to 30% linear forward movement
four Grand Slam professional tournaments), which is played • 10% linear backward movement
on a clay surface, a study was undertaken on 1540 strokes to
Applied Biomechanics of Tennis • CHAPTER 11 279
3000
Tennis Surfaces and How They Influence Movement 2500
Tennis is the only sport that is played on a number of different 2000
Force (N)
1500
playing surfaces, even at the professional level. Although there Fy
2000
are dozens of different surfaces around the world, for sake of 500
Fz
discussion, there are three major groups of surfaces that play- 0
ers typically compete on: hard courts, clay courts, and grass ⫺500 0 0.05 0.1 0.15 0.2 0.25
courts. These different court surfaces result in different move- A ⫺1000 Time (s)
ment requirements because of the speed, cushioning, and
friction of the court. Brody has found that the horizontal 3000
frictional force greatly affects ball speed and is a determining 2500
factor in court speed.79 There can be as much as a 15% differ- 2000
Force (N)
ence in ball speed after the bounce, depending on the court 1500
Fy
surface. Typically, a clay court is slower than a hard court. This 2000
Fz
500
reduction in ball speed allows athletes more time to reach the
0
ball, therefore lengthening the duration of points played on
⫺500 0 0.05 0.1 0.15 0.2 0.25
clay courts. A computerized notational analysis of 252 profes- B ⫺1000 Time (s)
sional singles matches found that rallies from women’s singles
matches (average 7.1 seconds) were significantly longer than 3000
rallies from men’s singles matches (5.2 seconds). Rallies on 2500
clay courts at the professional level were significantly longer 2000
Force (N)
than any other surface.80 At four Grand Slam events, 1500
Fy
O’Donoghue and Ingram found the following percentages 2000
Fz
for baseline rallies: (1) French Open (clay court): 51%; (2) 500
Australian Open (hard court): 46%; (3) US Open (hard 0
⫺500 0 0.05 0.1 0.15 0.2 0.25
court), 35%; and (4) Wimbledon (grass) 19%.80
C ⫺1000 Time (s)
Another interesting difference between surfaces is that
on hard courts, professional players are under increased
3000
time-pressure 45% of the time, whereas it is only 29% on
2500
clay courts.76 Therefore, court surfaces do play a role in the 2000
movement requirements of tennis athletes and training
Force (N)
1500
Fy
needs to be adapted based on these differences. 2000
More research is required before surfaces can be assessed Fz
500
using mechanical testing alone, especially in terms of the 0
effect that such mechanical test results have on human ⫺500 0 0.05 0.1 0.15 0.2 0.25
movement on the tennis court.81 D ⫺1000 Time (s)
Tennis players have been shown to subjectively rate cush- Figure 11-14
ioning of tennis surfaces that correlate highly with mechanical Typical vertical (Fz) and horizontal (Fy) ground reaction force profiles
testing. Peak and mean loading rates of vertical GRF, peak for the four surface conditions: A, baseline acrylic; B, rubber; C, thin
foam; D, thick foam. (From Stiles V, Dixon S: Biomechanical response
horizontal force, peak heel pressure, and rates of loading dem- to systematic changes in impact interface cushioning properties
onstrate significant correlations (p ⬍ 0.05) with the partici- while performing a tennis-specific movement, J Sport Sci 25[11]:
pant’s perceived levels of cushioning between four different 1229-1239, 2007.)
tennis court surfaces (acrylic, rubber, thin foam, and thick
foam) (Figure 11-14).81 Kinematic data for a running fore-
hand has not been shown to provide significantly different cortical response time improved in the gastrocnemius and
responses based on these four surfaces.81 medial hamstring (semimembranosus, semitendinosus).82
This is helpful when designing training programs in the gym,
as it should help to focus training on the specific muscle
Lateral Movement in Tennis (listed previously) along with movements that are performed
Because tennis movements are predominantly lateral in on court.
focus, the muscle recruitment patterns and mechanics of To aid in the understanding of tennis-distinct move-
lateral movements are discussed. ments during lateral displacement on court, there are three
With lateral-focused agility training, the spinal reflex times initiating movements that are usually used by players during
of the following muscles improve (vastus medialis and latera- baseline movement—jab step, pivot step, and the gravity
lis medialis because of anterior tibialis translation) and the step (Figure 11-15, Figure 11-16, and Figure 11-17).
280 SECTION II • Applied Biomechanics of Selected Sport Activities
Recovery Movement
Recovery movement occurs immediately after the athlete has
completed his or her stroke and is attempting to return to a
position that will allow for efficient movement toward the
next stroke. There are two typical movement patterns used
during the recovery after a stroke—the lateral crossover
(Figure 11-18) or the lateral shuffle (Figure 11-19). The
lateral crossover is more appropriate for movements that
require quicker responses and greater distances. The lateral
shuffle is more common when the athlete has a little extra
time to get back into position before having to explosively
move to the next shot.
Figure 11-16
Pivot step. (From Kovacs MS: Movement for tennis: The importance
of lateral training, Strength Cond J 31[4]:79, 2009.) Split Step Misconception
Because of the evolution of tennis and the reliance on speed
and power in today’s game, the movement patterns of play-
ers have adapted. Early descriptions of the split step
reported both feet landing on the court simultaneously, and
Applied Biomechanics of Tennis • CHAPTER 11 281
Figure 11-17
Gravity step. (From Kovacs MS: Movement for tennis: The importance of lateral training, Strength Cond J
31[4]:79, 2009.)
1 2
3 4
Figure 11-18
Lateral cross-over step. (Modified from Kovacs MS: Movement for tennis: The importance of lateral
training, Strength Cond J 31[4]:79, 2009.)
then the athlete would react left, right, forward, or backward ahead of the other foot. An example is that a right-handed
depending on the flight path, speed, direction, or spin of the athlete preparing to hit a forehand would land on the left
oncoming ball. However, because of advances in the speed foot first (Figure 11-20). Before the right foot touches the
of the sport and the technological advances available to ana- ground, the athlete subtly rotates the hip externally toward
lyze athletes using high-speed video, it has emerged that the intended movement of the ball. In the right-handed
elite players actually react in the air during the split and land player, this results in the right foot landing pointing out-
on the foot furthest from their intended target a split second wards (see Figure 11-20). The movement pattern described
282 SECTION II • Applied Biomechanics of Selected Sport Activities
1 2
3 4
Figure 11-19
Lateral shuffle step. (Modified from Kovacs MS: Movement for tennis: The importance of lateral training,
Strength Cond J 31[4]:80, 2009.)
previously has been a natural evolution to improve an ath- to improve reaction time should be a component of training
lete’s ability to react to the incoming ball and maximize the tennis movement, alongside technique, strength, and power.
movement/time ratio. In the training drills, a visual stimulus needs to be used to
help develop visual reaction time. An auditory stimulus
(e.g., whistle, voice, hand clap) is less tennis-specific than
Reaction Time the visual cue. A study looking at average reaction times
One other area that can have an immediate effect on how (from ball machine release to initial racquet movement) in
fast an athlete appears in short distances is the athlete’s reac- skilled tennis players’ volleys were 0.226 seconds for the
tion time. Reaction time is defined as the time from a forehand and 0.205 seconds for the backhand.91
stimulus (visual awareness of the opponent’s stroke or ball) After breaking inertia, the athlete’s aim is to increase
until the production of force.85 For more than 100 years, acceleration. Faster athletes have greater force production
the accepted figures for simple reaction times for college- and horizontal velocity than the slower athletes during the
age individuals has been approximately 190 ms (0.19 s) for last contact points on the ground.90 This means that the
light stimuli and approximately 160 ms (0.16 s) for sound power output at the last stage of ground contact is higher
stimuli.86,87 However, the fastest athletes in the world con- in faster athletes and this is an area that coaches should
sistently have reaction times less than 0.15 seconds.88,89 In focus on during training sessions. Developing this increased
identical events, women have been shown to have longer power output at ground contact will directly increase GRFs,
reaction times than men.90 However, reaction time does translating to quicker responses. Professional track sprinters
not correlate well with sprints lasting longer than a few running the 100 meter have movement velocities from a
seconds,89 yet it does correlate very well with distances standard block start of between 4.65 to 5.16 ms⫺1 for the
typically seen in tennis play.89 Therefore, training an athlete first ground contact and approximately 5.7 ms⫺1 at toe-off
Applied Biomechanics of Tennis • CHAPTER 11 283
1 2
3 4
Figure 11-20
Split step. (Modified from Kovacs MS: Movement for tennis: The importance of lateral training, Strength
Cond J 31[4]:80, 2009.)
for the second step from a block start.89,92,93 It is interesting example of a movement pattern during a long point) and
to compare this information with professional tennis players less than 30% of movements are linear (forward and back-
who have movement velocities that range substantially ward).77 It is imperative that the majority of training pro-
during any given point (Figure 11-21). grams are structured appropriately to train specifically for
Sprinting technique during an athlete’s acceleration is the movements experienced during tennis.
vastly different than that of an athlete who is running at or
near maximum velocity (Figure 11-22).94,95 Most competi-
tive athletes do not reach maximum velocity until 40 to Kinetic and Kinematic Data
60 meters (131 to 197 feet) (depending on training level Although extensive kinetic and kinematic data have been pre-
and genetic ability). As mentioned previously, tennis ath- sented analyzing tennis strokes in this chapter, currently there
letes typically move less than 2.5 meters (8.2 feet) and rarely is limited published kinetic and kinematic data on ennis-
exceed 5 meters (16.4 feet) (Figure 11-23 provides an specific movement. However, there is some information that
284 SECTION II • Applied Biomechanics of Selected Sport Activities
47. Ellenbecker TS: Clinical examination of the shoulder, Philadelphia, 71. Kovacs MS: A comparison of work/rest intervals in men’s profes-
2004, Elsevier Saunders. sional tennis, Med Sci Tennis 9(3):10–11, 2004.
48. Ellenbecker TS: Non-operative rehabilitation of the shoulder, 72. Kovacs MS: Applied physiology of tennis performance, Br J Sports
New York, 2006, Theime Publishers. Med 40(5):381–386, 2006.
49. Dillman CJ: Presentation on the upper extremity in tennis and 73. Roetert EP, Ellenbecker TS: Complete conditioning for tennis,
throwing athletes, United States Tennis Association National ed 2, Champaign, IL, 2007, Human Kinetics.
Meeting, Tucson, Arizona, March 1991. 74. Kovacs M, Chandler WB, Chandler TJ: Tennis training:
50. Andrews JR, Kupferman SP, Dillman CJ: Labral tears in throwing Enhancing on-court performance, Vista, CA, 2007, Racquet Tech
and racquet sports, Clin Sports Med 10:901–911, 1991. Publishing.
51. Chandler TJ, Kibler WB, Uhl TL, et al: Flexibility comparisons of 75. Ferrauti A, Weber K: Stroke situations in claycourt tennis,
junior elite tennis players to other athletes, Am J Sports Med Unpublished data, 2001.
18:134–136, 1990. 76. Pieper S, Exler T, Weber K: Running speed loads on clay and hard
52. Ellenbecker TS: Shoulder internal and external rotation strength courts in world class tennis, Med Sci Tennis 12(2):14–17, 2007.
and range of motion of highly skilled junior tennis players, 77. Weber K, Pieper S, Exler T: Characteristics and significance of
Isokinetics Exerc Sci 2:1–8, 1992. running speed at the Australian Open 2006 for training and injury
53. Ellenbecker TS, Roetert EP, Bailie DS, et al: Glenohumeral joint prevention, Med Sci Tennis 12(1):14–17, 2007.
total rotation range of motion in elite tennis players and baseball 78. Young WB, McDowell MH, Scarlett BJ: Specificity of sprint and
pitchers, Med Sci Sports Exerc 34(12):2052–2056, 2002. agility training methods, J Strength Cond Res 15(3):315–319,
54. Jobe FW, Bradley JP: The diagnosis and nonoperative treatment of 2001.
shoulder injuries in athletes, Clin Sports Med 8:419–439, 1989. 79. Brody H: Fast courts—slow courts, New York, 1995, United States
55. Groppel JL: The biomechanics of tennis: An overview, Int J Sport Tennis Association.
Biomech 2:141–155, 1986. 80. O’Donoghue P, Ingram B: A notational analysis of elite tennis
56. VanGheluwe B, DeRuysscher I, Craenhals J: Pronation and strategy, J Sports Sci 19:107–115, 2001.
endorotation of the racket arm in a tennis serve, In Jonsson B, 81. Stiles V, Dixon S: Biomechanical response to systematic changes in
editor: Biomechanics X-B, Champaign, IL, 1987, Human Kinetics. impact interface cushioning properties while performing a tennis-
57. Nirschl RP: Tennis elbow, Prim Care 4:367–382, 1977. specific movement, J Sport Sci 25(11):1229–1239, 2007.
58. Tyler TF, Nicholas SJ, Roy T, Gleim GW: Quantification of pos- 82. Wojtys EM, Huston LJ, Taylor PD, Bastian SD: Neuromuscular
terior capsular tightness and motion loss in patients with shoulder adaptations in isokinetic, isotonic, and agility training programs,
impingement, Am J Sports Med 28(5):668–673, 2000. Am J Sports Med 24(2):187–192, 1996.
59. Gerber C, Werner CML, Macy JC, et al: Effect of selective capsu- 83. Bragg RW, Andriacchi TP: The lateral reaction step in tennis foot-
lorraphy on the passive range of motion of the glenohumeral joint, work, XIX International Symposium on Biomechanics in Sports,
J Bone Joint Surg Am 85(1):48–55, 2003. San Francisco, 2001.
60. Harryman DT, Sidles JA, Clark JM, et al: Translation of the 84. Kraan GA, van Veen J, Snijders CJ, Storm J: Starting from
humeral head on the glenoid with passive glenohumeral motion, standing: Why step backwards, J Biomech 34:211–215, 2001.
J Bone Joint Surg Am 72:1334–1343, 1990. 85. Schmidt RA, Lee TD: Motor control and learning: A behavioral
61. Matsen FA III, Arntz CT: Subacromial impingement. In emphasis, ed 3, Champaign, IL, 1999, Human Kinetics.
Rockwood CA Jr, Matsen FA III, editors: The shoulder, ed 1, 86. Galton F: On instruments for (1) testing perception of differences
Philadelphia, 1990, WB Saunders. of tint and for (2) determining reaction time, J Anthropol Inst
62. Koffler KM, Bader D, Eager M, et al: The effect of posterior capsular 19:27–29, 1899.
tightness on glenohumeral translation in the late-cocking phase of 87. Brebner JT, Welford AT: Introduction and historical background
pitching: A cadaveric study, Abstract (SS-15) presented at Arthros- sketch. In Welford AT, editor: Reaction times, New York, NY,
copy Association of North America Annual Meeting, Washington, 1980, Academic Press.
DC, 2001. 88. Gambetta V, Winckler G: Sport specific speed: The 3S system,
63. Ellenbecker TS, Davies GJ, Rowinski MJ: Concentric versus Sarasota, FL, 2001, Gambetta Sports Training Systems.
eccentric isokinetic strengthening of the rotator cuff: Objective 89. Mero A, Komi PV: Reaction time and electromyographic activity
data versus functional test, Am J Sports Med 16:64–69, 1988. during a sprint start, Eur J Appl Physiol 61:73–80, 1990.
64. Ellenbecker TS: A total arm strength isokinetic profile of highly 90. Mero A, Komi PV, Gregor RJ: Biomechanics of sprint running,
skilled tennis players, Isokinetics Exerc Sci 1:9–21, 1991. Sports Med 13(6):376–392, 1992.
65. Koziris LP, Kraemer WJ, Triplett NT, et al: Strength imbalances in 91. Chow JW, Carlton LG, Chae WS, et al: Movement characteristics
women in tennis players (abstr), Med Sci Sports Exerc 23:253, of the tennis volley, Med Sci Sports Exerc 31(6):855–863, 1999.
1991. 92. Mero A: Force-time characteristics and running velocity of male
66. Ellenbecker TS, Roetert EP: Age specific isokinetic glenohumeral sprinters during the acceleration phase of sprinting, Res Q Exerc
internal and external rotation strength in elite junior tennis Sport 59(2):94–98, 1988.
players, J Sci Med Sport 6(1):63–70, 2003. 93. Schot P, Knutzen K: A biomechanical analysis of four sprint start
67. Ellenbecker TS, Roetert EP: Isokinetic muscular fatigue of the positions, Res Q Exerc Sport 2:137–147, 1992.
shoulder internal and external rotators, J Orthop Sports Phys Ther 94. USA Track and Field (USATF): Sprints and Hurdles, Starkville, MS,
29(5):275–281, 1999. 2004, United States Track and Field Level II Coaching School.
68. Ellenbecker TS, Roetert EP: Isokinetic profile of wrist and forearm 95. Kyröläinen H, Komi PV, Belli A: Changes in muscle activity pat-
strength in elite junior tennis players, Br J Sports Med 40(5): terns and kinetics with increasing running speed, J Strength Cond
411–414, 2006. Res 13(4):400–406, 1999.
69. Ellenbecker TS, Roetert EP: Isokinetic profile of elbow flexion 96. Strauss D: Biomechanical analysis of the impact characteristics of an
and extension strength in elite junior tennis players, J Orthop open stance forehand drive in tennis, Key Biscayne, FL, 2005,
Sports Phys Ther 33(2):79–84, 2003. USTA Sport Science.
70. Kovacs MS: Tennis physiology: Training the competitive athlete, 97. Cavanagh PR, Lafortune MA: Ground reaction forces in distance
Sports Med 37(3):1–11, 2007. running, J Biomech 13:397–406, 1980.
12
CHAPTER
287
288 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 12-1 kick (Table 12-2).5 The side-foot kick is more frequently used
Capability and Demand Definitions for short, precise passes and shooting, whereas the instep kick
is often used to propel the ball with high velocity.5 Although
Parameter Definition
such techniques have distinct goals, they are generally per-
Capability Ability (potential) of the musculoskeletal formed with similar biomechanical strategies, in which the key
system to generate, dissipate, and transfer function of the musculoskeletal system in kicking is to effi-
mechanical energy ciently transfer mechanical energy to the ball by imparting a
force to it with precise power and direction.
Demand Amount of stress applied to the musculoskeletal
system during a given activity Descriptions of the biomechanics of kicking have focused
on the behavior of the lower swing limb in the sagittal plane
and have divided this action into four consecutive phases:
backswing, leg cocking, leg acceleration, and follow-through
Biomechanics of Soccer (Figure 12-1, A).5-7 The backswing phase lasts from toe-off
Although soccer is composed of many skills, this section (which takes place just before the contact of the support limb
focuses only on the specific components that place the most with the surface) to the time of maximum hip extension.5
stress on the musculoskeletal system or are fundamental com- The swing limb is displaced backward in relation to the rest
ponents of the sport. Thus, this section concentrates on of the body, and there is hip extension and knee flexion.6 The
describing the biomechanics of kicking, heading, and cut- leg-cocking phase begins with maximum hip extension and
ting. For each of these tasks, subtasks or components are ends with maximum knee flexion of the swing limb and,
appropriately addressed when needed. For example, heading subsequently, the leg acceleration phase lasts until the contact
a ball requires jumping and landing, whereas cutting is of the swing foot with the ball.5 These last two phases are
embedded in pivoting, dribbling, and running. The selection characterized by the predominant anterior displacement and
of only kicking, heading, and cutting was made based on the acceleration of the swing limb, in the direction of the ball.6
fact that these components are crucial for soccer practice. During the leg-cocking phase, hip flexion and knee flexion
The focus on only these components facilitates a deeper continue to occur.7 During the leg-acceleration phase, the
understanding of their biomechanics and the demands that hip continues to flex and the knee begins to extend.7
they place on the musculoskeletal system. However, it is Finally, the follow-through phase lasts from ball contact to
worth remembering that, during a soccer match, these the end of the anterior displacement of the foot and is char-
activities occur in an overlapping manner and thus pose an acterized by the final deceleration of hip flexion and knee
even greater challenge to the musculoskeletal system. extension.5 The displacements at the ankle joint are minimal
Classical analyses of the biomechanics of a given sport in comparison with hip and knee, because the foot accompa-
frequently separate the kinematic and kinetic aspects of that nies shank linear and angular motions.
sport. In this section, a different approach is taken. Initially,
the components and their subphases are described, observ-
Clinical Relevance Summary - Kicking
ing the differences among existing styles. For example,
in this section, different types of kicking and cutting are • Analyses of the kicking action should include transverse and
described. Finally, the biomechanical description of each of sagittal plane motions of the upper body, in addition to sagittal
the soccer components introduced will focus on a global plane motions of the lower swing limb.
analysis of the demands and requirements of the task, con- • The contractile and passive properties of the myofascial structures
that interconnect the lower swing limb, pelvis, trunk, and nonkicking-
sidering simultaneously the kinematic and kinetic aspects of
side lower and upper limbs are crucial for kicking performance,
the soccer component. In this case, whenever possible, the
because the patterns of energy flow depend on the mechanical
energetics of the task (i.e., energy flow in the kinetic chain) interactions between these segments.
will be emphasized to allow a better understanding of the
musculoskeletal demands imposed from soccer practice.
Table 12-2
Biomechanics of Kicking Types of Kicking
Kicking is the playing action of soccer used to shoot the ball to Type of Kicking Definition
a desired direction, either to pass the ball to a teammate or in
an attempt to score a goal. This task is accomplished by hitting Side-foot kick Kick executed by striking the ball with
the ball with the foot of the swing limb while the support limb the medial aspect of the swing-limb
sustains the body. Kicking involves complex motions and large midfoot
demands on the musculoskeletal system, as it is one of the soc- Instep kick Kick executed by striking the ball with
cer components most related to noncontact injuries.2 The the dorsum of the swing-limb foot
main techniques of kicking are the side-foot kick and the instep
Applied Biomechanics of Soccer • CHAPTER 12 289
B SPRING DAMPING
Figure 12-1
Sagittal view of the kicking kinematics. Limbs in gray color are the kicking-side lower limb (swing limb)
and the nonkicking-side upper limb. A, Kicking phases related to the sagittal plane kinematics of the
swing limb. B, Kicking phases related to the main functions of the kinetic chain. (Redrawn from
Shan G, Westerhoff P: Full-body kinematic characteristics of the maximal instep soccer kick by
male soccer players and parameters related to kick quality, Sports Biomech 4(1):59-72, 2005.)
The musculoskeletal system may be understood as hav- certain amount of joint stiffness and stability and allows for
ing two major functions during kicking: the spring function adequate energy dissipation and transfer among segments.10
and the damping function (see Figure 12-1, B).8 According The differences between soccer players and nonplayers
to these functions, the kicking action can be divided into (i.e., between individuals who have, by practice, exploited
three main stages: an initial stage when potential energy is extensively their neuromusculoskeletal resources in the per-
stored (backswing), a second stage when the kinetic energy formance of kicking and those who have not) help clarify
involved in the anterior acceleration of the swing limb is the kicking demands. In soccer players, the antagonist
resultant from the conversion of the potential energy previ- muscles are more active than the agonist, whereas in non-
ously stored and from energy generation (i.e., leg cocking players, the opposite is true.11 Such differences indicate that
and leg acceleration), and a final stage when this energy eccentric contractions have essential roles in the spring
is absorbed and mostly dissipated with limb deceleration function12,13 by absorbing and storing energy during the
(i.e., follow-through). During the two initial stages, the backswing and by releasing it back to the system (energy
system works as a spring and during the third stage the return) during swing limb anterior acceleration. In the
damping (braking) function is predominant. Joint kinetics swing limb, the flexors, adductors, and anterior external
of the lower swing limb, estimated from inverse dynamics, rotators of the hip and extensors of the knee are mostly
reinforces such roles.5 During backswing, there is energy responsible for this function. Concentric contractions of
absorption and deceleration of hip extension and knee flex- these muscles are also required, mainly during the anterior
ion. During leg cocking and leg acceleration, there is energy acceleration of the swing limb, to add energy to the seg-
generation and acceleration of hip flexion and knee exten- ments.14 Limb anterior acceleration is enhanced by the
sion. Finally, during the follow-through, there is energy muscles’ previous eccentric contractions and myofascial
absorption and deceleration of hip flexion and knee exten- stretching.15 Eccentric contractions during the follow-
sion. This dynamic action is due to predominant hip flexor through are also essential for the kicking-damping
and knee extensor net torques during backswing, leg cock- function16 by dissipating mechanical energy for limb decel-
ing, and leg acceleration, and due to hip extensor and knee eration. This action has a crucial involvement of hip exten-
flexor net torques during the follow-through. At the ankle, sors and knee flexors in the swing limb.
the predominant net torque is dorsiflexion.5 It is important Another difference between players and nonplayers is
to recognize that inverse dynamics methods estimate only that, in general, players show less swing-limb muscle activa-
the joint torques necessary to generate the observed kine- tion (although they produce greater ball velocity) than non-
matics of an action, regardless of the structures and interac- players.11 This demonstrates that, in experienced players, the
tions that produce them.9 Thus, the torques and energetic demands of kicking are also met by efficiently using the pas-
changes described may be influenced by interactions with sive properties of the musculoskeletal system. The passive
other joints and segments within the chain. tension of myofascial structures and their resulting passive
The muscles of the swing and support limbs are active stiffness can be used for energy transfer among segments,
during the entire kicking cycle7 so that muscles that energy storage and return (stretching and shortening,
are agonist and antagonist to the occurring motion are co- respectively), and energy dissipation (tissue viscosity), with
contracted. This co-contraction allows the maintenance of a minimal metabolic cost.17,18
290 SECTION II • Applied Biomechanics of Selected Sport Activities
Segments other than the lower swing limb are also part the swing limb during kicking execution. Pelvic backward
of the kicking kinetic chain. The pelvis, trunk, contralateral rotation stretches the internal hip rotators of the support
upper limb and the support limb are involved in the function limb, which also participate in this force propagation
of transferring mechanical energy to the ball. Skilled players, pattern. Eccentric contractions of all of these muscles im-
compared to novice players, clearly show greater motions of prove energy absorption and storage.12 The motion of the
the upper body segments19 to take advantage of the great nonkicking-side upper limb increases the angular momen-
kinetic energy produced by the large masses of these seg- tum of the upper body,22 enhancing the superior inertial
ments. In preparation for kicking, soccer players often prefer anchoring of this ventral force propagation line and the
to walk or run toward the ball with a diagonal approach transfer of energy from the upper body to the swing lower
angle close to 45°.20 Such approach requires transverse plane limb. During leg cocking and leg acceleration, the potential
rotations of the body to shoot the ball forward. These rota- energy stored in these structures is returned, with great
tions take place at the hip joint of the support limb and at energy transfer to the swing limb. Concurrently, concentric
the trunk. During the backswing, the pelvis is rotated back- contractions of the involved muscles, enhanced by their
ward (toward the kicking side) (Table 12-3), with hip exter- previous stretching,15 reverse motion directions and add
nal rotation at the support limb, while the swing limb energy to the chain.
is displaced backwards.21 The upper trunk is rotated in the At ball contact, the stiffness of all tissues and joints
opposite direction, toward the nonkicking side, and there is involved in this mechanism must be high, from the kicking
trunk extension. The shoulder contralateral to the swing ankle to the nonkicking-side shoulder. Appropriate stiffness,
lower limb is abducted and extended.19,22 During the leg- provided both passively by tissue tension and actively
cocking and acceleration phases, the pelvis rotates forward through eccentric contractions and co-contractions, may
(toward the nonkicking side) (see Table 12-3), with internal produce a “sum of masses” of the segments involved in
hip rotation at the support limb, accelerating the swing limb kicking, allowing for greater energy transfer from the mus-
forward.21 The upper trunk is rotated toward the kicking culoskeletal system to the ball. The capability of using this
side and there is trunk flexion. The nonkicking side shoulder whole kinetic chain may explain the greater ball velocity
is adducted and flexed during the acceleration and follow- produced by the angled approach (45°) in comparison with
through phases.19,22 less angled approaches, even with similar anterior foot
The spring function of the system is also influenced by velocities before ball contact.24 It may also explain why
structures of the upper body that are stretched during the individuals who can kick the ball significantly farther do
backswing. During a kick, anterior muscles connected not necessarily have greater muscle strength in the lower
by fascia are stretched by the rotation of the upper trunk swing limb.25
toward the nonkicking side, extension of the trunk, exten- After ball contact, upper body structures also participate
sion and abduction of the nonkicking side shoulder, and in the damping function of the system. During the follow-
backward rotation of the pelvis. These muscles function as through, rotation of the upper trunk toward the kicking
an anterior force propagation line constituted by the rectus side, flexion of the trunk, flexion and adduction of the
abdominis, the kicking-side external obliquus abdominis, nonkicking-side shoulder, and forward rotation of the
and the nonkicking-side internal obliquus abdominis and pelvis19,21,22 stretch dorsal myofascial structures whose fiber
pectoralis major.23 These muscles are functionally continu- alignments make them capable of decelerating such
ous with hip flexors and adductors and knee extensors of motions. The nonkicking-side latissimus dorsi, the thoraco-
lumbar fascia, and the erector spinae muscles and the
kicking-side gluteus maximus, iliotibial band, and ham-
Table 12-3 strings constitute such a functional force propagation line.26
Pelvic Rotations in the Transverse Plane of Motion Pelvic forward rotation also stretches the external hip rota-
tors of the support limb. The passive tension and viscosity
Pelvic Motion
of all of these structures and the eccentric contractions of
in the Transverse
the muscles involved allow for the damping function of the
Plane Definition
system, with motion deceleration and energy absorption
Forward rotation The anterior face of the pelvic ring and dissipation.16,17
(pubis) rotates toward the nonkicking
side (kicking) or support-limb side
(cutting) Biomechanics of Cutting
Backward rotation The anterior face of the pelvic ring Cutting occurs frequently in sports activities such as soccer,
(pubis) rotates toward the kicking basketball, North American football, and handball. Specifi-
side (kicking) or swing-limb side cally in soccer, cutting is observed during dribbling maneu-
(cutting) vers. These maneuvers occur during offensive or defensive
strategies.27 During dribbling maneuvers in a game situation,
Applied Biomechanics of Soccer • CHAPTER 12 291
the athlete has to be able to run with the ball and abruptly
change direction, so cutting is an effective strategy used
to beat the opponent. Because of its relevance in different
situations, the biomechanics of cutting has received much
attention in scientific literature. In addition, cutting in
soccer games has a great potential to result in ligament
injuries,28-31 which reinforces the importance of studying
this motion. However, most studies on cutting focus only
on the biomechanics of the knee joint and neglect the con-
tribution of the whole kinetic chain to the execution of this
maneuver.
A
Cutting maneuvers are accomplished in two ways:
sidestep (outside) cutting and crossover (inside) cutting
(Table 12-4). The sidestep cut occurs when the direction
change proceeds away from the support limb side.32 For
example, a soccer player executes a sidestep cut when the
right foot is planted and the athlete cuts to the left, away
from the support foot (Figure 12-2, A).33 A crossover cut is
executed when, during running, the player plants one foot
and then crosses the contralateral lower extremity anteriorly
to provide acceleration to run in a new direction.31 For
example, when the player plants the left foot, the right
foot crosses over the left foot to change direction (see Figure
12-2, B).33 Thus, in a crossover cutting, the direction change
Table 12-4
Sidestep and Crossover Cutting Definitions
Type of Cutting Definition
occurs toward the support-limb side.32 In general, both sidestep cut movement is characterized by kinematic pat-
types of cutting are characterized by an abrupt direction terns of subtalar joint pronation, internal rotation of the
change named the plant-and-cut phase. This phase involves tibia and abduction of the knee joint, internal rotation
deceleration during the initial ground contact and accelera- of the femur (segment motion with respect to external
tion during propulsion in a new direction.31 The mecha- reference–global coordinate system) and rotation of the
nisms involved in body deceleration are very similar in both trunk and pelvis toward the new direction.28,36 The magni-
sidestep and crossover cutting. However, the biomechanical tudes of adduction and internal rotation torques on the
patterns during direction change and acceleration phases knee joint during sidestep cutting are greater than during
have marked differences between the two types of cutting. movements such as running and landing.38 This fact sug-
In this section, the biomechanical mechanisms involved in gests that cutting generates a great stability demand to
deceleration, direction change, and acceleration phases dur- the knee joint. Besier and colleagues38 demonstrated that,
ing cutting maneuvers are discussed in detail. during a sidestep cut, the torque on the knee joint is
The fast deceleration and subsequent acceleration approximately 150 Nm for an athlete with a body mass of
observed in the cut-and-plant phase of both cutting maneu- 75 kg. In addition, sidestep cutting produces the highest
vers impose great demands of absorption and generation overall pressure on the foot with the peak pressure observed
of energy on the musculoskeletal system. In both cutting in the medial forefoot and hallux.33
maneuvers, during deceleration following ground–foot The propulsive force necessary to accelerate the body
contact, there is a kinematic pattern in the sagittal plane of into a new direction during sidestep cutting is obtained
hip, knee, and ankle flexion movements. During this phase, by the energy storing and recovering mechanisms of the
the impact forces at initial ground contact are absorbed support limb.36 However, the movement efficiency and
through eccentric contraction of the hip, knee, and ankle stability observed in this phase also depends on the energy
extensor muscles of the support leg.34 This energy stored is generated by trunk and pelvic motions. Because these seg-
eventually released during the acceleration phase to add the ments are attachment sites for the largest muscles of the
mechanical energy necessary for the player to change direc- body, they generate a great portion of the mechanical
tion. This mechanism of storing and recovering energy in energy necessary to accelerate the body in the new direc-
the support limb is similar to a simple mass-spring system.35 tion. During sidestep cutting, the trunk and pelvis rotate
According to this view, the support limb behaves as a longi- toward the swing limb to change direction. This backward
tudinal spring, storing energy during the deceleration phase pelvic rotation produces external hip rotation (relative
(kinematic pattern of hip, knee, and ankle flexion with motion between two adjacent body segments) of the sup-
eccentric action of the opposing muscles)34,36 and returning port limb. Classical analysis of this motion indicates that the
the stored energy to provide a propulsive force in a new torque to rotate the pelvis and trunk is generated by exter-
direction (kinematic pattern of hip, knee, and ankle exten- nal hip rotator muscles.36 However, a complex pattern of
sion).36 The capability of the biological tissues to absorb force transmission is observed, because of the coupling be-
and to return energy depends on interaction between tween different anatomical structures.26,39 According to this
muscle activation and the viscoelastic properties of the view, the gluteus maximus “couples” with the contralateral
muscle and connective tissues, which determine tissue and latissimus dorsi via superficial thoracolumbar fascia and the
joint stiffness. Thus, soccer players with an adequate level of iliotibial band, transferring the kinetic energy of the trunk
lower limb stiffness take advantage of the properties of their to the supporting limb. Rotational force transmission is an
systems to efficiently exploit the elastic energy stored in the effective way of providing the mechanical energy necessary
support leg and reduce the muscle work necessary to to rotate the pelvis and trunk and, consequently, to change
change direction during cutting maneuvers. This role of the the athlete’s direction during sidestep cutting. This energy
support limb in generating part of the propulsive force in transfer mechanism is only possible as a result of fascial
cutting maneuvers is also observed during running on a organization of the tissues around the lower back.26 Thus
nonlinear (curved) pathway. In this activity, the ground the effect of a given muscle is not limited to moving the
reaction force (GRF) and the propulsive force in the outside joint or joints it crosses. In addition, eccentric contractions
limb accelerate the body toward the inside curve, suggest- of the adductor muscles decelerate the pelvic rotation and
ing a role of the musculature of the outside limb to generate hip abduction on the support limb. This mechanism helps
energy necessary to body acceleration.37 to explain the high rate of adductor muscle strains in activi-
ties that involve running with abrupt direction change.40
Sidestep Cutting The efficiency of the mechanisms related to generation
After terminal deceleration, the directional change in cut- and transference of energy through trunk and pelvis rota-
ting maneuvers and subsequent propulsion involve coordi- tion depend not only on the rotational force transmission
nated movements of body segments. However, the dynam- capacity, but also on the kinetic chain global stiffness. An
ics involved in the kinetic chain during this phase differ adequate level of hip joint stiffness, for example, allows the
for the two types of cutting. The direction change during necessary force transmission through the kinetic chain to
Applied Biomechanics of Soccer • CHAPTER 12 293
promote appropriate movement patterns and consequently that is also observed only during crossover cutting is hip
decrease the stress demand on the lower limb joints. On the adduction in the support leg when the contralateral leg is
other hand, diminished hip or subtalar joint stiffness can crossing the body. This movement is accompanied by eccen-
promote altered movement patterns that may increase stress tric contraction of the gluteus medius, a muscle that has its
demand on some joints of the lower limb. This excessive fascial sheet fused with the deep surface of the tensor fascia
energy flow through the kinetic chain (i.e., stress demand) lata.41 Thus, the lateral structures of the hip, including the
is among the main factors responsible for injury produc- gluteus medius and tensor fascia lata, must have adequate
tion.10 The role of stress demand in injury production dur- strength and stiffness to control excessive hip adduction and
ing cutting maneuvers is discussed in more detail in the to prevent the occurrence of injuries around the hip.
“Biomechanics of Soccer-Related Injuries” section in this Cutting mechanisms vary substantially among sports and
chapter. individuals. The variability observed in cutting biomechanics
reports are possibly due to differences among subjects in
Crossover Cutting terms of techniques, cutting angle, movement speed during
Similar to the sidestep cutting, in crossover cutting, the the maneuver, or the type of movement performed immedi-
direction change with subsequent body propulsion is accom- ately before the cutting maneuver (e.g., running or landing
plished by energy storing-and-recovering mechanisms in the from a jump). For example, cutting movements performed
support limb, trunk, and pelvis. However, during crossover with cutting angles at approximately 90° require greater
cutting, trunk and forward pelvis rotation toward the sup- values for the breaking and propelling forces.32 The presence
port limb are observed, which cause internal hip rotation on of a defensive opponent during the maneuvers can also alter
this limb. This trunk and pelvis rotation allow the contralat- the kinematic and kinetic parameters normally reported by
eral limb to swing forward in the direction of the new path- biomechanical investigations on cutting mechanisms. Larger
way. The mechanism related to directional change during medial GRFs and larger hip abduction and knee valgus an-
crossover cutting also involves rotational force transmission. gles are observed during sidestep cutting when the presence
In this case, force is transmitted between internal hip rotator of defensive opponent is simulated.42 In addition, parame-
muscles and obliquus abdominis muscles to provide the ters such as cutting technique can influence the athlete’s
mechanical energy necessary to rotate the trunk and pelvis performance. Besier and colleagues,38 demonstrated that
and accelerate the body in the new direction. This rotational athletes who perform the sidestep cutting with a knee joint
force transmission mechanism increases the efficiency of the varus moment maintained greater speeds and achieved
movement and diminishes demand on the joints of the lower greater cutting angles than those who performed the same
limb. As explained previously, this energy transference task with a valgus moment on the knee. Thus, cutting tech-
throughout the kinetic chain depends on an adequate level nique may affect not only the player’s performance but also
of hip joint stiffness. For example, if the hip joint has the loads placed on the knee joint.
low stiffness, the energy generated by the trunk and pelvis
motions is, in great part, absorbed at the hip, which
decreases the energy transference to the support limb. Biomechanics of Heading
This altered energy flow allows potentially injury-producing Soccer is the only contact sport in which players frequently
motions to occur, such as excessive internal hip rotation and hit the ball with their head, called heading the ball or head-
subtalar joint pronation. ing, during matches or training. Scoring a goal, defending,
Although there is hip internal rotation during crossover gaining control, or passing the ball with the head is an inte-
cutting, the trunk and pelvis movements impose an external gral part of soccer. To accomplish these tasks, different
rotational torque on the femur. Because the limb is main- types of headers are normally used in soccer.43 In a clearing
tained in relative internal rotation and the femur is externally header, the player has to impact the ball to produce maxi-
rotated over the tibia of the planted foot, the crossover cut- mum force to drive the ball back in a safe direction. A pass-
ting is described as the functional equivalent of a clinical pivot ing header advances the ball over a small distance toward an
shift maneuver used to test the integrity of the anterior cruci- open area or a teammate. Finally, a shooting header must
ate ligament (ACL) and for anterolateral rotary instability.31 drive the ball, with appropriate speed and direction, to
Thus, the crossover cutting, similar to sidestep, imposes a reach the goal accurately (Table 12-5).44 Heading in soccer
great demand on the knee joint. For example, torques on the may be performed in multiple ways, which depends on the
knee joint can reach 140 Nm for an athlete with 75 kg of aim of the action, the game situation (e.g., position of the
body mass.38 Although the demands on the knee joint are ball and of the player during heading), and the technique
similar in both cutting maneuvers, the foot loading character- used. Furthermore, players can head the ball while on the
istic is different in a crossover cutting as compared with ground, when running, jumping vertically, and diving. For
sidestep cutting. In crossover cutting, the load acts mainly on example, a shooting header can be performed with different
the lateral aspect of the foot and the peak pressure occurs on strategies. In a game situation in which the player is posi-
the lateral portion of forefoot.33 Another kinematic pattern tioned approximately perpendicular to the goal and the ball
294 SECTION II • Applied Biomechanics of Selected Sport Activities
A B C
Figure 12-3
Heading phases. A, Preparation phase. B, Impact phase. C, Follow-through phase. See text for details.
limit the capacity of the head-neck complex to generate sternocleidomastoid, are active during this phase43,45 to
inertial and active torques and to deal with energy flows create a flexor torque that offsets the extensor torques
between the body and the ball. To meet such mechanical produced by the head weight and moment of inertia
demands, the neuromusculoskeletal system exploits the (about the cervical axes of rotation). During the impact
greater masses and inertial properties of the other segments phase, the cervical joints must have the greatest amount
of the upper body. The cervical joints must have high stiff- of stiffness. Such behavior produces a “sum of masses,”
ness and stability to transfer mechanical energy from the which increases the kinetic energy of the head-neck-trunk
kinetic chain to the ball. Cervical stiffness is also needed to unit, allowing an effective transfer of mechanical energy
absorb and dissipate the energy transferred from the ball to from the kinetic chain to the ball. Great trunk stiffness is
the body originating from internal reactive forces.10 Cervi- also required for such function. High cervical stiffness
cal stability is required during the whole heading action, during impact also permits the energy transferred from
during which there is minimal cervical angular motion (i.e., the ball to the head to flow through the upper body.
motion of the head in relation to the trunk), making the Hence, the reaction forces imparted by the ball can be
head-neck-trunk complex move together as one single distributed and dissipated through the kinetic chain. This
unit.43 Consequently, the linear and angular motions of the energy flow prevents high rotational cervical accelerations
head (in a global coordinate system) accompany the trunk and excessive energy absorption by the cervical structures.
motion. Increased cervical stiffness during the impact moment is
During the preparation phase, appropriate neck mostly generated by co-contraction of the cervical flexors
stiffness is necessary to make the motions of the head- and extensors, which begins a few milliseconds before and
in phase with the trunk motion,43 and thus to take ends a few milliseconds after the impact.43,45 Because of
advantage of the acceleration produced at the hips the very short duration of the ball-impact phase, the
and trunk. The cervical flexor muscles, especially the muscles do not have enough time to generate responsive
296 SECTION II • Applied Biomechanics of Selected Sport Activities
contraction adjustments before the end of the phase.43 is positively correlated with jumping vertical height) by
Therefore, part of the increased cervical stiffness, espe- co-contraction.52
cially the stiffness generated at ball impact, relies on the Inverse dynamic calculations have estimated that the
inherent and pre-existing passive and architectural prop- percentage contribution of work done during jumping in
erties of the cervical myofascial structures.48 During the soccer players was 43% for the hip, 29% for the knee, and
follow-through phase, cervical stability is also necessary to 28% for the ankle. It has been shown that players who jump
allow the kinetic energy of the anterior displacement of higher than their teammates (10 cm or more) produce
the head-neck-trunk to be dissipated by the stretching greater power at the ankle joint.53 Because the energy flow
and by eccentric contractions16 of the extensor muscles of between anatomically close and remote segments and joints
the hips and trunk. The cervical extensor muscles, espe- and that the kinetic parameters of each joint, estimated
cially the trapezius, are active,43,45 producing an extensor through inverse dynamics, do not provide sufficient infor-
torque that offsets the flexor torques produced by the mation about the forces and energy sources that generate
head weight and moment of inertia (about the cervical such parameters, it is not possible to affirm that the hip
axes of rotation). muscles are required more than the knee and ankle mus-
The minimal cervical angular motion suggests that the cles.9 For example, a three-dimensional model of the mus-
muscle contractions during heading are predominantly culoskeletal system, which considers energy flows, indicates
isometric.43 However, some eccentric and concentric con- that the plantar flexors generate approximately twice the
tractions probably occur in different internal compart- power produced by the gluteus maximus.54 The energy
ments of these muscles (mainly during the perturbations produced at each joint flows through the kinetic chain, and
created by the ball impact). Thus, energy-generating, thus the torques produced at each joint may be influenced
energy-absorbing, and energy-dissipative capabilities of by the forces produced in all of the joints involved in the
the cervical muscles are also required for proper heading jumping dynamics.9 Therefore, the combined actions of the
performance. The impact force and the amount and tim- muscles of the hips, knees, and ankles are necessary to pro-
ing of muscle activation depend on the type of heading. duce an effective jump, without overloading any of these
For example, when the objective is to perform a passing joints.
header, the player must apply less force and allow motion There is a high variability of jump technique among soc-
at the neck to refine the action and obtain more preci- cer players. Some of them emphasize motion and force
sion.45 In this case, less coactivation of neck muscles will generation at the knee joint, whereas others generate more
be observed, as well as an uncoupling between trunk and forces at the hip joint. In addition, high values for work
neck motions. production at the hip joint has been associated with low
Heading is a skill that is frequently embedded in other values at the knee joint.53 The variability in jumping pattern
body motions. Jumping is a task that often occurs associ- indicates that soccer athletes exploit the strategy that is
ated with heading. For example, jumping as high as possible more compatible with their available force production capa-
to reach the ball is a common requirement for effective bilities.10 Therefore, it is important to consider the contri-
heading in soccer. In fact, the height achieved during a bution of three lower limb joints when planning jumping
vertical jump is a predictor of different performance levels training and injury prevention programs for soccer players.
among soccer players.49,50 From the initial lower limb flex- After jumping and heading the ball, the athletes land on
ion to the take-off phase of vertical jumps, the lower limbs the ground. Landing involves movements designed to dis-
go into a flexed position and from there, they have to gen- sipate the kinetic energy through muscle power and joint
erate the necessary force to propel the entire body into the torques of the lower extremity.55 On landing, the GRF
air. This mechanical function is similar to the vertical must be attenuated by ankle dorsiflexion and knee and hip
dynamics of a mass-spring model or a pogo stick.8,51 During flexion. This lower limb flexion acts like a damping spring
hip and knee flexion and ankle dorsiflexion, the lower limbs to decrease inertial torque of the landing player. In addi-
absorb and store potential energy. Subsequently, during tion, hip and knee joint flexion-extension angular velocities
extension of the hip and knee and plantar flexion of the at the initial foot contact with the ground significantly
ankle, this energy is returned and more energy is added to affect the peak GRF during landing. Thus, eccentric con-
the system according to the desired height to be achieved tractions of the hip and knee extensor muscles during land-
by the head. There are bilateral hip and knee extensor net ing are necessary to reduce knee joint resultant force.15,56
torques and ankle plantar flexion net torque during these During landing, there are external torques of hip adduc-
motions. Eccentric contractions followed by concentric tion and knee abduction (valgus).57 To land with an ade-
contractions and stretching followed by shortening of the quate lower limb alignment in the frontal and transverse
hip and knee extensors and ankle plantar flexors are the planes of movement, an adequate amount of strength and
main mechanisms of the mass-spring dynamics of jumping. proper activation timing of the muscles of the hip and knee
The activity of the antagonists of these muscle groups has is needed, especially the hip abductors and external rota-
a crucial role in increasing the joints’ stiffness (which tors. Strength and adequate stiffness of the hip muscles are
Applied Biomechanics of Soccer • CHAPTER 12 297
required to control the adduction and internal rotation situations in which injuries may occur, in this section, the
of the hip. In addition to this proximal-to-distal effect stress demand and musculoskeletal injuries for each compo-
observed during landing from a jump, distal-to-proximal nent of soccer (kicking, cutting, and heading) are discussed
effects may also happen. The vertically directed GRF nor- separately. Because many pathological conditions share
mally generates foot pronation during landing;58 however, common causal mechanisms, the approach taken in this sec-
it depends on the current foot position and on the ana- tion is to group some conditions into one description to
tomical alignment of the foot and tibia. Because the foot is avoid unnecessary repetition. However, some overlap
the first body segment to receive the impact force during among the soccer components may occur, as different
landing, alignment disorders of the foot and tibia may mechanisms or movement patterns may produce similar
induce excessive subtalar joint pronation or supination. pathological conditions.
Excessive foot pronation may lead to excessive hip adduc-
tion and internal rotation and knee abduction. These
abnormal joint actions may influence the alignment of the Kicking-Related Injuries
lower limbs and the patterns of force transmission along The musculoskeletal system must have the capability of
the kinetic chain. withstanding the mechanical demands inherent to the
kicking action by exploiting the whole kinetic chain to
execute the task with maximum performance and mini-
Biomechanics of Soccer-Related Injuries mum injury risk. The biomechanical characteristics of the
One of the basic objectives of studying soccer kinetic and player and the interactions with the performed task and
kinematic characteristics and, more specifically, the inter- the environmental conditions may increase the demands
play between the athlete’s capability and demand during imposed on the musculoskeletal system during kicking.
soccer is to provide information that may assist in reducing Kicking-related pathological conditions occur when kick-
the player’s susceptibility to injury and improving perfor- ing demands overcome the system’s capability and are
mance. In this view, injury prevention and performance often related to inappropriate energy flow between the
depend on the capability of the musculoskeletal system to upper body and the lower swinging limb. Impaired mus-
deal with the resulting stress caused by the flow of forces cle function and altered passive stiffness of myofascial
(energy) through the kinetic chain. Classic approaches structures at the trunk, pelvis, and support limb leads to
involve the identification of intrinsic and extrinsic factors compensatory changes in the lower swing-limb mechanics
associated with injury production, but capability-demand to allow for an effective kick. These compensations con-
reasoning recognizes that factors such as the player’s ana- stitute increased demands on lower limb structures. Al-
tomic characteristics, game versus practice situations, and though many acute, overuse, and contact injuries may be
the use of inadequate equipment or field conditions can related to the mechanics of kicking, this section focuses
produce increased demands on the body segments. On the on muscle strains, tendinopathies, painful hip and knee
other hand, adequate levels of strength, stiffness, and conditions, and lumbopelvic dysfunctions, which are some
endurance define the capability of the player’s musculosk- of the most common pathological conditions that affect
eletal system. When the stress (energy) applied to a soccer players.2,60,61
particular tissue exceeds a critical limit (i.e., above the
player’s capability), injury occurs. Therefore, the aim of
any injury prevention program should be to achieve a bal-
ance between the player’s capabilities and the demands
Clinical Relevance Summary – Kicking Injuries
imposed by the sport.
The most common injuries during soccer practice • Kicking-related pathological conditions are often related to inap-
involve the lower extremity.30 Upper extremity injuries are propriate energy flow between the upper body and the lower
less common than lower extremity injuries and usually swinging limb, which requires excessive locally generated torques
occur after a fall to the ground or collision with another and imposes increased demands on lumbopelvic, hip, and knee
structures.
player. In fact, upper extremity injuries are more common
• Injuries of the knee and hip joints of the lower swing limb and of
in goalkeepers than in any other soccer playing position.30
the lumbopelvic complex may arise as a result of eccentric and
The majority of injuries observed in soccer are traumatic. concentric weaknesses of muscles such as the oblique abdominis,
For example, a high proportion of ankle and foot injuries the nonkicking-side pectoralis major and hip internal rotators,
results from player-to-player contact in tackling events.59 during the backswing, leg-cocking, and leg-acceleration phases,
In general, tackling produces lateral or medial forces that respectively. Eccentric weakness of muscles such as the
create a great demand in eversion or inversion of the foot nonkicking-side latissimus dorsi and bilateral gluteus maximus
and ankle during weight-bearing.59 However, during soccer may also overload lower swing-limb structures, during the follow-
activity many musculoskeletal injuries are also related through phase.
to overuse mechanisms. Because of the great variability of
298 SECTION II • Applied Biomechanics of Selected Sport Activities
understanding of the causes and consequences of a local athlete functionally (training proper movement patterns) in
injury requires a global assessment of the player and the the sport components that are related to the injury process.
knowledge about the complex biomechanical interactions For example, a soccer player who has a complaint of groin
of the musculoskeletal system. pain may have the following mismatches between the sport
The previous sections of this chapter focused on outlin- demands and his or her musculoskeletal capacities:
ing the demands imposed by soccer components and how 1. A player frequently involved in running and cutting
they come about to produce pathological conditions. The actions that have a reduced range of hip internal ro-
other side of the story is the athlete. To play soccer properly tation (e.g., hip retroversion) will impose increased
and safely, the player must meet the demands that are torsional stress on the SI joint. If this player, at
frequently imposed by the execution of the soccer compo- the same time, has weak trunk or pelvic stabilizer
nents. The presence of a weak link in the player’s kinetic muscles, resulting excessive motion of the SI joint
chain may result in reduced performance or increased risk will lead to increased stress to the pubic symphysis.
of developing a given pathological condition. The ability of 2. A constant running player (midfield or backside) who
the player to generate and transfer the proper energy to the supinates the foot during heel strike because of inad-
required movement, or distribute the excessive forces equate lower limb alignment (e.g., rearfoot varus,
among all body parts to protect the musculoskeletal system with altered running line of progression) will have
defines the player capacity. It is in the understanding of the reduced shock absorption by the quadriceps muscles,
relationship between task demand and player’s capacity as a result of insufficient knee flexion. If the player has
that lies the main role of the rehabilitation professional. weak gluteal, latissimus dorsi, abdominals, or other
Reducing demands and increasing the player capacity are lumbothoracic fascia muscle stabilizers, the SI joint or
the foundations of an effective rehabilitation program di- lower back will be overstressed and pain may result.
rected toward reducing the risk of injuries or improving the 3. A soccer kicker who has inefficient movement patterns
player’s performance. caused by weakness of the oblique abdominals, pecto-
ralis major, or upper limb muscles will excessively use
the hip muscles to propel the ball during free kicks or
Clinical Point - Rehabilitation long passes. In this case, increased action of the hip
adductors is triggered by the lack of adequate force
Reducing demands and increasing the player capacity are the founda-
transmission through the kinetic chain, increasing the
tions of an effective rehabilitation program directed toward reducing
stress on the adductor muscles or pubic symphysis.
the risk of injuries or improving the player’s performance.
In all of the previous examples, local structures such as
hip adductors or pubic symphysis are not the source of the
problem, but only the location of the complaint. Initially, to
Classical biomechanical analysis considers that most of treat such patients, it is necessary to assess the kinetic chain
the forces applied to or produced by the body are solely capability in relation to the sport demand (global thinking).
transmitted through joints.9,14 Biomechanical models based Second, the rehabilitation team must work on weak struc-
on this assumption frequently find forces that easily exceed tures that were ascertained to require improvement (local
the capacity of any biological tissue to withstand them. acting). Finally, the proper movement patterns or skills
Conversely, it has been suggested that the human body acts must be trained according to the demands normally applied
in synergistic manner, in which its continuing connective functionally during soccer matches (global acting). This
tissue network (i.e., muscles, tendons, ligaments, capsules, type of approach indicates that the athlete, not the patho-
and fascia) acts to redistributes the forces among all body logic condition, is the focus of the intervention.
structures. Recent concepts derived from the works on The body is a continuous network of interconnected
tensegrity98-100 and myofascial force transmission101,102 seem elements. In soccer, the presence of weak links in this
to indicate that forces flow within the musculoskeletal sys- kinetic chain is the main threat to the musculoskeletal sys-
tem in an integral manner. This understanding shifts the tem. However, the failure of the rehabilitation professional
focus on the analysis and treatment of separated body parts to recognize the global nature of the injury-producing
to the assessment and rehabilitation of the whole. factors is an even greater threat to the player. The under-
Rehabilitation of the soccer athlete entails a clinical rea- standing of the complex relations among the sport require-
soning approach by the sport rehabilitation professional. In ments and the musculoskeletal system’s capability is the key
essence, clinical reasoning requires the practitioner to think factor for the proper treatment of the athlete. The
globally, act locally, and then act again globally. In clinical demands of soccer are multiple, as many of the sport com-
terms, it means that the rehabilitation team must understand ponents overlap during games and practices. However, the
the demands imposed by soccer; assess globally the athlete understanding of how the musculoskeletal system is orga-
(looking for weak links in the kinetic chain); treat locally nized to deal with the forces arising from the interaction
the areas that have inadequate strength, stiffness, endurance, between the athlete and environment is a primary step
or demonstrate improper alignment; and, finally, treat the toward planning an adequate intervention.
304 SECTION II • Applied Biomechanics of Selected Sport Activities
45. Bauer JA, Thomas TS, Cauraugh JH, et al: Impact forces and 66. Brown SH, McGill SM: How the inherent stiffness of the in vivo
neck muscle activity in heading by collegiate female soccer play- human trunk varies with changing magnitudes of muscular acti-
ers, J Sports Sci 19(3):171–179, 2001. vation, Clin Biomech (Bristol, Avon) 23(1):15–22, 2008.
46. Naunheim RS, Bayly PV, Standeven J, et al: Linear and angular 67. Howarth SJ, Beach TA, Callaghan JP: Abdominal muscles
head accelerations during heading of a soccer ball, Med Sci Sports dominate contributions to vertebral joint stiffness during the
Exerc 35(8):1406–1412, 2003. push-up, J Appl Biomech 24(2):130–139, 2008.
47. Tysvaer AT: Head and neck injuries in soccer. Impact of minor 68. Bonci CM: Assessment and evaluation of predisposing factors to
trauma, Sports Med 14(3):200–213, 1992. anterior cruciate ligament injury, J Athl Train 34(2):155–164,
48. Brown IE, Loeb GE: A reductionist approach to creating and us- 1999.
ing neuromusculoskeletal models. In Winters J, Crago P, editors: 69. Olsen OE, Myklebust G, Engebretsen L, et al: Injury mechanisms
Biomechanics and neuro-control of posture and movement, for anterior cruciate ligament injuries in team handball: A system-
New York, 2000, Springer-Verlag. atic video analysis, Am J Sports Med 32(4):1002–1012, 2004.
49. Smith R, Ford KR, Myer GD, et al: Biomechanical and perfor- 70. Yu B, Garrett WE: Mechanisms of non-contact ACL injuries,
mance differences between female soccer athletes in National Br J Sports Med 41 Suppl 1:i47–51, 2007.
Collegiate Athletic Association Divisions I and III, J Athl Train 71. Pollard CD, Sigward SM, Powers CM: Gender differences in hip
42(4):470–476, 2007. joint kinematics and kinetics during side-step cutting maneuver,
50. Wisloff U, Castagna C, Helgerud J, et al: Strong correlation of Clin J Sport Med 17(1):38–42, 2007.
maximal squat strength with sprint performance and vertical 72. Houck J, Yack HJ: Associations of knee angles, moments and
jump height in elite soccer players, Br J Sports Med 38(3): function among subjects that are healthy and anterior cruciate
285–288, 2004. ligament deficient (ACLD) during straight ahead and crossover
51. Laffaye G, Bardy BG, Durey A: Leg stiffness and expertise in cutting activities, Gait Posture 18(1):126–138, 2003.
men jumping, Med Sci Sports Exerc 37(4):536–543, 2005. 73. Lloyd DG: Rationale for training programs to reduce anterior
52. Nagano A, Komura T, Yoshioka S, et al: Contribution of non- cruciate ligament injuries in Australian football, J Orthop Sports
extensor muscles of the leg to maximal-effort countermovement Phys Ther 31(11):645–654; discussion 661, 2001.
jumping, Biomed Eng Online 4:52, 2005. 74. Ireland ML, Willson JD, Ballantyne BT, et al: Hip strength in
53. Vanezis A, Lees A: A biomechanical analysis of good and females with and without patellofemoral pain, J Orthop Sports
poor performers of the vertical jump, Ergonomics 48(11–14): Phys Ther 33(11):671–676, 2003.
1594–1603, 2005. 75. Cook JL, Khan KM: What is the most appropriate treatment for
54. Nagano A, Komura T, Fukashiro S: Optimal coordination of patellar tendinopathy? Br J Sports Med 35(5):291–294, 2001.
maximal-effort horizontal and vertical jump motions—A com- 76. Junge A, Dvorak J: Soccer injuries: A review on incidence and
puter simulation study, Biomed Eng Online 6:20, 2007. prevention, Sports Med 34(13):929–938, 2004.
55. Devita P, Skelly WA: Effect of landing stiffness on joint kinetics 77. Ergen E, Ulkar B: Proprioception and ankle injuries in soccer,
and energetics in the lower extremity, Med Sci Sports Exerc Clin Sports Med 27(1):195–217, 2008.
24(1):108–115, 1992. 78. Barker HB, Beynnon BD, Renstrom PA: Ankle injury risk factors
56. Yu B, Lin CF, Garrett WE: Lower extremity biomechanics dur- in sports, Sports Med 23(2):69–74, 1997.
ing the landing of a stop-jump task, Clin Biomech (Bristol, Avon) 79. Ibrahim A, Murrell GA, Knapman P: Adductor strain and hip
21(3):297–305, 2006. range of movement in male professional soccer players, J Orthop
57. Hewett TE, Myer GD, Ford KR, et al: Biomechanical measures Surg (Hong Kong) 15(1):46–49, 2007.
of neuromuscular control and valgus loading of the knee predict 80. Neptune RR, Wright IC, van den Bogert AJ: Muscle coordina-
anterior cruciate ligament injury risk in female athletes: A pro- tion and function during cutting movements, Med Sci Sports
spective study, Am J Sports Med 33(4):492–501, 2005. Exerc 31(2):294–302, 1999.
58. Kernozek TW, Torry MR, H Van Hoof, et al: Gender differences 81. Garrett WE, Jr.: Muscle strain injuries: Clinical and basic aspects,
in frontal and sagittal plane biomechanics during drop landings, Med Sci Sports Exerc 22(4):436–443, 1990.
Med Sci Sports Exerc 37(6):1003–1012; discussion 1013, 2005. 82. Mair SD, Seaber AV, Glisson RR, et al: The role of fatigue in
59. Giza E, Fuller C, Junge A, et al: Mechanisms of foot and ankle susceptibility to acute muscle strain injury, Am J Sports Med
injuries in soccer, Am J Sports Med 31(4):550–554, 2003. 24(2):137–143, 1996.
60. Lundin O, Hellstrom M, Nilsson I, et al: Back pain and radio- 83. Smodlaka VN: Medical aspects of heading the ball in soccer, Phys
logical changes in the thoraco-lumbar spine of athletes. A long- Sportsmed 12:127–131, 1984.
term follow-up, Scand J Med Sci Sports 11(2):103–109, 2001. 84. Aubry M, Cantu R, Dvorak J, et al: Summary and agreement
61. Volpi P, Melegati G, Tornese D, et al: Muscle strains in soccer: statement of the 1st International Symposium on Concussion in
A five-year survey of an Italian major league team, Knee Surg Sport, Vienna 2001, Clin J Sport Med 12(1):6–11, 2002.
Sports Traumatol Arthrosc 12(5):482–485, 2004. 85. Delaney JS, Frankovich R: Head injuries and concussions in soc-
62. Kujala UM, Kettunen J, Paananen H, et al: Knee osteoarthritis in cer, Clin J Sport Med 15(4):216–219; discussion 212–213,
former runners, soccer players, weight lifters, and shooters, Arthritis 2005.
Rheum 38(4):539–546, 1995. 86. Kirkendall DT, Jordan SE, Garrett WE: Heading and head inju-
63. Gabbe BJ, Bennell KL, Finch CF, et al: Predictors of hamstring ries in soccer, Sports Med 31(5):369–386, 2001.
injury at the elite level of Australian football, Scand J Med Sci 87. Kartal A, Yildiran I, Senkoylu A, et al: Soccer causes degenera-
Sports 16(1):7–13, 2006. tive changes in the cervical spine, Eur Spine J 13(1):76–82,
64. Major NM, Helms CA: Pelvic stress injuries: the relationship 2004.
between osteitis pubis (symphysis pubis stress injury) and sacro- 88. Zmurko MG, Tannoury TY, Tannoury CA, et al: Cervical sprains,
iliac abnormalities in athletes, Skeletal Radiol 26(12):711–717, disc herniations, minor fractures, and other cervical injuries in the
1997. athlete, Clin Sports Med 22(3):513–521, 2003.
65. Jansen JA, Mens JM, Backx FJ, et al: Diagnostics in athletes with 89. Alexander RM, Vernon A: The dimensions of knee and
long-standing groin pain, Scand J Med Sci Sports 18(6):679–690, ankle muscles and the forces they exert, J Hum Movement Stud
2008. 1:115–123, 1975.
306 SECTION II • Applied Biomechanics of Selected Sport Activities
90. Zhang SN, Bates BT, Dufek JS: Contributions of lower extremity 97. Joseph M, Tiberio D, Baird JL, et al: Knee valgus during drop
joints to energy dissipation during landings, Med Sci Sports jumps in National Collegiate Athletic Association Division I
Exerc 32(4):812–819, 2000. female athletes: The effect of a medial post, Am J Sports Med
91. Decker MJ, Torry MR, Wyland DJ, et al: Gender differences 36(2):285–289, 2008.
in lower extremity kinematics, kinetics and energy absorption dur- 98. Ingber DE: Tensegrity I. Cell structure and hierarchical systems
ing landing, Clin Biomech (Bristol, Avon) 18(7):662–669, 2003. biology, J Cell Sci 116(Pt 7):1157–1173, 2003.
92. Fonseca ST, Vaz DV, Aquino CF, et al.: Muscular co-contraction 99. Ingber DE: Tensegrity II. How structural networks influence
during walking and landing from a jump: Comparison between cellular information processing networks, J Cell Sci 116(Pt 8):
genders and influence of activity level, J Electromyogr Kinesiol 1397–1408, 2003.
16(3):273–280, 2006. 100. Levin SM: A different approach to the mechanics of the human
93. Ireland ML: Anterior cruciate ligament injury in female athletes: pelvis: Tensegrity. In: Vleeming A, Mooney V, Dorman TA, et al,
Epidemiology, J Athl Train 34(2):150–154, 1999. editors: Movement, stability and low back pain, New York, 1997,
94. Hewett TE, Paterno MV, Myer GD: Strategies for enhancing Churchill Livingstone.
proprioception and neuromuscular control of the knee, Clin 101. Huijing PA: Muscular force transmission necessitates a multilevel
Orthop Relat Res (402):76–94, 2002. integrative approach to the analysis of function of skeletal muscle,
95. Lephart SM, Ferris CM, Riemann BL, et al: Gender differences Exerc Sport Sci Rev 31(4):167–175, 2003.
in strength and lower extremity kinematics during landing, Clin 102. Huijing PA, Jaspers RT: Adaptation of muscle size and myofascial
Orthop Relat Res (401):162–169, 2002. force transmission: A review and some new experimental results,
96. Heinert BL, Kernozek TW, Greany JF, et al: Hip abductor Scand J Med Sci Sports 15(6):349–380, 2005.
weakness and lower extremity kinematics during running, J Sport
Rehabil 17(3):243–256, 2008.
13
CHAPTER
307
308 SECTION II • Applied Biomechanics of Selected Sport Activities
Figure 13-1
The running cycle and its various components.
Applied Biomechanics of Running • CHAPTER 13 309
at which time a new cycle is initiated. The primary purpose Table 13-1
of the flight or recovery phase is to add momentum to the Typical Range-of-Motion Values for the Lower Extremities
center of mass by means of the swinging limb. During Running
During the flight or recovery phase, the airborne or non-
Running
support period occurs. This is the period in which neither
Phase Joint Motion
foot is in contact with the ground, in contrast to walking
where one foot is always in contact with the ground. Foot Hip 45° to 20° flexion at midsupport
Because there is a brief period where neither foot is in con- strike* to Knee 20° to 40° flexion by midsupport
tact with the ground, when the swinging foot recontacts the midsupport† Ankle 5° plantar flexion to 10° dorsiflexion
ground at foot strike, the magnitude of ground reaction Midsupport Hip 20° flexion to 5° extension
force is substantially increased in comparison with walking. to takeoff‡ Knee 40° to 15° flexion
Various studies have indicated that the ground reaction Ankle 10° to 20° dorsiflexion
force during running may be as much as two to three times
Follow- Hip 5° to 20° hyperextension
greater than seen when walking.15,16 This increase in the
through§ Knee 15° to 5° flexion
magnitude of ground reaction force is an example of Ankle 20° to 30° plantar flexion
Newton’s second law of motion, which states that force is
equivalent to mass times acceleration. If an individual’s Forward Hip 5° to 20° hyperextension
swing¶ Knee 15° to 5° flexion
mass remains constant and he or she accelerates his or her
Ankle 20° to 30° plantar flexion
mass, then the ground reaction forces at foot strike will be
increased. This is certainly the case when going from walk- Foot Hip 65° to 40° flexion
ing to running. Furthermore, a by-product of this change descent|| Knee 130° to 20° flexion
in ground reaction force is an increase in both the ampli- Ankle 0° to 5° dorsiflexion to 5° plantar
tude and the rate of foot pronation during the support flexion
phase of running. These factors, which are unique to run-
* Foot strike begins when the foot first touches the ground and
ning, can combine to result in an injury that would not continues until the foot is firmly fixed.
necessarily occur during walking. †
Midsupport starts when the foot is fixed and continues until the
heel leaves the ground.
‡
Joint Movements During Running Take-off begins when the heel starts to rise and continues until
the toes leave the ground.
The amount of joint movement that occurs at the hip, §
Follow-through begins as the trailing foot leaves the ground and
knee, and ankle during the running cycle is different from continues until the foot ceases rearward motion. It includes the
that which occurs during the walking cycle. A summary of airborne period.
joint movements in the lower extremity during running is ¶
Forward swing starts with forward motion of the foot and stops
found in Table 13-1. As previously noted, overuse injuries when the foot reaches its most forward position.
||
Foot descent starts after the recovering foot has reached its most for-
to the knee region are commonly seen in runners. To
ward position, reverses direction, and then terminates with foot strike.
illustrate one of the major differences between running
and walking, the position of the knee joint when the foot
makes contact with the ground is significantly different.
During walking, the knee joint is either completely influences tibial internal rotation and supination influ-
extended or flexed approximately 5° at the time of heel ences tibial external rotation).
strike. In contrast, at the instant of foot strike while run- To effectively manage overuse injuries associated with
ning, the knee joint is already in at least 20° of flexion. running, it is important to have an understanding of the
This flexed position of the knee is important to assist the changes in range of motion at the hip, knee, and ankle
runner in attenuating impact forces that are being applied joints throughout the different phases of gait. From foot
through the lower extremity. Unfortunately, this greater strike to midsupport, hip joint flexion decreases from 45° to
degree of knee flexion also causes increased compressive 20°, whereas knee joint flexion increases from 20° to 40°.
forces between the patella and femur. This is an important The position of the ankle (talocrural) joint at foot strike is 5°
factor, considering the extremely high incidence of knee plantar flexed, with progression to 10° dorsiflexion by the
injuries in runners, particularly to the patellofemoral midsupport phase.
joint. This flexed position of the knee joint at foot strike From midsupport to takeoff, the hip joint moves from
also implies that the flexibility of the soleus muscle is just 20° of flexion to a 5° extended position, helping to propel
as important as the flexibility of the gastrocnemius when the runner’s mass forward in preparation for the next foot
assessing range of motion in runners. Furthermore, this strike. The knee joint decreases the amount of its flexion by
supports the importance that the subtalar joint has on the moving from a 40° to a 15° position. Finally, the talocrural
rotatory component of the tibia and the subsequent joint moves from a 10° dorsiflexed position to a 20° dorsi-
alignment and tracking of the patella (e.g., foot pronation flexed position.
310 SECTION II • Applied Biomechanics of Selected Sport Activities
During the flight or recovery phase, the swinging limb his or her stride length. By shortening his or her stride,
assists in increasing the forward momentum of the runner, the runner with a diagnosis of plantar fasciitis can enhance
thereby improving efficiency. During the follow-through the possibility of contacting the ground with the midfoot
phase of recovery, the hip joint, starting from a 5° position, rather than with the rearfoot, thereby decreasing impact
moves into further hyperextension of 20° supporting the stress to the heel tissues. This midfoot contact will also
importance of proper gluteus maximus strength and neuro- allow for a more efficient transition to the forefoot by not
muscular recruitment. The knee joint starts in a 15° flexed decelerating the body like runners who aggressively foot
position and moves to within 5° of full extension. The talo- strike on their heels with every stride.
crural joint moves from a 20° plantar flexed position to
approximately 30° of plantar flexion. As was previously
mentioned, during forward swing, the hip joint moves into Stride Length
its most maximally flexed position. Thus, the hip joint
moves a total of 85° from a 20° extended position into a Each runner has an optimal stride length and stride length changes
65° flexed position. At the same time, the knee joint under- (increases) as the runner’s speed increases and may vary if running
goes 125° of motion, moving from a 5° flexed position to surface is level, uphill, or downhill or on treadmill.
almost 130° of flexion. This amount of knee joint motion is
significantly greater than that during walking, which is only
65° to 70°, and is related to the greater amount of momen-
tum generated by the lower limbs during running. Finally, Finally, stride length can also vary depending on the com-
the talocrural joint will move from 30° of plantar flexion to fort level of a runner on a treadmill. For example, if an indi-
a position of neutral (0°). Finally, during foot descent, the vidual is uncomfortable or inexperienced on a treadmill
hip joint will move from a 65° flexed position to 40° of during a gait evaluation, that runner will often tend to
flexion, whereas the knee joint moves from 130° of flexion shorten his or her stride length. In some cases, the runner
to 20° of flexion in preparation for foot strike. The talocru- will actually present as a forefoot striker versus the natural
ral joint will move from 0° to 5° of dorsiflexion to 5° of “outdoor running” stride. This forefoot strike position is
plantar flexion in preparation for foot strike. inherently more rigid and provides increased stability for the
runner. This is an important factor that the clinician needs
Stride Length Characteristics to determine as it may influence any subsequent recommen-
A major issue when evaluating a client’s running cycle is dations on footwear or the need for a foot orthosis.
the optimal stride length for that individual runner, as
well as variations in stride length that can occur with Foot Placement During Running
different speeds of running. In general, stride length Another factor that differs between walking and running is
increases as the speed of the runner increases. However, a variation in the base of gait, or the distance between the
there are variations depending on whether the person is midpoints of the heels. Murray and colleagues reported
running on level ground, uphill, downhill, or on a tread- that in walking, the typical base of gait for both men and
mill. Cavanagh17 notes that when running uphill, stride women was approximately 2 to 4 inches (5 to 10 cm).20,21
length decreases, whereas during downhill running, stride However, in running, this value approaches zero or
length is typically increased. Landry and Zebas note that can even fall on or cross over the line of progression
improved running performance is generally associated (midline).17 The reason for this decrease in base of gait
with increased stride rate, but not necessarily with during running is because of an increase in the functional
increased stride length.18 Cavanagh and Williams demon- limb varus of the entire support leg. Functional limb varus
strated that at a specific running speed, each individual is defined as the angle between the bisection of the lower
has a stride length that appears to be optimal in terms of leg and the floor. An increase in functional limb varus
using the most efficient metabolic energy necessary for results during the period of single-limb support when the
running.19 Their study further showed that forcing an pelvis is shifted laterally over the single supporting lower
individual to lengthen or shorten his or her stride could extremity. During running, the entire center of mass of the
possibly increase energy cost by 1% to 2%. This is an body must be placed over the single support foot. During
important point for clinicians to remember when they are walking, however, even though there is a period of single
considering advising runners to decrease or increase their limb support, the movement of the body’s center of mass
stride length. In some cases, it might seem impractical to is not usually displaced completely over the single support
suggest that runners change their self-selected stride foot. Bogdan and colleagues were the first to report that
length because of the possibility of increasing energy there was an increase in functional limb varus during run-
costs, but certain injuries may dictate a recommendation ning.22 In their report, Bogdan and colleagues noted that
to modify stride length. For example, the individual who there was an approximate 10° increase in functional limb
is having heel pain might be advised to reduce or shorten varus in running as compared with walking.
Applied Biomechanics of Running • CHAPTER 13 311
McPoil and Cornwall assessed five female and five male The clinician must also consider the effect of functional
cross-country runners using two-dimensional videography limb varus on foot movement. If the amount of functional
to determine the change in functional limb varus during limb varus increases during running, a greater degree of
running in comparison with walking.23 The average increase foot pronation is required to allow the foot to remain plan-
in functional limb varus when going from walking to run- tigrade to the supporting surface. Thus, even if the runner
ning was approximately 5°. Figure 13-2 illustrates the in- does not excessively pronate during walking, the increase in
crease in functional limb varus in a runner while walking functional limb varus during the running cycle will cause a
and running. greater degree of pronation during running. This increased
Recognition of this increase in functional limb varus amount of foot pronation may lead to excessive soft tissue
by the clinician is important when evaluating the runner, stress in the lower extremity. The end result may lead to
as a change in alignment can increase both valgus stress the development of any number of pathological conditions
at the knee and pronation of the foot. The clinician involving the foot, lower leg, knee, thigh, hip, or pelvis.
should attempt to evaluate the change in the angle Because of the greater amount of foot pronation required
of the lower leg to the floor when evaluating runners with during running, clinicians should counsel their clients in the
lower extremity injuries. This is accomplished by having use of proper running footwear that matches their specific
the individual shift his or her weight laterally while foot type and biomechanics. Generally speaking, that is a
standing with both feet in contact with the ground shoe that has adequate rearfoot stabilization. Running
(Figure 13-3, A) and then assuming a position of single- shoes with enhanced rearfoot stabilization features can
limb support (see Figure 13-3, B). We have found that assist in controlling excessive foot pronation, thereby reduc-
the average increase in single-limb varus when shifting ing soft tissue stress while running. Further discussion on
from standing on both feet to standing on a single limb is footwear recommendations and foot orthotic management
approximately 5°. may be found in a later section.
Figure 13-2
The effect of walking and running on functional limb varus.
312 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 13-2
Clinical Example: Comparison of Early versus Late Pronation in Decision Making
Case Example Subtalar Joint Motion Clinical Observation Clinical Recommendations
Relaxed Partial
Stance* Squat†
“Early pronator” 10° of pronation 12° of pronation Of the 12° measured, the Try a footwear change to a
majority of the motion was stability shoe to control
observed early in the static rearfoot motion.
relaxed position consistent
with the period between
the foot-strike and midfoot
support phase of running.
“Late pronator” 5° of pronation 14° of pronation Of the 14° measured, the Consider the use of a foot
majority of the motion was orthosis with medial rear-
observed later in the static foot to forefoot posting to
partial-squat position assist with keeping the foot
consistent with the period in a more neutral position,
of take-off during running. along with a stability or
straight-last cushion shoe.
*Sell et al.34 method for evaluating subtalar joint pronation using an inclinometer in a relaxed weight-bearing position.
†
Modified technique using Sell et al.34 method of evaluating subtalar joint using an inclinometer in a dorsiflexed (partial squatting) position
of 20°.
Figure 13-5
Two-dimensional rear view analysis of downward pelvic obliquity.
A, Left stance leg measuring 3.5° of maximum downward pelvic
obliquity. B, Right stance leg measuring 10.3° of maximum
downward pelvic obliquity. (Reprinted with permission from
Agility Physical Therapy & Sports Performance, Portage,
Michigan.)
A B
activity, the lower extremity might compensate for frontal muscle is active during the early support phase and then
plane pelvic drop via increased genu valgum. These studies diminishes toward the end of the support phase.49-51 The
point toward a relationship between frontal plane pelvic lack of appreciable activity during the late support and early
drop and gluteus medius muscle fatigue. swing phases shows that muscle contraction is not respon-
In summary, excessive pelvic drop can potentially sible for limiting hip extension. The hip joint extensors,
increase the soft tissue stresses at the hip, knee, and foot specifically the gluteus maximus, demonstrate EMG activity
through the functional limb varus angulations. This is com- early in the foot-descent period, and this activity continues
monly attributed to lack of functional strength, neuromus- through the first 40% of the support phase.14 Whereas the
cular recruitment, or endurance of the gluteus medius on hip joint abductors demonstrate similar EMG activity in
the stance leg. both walking and running, the adductors show increased
EMG activity throughout the entire support phase.
Knee Joint
Important Clinical Point At the time of foot strike, the quadriceps muscle is very
The stance phase of running is a closed kinetic chain activity, which active in preparation for the rapid loading that occurs at this
requires proximal stability to control the absorption of contact forces. time. The quadriceps muscle group reaches peak activity
If proximal instability is present, the body may be put at a biome- during the early support phase.49-51 Quadriceps muscle
chanical disadvantage for absorbing contact forces, which, in turn, activity during this period of the running cycle facilitates the
can place the runner at an increased risk for lower extremity injury. shock attenuation process as the hip, knee, and ankle joints
Hip abductor weakness, specifically gluteus medius, has been found undergo flexion to create a shortening of the lower extrem-
to have an association with injury, and is therefore often addressed ity. The hamstring muscles have been shown to be active
during the rehabilitation of runners.7,38,46,47 from before foot strike until the hip joint completes its
period of extension later in the support phase.50,51 The ac-
tivity reported before foot strike is responsible for slowing
the rapidly extending knee in preparation for loading.50-52
Muscle Activity During Running The later activity helps to propel the runner’s body mass
In general, investigations of muscle action during running forward.
have demonstrated increased magnitudes of EMG activity
in comparison with walking.48 In addition, the duration of Ankle Joint
EMG activity has been found to be longer during the sup- The tibialis anterior muscle is active at the instant of
port phase of running in comparison with the stance phase foot strike so as to provide a stable base of support by
of walking.48 However, the reader should be aware that the co-contracting with the triceps surae muscles.50-52 The
majority of researchers have used surface electrodes, rather muscle’s activity during the early portion of the support
than indwelling or fine-wire electrodes, to study EMG phase is much more variable than at other times in the run-
activity because of the velocity and intensity of the motions ning cycle. The tibialis anterior muscle has been shown to
required for running. be both active as well as absent from foot strike until the
foot is plantigrade to the ground.50,51,53,54 The observed
Hip Joint absence of tibialis anterior activity might be caused by the
Hip joint flexors have been shown to have a greater period variation in foot placement at contact by different runners.
of EMG activity during the forward swing of running than A rearfoot striker may need the tibialis anterior muscle to
during the swing phase of walking. The rectus femoris contract eccentrically to allow smooth plantar flexion after
316 SECTION II • Applied Biomechanics of Selected Sport Activities
Running Kinetics
Influence of Ground Reaction Forces
During walking, the vertical component of the ground reac-
tion force acting through the lower extremity throughout
the stance phase is approximately 125% of body weight. The
vertical component of the ground reaction force is typically
greater during the latter half of the walking cycle when the
A
propulsion period is occurring. Several studies have shown
that the vertical component of ground reaction force during
distance running is usually 150% to 200% greater than dur-
ing slow walking.61,62 Cavanagh and LaFortune noted that
the typical distance runner who runs approximately 130 km
(80.8 miles) a week subjects each lower extremity to
approximately 40,000 such impacts over a 7-day period.61
Drez states that vertical force values of two to three times
body weight can occur at foot strike during running and
jogging.63 He further notes that there are approximately
800 foot strikes on each foot in a 1-mile run.
Drez also notes that for this reason, adequate midsole B
cushioning in a running shoe is necessary to help the body
attenuate or lessen the effect of these impact forces. Oth- Figure 13-6
ers are in agreement that a shock-absorbing orthoses Shock attenuation model. A, Diagram 1 illustrates a simple plunger
(semiflexible) is generally indicated versus a rigid device and cylinder system. Diagram 2 depicts the system with a shock
attenuation spring added. Diagram 3 shows the system compressed
in the management of lower extremity overuse injuries to under some compressive load (F). B, Diagrams 1 and 2 illustrate
assist in the attenuation of impact forces associated with the shock attenuation model applied to the lower extremities during
running.64-69 walking. See text for further explanation.
Applied Biomechanics of Running • CHAPTER 13 317
B
Figure 13-10
Surface area in a high-arch and a low-arch individual.
Q angle.82 Arch index, leg length, and ankle and knee range
of motion were not found to be significant discriminators. Foot Pronation
Moss and colleagues found that heavy subjects and those Abnormal foot pronation has been identified as a major
with a larger static quadriceps Q angle were more likely to cause of foot, lower leg, knee, thigh, and hip running inju-
have patellofemoral stress syndrome.83 Because an activity ries, including plantar fasciitis, ITB friction syndrome,
such as running involves numerous repetitions of knee ex- patellofemoral pain and medial shin pain (“shin splints” or
tension, Moss and colleagues83 noted that it was possible for medial tibial stress syndrome). Schuster, in describing the
a small variation in the Q angle to cause symptoms. influence of the environment on the foot of long distance
A more recent study, however, conducted by Caylor and runners, indicated that foot deformities, such as rearfoot
colleagues found no significant difference in the Q angle (calcaneal) varus, tibial varus, and forefoot varus, were a
between 52 patients with anterior knee pain syndrome and common cause of extreme structural imbalance within the
a control group of 50 subjects without anterior knee pain foot, causing excessive pronation.87 Excessive pronation
syndrome.84 The intratester reliability for the determination of both the rearfoot and midfoot during running causes
of the Q angle was quite good, but increased Q angles were increased stress on the soft tissues surrounding the various
not responsible for anterior knee pain syndrome in this joints of the foot, including the capsule, ligaments, and
group of patients. plantar aponeurosis. More importantly, there can be an
over-reliance on lower leg and foot musculature in an
attempt to control excessive foot mobility and provide a
Important Clinical Point: Managing Knee Pain more stabile foot structure. Thus, a thorough evaluation to
in Runners determine whether these various foot abnormalities exist
appears to be a sound method to predict which individuals
As running and multisport events have continued to increase in
might develop lower quarter injuries.
popularity, so has the incidence of knee pain. This common overuse
In a study that attempted to determine the causal factors
injury manifests itself in various forms or diagnoses, including patel-
lar tendinitis, patellofemoral pain syndrome, or iliotibial band (ITB) associated with selected running injuries, Messier and Pittala
friction syndrome. The causal factors for these types of injuries have collected anthropometric and motion data on runners
been discussed in the literature with a common consensus that there affected with ITB friction syndrome, shin splints, or plantar
may be a problem proximally or a problem distally. However, it is fasciitis.88 The groups studied consisted of a control group
astounding how many clinicians still continue to treat the symptoms of 19 healthy subjects, a shin splint group (17 subjects),
at the knee. It is critical in the successful management of running a plantar fasciitis group (15 subjects), and an ITB group
athletes to address the hip and the ankle and foot, as well as the (13 subjects). All of the runners underwent an evaluation
knee. Some key areas to evaluate: that included foot prints, determination of plantar flexion
Hip and dorsiflexion range of motion, hamstring and lower leg
• Gluteus medius and hip lateral rotator strength flexibility testing, and assessment of Q angle and leg length.
• Recruitment pattern for both gluteus maximus and medius The authors also determined total rearfoot motion and
• Flexibility of iliopsoas (can inhibit gluteus maximus function con- time from maximal pronation to maximal supination by ana-
sistent with lower crossed syndrome described by Janda85,86) lyzing film records. The results of their study indicated that
• Length flexibility and fascial mobility of the ITB the only significant discriminator between the plantar fasci-
Ankle and Foot itis group and the control group was that the fasciitis group
• Talocrural (ankle) joint mobility, especially dorsal glide had greater plantar flexion range of motion. No other
• The ability to “lock out” the oblique midtarsal joint with significant differences could be validated statistically. They
supination did note, however, that the ITB friction syndrome group
• Mobility assessment for subtalar joint, midtarsal joint and first ray had a significantly higher arch foot structure than the con-
• Appropriate shoe recommendations consistent with the runner’s trol group, and the shin splint and ITB friction groups had
foot type less ankle dorsiflexion range of motion than the control
• Foot orthosis recommendations considering both rearfoot and
group. The results of this study seem to question the
forefoot
accepted theory that structural deformities in the foot cause
There is sufficient research to support the need for the continued
drive toward evidence-based practice. Furthermore, the research a deviation in alignment leading to the development of foot
completed provides a foundation and a stimulus for further research problems.
to answer the “burning questions” that still exist. The chance of suc- Ross and Schuster conducted a similar study in which
cessfully managing a runner with ITB friction syndrome by simply they attempted to predict injuries in distance runners.89
performing ultrasound over the bursa, instructing him or her in They evaluated 63 runners, measuring inversion and ever-
seated isometric vastus medialis oblique (VMO) quadriceps sets, and sion of the subtalar joint, the position of the subtalar
recommending a motion-control shoe (without looking at the ath- joint (to determine whether a varus or valgus deformity of
lete’s feet) as a treatment plan is not only unlikely, it is a sign of poor the hindfoot existed), forefoot varus or valgus, and the
treatment. One should think “function” and look at the “big picture.” amount of available dorsiflexion at the ankle with the knee
joint both flexed and extended. They also performed two
Applied Biomechanics of Running • CHAPTER 13 321
weight-bearing measurements: resting calcaneal stance posi- to accurately predict which individuals will develop lower
tion and neutral calcaneal stance position. Based on their extremity overuse injuries. Furthermore, the literature
results and considering the cause of lower extremity injuries strongly suggests that it is extremely difficult to pinpoint
studied, the authors concluded that there was not one single the actual cause of an overuse injury. Often individuals
“cause-and-effect” factor responsible for running injuries. who exhibit the most profound lower extremity and
Warren and Jones attempted to determine those anatomic foot malalignments are asymptomatic, whereas those indi-
factors that could be used to predict plantar fasciitis in viduals with an “ideal” runner’s alignment—including
long distance runners.90 Forty-two runners were classified as symmetric hip rotation, no evidence of external or internal
(1) having no history of plantar fasciitis, (2) currently having malleolar torsion, and a “normal” foot structure with
plantar fasciitis, or (3) having recovered from plantar fasciitis. minimal pronation—can be highly susceptible to overuse
Various measurements were taken on each subject, including injuries. Because of these problems, we believe that a tissue
leg length, degree of pronation from neutral, arch height of stress model that is based on the load-deformation curve
the foot, and dorsiflexion and plantar flexion of the ankle. The can assist the clinician in understanding the effect of lower
results of the study were interesting in that the control group extremity and foot malalignments on the development of
who had never had a history of plantar fasciitis actually had a overuse injuries in runners.
greater degree of pronation than both of the other two groups. Each individual runner has his or her own level of toler-
These authors noted that perhaps plantar fasciitis was caused ance for the amount of tissue stress that can be withstood
by excessive overuse stress rather than faulty biomechanics. during the activity of running. The importance of this indi-
Little has been written regarding the runner with a high-arch vidual level of tissue stress tolerance can be illustrated using
and hypomobile foot structure. Schuster noted that runners the load-deformation curve (Figure 13-11). The load-
with high-arch foot structure had an extremely rigid foot, and deformation curve consists of two regions or zones: an
their joint ranges of motion were usually less than average.87 elastic region and a plastic region.91 A load-deformation
He further noted, as has been previously discussed, that they curve is commonly used by material engineers to explain the
had a much smaller weight-bearing pattern and difficulty in degree of deformation that occurs when a load is applied to
attenuating impact forces. Thus, the runner with limited rear- an object. The region or area separating the elastic and
foot motion could be classified as having decreased shock at- plastic regions is termed the microfailure zone. Although
tenuation and increased plantar pressures, especially in the deformation occurs when the load is applied, the object
forefoot, secondary to limited midfoot loading. being tested can completely recover from the deformation,
provided the deformation does not exceed the microfailure
Use of the Load-Deformation Curve zone. If deformation of the object exceeds the microfailure
zone and enters the plastic region, then permanent,
to Explain Running Injuries nonrecoverable deformation will occur.
Although numerous factors have been outlined as possible The deforming force may be from a single load or
causes of overuse injuries in the lower extremity and the summation of several loadings. To illustrate the effect
foot, it does not appear that any study to date has been able of loads applied to soft tissue during running, using the
Figure 13-11
Schematic of the load-deformation principle of soft tissue.
322 SECTION II • Applied Biomechanics of Selected Sport Activities
load-deformation curve, the elastic region represents the EVA or PU in combination with the existing cushioning
normal “give and take” of soft tissues as the foot is loaded materials. This type of construction is referred to as a dual
and unloaded during the running cycle. As long as the run- density midsole. Finally, the “upper” is the soft body of the
ner maintains the level of tissue stress within this elastic re- shoe that encloses the foot and is usually made of a combi-
gion, the amount of soft tissue stress will most likely be nation of materials, from lightweight, durable synthetic
tolerated and an overuse injury will be avoided. mesh to heavier materials such as leather. The materials and
The various factors that contribute to excessive tissue construction of the upper provide stability, comfort, and a
stress include the amount of stress applied to the soft tis- snug fit. Features to consider in the upper include the last
sues, the amount of extrinsic and intrinsic muscle activity (the shape of the shoe), the toe box (the front of the shoe),
required to enhance foot stability, and the degree of abnor- the heel counter (the part holding the heel, which can vary
mal lower extremity and foot alignment. If these factors can in stiffness for increased stability), and the Achilles notch
be balanced so that the tissues never go beyond the elastic (a groove in the heel piece to protect the tendon from
range and enter the microfailure zone, then injury will be irritation). Running footwear can be divided into four
avoided. If runners increase their running speed or the primary categories related to their overall cushioning and
training distance is accelerated too quickly, soft tissues may stability properties (Box 13-1). The shoe categories are
enter the microfailure zone, resulting in an overuse stress (1) light cushion, (2) straight last cushion, (3) stability, and
injury. If the runner does not rest the injured tissues when (4) motion control.
microtrauma is present, the stressed tissues can eventually A light cushion running shoe (Figure 13-12, A) is best
be taken beyond the microfailure zone and into the plastic for a true supinatory foot or for someone who is an under-
range, with the result being a breakdown of soft tissues, pronator. This foot type is generally fairly rigid in nature
muscle guarding, and pain. The load-deformation curve with pes cavus presentation, and thus does not absorb shock
also provides a model to explain the effectiveness of foot- during the initial contact phase of running. A light cushion
wear and foot orthoses in precluding excessive tissue stress running shoe is not a very substantial shoe and is con-
by restricting excessive motion and preventing soft tissues structed of single-density material for the midsole with
from entering the microfailure zone. minimal arch support. This shoe is extremely flexible
through the arch to allow the foot as much motion as pos-
Footwear Considerations sible. In general, a light cushion shoe will break down
rather quickly (typically in less than 400 miles [643 km]).
in the Management of Running Injuries A straight last cushion running shoe (see Figure 13-12, B)
It is evident that the cause of overuse running injuries is a is a newer category shoe, described by one author as a hy-
multifactorial problem and successful management often brid shoe that is a transition shoe between a light cushion
relies on sound decision-making by the clinician. One key shoe and a stability shoe (described in the following para-
factor is the consideration of matching the appropriate graph). This type of shoe is best for someone who is an
footwear to an individual’s foot classification, including underpronator, but still presents with some forefoot or
alignment, mobility and biomechanical factors related to rearfoot alignment concerns (e.g., forefoot varus or calca-
running. Clinically, footwear recommendations are a neces- neal varus). This foot type is generally somewhat rigid, but
sary complement to the various treatment approaches for more accurately does not have the necessary motion avail-
running injuries, including therapeutic exercise for lower able at the subtalar joint to accommodate for the positional
quarter imbalances, foot orthosis intervention, or the faults (e.g., uncompensated forefoot varus). This unique
judicious use of modalities. shoe still employs the single-density cushioning material for
To provide appropriate recommendations on running the midsole, while providing more inherent stability based
footwear, having a basic understanding of how the shoe is on the geometry of the shoe (straight last construction)
constructed is important. The key features of a running versus implementing a dual-density midsole or stability sys-
shoe include the outsole, midsole, and upper. The outsole tem commonly seen in the stability shoes. Clinically, this
is the bottom of the shoe and is generally made from carbon shoe provides a more stable platform for the foot and foot
or blown rubber. The midsole is the shock-absorbing layer orthosis to function without the extrinsic influence of the
between the outsole and the “upper” part of the shoe. This shoe, which may or may not be desirable.
midsole is the most important part of a running shoe, as the A stability running shoe (see Figure 13-12, C) is best for
construction and materials used will impact the levels of someone who is a mild to moderate overpronator. This type
both cushioning and stability in the shoe. The amount of of shoe generally has enough mobility in the subtalar joint
cushioning in the shoe is generally proportionate to the to assist in shock absorption during stance phase. This shoe
shoe’s heel height. The two types of cushioning generally encompasses some additional stability through the midsole
found in running shoes are ethylene vinyl acetate (EVA) with some type of added stability feature like a dual density
and polyurethane (PU). Increased stability in a shoe is ac- material found in most brands or the Graphite Rollbar sys-
complished through the incorporation of a heavier-density tem found exclusively in the New Balance shoes. A stability
Applied Biomechanics of Running • CHAPTER 13 323
Data from Gazelle Sports, Grand Rapids, Michigan and Agility Physical Therapy and Sports Performance, Portage, Michigan.
EVA, Ethylene vinyl acetate; PU, polyurethane.
*Board last construction primarily used with older running shoes and basketball shoes. Combination last primarily used now in newer running shoes.
324 SECTION II • Applied Biomechanics of Selected Sport Activities
A B
C D
Figure 13-12
Running shoe categories. A, Light cushion. B, Straight last cushion. C, Stability. D, Motion control.
(Reprinted with permission from Gazelle Sports, Grand Rapids, Michigan.)
shoe does allow for some flexibility through the midfoot, it is imperative that the individual’s foot type matches the
but has enough rigidity to provide pronation control. shoe by evaluating whether the runner has a flexible or rigid
Finally, a motion control shoe (see Figure 13-12, D) is foot type. Next, consider whether the runner has an overall
designed for the moderate-to-severe overpronator. This foot neutral, varus, or valgus alignment. In the case in which a
type generally has the same forefoot and rearfoot alignment runner has a forefoot varus combined with a rigid foot type,
concerns, but by stark contrast to the more rigid foot, has this is clinically a challenging foot type to manage. Further-
an excessive amount of subtalar or midtarsal joint motion more, overstabilizing someone’s foot can be just as detri-
available. A foot type that can compensate for a forefoot or mental to the soft tissue structures of the lower extremity as
calcaneal varus can present dynamically as an overpronator understabilizing the foot. Finally, consideration needs to be
(at midsupport) or as a late pronator (at takeoff). This made with an individual who has significantly different foot
causes the foot to roll inward, placing excessive stress on types (e.g., left foot is supinatory foot; right foot is an over-
soft tissue structures proximal to the foot, including lower pronator). In this example, the best clinical decision may be
leg, knee, hip, and back. Motion control shoes are straight- to understabilize the foot with a straight-last cushion shoe
lasted and have a very broad base for support. Motion and selectively increase the stability through a customized
control shoes are also constructed of either a dual density foot orthosis (Box 13-2).
midsole or a Graphite Rollbar system. This shoe is very rigid Other factors to take into consideration are the type of
through the midsole, much more so than the stability shoe, foot striker (e.g., midfoot versus forefoot); the distance the
to provide maximum pronation control. runner is training for (e.g., 5 K versus marathon); body
When making footwear recommendations, there are weight (e.g., heavier versus lighter runner); selecting a
several factors to consider that can influence the type of training shoe versus a racing shoe; the width of the runner’s
shoe that is ideal for each individual runner. Most important, foot (e.g., selecting the shoe manufacturer that has a wider
Applied Biomechanics of Running • CHAPTER 13 325
Box 13-2 Clinically Important Point: Possible Footwear Recommendations Based on Foot Type
Case Example Shoe Recommendation Orthosis Recommendation
#1 Rigid foot type (underpronator) Straight last cushion Semiflexible
Forefoot varus (uncompensated) Full-length device
Medial posting into the forefoot only
leaving the rearfoot in neutral
Clinical Rationale: This individual does not have enough motion to compensate for the forefoot deformity, so overstabilization of the rearfoot
(subtalar joint) is undesirable. By placing this individual in a straight last cushion shoe, a good stable foundation allows the orthosis to
function. By only posting the forefoot, the alignment concern will be addressed with less influence on the rearfoot.
#2 Left foot ⫽ underpronator Straight last cushion Semiflexible
Right foot ⫽ overpronator Full-length device
Forefoot varus bilaterally L⫽ Medial posting into the forefoot only
R ⫽ Medial posting from the rearfoot
to the forefoot
Clinical Rationale: This individual does not have enough motion to compensate for his or her forefoot deformity only on the left, but does
have the necessary available range of motion on the right in the subtalar joint. Placing the individual in a straight last cushion shoe will allow
a good stable foundation for the orthosis to function while not overstabilizing the left foot. The orthotic can then be individually
adjusted to meet the needs of each foot.
toe box); whether or not an orthosis will be used in the are present that predispose it to injury or exacerbation of
shoe; and the runner’s past history of running injuries. existing injuries. However, in many cases, when a lower
limb overuse injury is present, there are lower extremity
extrinsic or primary-foot abnormalities present. An
Footwear Recommendations orthosis can be used to control abnormal compensatory
movements of the foot by “bringing the floor to the
• Make sure foot type (e.g., flexible, rigid) matches type of shoe. foot.”101 This will allow the foot to function more effi-
• Determine whether athlete has a neutral, varus, or valgus foot. ciently in a subtalar-joint-neutral position and provide the
• Remember both feet may not be the same.
necessary support so that the foot does not have to move
• What type of foot striker is the runner (heel, micfoot, forefoot)?
abnormally.
• What distance does the runner run per week?
• What is the runner’s weight? When making a clinic decision regarding the type of device
• What type of shoe is needed? to use, it is important to have an understanding of how the
• Is there a history of past injuries? device is to function. There are two basic types of orthoses:
• Will the runner be wearing an orthotic in the shoe?
Table 13-3 lateral side of the forefoot and/or rearfoot to correct the
Rigid versus Semiflexible Orthoses—Advantages pathological deformities. The rigid-type shell can be made
and Disadvantages from carbon graphite, acrylic rohadur or (polyethylene) hard
plastic. The hard plastic shell is used when control require-
Type Advantage Disadvantage
ments are paramount to firmly restrain excessive foot motion.
Rigid Rearfoot—arch No forefoot support However their rigidity results in the loss of some shock
orthosis support or correction absorption and are most commonly used to correct walking
High control Sacrifices shock deformities. For the more active sports specific individuals, a
acquired absorption semirigid shell may be used. These shells are made from ther-
Several different More difficult to moplastic, rubber or leather. A semi-rigid device can provide
available materials make adjustments both shock absorption and motion control under increased
Intrinsic* Typically, not a loading while retaining its original shape. Flexible devices are
corrections from a comfortable with made of felt or dense foam and offer more shock absorption
neutral mold impact athletes
and less control but have a disadvantage in that they do not
Rigid materials less
likely to break
maintain their rigidity and wear out faster. The flexible devices
down are often used as a temporary correction or to determine if the
Able to get into a orthotic will correct the problem and, if so, then a semi-rigid
low-profile shoe device is made and used.99,102-104
Semiflexible Rearfoot–forefoot Semiflexible materials
orthosis support will eventually break
Accommodative Orthosis
Motion control down Accommodative orthoses are the flexible devices mentioned
acquired with Less likely to achieve in the biomechanical orthoses section above that allow the
shock absorption the high control foot to compensate but are not concerned about maintain-
Several different More difficult to get ing the foot in the subtalar neutral position. These devices
available materials into a lower profile are used in people with congenital malformations, restricted
Extrinsic† posting shoe ROM, neurological and neuromuscular problems, or physi-
on neutral module ological old age. Flexible, soft materials are used to fabricate
(shell) the shell (felt or dense foam) and are designed to yield to
Adjustments are the forces applied to the foot on weight bearing rather than
easy to accomplish
resist them.102-104
Typically more
When specifically dealing with running athletes, it is one
comfortable for
impact athletes author’s experience that a semiflexible, full-length device
Able to address (i.e., full length at the foot) using extrinsic posting on a
several forefoot neutral module (see Figure 13-13, C) is recommended for
abnormalities several clinical reasons. First, the functions of the foot dur-
ing the gait cycle are adaptation, shock absorption, rigid sup-
Data from Biocorrect Custom Foot Orthotics Lab, Kentwood, port for leverage, and torque conversion. More specifically,
Michigan. at foot strike, the foot acts as a shock absorber to the
*Intrinsic posting is a means of achieving the recommended
impact forces and then adapts to the uneven surfaces. If the
corrections by modifying the shape of the rigid material from the
original neutral mold. prescribed device is rigid (e.g., carbon fiber), this rigidity
†
Extrinsic posting is a means of achieving the recommended creates the potential for decreased shock absorption by the
corrections by adding different durometer (stiffness) materials to device attenuated through the soft tissue structures and
a neutral shell, which can be easily adjusted by using a grinder less ability for the foot to adapt to the surface. Further-
(to reduce) or by adding additional materials (to increase).
more, at take-off, the foot has to return to a rigid lever to
transmit the explosive force from the lower extremity to
the running surface. In cases in which the clinician has
Biomechanical Orthosis noted primary abnormalities of the foot related to the fore-
Biomechanical orthoses are either hard, semirigid or flexible foot (e.g., forefoot varus), consideration needs to be given
devices that are used to help maintain the foot at or near sub- to addressing this alignment issue with a full-length device
talar joint neutral (Figure 13-13). These rigid, semirigid or to assist in the transition back to a rigid foot from a supple
flexible “shells” are used to correct forefoot and/or rearfoot foot. Finally, most researchers concur that the use of
deformities that are thought to be causing pathology. The orthotic therapy is both a “science and an art.” There are
rigid and semirigid shells are molded from a neutral cast. advantages to using extrinsically posted, neutral-module
These shells use noncompressible postings (i.e., wedges of devices (versus intrinsically designed modules) such as ease
different angles to limit foot movement) on the medial or of modifications or adjustments. With extrinsically posted
Applied Biomechanics of Running • CHAPTER 13 327
References
1. James SL, Bates BT, Osternig LR: Injuries to runners, Am J
Sports Med 6:40–50, 1978.
2. Lutter LD: Injuries in the runner and jogger, J Am Podiatr Med
Assoc 70:45–50, 1980.
3. Kerner JA, D’Amico JC: A statistical analysis of a group of run-
C ners, J Am Podiatr Med Assoc 73:160–164, 1983.
4. Paluska SA: An overview of hip injuries in running, Sports Med
Figure 13-13 35:991–1014, 2005.
Biomechanical orthosis. A, Rigid, sulcus-length device. B, Semiflexible, 5. Yu B, Queen RM, Abbey AN, et al: Hamstring muscle kinematics
full-length device. C, Semiflexible, full-length device with rearfoot to and activation during overground sprinting, J Biomech 41:
forefoot medial posting. (Reprinted with permission from Biocorrect 3121–3126, 2008.
Custom Foot Orthotics Lab, Kentwood, Michigan.) 6. Sugiura Y, Saito T, Sakuraba K, et al: Strength deficits identified
with concentric action of the hip extensors and eccentric action
of the hamstrings predispose to hamstring injury in elite sprinters,
J Orthop Sports Phys Ther 38:457–464, 2008.
7. Niemuth PE, Johnson RJ, Myers MJ, Thieman TJ: Hip muscle
weakness and overuse injuries in recreational runners, Clin J
Sports Med 15:14–21, 2005.
328 SECTION II • Applied Biomechanics of Selected Sport Activities
8. Kocher MS, Tucker R: Pediatric athlete hip disorders, Clin Sports 34. Sell KE, Verity TM, Worrell TW, et al: Two measurement tech-
Med 25:241–253, 2006. niques for assessing subtalar joint position: a reliability study,
9. Clement DB, Ammann W, Taunton JE, et al: Exercise-induced J Orthop Sports Phys Ther 19:162–167, 1994.
stress injuries to the femur, Int J Sports Med 14:347–352, 35. Novacheck TF: The biomechanics of running, Gait Posture
1993. 7:77–95, 1998.
10. Slocum DB, James SL: Biomechanics of running, JAMA 205: 36. Schache AG, Bennell KL, Blanch PD, Wrigley TV: The coordi-
97–100, 1968. nated movement of the lumbo-pelvic-hip complex during run-
11. James SL, Brubaker CE: Biomechanics of running, Orthop Clin ning: a literature review, Gait Posture 10:30–47, 1999.
North Am 4:605–611, 1973. 37. Schache AG, Blanch PD, Rath D, et al: Three-dimensional angu-
12. Adrian MJ, Kreighbaum E: Mechanics of distance-running dur- lar kinematics of the lumbar spine and pelvis during running,
ing competition. In Jokl E, editor: Biomechanics III, Baltimore, Human Mov Sci 21:273–293, 2002.
1973, University Park Press. 38. Fredericson M, Cookingham CL, Chaudhari AM, et al: Hip
13. Deshon DE, Nelson RC: A cinematographical analysis of sprint abductor weakness in distance runners with iliotibial band
running, Res Q 35:451–455, 1964. syndrome, Clin J Sports Med 10:169–175, 2000.
14. Mann RA, Hagy J: Biomechanics of walking, running and sprint- 39. Cichanowski HR, Schmitt JS, Johnson RJ, Niemuth PE: Hip
ing, Am J Sports Med 8:345–350, 1980. strength in collegiate female athletes with patellofemoral pain,
15. Roy B: Caracteristiques biomecaniques de la course d’endurance, Med Sci Sports Exerc 39:1227–1232, 2007.
Can J Appl Sports Sci 7:104–116, 1982. 40. Beckman SM, Buchanan TS: Ankle inversion injury and hyper-
16. Sprague P, Mann RV: The effects of muscular fatigue on the kinet- mobility: Effect on hip and ankle muscle electromyography onset
ics of sprint running, Res Q Exerc Sport 54:60–66, 1983. latency, Arch Phys Med Rehabil 76:1138–1143, 1995.
17. Cavanagh PR: The biomechanics of lower extremity action in 41. Sims KJ, Richardson CA, Brauer SG: Investigation of hip abduc-
distance running, Foot Ankle 7:197–217, 1987. tor activation in subjects with clinical unilateral hip osteoarthritis,
18. Landry M, Zebas CJ: Biomechanical principles in common running Ann Rheum Dis 61:687–692, 2002.
injuries, J Am Podiatr Med Assoc 75:48–52, 1985. 42. Long WT, Dorr LD, Healy B, Perry J: Functional recovery of
19. Cavanagh PR, Williams KW: The effect of stride length variation noncemented total hip arthroplasty, Clin Orthop Relat Res
on oxygen uptake during distance running, Med Sci Sports Exerc 288:73–77, 1993.
14:30–34, 1982. 43. Watanabe H, Shimada Y, Sato K, et al: Gait analysis before or
20. Murray MP, Drought AB, Kory RC: Walking patterns of normal after varus osteotomy of the femur for hip osteoarthritis, Biomed
men, J Bone Joint Surg Am 46:335–360, 1964. Mater Eng 8:177–186, 1998.
21. Murray MP, Kory RC, Sepic BS: Walking patterns of normal 44. Jacobs C, Uhl TL, Seeley M, et al: Strength and fatigability of
women, Arch Phys Med Rehabil 51:637–650, 1970. the dominant and nondominant hip abductors, J Athl Train
22. Bogdan RJ, Jenkins D, Hyland T: The runner’s knee syndrome. 40:203–206, 2005.
In Rinaldi RR, Sabia M, editors: Sports medicine, Mount Kisco, 45. Eggen JM, Carcia CR, Gansneder BM, Shultz SJ: Hip abductor
NY, 1978, Futura Publishing. fatigue affects knee motion during the landing phase of a drop
23. McPoil TG, Cornwall MW: Influence of running on functional jump, J Athl Train 38(2, Suppl):S22, 2003.
limb varus, Unpublished data, 1992. 46. Ireland ML, Willson JD, Ballantyne BT, Davis IM: Hip strength
24. Bates BT, Osternig LR, Mason BR, et al: Functional variability of in females with and without patellofemoral pain, J Orthop Sports
the lower extremity during the support phase of running, Med Sci Phys Ther 33(11):671–676, 2003.
Sports Exerc 11:328–331, 1979. 47. Leetun DT, Ireland ML, Wilson JD, et al: Core stability mea-
25. Areblad M, Nigg BM, Ekstrand J, et al: Three-dimensional sures as risks for lower extremity injury in athletes, Med Sci Sports
measurement of rearfoot motion during running, J Biomech Exerc 36(6):926–934, 2004.
23:933–940, 1990. 48. Boden F, Volkert R, Menke W, et al: Computer-assisted electro-
26. Soutas-Little RW, Beavis GC, Verstraete MC, et al: Analysis of myographic running studies of athletic shoes with various sole
foot motion during running using a joint co-ordinate system, configurations. In Segesser B, Pforringer W, editors: The shoe in
Med Sci Sports Exerc 19:285–293, 1987. sport, Chicago, 1989, Year Book Medical.
27. Engsberg JR, Andrews JG: Kinematic analysis of the talocalca- 49. Brandell BR: An analysis of muscle coordination in walking and
neal/talocrural joint during running support, Med Sci Sports Exerc running gaits. In Jokl E, editor: Biomechanics III, Baltimore,
19:275–284, 1987. 1973, University Park Press.
28. Rodgers MM, LeVeau BF: Effectiveness of foot orthotic devices 50. Elliott BC, Blanksby BA: A biomechanical analysis of the male
used to modify pronation in runners, J Orthop Sports Phys Ther jogging action, J Hum Mov Stud 5:42–51 1979.
4:86–90, 1982. 51. Elliott BC, Blanksby BA: The synchronization of muscle activity
29. Nigg BM, Herzog W, Read LJ: Effect of viscoelastic shoe insoles and body segment movements during a running cycle, Med Sci
on vertical impact forces in heel-toe running, Am J Sports Med Sports Exerc 11:322–327, 1979.
16:70–76, 1988. 52. Frigo C, Pedotti A, Santambrogio G: A correlation between
30. Nigg BM, Morlock M: The influence of lateral heel flare of run- muscle and ECG activities during running. In Terauds J, Dale G,
ning shoes on pronation and impact forces, Med Sci Sports Exerc editors: Science in athletics, Del Mar, CA, 1979, Academic
19:294–301, 1987. Press.
31. Stacoff A, Reinschmidt C, Stussi E: The movement of the heel 53. Mann RA, Hagy JL: The function of the toes in walking, jog-
within a running shoe, Med Sci Sports Exerc 24:695–701, ging, and running, Clin Orthop Relat Res 142:24–29, 1994.
1992. 54. Dietz V, Schmidtbleicher D, Noth J: Neuronal mechanisms of
32. Clarke TE, Frederick EC, Hamill CL: The effects of shoe design human locomotion, J Neurophysiol 42:1212–1222, 1979.
parameters on rearfoot control in running, Med Sci Sports Exerc 55. Williams KR: Biomechanics of running, Exerc Sports Sci Rev
15:376–381, 1983. 13:389–441, 1985.
33. Reinschmidt C, Stacoff A, Stussi E: Heel movement within a 56. Miyashita M, Matsui M, Miura M: The relation between
court shoe, Med Sci Sports Exerc 24:1390–1395, 1992. electrical activity in muscle and speed of walking and running.
Applied Biomechanics of Running • CHAPTER 13 329
In Vredenbregt J, Wartenweiler JW, editors: Biomechanics II, 79. James SL: Chondromalacia of the patella in the adolescent. In
Baltimore, 1971, University Park Press. Kennedy JC, editor: The injured adolescent knee, Baltimore,
57. Hoshikawa T, Matsui H, Miyashita M: Analysis of running pat- 1979, Williams & Wilkins.
tern in relation to speed. In Jokl E, editor: Biomechanics III, 80. Buchbinder MR, Napora NJ, Biggs EW: The relationship of
Baltimore, 1973, University Park Press. abnormal pronation to chondromalacia of the patella in distance
58. Komi PV: Biomechanical features of running with special empha- runners, J Am Podiatr Med Assoc 69:159–162, 1979.
sis on load characteristics and mechanical efficiency. In Nigg B, 81. Heil B: Running shoe design and selection related to lower limb
Kerr B, editors: Biomechanical aspects of sport shoes and playing biomechanics, Physiotherapy 78:406–412, 1992.
surfaces, Calgary, 1983, University of Calgary, 1983. 82. Messier SP, Davis SE, Curl WW, et al: Etiologic factors associated
59. Knuttgen HG: Oxygen uptake and pulse rate while running with with patellofemoral pain in runners, Med Sci Sports Exerc
undetermined and determined stride lengths at different speeds, 23:1008–1015, 1991.
Acta Physiol Scand 52:366–371, 1961. 83. Moss RI, DeVita P, Dawson ML: A biomechanical analysis of
60. Ito A, Fuchimoto T, Kaneko M: Quantitative analysis of EMG patellofemoral stress syndrome, J Athl Training 27:64–69, 1992.
during various speeds of running. In Winter DA, Normal RW, 84. Caylor D, Fites R, Worrell TW: The relationship between quad-
Wells RP, et al, editors: Biomechanics IX, Champaign, IL, 1985, riceps angle and anterior knee pain syndrome, J Orthop Sports
Human Kinetics Publishers. Phys Ther 17:11–16, 1993.
61. Cavanagh PR, LaFortune MA: Ground reaction forces in dis- 85. Janda V, editor: Movement patterns in the pelvic and hip region
tance running, J Biomech 13:397–406, 1980. with special reference to pathogenesis of vertebrogenic disturbances,
62. Dickinson JA, Cook SD, Leinhardt TM: The measurement of Prague, Czechoslovakia, 1964, Charles University.
shock waves following heel strike while running, J Biomech 86. Jull GA, Janda V: Muscles and motor control in low back pain:
18:415–422, 1985. assessment and management. In Twomey LT, Taylor JR, editors:
63. Drez D: Running footwear: Examination of the training shoe, Physical therapy of the low back, New York, 1987, Churchill-
the foot, and functional orthotic devices, Am J Sports Med Livingstone.
8:140–141, 1980. 87. Schuster RO: Foot types and the influence of environment on the
64. Michaud TC, Nawoczenski DA: The influence of two different foot of the long distance runner, Ann NY Acad Sci 301:881–887,
types of foot orthoses on first metatarsophalangeal joint kinemat- 1977.
ics during gait in a single subject, J Manipulative Physiol Ther 29: 88. Messier SP, Pittala KA: Etiologic factors associated with selected
60–65, 2006. running injuries, Med Sci Sports Exerc 20:501–505, 1988.
65. Saxena A, Haddad J: The effect of foot orthoses on patellofemoral 89. Ross CF, Schuster RO: A preliminary report on predicting injuries
pain syndrome, J Am Podiatr Med Assoc 93:264–271, 2003. in distance runners, J Am Podiatr Med Assoc 73:275–277, 1983.
66. MacLean CL, Davis IS, Hamill J: Short- and long-term influences 90. Warren BL, Jones CJ: Predicting plantar fasciitis in runners, Med
of a custom foot orthotic intervention on lower extremity dynamics, Sci Sports Exerc 19:71–73, 1986.
Clin J Sport Med 18:338–343, 2008. 91. Cornwall MW: Biomechanics of noncontractile tissue: A review,
67. McNicol K, Taunton JE, Clement DB: Iliotibial tract friction Phys Ther 64:1869–1873, 1984.
syndrome in athletes, Can J Appl Sport Sci 6:76–80, 1981. 92. Bates BT, Osternig L, Mason B: Foot orthotic devices to modify
68. Gross ML, Napoli RC: Treatment of lower extremity injuries selected aspects of lower extremity mechanics, Am J Sports Med
with orthotic shoe inserts. An overview, Sports Med 15:66–70, 7:338–342, 1979.
1993. 93. Cavanaugh PR: An evaluation of the effects of orthotics force distri-
69. Gross ML, Davlin LB, Evanski PM: Effectiveness of orthotic shoe bution and rearfoot movement during running. Paper presented
inserts in the long-distance runner, Am J Sports Med 19:409–412, at meeting of American Orthopedic Society for Sports Medicine,
1991. Lake Placid, 1978.
70. Dillman CJ: A kinetic analysis of the recovery leg during sprint 94. Collona P: Fabrication of a custom molded orthotic using an
running. In Cooper J, editor: Biomechanics, Chicago, 1971, intrinsic posting technique for a forefoot varus deformity, Phys
Athletic Institute. Ther Forum 8:3, 1989.
71. Hamill J, Bates BT, Knutzen KM, et al: Variations in ground 95. Gill E: Orthotics, Runner’s World, Feb:55–57, 1985
reaction force parameters at different running speeds, Hum 96. Itay S: Clinical and functional status following lateral ankle
Movement Sci 2:47–56, 1983. sprains: Follow-up of 90 young adults treated conservatively,
72. Nigg BM: Biomechanics of running shoes, Champaign, IL, 1986, Orthop Rev 11:73–76, 1982.
Human Kinetics Publishers. 97. Rogers MM, LeVeau BF: Effectiveness of foot orthotic devices
73. Heil B: Lower limb biomechanics related to running injuries, used to modify pronation in runners, J Orthop Sports Phys Ther
Physiotherapy 78:400–406, 1992. 4:86–90, 1982.
74. Becker N-L: Specific running injuries and complaints related to 98. Subotnick SI: The flat foot, Phys Sports Med 9:85–91, 1981.
excessive loads: Medical criteria of the running shoe. In Segesser 99. Subotnick SI, Newell SG: Podiatric sports medicine, Mt Kisko,
B, Pforringer W, editors: The shoe in sport, Chicago, 1987, Year NY, 1975, Futura.
Book Medical. 100. Williams JGP: The foot and chondromalacia—a case of biome-
75. McMahon TA, Valiant G, Frederick EC: Groucho running, chanical uncertainty, J Orthop Sports Phys Ther 2:50–51, 1980.
J Appl Physiol 62:2326–2337, 1987. 101. Hunter S, Dolan M, Davis M: Foot orthotics in therapy and sports,
76. Nachbauer W, Nigg BM: Effects of arch height of the foot Champaign, IL, 1996, Human Kinetics Publishers.
on ground reaction forces in running, Med Sci Sports Exerc 102. American Physical Rehabilitation Network: When the feet hit the
24:1264–1269, 1992. ground . . . everything changes. Program outline and prepared
77. Root ML, Orien WP, Weed JH: Clinical biomechanics, Vol 2: notes—a basic manual, Sylvania, OH, 2000.
Normal and abnormal function of the foot, Los Angeles, 1977, 103. American Physical Rehabilitation Network: When the feet hit the
Clinical Biomechanics Corporation. ground . . . take the next step. Program outline and prepared
78. McConnell J: The management of chondromalacia patellae: notes—an advanced manual, Sylvania, OH, 1994.
A long term solution, Aust J Physiother 32:215–223, 1986. 104. Voight M, Hoogenboom B, Prentice W: Musculoskeletal interventions:
techniques for therapeutic exercise, New York, McGraw-Hill, 2006.
330 SECTION II • Applied Biomechanics of Selected Sport Activities
331
332 SECTION II • Applied Biomechanics of Selected Sport Activities
During the freestyle stroke, 70% of the “most pain” and two demonstrated bursal contact only.2 Two of the
occurred during the first half of pull-through.2 Another specimens with intra-articular cuff contact demonstrated
vulnerable point of the stroke appeared during the first half greater tuberosity contact with the acromion. The site
of recovery (18% of the symptoms were elicited during this of intra-articular contact was the most common in the
phase) (Figure 14-1). During the first half of the pull- anterior-superior labrum (five specimens). Cadaver speci-
through, the arm is unilaterally pulling the body over the mens greatly simplify the issue of shoulder problems in
arm as the arm generates the propulsive force. The humerus swimmers because they cannot account for the inflammation
has a common tendency to be hyperextended relative to the that would accompany the microtrauma of injury. The
trunk rotation toward the submerged side (Figure 14-2, A). inflammation could cause more, or different, areas of con-
In this position, the humeral head is pushing anteriorly. Any tact. The cadavers cannot account for any pathological insta-
anterior impingement, labral damage, or inflammation bility or muscular fatigue or substitution mechanics that may
would be aggravated in this position. occur. Although simplified, this cadaver model allows a clini-
Toward midrecovery, the humerus is swinging the fore- cian to understand the multiplicity of anatomical contact
arm forward. When the elbow is too high and close to the areas (bursal and intra-articular areas) during the most
body, the humerus is in hyperextension, which is most likely painful phase of the freestyle stroke.
causing the pain. It has been suggested that the humerus is
moving into maximal external rotation, and this has been
equated to the late cocking phase of the baseball pitch.
The Strokes
Although it is true that at this point the humerus is as far The shoulder is the primary area of interest to clinicians
into external rotation as it goes during the freestyle stroke, working with swimmers because of its vulnerability to
it is nowhere near the degree of maximal external rotation injury. The visually apparent mechanics related to potential
required during the baseball pitch. During the midrecovery shoulder injury in the freestyle, backstroke, and butterfly
phase of the freestyle stroke, the humerus is closer to neu- strokes is that of humeral position relative to the axis of the
tral rotation than it is to “maximal” external rotation. This body. Figures 14-2, these three strokes and demonstrates
singular fact underscores the issue that the mechanics of the problem of humeral hyperextension relative to body
injury in the swimmer are unique for that sport; indeed, axis. For the purposes of this chapter, humeral hyperexten-
they are unique for each stroke within swimming. A group- sion is defined as a combination of humeral abduction and
ing of all overhead athletes does injustice to the understand- extension (i.e., the humerus is behind the long-axis of the
ing of specific injury mechanics. body while the arm is abducted). This position places stress
Based on the knowledge of where the shoulder hurt on the anterior joint structures. Too much or too little body
during swimming and which phase of the stroke provoked rotation changes the position of the humerus relative to the
the injury, an anatomical study was designed to determine body axis, and thus is related to humeral hyperextension.
the proximity of soft tissues with skeletal tissue. Nine cadaver Whether these faulty mechanics cause the pathological
shoulders were placed in the positions during the first half of muscle firing patterns or whether weak or fatigued muscles
pull-through, and cross-sections were taken. Five of the cause these faulty mechanics is a bit like the issue of the
specimens exhibited bursal and intraarticular contact with chicken and the egg. The changes in muscle firing patterns
the rotator cuff. This is now called a double squeeze (of the are not as visually apparent as is the body rotation; however,
rotator cuff). Three of these specimens also revealed the knowledge of the faulty muscle firing patterns defines the
biceps tendon in contact with the coracoacromial arch. Two underlying issues and allows the clinician to effectively and
other specimens demonstrated intra-articular contact only, efficiently diagnose and treat the problem.
70% 18%
Hand entry Forward reach Pull-through Middle pull-through Hand exit Middle recovery
Figure 14-1
Painful phases of the freestyle stroke. Seventy percent of painful symptoms are identified during the first
half of pull-through. Eighteen percent of symptoms are identified during the first half of recovery. (From
Pink MM, Tibone JE: The painful shoulder in the swimming athlete, Orthop Clin North Am 31[2]:248,
2000.)
Applied Biomechanics of Swimming • CHAPTER 14 333
figure 1
figure 2
figure 1
figure 2
figure 3
figure 4
figure 1
figure 2
C
Figure 14-2
Humeral hyperextension. A, During the freestyle stroke. Hand exit (left) and hand entry (right).
B, During the butterfly stroke.C, During the backstroke.
334 SECTION II • Applied Biomechanics of Selected Sport Activities
The following is intended to be a synopsis of the As previously mentioned, it has been noted that shoul-
key factors in each of the four competitive strokes. There der pain occurs most frequently in two phases of the
are multiple excellent books and articles on swimming stroke: (1) the early pull-through to mid pull-through
mechanics for those with an interest in more detail. Some and (2) hand exit to mid-recovery.2 There is potential in
of the articles are referenced herein. Two books on basic both of these phases for humeral hyperextension that
swim mechanics are those by Ernest Maglischo3 and could likely cause pain (see Figure 14-2, A). When adjust-
Cecil M. Colwin.4 ing to mitigate the pain, the swimmer will most likely seek
a path of least resistance and decrease efficiency of the arm
stroke while shortening the pull-through phase. One of
Freestyle Stroke the easiest ways to see this is during an increase in stroke
Mechanics count.
The basic arm mechanics—with the arm position marking Swimmers with painful shoulders may begin to use a
different phases of the freestyle stroke—are as follows wider hand-entry and a wider pull-through to diminish the
(Figure 14-3): pinching of an inflamed supraspinatus. A wide hand-entry
1. The arm enters the water and extends forward in and wide pull-through, combined with the body rotation,
front of the shoulder. The underwater pull-through can increase the likelihood of humeral hyperextension.
starts with the early pull-through phase, which is It is important to take notice of the shoulder complex
marked by the initiation of the backward arm move- in relation to trunk rotation when a swimmer takes a
ment. The palm and forearm should face the back- breath. Observations of elite swimmers from an underwa-
ward direction with the fingertips pointing down for ter front view shows a maximum trunk rotation of
as long as possible. approximately 30° to 40° down from the surface of the
2. The point at which the humerus is perpendicular to water on each side. The purpose of the rotation should be
the body is called the mid pull-through. to aid in the forward progression, not to rotate the body
3. Subsequent to mid pull-through is the late pull- onto its side. It is common for a swimmer to rotate exces-
through. The hand continues back and passes next sively during a breathing cycle, sometimes rotating as
to the hip until it exits the water, leading with the much as 90°. In other words, if a swimmer breathes to the
elbow. right side, there will be a tendency to rotate onto the left
4. After the arm exits the water, the recovery phase side too much. A situation of over-rotating like this is a
begins, when the arm is swung above the water to no-win situation. If the swimmer maintains the optimal
bring the arm into position to pull once again. pull-through mechanics, the excessive trunk rotation may
The arm motion is accompanied by axial rotation of lead to humeral hyperextension. If the swimmer avoids
the body. Many swimmers are taught to rotate, yet some the humeral hyperextension by keeping the arm in front
degree of rotation will naturally occur toward the side of of the body, it is a major mechanical flaw that will not
arm entry. As the arm is entering and the elbow is extend- maximize propulsion.
ing, the shoulder and side of the body rotate below the Another way that the injured swimmer may reduce
surface of the water. During the recovery, that same humeral hyperextension is to adjust the timing of the arm
shoulder and side of the body begin to counter-rotate strokes to a “catch-up” timing as opposed to being sym-
above the surface of the water (while the opposite shoul- metrically opposite each other. “Catch-up” timing is when
der is rotated down). the arm phases overlap slightly, so that the recovery arm is
on the late recovery while the underwater arm is still in the
early pull-through. This reduces body rotation during the
early to mid pull-through, thus decreasing the chances for
humeral hyperextension.
During the hand exit to mid-recovery, humeral hyperex-
tension can be reduced by swinging the arm wider and
decreasing elbow flexion. The elbow does not have to be
very high or close to the body (i.e., the emphasis should
not be on a high elbow recovery). The recovery should be
relaxed and controlled, and it is acceptable to swing the
hand around to the side.
The recovery phase should be led by the elbow. Some
swimmers try to lead with the hand. They overemphasize
Figure 14-3
Phases of the swimming stroke. (From Pink M, Perry J, Browne A, et
the finish motion of the pull-through and actively flick the
al: The normal shoulder during freestyle swimming, Am J Sports Med wrist out of the water upon exit. When they flick the wrist,
19:569–576, 1991.) they are also typically increasing the humeral hyperextension,
Applied Biomechanics of Swimming • CHAPTER 14 335
which increases the vulnerability of the shoulder. Also, it the butterfly stroke typically consisting more of an S-shaped
typically changes the initiation of recovery by increasing pulling pattern (Figure 14-5) and the upper body pivoting
humeral internal rotation. up and down about the hips, instead of rotating about the
central axis as in freestyle and backstroke.
Muscle Activity The hands enter the water with the arms extended for-
Clinically, the key to potential pathological conditions in the ward and in front of the shoulder. The upper body presses
shoulder during the freestyle stroke may be related to the down at the same time the arms enter the water to generate
serratus anterior. In swimmers with normal shoulders, the a more dynamic motion on entry and support the swim-
serratus anterior continually fires above 20% of its maxi- mer’s forward motion. The hands and arms should remain
mum.5 This muscle appears to be stabilizing the scapula in a extended forward during the upper body press, as opposed
protracted position as the arm pulls the body over itself. to aiming downward. This being the case, the magnitude of
When a muscle continually fires above 20%, it is susceptible the upper body press has a great influence on the subse-
to fatigue.6 With the distances required during swim training, quent motion of the early pull-through and on susceptibil-
the serratus anterior is certainly vulnerable to fatigue. Indeed, ity to shoulder pain. Swimmers who press the chest down
in swimmers with painful shoulders, the serratus anterior such that the hands and arms are above the torso are gener-
demonstrates significantly less muscle action during a large ally in a more risky shoulder position in the early pull-
portion of pull-through (Figure 14-4, A). Although the through because this leads to the humeral hyperextension
serratus anterior diminishes its action during pull-through, (the humerus is behind the axis of the body). The pulling
the rhomboids increase their activity (Figure 14-4, B). It may pattern for a swimmer with a deep upper body press tends
be that, in an attempt to stabilize the scapula during the ab- to go wide and well outside the shoulder on the early pull-
sence of the serratus anterior, the primary muscles available through. If a swimmer is experiencing shoulder pain in the
are the rhomboids. Yet the action of the rhomboids (retrac- early pull-through, a possible corrective measure for the
tion and downward rotation of the scapula) is the exact mechanics is a change in the depth of the upper body press
opposite of the serratus anterior (protraction and upward and focusing on keeping the arms in line or in front of
rotation). This may well be positioning the acromion to im- the body.
pinge on the rotator cuff. During late pull-through and the beginning of the
Another muscle to consider when studying muscle activ- recovery phase, there is also a chance for the shoulder to be
ity during the freestyle stroke is the subscapularis. In swim- at risk. At the beginning of the late pull-through, the arms
mers with normal shoulders, this muscle also continually are bent and the hands are underneath the hips. The arms
fires above 20% of its maximum.5 And, in swimmers with then extend, with the hands sweeping outward and the
painful shoulders, there is significantly less activity during arms lifting upward to exit the water and transition into the
pull-through (Figure 14-4, C).7 recovery phase. There is potential for the humerus to be
Of interest, the primary “power” muscles of the shoul- internally rotated during the arm exit and early recovery
der during swimming (the latissimus dorsi and the pecto- phase. A swimmer should not overemphasize the end of late
ralis major) demonstrate no significant differences when pull-through and lift the hands out of the water too high;
comparing normal versus painful shoulders. So it appears instead, he or she should keep his or her hands as close to
that these muscles may not be integral in the prevention the surface of the water as possible in the early recovery
of injury (Figures 14-4, D and 14-4, E).7 Also of note, phase.
neither the supraspinatus, teres minor, nor posterior With the undulating body motion in the butterfly, the
deltoid exhibit any significant differences in muscle activ- swimmer takes a breath by lifting the upper body upward
ity between painful and nonpainful or normal shoulders throughout the underwater pull-through. The swimmer
(Figures 14-4, F–H).7 should use the forces generated by the pull-through to lift
As a clinician, one application of this research information the upper body just enough for the shoulders and head to
is to ensure there is both a strengthening and endurance clear the surface, but it is common for swimmers to force-
component for the serratus anterior and the subscapularis in fully arch the back and throw the head upward to do this.
a swimmer’s conditioning program. Another application is This action, followed by lunging forward on arm entry, can
to watch for the initial signs of fatigue in these muscles, as stress the spine and lower back.
that may be the start of a chain of injury.
Muscle Activity
As with the freestyle stroke, the pattern of disruptive
Butterfly muscle firing patterns during the butterfly are primarily
Mechanics seen in the muscles attaching to the scapula. The two
The butterfly stroke is a bilateral activity, as opposed to a muscles with clinically relevant muscle firing changes in the
reciprocal, unilateral pattern in the freestyle and backstroke. painful shoulder during the butterfly are the serratus anterior
The pull pattern and body motion are also different, with and the teres minor.8 In swimmers with painful shoulders,
336 SECTION II • Applied Biomechanics of Selected Sport Activities
60 60
40 40
20 20
0 0
EARLY LATE EARLY LATE EARLY LATE EARLY LATE
PULL-THROUGH RECOVERY PULL-THROUGH RECOVERY
A PHASE B PHASE
NORMAL AND PAINFUL - SUBSCAPULARIS NORMAL AND PAINFUL - PECTORALIS MAJOR
100 100
AVE MUSCLE ACTIVITY
60 60
40 40
20 20
0 0
EARLY LATE EARLY LATE EARLY LATE EARLY LATE
PULL-THROUGH RECOVERY PULL-THROUGH RECOVERY
C PHASE D PHASE
NORMAL AND PAINFUL - LATISSIMUS DORSI NORMAL AND PAINFUL - SUPRASPINATUS
100 100
AVE MUSCLE ACTIVITY
NORMAL NORMAL
80 PAINFUL 80 PAINFUL
60 60
40 40
20 20
0 0
EARLY LATE EARLY LATE EARLY LATE EARLY LATE
PULL-THROUGH RECOVERY PULL-THROUGH RECOVERY
E PHASE F PHASE
NORMAL AND PAINFUL - TERES MINOR NORMAL AND PAINFUL - POSTERIOR DELTOID
100 100
AVE MUSCLE ACTIVITY
NORMAL NORMAL
80 PAINFUL 80 PAINFUL
60 60
40 40
20 20
0 0
EARLY LATE EARLY LATE EARLY LATE EARLY LATE
PULL-THROUGH RECOVERY PULL-THROUGH RECOVERY
G PHASE H PHASE
Figure 14-4
Normal and painful shoulders muscle firing during the freestyle. A, Serratus anterior. B, Rhomboids.
C, Subscapularis. D, Pectoralis major. E, Latissimus dorsi. F, Supraspinatus. G, Teres minor. H, Posterior
deltoid. (From Scovazzo ML, Browne A, Pink M, et al: The painful shoulder during freestyle swimming:
An electromyographic cinematographic analysis of twelve muscles, Am J Sports Med 19[6]:579-581, 1991.)
Applied Biomechanics of Swimming • CHAPTER 14 337
Backstroke
the hand entry is wider than that of the swimmers with Mechanics
normal shoulders. This is also one of the two common The backstroke is similar to the freestyle stroke in that the
points at which swimmers experience shoulder pain during arms stroke reciprocally and are supported by a trunk rota-
the butterfly stroke.2 With the wider hand entry, the tion and a leg kick. Obviously, the major difference between
scapula does not need as much upward rotation or protrac- the backstroke and the freestyle is that the backstroke is
tion, as evidenced by the decreased activity in the serratus performed supine. In the backstroke, the shoulder is vulner-
anterior. The teres minor also reveals significantly less able to injury similarly to the freestyle, and the relationship
action, most likely caused by the altered scapular and hu- between the arm and the body orientation is important
meral position. to note.
During the powerful pulling in the butterfly stroke, the The phases are the same for the two strokes. The begin-
swimmers with painful shoulders continue to demonstrate ning of the pull-through is marked by the hand entry of the
Figure 14-6
With a floating scapula during the butterfly stroke there is no stable base and the teres minor and serratus
anterior cannot function adequately.
338 SECTION II • Applied Biomechanics of Selected Sport Activities
swimmer with the arm extended above the head. The arm
becomes submerged and the hand and arm press toward the Muscle Activity
feet. The mid pull-through phase begins when the humerus The muscle action during the backstroke, by mere virtue of
is perpendicular to the body. The arm continues to move the swimmer being on his or her back, is widely different
toward the feet, and at the end of the late pull-through, the from that of the other strokes. The muscles most active dur-
elbow straightens out with a slight downward press before ing the powerful pull-through are the teres minor and the
lifting out of the water to start the recovery phase. The subscapularis9; and obviously, these two muscles were not
elbow is fully extended throughout the recovery phase and designed for power. Even during the peak moments of pull-
travels straight over the top of the water and overhead to ing, the latissimus dorsi reveals 30% less action than does
the point of hand entry. the teres minor and the subscapularis in swimmers with
The timing of the body rotation as it relates to the arm normal shoulders. So, not only is the backstroke swimmer
entry and early pull-through is important. To maximize at risk because of the aforementioned humeral hyperexten-
performance and minimize shoulder vulnerability, the body sion and levering of the humeral head anteriorly, but these
should be rotating in synchrony with the arm. In other athletes require the small rotator cuff muscles to perform as
words, if the humerus is oriented 30° below the surface, the power muscles.
torso should be rotated a similar amount below the surface In addition, during pull-through, the teres minor and
at that time. However, oftentimes this is not the case, subscapularis are constantly active at approximately 30%
because it is typical for the timing of the body rotation to maximum voluntary contraction. Thus it appears that these
lag behind the arm mechanics. Common symptoms of a late two rotator cuff muscles are functioning as power drivers as
body rotation are a hand entry that crosses inside the shoul- well as endurance muscles.
der width and a hand entry with the back of the hand. At the same time as the depressed activity in the teres
In this situation, in which the arm stroke leads the body minor in the backstrokers with painful shoulders, the rhom-
rotation, the humerus is hyperextended. For the body rota- boids also exhibit less action.10 Apparently, the scapula is not
tion and arm motion to be in sync, it is important that the retracted properly in early recovery and hence there may be
body rotation is initiated at the mid-recovery phase so that less clearance for the humeral head under the acromion.
at hand entry, the shoulders are horizontal in the water. The A third rotator cuff muscle, the supraspinatus, demon-
body rotation continues as the arm is submerged and the strates suppressed activity toward mid pull-through in the
early pull-through is started. The swimmer should rely on swimmers with painful shoulders.10 Given the decreased
the leg kick and the late pull-through to properly execute action in three of the four rotator cuff muscles, one can
the body rotation. reasonably conclude that there could be difficulty in
Variations across swimmers in the mechanics of the early depressing the humeral head for adequate clearance of the
pull-through phase can also affect the degree of shoulder acromion during pull-through.
vulnerability. After the hand enters the water, the early pull-
through can vary in depth, palm orientation, and direction
of the initial motions. Although observations of today’s Breaststroke
elite backstrokers show that their palms rotate toward the Mechanics
feet very shortly after hand entry and their arms stay to the The breaststroke is the oldest of all competitive swim
side of the body, many swimmers have been taught to press strokes, and it is unique in that the arms do not exit the
downward immediately after entry to have a deep pull. water. In this stroke, the legs are more of the propeller or
A deep, early pull-through can lead to a humeral hyperex- power drivers than are the arms. It appears that the least
tension because the body is not rotated enough—or soon number of complaints of shoulder pain appear to occur with
enough. If a swimmer is experiencing shoulder pain in the the breaststroke. And, the issue of body rotation along with
early pull-through phase of backstroke and the swimmer is humeral hyperextension is minimal. This stroke uses a bilat-
observed to have a straight arm and deep initial pull, eral arm motion in which the arms reach forward and then
then some stress on the shoulder may be relieved with a sweep outward (the beginning of the pull-through), while
suggestion to keep the pull more shallow and the arm closer the elbows begin to flex. When the hands are in line with
to the body. the mid-chest, the hands move inward in a circular pattern
At the end of the late pull-through, when the hand exits until they meet in front of the chest and are thrust forward
the water, it is important that the hand exit the water with (recovery) once again. Because the arms remain in front of
the thumb first. Lifting the arm out with the pinky first will the body at all times, the shoulders are not at high risk in
result in excessive humeral internal rotation. This will the breaststroke.
increase the pinching of the supraspinatus on the undersur- Just like the butterfly, the body motion in the breast-
face of the acromion. The hand then rotates during stroke is centered around the hips. The swimmer breathes
mid-recovery so that the hand can enter the water with the by lifting the head up as well, but because the breaststroke
pinky first and the palm rotated out. arm motion leads to a much more natural lifting of the
Applied Biomechanics of Swimming • CHAPTER 14 339
upper body, the spine and lower back are not as susceptible feet and knee orientation during the propulsive portion of
to pain as in the butterfly stroke. the kick can create issues with the knee, and the forceful
The kicking motion most frequently used in competition inward motion can lead to a pulled groin muscle. A swim-
is the whip kick, a symmetric, bilateral action (Figure 14-7). mer can reduce the risk of injury in these cases with
The kick motion starts with the legs fully extended proper warm-up and conditioning.
horizontally. The knees bend and move forward as the
heels are brought as close to the buttocks as possible. Muscle Activity
When the heels reach their highest point, the feet rotate During pull-through, breaststroke swimmers with painful
outward so that the toes point to the side, and will also shoulders demonstrate an increase in activity in the sub-
move wide of the knees. The knees and feet push back- scapularis and the latissimus dorsi.11 The increased sub-
ward and inward from that position until reaching full scapularis activity, along with a decrease in the action of the
extension with the legs together again. Forward propul- teres minor, leads to a relative increase in internal rotation.
sion is generated primarily by the force of the inside of the The increased internal rotation places the arm in a position
feet and lower leg pushing directly against the water. The that is vulnerable to impingement. The increase in latissi-
mus dorsi action may assist with humeral head depression to
relieve the impingement.
with high-level training to ultimately make them stronger. the intensity of pain on the scale, the athlete may progress
In the case of the swimmer, this is usually mid-season. to “shampoo arm syndrome” (i.e., it is hard for the athlete
Pain exists on a continuum—and yet with our interpreta- to lift his or her arm to shampoo his or her hair in the
tion and discussion of pain, we are trying to fit it into shower after workout) and faulty mechanics by the end of
categories. Although the categorization of pain is easiest for the workout. As the athlete reaches a level 3 pain, ice is
discussion purposes, it is not entirely accurate. So, when recommended, and the athlete needs to make certain he or
combining the categorical discussion along with societal she is performing his or her conditioning program appro-
influence, interpretation of a pain scale can be difficult in priately. At this point, mechanics are normal at the begin-
this population. The true accuracy comes from an integra- ning of the workout, and may have adapted by the end of
tion of the pain scale with observations of the athlete, the the workout because of fatigue. Within this zone, the
on-deck personnel, and the medical professionals. athlete is still able to complete a full workout but may need
to minimize certain strokes to avoid pain. Pain may last 2 to
Athlete’s Pain Scale 4 hours after practice, but is resolved upon waking the
An athlete’s pain scale is suggested in Figure 14-8. This scale next day.
is currently under investigative study, and hence the reliabil- Yellow Zone (4-5). The yellow zone is the “heads-up”
ity and validity are unknown. The authors choose to present zone, signaling caution, yet basically managed by the ath-
it, however, to make the point of differentiating pain from lete and the coach. Almost all competitive athletes reach
soreness, as well as the point that an athlete’s perception of this zone at some point in the season. The coach is trying
pain may well require a different interpretation from that of to break down the athlete so that he or she can then pro-
a nonathlete. gress to the next level of performance. If the athlete’s pain
The standard 10-cm horizontal line is used for this pain increases throughout this zone, his or her mechanics may
scale, which has a mark at every centimeter, with the 0 and become faulty, stroke disciplines modified, and workout
the 10 numerically identified (see Figure 14-8). The differ- distances decreased. Minor performance inconsistencies
ent zones of white to red are used for the purpose of com- develop early in this zone, yet the athlete can still com-
municating with the health care professional. The color pete well enough to win. As this zone progresses, the
codes are not necessarily presented to the athlete. performance diminishes. Pain may be experienced with
White Zone (0-3). Symptoms in the white zone indi- forceful arm movements during swimming. Pain may last
cate fatigue and soreness from training rather than true 4 to 8 hours following a workout, and could be experi-
pain. This zone is a normal part of the intensity of training enced on waking the next day. Management strategies for
in a competitive athlete. The athlete can continue to train this zone include a longer-than-normal warmup with slow
and continue with his or her exercise conditioning program swimming. It is recommended that sprint sets and hand
when pain is reported in this zone. As the athlete increases paddles be eliminated from practice. Fins can be used during
0 10
White Zone (0-3): Normal level
- continue to train
- fatigue and soreness during and post-workout
- handle with coach and athlete
practice to unweigh the shoulders. To maintain a feel of video analysis software can aid a coach and clinician to
the water, the athlete can kick in a side-lying or vertical diagnose mechanics.
position, but with the involved arm down by the side. Because the medical personnel are not typically on-deck
The conditioning program should be reviewed with the with the swimmers and coaches, it behooves sports
athlete before and after a workout with a level 4 pain. clinicians to be a bridge between the clinics and the deck.
Once again, adaptations in the program performed after Thus, it is important that sports clinicians converse with the
the workouts are probably secondary to fatigue (and coaches and on-deck personnel about the subtle mechanical
simple planar motions may exhibit scapular asymmetry), changes that may lead to anatomical damage.
whereas substitution patterns in the program before a Because the freestyle is the most used stroke, the me-
workout need attention. The true pain is probably local- chanical changes caused by fatigue, soreness, and pain are
ized (the soreness and fatigue are generalized). Ice is noted herein for that stroke. Table 14-1 presents some of
recommended after practice and before bedtime. If the the more common potential mechanical changes in the
athlete cannot return to pain-free swimming within 7 to freestyle stroke.
10 days of modifying the stroke, workout, and condition-
ing program, referral to sports medicine staff may be
appropriate.
Clinical Implications
Orange Zone (6-8). The orange zone is the rehabili- Repetitive overuse appears to be a major contributor to
tation zone. Once the pain duration consistently spills shoulder pain in swimmers. In addition to the aforemen-
into the next day (level 6), the swimmer should be tioned mechanics, which can lend to impingement, other
referred to sports medicine staff. This could be the start of contributing factors for swimmer’s shoulder include
potential anatomical damage. The power portion of the (1) overuse and subsequent fatigue of the muscles around
upper-extremity conditioning program should be consid- the shoulder, scapula, and upper back; and (2) glenohu-
ered and probably discontinued by the time the swimmer’s meral laxity. These factors are all related, because impinge-
pain is in this zone. Early in this zone (level 6), the coach ment may be caused by altered glenohumeral kinematics
may want to consider a 3-day rest from workouts. If the resulting from muscle fatigue or glenohumeral laxity.
swimmer does not improve with a 3-day rest, then a referral Other associated findings include muscle imbalances and
to a physician is appropriate. inflexibility, such as tightness of the pectoral muscles,
Red Zone (9-10). This zone represents anatomical and sometimes inflexibility of the posterior capsule and
damage. The athlete is unable to perform at a competitive posterior rotator cuff.
level, must stop swimming altogether for an undetermined
period, and needs to be under the care of a physician,
physical therapist, or athletic trainer. Muscle Fatigue and Dysfunction
Because the shoulder is an inherently unstable joint, muscle
forces are critical for maintaining stability, proper motion,
Mechanical Changes and painless function. As previously discussed, performance
Mechanical changes in the body go hand-in-hand with of the swimming stroke requires a highly coordinated
fatigue, soreness, and pain. Swimmers will modify their pattern of muscles firing at precisely the right time to pro-
stroke because of these factors before they decrease work- vide the most efficient and powerful stroke. If one muscle
outs. The mechanical changes caused by fatigue are identi- fatigues, it is as if one cog in a machine is malfunctioning.
fied prior to the pain modifications. These alterations obvi- When that one muscle fatigues, it affects the function of
ously show up toward the end of the workout as fatigue other muscles in the kinetic chain.
increases. When the fatigue-induced mechanical changes Muscle dysfunction increases impingement by loss of the
show up early in the workout, then the swimmer may need humeral head depressor function of the rotator cuff and loss
a recovery workout or a day of rest. The butterfly is likely of upward rotation and elevation of the scapula. Loss of the
the first stroke to demonstrate mechanical changes, stabilizing effect of muscles may be especially problematic
followed by the freestyle and the backstroke. The breast- in swimmers with associated shoulder laxity (discussed in
stroke is likely the most mechanically enduring stroke the following section). Fatigue of the abdominal and pelvic
related to fatigue, soreness, and pain. muscles may also contribute by affecting scapular kinemat-
Mechanical flaws and adaptations are easiest to see from ics and body position in the water.
the underwater vantage point. Ideally, all pools would have
underwater windows, both laterally and under the pool.
A more practical solution is the use of underwater video, Laxity
which has become an affordable and valuable analysis tool. Many competitive swimmers have an element of shoulder
The most subtle changes in mechanics will be very difficult laxity.12,13 A certain degree of laxity may be advantageous by
for a relatively naïve eye to catch, and the use of digital allowing a swimmer to achieve both a body position that
342 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 14-1
Common Freestyle Mechanical Changes Caused by Fatigue, Soreness, and Pain
Mechanical Change Effect on Stroke
Wider hand entry and lateral underwater hand Hand starts wide and “slides” under the belly
motion Less force on the shoulder
Flatter hand entry
Avoids Neer and Hawkins impingement positions
Shorten underwater reach after hand entry Hand does not extend as far forward under water after hand entry
Avoids positions that mimic Neer and Hawkins impingement positions
Leading with elbow rather than hand during Attempts to decrease amount of force on hand and forearm
catch and early pull-through
Early hand exit Minimizes humeral internal rotation
Looks similar to hand exit with butterfly stroke
Decreased trunk rotation Related to shorter underwater reach and early hand exit
Attempts maintain stroke rate
Premature rotation and lifting of head prior to Attempts to get arm out of water earlier and with less force in final
breathing position of stroke
“Dropped” elbow on recovery Decreased elbow flexion and height
More lateral swing
Attempts to avoid painful internal rotation of humerus
reduces drag and a longer sweep during the pull-through instability symptoms, although less common, may be
phase. It is well-established that there is a narrow distinc- exacerbated because of the position of the arm in flexion,
tion between physiological laxity (normal) and pathological adduction, and internal rotation.
instability (abnormal). Normal laxity may increase over time
because of repetitive overuse and eventually become a
pathological condition. Shoulder stability is controlled by Impingement
static (i.e., glenohumeral ligaments and capsule) and Swimmers usually have a nonoutlet type of impingement, in
dynamic (rotator cuff muscles) factors. Loss of the static which altered kinematics rather than subacromial pathological
component (i.e., glenohumeral capsular laxity) requires a changes (i.e., acromial osteophyte or coracoacromial ligament
greater contribution from the rotator cuff, which can result abnormalities) results in abnormal contact. Such impinge-
in muscle overload and eventual muscle fatigue, as ment may be subacromial (the bursal surface of the rotator
described previously. The challenge for the clinician is to cuff against the anteroinferior acromion) or intra-articular
distinguish between normal laxity and abnormal instability. (the articular surface of the rotator cuff or biceps tendon
Previous studies have documented the presence of impinges on the anterosuperior glenoid and labrum). The
increased joint laxity and glenohumeral instability in swim- position of the shoulder during the recovery phase of the
mers. Bak and Faunø reported that 37 out of 49 competi- stroke (forward flexion and internal rotation) is a classic
tive swimmers had increased humeral head translation with position for subacromial impingement. At the end of the pull-
associated apprehension.14 Furthermore, McMaster and through phase of the stroke, the arm goes into hyperexten-
colleagues found a significant correlation between shoulder sion, which pushes the humeral head anteriorly, which also
laxity and shoulder pain in a group of 40 elite-level exacerbates impingement. Use of a video analysis system to
swimmers.15 The presence of underlying generalized joint document impingement during the freestyle stroke found that
hypermobility was reported by Zemek and Magee.13 These impingement occurred when the hand entered the water and
authors reported both increased glenohumeral laxity and in the middle of the recovery phase.16 The mean duration of
increased generalized joint hypermobility in elite swimmers. impingement was nearly 25% of the total stroke time. This
These studies suggest that a combination of acquired and study demonstrated that impingement was most likely in
inherent factors contribute to shoulder laxity in swimmers. swimmers who have excessive internal rotation during the
The most common pattern of instability is anteroinferior, pulling phase, delayed initiation of external rotation of the
but there is often a component of multidirectional instabil- arm during the recovery phase, and decreased upward scapu-
ity. Subluxation can occur during the backstroke as the lar rotation.17 Hydrodynamic forces exerted by the water may
hand enters the water with the swimmer on his or her back also exacerbate impingement. At the point at which the hand
with the arm in full flexion and external rotation. Posterior enters the water, the hydrodynamic force exerted on the hand
Applied Biomechanics of Swimming • CHAPTER 14 343
generates a large moment about the shoulder joint caused by reason to consider an excessive stretching program for
the long moment arm in this position. This moment will forc- swimmers. As a matter of fact, the stretching performed by
ibly elevate the arm, possibly increasing impingement.16 many swimmers may actually be harmful to the capsuloliga-
Alternatively, intra-articular impingement may occur mentous structures. Thus, it is probably more important for
during the swimming stroke as the articular surface of the swimmers to stop traditional stretching practices than it is
rotator cuff can impinge against the anterosuperior labrum to begin proper stretching based on individual physiology.
adjacent to the biceps attachment as the arm is placed into The four stretches demonstrated in Figure 14-9 should no
forward flexion and internal rotation. Such a mechanism longer be considered in a dry-land program for swimmers.
could account for the frequent localization of pain around Stretching is athlete-specific. A simple shoulder screen
the biceps tendon in swimmers. The position of forward (Figure 14-10) for coaches and on-deck personnel has been
elevation, adduction, and internal rotation may also result developed to review the flexibility of all members of the
in impingement of the coracoid process on the lesser tuber- team effectively and efficiently. There are three positions for
osity and subscapularis tendon. each athlete to review:
Muscle fatigue caused by overuse may also contribute to
impingement. The normal rotator cuff functions to stabilize
the glenohumeral joint and acts as a humeral head depres- Suggested Flexibility Screen for Swimmers
sor, preventing subacromial impingement. It is known that
loss of the humeral head depressor function of the rotator • Tight streamline position (see Figure 14-10)
cuff results in superior migration of the humeral head and • 90/90 position (see Figure 14-10)
increases the risk of impingement.18 • 45° position (see Figure 14-10)
Conditioning, Prevention,
and Rehabilitation 1. Tight Streamline Position—1⁄2 Sit Against the
Wall. This position is a sport-specific, functional posi-
Stretching tion that assesses mobility in the scapulothoracic and
Given the discussion on laxity as well as underwater videog- glenohumeral joints as well as the length of the latis-
raphy indicating that no extraordinary shoulder joint simus dorsi. The swimmer should be able to complete
motion is necessary for a fast, efficient stroke, there is little this desired motion without difficulty with the lumbar
Figure 14-9
Stretches that swimmers should NOT do.
344 SECTION II • Applied Biomechanics of Selected Sport Activities
Tight Streamline –1/2 Sit Against Wall: Assume the following tight
streamline position.
(In order to ‘pass’ this position, all of the 5 questions in this section must
be answered with a ‘Yes’.)
90/90 Position: Lie supine with knees bent and feet on surface. Assume
90° of shoulder abduction in the coronal plane and 90° of glenohumeral
external rotation.
(In order to ‘pass’ this position, all 4 of the questions in this section must
be answered with a ‘Yes’.)
If a swimmer is able to achieve at least two of the positions above, then he/she is well served with the stretching program herein. If
the swimmer fails in 2 or all of the positions, then a customized stretching routine from a health care professional is recommended.
Figure 14-10
Shoulder range of motion screen for swimmers.
Applied Biomechanics of Swimming • CHAPTER 14 345
spine flat against the wall, full elbow extension, and Based on these observations and if the swimmer “passes”
clasped hands against the wall. the shoulder screen in Figure 14-10, an appropriate
2. 90/90 Position. This position is completed in dry-land stretching routine can be found in Figure 14-11.
supine position. It assesses mobility of the inferior It is recommended that swimmers stretch at a time
and anterior glenohumeral joint capsule as well as the unrelated to working out or racing (at least several hours
blended anterior band of the inferior glenohumeral prior to getting in the water). Pre-exercise stretching has
and the middle glenohumeral ligaments.19 Shorten- been found to compromise muscle performance for up to
ing of the pectoralis group is also identified with this 1 hour.20-25 Postexercise stretching is not encouraged.
position. The swimmer should be able to rest his or Stretching fatigued muscles tends to facilitate muscle
her forearm, wrist, and elbow comfortably on the spindle and inhibit Golgi tendon organ firing.26,27 General
floor in this position while maintaining 90° of elbow guidelines for stretching include completing a specific
flexion and 90° of glenohumeral abduction. The pos- static stretch that targets muscle tissue one to three times
terior shoulder joint muscles should be in contact for 15 to 30 seconds each, approximately 5 days a week is
with the floor or table. appropriate.28-31 Instead of pre-exercise stretching, a
3. 45° Position. This position specifically assesses the longer warmup in the water with increasing intensity is
length of the subscapularis. A competitive swimmer recommended.
needs to be able to achieve this position with 45° of
external rotation while keeping the humerus in an
adducted position. Conditioning the Uninjured Swimmer
If the swimmer is able to achieve at least two of these Given the muscle functions described previously, the fol-
positions, then the athlete is well served with the stretching lowing is an offered infrastructure intended to assist the
program described in Figure 14-11. If the swimmer is health care professional in designing a conditioning pro-
unable to achieve two or more of the positions in the gram for the uninjured swimmer that is specific not only to
shoulder screen, then consultation with a sports medicine swimming, but also specific for the individual’s competitive
professional is encouraged to help identify the origin of the strokes. Numerous studies identify optimal exercises for the
restriction and develop a customized stretching program different muscles.32-41 The suggested optimal exercises are
for that individual. simply that: a suggestion for a starting point in considering
Based on the physical demands of swimming, under- the conditioning program.
standing the biomechanics of the stroke and respecting A program for competitive butterfly, backstroke, and
the capsuloligamentous structures, the focus of the rec- breaststroke swimming will, most likely, include the exercises
ommended stretches is to target the at-risk connective for the freestyle stroke because most swimmers (regardless of
tissue while avoiding insult to the static stabilizers. Obser- competitive strokes) put in large distances with the freestyle.
vationally, it appears that only three muscle groups of the Coaches are encouraged to implement the strength and
glenohumeral joint may be at risk of shortening in the endurance program after practice or several hours before
swimmer. Those three groups are the (1) pectoralis mus- practice (Table 14-2). Exercising the muscles of the shoulder
cles, (2) latissimus dorsi, and (3) subscapularis. If these complex directly before practice may lead to fatigue and
muscles have been tight for a prolonged period, there subsequent faulty stroke mechanics.7
is also a risk of tightness in the capsuloligamentous
complex.
However, swimmers tend to have more tightness in the Rehabilitation
low back than in the shoulder. Although the back is not Given the currently known specificity of muscle require-
necessarily at risk during the swim stroke, the “common” ments in the competitive swimmer, the work of the reha-
posture of the swimmer with forward shoulders, lordotic bilitation professional can be much more focused than ever
back, and genu recurvatum indicates that the soft tissue before. The intent of these few paragraphs is to give the
structures in the lumbar spine may shorten. In the professional the scaffolding on which to build the nonsurgi-
long run, this is known to be a potential cause of back cal rehabilitation program.
problems. A swimmer’s inflamed shoulder is treated the same as the
Although there is little, if any, research literature inflamed shoulder of any individual. Rest from offending
on the musculoskeletal requirements and common limita- activities, ice, and anti-inflammatory medication may be
tions of the lower extremity, a swimmer ideally has necessary as well as potential application of modalities such
good range of motion (ROM) at the hip and at the ankle. as iontophoresis, ultrasound, or high-voltage galvanic stim-
If there are tight hip flexors, they could contribute to ulation. Once the inflammatory process is halted, gentle
a low back problem. And if there is a limitation in stretches such as those described in the conditioning pro-
ankle plantar flexion ROM, kicking efficiency could be gram are suggested. Consideration needs to be given to safe
decreased. arcs of motion for the stretches. Identification of the weak
346 SECTION II • Applied Biomechanics of Selected Sport Activities
Figure 14-11
Dry-land stretching recommendations for swimmers.
muscles begins at this stage. As reinforcement to the afore- eration not only those exercises that optimally recruit the
mentioned material, each swimming stroke carries different specific muscles within a safe and efficient range, but they
muscle injury risk requiring varying levels of strength and also use the most effective type of contraction (i.e., isomet-
endurance. ric or concentric). For example, if the rhomboids were
Once the weak components for the glenohumeral muscles needing strengthening, the optimal exercise is an
muscles are identified, the specific exercise program can be isometric contraction while the muscles are in the maxi-
developed. The optimal exercise program takes into consid- mally shortened state. Although it is beyond the scope of
Applied Biomechanics of Swimming • CHAPTER 14 347
Table 14-2
Muscles at Risk During the Swim Stroke and Suggested Exercises
Stroke Muscles at Risk Strength or Endurance Suggested Optimal Exercises
Table 14-3
Return to Swimming Benchmarks
Criteria to Allow Swimming Swimming Activity Allowed
Benchmark 1
Reach above shoulder height pain free Swim 1000-2000 yards slowly and comfortably while
Pain-free resisted movements 0° to 90° avoiding antagonizing swim strokes and sprint sets
Benchmark 2
Pain free with resisted shoulder motions Add 500 yards every three workouts
Pain free with most activities of daily living Avoid double workouts at this time
Pain free with swimming 2000 yards
Benchmark 3
Pain free swimming 4000 to 5000 yards Short sprint sets
Incorporate all swim strokes
this chapter to discuss the specific muscle physiology for sia, and selected muscle performance in a group of Division
each muscle, health care practitioners have such informa- I female swimmers. After a 6-week period of a plyometric
tion available to them. training program that focused on the internal rotators of
Any individual with shoulder problems benefits from the shoulder complex, both proprioception and kinesthesia
cardiovascular and muscle endurance rehabilitation. Walk- significantly improved. The Swanik study confirmed that
ing, rowing, stationary bicycling, and use of the elliptical plyometric exercises for the competitive swimmer helps
are all ways to maintain aerobic conditioning. Muscle to promote endurance, glenohumeral joint stability, and
endurance training is another integral part of the reha- neuromuscular efficiency.
bilitation program for swimmers. Endurance training can
be addressed with low-resistance and high-repetition ac- Return to Swimming Program
tivities. Maintaining a feel for the water is critical during the reha-
Plyometric training has also been found to improve bilitation process and, as a result, coordinating a timely
endurance. Swanik and colleagues42 studied the effect of return to the pool is essential. There are specific benchmarks
plyometric training on shoulder proprioception, kinesthe- in the swimmer’s return to a pool program (Table 14-3)
348 SECTION II • Applied Biomechanics of Selected Sport Activities
based on their progress. Adherence to a slow, progressive 17. Yanai T, Hay JG: Shoulder impingement in front-crawl swimming:
program ensures a healthy return to the sport they love. II. Analysis of stroking technique, Med Sci Sports Exerc 32(1):
30–40, 2000.
18. Paletta GA Jr., Warner JJ, Warren RF, et al: Shoulder kinematics
Conclusion with two-plane x-ray evaluation in patients with anterior instability
or rotator cuff tearing, J Shoulder Elbow Surg 6(6):516–527,
The mechanics of swimming are different from that of the 1997.
“overhead” athlete. Indeed each of the four swim strokes 19. Turkel SJ, Panio MW, Marshall JL, Girgis FG: Stabilizing mecha-
nisms preventing anterior dislocation of the glenohumeral joint,
need to be considered independently. With the high rate
J Bone Joint Surg 63: 1208–1217, 1981.
of injury and reinjury, it is important for clinicians to un- 20. Knudson DV, Magnusson P, McHugh M: Current issues
derstand the mechanics and the cause of injury and rein- in flexibility fitness, Pres Council Phys Fitness Sports 3:1–6,
jury for each stroke. Such an understanding will not only 2000.
allow the clinician and on-deck personnel to catch the 21. Kokkonen JA, Nelson AG, Cornwell A: Acute muscle stretching
inhibits maximal strength performance, Res Q Exerc Sport 69:
subtle signs of injury, but it will also minimize the risk of
411–415, 1998.
potential injury and maximize the rehabilitative out- 22. Fowles JR, Sale DG, MacDougall JD: Reduced strength after
comes. passive stretch of the human plantar flexors, J Appl Physiol
89:1179–1188, 2000.
23. Cornwell AG, Nelson A, Heise G, Sidaway B: Acute effects of
References passive muscle stretching on vertical jump performance, J Hum
Mov Stud 40:307–324, 2001.
1. Stocker D, Pink MM, Jobe FW: Comparison of shoulder injury in 24. Knudson D, Bennett K, Corn R, et al: Acute effects of stretching
collegiate and masters level swimmers, Clin J Sports Med 5:4–8, are not evident in the kinematics of the vertical jump, J Strength
1995. Cond Res 15(1):98–101, 2001.
2. Pink MM, Tibone JE: The painful shoulder in the swimming athlete, 25. Cramer JT, Housh TJ, Johnson GO, et al: Acute effects of static
Orthop Clin North Am 31(2):247–261, 2000. stretching on peak torque in women, J Strength Cond Res
3. Maglischo EW: Swimming fastest, Champaign, IL, 2003, Human 18(2):236–241, 2004.
Kinetics. 26. Nelson HL, Hutton RS: Dynamic and static stretch responses in
4. Colwin CM: Breakthrough swimming: stroke mechanics, training muscle spindle receptors in fatigued muscle, Med Sci Sports Exerc
methods, racing techniques, Champaign, IL, 2002, Human 17:445–450, 1985.
Kinetics. 27. Hutton RS, Nelson DL: Stretch sensitivity of Golgi tendon organ
5. Pink M, Perry J, Browne A, et al: The normal shoulder during in fatigued gastrocsoleus muscle, Med Sci Sports Exerc 18:69–74,
freestyle swimming, Am J Sports Med 19:569–576, 1991. 1986.
6. Monad H: Contractility of muscle during prolonged static and 28. Decoster LC, Scanlon RL, Horn KD, Cleland J: Standing and
static dynamic activity, Ergonomics 28:81, 1985. supine hamstring stretching are equally effective, J Athl Train
7. Scovazzo ML, Browne A, Pink M, et al: The painful shoulder 39(4):330–334, 2004.
during freestyle swimming: an electromyographic and cinemato- 29. Bandy WD, Irion JM, Briggler M: The effect of time and
graphic analysis of twelve muscles, Am J Sports Med 19: frequency of static stretching on flexibility of the hamstring
577–582, 1991. muscles, Phys Ther 77:1090–1096, 1997.
8. Pink M, Jobe, FW, Perry J, et al: The painful shoulder during the 30. Bandy WD, Irion JM: The effect of time on static stretch on the
butterfly stroke: an electromyographic and cinematographic analysis flexibility of the hamstring muscles, Phys Ther 74:845–852,
of twelve muscles, Clin Orthop Relat Res 288:60–72, 1993. 1994.
9. Pink M, Jobe FW, Perry J, et al: The normal shoulder during the 31. Bandy WD, Irion JM, Briggler M: The effect of static stretch
backstroke: an EMG and cinematographic analysis of twelve muscles, and dynamic range of motion training on the flexibility of the
Clin J Sports Med 2:6–12, 1992. ham string muscles, J Orthop Sports Phys Ther 27:295–300,
10. Perry J, Pink M, Jobe FW, et al: The painful shoulder during the 1998.
backstroke: an EMG and cinematographic analysis of twelve 32. Blackburn TA, McLeod WD, White B, Wofford L: EMG analysis
muscles, Clin J Sports Med 2:13–20, 1992. of posterior rotator cuff exercises, J Athl Train 25:40–45,
11. Ruwe PA, Pink M, Jobe FW, et al: The normal and painful shoulder 1990.
during the breaststroke: an EMG and cinematographic analysis of 33. Moseley JB, Jobe FW, Pink M, et al: EMG analysis of the scapular
twelve muscles, Am J Sports Med 6:709–796, 1993. muscles during a shoulder rehabilitation program, Am J Sports
12. Rupp S, Berninger K, Hopf T: Shoulder problems in high level Med 20(2):128–134, 1992.
swimmers—impingement, anterior instability, muscular imbalance? 34. Wilk KE, Arrigo C: Current concepts in the rehabilitation of the
Int J Sports Med 16(8):557–562, 1995. athletic shoulder, J Orthop Sports Phys Ther 18:365–378, 1993.
13. Zemek MJ, Magee DJ: Comparison of glenohumeral joint laxity 35. Lear LJ, Gross MT: An electromyographical analysis of the scapular
in elite and recreational swimmers, Clin J Sport Med 6(1):40–47, stabilizing synergists during a push-up progression, J Orthop Sports
1996. Phys Ther 28(3):146–157, 1998.
14. Bak K, Faunø P: Clinical findings in competitive swimmers with 36. Kibler WB: Shoulder rehabilitation: principles and practice, Med
shoulder pain, Am J Sports Med 25(2):254–260, 1997. Sci Sports Exerc 30:540–550, 1998.
15. McMaster WC, Roberts A, Stoddard T: A correlation between 37. Decker MJ, Hintermeister RA, Faber KJ, Hawkins RJ:. Serratus
shoulder laxity and interfering pain in competitive swimmers, Am anterior muscle activity during selected rehabilitation exercises,
J Sports Med 26(1):83–86, 1998. Am J Sports Med 27(6):784–791, 1999.
16. Yanai T, Hay JG, Miller GF: Shoulder impingement in front-crawl 38. Blackburn TA, Guido TA: Rehabilitation after ligamentous and
swimming: I. A method to identify impingement, Med Sci Sports labral surgery of the shoulder: guiding concepts, J Athl Train
Exerc 32(1):21–29, 2000. 35(3):373–381, 2000.
Applied Biomechanics of Swimming • CHAPTER 14 349
39. Voight ML, Thomson BC: The role of the scapula in the reha- 41. Reinold M, Wilk KE, Fleisig GS, et al: Electromyographic analysis of the
bilitation of shoulder injuries, J Athl Train 35(3):364–372, rotator cuff and deltoid musculature during common shoulder external
2000. rotation exercises, J Orthop Sports Phys Ther 34:385–394, 2004.
40. Ekstrom R, Donatelli R, Soderberg G: Surface electromyo- 42. Swanik KA, Lephart SM, Swanik CB, et al: The effects of shoulder
graphic analysis of exercises for the trapezius and serratus plyometric training on proprioception and selected muscle perfor-
anterior muscles, J Orthop Sports Phys Ther 33:247–258, mance characteristics, J Shoulder Elbow Surg 11(6):579–586,
2003. 2002.
15
CHAPTER
350
Applied Biomechanics of Baseball Pitching • CHAPTER 15 351
90°
90° 180°
135°
60°
40° 0° 40°
0°
A B C D
0°
30° 0° 20° UT
0°
P
40° 90°
90°
E F G H
Figure 15-2
Definition of kinematic parameters. A, Elbow flexion. B, Shoulder external and internal rotation.
C, Shoulder abduction. D, Shoulder horizontal adduction (positive values) and horizontal abduction
(negative values). E, Lead knee flexion. F, Forward trunk tilt. G, Lateral trunk tilt. H, Pelvis angular
velocity (P) and upper torso angular velocity (UT). (From Escamilla RF, Fleisig GS, Barrentine SW, et al:
Kinematic comparison of throwing different types of baseball pitches, J Appl Biomech 14:1-23, 1998.)
352 SECTION II • Applied Biomechanics of Selected Sport Activities
Upper torso/pelvis
separation
Horizontal
Upper torso
abduction
orientation
Pelvis
orientation Elbow flexion
Trunk lateral tilt
Horizontal
adduction
Stride length
Shoulder
abduction
Shoulder
external rotation
Knee flexion
Foot orientation
Foot placement
Figure 15-3
Definition of kinematic parameters (continued): Stride length, horizontal abduction and adduction,
upper torso orientation, pelvis orientation, foot placement, foot orientation. (From Chu Y, Fleisig GS,
Simpson KJ, et al: Biomechanical comparison between elite female and male baseball pitchers, J Appl
Biomech 25:22-31, 2009.)
Superior
Internal
Proximal rotation
Horizontal
adduction
Anterior
Abduction
A B
Anterior
Flexion
Proximal
Varus
D
Medial C
Figure 15-4
Definition of kinetic parameters. A, Forces applied by the trunk to the upper arm at the shoulder.
B, Torques applied by the trunk to the upper arm about the shoulder. C, Forces applied by the upper
arm to the forearm at the elbow. D, Torques applied by the upper arm to the forearm about the elbow.
(From Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF: Kinetics of baseball pitching with implications
about injury mechanisms, Am J Sports Med 23:233-239, 1995.)
A B C D E F G
H I J K L
Table 15-1
Kinematic and Temporal Measurements (Mean ⫾ SD) During American Professional Baseball Pitching
Kinematic Parameter Temporal Parameter
(n ⫽ 11) (n ⫽ 11)
Lead Foot Contact
Arm-Cocking Phase
Arm-Acceleration Phase
From Escamilla RF, Fleisig GS, Barrentine SW, et al: Kinematic and kinetic comparisons between American and Korean professional baseball
pitchers, Sports Biomech 1:213-228, 2002.
NA, Not applicable; SD, standard deviation.
Note: Temporal parameters were defined as a percentage of the pitch completed, measured from lead foot contact to the kinematic parameter
shown, in which 0% corresponded to lead foot contact and 100% corresponded to the instant of ball release.
foot is positioned excessively open, pelvis rotation may to home plate for a right-handed pitcher). For example, a
occur too early. This results in improper timing, causing 20-cm (8-inch) open foot placement would result in an
energy from pelvis rotation to be applied to the upper trunk estimated 60-N increase in shoulder anterior force. Because
prematurely.26 Consequently, the pitcher may throw with the mean shoulder anterior force in adult pitching is
too much “arm,” because the energy generated from the approximately 380 N during the arm cocking phase (see
pelvis rotation may be dissipated instead of being applied up Table 15-2), a 60-N increase results in approximately a 15%
the kinetic chain to the throwing arm. increase in shoulder anterior force.
Improper foot placement and orientation at lead foot An open foot orientation (i.e., foot points out [externally
contact can also result in increased shoulder forces during rotated], which is the opposite of the illustration shown in
the arm-cocking phase. Fleisig9 demonstrated that shoulder Figure 15-7) can also result in increased shoulder anterior
anterior force increased 3 N during the arm-cocking phase force. Fleisig9 demonstrated that shoulder anterior force
for every centimeter (approximately 0.5 inch) that foot increased 2 N during the arm-cocking phase for every
placement was in the open position at lead foot contact (from degree that the foot orientation is externally rotated at lead
Figure 15-7, the foot is positioned in an open placement foot contact. For example, a 45° open foot orientation
position, which is to the left of a line drawn from the rubber would result in an estimated 90-N increase in shoulder
356 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 15-2
Kinetic Measurements (Mean ⫾ SD) During American Professional and Collegiate Baseball Pitching
Fleisig et al.10 Werner et al.35 Feltner and Dapena36
Parameter (n ⫽ 26) (n ⫽ 7) (n ⫽ 8)
Arm-Cocking Phase
Shoulder Kinetics
Elbow Kinetics
Arm-Acceleration Phase
Elbow Kinetics
Arm-Deceleration Phase
Shoulder Kinetics
Elbow Kinetics
Data from Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF: Kinetics of baseball pitching with implications about injury mechanisms, Am J
Sports Med 23:233-239, 1995; Werner SL, Fleisig GS, Dillman CJ, Andrews JR: Biomechanics of the elbow during baseball pitching, J Orthop
Sports Phys Ther 17(6):274-278, 1993; Feltner M, Dapena J: Dynamics of the shoulder and elbow joints of the throwing arm during a baseball
pitch, Int J Sports Biomech 2:235-259, 1986.
SD, Standard deviation.
anterior force, which is approximately a 25% increase in serratus anterior have moderate to high activity as they assist
shoulder anterior force. in stabilizing, upward rotating, and elevating the scapula.
During the stride, both shoulders abduct, externally At lead foot contact, shoulder abduction is approximately
rotate, and horizontally abduct as a result of the concentric 80° to 100° (Figure 15-8; see Table 15-1).5,12 The shoulder
muscle action of several muscles, including the deltoids, abductors are responsible for abducting and holding the
supraspinatus, infraspinatus, teres major, serratus anterior, arm in this position, while the rotator cuff muscles help
and upper trapezius (see Table 15-3). The supraspinatus has maintain proper humeral head position within the glenoid
its highest activity during the stride phase as it works to not fossa.19
only abduct the shoulder but also to help compress and At lead foot contact, the throwing arm is positioned
stabilize the glenohumeral joint.19 The deltoids exhibit high slightly behind the trunk in approximately 10° to 35° of
activity during this phase to initiate and maintain the shoul- horizontal abduction (see Table 15-1, Figure 15-3, and
der in an abducted position.19 Moreover, the trapezius and Figure 15-8).5,25 The posterior deltoid, latissimus dorsi,
Applied Biomechanics of Baseball Pitching • CHAPTER 15 357
Table 15-3
Muscle Activity (Mean ⫾ SD) During the Phases of Baseball Pitching, Expressed as % MVIC
Arm- Arm- Arm- Follow-
Cocking Acceleration Deceleration Through
Muscles N Windup Stride Phase Phase Phase Phase
Scapular
Upper trapezius 11 18 16 64 53 37 29 69 31 53 22 14 12
Middle trapezius 11 7 5 43 22 51 24 71 32 35 17 15 14
Lower trapezius 13 13 12 39 30 38 29 76 55 78 33 25 15
Serratus anterior (sixth rib) 11 14 13 44 35 69 32 60 53 51 30 32 18
Serratus anterior (fourth rib) 10 20 20 40 22 106 56 50 46 34 7 41 24
Rhomboids 11 7 8 35 24 41 26 71 35 45 28 14 20
Levator scapulae 11 6 5 35 14 72 54 76 28 33 16 14 13
Glenohumeral
Anterior deltoid 16 15 12 40 20 28 30 27 19 47 34 21 16
Middle deltoid 14 98 44 19 12 17 36 22 59 19 16 13
Posterior deltoid 18 65 42 26 28 27 68 66 60 28 13 11
Supraspinatus 16 13 12 60 31 49 29 51 46 39 43 10 9
Infraspinatus 16 11 9 30 18 74 34 31 28 37 20 20 16
Teres minor 12 56 23 15 71 42 54 50 84 52 25 21
Subscapularis (lower third) 11 79 26 22 62 19 56 31 41 23 25 18
Subscapularis (upper third) 11 78 37 26 99 55 115 82 60 36 16 15
Pectoralis major 14 66 11 13 56 27 54 24 29 18 31 21
Latissimus dorsi 13 12 10 33 33 50 37 88 53 59 35 24 18
Triceps brachii 13 4 6 17 17 37 32 89 40 54 23 22 18
Biceps brachii 18 8 9 22 14 26 20 20 16 44 32 16 14
Brachialis 13 8 5 17 13 18 26 20 22 49 29 13 17
Brachioradialis 13 5 5 35 20 31 24 16 12 46 24 22 29
Pronator teres 14 14 16 18 15 39 28 85 39 51 21 21 21
Supinator 13 9 7 38 30 54 38 55 31 59 31 22 19
Modified from Fleisig GS, Escamilla RF, Andrews JR: Biomechanics of throwing. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic
injuries and rehabilitation, p 338, Philadelphia, 1996, WB Saunders. Adapted from DiGiovine NM, Jobe FW, Pink M et al: An electromyographic
analysis of the upper extremity in pitching, J Shoulder Elbow Surg 1:15-25, 1992.
SD, standard deviation.
Windup, From initial movement to maximum knee lift of stride leg; stride, from maximum knee lift of stride leg to when lead foot of stride leg
initially contacts the ground; arm-cocking phase, from when lead foot of stride leg initially contacts the ground to maximum shoulder external
rotation; arm-acceleration phase, from maximum shoulder external rotation to ball release; arm-deceleration phase, from ball release to maximum
shoulder internal rotation; follow-through phase, from maximum shoulder internal rotation to maximum shoulder horizontal adduction.
358 SECTION II • Applied Biomechanics of Selected Sport Activities
Figure 15-6
Approximate time lengths for pitching phases: wind-up, stride, arm cocking (COCK), arm acceleration
(ACC), arm deceleration (DEC), and follow-through. Events shown separating phases: hand out of
glove, foot contact (FC), maximum shoulder external rotation (MER), ball release (REL), and maximum
internal rotation (MIR).
teres major, and posterior rotator cuff (i.e., infraspinatus of 0° (i.e., forearm parallel with ground) at lead foot con-
and teres minor) are responsible for horizontally abducting tact would result in an increase in shoulder proximal force
the shoulder, while the rhomboids and middle trapezius of 70 N during arm cocking. Given a mean shoulder proxi-
retract the scapula (see Table 15-3).19 At lead foot contact, mal force of 660 N during arm cocking (see Table 15-2),10
the pelvis orientation is in an open position (positive values, a 70-N increase results in a 10% increase in shoulder proxi-
as shown in Figure 15-3) of approximately 20° to 30°,25,26 mal force.
and the upper torso orientation is in a closed position Elbow flexion of the throwing arm at foot contact is
of approximately 10° to 20° (negative values, as shown in approximately 80° to 100° (see Table 15-1).5,12 Eccentric
Figure 15-3).25,26 The closed upper torso orientation places and isometric actions from the elbow extensors of the
the trunk musculature, such as the abdominals, obliques, throwing arm help control elbow flexion, while the prona-
and paraspinal muscles, on stretch. Moreover, the horizon- tor muscles pronate the forearm as the shoulder abducts
tally abducted shoulder places the horizontal shoulder and externally rotates (see Table 15-3).19 EMG has shown
adductors on stretch. Therefore, the elastic energy stored in that the wrist and finger extensors have very high activity
these muscles and associated connective tissue caused by during the stride, causing the wrist to move from a position
being stretched can be transferred up the kinetic chain dur- of slight flexion to a position of hyperextension (see Table
ing the arm-cocking phase. The stretch reflex may also be 15-3).19 These muscles act concentrically as they work
evoked as these muscles are quickly stretched, summating against gravity, with the throwing palm and ball initially
the energy that can be transferred up the kinetic chain dur- facing downward as the shoulder abducts.
ing the arm-cocking phase. This elastic energy may not be
generated and transferred appropriately in a pitcher who
does not exhibit a normal sequence of pelvis, upper torso, Arm Cocking
and shoulder spatial orientations. Arm cocking begins at lead foot contact and ends at maxi-
A shoulder external rotation of approximately 45° to 70° mum shoulder external rotation, as the upper body is
at lead foot contact (Figure 15-9; see Table 15-1) causes rotated to face the target (see Figure 15-5 F, G). This phase
the forearm to rotate up toward a vertical position.5,12 If the lasts between 0.10 to 0.15 seconds (see Figure 15-6).7,12
arm is late in rotating upward, shoulder proximal (i.e., the High to very high forces, torques, and muscle activity typi-
force that resists shoulder distraction) force may increase. cally occur during this phase.10,19
Fleisig9 demonstrated for every degree the arm is late rotat- The quadriceps of the lead leg initially exhibit an eccen-
ing up at lead foot contact, shoulder proximal force tric action to decelerate knee flexion after lead foot contact,
increased 1.5 N during the arm-cocking phase. For exam- and then an isometric action to stabilize the lead leg. High
ple, given a mean shoulder external rotation of 45° at lead activity from the gluteus maximus also occurs to help stabi-
foot contact (see Table 15-1), a shoulder external rotation lize the hip.27 This emphasizes the importance of lower
Applied Biomechanics of Baseball Pitching • CHAPTER 15 359
Figure 15-8
Shoulder abduction and horizontal adduction. Acc, Arm acceleration;
Cocking, arm cocking; Dec, arm deceleration; FC, time of foot contact;
F-T, follow-through; MER, maximum shoulder external rotation;
MIR, maximum internal rotation; REL, ball release. (From Dillman
CJ, Fleisig GS, Andrews JR: Biomechanics of pitching with emphasis
upon shoulder kinematics, J Orthop Sports Phys Ther 18:402-408,
1993.)
Figure 15-7
Stride length, foot placement, and foot orientation measurements
during baseball pitching. (Modified from Dillman CJ, Fleisig GS,
Andrews JR: Biomechanics of pitching with emphasis upon shoulder
kinematics, J Orthop Sports Phys Ther 18:402-408, 1993.)
ball release (see Table 15-1).12,26 As the hips rotate to face phase (see Table 15-3).19 High activity from these muscles
the target, the trunk rotators are placed on stretch, which is needed to stabilize the scapula and properly position the
will produce a recoil effect for the subsequent shoulder scapula in relation to the horizontally adducting and rotat-
rotation. Shortly after the pelvis begins its rotation, the ing shoulder.19 The scapular protractors are especially
upper torso begins transverse rotation about the spinal col- important during this phase to resist scapular retraction by
umn (see Table 15-1).12,26 Maximum upper torso angular eccentric and isometric action during the early part of this
velocity of approximately 900 deg/sec to 1300 deg/sec phase, and cause scapular protraction by concentric action
(approximately twice as large as pelvis angular velocity) is during the latter part of this phase. The serratus anterior is
achieved.7,12 This action occurs 0.05 to 0.07 seconds after the most active, as it provides both stabilization and pro-
lead foot contact, which is approximately 50% of the time traction to the scapula (see Table 15-3).19 During late arm
from lead foot contact to ball release (see Table 15-1).12,26 cocking, the serratus anterior is important in providing up-
The sequence of attaining maximal pelvis rotation prior to ward rotation and protraction of the scapula, allowing the
maximal upper torso rotation is important in establishing scapula to move with the horizontally adducting humerus.
proper timing and coordination for subsequent portions of The middle trapezius, rhomboids, and levator scapulae,
the throw, and can also affect ball velocity.26 Moreover, which oppose the scapular motion created by the serratus
pitchers who delay upper torso rotation as late as possible anterior, have also been shown to be quite active (see Table
(typically higher-skilled professional pitchers) minimize 15-3).19 Dysfunction of the scapula muscles may adversely
shoulder internal rotation torque.30 When maximum shoul- affect normal function of the glenohumeral muscles. More-
der external rotation occurs, both the pelvis and the upper over, scapular muscle imbalances may lead to abnormal
torso are rotated approximately 90° and now face the scapular movement and position relative to the humerus,
hitter.26 The abdominal and oblique musculature are also increasing injury risk to the shoulder.
placed on stretch because of the hyperextension of the lum- Gowan and colleagues31 demonstrated that subscapularis
bar trunk that occurs as the upper torso rotates. High activ- activity is nearly twice as great in professional pitchers as
ity from the abdominals, obliques, and lumbar paraspinal in amateur pitchers during this phase. In contrast, muscle
muscles have been reported during the arm-cocking phase, activity from the pectoralis major, supraspinatus, serratus
which emphasizes the importance of strong trunk muscula- anterior, and biceps brachii was approximately 50% greater
ture in overhead pitching.27 in amateur pitchers than in professional pitchers. From
As the trunk rotates to face the target, the throwing shoul- these data, professional pitchers may exhibit better pitching
der horizontally adducts, moving from a position of 20° to efficiency, requiring less muscular activity compared with
30° of horizontal abduction at lead foot contact to a position amateurs.
of 15° to 20° of horizontal adduction at the time of maxi- Glousman and colleagues32 compared shoulder muscle
mum shoulder external rotation (see Table 15-1 and Figure activity between healthy pitchers with no pathologic, condi-
15-8).7,12 During this time, a maximum shoulder horizontal tions of the shoulder to pitchers with chronic anterior shoul-
adduction velocity (relative to the trunk) of approximately der instability caused by anterior glenoid labral tears. Pitch-
500 deg/sec to 650 deg/sec is obtained.7 Consequently, ers diagnosed with chronic anterior instability exhibited
high to very high shoulder muscle activity is needed to keep greater muscle activity in the biceps brachii and supraspina-
the arm moving with the rapidly rotating trunk (see Table tus and less muscle activity in the pectoralis major, subscapu-
15-3),19 as well as control the resulting shoulder external laris, and serratus anterior. Chronic anterior instability
rotation, which peaks near 180° (see Figure 15-9).7 results in excessive stretch of the anterior capsule, which may
The multiple functions of muscles are clearly illustrated stimulate mechanoreceptors within the capsule, resulting in
during arm cocking. For example, the pectoralis major, excitation of the biceps brachii and supraspinatus and inhibi-
anterior deltoid, and subscapularis act concentrically to tion of the pectoralis major, subscapularis, and serratus ante-
horizontally adduct the shoulder and act eccentrically to rior.32 Increased activity in the biceps brachii and supraspina-
control shoulder external rotation. The dual function of tus help compensate for anterior shoulder instability as
these muscles helps maintain an appropriate length-tension these muscles enhance glenohumeral stability. Rodosky and
relationship by simultaneously shortening and lengthening, colleagues33 reported that as the humerus abducts and
which implies that these muscles may be maintaining a near- maximally externally rotates, the long head of the bicep
constant length. Therefore, some muscles that have duel helps enhance anterior stability of the glenohumeral joint
functions and simultaneously shorten and lengthen as the and decreases stress placed on the inferior glenohumeral
shoulder performs dual actions at the same time may in ligament. Decreased activity from the pectoralis major and
effect be acting isometrically. Muscle actions during pitching subscapularis, which act eccentrically to decelerate the exter-
have important implications in training and rehabilitation. nally rotating shoulder, may accentuate shoulder external
The shoulder girdle muscles (i.e., levator scapulae, ser- rotation and increase the stress on the anterior capsule.32
ratus anterior, trapezius, rhomboids, and pectoralis minor) Decreased activity in the serratus anterior may cause the
show high to very high activity during the arm cocking scapula to be abnormally positioned relative to the externally
Applied Biomechanics of Baseball Pitching • CHAPTER 15 361
Figure 15-12
Shortly before maximum external rotation is achieved, a critical
instant occurs; at this instant, a pitcher’s shoulder is externally rotated
165°, and the elbow is flexed 95°. Among the loads generated at this
time are 67 Nm of internal rotation torque, 310 N of anterior force
at the shoulder, and 64 Nm of varus torque at the elbow. (From
Fleisig GS, Andrews JR, Dillman CJ, Escamilla RF: Kinetics
of baseball pitching with implications about injury mechanisms, Am J
Sports Med 23:233-239, 1995.)
Moderate to high muscle activity occurs during this scapula stabilization are crucial during this phase. How-
phase as the arm accelerates forward both linearly and ever, Gowan31 has demonstrated that rotator cuff activity
angularly (see Table 15-3).19,22,23 is significantly different between professional and amateur
Just prior to maximum shoulder external rotation, pitchers. Muscle activity in infraspinatus, teres minor,
elbow extension begins (see Figure 15-13).7 This move- supraspinatus, and biceps were two to three times higher
ment is followed immediately by the onset of shoulder in amateur pitchers. In contrast, the muscle activity of the
internal rotation.7 The initiation of elbow extension subscapularis, serratus anterior, and latissimus dorsi were
before shoulder internal rotation allows the thrower to greater in professional pitchers. These findings may imply
reduce the rotational inertia around the arm’s longitudi- that professional pitchers better coordinate the move-
nal axis, resulting in greater internal rotation velocity. The ments of their body segments to increase pitching
shoulder internal rotators act concentrically to help efficiency. This improved efficiency may minimize gleno-
produce an extremely high maximal internal rotation humeral instability during the arm cocking and accelera-
velocity of approximately 7000 deg/sec to 8000 deg/sec tion phases, thus less rotator cuff muscle activity is
(see Table 15-1),5,12 which is one of the fastest known needed. These findings also appear to support the results
movements in sports. Maximal shoulder internal rotation of previous EMG studies.22,23
angular velocity occurs at approximately ball release.5,12 Maximum elbow angular velocity during pitching occurs
EMG data show that the subscapularis is the most active approximately half way through the acceleration phase, and
shoulder internal rotator, followed by the latissimus dorsi reaches a peak of approximately 2100 deg/sec to 2400 deg/
and pectoralis major (see Table 15-3).19,31,42 sec (see Table 15-1).5,35 This rapid elbow extension may
As the elbow extends and the shoulder internally rotates, primarily be due to “centrifugal” force acting at the elbow
the trunk flexes forward from its hyperextended position to as the trunk and arm rotate, for it is unlikely that the elbow
a neutral position at ball release.5,12 High muscle activity extensors can shorten fast enough to generate the high
from the trunk flexors (i.e., rectus abdominals and obliques) angular velocity measured at the elbow.
has been demonstrated during the acceleration phase, as Several studies have examined the role of the triceps
well as from the lumbar paraspinal muscles and gluteus brachii in extending the elbow during the acceleration
maximus.27 Forward trunk tilt achieves a maximal angular phase of pitching. Roberts41 reported that a pitcher with a
velocity of approximately 300 deg/sec to 450 deg/sec.5 paralyzed triceps caused by a differential nerve block was
Forward flexing of the trunk is enhanced by lead knee ex- able to throw a ball more than 80% of the speed attained
tension, providing a stable base around which the trunk prior to the paralysis of the triceps brachii. This seems to
rotates.5 The lead knee extends approximately 15° to 20° support the concept that concentric action of the triceps
from lead foot contact to ball release (see Table 15-1).5 brachii does not generate all of the elbow extension angular
Forward trunk tilt may decrease (i.e., be more erect) if the velocity, and that “centrifugal” force may be a major factor.
lead knee continues flexing and moving forward, and in EMG has shown high triceps brachii and anconeus activity
such cases ball velocity also is diminished.28 This again il- during the arm-acceleration phase, suggesting that the
lustrates the importance of lower extremity strength in the triceps brachii probably initiate or contribute to the angular
overhead thrower. At ball release, the trunk of a baseball velocity generated during this phase.19,22,24,35 However,
pitcher is normally flexed forward from a vertical position these muscles may function more as arm stabilizers than as
approximately 30° to 40° (see Table 15-1).5 accelerators.36
The throwing shoulder remains abducted approximately Toyoshima and colleagues29 compared “normal throw-
80° to 100° throughout the acceleration phase, which ing” (i.e., using the entire body) to throwing using only the
implies that this is a strong position for the shoulder (see forearm to extend the elbow. The latter “forearm throw”
Table 15-1 and Figure 15-8).7 This is true regardless of the involved a maximum voluntary effort to extend the elbow
type of pitching delivery (i.e., sidearm, three-quarters, with the upper arm immobilized. If it is assumed that the
or overhand) that occurs.39 It is lateral trunk tilt, not shoul- triceps brachii shortened as fast as voluntarily possible during
der abduction, that changes with varying types of pitching the “forearm throw,” the resulting elbow angular velocity
deliveries, with an overhand thrower tilting the trunk to the would be the maximum possible given a maximum triceps
contralateral side (i.e., away from the throwing arm) brachii contraction. Their results demonstrated that “normal
more than a sidearm or three quarters thrower. In overhead throwing” generated approximately twice the elbow exten-
pitching, trunk tilt normally deviates from a vertical sion angular velocity as could be achieved during the “fore-
position 20° to 30° away from the throwing arm (see arm throw.” It was concluded that the elbow was swung
Table 15-1).7 open like a whip when the entire body was involved in the
The rotator cuff muscles, trapezius, serratus anterior, throw, and that the elbow extension angular velocity that
rhomboids, and levator scapula have all demonstrated occurred during “normal throwing” was due more to the
high levels of activity during the acceleration phase (see rotary actions of other parts of the body, such as the hips,
Table 15-3).19 This implies that humeral head control and trunk, and shoulder, rather than by the elbow-extending
Applied Biomechanics of Baseball Pitching • CHAPTER 15 365
capabilities of the triceps brachii. It was further stated that in ment to impart force to the ball is the hand, which moves
“normal throwing” the elbow contributed less than 43% to from a hyperextended wrist position at maximum shoulder
ball velocity, and that a larger contribution percentage to external rotation to a neutral wrist position at ball release.45
ball velocity resulted from “body” rotations. The wrist flexors (i.e., flexor carpi radialis, flexor carpi ulna-
Ahn43 used computer simulations and optimization tech- ris, and flexor digitorum) have been shown to be active
niques to compare theoretical data with experimental data during this phase of pitching (see Table 15-3).19 Their
during baseball pitching. His data demonstrated that hand activity may initially be eccentric to slow down the hyperex-
velocity at ball release was approximately 80% of the ex- tending wrist at the beginning of the acceleration phase.45
perimental result when the resultant elbow joint torque was However, as they continue to fire, they concentrically con-
set to zero, approximately 95% of the experimental value tract and flex the wrist as ball release is approached.45 In
when the resultant wrist joint torque was set to zero, and addition, the pronator teres is also active during this
approximately 75% of the experimental value when both the phase to pronate the forearm (see Table 15-3).19 Mean ball
resultant elbow and wrist joint torques were set to zero. He velocity for college and professional pitchers average
concluded that ball velocity at ball release was generated approximately 75 to 85 mph (see Table 15-1).5,12
primarily by body segments other than the upper extremity,
such as the legs, hips, and trunk.
At ball release, the elbow is almost fully extended, and Arm Deceleration
positioned slightly anterior to the trunk. At release, This arm-deceleration phase, which lasts between 0.03 to
the elbow is slightly flexed approximately 20°, and shoul- 0.05 seconds (see Figure 15-6), goes from ball release to
der horizontal adduction is approximately 5° to 10° (see maximum shoulder internal rotation (see Figure 15-5 I).
Table 15-1). The trunk and hips continue to flex and the lead knee and
Shoulder internal rotation torque and elbow varus throwing elbow continue to extend until almost full exten-
torque decrease during the arm acceleration phase as the sion is reached. Moderate to high activity has been reported
arm begins rotating forward and generating speed (see in the lumbar paraspinals, abdominal and oblique muscles,
Figures 15-11 and 15-13).10 However, because the valgus and gluteus maximus.27 The stance leg now starts moving
stress at the elbow is near maximum at the beginning of the upward in reaction to the flexing trunk and hips. The mov-
arm-acceleration phases when the elbow is extending, a ing of the arm forward, down, and across the body may be
wedging of the olecranon against the medial aspect of the a natural occurrence in pitching to minimize injury poten-
trochlear groove and the olecranon fossa can occur. This tial at the elbow and shoulder.46
impingement leads to osteophyte production at the poste- Shoulder internal rotation continues until approximately
rior and posteromedial aspect of the olecranon tip and can 0° (i.e., neutral position). Pronation occurs at the radioul-
cause chondromalacia and loose body formation.4 Figure nar joint,45 with the pronator teres exhibiting moderate
15-13 demonstrated substantial varus torque being gener- activity (see Table 15-3).19 The biceps brachii and supinator
ated throughout the arm-cocking and arm-acceleration muscles act eccentrically to decelerate the rapidly pronating
phases to resist this valgus stress. During arm cocking and forearm (see Table 15-3).19 The biceps brachii also act
acceleration, the elbow extends from approximately 85° to eccentrically to decelerate elbow extension, as does the
20° of elbow flexion (see Figure 15-13).10 This combina- brachialis.
tion of elbow extension and resistance to valgus stress The posterior muscles of the shoulder have been identi-
supports the “valgus extension overload” mechanism de- fied as having a paramount role in resisting shoulder distrac-
scribed by Wilson and colleagues.4 In addition, Campbell tion and anterior subluxation forces.5,10,22,23 These muscles
and colleagues44 found greater valgus torque (normalized include the infraspinatus, supraspinatus, teres major and
by body weight height) in 10-year-old pitchers than in minor, latissimus dorsi, and posterior deltoid. Contraction
professional pitchers at the instant of ball release, which of the teres major, latissimus dorsi, and posterior deltoid
they felt may be related to “little league” elbow syndrome also helps to decelerate the shoulder abduction that occurs
in young pitchers. during this phase. The lower trapezius, rhomboids, and
A maximum elbow proximal force of approximately 800 serratus anterior have all been shown to be quite active, thus
to 900 N is produced at the elbow to prevent distraction of providing stability to the scapula (see Table 15-3).19 The
the forearm resulting from the “centrifugal” force acting on teres minor, which is often an isolated source of rotator cuff
the forearm (see Table 15-2 and Figure 15-10).10 In addi- pain, has demonstrated the highest activity of all the gleno-
tion, a maximum elbow flexor torque of approximately humeral muscles during this phase (see Table 15-3), provid-
50 to 60 Nm (see Table 15-2 and Figure 15-13)10,35 ing a posterior restraint that may limit humeral head
is generated by low to moderate activity from the elbow anterior translation, horizontal adduction, and shoulder
flexors.19,24 Contraction of the elbow flexors in this phase internal rotation.19,23
resists elbow distraction, enhancing elbow joint stability, Comparing professional and amateur pitchers, Gowan
and also controls the rate of elbow extension. The final seg- and colleagues31 reported that amateur pitchers had more
366 SECTION II • Applied Biomechanics of Selected Sport Activities
than twice as much muscle activity in the biceps and poste- The serratus anterior has demonstrated the highest activ-
rior deltoid. This may imply that amateur pitchers incur ity of all scapular rotators in this phase (see Table 15-3),19
greater posterior shoulder stress compared with professional acting concentrically or isometrically. However, the middle
pitchers because of a less efficient throwing pattern. trapezius and rhomboids act eccentrically to decelerate
The wrist and finger flexors also had very high muscle scapular protraction (see Table 15-3).19 As in the decelera-
activity during this phase (see Table 15-3).19 These muscles tion phase, EMG has shown that the wrist and finger exten-
continue contracting and flexing the wrist. In addition, the sor muscles had low to moderate activity during the follow-
wrist and finger extensor muscles demonstrate low to mod- through, implying that they act eccentrically to decelerate
erate activity (see Table 15-3),19 perhaps acting eccentrically the flexing wrist (see Table 15-3).19
to decelerate the flexing wrist and fingers.
Large shoulder and elbow forces and torques are
needed during arm deceleration to slow the rapidly mov- Kinematic and Kinetic Comparisons
ing arm (see Table 15-2).5,10 Maximum proximal forces of Among Fastball, Curveball, Slider,
approximate body weight are needed at both the elbow
(800 to 1000 N) and shoulder (1000 to 1200 N) to
and Change-Up Baseball Pitches
prevent distraction at these joints (see Table 15-2, Figure Kinematic (Table 15-4), temporal (Table 15-5), and
15-10, and Figure 15-13).10,35 These shoulder and elbow kinetic (Table 15-6) differences among fastball, curveball,
proximal forces are two to three times greater than other slider, and change-up pitches in adult pitchers have been
shoulder and elbow forces generated during pitching (see reported by Escamilla and colleagues,7 Barrentine and
Table 15-2).10,35 colleagues,45 and Fleisig and colleagues.17 Fleisig and col-
A maximum shoulder posterior force of approximately leagues reported that 10 of 15 kinematic variables mea-
310 to 490 N and a maximum shoulder horizontal abduc- sured demonstrated significant differences among the four
tion torque of approximately 75 to 125 Nm are applied to pitch variations (see Table 15-4). Most significant differ-
the arm to resist shoulder horizontal adduction and anterior ences among pitches were at the instant of ball release.
humeral head translation (see Table 15-2 and Figure Elbow flexion, shoulder horizontal adduction, and knee
15-11).5,10 In addition, a maximum shoulder inferior force flexion were greater in the change-up than in the other
of approximately 230 to 390 N and a maximum shoulder pitches. The curveball demonstrated greater forward and
adduction torque of approximately 60 to 110 Nm are lateral trunk tilt compared with the fastball and change-up.
produced to resist shoulder abduction and superior Similarly, Escamilla and colleagues7 also reported that
humeral head translation (see Table 15-2, Figure 15-10, approximately two thirds (18 of 26) of the kinematic vari-
and Figure 15-11).5,10 ables measured demonstrated significant differences among
the four pitch variations. The greatest number of kinematic
differences (14 of 26) occurred between the fastball and
Follow-Through change-up groups, which implies that disguising the
The follow-through phase begins at the time of maximum change-up to look like the fastball may be challenging, but
shoulder internal rotation and ends when the arm com- it is important for the fastball and change-up to look simi-
pletes its movement across the body and a balanced position lar to fool the hitter. The fewest kinematic differences (2 of
is obtained (see Figure 15-5). This phase typically lasts 26) occurred between the fastball and slider groups.
approximately 1 second (see Figure 15-6). Energy in the The change-up group had the smallest knee and elbow
throwing arm continues to be dissipated back through the flexion at lead foot contact and the greatest knee and elbow
kinetic chain. A long arc of deceleration from the throwing flexion at ball release. During the arm-cocking and arm-
arm, as well as sufficient forward tilting of the trunk, allows acceleration phases, peak shoulder, elbow, and trunk
energy to be absorbed by the large musculature of the trunk angular velocities were generally greatest in the fastball
and legs. This absorption helps reduce the stress placed on and slider groups and smallest in the change-up group. At
the throwing arm. All the body’s weight is now borne by a ball release, the change-up group had the most upright
straight or almost-straight lead leg. The trunk and hips trunk and the greatest horizontal shoulder adduction,
continue flexing and the stance leg continues moving whereas the curveball group had the most lateral trunk tilt.
upward (see Figure 15-5). Understanding kinematic differences can help a pitcher
As in the deceleration phase, the posterior shoulder select and learn different pitches, and help a batter learn
muscles continue to act eccentrically, continuing to deceler- how to identify different pitches.
ate the horizontally adducting shoulder. Shoulder joint Forearm, wrist, and hand kinematics have also been
forces and torques generated during the follow-through are reported during different pitch types.45,47 The forearm
generally lower than joint forces and torques generated dur- is supinated more during the arm-cocking phase for a
ing the deceleration phase (see Figures 15-10, 15-11).10 curveball (approximately 40°) compared with a fastball
Applied Biomechanics of Baseball Pitching • CHAPTER 15 367
Table 15-4
Kinematic Comparisons (Mean ⫾ SD) Among Fastball, Curveball, Change-Up, and Slider Baseball Pitches
in Collegiate Baseball Pitchers
Fastball Curveball Change-Up Slider
(n ⫽ 21) (n ⫽ 20) (n ⫽ 19) (n ⫽ 6) Comparison*
Lead Foot Contact
Arm-Cocking Phase
Ball Release
From Fleisig GS, Kingsley DS, Loftice JW et al: Kinetic comparison among the fastball, curveball, change-up, and slider in collegiate baseball
pitchers, Am J Sports Med 34:423-430, 2006.
SD, Standard deviation.
*Significant difference (p 0.01) among fastball, curveball, and change-up. Post-hoc pair-wise significant difference (p 0.05): a, fast versus
curve; b, fast versus change; c, fast versus slider; d, slider versus curve; e, slider versus change; f, change versus curve
(approximately 20°), which may also may be related to the significantly less angular velocities in the upper trunk,
risk of injury.47 The wrist was extended more in the fastball elbow, and shoulder than the three other pitch types. There
(approximately 40°) compared with the curveball (approxi- were no significant differences in any of the temporal
mately 30°) during late cocking and acceleration phases.47 parameters.
Moreover, Barrentine and colleagues45 and Sakurai and Kinetic measurements among pitch type variations are
colleagues47 reported that during arm cocking, peak wrist shown in Table 15-6. There was only one significant
extension for the fastball and change-up was greater than kinetic difference between the fastball and curveball and
for the curveball, whereas forearm supination was greater between the fastball and the slider. Shoulder and elbow
in the curveball compared with the fastball and change-up. kinetics were significantly less for the change-up com-
At ball release, the forearm was in a supinated position for pared with the fastball, curveball, and slider. This implies
the curveball, but a fairly neutral position for the fastball that the change-up may have a lower injury risk potential
and change-up. to the shoulder and elbow compared with the other three
Angular velocity kinematic and temporal measurements pitches, and the fastball and curveball may have similar
among pitch type variations are shown in Table 15-5. Ball injury risk potential because of the similar joint loads they
velocity decreased significantly from fastball to slider to produce.
change-up to curveball. Although the curveball had the Perhaps nowhere is the topic of pitch types as impor-
lowest ball velocity, it was the change-up that generated tant as it is with youth baseball. Even though previous
368 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 15-5
Magnitude and Timing of Maximum Velocity Comparisons (Mean ⫾ SD) Among Fastball, Curveball, Change-Up, and Slider
Baseball Pitches in Collegiate Baseball Pitchers
Fastball Curveball Change-Up Slider
(n ⫽ 21) (n ⫽ 20) (n ⫽ 19) (n ⫽ 6) Comparison*
Arm-Cocking Phase
Maximum pelvis angular velocity (°/s) 596 112 562 91 536 89 546 42 *(a,b)
Maximum pelvis angular velocity 30 17 34 17 29 15 38 18
(% of pitch)
Maximum upper trunk angular 1120 95 1071 85 1025 65 1107 60 *(a,b,e,f)
velocity (°/s)
Maximum upper trunk angular 50 9 51 6 49 10 52 9
velocity (% of pitch)
Arm-Acceleration Phase
Maximum elbow extension angular 2206 263 2160 234 1971 215 2264 158 *(b,e,f)
velocity (°/s)
Maximum elbow extension angular 93 3 93 3 94 2 93 3
velocity (% of pitch)
Ball velocity (m/s) 77 3 64 3 67 3 70 4 *(a,b,c,d,f)
Arm-Deceleration Phase
Maximum shoulder internal rotation 6518 946 6484 857 5799 778 6356 721 *(b,e,f)
velocity (°/s)
Maximum internal rotation velocity 104 2 104 2 105 2 102 2
(% of pitch)
From Fleisig GS, Kingsley DS, Loftice JW et al: Kinetic comparison among the fastball, curveball, change-up, and slider in collegiate baseball
pitchers, Am J Sports Med 34:423-430, 2006.
SD, Standard deviation.
*Significant difference (p 0.01) among fastball, curveball, and change-up. Post-hoc pair-wise significant difference (p 0.05): a, fast versus
curve; b, fast versus change; c, fast versus slider; d, slider versus curve; e, slider versus change; f, change versus curve.
Note: Timing parameters expressed on a normalized time scale as a percent of pitch, in which 0% was the time of lead foot contact and 100%
was the time of ball release.
studies showed no significant increases in elbow and Baseball Pitching Kinematic and Kinetic
shoulder kinetics with breaking pitches, many people be- Comparisons Among Youth, High School,
lieve that curveballs are more stressful than fastballs in
younger, less experienced pitchers. Dun and colleagues48
College, and Professional Levels
repeated the biomechanical comparison among pitch Kinematic (Table 15-8), temporal (Table 15-9), and kinetic
types with adults,7,17 but this time, youth pitchers (10 to (Table 15-10) differences among youth, high school, col-
15 years old) were employed. Once again, elbow and lege, and professional pitchers have been reported by Fleisig
shoulder forces and torques were less in the change-up and colleagues.12 Of the 16 position and velocity parameters
than in the fastball and curveball (Table 15-7).48 Further- tested, six had significant differences among competition
more, forces and torques for youth pitchers were signifi- levels (see Table 15-8). Five of the six parameters that
cantly less during the curveball than during the fastball. exhibited significant differences were velocity parameters,
These results suggest that the curveball is not a primary which were generally significantly greater in college and
contributor to elbow injuries in youth pitchers. Avoiding professional pitchers compared with youth and high
overuse (such as high pitch counts, year-round baseball, school pitchers. No significant differences were observed in
and multiple teams) and poor mechanics are most likely temporal measurements (see Table 15-9).
more important for minimizing the risk of youth pitching All eight kinetic parameters were significantly different
injuries.6,12,49,50 among youth, high school, college, and professional
Applied Biomechanics of Baseball Pitching • CHAPTER 15 369
Table 15-6
Joint Kinetic Comparisons (Mean ⫾ SD) Among Fastball, Curveball, Change-Up, and Slider Baseball Pitches in Collegiate
Baseball Pitchers
Fastball Curveball Change-Up Slider
(n ⫽ 21) (n ⫽ 20) (n ⫽ 19) (n ⫽ 6) Comparison*
Arm-Cocking Phase
Arm-Acceleration Phase
Wrist flexion (Nm) 0.4 0.3 0.5 0.3 0.4 0.3 0.5 0.2
Elbow flexion torque (Nm) 40 9 41 16 32 9 37 14 *(f)
Elbow proximal force (N) 988 110 934 103 857 138 1040 53 *(a,b,e,f)
Shoulder horizontal adduction torque (Nm) 111 29 109 20 98 20 130 35 *(b,c,d,e,f)
Shoulder proximal force (N) 1056 157 998 155 910 169 1145 113 *(b,d,e,f)
Arm-Deceleration Phase
From Fleisig GS, Kingsley DS, Loftice JW et al: Kinetic comparison among the fastball, curveball, change-up, and slider in collegiate baseball
pitchers, Am J Sports Med 34:423-430, 2006.
SD, Standard deviation.
*Significant difference (p 0.01) among fastball, curveball, and change-up. Post-hoc pair-wise significant difference (p 0.05): a, fastball versus
curveball; b, fastball versus change-up; c, fastball versus slider; d, slider versus curveball; e, slider versus change-up; f, change-up versus curveball.
Table 15-7
Joint Kinetic Comparisons (Mean ⫾ SD) Among Fastball, Curveball, and Change-Up Baseball Pitches
in Youth (10 to 15 Years Old) Baseball Pitchers
Fastball Curveball Change-Up Comparison*
(N ⫽ 29) (N ⫽ 29) (N ⫽ 29) (N ⫽ 29)
Arm-Cocking Phase
Elbow varus torque (Nm) 34.8 15.4 31.6 15.2 29.0 14.8 a, b, c
Shoulder internal rotation torque (Nm) 35.2 15.6 31.9 15.3 29.5 15 a, b, c
Arm-Acceleration Phase
Wrist flexion torque (Nm) 1.5 1.3 2.3 1.9 1.1 1.1 a, b, c
Forearm supination torque (Nm) 0.9 0.7 1.2 0.9 0.7 0.6 a, b, c
Elbow flexion torque (Nm) 16.4 7.2 14.4 7.5 12.9 6.8 a, b
Elbow proximal force (N) 461.9 163.2 428.2 164.3 377.9 164.9 a, b, c
Shoulder horizontal adduction torque (Nm) 39.1 18.7 38.2 18.9 32.9 17.6 b, c
Shoulder proximal force (N) 465.6 169.9 433.3 170.7 384.2 165.4 a, b, c
Arm-Deceleration Phase
From Dun S, Loftice J, Fleisig GS et al: A biomechanical comparison of youth baseball pitches: Is the curveball potentially harmful? Am J Sports
Med 36(4):686-692, 2008.
SD, Standard deviation.
*Significant difference (P 0.01) among pitch types. Post-hoc pair-wise significant difference (p 0.05): a, fastball versus curveball; b, fastball
versus change-up; c, curveball versus change-up.
370 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 15-8
Kinematic Differences (Mean ⫾ SD) Among Youth, High School, College, and Professional Baseball Pitchers
Youth High School College Professional Significant
(n ⫽ 23) (n ⫽ 33) (n ⫽ 115) (n ⫽ 60) Differences
Lead Foot Contact
Arm-Cocking Phase
Arm-Acceleration Phase
Maximum elbow extension angular 2230 300 2180 340 2380 300 2320 300 †
b, d, e
velocity (°/s)
Maximum shoulder internal rotation 6900 1050 6820 1380 7430 1270 7240 1090 *d
angular velocity (°/s)
Ball Release
From Fleisig GS, Barrentine SW, Zheng N et al: Kinematic and kinetic comparison of baseball pitching among various levels of development,
J Biomech 32:1371–1375, 1999.
SD, Standard deviation.
*Significant differences (p 0.05) among four levels.
†
Significant differences (p 0.01) among four levels.
Post-hoc pair-wise significant difference (p 0.05) between a, youth and high school; b, youth and college; c, youth and professional; d, high
school and college; e, high school and professional; and f, college and professional.
pitchers (see Table 15-10).12 Joint forces and torques adjacent body segments. Furthermore, the magnitude of
increased with each level of competition, which may be force needed to produce injury most likely varies among
due to greater muscle strength at each higher level. The levels of competition, because of differences in muscle
greater shoulder and elbow angular velocities produced mass and tissue strength.
by higher-level pitchers were most likely caused by the Although increased kinetics cannot be proven to increase
greater joint forces and torques generated during the the risk of injury, interpretation of the data with knowledge of
arm-cocking and arm-acceleration phases. Because joint functional anatomy can be insightful. For example, elbow
kinetics increased with the level of competition, a higher- varus torque is produced by tension in the UCL, tension in
level pitcher may be more susceptible to arm injury. How- the flexor-pronator muscle mass, and compression in the
ever, such relationships can only be discussed in theory, radiocapitellar joint.10,36 Thus, greater varus torque generated
as joint kinetic values represent the combination of forces by college and professional pitchers (see Table 15-10) may
in muscles, tendons, ligaments, and bone that connect imply that they are at higher risk for UCL tear, muscle strain,
Applied Biomechanics of Baseball Pitching • CHAPTER 15 371
Table 15-9
Temporal Differences (Mean ⫾ SD) Among Youth, High School, College, and Professional Baseball Pitchers
Youth High School College Professional
(n ⫽ 23) (n⫽ 33) (n ⫽ 115) (n ⫽ 60)
Arm-Cocking Phase
Arm-Acceleration Phase
Arm-Deceleration Phase
From Fleisig GS, Barrentine SW, Zheng N et al: Kinematic and kinetic comparison of baseball pitching among various levels of development,
J Biomech 32:1371-1375, 1999.
SD, Standard deviation.
Note: No significant differences (p 0.05) found.
Note: Timing parameters expressed on a normalized time scale as a percent of pitch, in which 0% was the time of lead foot contact and 100%
was the time of ball release.
Table 15-10
Kinetic Differences (Mean ⫾ SD) Among Youth, High School, College, and Professional Baseball Pitchers
Youth High School College Professional Significant
(n ⫽ 23) (n ⫽ 33) (n ⫽ 115) (n ⫽ 60) Differences
Arm Cocking Phase
Arm-Acceleration Phase
Arm-Deceleration Phase
Elbow proximal force (N) 400 100 630 140 770 120 910 140 †
a, b, c, d, e
Shoulder proximal force (N) 480 100 750 170 910 130 1070 190 †
a, b, c, d, e
Shoulder posterior force (N) 160 70 280 100 350 160 390 240 †
a, b, c, d, e
†
Shoulder horizontal abduction torque (Nm) 4014 6925 8949 10985 b, c, e, f
From Fleisig GS, Barrentine SW, Zheng N et al: Kinematic and kinetic comparison of baseball pitching among various levels of development,
J Biomech 32:1371-1375, 1999.
SD, Standard deviation.
†
Significant differences (p 0.01) among four levels.
Post-hoc pair-wise significant differences (p 0.05) between a, youth and high school; b, youth and college; c, youth and professional; d, high
school and college; e, high school and professional; and f, college and professional.
372 SECTION II • Applied Biomechanics of Selected Sport Activities
avascular necrosis, osteochondritis dissecans, or osteochondral fer results in high distal segment angular velocities and
chip fractures.51-54 Furthermore, the combination of varus ultimately high ball velocities.
torque and elbow extension may lead to osteophyte produc- Dun and colleagues57 investigated the effects of age on
tion at the posterior and posteromedial aspect of the olecra- the pitching kinematics among younger (20 years of age or
non tip, which can cause chondromalacia and loose body younger) and older (27 years of age or older) professional
formation.51-54 These common elbow injuries will be dis- baseball pitchers. Six position variables were found to be
cussed subsequently in the “Common Elbow Injuries in significantly different between the two groups. At the instant
Throwing” section of this chapter. of lead foot contact, the older group had a shorter stride, a
Because kinetics are different between youth and adult more closed pelvis orientation, and a more closed upper
pitching, and because both levels throw the same size and trunk orientation. The older group also produced less shoul-
weight ball, Fleisig and colleagues18 investigated kinemat- der external rotation during the arm-cocking phase, more
ics and kinetics of youth baseball pitching using standard lead knee flexion at ball release, and less forward-trunk tilt at
and lightweight baseballs. Pitching the lightweight ball ball release. Ball velocity and body segment velocity variables
produced no difference in arm position, but greater showed no significant differences between the two groups.
shoulder, elbow, and ball velocities. With the lightweight Thus, differences in specific pitching kinematic variables
ball, pitchers produced decreased kinetics, such as signifi- among professional baseball pitchers of different age groups
cant decreases in elbow varus torque and shoulder inter- were not associated with significant differences in ball ve-
nal rotation torque. These data suggest that playing locities between groups. The current results suggest that
with lightweight baseballs may reduce the risk of overuse both biological changes and technique adaptations occur
injury in the youth pitcher and also help develop during the career of a professional baseball pitcher.
arm speed. However, before introducing lightweight
baseballs into the youth game, the effect of lighter, faster- Kinematic and Kinetic Comparisons
pitched balls for the batters and fielders should also be
considered.
Between Adult Male and Female Pitchers
Fleisig and colleagues13 reported a trend of decreased Chu and colleagues25 performed a biomechanical compari-
variability in kinematics with development level. Most of son between elite female and male baseball pitchers, report-
the significant improvements in kinematic consistency ing kinematic (Table 15-11), temporal (Table 15-12), and
occurred from the youth to high school level. To help kinetic (Table 15-13) differences. Results demonstrated
increase consistency in the younger pitcher, coaches may that females had general similarities to males in pitching
focus on a more consistent and stable windup and stride. kinematics, but there were some differences. At lead foot
Particular attention can be given to the positioning of the contact, the female pitcher had a shorter and more open
front leg as it lands on the front of the mound. In general, stride and less separation between pelvis and upper torso
increased consistency with higher levels (college and orientations (see Table 15-11). The female athlete had
professional) is most likely a natural process acquired lower peak angular velocities for throwing elbow extension
from experience and physical development. Furthermore, and lead knee extension (see Table 15-11). At the instant of
young pitchers who do not achieve consistent mechanics ball release, the female had greater lead knee flexion and less
may not perform well enough to advance to higher ball velocity (see Table 15-11). The time from lead foot
levels. contact to ball release took longer in females, and females
Stodden and colleagues55,56 investigated kinematic con- achieved peak knee extension angular velocity later com-
straints associated with the acquisition of overarm throwing pared with males (see Table 15-12). Peak shoulder and
in boys and girls approximately 10 years of age. These elbow forces and torques were considerably less in females
authors reported that step, trunk, humerus, and forearm compared with males (see Table 15-13). However, it is
kinematics progress through developmental levels. The dif- unclear whether these lower kinetics in females equate to a
ferences in kinematics between levels reflect increased lower risk of injury to the shoulder and elbow.
energy that is generated and transferred within the system.
Taking a contralateral step and increasing stride length pro-
mote increased linear and angular rotation velocities of the Kinematic and Kinetic Comparisons
trunk, which provide increased energy that can be trans- Between Baseball Pitching
ferred to the upper extremity. To optimize the use of this
increased energy, it is vital to have the humerus and forearm
and Football Passing
in proper position at stride foot contact. Higher-skilled Fleisig and colleagues15 compared pitching kinematics and
throwers exploit certain mechanical and neuromuscular kinetics between 26 baseball pitchers and 26 football quar-
principles such as segmental inertial characteristics and the terbacks at high school and college levels. Of 21 kinematic
stretch-reflex mechanism, which promote increased energy parameters, 20 were significantly different between base-
generation and transfer to the ball. Increased energy trans- ball pitchers and football passers (Table 15-14). At lead
Applied Biomechanics of Baseball Pitching • CHAPTER 15 373
Table 15-11
Kinematic Comparisons (Mean ⫾ SD) Between Male and Female Adult Baseball Pitchers
Variable Female Male P value
Balance Position (Windup)
Arm-Cocking Phase
Maximum upper torso angular velocity (°/s) 1190 240 1250 20 0.519
Maximum shoulder external rotation (°) 180 10 171 8 0.095
Arm-Acceleration Phase
Maximum shoulder internal rotation angular velocity (°/s) 5630 1590 5850 2400 0.807
Maximum shoulder horizontal adduction angular velocity (°/s) 660 250 750 240 0.384
Maximum elbow extension angular velocity (°/s) 2060 370 2980 740 0.001*
Ball Release
From Chu Y, Fleisig GS, Simpson KJ et al: Biomechanical comparison between elite female and male baseball pitchers, J Appl Biomech 25:22-31,
2009.
N/A, Not available; SD, standard deviation.
*Female and male groups significantly different (p 0.05).
374 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 15-12
Temporal Comparisons (Mean ⫾ SD) Between Male and Female Adult Baseball Pitchers
Variables Female Male p value
Time from lead foot contact to ball release (seconds) 0.163 0.026 0.141 0.021 0.048*
Arm-Cocking Phase
Arm-Acceleration Phase
Arm-Deceleration Phase
From Chu Y, Fleisig GS, Simpson KJ et al: Biomechanical comparison between elite female and male baseball pitchers, J Appl Biomech 25:22-31,
2009.
SD, Standard deviation.
*Female and male groups significantly different (p 0.05).
Note: Timing parameters expressed on a normalized time scale as a percent of pitch, in which 0% was the time of lead foot contact and 100%
was the time of ball release.
Table 15-13
Kinetic Comparisons (Mean ⫾ SD) Between Female Adult Baseball Pitchers and Previously Reported Values
for Male Adult Baseball Pitchers
Variables Female Fleisig et al.10a Fleisig et al.12b Escamilla et al.5c
Arm-Cocking Phase
Arm-Deceleration Phase
From Chu Y, Fleisig GS, Simpson KJ et al: Biomechanical comparison between elite female and male baseball pitchers, J Appl Biomech 25:22-31,
2009.
SD, Standard deviation.
a
26 professional and college participants.
b
115 college participants.
c
11 professional participants.
Applied Biomechanics of Baseball Pitching • CHAPTER 15 375
Table 15-14
Kinematic Differences (Mean ⫾ SD) Between Baseball Pitching and Football Passing
Pitching Passing
Parameter (n ⫽ 26) (n ⫽ 26)
Lead Foot Contact
Arm-Cocking Phase
Arm-Acceleration Phase
Maximum elbow extension angular velocity (°/s)† 2340 300 1760 210
Average shoulder abduction (°)† 93 9 108 8
Ball Release
Arm-Deceleration Phase
Maximum shoulder internal rotation angular velocity (°/s)† 7550 1360 4950 1080
Minimum elbow flexion (°)† 18 5 24 5
From Fleisig GS, Escamilla RF, Andrews JR et al: Kinematic and kinetic comparison between baseball pitching and football
passing, J Appl Biomech 12: 207-224, 1996.
SD, Standard deviation.
*p 0.01.
†
p 0.001.
foot contact, baseball pitchers had a greater stride length, adduction and elbow flexion (see Table 15-14).15 More-
shoulder horizontal abduction, elbow flexion, and lead over, compared with passers, maximum pelvis and upper
knee flexion, and less shoulder external rotation, compared torso angular velocities in pitchers occurred earlier in
with football passers. These data imply that, compared with arm cocking and maximum shoulder external rotation
baseball pitchers, football passers rotate their arms up occurred later in arm cocking (Table 15-15). During the
quicker, lead with the elbow, and flex the lead knee and arm-acceleration phase, baseball pitchers had greater
elbow less. elbow extension angular velocity and less shoulder abduc-
During the arm-cocking phase, baseball pitchers tion compared with football passers (see Table 15-14).
rotated their pelvis and upper torso with greater angular Compared with passers, maximum elbow extension angu-
velocity and had greater shoulder external rotation, lar velocity in pitchers occurred earlier in the arm accel-
whereas football passers had greater shoulder horizontal eration phase (see Table 15-15). At ball release, baseball
376 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 15-15
Temporal Comparisons (Mean ⫾ SD) Between Baseball Pitching and Football Passing
Variables Pitching (n 26) Passing (n 26)
Time from lead foot contact to ball release (seconds)* 0.145 0.022 0.207 0.037
Arm-Cocking Phase
Arm-Acceleration Phase
Arm-Deceleration Phase
From Fleisig GS, Escamilla RF, Andrews JR et al: Kinematic and kinetic comparison between baseball pitching and football passing, J Appl
Biomech 12:207–224, 1996.
SD, Standard deviation.
*p 0.001.
†
p 0.01.
Note: Timing parameters expressed on a normalized time scale as a percent of pitch, where 0% was the time of lead foot contact and 100% was
the time of ball release.
pitchers had greater ball velocity, lateral trunk tilt, for- incidence of shoulder and elbow injuries is lower for quar-
ward trunk tilt, and lead knee flexion, whereas football terbacks than pitchers is that passers exhibit less motion in
passers had greater shoulder horizontal adduction and their legs, pelvis, and upper torso compared with pitchers.
elbow flexion (see Table 15-14). Just after ball release, Another justification for the lower incidence of injury in
during arm deceleration, baseball pitchers had greater passers is that quarterbacks throw much less than pitchers,
shoulder internal rotation angular velocity and less play in fewer games, and have a greater rest period between
elbow flexion. Maximum shoulder internal rotation angu- games.
lar velocity and minimum elbow flexion occurred earlier
in pitchers compared with passers.
Of 11 kinetic variables, only three demonstrated signifi-
Common Shoulder Injuries in Pitching
cant differences (Table 15-16).15 The lower incidence of Pathological conditions in the thrower’s shoulder are often
rotator cuff injury in passers compared with pitchers may be complex and multifaceted, involving the rotator cuff, the
related to less shoulder proximal force in passers (660 labrum-biceps complex, and the capsule. Both static (capsu-
120 N) compared with pitchers (850 140 N). The risk of lolabral complex) and dynamic stabilizers (rotator cuff and
subacromial impingement may also be less in football pass- scapular rotators) control the movement and stability of the
ers compared with pitchers because they do not externally humeral head within the glenoid cavity. A summary of
rotate their shoulders as much during the arm-cocking pathomechanics associated with increased shoulder kinetics
stage (see Table 15-14). The lower incidence of elbow in- and decreased ball velocity is shown in Table 15-17.
jury in passers compared with pitchers may be related to less Internal impingement, in which the supraspinatus or infra-
elbow proximal force in passers (620 110 N) compared spinatus tendons impinge on the posterosuperior labrum, is
with pitchers (710 110 N). one of the most common soft tissue injuries seen in
The kinetic data (see Table 15-16) show that football throwers.58,59 With a capsular injury, internal impingement
passing did not produce higher forces or torques compared may result secondary to excessive anterior humeral head trans-
with baseball pitching.15 One explanation for why the lation. Contributing factors to internal impingement include
Applied Biomechanics of Baseball Pitching • CHAPTER 15 377
Table 15-16
Kinetic Differences (Mean ⫾ SD) Between Baseball Pitching and Football Passing
Parameter Pitching (n 26) Passing (n 26)
Arm-Cocking Phase
Arm-Acceleration Phase
Arm-Deceleration Phase
Follow-Through Phase
From Fleisig GS, Escamilla RF, Andrews JR et al: Kinematic and kinetic comparison between baseball pitching and football passing,
J Appl Biomech 12:207-224, 1996.
SD, Standard deviation.
*p 0.01.
†
p 0.001.
excessive shoulder external rotation, internal rotation deficit undersurface of the acromion, is a common soft tissue
caused by posterior cuff or capsule tightness, anterior capsule- injury seen in older throwers, but typically not common
labrum injuries, excessive shoulder horizontal abduction, in younger throwers.10,34,64 The rotator cuff muscles gen-
muscle imbalances, and scapular dyskinesis.58,60,61 A protective erate shear and compressive forces to depress, rotate, and
factor in helping to prevent internal impingement is humeral center the humeral head within the glenoid fossa. Conse-
head and glenoid retroversion, which is believed to occur by quently, they help prevent superior translation of the hu-
throwing in childhood.62,63 meral head caused largely by deltoid activity. When these
muscles function abnormally, such as when a partial or
complete rotator cuff thickness tear occurs, superior
Shoulder Injuries in Pitchers translation of the humeral head may occur as the result of
muscle fatigue and weakness, causing the bursal surface of
• Posterior internal impingement
the supraspinatus, the subacromial bursa, and the long
• Anterior instability
• Strain of posterior shoulder muscles
biceps tendon to abrade against the undersurface of the
• Superior labrum anterior-posterior (SLAP) tears acromion.
• Stress fracture of proximal humeral physis Anterior shoulder instability is also common in throwers,
• Spiral humeral fractures especially baseball pitchers. During shoulder external rota-
• Suprascapular nerve entrapment tion, the anterior capsule and anterior band of the inferior
• Quadrilateral space syndrome glenohumeral ligament are stretched and help resist
• Snapping scapula humeral head anterior translation. Repeated stretching of
the anterior capsule can further stress the joint, leading to
chronic inflammation and damage to the anterior capsular
structures and anterior labrum. Laxity within the joint can
External (subacromial) impingement, in which the exacerbate this problem, resulting in further anterior shoul-
bursal surface of the supraspinatus tendon, the subacro- der instability. Muscle imbalances, such as overpowering
mial bursa, and the long biceps tendon impinge on the anterior shoulder muscles and weak posterior shoulder
378 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 15-17
Summary of Pathomechanics Associated With Increased Kinetics and Decreased Ball Velocity
Phase/Event Proper Mechanics Pathomechanics n Consequences
Stride Front leg goes down and forward g Push off rubber, g ball velocity
Arms separate, swing down,
and up
Lead foot contact Front foot is planted slightly to g Stride length, g ball velocity
third-base side (for a right-handed Front foot open (position or angle)
pitcher) h Shoulder and elbow force
Front foot is pointed slightly Improper shoulder external rotation
inward h Shoulder and elbow kinetics
Shoulder is abducted Excessive shoulder external rotation g ball
approximately 90°, with velocity
approximately 60° of external g Shoulder horizontal abduction g ball
rotation velocity
Arm-cocking phase Pelvis rotation, followed by upper Early pelvis rotation g ball velocity
trunk rotation Late pelvis rotation h shoulder and elbow
Shoulder externally rotates, and kinetics
trunk arches g Pelvis rotation velocity g ball velocity
Poor timing between pelvis rotation and
upper trunk rotation g ball velocityPoor
timing between pelvis rotation and
upper trunk rotation h shoulder internal
rotation torque
Maximum shoulder external rotation Shoulder external rotation is g Shoulder external rotation h ball
approximately 180° velocity
Elbow flexion is approximately 90° Excessive shoulder horizontal adduction
and elbow flexion h shoulder kinetics
Applied Biomechanics of Baseball Pitching • CHAPTER 15 379
Table 15-17
Summary of Pathomechanics Associated With Increased Kinetics and Decreased Ball Velocity—cont’d
Phase/Event Proper Mechanics Pathomechanics n Consequences
From Fortenbaugh D, Fleisig GS, Andrews JR: Baseball pitching biomechanics in relation to injury risk and performance, Sports Health:
A Multidisciplinary Approach 1:314-320, 2009.
g Decreased; h increased.
muscles, can also contribute to the humeral head being This action can place abnormal stress on the posterior cap-
pulled forward within the glenoid. sule and lead to “posterior capsule syndrome.”3 Repeated
Because of the large eccentric loads on the posterior abrasions of the posteroinferior capsule structures has been
shoulder muscles during the deceleration and follow- described as creating an exostosis of the posteroinferior
through phases, these muscles are frequently injured during glenoid.58
pitching. Most rotator cuff injuries in pitching are partial- Although the biceps has been considered to function
thickness undersurface tears, which do not heal well.10 primarily at the elbow, the biceps also contributes to shoul-
If the rotator cuff muscles and other posterior shoulder der abduction and flexion, especially when the shoulder is
muscles are weak, fatigued, or injured, the humeral head externally rotated and the forearm is supinated. Biceps ac-
will distract and anteriorly translate out of the glenoid fossa. tivity, especially the long head, has been shown to be a
380 SECTION II • Applied Biomechanics of Selected Sport Activities
significant contributor to shoulder abduction and flexion in meral capsule, it tightens with horizontal adduction and
a compromised shoulder, such as a torn rotator cuff.32 internal rotation, thus compressing the nerve. Stretching
Because the biceps long head originates at the anterosupe- of the nerve may be exacerbated by rapid scapular protrac-
rior glenoid labrum, its contraction could abnormally stress tion combined with infraspinatus and supraspinatus con-
this portion of the labrum. This is especially true in pitch- tractions, which pull the nerve medially as it is tethered
ing, because the biceps has been shown to eccentrically laterally.
contract in decelerating the rapidly extending elbow. Quadrilateral space syndrome can occur when the axil-
Andrews and colleagues2,65 arthroscopically observed lary nerve and posterior humeral circumflex artery are
73 throwing athletes who had labrum tears in their throw- entrapped in the quadrilateral space between the teres mi-
ing shoulders. The long head of the biceps tendon appeared nor above, teres major below, long triceps brachii head
to have pulled the anterosuperior portion of the labrum off medially, and humerus laterally.70 This entrapment can
the glenoid, resulting in a superior labrum tear that is ante- result in atrophy of the teres minor and deltoid with con-
rior to posterior in direction. This observation was verified comitant loss of shoulder abduction and external rotation
arthroscopically by electrically stimulating the biceps strength, as well as diminished sensation over lateral del-
muscle. When stimulated, the tendinous portion became toid. Tenderness and pain in quadrilateral space, especially
taut near its attachment to the labrum, and actually lifted during late arm cocking, may also occur.
the labrum off the glenoid.2,65 A “snapping scapula” can also occur from repetitive pitch-
Several other injuries may occur during overhead ing, especially during the deceleration and follow-through
pitching. In youth, a common overuse injury is “little phases.71,72 This pathological condition, which can be quite
league shoulder,”66 which involves a stress fracture of the painful, is the result of an inflamed bursa located beneath
proximal humeral physis. This can be caused by large ro- the medial border of the scapula. This bursa provides lubrica-
tational forces (torques) applied to humerus during shoul- tion as the scapula moves in relation to the thorax. During
der external and internal rotation, resulting in humeral repeated and overuse conditions, bursitis can develop, result-
torsion. Excessive pitching during a game or a season, ing in both pain and a “snapping” sound as the swollen tissue
poor pitching mechanics, or throwing high-stress pitches impinges upon the thorax. A good follow-through can help
(e.g., a curveball or slider) can exacerbate or cause little minimize injury potential of the shoulder. A long arm arc of
league shoulder. deceleration and sufficient forward trunk tilt (trunk approxi-
Spiral fractures of the humeral shaft occasionally occurs mately in a horizontal position) may help minimize stress on
in overhead pitching.67 These injuries occur because of the shoulder complex.
large rotational torques applied to the humerus.5,68 They
are more common in adults than children, and more
common with excessive pitching and overuse. Spiral frac-
Common Elbow Injuries in Pitching
tures are more common in throwing maximum-effort Musculotendinous, joint, and neural injuries are the most
fastball, curveball, and slider pitches because of the common problems that occur in the throwing elbow.51-54
greater shoulder internal rotation torques generated A summary of pathomechanics associated with increased
by these pitches.17 The fracture occurs during the arm- elbow kinetics and decreased ball velocity is shown in Table
cocking or arm-acceleration phases, and is associated with 15-17.73 Pathological conditions of the elbow caused by
improper warmup and deconditioned pitchers. Moreover, pitching can be categorized into four areas.
they are common in older ( 30) recreational pitchers
who pitch infrequently, and seldom occur in younger,
well-conditioned pitchers. Medial Compartment
Suprascapular nerve entrapment can occur in pitchers Medial musculotendinous injuries are quite common, espe-
as the suprascapular nerve becomes entrapped in the cially involving the muscles that originate at the medial
suprascapular or spinoglenoid notches, resulting in atrophy epicondyle (medial epicondylitis).51-54 These muscles, which
and weakness in supraspinatus or infraspinatus muscles, are collectively referred to as the flexor/pronator mass, are
and possible posterolateral shoulder pain if the entrapment composed primarily of the pronator teres, flexor carpi radia-
occurs in the suprascapular notch.69 If the entrapment lis, flexor digitorum superficialis, and flexor carpi ulnaris.
occurs at the spinoglenoid notch, isolated atrophy occurs in During pitching, pain and tenderness can occur in the
the infraspinatus. It is believed to occur in approximately 5% medial epicondyle region.51-54 The flexor-pronator mass
of major league starting pitchers at the end of the season.69 is loaded as a result of tensile force during the late arm-
When pitching, the suprascapular nerve is susceptible to cocking and early acceleration phases of pitching. These
compressive and tensile loads because of its relatively fixed dynamic contractile structures must apply a varus torque to
position under the rotator cuff and ligaments. Because the the forearm to resist the valgus stress created by the throw-
spinoglenoid ligament inserts into the posterior glenohu- ing motion.
Applied Biomechanics of Baseball Pitching • CHAPTER 15 381
23. Jobe FW, Tibone JE, Perry J, Moynes D: An EMG analysis of the 45. Barrentine SW, Matsuo T, Escamilla RF, et al: Kinematic analysis
shoulder in throwing and pitching. A preliminary report, Am J of the wrist and forearm during baseball pitching, J Appl Biomech
Sports Med 11(1):3–5, 1983. 14(1):24–39, 1998.
24. Sisto DJ, Jobe FW, Moynes DR, Antonelli DJ: An electromyo- 46. Dillman CJ, Fleisig GS, Andrews JR: Biomechanics of pitching
graphic analysis of the elbow in pitching, Am J Sports Med with emphasis upon shoulder kinematics, J Orthop Sports Phys Ther
15(3):260–263, 1987. 18(2):402–408, 1993.
25. Chu Y, Fleisig GS, Simpson KJ, Andrews JR: Biomechanical com- 47. Sakurai S, Ikegami Y, Okamoto A, et al: A three-dimensional
parison between elite female and male baseball pitchers, J Appl cinematographic analysis of upper limb movement during fastball
Biomech 25:22–31, 2009. and curveball baseball pitches, J Appl Biomech 9:47–65, 1993.
26. Stodden DF, Fleisig GS, McLean SP, et al: Relationship of pelvis 48. Dun S, Loftice J, Fleisig GS, et al: A biomechanical comparison of
and upper torso kinematics to pitched baseball velocity, J Appl youth baseball pitches: Is the curveball potentially harmful? Am J
Biomech 21:164–172, 2005. Sports Med 36(4):686–692, 2008.
27. Watkins RG, Dennis S, Dillin WH, et al: Dynamic EMG analysis 49. Lyman S, Fleisig GS, Andrews JR, Osinski ED: Effect of pitch
of torque transfer in professional baseball pitchers, Spine type, pitch count, and pitching mechanics on risk of elbow and
14(4):404–408, 1989. shoulder pain in youth baseball pitchers, Am J Sports Med
28. Matsuo T, Escamilla RF, Fleisig GS, et al: Comparison of kine- 30(4):463–468, 2002.
matic and temporal parameters between different pitch velocity 50. Petty DH, Andrews JR, Fleisig GS, Cain EL: Ulnar collateral
groups, J Appl Biomech 17:1–13, 2001. ligament reconstruction in high school baseball players: Clinical
29. Toyoshima S, Hoshikawa T, Miyashita M, Oguri T: Contribution results and injury risk factors, Am J Sports Med 32(5):1158–1164,
of the body parts to throwing performance. In Nelson RC, 2004.
Morehouse CA, editors: Biomechanics IV, Baltimore, 1974, 51. Andrews JR, Whiteside JA: Common elbow problems in the
University Part Press. athlete, J Orthop Sports Phys Ther 17(6):289–295, 1993.
30. Aguinaldo AL, Buttermore J, Chambers H: Effects of upper trunk 52. Azar FM, Andrews JR, Wilk KE, Groh D: Operative treatment of
rotation on shoulder joint torque among baseball pitchers of ulnar collateral ligament injuries of the elbow in athletes, Am J
various levels, J Appl Biomech 23(1):42–51, 2007. Sports Med 28(1):16–23, 2000.
31. Gowan ID, Jobe FW, Tibone JE, et al: A comparative electromyo- 53. Cain EL Jr., Dugas JR, Wolf RS, Andrews JR: Elbow injuries in
graphic analysis of the shoulder during pitching. Professional ver- throwing athletes: A current concepts review, Am J Sports Med
sus amateur pitchers, Am J Sports Med 15(6):586–590, 1987. 31(4):621–635, 2003.
32. Glousman R, Jobe F, Tibone J, et al: Dynamic electromyographic 54. Jobe FW, Nuber G: Throwing injuries of the elbow, Clin Sports
analysis of the throwing shoulder with glenohumeral instability, Med 5(4):621–636, 1986.
J Bone Joint Surg Am 70(2):220–226, 1988. 55. Stodden DF, Langendorfer SJ, Fleisig GS, Andrews JR: Kinematic
33. Rodosky MW, Harner CD, Fu FH: The role of the long head of constraints associated with the acquisition of overarm throwing part
the biceps muscle and superior glenoid labrum in anterior stability I: Step and trunk actions, Res Q Exerc Sport 77(4):417–427, 2006.
of the shoulder, Am J Sports Med 22(1):121–130, 1994. 56. Stodden DF, Langendorfer SJ, Fleisig GS, Andrews JR: Kinematic
34. De Wilde L, Plasschaert F, Berghs B, et al: Quantified measurement constraints associated with the acquisition of overarm throwing
of subacromial impingement, J Shoulder Elbow Surg 12(4):346–349, part II: Upper extremity actions, Res Q Exerc Sport 77(4):
2003. 428–436, 2006.
35. Werner SL, Fleisig GS, Dillman CJ, Andrews JR: Biomechanics of 57. Dun S, Fleisig GS, Loftice J, et al: The relationship between age
the elbow during baseball pitching, J Orthop Sports Phys Ther and baseball pitching kinematics in professional baseball pitchers,
17(6):274–278, 1993. J Biomech 40(2):265–270, 2007.
36. Feltner ME, Dapena J: Dynamics of the shoulder and elbow joints 58. Meister K, Andrews JR, Batts J, et al: Symptomatic thrower’s
of the throwing arm during a baseball pitch, Int J Sport Biomech exostosis. Arthroscopic evaluation and treatment, Am J Sports Med
2:235–259, 1986. 27(2):133–136, 1999.
37. Werner SL, Murray TA, Hawkins RJ, Gill TJ: Relationship 59. Paley KJ, Jobe FW, Pink MM, et al: Arthroscopic findings in the
between throwing mechanics and elbow valgus in professional overhand throwing athlete: Evidence for posterior internal
baseball pitchers, J Shoulder Elbow Surg 11(2):151–155, 2002. impingement of the rotator cuff, Arthroscopy 16(1):35–40, 2000.
38. Morrey BF, An KN: Articular and ligamentous contributions to the 60. Meister K: Injuries to the shoulder in the throwing athlete. Part
stability of the elbow joint, Am J Sports Med 11(5):315–319, 1983. one: Biomechanics/pathophysiology/classification of injury, Am J
39. Dillman CJ, Smutz C, Werner S: Valgus extension overload in Sports Med 28(2):265–275, 2000.
baseball pitching, Med Sci Sports Exerc 23(suppl 4):S135, 1991. 61. Meister K: Injuries to the shoulder in the throwing athlete. Part two:
40. Buchanan TS, Delp SL, Solbeck JA: Muscular resistance to varus Evaluation/treatment, Am J Sports Med 28(4):587–601, 2000.
and valgus loads at the elbow, J Biomech Eng 120(5):634–639, 62. Crockett HC, Gross LB, Wilk KE, et al: Osseous adaptation and
1998. range of motion at the glenohumeral joint in professional baseball
41. Roberts EM: Cinematography in biomechanical investigation, In pitchers, Am J Sports Med 30(1):20–26, 2002.
Proceedings of the CIC Symposium on Biomechanics, Chicago, 63. Osbahr DC, Cannon DL, Speer KP: Retroversion of the humerus
1971, The Athletic Institute. in the throwing shoulder of college baseball pitchers, Am J Sports
42. Moynes DR, Perry J, Antonelli DJ, Jobe FW: Electromyography Med 30(3):347–353, 2002.
and motion analysis of the upper extremity in sports, Phys Ther 64. Park SS, Loebenberg ML, Rokito AS, Zuckerman JD: The shoulder
66(12):1905–1911, 1986. in baseball pitching: Biomechanics and related injuries—Part 1, Bull
43. Ahn BH: A model of the human upper extremity and its application Hosp Jt Dis 61(1–2):68–79, 2002.
to a baseball pitching motion, East Lansing, 1991, Michigan State 65. Andrews JR, Broussard TS, Carson WG: Arthroscopy of the
University. shoulder in the management of partial tears of the rotator cuff:
44. Campbell KR, Hagood SS, Takagi Y: Kinetic analysis of the elbow A preliminary report, Arthroscopy 1(2):117–122, 1985.
and shoulder in professional and little league pitchers, Med Sci 66. Carson WG Jr, Gasser SI: Little Leaguer’s shoulder. A report of
Sports Exerc 26:S175, 1994. 23 cases, Am J Sports Med 26(4):575–580, 1998.
384 SECTION II • Applied Biomechanics of Selected Sport Activities
67. Ogawa K, Yoshida A: Throwing fracture of the humeral shaft. An 71. Milch H: Snapping scapula, Clin Orthop 20:139–150, 1961.
analysis of 90 patients, Am J Sports Med 26(2):242–246, 1998. 72. Sisto DJ, Jobe FW: The operative treatment of scapulothoracic bursitis
68. Sabick MB, Torry MR, Kim YK, Hawkins RJ: Humeral torque in in professional pitchers, Am J Sports Med 14(3):192–194, 1986.
professional baseball pitchers, Am J Sports Med 32(4):892–898, 73. Fortenbaugh D, Fleisig GS, Andrews JR: Baseball pitching biome-
2004. chanics in relation to injury risk and performance, Sports Health:
69. Cummins CA, Messer TM, Schafer MF: Infraspinatus muscle A Multidisciplinary Approach 1:314–320, 2009.
atrophy in professional baseball players, Am J Sports Med 32(1): 74. Matsuo T, Fleisig GS: Influence of shoulder abduction and lat-
116–120, 2004. eral trunk tilt on peak elbow varus torque for college baseball
70. Redler MR, Ruland LJ, McCue FC: Quadrilateral space syndrome pitchers during simulated pitching, J Appl Biomech 22(2):
in a throwing athlete, Am J Sports Med 14(6):511–513, 1986. 93–102, 2006
16
CHAPTER
385
386 SECTION II • Applied Biomechanics of Selected Sport Activities
the transverse abdominis, lumbar multifidus (LM), inter- trunk stability have been shown to rotate among the many
nal oblique, diaphragm, and the muscles of the pelvic muscles.18,19 Whereas ES muscle activation occurs primarily
floor.1,16,17 to maintain appropriate lumbar spine posture, other mus-
cles function primarily to generate torque.20-22 Because it
has been determined that no one or two muscles were con-
Local Stabilizer Muscles sistently active across all of the various tasks required of
human function19,23 and in deference to the proposal that
• Transverse abdominus the exercises themselves are the most important component
• Lumbar multifidus of spinal stability,24 we delineate the specific spinal stabiliza-
• Internal oblique tion exercises as they have been reported.
• Diaphragm
• Pelvic floor muscles
Specific Exercise Examples Including Kinetics,
Kinematics, and Pathomechanics
Squat Exercise
Clinical Point The squat exercise has been advocated as an important
method for hip, knee, and back muscle training.25-28 Weight-
Local stabilizer muscles provide stability to the lumbar spine while lifters and powerlifters use squatting as one of the most
allowing movement of peripheral joints. important parts of their training programs, and for the
powerlifters, squatting is directly included during their
competition performance.29-31 Most research regarding
kinetics, kinematics, and muscle EMG activity for the squat
The global muscle system, or outer muscle unit, is pre- exercise has been devoted to the lower extremities, and
dominantly responsible for movement and consists of more therefore greater detail is devoted to this particular exercise
superficial musculature that attaches from the pelvis to the in that section of this chapter.
rib cage or lower extremities. Major muscles in this group It has been a long-held belief that, during the lifting task,
include the rectus abdominis, external oblique, erector spi- the ES muscles provide the extensor force necessary to resist
nae (ES), hamstrings, gluteus maximus, latissimus dorsi, hip the weight of the upper body and any external loads in the
adductors, and quadriceps.1,16,17 These muscles transfer and hands.32,33 ES muscle activity was found to be reduced
absorb forces from the upper and lower extremities to the in kyphotic postures during the squat type of lifting.34-36
pelvis.1 Kyphotic postures during a squat movement were found to
demonstrate peak EMG activity of the ES muscle in the
middle of the lift, whereas a lordotic posture demonstrated
Global Stabilizer Muscles peak ES muscle EMG activity early in the lift.36 As an indi-
vidual continues deeper into his or her squat posture, the
• Rectus abdominus ES muscles undergo a “silent phase” of EMG activity
• External oblique known as flexor relaxation.37,38 It has since been discovered
• Erector spinae that the extensor function of the lumbar part of the ES
• Hamstrings
muscles is then taken over by the thoracic part of the ES,39
• Gluteus maximus
although the EMG activity of the entire ES muscle group
• Latissimus dorsi
• Hip adductors decreases as the spine flexes (Figure 16-1).
• Quadriceps It is generally accepted that the closer the load is placed
to the body, the more significantly diminished are the resul-
tant compressive forces to the lumbar spine (Figure 16-2).
This is a strategy that is employed more effectively in the
semi–squat lift (load between the feet and knees) than with
Clinical Point the stoop or squat lift (Figure 16-3). This posture has
Global stabilizers transfer and absorb forces from the upper and
traditionally been accepted as the norm for these reasons.
lower extremities to the pelvis. Conflicting findings regarding the specific type of
lift posture with static lifting tasks have been discovered.
Although lumbar flexion was much greater in lifts from the
kyphotic initial position, the torques required around L3
Trunk muscles often perform several functions simulta- were similar between the two different postures (kyphotic
neously, depending on instantaneous demands. It should and lordotic), although somewhat larger initially in
also be recognized that the most important muscles for lifts from a kyphotic posture.36 The largest torques were
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 387
450
400
350
EMG-amplitude (a.u.)
300
250
200
150
100
50
0
135 130 125 120 115 110 105 100 95
sustained by flexed lumbar spines during periods of little or Adding to the potential for injury is the fact that
no ES muscle activity.36 More recent results40 suggest that the compressive loads sustained during squatting can be
the tensile strain on tissues in the lower lumbar spine was extremely high. Half-squats performed with barbell
not affected by lift style. Squat lifting over stoop lifting loads of 0.8 to 1.6 times body weight (BW) demonstrated
(Figure 16-4) as the technique of choice resulted in reduced compressive loads between 6 to 10 times BW.47 Even
net moments, muscle forces, and internal spinal loads,41-43 higher compressive loads were found in powerlifters.48
although a freestyle lifting mechanism has also been advo- Cholewicki and colleagues48 estimated compressive loads
cated.44 Most recently, in a comparison study between the on L4 and L5 of powerlifters to be up to 17,192 N.
squat and stoop lift, it was concluded that although the Because the spine is inherently unstable, as previously
range of motion (ROM) at the waist, hip, knee, and ankle described in this chapter, how the spine can withstand
was different between squat and stoop lifts, the maximum such forces might be questioned. Motor control of trunk
lumbar joint movement was not significantly different flexion posture, advanced technique with such lifts, and
between the two lifting methods when lifting three differ- systematic training of the spinal musculature over years has
ent box loads (5, 10, and 15 kg [11, 22, and 33 lb]) (Figure been postulated to account for high-level athletes’ ability
16-5, also see Figure 16-4).45 to successfully perform such lifts without injury.24 Adams
Trunk muscle coactivation is thought to increase trunk and colleagues49 suggested that a fully flexed spine is
stiffness and potentially reduce risk of injury, even in flexed weaker than one that is moderately flexed. In a strictly
or kyphotic postures. Increasing torso muscle coactivation biomechanical model analysis, Gunning and colleagues50
leads to a linear-type increase in trunk stiffness throughout used a porcine spine model to demonstrate that a fully
trunk extension ROM.41 Stiffness in trunk flexion and lateral flexed spine is 20% to 40% weaker than if it were in a neu-
flexion, however, only increased with muscle coactivation tral posture. A more neutral spine posture is also more
until approximately 40% and 60% of ROM respectively.46 effective at reducing total joint shear, compared with a
A “yielding” phenomenon similar to the “flexor relaxation” flexed spine posture straining the interspinous ligament
phenomenon previously described was seen after these complex and therefore imposing an anterior shear force on
points in each respective ROM.41 the superior vertebra (Figure 16-6).51
388 SECTION II • Applied Biomechanics of Selected Sport Activities
B 18.4 cm
L5/SI
disc
500N
1800N B 15.3 cm
350N
2700N
35.0 cm
H 50.9 cm
150N H 150N
Figure 16-2
An approximate 50% variance in lumbar movements at the L5/S1 segments when comparing squat and
stoop lifts. (From Chaffin DB, Andersson GB: Occupational biomechanics, ed 2, New York, 1991,
John Wiley & Sons.)
Figure 16-4
Joint angles in sagittal plane during squat and stoop lifting. (From Hwang S, Kim Y, Kim Y: Lower extremity
joint kinetics and lumbar curvature during squat and stoop lifting, BMC Musculoskel Dis 10:15, 2009.)
Figure 16-5
Joint moments during squat and stoop lifting at various loads. (From Hwang S, Kim Y, Kim Y: Lower
extremity joint kinetics and lumbar curvature during squat and stoop lifting, BMC Musculoskel Dis
10:15, 2009.)
390 SECTION II • Applied Biomechanics of Selected Sport Activities
700
Rect. ab
600
Ext. oblique
Int. oblique
500
Lumbar erectors
Lat. dorsi
Force (N)
400
Thoracic erectors
300
200
100
3
Force (kN)
cmp
2
shrs
0
0 1 2 3 4 5
Time (s)
Figure 16-6
Comparison of a fully flexed spine versus a more neutral posture associated with myoelectric silence
in the back extensors, loaded posterior passive tissues, and shearing forces on the lumbar spine. (From
McGill SM: Biomechanics of low back injury: Implications on current practice and the clinic, J Biomech
30[5]:465-475, 1997.)
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 391
the experience level and technique of the participant. Tech- with L4-L5 compressive forces as high as 4328 N.59 The
nique especially was found to influence the amount of load- rectus abdominis and external and internal oblique muscles
ing of the spine.53 Novice lifters were particularly vulnerable exhibited a continuous activation pattern, independent of
to increased compressive loads with a push-and-pull exer- the oscillation plane, whereas the LM and ES changed from
cise when compared with more experienced individuals.53 continuous activation in the horizontal plane to phasic pat-
Rowing is another exercise that involves trunk flexion terns in the vertical plane with the oscillating pole.60 Com-
and therefore the potential of the flexor relaxation phenom- pressive loads were not measured with the oscillating pole.
enon. The potential for this phenomenon is actually much
greater because of repeated trunk flexion of extreme ROM.
Lumbar flexion has been shown to increase significantly
during a rowing trial, as was the magnitude of EMG activity Clinically Relevant Points Regarding Push-Pull
of the LM and other ES musculature.54,55 Findings showed Activities
that young adult rowers attained relatively high levels of
• 9% to 20% of low back injuries may be associated with push-pull
lumbar flexion during the rowing stroke, and these levels activities
continued to increase during the course of the rowing • Spinal compressive loads are also significant with push-pull
trial.55 activities
Spinal compressive forces are also a significant issue with • Spinal compressive loads and spine musculature activation varies
rowing, even though the individual is not in an upright pos- with the type of push-up exercise performed
ture. Peak spinal compressive forces as high as 6066 N for
men and 5031 for women have been measured in rowers.54
The combination of increased hip flexion, increased EMG
activity of the lumbar ES and LM, and particularly the
exceedingly high compressive forces encountered during Trunk Flexion Exercises
this activity should caution the clinician as the application of Bent-knee sit-ups have been recommended to decrease
such an exercise in a rehabilitation continuum. psoas muscle activity and decrease its resultant compressive
Spinal loading during many forms of the push-up is sub- force on the lumbar spine caused by length-tension rela-
stantial. Plyometric forms of the push-up require much tionships. Juker and colleagues61 found psoas muscle activa-
higher levels of muscle activity and therefore result in tion levels to be higher during bent-knee sit-ups than with
higher spine loading.24 Compression loads have been mea- straight-knee sit-ups. It is postulated that the shortened
sured in various forms of the push-up: 1838 N with a tradi- psoas muscle must contract to higher levels of activation
tional push-up, 2840 N with both hands on a ball-type of given its compromised length with the bent-knee situp.61
push-up, 4699 N with a clapping push-up, and as high as This bent-knee position for sit-ups also imposes approxi-
5848 N of compression force on the spine with a one-arm mately 3300 N of compression force on the spine.62 A bent-
push-up.57 Performing push-ups on labile surfaces only knee sit-up in which the client first isometrically contracts
moderately increased spinal compressive loads.57 EMG the hamstrings was originally thought to inhibit the psoas
activity of the contralateral rectus abdominis was higher muscle, but actually was found to produce some of the
than the ipsilateral rectus abdominis in a staggered-hand- highest levels of psoas muscle activation of any sit-up exer-
placement push-up (i.e., right hand more cranial than left cise as a result of the psoas requirement to overcome the
and vice versa).57 Moderate activation levels in the trunk trunk extensor movement created by the hamstring con-
flexors and lower activation in the trunk extensors has been traction.62 Abdominal curls or “crunches,” although going
suggested to challenge the musculature surrounding the through a much smaller amplitude of motion, still demon-
lumbar spine with a standard push-up, provided that a neu- strated large compressive forces on the L4-L5 in at least one
tral spine posture is maintained.57 For lumbar spine verte- study,19 with values ranging from 2615 N to 3422 N. The
bral joint rotational stiffness, the abdominal muscles con- EMG MVIC values ranged from 30% to 32% for the rectus
tributed 64.32 8.5%, 86.55 1.13%, and 83.84 1.95% abdominis to 30% for left internal oblique and 44% for right
on average around the sagittal, frontal, and transverse axes internal oblique with the same exercise.19 Higher MVIC
respectively.58 The muscles primarily involved were the values for upper rectus abdominis (62%), lower rectus ab-
rectus abdominis and external and internal obliques, with dominis (55%), and external oblique (52%) have been re-
minimal contribution from the transverse abdominis, LM, ported with the curl-up exercise in another study.63
and ES.58
A vertically oriented Bodyblade with large-amplitude Trunk Extension Exercises
oscillation resulted in the greatest activation levels of the Recent EMG comparison analysis with various exercises has
internal oblique and external oblique muscles (48% and supported an interaction between various muscle groups in
46% of maximum voluntary isometric contraction [MVIC] affording stability to the lumbar spine. Using EMG during
respectively). This particular technique was also associated three bridging exercises, Stevens and colleagues found that
392 SECTION II • Applied Biomechanics of Selected Sport Activities
the relative muscle activity and the ratio of the abdominal of compressive force on the lumbar spine. The “bird dog”
obliques seemed to alter depending on the task and the pre- or quadruped exercise, in which contralateral upper and
sumable need for stability.64 These authors concluded that lower extremity are lifted to horizontal from the quadruped
their findings supported the assumption that during these position, has been advocated as an alternative to the prone
bridging exercises, all back muscles contribute in a similar “Superman” exercise in which bilateral upper and lower
way to control spine positions and movements in a healthy extremities are lifted simultaneosly.24 The “bird dog” exer-
population.64 Mean EMG amplitudes of the longissimus cise decreased the load to 3000 N while still producing a
thoracis (LT) and LM MVIC values during various bridging maximum voluntary contraction range of 30% to 40% in the
exercises has been investigated by multiple authors.65-67 primary muscles involved.19 Other MVIC percentage values
Performing a bridging movement varied slightly depending of various trunk muscles are listed in Table 16-2.
on how it was performed (Table 16-1). Compressive loads
on the spine were not measured in any of these studies. Unstable Surface Exercises
Average compression loads on L4-L5 have been measured The use of changing unstable surfaces is also an increasing
with supine bridging to neutral with bilateral shoulders on trend in stabilization training programs. EMG analysis
ground and lifting pelvis with either one or both legs.19 comparing a curl-up exercise found increased abdominal
Values ranged from 2387 N to 3231 N for bridging with activity when the exercise was performed on the unstable
bilateral legs and from 2707 N to 3656 N for bridging with surfaces. It was concluded that much higher demands were
one leg on the ground and the other extended.19 placed on the motor control system when on unstable
The “dying bug” or “dead bug” exercise in which the surfaces and therefore these exercises were more likely
contralateral upper and lower extremity is lifted from the appropriate for later stages of rehabilitation.72 In addition,
supine position has been advocated as an integral part of a performing stabilization exercises on exercise balls has also
properly designed stabilization program. EMG analysis been a popular method of stabilization training. No change
established that the rectus abdominis and oblique muscles in the internal oblique/rectus abdominis ratio between
were equally active with three different progression levels of stabilization exercises performed on or off a ball was found.
this exercise.68 The same authors also assessed three different Significant increase in activation of the rectus abdominis
progression levels of exercises in the quadruped position. with performance of a single–leg hold and at the top of a
They concluded that the ES and gluteus maximus both dem- hook-lying press-up on the ball was identified.73 Although
onstrated significant activation above resting, especially with trunk strengthening demonstrated improvement on
elevation of ipsilateral lower extremity, although neither unstable surfaces in normals73,74 and nonspecific chronic
muscle exceeded 41% of MVIC. The authors speculated that low back pain patients were reported to have trunk muscle
these relatively low levels of activation would most likely not activation levels similar to normals,75 the assumption that
be sufficient to produce strengthening in healthy subjects.68 the use of an exercise ball will always create a greater
The “Superman” exercise (prone lying, arms above challenge for the musculoskeletal system is not universally
head) exerts more than 6000 N or more than 1300 pounds supported.69
Table 16-1
Mean MVIC Values (%) of Longissimus Thoracis and Lumbar Multifidus Muscles During Various Bridging Exercises
Exercise Muscle %MVIC
LM, Lumbar multifidus; LT, longissimus thoracis; MVIC, maximum voluntary isometric contraction; NWB, nonweight bearing; WB, weightbearing.
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 393
Table 16-2
Mean MVIC Values (%) of Various Muscles During Various Quadruped Exercises
Exercise Muscle %MVIC
EO, External oblique; LM, lumbar multifidus; LT, longissimus thoracis; MVIC, maximum voluntary isometric contraction; RA,
rectus abdominus.
Commercial Devices
There are multiple commercial devices advocating improved
Clinically Relevant Points Regarding Stabilization
core strengthening. Limited research is available for support Exercises for the Spine
of such claims. The Power Wheel and hanging knee-up with • Involve various movements (flexion and extension primarily
straps recruited greater abdominal muscle activity than a discussed in the literature)
traditional crunch, bent-knee sit-up, or reverse crunch in a • MVIC values of various muscles vary amongst different forms of
study comparing various devices with traditional exercises.76 the same type of exercise
In another study with similar comparisons, the Ab Slide and • MVIC values of various muscles also vary amongst different
Torso Track activated trunk abdominal musculature to a exercises
greater degree than the crunch or bent-knee sit-up while • Can be performed on unstable surfaces
• Can be performed with various commercial devices
minimizing low back and hip flexion activity.77 The authors
MVIC, Maximum voluntary isometric contraction.
concluded that the Power Wheel, reverse crunch, and bent-
knee sit-up may be problematic for some individuals with
low back pain because of the relatively high rectus femoris
muscle activity.76
squat short (with the feet positioned half the distance Compared with using BW as resistance, using the 12 RM as
from the wall compared with the wall squat long so resistance resulted in 70% to 100% greater quadriceps activ-
that at 90° knee flexion, the knees are positioned ap- ity, 60% to 70% greater hamstrings and thigh adductor
proximately 8 to 10 cm [approximately 3 to 4 inches] activity, and 150% to 200% greater gastrocnemius and
beyond the toes) gluteus maximus activity.
• Ball squat long and ball squat short, which are Quadriceps and hamstrings activity was greatest in the
performed in a similar fashion as the wall squat long one-leg squat and side-lunge exercises, which produced
and wall squat short except the client rolls up and high quadriceps activity and moderate hamstrings activity
down the wall using a Swiss ball positioned between (see Table 16-3). The remaining exercises in Table 16-3
the back and the wall, instead of sliding up and down produced moderate quadriceps activity and low to moder-
the wall ate hamstrings activity. Moreover, gluteus maximus activity
• Forward lunge long (a long stride is used so when the was greatest in the one-leg squat, producing moderate
lead knee is flexed 90°, the lead tibia is in a vertical muscle activity, whereas thigh adductor activity was greatest
position) and forward lunge short (a forward lunge in the forward lunge with a long stride, producing moder-
with a stride length half the distance of the forward ate muscle activity. Gastrocnemius activity was low in all
lunge long) so that at 90° lead knee flexion, the exercises.
lead knee is positioned approximately 8 to 10 cm Quadriceps and gluteus maximus activity was greatest in
(approximately 3 to 4 inches) beyond the toes of the the forward lunge long and forward lunge short, which
same leg produced very high quadriceps activity, whereas hamstrings
• Side lunge activity was greatest in the convention and sumo style dead-
• Barbell deadlift (both sumo and conventional styles) lifts, which produced moderate to high hamstrings activity
(see Table 16-4). The remaining exercises in Table 16-4
produced moderate to high quadriceps activity and low to
moderate hamstrings activity. Moreover, hip adductor activ-
ity was greatest in the side lunge, producing moderate to
Lower-Limb Weightlifting Exercises
high muscle activity, whereas gastrocnemius activity was
• Barbell squat (flat surface) greatest in the conventional style deadlift, producing mod-
• Barbell squat (on balance ball) erate muscle activity. Data from Table 16-4 demonstrates
• Wall squat long that squat, lunge, and deadlift exercises collectively are very
• Wall squat short effective in recruiting the quadriceps musculature, and
• Ball squat long moderately effective in recruiting the hamstrings, gluteus
• Ball squat short
maximus, hip adductors, and gastrocnemius.
• Forward lunge long
• Forward lunge short
In addition to the squat data provided in Tables 16-3 and
• Side lunge 16-4, several other papers have reported lower-extremity
• Barbell deadlift (Sumo and conventional) muscle activity during squat exercises.81-96 Escamilla and
colleagues83 and Wilk and colleagues93 quantified quadri-
ceps, hamstring, and gastrocnemius activity using a 12-RM
load during the barbell squat. Quadriceps activity progres-
sively increased as the knee flexed and decreased as the knees
extended, with peak activity occurring at approximately
Muscle Activity During Squat, Deadlift, 80° to 90° of knee flexion. Similar results were observed in
and Lunge Exercises several other studies.84,86,89,91,92,95 Quadriceps activity
Mean muscle activity, quantified by EMG and normalized by remained fairly constant beyond 80° to 90° knee flexion,
MVIC, are shown in Table 16-3 and Table 16-4 for a variety which has also been observed in other studies.92,95,96 Hence,
of squat,78 deadlift,79 and lunge78 exercises. As previously descending beyond 90° knee flexion, which is near the
defined, EMG between 0% to 20% of an MVIC represents parallel squat position, may not enhance quadriceps
low muscle activity, 21% to 40% of an MVIC represents development.
moderate muscle activity, 41% to 60% of an MVIC repre- Escamilla and colleagues83 reported that the two vasti
sents high muscle activity, and 61% to 100% of an MVIC muscles produce 40% to 50% more activity than the rectus
represents very high muscle activity.80 Table 16-3 displays femoris, which is in agreement with squat data from
muscle activity using BW only as external resistance, and Escamilla and colleagues,84 Wretenberg and colleagues,94
Table 16-4 displays muscle activity using a 12-repetition Wright and colleagues,96 and Isear and colleagues.86 The
maximum (12 RM) as external resistance. lower activity observed in the rectus femoris compared with
Not surprisingly, muscle activity was greater when the the vasti muscles may be due to its biarticular function as
12 RM was employed as resistance compared with BW. both a hip flexor and knee extensor. Increased activity from
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 395
Table 16-3
Lower Extremity Mean (SD) EMG Activity Expressed as a Percent of a Maximum Isometric Voluntary Contraction
During the Knee Extending (90° to 0°) Ascent Phase of Squat and Lunge Exercises Using Bodyweight Only as Resistance
Rectus Vastus Vastus Lateral Medial Gluteus
Femoris Medialis Lateralis Hamstrings Hamstrings Gastrocnemius Maximus Adductors
One-leg squat on 33(23) 51(34) 47(29) 19(16) 17(14) 11(9) 20(15) 24(16)
ground
One-leg squat on 37(26) 57(38) 50(33) 20(17) 19(15) 12(12) 24(20) 21(17)
balance ball
Two-leg squat on 20(15) 29(21) 23(17) 11(11) 8(6) 5(6) 9(7) 9(7)
ground
Two-leg squat on 23(19) 29(21) 21(15) 15(16) 14(14) 8(8) 10(10) 11(8)
balance ball
Wall squat short 26(21) 35(28) 33(26) 10(9) 8(9) 7(7) 9(9) 13(11)
Wall squat long 20(15) 33(25) 28(20) 10(9) 11(12) 6(7) 11(11) 10(8)
Ball squat short 22(15) 30(22) 26(18) 9(8) 6(6) 6(5) 7(8) 9(6)
Ball squat long 21(16) 30(22) 26(17) 8(9) 6(6) 5(5) 7(7) 9(7)
Forward lunge 26(22) 41(30) 38(29) 12(10) 11(8) 8(8) 17(17) 17(12)
short with stride
Forward lunge 28(28) 44(39) 38(30) 16(13) 15(12) 9(8) 18(19) 25(19)
long with stride
Forward lunge 29(23) 37(31) 31(26) 12(11) 11(9) 7(7) 17(18) 17(14)
short with stride
up to 4" bench
Forward lunge 26(21) 46(38) 32(28) 16(12) 15(12) 8(7) 19(19) 26(20)
long with stride
up to 4" bench
Side lunge with 36(28) 49(37) 47(38) 17(15) 14(12) 9(8) 18(17) 18(14)
stride
Side lunge with 37(30) 50(41) 41(29) 17(15) 17(15) 9(9) 18(17) 16(13)
stride up to 4"
bench
the rectus femoris would increase hip flexor torque, with a colleagues,86 Ninos and colleagues,89 and Stuart and
concomitant increase in the amount of hip extensor torque colleagues.92 The lower hamstring activities in these latter
needed from the hamstrings, gluteus maximus, and adduc- studies are probably due to subjects squatting with a lower
tor magnus (ischial fibers) to extend the hip. The rectus relative external load, and perhaps squatting with a more
femoris is probably more effective as a knee extensor during erect trunk. Subjects in the Isear and colleagues86 study
the squat when the trunk is more upright, because it is in a used no external lifting load, whereas subjects in the Ninos
lengthened position compared with when the trunk is tilted and colleagues89 and the Stuart and colleagues92 studies
forward in hip flexion. Compared to each other, the VM used lifting loads of 25% BW and 28% BW, respectively,
and VL produced approximately the same amount of while subjects in Escamilla and colleagues83,84 studies lifted
activity, which is in agreement with data from other loads equal to 140% to 160% BW. Because many of the
studies.84,88,91,93 subjects in the Escamilla and colleagues studies83,84 were
Hamstring activities from Escamilla and colleagues83,84 powerlifters and used the power squat position with the
and Wilk and colleagues93 were highest during the squat trunk tilted forward 30° to 45° from vertical, greater ham-
ascent, with the lateral hamstrings showing greater overall string activity was generated. Greater hamstring activity
activity than the medial hamstrings. Peak hamstring activity with greater forward trunk tilt during the squat has also
between approximately 30% to 80% of a MVIC, occurs near been reported by Ohkoshi and colleagues.97
50° to 70° knee flexion. In contrast, peak hamstring activity Several studies have reported gastrocnemius activity and
was approximately 12% MVIC, 15% MVIC, and 20% force during the squat.82-84,86 Escamilla and colleagues83
MVIC, respectively, with peak values occurring between observed moderate gastrocnemius activity during the squat,
10° and 60° knee flexion based on data from Isear and which progressively increased as the knees flexed and
396 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 16-4
Lower Extremity Mean (SD) EMG Activity Expressed as a Percent of a Maximum Isometric Voluntary Contraction During
the Knee Extending (90° to 0°) Ascent Phase of Squat, Lunge, and Deadlift Exercises Using Each Subject’s 12-Repetition
Maximum as Resistance
Rectus Vastus Vastus Lateral Medial Gluteus
Femoris Medialis Lateralis Hamstrings Hamstrings Gastrocnemius Maximus Adductors
One-leg squat on 47(15) 79(20) 78(22) 29(12) 25(14) 25(9) 57(24) 26(11)
ground
Wall squat short 51(17) 71(24) 70(17) 12(9) 7(5) 16(8) 24(12) 17(10)
Wall squat long 48(15) 69(19) 67(16) 12(7) 10(5) 8(6) 28(12) 20(12)
Ball squat short 47(29) 58(37) 48(33) 16(13) 11(9) 7(6) 21(20) 17(11)
Ball squat long 39(26) 53(35) 45(34) 13(11) 10(8) 6(6) 17(13) 16(10)
Forward lunge 50(20) 75(23) 76(23) 16(8) 14(7) 19(9) 53(31) 22(15)
short without
stride
Forward lunge 67(32) 88(31) 84(29) 16(11) 16(12) 21(11) 64(32) 28(15)
short with stride
Forward lunge 32(11) 63(20) 62(19) 23(11) 21(10) 20(11) 50(29) 28(14)
long without
stride
Forward lunge 67(30) 104(36) 102(30) 31(17) 27(17) 29(16) 62(29) 37(18)
long with stride
Side lunge with- 43(16) 77(18) 72(15) 22(13) 18(11) 19(9) 41(23) 30(13)
out stride
Side lunge with 55(25) 87(22) 92(27) 31(12) 23(16) 25(12) 52(21) 42(22)
stride
Sumo-style 24(14) 63(21) 59(27) 41(16) 40(23) 31(18) 38(26) 26(19)
deadlift
Conventional- 26(18) 56(19) 54(27) 41(15) 37(24) 39(24) 32(22) 21(19)
style deadlift
decreased as the knees extended. Escamilla and colleagues83 and foot turned outward 30°). Hung and Gross85 examined
and Isear and colleagues86 reported peak gastrocnemius the effects of foot wedges on VM oblique (VMO) and VL
activity between 60° to 90° knee flexion. Because the ankle activity. Their study varied foot angle by changing forefoot
dorsiflexes during the descent and plantar flexes during the inversion and eversion (by using 10° medial and lateral
ascent, it is a common belief that the gastrocnemius wedges) rather than changing forefoot adduction and ab-
contracts eccentrically during the descent to help control duction. These authors reported no significant EMG differ-
the rate of ankle dorsiflexion, and concentrically during the ences in VMO/VL ratios among the foot positions. EMG
ascent to aid in ankle plantar flexion. data from the aforementioned studies demonstrate that
Several studies have investigated the effects of varying varying foot positions do not appear to affect quadriceps,
foot positions on quadriceps, hamstrings, and gastrocne- hamstrings, or gastrocnemius activity during the squat.
mius activity.84,85,89,90 Escamilla and colleagues84 reported Several studies have investigated the effects of stance
no significant differences in quadriceps, hamstrings, or width (narrow stance and wide stance) on knee muscle ac-
gastrocnemius activity between two foot positions (feet tivity during the squat.84,87,98,99 Escamilla and colleagues84
pointing straight ahead and feet turned outward 30°). found that gastrocnemius activity was 21% greater in the
Signorile and colleagues90 reported no significant differ- narrow-stance barbell squat compared with the wide-stance
ences in VM, VL, and rectus femoris activity among three barbell squat. In addition, there was no significant differ-
foot positions (feet pointing straight ahead, toes pointed ences in quadriceps or hamstrings activity between narrow-
outward as far as possible, and toes pointed inward and wide-stance squats, which is in agreement with EMG
approximately 30°). Ninos and colleagues89 reported no data from McCaw and Melrose,87 which also employed
significant differences in quadriceps or hamstrings activity similar narrow and wide stances. Tesch,99 using magnetic
between two foot positions (self-selected neutral position resonance imaging immediately after performing the squat,
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 397
also showed no differences in quadriceps or hamstrings unload the ACL by producing a posterior-directed force to
activity between narrow- and wide-stance squats. Anderson the leg throughout the knee movement.97,108-112 Quadri-
and colleagues98 found no significant differences in VMO/ ceps activity also affects the strain on the cruciate ligaments.
VL ratios between narrow and wide stances during the BW Quadriceps force, via the patella tendon, exerts an anterior
squat, but did report significantly greater VMO/VL ratios directed force on the leg (ACL loading) when the knee is
with increasing knee flexion angles (0° to 30°, 0° to 60°, flexed between 0° to 50°, and a posterior directed force on
0° to 90°). These results imply that increasing knee flexion the leg (PCL loading) when the knee is flexed greater than
angles during the BW squat elicited greater activity of the 50° to 60°.113,114
VMO relative to the VL. One additional study81 investi- Escamilla and colleagues83,84 reported cruciate ligament
gated the effects of moving the feet forward while perform- loading during the barbell squat with a 12-RM intensity.
ing a machine squat exercise. This author reported that During the squat ascent, a mean peak PCL tensile force of
a more forward foot position during a machine squat 1868 878 N occurred at 63° knee flexion, whereas a
increased quadriceps and hamstrings activity. mean peak compressive force of 3134 1040 N occurred
In addition to the lunge data provided in Tables 16-3 at 53° knee flexion. During the descent, a mean peak PCL
and 16-4, a few other studies have reported lower-extremity tensile force of 1635 369 N occurred at 95° knee flexion,
muscle activity during lunge exercises.92,100,101 Farrokhi and whereas a mean peak compressive force of 2192 930 N
colleagues100 reported that performing the forward lunge occurred at 81° knee flexion. There were no significant dif-
with the trunk tilted forward significantly increased gluteus ferences in compressive forces and PCL tensile forces
maximus and biceps femoris EMG compared with perform- between two foot angle conditions (feet straight and turned
ing the forward lunge with the trunk erect. These lunge out 30°), and no significant differences in PCL tensile
EMG data are similar to squat EMG data reported by forces between two stance conditions (narrow stance and
Ohkoshi and colleagues.97 Both Hefzy and colleagues101 wide stance). However, the wide stance generated 15% to
and Stuart and colleagues92 reported co-contraction of the 16% significantly greater tibiofemoral compressive forces
quadriceps and hamstrings during the lunge, although than the narrow stance. It is currently unknown at what
Stuart and colleagues92 reported increased quadriceps activ- magnitude tibiofemoral compressive force becomes injuri-
ity with decreased hamstrings activity. Because trunk posi- ous to knee structures, such as menisci and articular carti-
tion was not reported by Stuart and colleagues,92 the lage. Excessive loading of the menisci and articular cartilage
decreased hamstrings activity may have resulted from main- can lead to degenerative changes. However, compressive
taining an erect trunk position during the lunge. forces have been demonstrated to be an important factor in
knee stabilization by resisting shear forces and minimizing
tibia translation relative to the femur.115-118
Kinetics and Pathomechanics During Squat Escamilla and colleagues119 reported cruciate ligament
Exercises loading during the wall squat and one-leg squat with a
Tibiofemoral Forces 12-RM intensity (Table 16-5). During the squat-ascent
Several studies have quantified tibiofemoral shear (anterior phase, mean PCL forces were significantly greater during the
cruciate ligament [ACL] and posterior cruciate ligament wall squat long compared with the wall squat short between
[PCL] loading) or compressive forces during squat 70° and 0° knee angles, significantly greater in the wall squat
exercises.82-84,92,93,102-107 These studies reported low to mod- long compared with the one-leg squat between 90° and
erate posterior shear forces and PCL loading during the 60° and 20° and 0° knee angles, and significantly greater in
squat, with PCL loading increasing as knee flexion the wall squat short compared with the one-leg squat
increased. A few of these studies also showed low ACL between 90° and 70° and 0° knee angles. For all three squat
loading during the squat,104-107 but only at knee flexion exercises, mean peak PCL force magnitudes occurred be-
angles between 0° to 60°. When tibiofemoral forces were tween 80° and 90° knee angles during the squat ascent, and
normalized as a percent of BW plus load lifted, the normal- were 723 127 N for the wall squat long, 786 197 N for
ized peak posterior shear forces (PCL loading) ranged from the wall squat short, and 414 133 N for the one leg squat.
29% to 99%, normalized peak anterior forces (ACL loading) ACL forces, which were generated only during the one leg
ranged from 4% to 14%, and normalized compressive force squat (31 to 59 N range), occurred between 0° and 40° knee
ranged from 54% to 367%. It can be concluded from these angles. The mean peak ACL force magnitude during the one
data that squat exercises moderately compress the tibio- leg squat was 59 52 N and occurred at 30° knee angle.
femoral joint (primarily at higher knee angles), moderately The mean peak PCL forces of approximately 400 N dur-
load the PCL (primarily at higher knee angles), and mini- ing the one-leg squat and approximately 750 N during
mally load the ACL (primarily at lower knee angles). the wall squat exercises may be problematic early after PCL
The relatively low ACL forces observed during the squat reconstruction when the graft site is still healing. Moreover,
may in part be due to moderate hamstring activity, because during PCL reconstruction, at any given exercise intensity,
several studies have demonstrated that the hamstrings help it may be appropriate to employ the one-leg squat prior to
398 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 16-5
Mean (⫾SD) Cruciate Ligament Forces (N) Among the Three Squat Types, Wall Squat Long, Wall Squat Short, and One-Leg
Squat, and Between the Two Squat Phases (Squat Descent and Squat Ascent) as a Function of Knee Angle
Knee Angles Wall Squat Wall Squat One-Leg Significant Differences (P ⬍ 0.05) Between
for Descent Phase Long Short Squat Squat Types
0° 482 209 297 152 31 52 WSL WSS (p 0.002); WSL OLS
(p 0.001); WSS OLS (p 0.001)
10° 423 205 243 140 36 54 WSL WSS (p 0.011); WSL OLS
(p 0.001); WSS OLS (p 0.001)
20° 316 135 143 131 51 77* WSL WSS (p 0.049); WSL OLS
(p 0.001); WSS OLS (p 0.004)
30° 261 124 100 100 59 52* WSL WSS (p 0.023); WSL OLS (p 0.001)
40° 259 121 109 77 22 66* WSL WSS (p 0.014); WSL OLS (p 0.002)
50° 295 122 157 70 64 93* WSL WSS (p 0.005); WSL OLS (p 0.001)
60° 348 133* 231 81 160 97* WSL WSS (p 0.034); WSL OLS (p 0.001)
70° 445 136* 324 101* 227 81* WSL WSS (p 0.022); WSL OLS (p 0.001)
80° 573 149* 439 129* 326 118 WSL WSS (p 0.017); WSL OLS (p 0.001)
90° 659 150 578 158* 386 121 WSL OLS (p 0.001); WSS OLS (p 0.003)
Knee Angles Wall Squat Wall Squat One-Leg Significant Differences (p ⬍ 0.05) Between
for Ascent Phase Long Short Squat Squat Types
90° 723 127 786 197* 414 133 WSL OLS (P 0.001); WSS OLS (P 0.001)
80° 757 185* 702 200* 391 169 WSL OLS (P 0.001); WSS OLS (P 0.001)
70° 714 181* 529 177* 368 157* WSL WSS (P 0.001); WSL OLS
(P 0.001); WSS OLS (P 0.035)
60° 542 144* 366 146 374 178* WSL WSS (P 0.001); WSL OLS (P 0.002)
50° 408 137 267 141 329 172* WSL WSS (P 0.001)
40° 355 120 223 174 266 159* WSL WSS (P 0.020)
30° 363 141 206 158 231 132* WSL WSS (P 0.007)
20° 436 180 222 139 209 142* WSL WSS (P 0.001); WSL OLS (P 0.005)
10° 539 223 253 155 88 130 WSL WSS (P 0.001); WSL OLS (P 0.001)
0° 529 249 274 178 37146 WSL WSS (P 0.003); WSL OLS
(P 0.001); WSS OLS (P 0.001)
N, Ligament forces; OLS, one-leg squat; WSL, wall squat long; WSS, wall squat short.
Note: Anterior cruciate ligament forces are listed as negative values and posterior cruciate ligament forces are listed as positive values. An asterisk
(*) indicates that there is a significant difference (p 0.05) in cruciate ligament force at the specified knee angle between the squat descent and
the squat ascent phases of a squat exercise.
wall squat exercises because there is less PCL loading during angles (e.g., 50° to 100°) before progressing to smaller
the one leg squat. In addition, it may be prudent to employ knee angles (e.g., 0° to 50°) because ACL forces may be
smaller knee angles (e.g., 0° to 50°) before progressing to generated at smaller knee angles less than 50°.
larger knee angles (e.g., 50° to 100°) because PCL forces During the one leg sit-to-stand, which is similar to the
generally increase as knee angle increases. In contrast, wall ascent phase of the one leg squat, Heijne and colleagues121
squat exercises may be a better choice compared with the reported a peak 2.8% ACL strain (calibrated to approxi-
one-leg squat early after ACL reconstruction because of mately 100 N) at 30° knee angle. Moreover, Kvist and
ACL forces generated during the one-leg squat. However, Gillquist122 reported a peak anterior shear ACL force of less
because peak ACL force during the one-leg squat were only than 90 N at 30° knee angle during the one leg BW squat,
approximately 60 N, it is not likely that the one-leg squat which is similar to the results in the Heijne and colleagues
will produce forces that would be injurious to the healing study.121 Moreover, ACL forces as a function of knee angle
ACL graft, and mild strain to the graft may enhance in Escamilla and colleagues119 are similar to ACL forces and
the healing process.120 Nevertheless, after ACL reconstruc- knee angles reported by other authors.104,106,107,121
tion it may be safer to start with wall squat exercises The ACL and PCL forces that are generated while per-
and progress to the one-leg squat, and employ larger knee forming squat exercises depend on which exercise technique
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 399
75° and 110° because of similar magnitudes of patellofemoral at 70° and 80° knee angles in the wall squat short and
stress during these knee angles, with the benefit of increased long compared with the one-leg squat, and significantly greater
quadriceps, hamstrings, and gastrocnemius activity when at 60° knee angle in the wall squat long compared with the wall
training at higher knee angles (75° to 110°) compared with squat short and one-leg squat.124 The primary cause of the
training at lower knee angles (0° to 70°).83 greater patellofemoral force and stress between 90° and 70°
Escamilla and colleagues124 compared patellofemoral knee angles in the wall squat short compared with the one-leg
force and stress among wall squat (wall squat long and squat was 30% to 40% greater estimated quadriceps force and
short) and one-leg squat exercises using dumbbell weights, 60% to 70% less estimated hamstrings force during the wall
and these results are shown in Figure 16-7 and Figure 16-8. squat short compared with the one-leg squat.124 One reason for
Like the barbell squat, patellofemoral force and stress gen- greater quadriceps force and less hamstrings force in the wall
erally increased with greater knee angles and decreased with squat short compared with the one-leg squat is because the
smaller knee angles. For example, during the squat-ascent trunk is erect in the wall squat short (more conducive to greater
phase of the wall squat short, patellofemoral force ranged quadriceps activity and less hamstrings activity) and tilted for-
from approximately 75 to 1400 N between 0° and 50° knee ward 30° to 40° in the one-leg squat (more conducive to
angle and from approximately 2100 to 3650 N between greater hamstrings activity and less quadriceps activity).
60° and 90° knee angles, and patellofemoral stress ranged Unfortunately, it is currently unknown how much patel-
from approximately 0.5 to 4.4 MPa between 0° and lofemoral compressive force and stress is detrimental to the
50° knee angles and from approximately 5.9 to 8.9 MPa patellofemoral joint. There are many factors that may con-
between 60° and 90° knee angles. Therefore, performing tribute to patellofemoral pathological conditions, such as
the squat in the functional range between 0° and 50° of overuse or trauma, dysfunctional extensor mechanism,
knee flexion may be more appropriate for patellofemoral weakness in the quadriceps or hip external rotators, tight
patients, because only low to moderate patellofemoral quadriceps, hamstrings, or iliotibial band, lower-extremity
compressive forces were generated in this range. malalignment, and excessive rear-foot pronation. Neverthe-
Patellofemoral force and stress were significantly greater less, clinicians can use information regarding patellofemoral
at 90° knee angle during the wall squat short compared joint force and stress magnitudes among different weight-
with wall squat long and one-leg squat, significantly greater bearing exercises, technique variations, and functional
Figure 16-7
Mean (standard deviation) patellofemoral compressive force during the one leg squat and the wall squat.
(From Escamilla RF, Zheng N, Imamura R, et al: Patellofemoral compressive force and stress during the
one leg squat and wall squat, Med Sci Sports Exerc 41[4],879-888, 2009.)
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 401
Figure 16-8
Mean (standard deviation) patellofemoral stress during the one-leg squat and the wall squat. (From
Escamilla RF, Zheng N, Imamura R, et al: Patellofemoral compressive force and stress during the one
leg squat and wall squat, Med Sci Sports Exerc 41[4],879-888, 2009.)
Table 16-6
Mean (⫾ SD) Cruciate Ligament Force (N) Values Between Forward Lunge Step Length Variations and Between Forward
Lunge Stride Variations
Step Length Variations Stride Variations
Knee Angles for
Descent Phase Long Step Short Step p Value With Stride Without Stride p Value
90° 682 275 612 157 0.326 602 174 691 262 0.046
80° 740 247 610 196 0.020 663 224 686 241 0.539
70° 765 220 549 195 0.001* 681 248 632 218 0.301
60° 744 233 485 194 0.001* 669 266 560 223 0.056
50° 706 264 452 219 0.001* 642 281 514 251 0.005
40° 676 279 390 184 0.001* 563 285 509 269 0.224
30° 657 259 375 201 0.001* 515 285 522 261 0.675
20° 580 268 340 163 0.001* 418 263 502 239 0.355
10° 488 212 279 142 0.001* 305 168 448 216 0.015
0° 412 185 219 150 0.001* 266 183 360 193 0.126
N, Ligament forces
*Significant difference (p 0.0025) between step length variations or stride variations.
Note: Anterior cruciate ligament forces represent negative values and posterior cruciate ligament forces represent positive values.
Note: The mean values given for the two step length variations (long step and short step) were collapsed across the two stride variations
(with stride and without stride), and the mean values given for the two stride variations were collapsed across the two step length variations.
loading is different between the forward lunge short and performing a forward lunge exercise using a 50 N barbell,
the forward lunge long. which support the results of Escamilla and colleagues.128
When the goal is to minimize ACL loading, such as after During a BW lunge with a stride (step length was not
ACL reconstruction, the forward lunge long may be a more measured), Heijne and colleagues121 reported a mean ACL
appropriate and safer choice compared with the forward strain of approximately 1% or less (approximately 40 N or
lunge short, especially the forward lunge short with stride, less) at knee angles less than 60° (i.e., no ACL strain at knee
which was the only lunge variation that generated ACL flexion angles greater than 60°), and a peak ACL strain of
loading.128 Moreover, performing the lunge throughout a 1.8% (approximately 75 N) between 0° and 30° knee flex-
higher knee angle range may be preferred compared with ion. By comparison, the peak ACL force found by Escamilla
a lower knee angle range, because ACL forces were only and colleagues128 was approximately 50 N in the forward
generated at smaller knee angles.128 lunge short with stride between 0° and 10° knee flexion
When the goal is to minimize PCL loading, such as after angles. This demonstrates a remarkable similarity between
PCL reconstruction, all lunge variations should be used the ACL lunge data between Escamilla and colleagues,128
cautiously, especially the forward lunge long at higher knee who calculated ACL loading by knee biomechanical model-
angles between 60° and 90°, where mean PCL forces ing techniques, and the ACL strain lunge data by Heijne
ranged between 475 to 775 N.128 Mean PCL forces ranged and colleagues,121 who calculated ACL loading by direct
between 250 and 600 N for the forward lunge short.128 measurement using force sensors within the ACL. The sub-
Stuart and colleagues92 also reported tibial posterior shear jects in Heijne and colleagues’ study121 were patients who
loads (i.e., PCL loading) throughout the knee ROM while had force sensors implanted within the anteromedial bundle
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 403
of a healthy ACL during arthroscopic surgery to repair of the healthy PCL is approximately 4000 N,130 all four
damaged knee structures (partial meniscectomies, capsule lunge variations appear appropriate for healthy individuals.
and patellofemoral joint debridement). Immediately after However, although the reconstructed PCL typically has
surgery, these patients were asked to perform a variety of equal or greater ultimate strength compared with the
exercises, including the lunge, and the strain within the healthy PCL, it is unclear how much PCL loading may
anteromedial bundle of the ACL was measured and refer- become injurious to the healing graft site during PCL
enced to an instrumented Lachman test. Unfortunately, rehabilitation.
Heijne and colleagues121 did not measure PCL strain, so Escamilla and colleagues129 compared cruciate ligament
PCL loads cannot be compared among studies. loading between the forward lunge and side lunge both
Estimated hamstring forces calculated by Escamilla and with and without a stride. Mean PCL forces ranged from
colleagues128 during the forward lunge were 50% to 60% 205 to 765 N, and were significantly greater in the forward
greater in the forward lunge long compared with the for- lunge compared with the side lunge between 40° and 80°
ward lunge short, which helps explain the greater PCL knee flexion angles. When the goal is to minimize PCL
forces generated in the forward lunge long. Because the loading, the side lunge may be a better choice than the
same trunk position was used during the forward lunge forward lunge.
long and short, the greater hamstrings force during the
forward lunge long appears to be related to a longer step
length during the lunge. Trunk position may also affect
Clinically Relevant Points Regarding Lower-
cruciate ligament loading during the lunge. Farrokhi and
colleagues100 demonstrated that, compared with perform-
Extremity Muscle Activity During Lunge Exercises
ing a forward lunge with a relatively erect trunk, perform- Lunging without Resistance (Bodyweight Only)
ing the lunge with the trunk tilted forward approximately • Moderate quadriceps activity occurs regardless of technique
30° to 45° resulted in significantly greater hip extensor employed
impulse and significantly greater hamstrings activity. This • Hamstrings, gluteus maximus, and hip adductor activities were
greater hamstrings activity would likely result in an increase low during the forward lunge and side lunge
in hamstrings force compared with performing the lunge • Hamstrings and hip adductor activities were slightly greater in the
forward lunge long than the forward lunge short
with a more erect trunk, which may result in greater PCL
• Low gastrocnemius activity occurs during all lunging techniques
loading and less ACL loading.
Comparing with and without stride techniques, PCL Lunging with Resistance (12-Repetition Maximum Intensity)
forces were significantly greater without a stride between • High quadriceps activity occurs in all lunging techniques
0° and 20° knee angles.128 Conversely, ACL forces were employed
significantly greater with a stride compared to without a • Quadriceps activity was greater in the forward and side lunge with
a stride compared to without a stride
stride, but only between 0° and 10° knee-flexion angles
• Quadriceps activity was greater in the forward lunge long with
during the forward lunge short with stride, in which ACL
stride compared with the forward lunge short with stride, but
forces were between 0° and 50 N. One possible explanation quadriceps activity was less in the forward lunge long without
for greater ACL forces with a stride and greater PCL forces stride compared with the forward lunge short without stride
without a stride is that with a stride produced 15% to 30% • Quadriceps activity was greater in the forward lunge long with
greater quadriceps forces between 0° and 20° knee flexion stride compared with the side lunge with stride, but quadriceps
angles,128 and higher quadriceps force at these lower knee activity was less in the forward lunge long without stride
angles has been shown to result in greater ACL loading.114 compared with the side lunge short without stride
Just after lead foot contact during the descent, when the • Moderate hamstrings activity occurs during the forward and side
knee was flexed 0° to 20°, peak ground reaction forces act- lunge
ing on the lead foot were 15% to 20% greater with a stride, • Hamstrings activity is greater in forward lunge long compared with
the forward lunge short
because the body had more forward and downward accel-
• Hamstrings activity is similar between the forward lunge and side
eration compared to without a stride. Therefore, with a
lunge
stride the lead foot had to push harder into the ground to • High gluteus maximus activity occurs in the forward lunge,
slow down and control the rate of lead knee flexion, causing whereas moderate gluteus maximus activity occurs in the side
greater quadriceps activity. Therefore, when the goal is to lunge
minimize ACL loading, lunging without a stride may be • Gluteus maximus activity is greater in the forward lunge long
a safer choice compared with lunging with a stride, because compared than the side lunge
the ACL is less likely to be loaded without a stride • Moderate hip adductor activity occurs in the forward lunge and
compared to with a stride.128 side lunge
Like the reconstructed ACL, it is unknown how much • Low to moderate gastrocnemius activity occurs during all lunging
loading can safely occur in the reconstructed PCL, and graft techniques
type must also be considered. Because the ultimate strength
404 SECTION II • Applied Biomechanics of Selected Sport Activities
Figure 16-9
Mean (standard deviation) patellofemoral compressive force during the forward lunge long and short
with a stride. (From Escamilla RF, Zheng N, Macleod TD, et al: Patellofemoral joint force and stress
between a short- and long-step forward lunge, J Orthop Sports Phys Ther 38[11]:681-690, 2008.)
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 405
Figure 16-10
Mean (standard deviation) patellofemoral stress during the forward lung long and short with a stride.
(From Escamilla RF, Zheng N, Macleod TD, et al: Patellofemoral joint force and stress between a
short- and long-step forward lunge, J Orthop Sports Phys Ther 38[11]:681-690, 2008.)
when patellofemoral joint force and stress are initially the knee extensors, are approximately 15% to 20% greater
greater in the forward lunge short compared with the for- with a stride compared to without a stride between 10° and
ward lunge long.132 The lead knee continues translating 40° knee angles.132 This occurs because with a stride the
beyond the toes as the lead knee continues flexing, translat- subjects have to forcefully push off the force platform to
ing 8 3 cm (3 1 inches) beyond the distal toes at accelerate the body backward and upward and return the
maximum lead knee flexion.132 These results support the body back to the upright starting position. Because lunging
belief of many clinicians and trainers that anterior lead knee without a stride results in both feet remaining stationary
translation beyond the toes during the forward lunge may throughout the lunging motion, acceleration is minimal.
be harmful to the patellofemoral joint, and should Escamilla and colleagues131 reported patellofemoral force
be avoided. In contrast, the lead knee did not translate and stress magnitudes between a forward and side lunge
beyond the toes throughout the knee ROM during the with and without a stride. They reported that patellofemo-
forward lunge long.132 Because significantly greater patel- ral force and stress were greater in the side lunge compared
lofemoral joint force and stress occur between 70° to with the forward lunge between 80° and 90° knee angles,
90° knee angles during the forward lunge short compared and greater with a stride compared to without a stride
with the forward lunge long, there appears to be a relation- between 10° and 50° knee flexion angles. From these data,
ship between anterior knee translation and increased it can be concluded that loading the patellofemoral joint is
patellofemoral joint force and stress. similar between forward and side lunges except at higher
The greater patellofemoral force and stress in the knee angles, in which patellofemoral loading is greater in
forward lunge short compared with the forward lunge long, the side lunge. Performing forward and side lunges without
and with a stride compared to without a stride, is primarily a stride within a smaller knee angle range (e.g., 0° to 50°)
the result of approximately 20% to 30% greater quadriceps may be easier and safer to start with earlier during patello-
forces in the forward lunge short compared with the for- femoral rehabilitation when the goal is to minimize patel-
ward lunge long, and approximately 40% greater quadriceps lofemoral compressive force and stress, whereas performing
force with a stride compared to without a stride.132 Quadri- forward and side lunges with a stride may be more appro-
ceps forces are greater with a stride because peak ground priate later during patellofemoral rehabilitation because
reaction forces acting on the lead foot, which generates a of greater patellofemoral compressive force and stress
knee flexor torque throughout the lunge that is opposed by compared to without a stride.
406 SECTION II • Applied Biomechanics of Selected Sport Activities
rotated laterally in the transverse plane. Because of the ori- type A and B trajectories appear to be most common in
entation of the lower extremity, the sequence of this pull world champions.31,144,153,154 Type A and B trajectories are
involves predominantly knee extension followed by hip fairly similar, in that both are an S-shaped curve with the
extension.138,139,143,144 A majority of elite lifters use the barbell pulled toward the lifter during the FP, followed by a
double knee bend pull, and empirical evidence from recent forward trajectory during the end of the SKB and start of
major international events (world championships and Olym- the SP, after which it arcs back toward the lifter during the
pic Games) has found no lifters using the frog-style pull. pull-under phase. In the type A trajectory, the forward
Therefore, this discussion of the snatch and clean focuses on trajectory during the SKB and SP pushes the barbell forward
the double knee bend technique. of the vertical reference line, whereas the barbell always
Both the snatch (Figure 16-11) and clean (Figure 16-12) remains behind the vertical reference line in a type B trajec-
can be broken into seven distinct phases based on segment tory. Type B trajectories are typically accompanied by the
kinematics and kinetics and muscle activation.146-148 These feet jumping backward.152,155 Type C trajectories are gener-
phases are (1) pre-lift, (2) first pull (FP), (3) second knee ally considered improper because the amount of horizontal
bend (SKB), (4) second pull (SP), (5) pull under the barbell, motion increases the work performed in lifting the
(6) amortization phase, and (7) recovery. The FP, SKB, and barbell.144,156
SP are collectively referred to as the pulling phase,145 and the To initiate the lift, the lifter assumes a partial squat posi-
majority of research in weightlifting has analyzed the pulling tion, in which the knee and shoulder are over or forward of
phase. The duration of phases two through six are detailed the barbell. The shanks (tibia) are rotated forward approxi-
in Table 16-7. mately 25°, the angle of the knees is 70° to 75° in the
When performed properly, the barbell follows a charac- snatch and 80° to 85° in the clean, and the angle of the hips
teristic trajectory during the pulling phase. Vorobyev149 45° to 50° (note that joint angles refers to the angle
categorized pulling trajectories based on the initial direction between two adjacent segments). Gourgoulis et al.157 ob-
of the barbell and the number of horizontal crossings of the served that elite Greek women weightlifters had an initial
barbell relative to an imaginary vertical line projected from knee angle of 60°. Center of pressure is located toward the
the initial barbell position (Figure 16-13). Although there is forefoot, 30% to 50% behind the front of the feet.158,159 In
considerable dissent over which trajectory is optimal,150-152 lifting the barbell from the ground, a static or dynamic start
Figure 16-11
The seven phases of the snatch using the double knee bend pull.
408 SECTION II • Applied Biomechanics of Selected Sport Activities
Figure 16-12
The seven phases of the clean using the double knee bend pull.
may be employed. The static start involves pulling from the Peak knee flexor NJM (0.5 to 1.5 NmkgBM1) oc-
aforementioned positions, whereas a dynamic start may curs before the end of the FP.138 The FP is completed when
involve starting in a deeper squat and rising to these posi- the knees reach their first maximum extension. Elite weight-
tions or performing a countermovement. There does not lifters extend their knees to an angle of approximately 145°
appear to be a clear advantage or disadvantage for any of at the completion of the FP154,157,165-167; however, it has
these starting methods.160 been noted that lower-caliber men lifters only reach 135°
As the barbell is lifted from the ground, the hips and knees and elite women 130°.157,165 The angle of the trunk relative
extend and the ankles plantar flex. The hip extensors have the to the ground remains relatively constant throughout the
largest net joint moment (NJM) (3.5 to 5.5 NmkgBM1), FP; therefore, as the knees extend, it becomes increasingly
which increases during the pre-lift phase and reaches a peak difficult to continue elevating the bar relying primarily on
during the FP.138,153,161 The knee extensor (1.0 to 2.2 Nm- the hip extensors,138,139,145 which include the biarticular
kgBM1) and ankle plantar flexor (1.4 to 2.5 NmkgBM1) hamstring muscles. Therefore, it is likely that in lower-
NJM also reach a peak shortly after lift-off. The lifter’s center caliber men and elite women, the hamstring muscles are not
of pressure shifts from the fore to rear foot, resulting in the strong enough to extend the knee and hip joints, resulting
initial posterior trajectory of the barbell.158 As the barbell in less extension at the end of the FP. Numerous studies have
passes mid-shank, the knees shift from an extensor NJM to a found lower relative strength of the hamstring muscles in
flexor NJM.161-163 The knees, however, continue to extend; women compared with men.168,169
thus, the knee flexor musculature is acting eccentrically. It is As the SKB begins, the knee NJM is still flexor-dominant
important to note that throughout the FP, the knee extensor as the knees begin to flex. Thus, the knee flexors shift from
and knee flexor muscles are co-contracting, with the extensors an eccentric to concentric action.161-163 This concentric knee
showing greater activation initially and the flexors increasing flexor action, however, is short-lived, as the knee NJM shifts
activation toward the end of the FP.162,164 The magnitude of from flexor to extensor.161-163 As the knees continue to flex,
co-contraction suggests that the actual muscle movement the knee extensors are now acting eccentrically. The SKB
generated by the knee extensors is considerably larger than generates approximately 20° flexion of the knee, resulting in
the NJM indicates.138,162,163 In addition, the biarticular ham- a knee angle of approximately 125°.147,148,153,154,157,166,167 It
string muscles are likely also contributing to hip extension is interesting to note that elite male lifters during the early
during the FP. 1970s flexed their knees up to 30° during the SKB.165 The
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 409
Table 16-7
Duration of Phases 2 Through 6 in the Snatch and Clean, Observed in Laboratory and Competition Investigations
Duration
First Pull Second Knee Second Pull Under Amortization
Weightlifters Lift—Conditions (s) Bend (s) Pull (s) the Bar (s) (s)
Greek National Men’s Snatch—Laboratory 0.48 0.07 0.14 0.01 0.15 0.01 0.24 0.03
Team167
Greek Junior National Snatch—Laboratory 0.51 0.10 0.13 0.02 0.26 0.23 0.46 0.05
Men’s Team167
Y. Zakharevich Snatch—World record 0.37 0.08 0.17 0.20 0.33
(USSR)—World in competition
Record166
Finnish National Men’s Snatch—Laboratory 0.54 0.23 0.13 0.04 0.20 0.03 0.17 0.02
Team148
Finnish Non-Elite148 Snatch—Laboratory 0.57 0.09 0.14 0.03 0.17 0.03 0.18 0.04
Finnish National Men’s Clean—Laboratory 0.64 0.18 0.13 0.03 0.19 0.04 0.17 0.03
Team148
Finnish Non-Elite148 Clean—Laboratory 0.78 0.18 0.14 0.04 0.17 0.03 0.16 0.02
Greek National Men’s Snatch—Laboratory 0.45 0.04 0.15 0.01 0.16 0.01 0.23 0.01
Team157
Greek National Snatch—Laboratory 0.45 0.04 0.14 0.02 0.18 0.02 0.26 0.02
Women’s Team157
Greek National Men’s Snatch—Competition 0.47 0.06 0.16 0.01 0.15 0.01 0.23 0.02
Team154
European Junior Snatch—European 0.48 0.04 0.14 0.02 0.16 0.03 0.36 0.02 0.14 0.06
Men—56 kg & junior championships
62 kg175
European Junior Snatch—European 0.54 0.03 0.12 0.02 0.16 0.03 0.37 0.02 0.15 0.06
Men—85 kg & junior championships
105 kg175
Note: Some investigations did not report data for all phases.
rationale for the greater knee flexion is unknown, but would barbell being purposely pulled rearward and violently
be expected to increase the loading on the hip, knee, and colliding with the thighs or pelvis.
ankle musculature. This style of lifting may be a residual The change in segment orientations during the SKB
effect of the press era when greater emphasis was placed on repositions the body into a mechanically advantageous posi-
strength than speed strength.140 Lower caliber men and elite tion to impart vertical momentum to the barbell during the
women flex their knees 10° to 15° during the SKB, resulting SP.139,145 The knees shift from an eccentric action during
in a similar knee angle to elite men at the end of the SKB the SKB to a concentric action during the SP, similar to the
and start of the SP.157,165 stretch-shortening cycle phenomenon observed during a
In addition to knee flexion, the SKB is characterized by countermovement jump.162,163,170,171 In the SP, the hips and
a repositioning of the body.145 As the knees flex, the ankles knees extend, and the ankles plantar flex in a rapid manner
dorsiflex and the center of pressure shifts from the rear to to increase the vertical velocity of the barbell. A second peak
mid-foot.158,159 The trunk repositions from an inclined to in the knee extensor (1.5 to 2.5 NmkgBM1) and ankle
vertical position. These events increase the ankle plantar plantar flexor (0.6 to 2 NmkgBM1) NJM occurs.138,153,161-
163
flexion and knee extensor NJM and decrease the hip exten- In a longitudinal analysis of national and international
sor and lumbar spine NJM.138,145,153,161,163 The dorsiflexion caliber lifters, Garhammer133,156 observed that the knee
at the ankles results in anterior translation of the tibia, extensor NJM was particularly reflective of changes in per-
thigh, and pelvis, and it is during this phase that the barbell formance (whether positive or negative). As load increases,
makes contact with the upper thighs or pelvis. It is impor- knee extensor joint angular power during the SP also
tant to consider that at this point, the barbell has reached increases, but not ankle plantar-flexor or hip extensor joint
its maximum posterior horizontal displacement. Therefore, angular power.163 Knee extensor joint angular power (NJM
as the barbell continues to travel vertically, it brushes against joint angular velocity) is also less variable than either hip
the forward-moving thighs and pelvis, as opposed to the extensor or ankle plantar flexor joint angular power.172
410 SECTION II • Applied Biomechanics of Selected Sport Activities
These data highlight the importance of the knee extensors System Mechanics of the Snatch and Clean
for generating propulsion during the SP. The systematic activation of muscles during the first five
The SP is completed when the barbell reaches maximum phases of the snatch and clean result in a coordinated move-
vertical velocity. Contrary to popular belief, the knees do ment designed to displace a barbell of maximum weight in
not fully extend at the end of the SP.153,154,157,166,167 For elite the vertical and horizontal directions such that the lifter can
men lifters, the angle of the knees at the end of the SP is receive the barbell overhead or on the shoulders.146,149,166 In
approximately 160°, whereas lower caliber men lifters reach the snatch, the barbell must be raised vertically to approxi-
a knee angle of 145° to 150° and elite women approxi- mately 60% of the lifter’s height, whereas for the clean, the
mately 165°. Simultaneous to knee extension, the hips fully barbell must be raised to approximately 50% of the lifter’s
extend (reaching 180° 10°) and the ankles reach 20° to height.153,177 Mechanically, the work performed to raise the
30° of plantar flexion, with the heels raising off the barbell these distances is a combination of a change in
ground.153,154,157,165-167 At the end of the SP, the knee NJM potential and kinetic energies.177,178 The change in potential
shifts from extensor to flexor.162 The knee flexor NJM likely energy of the barbell is calculated from the displacement of
prevents hyperextension of the knee and prepares the lifter the barbell from the floor to the height attained at the end
for the pulling-under-the-bar phase. of the SP and the change in kinetic energy is calculated from
Although the vertical momentum generated during the the peak vertical velocity minus the initial velocity of the
SP results in additional gain in barbell height, the lifter must barbell.30,178,179 As the lifter’s body rises, there is a change
rapidly reposition the body under the barbell to receive it in potential energy to elevate the lifter’s center of mass.30,178
overhead or on the shoulders. The acceleration of the Work performed and changes in energy can also be
lifter’s center of mass during the pull under phase calculated for a specific phase of the snatch or clean, such as
approaches 15 ms2, indicating that he or she is not in free the SP.30,157,178,179
fall, but is actively interacting with the barbell.173 As with The majority of the work performed during the pulling
any object in free fall, the center of mass of the system obeys phase is to elevate the barbell, followed by work performed
the principles of projectile motion; however, the lifter is able to raise the lifter’s center of mass and finally work per-
to reposition his or her body relative to the barbell by formed to achieve the peak vertical velocity of the bar-
actively pulling on the barbell. The negative acceleration of bell.178 A small amount of work is also performed to move
the barbell is offset by the active interaction between the the barbell in the anterior-posterior directions; however,
lifter with the barbell. This motion is aided by the with type A and B trajectories, this work should be mini-
hamstring, tibialis anterior, trapezius, and biceps brachii mal. From analysis of elite weightlifters at the national and
muscles.147,164,174 international level, greater than 95% of the total work done
When performed properly, the lifter receives the barbell in the snatch and clean should be performed in the vertical
in the overhead or front squat position and transitions from direction.144,156 Greater horizontal work is performed when
the pull-under to the amortization phase when the barbell a lifter uses the type C trajectory as well as deviations of the
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 411
typical type A and B trajectories, as did Zaitsev, of the taller lifters requiring greater barbell velocity than shorter
Soviet Union, in the 1978 World Weightlifting Champion- lifters.31,144,153,154,157,167
ships. While winning the 110-kg class in 1978, Zaitsev Women tend to achieve greater peak vertical velocities
employed an uncharacteristic type-A trajectory, with the when compared with men, despite being slightly shorter than
barbell being caught forward of the vertical reference men.157 This translates to a greater relative peak barbell
line.144 It should be noted that in the same year, Rigert, height, resulting in the barbell falling a greater distance to the
also of the Soviet Union, cleaned a then–world record lowest position in the amortization phase. Based on elite men
223 kg weighing 94.4 kg with a 97% efficiency compared weightlifters, an acceptable drop distance in either the snatch
with Zaitsev, who cleaned 220 kg weighing 109 kg with or clean is 10 to 15 cm (3.9 to 5.9 inches),153,154,157,167,175
90% efficiency.144 Rigert’s lift was performed with a type-B whereas elite women are observed to have a drop distance
trajectory. ranging from 19 to 47 cm (7.5 to 18.5 inches).157,173,180 This
An additional source of inefficient energy expenditure suggests that women should be capable of lifting heavier
arises from elevating the barbell higher than is required to weights; however, the technical differences discussed previ-
receive it in either the overhead or front squat position. This ously (i.e., less knee extension during the FP) may be a limit-
can occur either by extending the knees beyond 160° while ing factor in pulling heavier weights during the FP and into
generating propulsion during the SP or by reaching an the SP position.
excessive peak vertical barbell velocity. The former has been A consideration of power output during the pulling phase
observed in elite Greek women compared with elite Greek provides useful information about differences between men
men,157 and college versus international165 weightlifters. and women. Power is calculated from the mechanical work
The latter is often observed in women157,173,180 as well as performed divided by the time required to perform work.30,179
during submaximal attempts.147,181 In both laboratory in- Typically, power has been calculated for the entire pulling
vestigations and studies of lifters in competition, peak verti- phase (i.e., from lift-off to peak vertical barbell velocity)
cal barbell velocity is lower for maximum attempts than and during the SP only (Table 16-8).30,31,144,178 For ease
submaximum attempts.147,182 The lower barbell velocity of analysis, work performed and power generated on the
also corresponds to changes in vertical ground reaction barbell rather than the lifter-barbell system can also be
forces, which decrease with increasing load.147,182 In addi- determined.142,157,178,179,183 It should be noted that this
tion, the shape of the force-time curve appears as a “U” calculation results in the average power during the given
shape as opposed to a “V” shape for maximum lifts, phase, and not the peak power generated. For elite men
indicating that rather than higher peak forces, heavier weightlifters, power output during the snatch and clean is
lifts are characterized by near-maximal force applied for a similar for the same individual, whether evaluating the entire
longer period (Figure 16-14).171 Elevating the barbell to a pulling phase or the SP alone.30,144 This suggests that at the
greater height by an increase in either or both potential elite level, technical abilities have been optimized and that the
or kinetic energies requires greater work to be performed. limiting factor in the snatch and clean is the ability for muscles
This greater amount of work, however, could be performed to perform work. For lower caliber lifters, differences in
on a heavier barbell, lifting it to the minimum height power generated during maximum snatch and clean attempts
required to pull under and receive the barbell. A peak may be indicative of technical errors; therefore, assessing
vertical barbell velocity of 1.6 to 2 ms1 in the snatch and power generating capability can be used as a pedagogical
1.4 to 1.8 ms1 in the clean appears to be sufficient, with tool.30,178
Figure 16-14
Theoretical shift from V- to U-shaped force-time curve. (Adapted from Garhammer J, Gregor R:
Propulsion forces as a function of intensity for weightlifting and vertical jumping, J Appl Sport Sci
Res 6[3]:131, 1992, using data from Häkkinen, et al, Scand J Sports Sci 6[2]:57-66, 1984.)
412 SECTION II • Applied Biomechanics of Selected Sport Activities
Table 16-8
Average Barbell Power for World and Olympic Champions During the Snatch, Clean, and Jerk
Average Power Output (W)
67.5 82.5 110⫹
Competition Lift 52 kg 56 kg 60 kg kg 75 kg kg 90 kg 100 kg 110 kg kg
1978 World Snatch—pull 1619 2018 2460 2675 3057 3139 3216 3542 4021
Championships144 Snatch— 2784 3187 3239 3892 4765 4976 5243 5212 6088
Second pull
Clean—pull 1453 2200 2149 2803 2858 2837 3246 3877
Clean— 2470 3364 2762 4846 4630 4700 5291 4387
Second pull
Jerk 2515 3451 2948 5060 4495 5072 5080
1984 Olympic Snatch—pull 1770 2533 2423 2920 3671
Games31 Snatch— 3190 4052 3689 4714 5442
Second pull
Clean—pull 1677 2600 2268 2772 3360
Clean— 3142 3877 3543 4983 6120
Second pull
Jerk 2825 3804 3548 4170 4321
Note: Data were not available for each lift for every athlete.
In elite men weightlifters, 31 to 37 WkgBM1 power in eccentrically extending the knee and concentrically
is generated during the entire pulling phase and 45 to extending the hip at the end of the FP.161-163
60 WkgBM1 during the SP.144 Power output for elite men
weightlifters has remained relatively constant since the late
1970s, which parallels the small increases in the world Clinically Relevant Points Regarding the Snatch
records to the present day.150 In the inaugural women’s and Clean
world championships in 1987, power output averaged 62%
for the entire pulling phase and 73% for the SP relative to • Consist of seven distinct phases
power generated by men (Table 16-9).141 At the same time, • The pulling phases (first pull, second knee bend, second pull)
require muscle forces to elevate the lifter and barbell (i.e.,
the women’s world records in the long jump and high jump
propulsion)
were 85% of the records for men.141 Given that the BW of
• The pull under and amortization phases require muscle forces to
elite women jumpers at the time was 85% that of men, it can absorb impulse (i.e., braking)
be estimated that women generated approximately 72% • Requires a coordinated sequence of muscle actions to lift the
(85% jump 85% BW) as much power as men in perform- barbell through an appropriate trajectory
ing world record jump attempts.141 Thus, the power output • Excessive elevation of the barbell is energetically inefficient
generated during the SP is appropriate given physiological • The hip extensor and ankle plantar-flexor muscles are primarily
differences between men and women. However, the power used to maintain proper body posture during the pulling phase
generated during the FP and entire pulling phase is lower • The quadriceps and hamstrings are primarily used to generate
than would be expected. propulsion during the pulling phase
Analysis of more recent lifts by women indicate that • In receiving the barbell, a lifter actively repositions the body from
an upright to a squatting position
power generated during the SP approaches 80% of power
generated by men158,183; however, power generated during
the FP and entire pulling phase has not increased, despite a
considerable increase in the women’s world records for
the snatch and the clean and jerk. Thus, while women are Segment Mechanics of the Split Jerk
capable of generating large muscular forces during the Considerably less research exists for the jerk than the snatch
mechanically advantageous SP, they are limited by their or clean. A major difference between the jerk versus the
ability to generate muscular forces during the mechanically snatch and clean is that the lifter begins the jerk movement
disadvantageous FP. In particular, the strength of the ham- in an upright posture, which reduces the importance of the
string muscles should be considered because of its role hip and back extensor musculature that are essential for the
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 413
FP and SKB. The jerk has been broken into seven distinct mum velocity. The peak downward velocity of the barbell
phases: (1) preliminary half squat, (2) active half squat, ranges from 0.9 to 1 ms1 and the knees reach an angle of
(3) braking, (4) thrust, (5) push under the bar, (6) support, approximately 130°.148,185 Elite lifters have been observed
and (7) recovery (Figure 16-15).184,185 Weightlifting coaches performing these phases faster than lower-caliber lifters,
often refer to the jerk as a dip and drive and split. The dip achieving a higher downward barbell velocity and displaying
consists of phases 1 and 2, the drive phases 3 and 4, and the a shorter time to peak velocity.185,186 During the preliminary
split phases 5, 6, and 7. half-squat phase of the jerk, and the mechanically similar
The preliminary half squat consists of the lifter flexing push press, a knee flexor NJM is observed.137,187,188 No seg-
the knees and dorsiflexing the ankles, ending when the bar- ment kinetic analyses of the hip and ankle exist for the jerk;
bell begins to move downward. This initiates the active half however, an analysis of the push press, which involves a similar
squat, which ends when the falling barbell reaches maxi- dip and drive motion found minimal ( 0.5 NmkgBM1)
Table 16-9
Comparison of Relative Power Output for Men and Women World Champions in the Snatch and Clean
Average Power Output (WkgBM1)
Snatch—Pull Snatch—Second Pull Clean—Pull Clean—Second Pull
Men—1978 World 34.4 2.5 52.7 4.5 34.2 3.6 52.5 8.9
Champions
Women—1987 World 22.5 1.7 40.1 5.0 21.0 1.8 38.2 3.3
Champions
% (Women/men) 65.4 76.1 61.4 72.8
Data from Garhammer J: A comparison of maximal power outputs between elite male and female weightlifters in competition, Int J Sport
Biomech 7:3–11, 1991.
Figure 16-15
The seven phases of the split jerk.
414 SECTION II • Applied Biomechanics of Selected Sport Activities
hip extensor and ankle plantar flexor NJM during the initial under the barbell, accelerating his or her body downward at
dip motion.137 The knee flexor NJM likely increases the rate 14 ms-2, which imparts additional vertical impulse to the
of performing the half squat, whereas the low hip and ankle barbell.173 If performed properly, the barbell should be
NJM minimize resistance to movement. received overhead at the instant it reaches its apex.
As the barbell attains maximum downward velocity, the
braking phase begins, ending when the knees reach maxi-
mum flexion. An additional 10° knee flexion occurs during System Mechanics of the Split Jerk
the braking phase, with the knee extensors actively resist During the “dip and drive” in the jerk, the optimal down-
further flexion.159 A rapid rise in the knee extensor NJM ward displacement of the lifter’s center of mass ranges from
has been observed during this phase of the jerk and push 10% to 12% of the lifter’s height.186,190 A larger downward
press, as well as a large increase in vertical ground reaction displacement indicates that the half squat was not per-
force during the jerk.137,147,148,187,188 The rapid rise in formed rapidly enough or insufficient muscular force was
ground reaction force during the braking phase is similar to generated during the braking phase. The larger downward
what is observed during the SKB phase of the snatch and displacement results in longer thrust duration.185 Interest-
clean, as well as during the squat in a countermovement ingly, longer thrust duration is associated with higher peak
jump.145,147,148,171 The combined knee flexion with a rap- vertical barbell velocity and a higher peak height of the
idly increasing knee extensor NJM is indicative of a stretch- barbell; however, these are characteristic of low caliber
shortening cycle movement. Shortly after maximum knee rather than elite weightlifters.185 These data are indicative of
flexion is attained, there is elastic deformation of the ends the importance of the push-under-the-bar phase, which,
of the barbell, resulting in the ends of the barbell dropping when performed properly, imparts sufficient vertical mo-
lower than the center, increasing the load on the knee mentum to the barbell that the athlete is able to reposition
extensors.188 into the split position and receive the barbell overhead.190
As the ends of the barbell reach their minimum height, The longer-duration thrust phase may be an indicator
the knees begin to extend, initiating the thrust phase. Simi- of inefficient energy expenditure.178 The greater change
lar to the SP in the snatch and clean, the end of the jerk in potential energy during the thrust phase, and higher
thrust phase occurs when the barbell has reached maximum peak vertical barbell velocity at the end of the thrust phase
velocity.30 The peak vertical velocity of the barbell should increase the mechanical work that must be performed;
exceed 1.6 ms1, with taller lifters requiring a greater veloc- however, power output is lower. As with the snatch and
ity than shorter lifters.144,185,186 It has been observed that clean, it is preferable to perform the same amount of work
the ratio between the peak upward velocity to the peak to lift a heavier barbell, rather than to lift a lighter barbell
downward velocity increases with the caliber of athlete.186 to a greater height. A long duration of the thrust phase
As peak downward velocity is also higher for better will also reduce power output during the jerk. Typically,
lifters,185,186 it highlights the importance of applying a large in elite lifters, the average power during the jerk is com-
impulse to impart momentum to the barbell. This impulse parable to the power generated during the SP of the
is predominantly generated by the knee extensor and ankle snatch and clean.30,144 However, some elite lifters gener-
plantar flexor muscles.137,187,188 The large co-contraction of ate considerably less power during the jerk than either the
the quadriceps and hamstring muscles147,148 combined with snatch or clean, which may suggest a technical fault, such
the high knee extensor NJM (4 NmkgBM1)187,188 indi- as dipping too low or extending the duration of the thrust
cate that the muscular force generated by the quadriceps phase.30,178
during the jerk is considerably high.
As with the snatch and clean SP, the knees do not fully
extend during the jerk thrust. At the end of the thrust phase Clinically Relevant Points Regarding the Split Jerk
and start of the push-under-the-bar phase, the knees are
• The jerk requires the rapid reversal of knee flexion to knee exten-
extended to approximately 150° to 160°.185,186 An increase
sion to apply vertical impulse to the barbell
in the ankle plantar flexor NJM137 indicates that the lifter
• During this knee flexion and extension, the quadriceps are active,
raises onto his or her toes; however, this may not be occur- first eccentrically then concentrically, to generate propulsion
ring to increase the height of the barbell. Rather, as in • The contribution of the arms to elevating the barbell is minimal
walking and running, the activation of the biarticular gas- • Excessive elevation of the barbell is energetically inefficient
trocnemius muscle at toe-off may contribute to flexing the • The lifter begins to split his or her legs fore and aft before the
knee for the forward step.189 Similarly, the knee of the rear- knees fully extend
moving leg must also flex. As the feet are rapidly removed • The splitting motion applies additional vertical impulse to elevate
from the platform, additional impulse is applied to the bar- the barbell
bell, increasing its vertical momentum.190 Prior to the • The arms are used to push the lifter under the barbell
barbell leaving the shoulders, the lifter aggressively pushes
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 415
in the sport prior to 1972, when the press was used in com-
Injuries in Weightlifting petition. During the decade preceding its removal from
There is considerable discussion of the potential for injuries competition, the press had evolved from a strict upright
when performing weightlifting movements and their pressing motion to one that involved an initial hyperex-
variations.191-199 In considering the incidence of injuries, it tended trunk that preceded a rapid hip flexion–hip exten-
is important to distinguish weightlifting, either as a sport or sion motion sequence. It was speculated that the hyperex-
as training exercises, from other forms of resistance exercise tension under load would injure the low back.191 In 1978,
because the muscles and joints stressed as well as the nature Rossi197 reported 21 of 58 weightlifters with low back pain
of the stresses are often different. Long-term assessments of had spondylolysis; however, in a follow-up paper in 1990,209
weightlifters of varying abilities indicate that the incidence an additional 39 weightlifters presented with low back pain,
of injuries ranges from 2.4 to 3.3 per one thousand partici- but only one had spondylolysis. This provides support for
pation hours.191,196 The incidence of injuries in youth and the notion that the press contributed to the incidence of
adolescents is considerably lower.199,200 Injuries in weight- spondylolysis, and not the snatch, clean, or jerk movements.
lifting appear to be influenced by the weight of the barbell, In today’s weightlifter, the majority of injuries appear to
and acute and long-term fatigue.191,198 The most common be muscle strains as a result of the high training volumes
injuries involve the low back and knee followed by the typically used.191
shoulder, wrist, and hand.191,196,198,201 The majority of these Similarly, the majority of knee injuries appear to be
injuries are acute (60%) rather than chronic (30%) or recur- strains to the quadriceps tendon or patellar ligament.191 It
ring (10%).61 Most injuries to the low back (87%), knee is commonly believed that the “bouncing” nature of the
(95%), and shoulder (92%) required less than one day to amortization phase of the clean, snatch, and jerk will re-
resolve and rarely more than one week.191 Typically, these sult in injury to the knee joint, particularly the patellar
injuries were classified as a muscle strain or tendinitis.191 ligament.211 Zernicke and colleagues188 reported a patel-
More serious, although rare, injuries have been reported in lar ligament rupture during the braking phase of an
competition, which include dislocation of the lunate,202,203 attempted jerk of 175 kg by an 82.5-kg lifter in competi-
wrist fractures,204,205 dislocation of the elbow,195 and rup- tion, in which the knee extensor NJM was 550 to
ture of the patellar ligament.188 560 Nm and the tension in the ligament was estimated to
be 14.5 KN. Prior to the moment of rupture, the knee
extensor NJM peaked at 400 Nm and began to decrease
as the barbell oscillated, first downward, then upward.
However, a second downward oscillation of the barbell
Injuries in Weightlifting
led to a rapid increase in the knee extensor NJM, result-
Chronic ing in rupture of the patellar ligament 0.06 seconds later.
• Tendinosis—quadriceps tendon, patellar ligament An analysis of a 165-kg jerk by a 104-kg lifter in a labora-
• Spondylolysis (Note: the incidence of spondylolysis in weightlifting tory setting reported a peak knee extensor NJM of
has rarely been reported since the elimination of the clean and 350 Nm.187 Knee extensor NJM during the amortization
press from competition in 1972) phase of the clean preceding the 165-kg jerk peaked at
Acute 400 Nm.187 Normally, the braking phase of the jerk and
• Tendinitis—quadriceps tendon, patellar ligament, shoulder rotator amortization phase of the snatch and clean is reportedly
cuff tendons and biceps tendon at least 2.5 times longer than that found during the
• Muscle strains—quadriceps, shoulder muscles especially biceps ligament rupture, which would result in a substantially
and rotator cuff, lumbar spine muscles lower loading rate and less peak demand on the quadri-
• Fractures/dislocations—carpal bones, elbow (Note: these injuries ceps tendon and patellar ligament.159,175,185,186 Thus, the
are not common and are typically associated with maximum lifts
second oscillation of the barbell may have been abnormal,
in competition)
and its high loading rate ultimately led to the patellar
ligament rupture.188
When evaluating the potential for knee injuries during
weightlifting, two factors must be considered when as-
A potential concern in the low back is spondylolysis sessing the supposed stress due to “bouncing.” First, the
(fracture of the pars interarticularis), which was reported to ultimate tensile strength of viscoelastic tissues, such as the
have a high incidence in the 1970s and 1980s.197,206-209 The patellar ligament, increases with strain rate.188,212,213 While
mechanism of injury for pars interarticularis fracture is spi- the loading rate reported by Zernicke and colleagues188
nal hyperextension, which is augmented by heavy load- was high, it appears to be considerably higher than that
ing.210 It should be noted, however, that a majority of observed during normal performance of the jerk, as well
weightlifters examined in these investigations participated for the snatch and clean.137,153,163-165,187 Thus, a controlled
416 SECTION II • Applied Biomechanics of Selected Sport Activities
“bounce” may actually afford greater protection for the to the article date (1982); thus, if they were competitive
quadriceps tendon and patellar ligament than a slower weightlifters, they would have competed in the press.
descent. In addition, slower squats are more likely to Because of the similarity in motion for the press and
avulse the bony attachment than rupture the tendon and bench press, it is reasonable to expect that similar injuries
ligament midsubstance because of the different viscoelas- may occur for both exercises. However, the propulsive
tic properties of tendon and ligament compared with forces during the jerk are generated primarily by the lower
bone.212,214 With advances in modeling technology, future extremities163,187,188 and the weight of the barbell is only
research should investigate the stresses imposed on these supported by the shoulders in the extended position,
and other soft tissues during rapid dynamic movements as opposed to when flexed as occurs during pressing
such as those occurring in weightlifting. exercises.
The second factor to consider is the soft tissue reaction Retrospective assessments of active and retired weight-
forces that occur in a deep squat. Zelle and colleagues176 lifters supports the notion that weightlifting exercises are
found that in an unloaded deep squat, thigh-calf contact not inherently dangerous, nor do injuries during weight-
resulted in reaction forces of 34% of BW, acting approxi- lifting result in long-term disability.192,193,221 The inci-
mately 15 cm (5.9 inches) from the knee axis of rotation. dence of low back, hip, knee and shoulder osteoarthritis
This would result in a moment extending the knee of ap- is no greater and in some cases less than the general
proximately 0.5 NmkgBM1, whereas the NJM flexing population.193 The use of free weight training alone is
the knee in an unloaded squat with thigh contact is ap- associated with a low relative risk for lumbar and cervical
proximately 1 NmkgBM1.215 Although it is unknown disc herniation.221 Kujala et al.194 has reported a higher
what the effect of soft tissue contact is on knee extensor incidence of tibiofemoral joint osteoarthritis in weight-
NJM during the snatch and clean, this factor may consid- lifters than in runners and shooters, and patellofemoral
erably reduce the stress imposed on the quadriceps tendon joint osteoarthritis than runners, shooters, and soccer
and patellar ligament during these movements. Clearly, players. However, the 29 weightlifters selected for
more research is required on this topic to assess the practi- this investigation were a subsample of 40 weightlifters
cal implications of soft tissue contact during human who had responded to an initial survey, which may
movement. skew the actual incidence of these degenerative condi-
A recent case study has cast doubt on whether chronic tions. The results are further confounded by the number
pain and morphological changes to the patellar ligament of years the weightlifters participated in occupations
result in weakening of the tissue.216 Patellar tendinosis was involving kneeling and squatting and heavy labor com-
diagnosed in an international caliber weightlifter from ultra- pared with the other athlete groups. Finally, as the
sound evidence of local widening of the ligament with focal technique and mechanics of weightlifting have evolved
hypoechoic areas, irregular fiber structure, and neovascular- since 1972, it is important to continue to assess the
ization. Treatment of the neovascularization with a scleros- long-term effect of training and competition on joint
ing agent (polidocanol) resulted in a decrease in pain and health.
return to training in 2 weeks (including performing deep
squats with 240 kg). Ligament morphology was unchanged
at 2- and 4-month follow-ups, except a reduction of neo-
Conclusion
vascularization. Similar results were reported in a larger The biomechanics of weight training is complex because
study of various athletes who returned to physical activity of the various kinetics, kinematics, muscle activity, and
after sclerosing treatment without ligament morphological pathological conditions of each respective body part.
changes.217 Significant muscle activity is relevant to specific tasks and
The incidence of shoulder instability has been reported movements, as is the coordination of muscles activated.
to be high in weightlifters.196 However, most of these Compressive, tensile, and shear forces can be high with
reports have generally presented cases of recreational various forms of specific exercises, which may be signifi-
weight trainers and not competitive weightlifters.218-220 cant for individuals with pre-existing pathological condi-
Cahill218 reported 19 cases of osteolysis of the distal tions. It is recommended the clinician use the included
clavicle requiring surgery, of which all performed weight information in this chapter to prescribe the most effica-
training, and four were identified as “competitive weight- cious exercise program for their clients. In particular, cli-
lifters.” However, the bench press and parallel bar dip nicians should consider how the mechanics of an exercise
exercises were implicated as contributing to most of these load the body, as well as how modifications of these
injuries. As these exercises are rarely performed by com- mechanics may increase effectiveness and reduce risk of
petitive weightlifters,134,140,190 it is possible that some or injury. This is especially relevant for those clients with a
all of these four cases were powerlifters. Furthermore, pathologic conditions of a particular body part that may
three of the four were followed up for 10 to 11 years prior respond less favorably to excessive forces.
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 417
References 22. McGill SM: Electromyographic activity of the abdominal and low
back musculature during the generation of isometric and
1. Bergmark A: Stability of the lumbar spine. A study in mechanical dynamic axial trunk torque: Implications for lumbar mechanics,
engineering, Acta Orthop Scand [Suppl] (230):1–54, 1989. J Orthop Res, 9:91–103, 1991.
2. Crisco JJ 3rd, Panjabi MM: The intersegmental and multiseg- 23. Cholewicki J, Van Velt JJ: Relative contribution of trunk muscles
mental muscles of the lumbar spine, A biomechanical model to the stability of the lumbar spine during isometric exertions,
comparing lateral stabilizing potential, Spine 16:793–799, 1991. Clin Biomech 17:99–105, 2002.
3. Gardner-Morse M, Stokes IA, Laible JP: Role of muscles in lum- 24. McGill SM. Ultimate back fitness and performance, Waterloo,
bar spine stability in maximum extension efforts, J Orthop Res Ontario, Canada, 2004.Wabuno.
13:802–808, 1995. 25. Chandler TJ, Stone MH: The squat exercise in athletic conditioning:
4. Cholewicki J, McGill SM: Mechanical stability of the in vivo A review of the literature, Natl Strength Condit Assoc J 13:52–58,
lumbar spine: Implications for injury and chronic low back pain, 1991.
Clin Biomech 11:1–15, 1996 26. Hattin HC, Pierrynowski MR, Ball KA: Effect of load, cadence,
5. Cholewicki J, Panjabi MM, Khachatryan A: Stabilizing function and fatigue on tibio-femoral joint force during a half squat, Med
of trunk flexor-extensor muscles around a neutral spine posture, Sci Sports Exerc 5:613–618, 1989.
Spine 22:2207–2212, 1997. 27. McLaughlin TM, Dillman CJ, Lardner TJ: A kinematic model of
6. Granata KP, Marras WS: Cost-benefit of muscle cocontraction in performance in the parallel squat by champion powerlifters, Med
protecting against spinal instability, Spine 25:1398–1404, 2000. Sci Sports 2:128–133, 1977.
7. Magnusson ML, Aleksiev A, Wilder DG, et al: Unexpected load 28. McLaughlin TM, Lardner TJ, Dillman CJ: Kinetics of the parallel
and asymmetric posture as etiologic factors in low back pain, Eur squat, Res Q 2:175–189, 1978.
Spine J 5:23–35, 1996. 29. Coaches’ Roundtable. The squat and its application to athletic
8. Hodges PW, Richardson CA: Delayed postural contraction of performance, Natl Strength Condit Assoc J 6:10–22, 1984.
transversus abdominis in low back pain associated with move- 30. Garhammer J: Power production by Olympic weightlifters, Med
ment of the lower limb, J Spinal Disor 11:46–56, 1998. Sci Sports Exerc 1:54–60, 1980.
9. Hodges PW, Richardson CA: Altered trunk muscle recruitment 31. Garhammer J: Biomechanical profiles of Olympic weightlifters,
in people with low back pain with upper limb movement at Int J Sports Biomech 1:122–130, 1985.
different speeds, Arch Phys Med Rehabil 80:1005–1012, 32. Hutton WC, Adams MA: Can the lumbar spine be crushed in
1999. heavy lifting? Spine 7:586–590, 1982.
10. Radebold A, Cholewicki J, Panjabi MM, Patel TC: Muscle 33. Schultz AB, Andersson GBJ: Analysis of loads on the lumbar
response pattern to sudden trunk loading in healthy individuals spine, Spine 6:76–82, 1981.
and in patients with chronic low back pain, Spine 25:947–954, 34. Delitto RS, Rose SJ, Apts DW, Electromyographic analysis of two
2000. techniques for squat lifting, Phys Ther 67:1329–1334, 1987.
11. Panjabi MM: The stabilizing system of the spine. Part I. Function 35. Hart DL, Stobbe TJ, Jaraiedi M: Effect of posture on lifting,
dysfunction, adaptation, and enhancement, J Spinal Disord Spine 12:138–145, 1987.
5:383–389, 1992. 36. Holmes JA, Damaser MS, Lehman SL: Erector spinae activation
12. Lucas DB, Bresler B: Stability of the ligamentous spine, Report no. and movement dynamics about the lumbar spine in lordotic and
40 from the Biomechanics Laboratory, University of California, kyphotic squat-lifting, Spine 17(3):327–334, 1992.
San Francisco, Berkeley, 1961. 37. Floyd WF, Silvers PHS: The function of the erector spinae
13. Crisco JJ, Panjabi MM, Yamamoto I, et al: Euler stability of muscles in certain movements and postures in man, J Physiol
the human ligamentous lumbar spine: Part II experiment, Clin 129:184–203, 1955.
Biomech 7:27–32, 1992. 38. Floyd WF, Silvers PHS: Function of erector spinae in flexion of
14. Cromwell R, Schultz AB, Beck R, et al: Loads on the lumbar the trunk, Lancet 1:133–134, 1951.
trunk during level walking, J Orthop Res 7:371–377, 2005. 39. Toussaint HM, de Winter AF, de Haas Y, et al: Flexion relaxation
15. El-Rich M, Shirazi-Adl A, Arjmand N: Muscle activity, internal during lifting: Implication for torque production by muscle activ-
loads, and stability of the human spine in standing postures: ity and tissue strain at the lumbo-sacral joint, J Biomechanics
Combined model and in vivo studies, Spine 29:2633–2642, 28(2):199–210, 1995.
2004. 40. Gill KP, Bennett SJ, Savelsbergh GJP, et al: Regional changes in
16. Gibbons SGT, Comerford MJ: Strength versus stability. Part 1: spine posture at lift onset with changes in lift distance and lift
Concept and terms, Orthop Division Rev March/April:21–27, style, Spine 32(15):1599–1604, 2007.
2001. 41. Shirazi-Adl A, El-Rich M, Pop DG, Parninpour M: Spinal muscle
17. Solomonow M, Zhou B-H, Bratta RV, et al: Biomechanics and forces, internal loads and stability in standing under various pos-
electromyography of a cumulative lumbar disorder: Response to tures and loads-application of kinematics-based algorithm, Eur
static stretching, Clin Biomech 18:890–898, 2003. Spine J 14(4):381–392, 2005.
18. Lavender SA, Tsuang YH, Andersson GB, et al: Trunk muscle 42. Bazrgari B, Shirazi-Adl A, Arjmand N: Analysis of squat and
cocontraction: The effects of moment direction and moment stoop dynamic liftings: Muscle forces and internal spinal loads,
magnitude, J Orthop Res 10:691–700, 1992. Eur Spine J 16(5):687–699, 2007.
19. Kavcic N, Grenier S, McGill SM: Determining the stabilizing 43. Bazrgari B. Shirazi-Adl A: Spinal stability and role of passive
role of individual torso muscles during rehabilitation exercises, stiffness in dynamic squat and stoop lifts, Comput Methods
Spine 29:1254–1265, 2004. Biomech Biomed Engin 10(5):351–360, 2007.
20. Pope MH, Andersson GB, Broman H, et al: Electromyographic 44. Arjmand N, Shirazi-Adl A: Biomechanics of changes in lumbar
studies of the lumbar trunk musculature during the development posture in static lifting, Spine 30(23):2637–2648, 2005.
of axial torques, J Ortho Res 4:288–297, 1986. 45. Hwang S, Kim Y, Kim Y: Lower extremity joint kinetics and lum-
21. Aspden RM: The spine is an arch. A new mathematical model, bar curvature during squat and stoop lifting, BMC Musculoskel Dis
Spine 14:266–274, 1989. 10:15, 2009.
418 SECTION II • Applied Biomechanics of Selected Sport Activities
46. Brown SHM, McGill SM: How the inherent stiffness of the in 67. Arokoski JP, Valta T, Airaksinen O, et al: Back and abdominal
vivo human trunk varies with changing magnitudes of muscular muscle function during stabilization exercises, Arch Phys Med
activation, Clin Biomech 23:15–22, 2008. Rehabil 82:1089–1098, 2001.
47. Cappozzo A, Felici F, Figura F, et al: Lumbar spine loading 68. Souza GM, Baker LL, Powers CM: Electromyographic activity of
during half-squat exercises, Med Sci Sports Exerc 17:613–620, selected trunk muscles during dynamic spine stabilization exercises,
1985. Arch Phys Med Rehabil 82:1551–1557, 2001.
48. Cholewicki J, McGill SM, Norman RW: Lumbar spine loads 69. Drake JDM, Fischer SL, Brown SHM, et al: Do exercise balls
during the lifting of extremely heavy weights, Med Sci Sports provide a training advantage for trunk extensor exercises? A bio-
Exerc 23:1179–1186, 1991. mechanical evaluation, J Manipulative Physiol Ther 29:354–362,
49. Adams MA, McNally DS, Chinn H, et al: Posture and the 2006.
compressive strength of the lumbar spine, Clin Biomech 9:5–14, 70. Stevens VK, Vleeming A, Bouche KG, et al: Electromyographic
1994. activity of trunk and hip muscles during stabilization exercises
50. Gunning JL, Callaghan JP, McGill SM: The role of prior loading in four-point kneeling in healthy volunteers, Eur Spine J 16:
history and spinal posture on the compressive tolerance and type 711–718, 2007.
of failure in the spine using a porcine trauma model, Clin 71. Arokoski JPA, Kankaanpää M, Valta T, et al: Back and hip exten-
Biomech 16(6):471–480, 2001. sor muscle function during therapeutic exercises, Arch Phys Med
51. McGill SM: Biomechanics of low back injury: Implications on Rehabil 80:842–850, 1999.
current practice and the clinic, J Biomech 30(5):465–475, 72. Vera-Garcia FJ, Grenier SG, McGill SM: Abdominal muscle
1997. response during curl-ups on both stable and labile surfaces, Phys
52. Kumar S: Upper body push-pull strength of normal young Ther 80:564–569, 2000.
adults in sagittal plane at three heights, Ind Ergon 15:427–436, 73. Marshall PW, Murphy BA: Core stability exercises on and off a
1995. Swiss ball, Arch Phys Med Rehabil 86:242–249, 2005.
53. Caldwell JS, McNair PJ, Williams M: The effects of repetitive 74. Behm DG, Leonard AM, Young WB, et al: Trunk muscle
motion on lumbar flexion and erector spinae muscle activity in electromyographic activity with unstable and unilateral exercises,
rowers, Clin Biomech 18(8):704–711, 2003. J Strength Cond Res 19(1):193–201, 2005.
54. Anderson K, Behm DG: Maintenance of EMG activity and loss 75. Arokoski JPA, Valta T, Kankaanpää M, et al: Activation of lumbar
of force output with instability, J Strength Cond Res 18:637–640, paraspinal and abdominal muscles during therapeutic exercises in
2004. chronic low back pain patients, Arch Phys Med Rehabil 85:
55. Schibye B, Sogaaro K, Martinsen D, et al: Mechanical load on 823–832, 2004.
the low back and shoulders during pushing and pulling of two 76. Escamilla RF, Babb E, DeWitt R, et al: Electromyographic analy-
wheeled waste containers compared with lifting and carrying of sis of traditional and nontraditional abdominal exercises: Implica-
bags and bins, Clin Biomech 16:549–559, 2001. tions for rehabilitation and training, Phys Ther 86(5):656–671,
56. Lett KK, McGill SM: Pushing and pulling: Personal mechanics 2006.
influence spine loads, Ergonomics 49(9):895–908, 2006. 77. Escamilla RF, McTaggart MSC, Fricklas EJ, et al: An electromyo-
57. Freeman S. Karpowicz A, Gray J, et al: Quantifying muscle graphic analysis of commercial and common abdominal exercises:
patterns and spine load during various forms of the pushup, Med Implications for rehabilitation and training, J Orthop Sports Phys
Sci Sports Exerc 38(3):570–577, 2006. Ther 36(2):45–57, 2006.
58. Howarth SJ, Beach TAC, Callaghan JP: Abdominal muscles 78. Escamilla RF, Bonacci L, Burnham T, et al: A biomechanical
dominate contributions to vertebral joint stiffness during the analysis of squatting and lunging type exercises, Med Sci Sports
push-up, J Appl Biomech 24:130–139, 2008. Exerc 38(5):S97, 2006.
59. Moreside JM, Vera-Garcia FJ, McGill SM: Trunk muscle activa- 79. Escamilla RF, Francisco AC, Fleisig GS, et al: A three-dimensional
tion patterns, lumbar compressive forces, and spine stability when biomechanical analysis of sumo and conventional style deadlifts,
using the Bodyblade, Phys Ther 87(2):153–163, 2007. Med Sci Sports Exerc 32(7):1265–1275, 2000.
60. Anders C, Wenzel B, Scholle HC: Activation characteristics of 80. DiGiovine NM, Jobe FW, Pink M, Perry J: Electromyography of
trunk muscles during cyclic upper-body perturbations caused by upper extremity in pitching, J Shoulder Elbow Surg 1:15–25,
an oscillating pole, Arch Phys Med Rehabil 89:1314–1322, 2008. 1992.
61. Juker D, McGill SM, Kropf P, et al: Quantitative intramuscular 81. Blanpied PR: Changes in muscle activation during wall slides and
myoelectric activity of lumbar portions of psoas and the abdominal squat-machine exercise, J Sport Rehabil 8(2):123–134, 1999.
wall during a wide variety of tasks, Med Sci Sports Exerc 30(2): 82. Dahlkvist NJ, Mayo P, Seedhom BB: Forces during squatting and
301–310, 1998. rising from a deep squat, Eng Med 11(2):69–76, 1982.
62. Axler C, McGill SM: Low back loads over a variety of abdominal 83. Escamilla RF, Fleisig GS, Zheng N, et al: Biomechanics of the
exercises: Searching for the safest abdominal challenge, Med Sci knee during closed kinetic chain and open kinetic chain exercises,
Sports Exerc 29(6):804–811, 1997. Med Sci Sports Exerc 30(4):556–569, 1998.
63. Willett GM, Hyde JE, Uhrlaub MB, et al: Relative activity of 84. Escamilla RF, Fleisig GS, Zheng N, et al: Effects of technique
abdominal muscles during commonly prescribed strengthening variations on knee biomechanics during the squat and leg press,
exercises, J Strength Cond Res 15(4):480–485, 2001. Med Sci Sports Exerc 33(9):1552–1566, 2001.
64. Stevens VK, Bouche KG, Mahieu NN, et al: Trunk muscle activ- 85. Hung YJ, Gross MT: Effect of foot position on electromyo-
ity in healthy subjects during bridging stabilization exercises, graphic activity of the vastus medialis oblique and vastus lateralis
BMC Musculoskelet Disord 20:75, 2006. during lower-extremity weight- bearing activities, J Orthop Sports
65. Ekstrom RA, Osborn RW, Hauer PL: Surface electromyographic Phys Ther 29(2):93–105, 1999.
analysis of the low back muscles during rehabilitation exercises, 86. Isear JA Jr., Erickson JC, Worrell TW: EMG analysis of lower
J Orthop Sports Phys Ther 38(12):736–745, 2008. extremity muscle recruitment patterns during an unloaded squat,
66. Ekstrom RA, Donatelli RA, Carp KC: Electromyographic Med Sci Sports Exerc 29(4):532–539, 1997.
analysis of core trunk, hip, and thigh muscles during 9 reha- 87. McCaw ST, Melrose DR: Stance width and bar load effects on
bilitation exercises, J Orthop Sports Phys Ther 37(12):754–762, leg muscle activity during the parallel squat, Med Sci Sports Exerc
2007. 31(3):428–436, 1999.
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 419
88. Mirzabeigi E, Jordan C, Gronley JK, et al: Isolation of the vastus 107. Toutoungi DE, Lu TW, Leardini A, et al: Cruciate ligament
medialis oblique muscle during exercise, Am J Sports Med forces in the human knee during rehabilitation exercises, Clin
27(1):50–53, 1999. Biomech 15(3):176–187, 2000.
89. Ninos JC, Irrgang JJ, Burdett R, Weiss JR: Electromyographic 108. Aune AK, Ekeland A, Nordsletten L: Effect of quadriceps or
analysis of the squat performed in self-selected lower extremity hamstring contraction on the anterior shear force to anterior
neutral rotation and 30 degrees of lower extremity turn- out cruciate ligament failure. An in vivo study in the rat, Acta Orthop
from the self-selected neutral position, J Orthop Sports Phys Ther Scand 66(3):261–265, 1995.
25(5):307–315, 1997. 109. More RC, Karras BT, Neiman R, et al: Hamstrings—An anterior
90. Signorile JF, Kwiatkowski K, Caruso JF, Robertson B: Effect of cruciate ligament protagonist. An in vitro study, Am J Sports Med
foot position on the electromyographical activity of the superficial 21(2):231–237, 1993.
quadriceps muscles during the parallel squat and knee extension, 110. Ortiz GJ, Schmotzer H, Bernbeck J, et al: Isometry of the
J Strength Cond Res 9(3):182–187, 1995. posterior cruciate ligament. Effects of functional load and muscle
91. Signorile JF, Weber B, Roll B, et al: An electromyographical force application, Am J Sports Med 26(5):663–668, 1998.
comparison of the squat and knee extension exercises, J Strength 111. Yasuda K, Sasaki T: Muscle exercise after anterior cruciate
Cond Res 8(3):178–183, 1994. ligament reconstruction. Biomechanics of the simultaneous iso-
92. Stuart MJ, Meglan DA, Lutz GE, et al: Comparison of interseg- metric contraction method of the quadriceps and the hamstrings,
mental tibiofemoral joint forces and muscle activity during Clin Orthop (220):266–274, 1987.
various closed kinetic chain exercises, Am J Sports Med 24(6): 112. Yasuda K, Sasaki T: Exercise after anterior cruciate ligament
792–799, 1996. reconstruction. The force exerted on the tibia by the separate
93. Wilk KE, Escamilla RF, Fleisig GS, et al: A comparison of tibio- isometric contractions of the quadriceps or the hamstrings, Clin
femoral joint forces and electromyographic activity during open Orthop (220):275–283, 1987.
and closed kinetic chain exercises, Am J Sports Med 24(4): 113. Castle TH Jr., Noyes FR, Grood ES: Posterior tibial subluxation
518–527, 1996. of the posterior cruciate-deficient knee, Clin Orthop (284):
94. Wretenberg P, Feng Y, Arborelius UP: High-and low-bar squat- 193–202, 1992.
ting techniques during weight-training, Med Sci Sports Exerc 114. Herzog W, Read LJ: Lines of action and moment arms of the
28(2):218–224, 1996. major force-carrying structures crossing the human knee joint,
95. Wretenberg P, Feng Y, Lindberg F, Arborelius UP: Joint mo- J Anat 182:213–230, 1993.
ments of force and quadriceps activity during squatting exercise, 115. Hsieh HH, Walker PS: Stabilizing mechanisms of the loaded and
Scand J Med Sci Sports 3:244–250, 1993. unloaded knee joint, J Bone Joint Surg Am 58(1):87–93, 1976.
96. Wright GA, Delong TH, Gehlsen G: Electromyographic activity 116. Shoemaker SC, Markolf KL: Effects of joint load on the stiffness
of the hamstrings during performance of the leg curl, stiff-leg and laxity of ligament-deficient knees. An in vitro study of the
deadlift, and back squat movements, J Strength Cond R anterior cruciate and medial collateral ligaments, J Bone Joint
13(2):168–174, 1999. Surg Am 67(1):136–146, 1985.
97. Ohkoshi Y, Yasuda K, Kaneda K, et al: Biomechanical analysis of 117. Markolf KL, Bargar WL, Shoemaker SC, Amstutz HC: The
rehabilitation in the standing position, Am J Sports Med role of joint load in knee stability, J Bone Joint Surg Am
19(6):605–611, 1991. 63(4):570–585, 1981.
98. Anderson R, Courtney C, Carmeli E: EMG analysis of the vastus 118. Yack HJ, Washco LA, Whieldon T: Compressive forces as a limit-
medialis/vastus lateralis muscles utilizing the unloaded nar- ing factor of anterior tibial translation in the ACL-deficient knee,
row-and wide-stance squats, J Sport Rehabil 7(4):236–247, Clin J Sports Med 4:233–239, 1994.
1998. 119. Escamilla RF, Zheng N, Imamura R, et al: Cruciate ligament
99. Tesch PA: Muscle meets magnet, Stockholm, 1993, PA Tesch AB. force during the wall squat and one leg squat, Med Sci Sports
100. Farrokhi S, Pollard CD, Souza RB, et al: Trunk position influ- Exerc 41(2):408–417, 2009.
ences the kinematics, kinetics, and muscle activity of the lead 120. Fitzgerald GK: Open versus closed kinetic chain exercise: Issues
lower extremity during the forward lunge exercise, J Orthop in rehabilitation after anterior cruciate ligament reconstructive
Sports Phys Ther 38(7):403–409, 2008. surgery, Phys Ther 77(12):1747–1754, 1997.
101. Hefzy MS, al Khazim M, Harrison L: Co-activation of the 121. Heijne A, Fleming BC, Renstrom PA, et al: Strain on the anterior
hamstrings and quadriceps during the lunge exercise, Biomed Sci cruciate ligament during closed kinetic chain exercises, Med Sci
Instrum 33:360–365, 1997. Sports Exerc 36(6):935–941, 2004.
102. Andrews JG, Hay JG, Vaughan CL: Knee shear forces during a 122. Kvist J, Gillquist J: Sagittal plane knee translation and electro-
squat exercise using a barbell and a weight machine. In Matsui myographic activity during closed and open kinetic chain exer-
H, Kobayashi K, editors: Biomechanics VIII-B, Champaign, cises in anterior cruciate ligament-deficient patients and control
1983, Human Kinetics. subjects, Am J Sports Med 29(1):72–82, 2001.
103. Ariel BG: Biomechanical analysis of the knee joint during 123. Zernicke RF, Garhammer J, Jobe FW: Human patellar-tendon
deep knee bends with heavy loads. In Nelson R, Morehouse C, rupture: A kinetic analysis, J Bone Joint Surg Am 59(2):179–183,
editors: Biomechanics IV, Baltimore, 1974, University Park 1977.
Press. 124. Escamilla RF, Zheng N, Imamura R, et al: Patellofemoral
104. Beynnon BD, Johnson RJ, Fleming BC, et al: The strain behavior compressive force and stress during the one leg squat and wall
of the anterior cruciate ligament during squatting and active squat, Med Sci Sports Exerc 41(4):879–888, 2009.
flexion-extension. A comparison of an open and a closed kinetic 125. Reilly DT, Martens M: Experimental analysis of the quadriceps
chain exercise, Am J Sports Med 25(6):823–829, 1997. muscle force and patello-femoral joint reaction force for various
105. Hattin HC, Pierrynowski MR, Ball KA: Effect of load, cadence, activities, Acta Orthop Scand 43(2):126–137, 1972.
and fatigue on tibio-femoral joint force during a half squat, Med 126. Nisell R, Ekholm J: Patellar forces during knee extension, Scand
Sci Sports Exerc 21(5):613–618, 1989. J Rehabil Med 17(2):63–74, 1985.
106. Nisell R, Ekholm J: Joint load during the parallel squat in pow- 127. Salem GJ, Powers CM: Patellofemoral joint kinetics during
erlifting and force analysis of in vivo bilateral quadriceps tendon squatting in collegiate women athletes, Clin Biomech (Bristol,
rupture, Scand J Sports Sci 8(2):63–70, 1986. Avon) 16(5):424–430, 2001.
420 SECTION II • Applied Biomechanics of Selected Sport Activities
128. Escamilla RF, Zheng N, Hreljac A, et al: Cruciate ligament force 149. Vorobyev AN: A textbook on weightlifting, Budapest, 1978,
between the forward lunge long and short with and without a International Weightlifting Federation. Translated by WJ
stride, In Annual Meeting of the American Society of Biomechanics, Brice.
Palo Alto, CA, 2007. 150. Garhammer J: Weightlifting performance and techniques of men
129. Escamilla RF, Zheng N, Macleod TD, et al: Cruciate ligament and women, In Proceedings of the International Conference
tensile forces during lunging with varying techniques, Med Sci on Weightlifting and Strength Training, Lahti, Finland, 1998,
Sports Exerc 41(5):S81, 2009. Gummerus Printing.
130. Race A, Amis AA: The mechanical properties of the two bundles 151. Newton H: Explosive lifting for sports, Champaign, IL, 2002,
of the human posterior cruciate ligament, J Biomech 27(1): Human Kinetics.
13–24, 1994. 152. Stone MH, O’Bryant HS, Williams FE, et al: Analysis of bar
131. Escamilla RF, Zheng N, MacLeod TD, et al: Patellofemoral paths during the snatch in elite male weightlifters, Strength Cond
compressive force and stress during the forward and side lunges 20(4):30–38, 1998.
with and without a stride, Clin Biomech (Bristol, Avon) 153. Baumann W, Gross V, Quade K, et al: The snatch technique of
23(8):1026–1037, 2008. world class weightlifters at the 1985 World Championships, Int J
132. Escamilla RF, Zheng N, Macleod TD, et al: Patellofemoral joint Sport Biomech 4:68–89, 1988.
force and stress between a short- and long-step forward lunge, 154. Gourgoulis V, Aggeloussis N, Mavromatis G, et al: Three-
J Orthop Sports Phys Ther 38(11):681–690, 2008. dimensional kinematic analysis of the snatch of elite Greek weight-
133. Garhammer J: Weight lifting and training. In Vaughan CL, lifters, J Sport Sci 18:643–652, 2000.
Editor: Biomechanics of sport, Boca Raton, 1989, CRC Press. 155. Schilling BK, Stone MH, O’Bryant HS, et al: Snatch technique
134. Garhammer J, Takano B: Training for weightlifting, In Komi PV, of collegiate national level weightlifters, J Strength Cond Res
Editor: Strength and power in sport, Oxford, 2003, Blackwell 16(4):551–555, 2002.
Scientific. 156. Garhammer J: Performance evaluation of Olympic weightlifters,
135. Newton H: Weightlifting? Weight Lifting? Olympic Lifting? Med Sci Sports 11(3): 284–287, 1979.
Olympic Weightlifting? Strength Cond J 21(3):15–16, 1999. 157. Gourgoulis V, Aggeloussis N, Antoniou P, et al: Comparative
136. Chiu LZF, Schilling BK: A primer on weightlifting: From sport 3-dimensional kinematic analysis of the snatch technique in elite
to sports training, Strength Cond J 27(1):42–48, 2005. male and female Greek weightlifters, J Strength Cond Res
137. Chiu LZF, Salem GJ: Comparison of joint kinetics during free 16(3):359–366, 2002.
weight and flywheel resistance exercise, J Strength Cond Res 158. Garhammer J, Taylor L: Center of pressure movements during
20(3):555–562, 2006. weightlifting, In Proceedings of the 2nd International Symposium
138. Garhammer J: Biomechanical analysis of selected snatch lifts at the on Biomechanics in Sports, Colorado Springs, CO, 1984.
U.S. Senior National Weightlifting Championships, In Proceed- 159. Breniére Y, Do MC, Gatti L, et al: A dynamic analysis of the
ings of the International Congress of Physical Activity, Quebec squat snatch, In Biomechanics VII-B, Baltimore, MD, 1981,
City, QC, 1976, Symposia Specialists Inc. University Park Press.
139. Garhammer J: Energy flow during Olympic weight lifting, Med 160. Lee Y-H, Huwang C-Y, Tsuang Y-H: Biomechanical characteris-
Sci Sports Exerc 14(5):353–360, 1982. tics of preactivation and pulling phases of snatch lift, J Appl
140. Laputin NP, Oleshko VG: Managing the training of weightlifters Biomech 11:288–298, 1995.
[Russian]. Kiev, 1982, Zdorov’ya Publishers. Translated by A. 161. Chiu LZF: Acute Physiologic and Neuromuscular Responses to High-
Charniga Jr. Power Resistance Exercise, Unpublished Doctoral Dissertation,
141. Garhammer J: A comparison of maximal power outputs between Division of Biokinesiology and Physical Therapy, University of
elite male and female weightlifters in competition, Int J Sport Southern California, Los Angeles, 2008.
Biomech 7:3–11, 1991. 162. Enoka RM: Muscular control of a learned movement: The
142. Garhammer J, Kauhanen H, Häkkinen K: A comparison of perfor- speed control system hypothesis, Exper Brain Res 51:135–145,
mances by women at the 1987 and 1998 World Weightlifting 1983.
Championships, In Proceedings of the Science for Success 163. Enoka RM: Load- and skill-related changes in segmental contri-
Congress, Jyväskylä, Finland, 2002. butions to a weightlifting movement, Med Sci Sports Exerc
143. Garhammer J: Longitudinal analysis of highly skilled Olympic 20(2):178–187, 1988.
weightlifters. In Terauds J, Editor: Science in weightlifting, Del 164. Connan A, Moreaux A, Van Hoecke J: Biomechanical analysis of
Mar, CA, 1979. the two-hand snatch, In Biomechanics VII-B, Baltimore, MD,
144. Garhammer J: Biomechanical characteristics of the 1978 world 1981, University Park Press.
weightlifting champions, In Biomechanics VII-B, Baltimore, 165. Burdett RG: Biomechanics of the snatch technique of highly
1981, University Park Press. skilled and skilled weightlifters, Res Q Exerc Sport 53(3):
145. Enoka RM: The pull in Olympic weightlifting, Med Sci Sports 193–197, 1982.
11(2):131–137, 1979. 166. Roman RA, Treskov VV: Snatch technique of world record
146. Frolov VI, Lelikov SI, Efimov NM, et al: Snatch technique of holder Yuri Zakharevich [Russian], Tyazhelaya Atletika 1:10–16,
top-class weightlifters [Russian], Teoriya i Praktika Fizicheskoi 1983. Translated by M. Yessis.
Kultury 6:59–61, 1977. Translated by M. Yessis. 167. Gourgoulis V, Aggeloussis N, Kalivas V, et al: Snatch lift kinemat-
147. Häkkinen K, Kauhanen H, Komi PV: Biomechanical changes in ics and bar energetics in male adolescent and adult weightlifters,
the Olympic weightlifting technique of the snatch and clean and J Sports Med Phys Fit 44:126–131, 2004.
jerk from submaximal to maximal loads, Scand J Sports Sci 168. Lephart SM, Ferris CM, Riemann BL, et al: Gender differences
6(2):57–66, 1984. in strength and lower extremity kinematics during landing, Clin
148. Kauhanen H, Häkkinen K, Komi PV: A biomechanical analysis Orthop Rel Res 401:162–169, 2002.
of the snatch and clean & jerk techniques of Finnish elite and 169. Pincivero DM, Campy RM, Coelho AJ: Knee flexor torque and
district level weightlifters, Scand J Sports Sci 6(2):47–56, perceived exertion: A gender and reliability analysis, Med Sci
1984. Sports Exerc 35(10):1720–1726, 2003.
Applied Biomechanics of Common Weight Training Exercises • CHAPTER 16 421
170. Bosco C, Komi PV: Potentiation of the mechanical behavior of 192. Fitzgerald B, McLatchie GR: Degenerative joint disease in
the human skeletal muscle through prestretching, Acta Physiol weight-lifters: Fact or fiction? Br J Sports Med 14(2–3):97–101,
Scand 106(4):467–472, 1979. 1980.
171. Garhammer J, Gregor R: Propulsion forces as a function of 193. Granhed H, Morelli B: Low back pain among retired wrestlers
intensity for weightlifting and vertical jumping, J Appl Sport Sci and heavyweight lifters, Am J Sports Med 16(5):530–533,
Res 6(3):129–134, 1992. 1988.
172. Kipp K, Harris C, Sabick M, et al: Lower extremity joint power 194. Kujala UM, Kettunen J, Paananen H, et al: Knee osteoarthritis in
production during Olympic weightlifting exercise [abstract], Med former runners, soccer players, weight lifters, and shooters,
Sci Sports Exerc 38(5):S296, 2006. Arthritis Rheum 38(4):539–546, 1995.
173. Deming L, Kangwei A, Yunde W: Three dimensional analysis of the 195. Kuland DN, Dewey JB, Brubaker CE, et al: Olympic weight-
clean and jerk techniques for female elite Chinese weightlifters, In lifting injuries, Phys Sports Med 6(11):111–119, 1978.
Proceedings of the 11th International Symposium on Biomechanics 196. Raske Å, Norlin R: Injury incidence and prevalence among elite
in Sports, Amherst, MA, 1993. weight and power lifters, Am J Sports Med 30(2):248–256,
174. Lehr RP, Poppen R: An electromyographic analysis of Olympic 2002.
power and squat clean, In Terauds J, Editor: Science in weightlift- 197. Rossi F: Spondylolysis, spondylolisthesis and sports, J Sports Med
ing, Del Mar, CA, 1979, Academic Publishers. Phys Fitness 18(4):317–340, 1978.
175. Campos J, Poletaev P, Cuesta A, et al: Kinematical analysis of the 198. Stone MH, Fry AC, Ritchie M, et al: Injury potential and safety
snatch in elite male junior weightlifters of different weight cate- aspects of weightlifting movements, Strength Cond 16(3):15–21,
gories, J Strength Cond Res 20(4):843–850, 2006. 1994.
176. Zelle J, Barink M, Loeffen R, et al: Thigh-calf contact force 199. Hamill BP: Relative safety of weightlifting and weight training,
measurements in deep knee flexion, Clin Biomech 22:821–826, J Strength Cond Res 8(1):53–57, 1994.
2007. 200. Byrd R, Pierce K, Rielly L, et al: Young weightlifter’s perfor-
177. Nelson RC, Burdett RG: Biomechanical analysis of Olympic mance across time, Sports Biomech 2(1):133–140, 2003.
weightlifting, In Proceedings of the International Congress of 201. Mölsä J, Kauhanen H, Häkkinen K: Sports injuries among junior
Physical Activity, Quebec City, QC, 1976. weightlifters, In Proceedings of the International Conference on
178. Garhammer J: A review of power output studies of Olympic and Weightlifting and Strength Training, Lahti, Finland, 1998.
powerlifting: Methodology, performance prediction, and evalua- 202. Miller SJ, Smith PA: Volar dislocation of the lunate in a weight
tion tests, J Strength Cond Res 7(2):76–89, 1993. lifter, Orthopedics 19(1):61–63, 1996.
179. Chiu LZF, Schilling BK, Fry AC, et al: The influence of deforma- 203. Wooten JR, Jones DH: An unusual weightlifting injury, Injury
tion on barbell mechanics during the clean pull, Sports Biomech 19:446–454, 1988.
7(2):260–273, 2008. 204. Gumbs VL, Segal D, Halligan JB, et al: Bilateral distal radius and
180. Hoover DL, Carlson KM, Christensen BK, et al: Biomechanical ulnar fractures in adolescent weight lifters, Am J Sports Med
analysis of women weightlifters during the snatch, J Strength 10(6):375–379, 1982.
Cond Res 20(3):627–633, 2006. 205. Lewis DC, Johnson SR: Spontaneous dislocation of the lunate in
181. Campbell DE, Pond JW, Trenbeath WG: Cinematographic analysis a weightlifter, Injury 21(4):252–254, 1990.
of varying loads of the power clean, In Terauds J, Editor: Science in 206. Aggrawal ND, Kaur R, Kumar S, et al: A study of changes in the
weightlifting, Del Mar, CA, 1979, Academic Publishers. spine in weight lifters and other athletes, Br J Sports Med 13:
182. Campillo P, Chollet D, Micallef JP: Localisation de points cri- 58–61, 1979.
tiques lors du tirage à l’arraché en haltérophilie, Sci Sports 207. Dangles CJ, Spencer DL: Spondylolysis in competitive weight
13:90–92, 1998. lifters [abstract], Am J Sports Med 15(6):624–625, 1987.
183. Garhammer J: Barbell trajectory, velocity and power changes: 208. Kotani PT, Ichikawa N, Wakabayashi W, et al: Studies of spondy-
Six attempts and four world records, Weightlifting USA 19(3): lolysis found among weight lifters, Br J Sports Med 6(1):4–8,
27–30, 2001. 1971.
184. Frolov VI, Levshunov NP: The phasic structure of the jerk from the 209. Rossi F, Dragoni S: Lumbar spondylolysis: Occurrence in
chest [Russian], Tyazhelaya Atletika 11:25–28, 1982. Translated competitive athletes, J Sports Med Phys Fitness 30:450–452,
by A Charniga Jr. 1990.
185. Grabe SA, Widule CJ: Comparative biomechanics of the jerk in 210. Alexander MJL: Biomechanical aspects of lumbar spine
Olympic weightlifting, Res Q Exerc Sport 59(1):1–8, 1988. injuries in athletes: A review, Can J Appl Sport Sci 10(1):1–20,
186. Roman RA, Shakirzyanov MS: The snatch, the clean & jerk 1985.
[Russian]. Moscow, 1978, Fizkultura I Sport. Translated by A 211. Ariel BG: Biomechanical analysis of the knee joint during deep
Charniga Jr. knee bends with heavy loads. In Nelson RC, Morehouse C,
187. Whittle MW, Sargeant AJ, Johns L: Computerised analysis of Editors, Biomechanics IV, Baltimore, MD, 1974, University Park
knee moments during weightlifting, In de Groot G, Hollander Press.
AP, Huijing PA, et al, Editors: Biomechanics XI-B, Amsterdam, 212. Whiting WC, Zernicke RF: Biomechanics of musculoskeletal
1988, Free University Press injury, ed 2, Champaign, IL, 2008, Human Kinetics.
188. Zernicke RF, Garhammer J, Jobe FW: Human patellar-tendon 213. Yamamoto N, Hayashi K: Mechanical properties of rabbit patel-
rupture, J Bone Joint Surg Am 59(2):179–183, 1977. lar tendon at high strain rate, Biomed Mater Eng 8(2):89–90,
189. Neptune RR, Kautz SA, Zajac FE: Contributions of the individual 1998.
ankle plantar flexors to support, forward progression and swing 214. Grenier R, Guimont A: Simultaneous bilateral rupture of the
initiation during walking, J Biomech 34:1387–1398, 2001. quadriceps tendon and leg fractures in a weightlifter: A case
190. Roman RA: The training of the weightlifter [Russian]. Moscow, report, Am J Sports Med 11(6):451–453, 1983.
1986, Fizkultura I Sport. Translated by A Charniga Jr. 215. Fry AC, Smith JC, Schilling BK: Effect of knee position on hip
191. Calhoon G, Fry AC: Injury rates and profiles of elite competitive and knee torques during the barbell squat, J Strength Cond Res
weightlifters, J Athl Tr 34(3):232–238, 1999. 17(4):629–633, 2003.
422 SECTION II • Applied Biomechanics of Selected Sport Activities
216. Gisslén K, Öhberg L, Alfredson H: Is the chronic painful 219. Fees M, Decker T, Snyder-Mackler L, et al.: Upper extremity
tendinosis tendon a strong tendon? Knee Surg Sports Traumatol weight-training modifications for the injured athlete: A clinical
Arthrosc 14:897–902, 2006. perspective, Am J Sports Med 26(5):732–742, 1998.
217. Alfredson H, Öhberg L: Neovascularisation in chronic painful 220. Neviaser TJ: Weight lifting. Risk and injuries to the shoulder,
patellar tendinosis—Promising results after sclerosing neovessels Clin Sports Med 10(3):615–620, 1991.
outside the tendon challenge the need for surgery, Knee Surg 221. Mundt DJ, Kelsey JL, Golden AL, et al: An epidemiologic study
Sports Traumatol Arthrosc 13(2):74–80, 2005. of sports and weight lifting as possible risk factors for herniated
218. Cahill BR: Osteolysis of the distal part of the clavicle in male lumbar and cervical discs, Am J Sports Med 21(6):854–860,
athletes, J Bone Joint Surg Am 64(7):1053–1058, 1982. 1993.
17
CHAPTER
423
424 SECTION III • Management of Sports Injury and Illness
Clinical Point
Delayed onset muscle soreness can be generally considered a
temporary subjective condition that will resolve itself over several
days and without intervention.
Protease Protease
Kininogen
Models to Study Muscle Soreness
To produce DOMS in humans, activated or contracted
Serotonin Bradykinin H+
muscles are stretched (lengthening contractions) using a
Figure 17-2 variety of methods ranging from free weights31 to dyna-
Resident mast cells and infiltrating neutrophils can produce substances mometers.32 Generally, many repetitions with short rest
that are hyperalgesic such as bradykinin and serotonin.
times between contractions are used with single-joint move-
ments (e.g., lengthening of active knee extensor or elbow
flexor muscles) or complex limb movements such as
junction would be more prone to damage caused by a downhill walking or running.
concentration of forces at that region has gained favor as Because DOMS is subjectively experienced by humans,
the distal portion of some muscles appeared to be more researchers rely on reports of resting pain via visual analog
sensitive to DOMS.19 However, alterations in pressure- scales (VASs) or pain evoked by pressure (pressure-
pain threshold can be measured in other areas, including pain threshold) or movement. Two types of protocols are
the more central region of the biceps brachii muscles.20 commonly used in humans to produce DOMS: (1) voluntary
Attempts have been made to map the soreness as a func- or electrically activated skeletal muscles exposed to repeated
tion of the surface area of quadriceps muscles using a lengthening contractions33 (Figure 17-3) using typically the
standardized grid placed on the leg and a threshold force elbow flexor, knee extensor, or ankle dorsiflexor muscles; and
of 50 N. These studies revealed regional differences do (2) downhill running, stepping, or walking. Because these
exist.21 For example, the location of the soreness was activities recruit different muscle fibers within different ana-
found in the distal portion of the vastus medialis and the tomical muscles with diverse architecture and fascial compart-
proximal part of the vastus lateralis, whereas the rectus ments, outcome measures would be expected to have large
femoris was absent of muscle soreness.22 Regional differ- variability. For example, it is quite easy to produce extreme
ences were also noted in the quadriceps muscles before soreness in the elbow flexor muscles of untrained individuals
and after a bout of downhill running—proximal and distal with only 30 repetitions.33 However, to produce DOMS in
regions were more sensitive.23 For practical reasons, most the knee extensor muscle, used more frequently in activities of
investigators choose a point that is easily located and daily living, hundreds of repetitions were used34,35 and down-
reproduced in repeated trials, but may be problematic if hill running required 15 bouts of 10 floor descents.36 Surpris-
regional differences do exist or change with time. ingly, even repeated isometric muscle actions at long muscle
426 SECTION III • Management of Sports Injury and Illness
Repeated Lengthening Contractions loads of 84% and 112% of MVC.39 Also, using two different
protocols, another study found that using 10% of isometric
elbow flexor strength with 600 repetitions was no different
Stretch-Activated Membrane Force Deficit of 50%= in producing DOMS than using 30 repetitions at 100%.32
Calcium Channels Damage Muscle weakness
Velocity of Movement
lengths of the elbow flexor muscles can produce damage and Unlike studies on animals, the effect of velocity of movement
soreness.37 Other models for inducing muscle soreness in- with maximally activated muscles has not been performed in
clude injections of noxious materials into human muscles14,38 humans without additional confounding variables. Using rela-
and are beyond the scope of this discussion. tively low angular velocities of elbow movement, faster veloci-
ties produced greater DOMS than lower velocities.43 Similar
findings were reported for differences between 30° and 210°
Relationship Between Load, Repetition per second using an isokinetic dynamometer and human
Number, Velocity of Movement elbow flexor muscles.44 Unfortunately, the study standardized
the total time under contraction by using different numbers of
and Muscle Length repetitions for the two groups. Thus, repetition number alone
It is common experience that low loads, small numbers of could have resulted in the same outcome.
repetitions and slow velocities of movement do not always
result in DOMS. However, only a few studies have evalu-
ated the effects of submaximal protocols;32,39-41 a systematic Muscle Length
study of load and repetition number on DOMS has not Early studies on the role of mechanical factors in the
been undertaken. From the studies available, it appears that development of DOMS revealed that there was a length-
the minimum number of maximal lengthening contractions dependent component.45 Exercises at longer muscle lengths
of the elbow flexor muscles required to produce DOMS was produced more soreness.37 Partial range-of-motion (ROM)
two repetitions41 and a load of only 10% of maximum if the exercises have been used for knee extension (150°to 80°)46
number of repetitions was large.32 and elbow flexion (120° to 180°)32 to produce soreness.
Most studies use large ROM exercises for the elbow flexor
muscles.
Load Thus, load and repetition number are important factors
in magnitude of the DOMS reported, but large variability
Factors That Can Lead to DOMS
between subjects prevents conclusive statements. Large
• Load variability is not the result of total work performed or peak
• Number of repetitions torque.47
• Velocity of movement
• Length of muscle
Performance Deficit
In 1902, Hough48 first hypothesized that the muscle dam-
The magnitude of the load or level of muscle contraction age that occurred following unaccustomed exercise was the
(percent of maximum voluntary contraction [MVC]) as a result of mechanical stress to the muscles (see Figure 17-3).
determinant for DOMS has been studied. Differences in pain Working with simple equipment and using himself as a sub-
during straightening of the injured elbow flexor muscles, but ject, Hough described his experience and functional out-
not during palpation (although a trend was clearly evident), come of this type of exercise-induced muscle damage and
were reported following 36 lengthening contractions using hypothesized the mechanism of injury. Hough observed
Delayed-Onset Muscle Soreness • CHAPTER 17 427
that the reduction in muscle force immediately after exer- processes occurring over time: contraction failure and histo-
cise preceded the onset of muscle soreness, which began the pathological changes (see Figure 17-3). Contraction failure
day after the exercise session. It is remarkable that contin- results primarily from mechanical events occurring more
ued exercise with sore, weakened elbow flexor muscles did prominently during the early repetitions while the events,
not exacerbate the injury or alter the repair process.49,50 eventually leading to histopathological changes, increase in
The decrease in muscle performance or loss of function, magnitude throughout the course of repeated lengthening
usually measured as a decreased maximal isometric force contractions. Thus, it is not surprising that the magnitude
(weakness), is due to a reduction in the muscles intrinsic of the force deficit does not correlate with soreness or mark-
ability to produce force (see Figure 17-3).51 The majority of ers of muscle damage such as creatine kinase (CK).63 In
the force decrement occurs early in a series of repeated addition, in animal studies, weakness could be produced
lengthening contractions in both voluntary and electrically from 30 lengthening contractions with or without histo-
active muscles in humans33 and in electrically active muscles pathological changes.52 Perhaps the soreness would corre-
in animals.52-55 late best with the degree of histopathologic changes that, in
More detailed studies on animals have revealed that turn, varies with the loss of cellular integrity. Loss of cellular
force-generating56 and transmitting components57 of skele- integrity may increase with repetition number.
tal muscles are compromised with repeated lengthening Following lengthening contractions, the membrane-
contractions. Both the force generator (sarcomere) and ac- associated protein, dystrophin, is lost64-66 indicating a loss of
tivating system (excitation-contraction [E-C] coupling) cell membrane integrity (Figure 17-4). Such membrane
have been observed to be disrupted following repeated disruptions can lead to cell death caused by calcium over-
lengthening contractions (see Figure 17-3).58 Of these two, load67 as high concentrations of extracellular calcium enter
E-C coupling damage perhaps is responsible for 75% of the the cell (see Figure 17-4) and overcome the cellular buffer-
force decline.59 During the early contractions, it is probable ing capacity leading to cell death.68 Dead cells become
that unstable sarcomeres become overstretched (sarcomere necrotic and require phagocytic cell action to remove the
popping),58 which, in turn, causes the transverse (T) tubule, cellular debris. Necrotic myofibers can be easily observed in
structurally associated with the sarcomere, to shear,60 dis- rat muscles 48 hours after a single bout of repeated length-
connecting it from the sarcolemma. Thus, the T tubule and ening contractions52,66,69 and after long-distance running in
associated sarcoplasmic reticulum, called a triad, would humans.70 Some of these necrotic myofibers are infiltrated
become functionally detached from the sarcolemma and by phagocytic cells (neutrophils and macrophages) but still
unable to respond to subsequent action potentials. The contain some detectable myosin.52 Thus, histopathological
reduction in release-activator calcium from disconnected changes appear to result from loss of myofiber integrity.
triads would result in a decline in force output or weakness. Evidence for loss of myofiber integrity following a bout
Although these cellular disruptions would alter the force- of repeated lengthening contractions is provided by observa-
producing capability of muscle, they would not necessarily tions of extracellular dyes,71 technetium pyrophosphate,70
lead to plasma membrane rupture unless the overstretched and proteins such as albumin72 and fibronectin70 inside myo-
sarcomeres are attached to the plasma membrane via costa- fibers. These perturbations of the cell membrane also allow
meres.61 Some type of membrane damage is presumed to be intracellular, muscle-specific proteins to exit. Many studies
a precursor for myofiber necrosis and subsequent inflamma- have provided evidence for myofiber injury as muscle specific
tion (see Figure 17-3). proteins such as creatine kinase (CK) (see Figure 17-4),
It has been shown in rats that increasing the rest interval myoglobin and myosin fragments could be measured in the
between successive lengthening contractions prevented blood following different protocols known to contain exer-
histopathological changes in spite of a 50% decrease in cises that produce muscle injury.73 Myoglobin appears early
muscle force.52 Thus, muscle weakness occurred without
evidence of cellular pathology. What appears to be lacking
in human studies has been efforts to define the threshold Arachidonic Acid Calcium Creatine Kinase
for muscle soreness. Although tissue damage may be a pre-
requisite for DOMS, the factors involved in muscle weak-
ness can occur independently from those that produce
FORCE
FORCE
INJURY
soreness (see Figure 17-3).
Histopathological Changes
Skeletal muscle
Although the magnitude of the force deficit (weakness)
Figure 17-4
diminishes with increasing repetition number in humans62 Skeletal muscle injury can result in plasma membrane injury and
and animals,52 the amount of cellular pathology continues the production of arachidonic acid, increased influx of extracellular
to increase,54 providing indirect support for two distinct calcium, and release of intracellular proteins such as creatine kinase.
428 SECTION III • Management of Sports Injury and Illness
in the blood and could be a direct indicator of myofiber 300 repeated lengthening contractions of the knee extensor
injury as it can pass easily the capillary wall.74 With a similar muscles, the entire muscle contained WBCs at 24 hours
time course, fatty acid–binding protein appears in the blood later together with an increase in DOMS.34 In a subsequent
with a peak between 2 to 4 hours.73 CK appears later,73 study, labeled neutrophils were used to provide evidence
perhaps requiring lymphatic clearance75 to arrive in the that DOMS is associated with inflammation but not with
circulation. Lastly, the time course of myosin fragments73 muscle damage.78
might support a role in neutrophil action as the proteases Because neutrophils and macrophages can be identified
released from neutrophils during removal of cellular debris in injured muscles,52,78,79 chemoattractants such as leukotri-
would be capable of fragmenting but not completely ene B4 released by injured cells may play a role in their
degrading contractile proteins. The protein fragments could recruitment80 (Figure 17-5). Unfortunately, no attempts at
then pass directly into the blood. measuring leukotrienes in injured skeletal muscles in vivo
have been reported and inhibition of lipoxygenase (LIPOX)
has only been reported for isolated rat muscles.81 Thus,
Inflammation the role of LIPOX must be inferred from the presence
Because the weakness observed as a function of lengthening of neutrophils in injured human muscle. However, activa-
contractions would not produce DOMS, developing inflam- tion of LIPOX initially depends on the production of
mation following associated tissue damage is a likely candi- arachidonic acid.
date (see Figure 17-3). Inflammation is a complex cellular The production of arachidonic acid (see Figure 17-5) and
and chemical reaction in blood vessels and adjacent tissues to the generation of inflammation results from the activation of
an injury. Typically, acute inflammation is characterized by the enzyme, phospholipase A2. In turn, arachidonic acid
hyperemia, edema, and diapedesis of neutrophils and macro- results in the activation of 5-LIPOX and cyclo-oxygenase
phages. Inflammation is commonly accompanied by pain. (COX). The activation of COX leads to the production of
Although others have presented arguments to the contrary,76 prostaglandins, which could contribute to pain, edema, and
the arrival of inflammatory cells into the injured muscle espe- vasodilation—typical of inflamed tissue.
cially around blood vessels, may be the prerequisite for pain.
Evidence of an inflammation state in injured muscles has
been long appreciated (see review77); both vascular and cel-
Mast Cells
lular responses have been identified. Unlike studies on the One additional candidate for the production of sensitizing
location of muscle pain, inflammation was distributed agents is mast cell degranulation. Human mast cells con-
throughout the muscle.34 When technetium-99m–labeled tain proteolytic enzymes that could activate kininogens
white blood cells (WBCs) were given to subjects prior to leading to bradykinin production82 and have been shown
Blood vessel
Monocytes
PMN Plasma
INJURY
Skeletal muscle
Figure 17-5
Membrane injury can lead to the release of arachidonic acid from muscle resulting in cellular infiltration
mediated by leukotriene signaling and protein extravasation by prostaglandin interaction with vascular
endothelial cells. The infiltrating neutrophils and macrophages can release enzymes such as proteases.
Delayed-Onset Muscle Soreness • CHAPTER 17 429
to release stored serotonin83 (see Figure 17-2). Thus, mast activation of resident cells in the matrix may be necessary
cell degranulation could provide the necessary chemical for DOMS.93 Thus, the connective tissue surrounding the
mediators for sensitization even in the absence of loss of myofibers could play a major role in DOMS and may also
myofiber integrity. help explain why markers of myofiber injury do not corre-
Some evidence exists for mast cell degranulation follow- late with the magnitude of DOMS.
ing repeated lengthening contractions in both animal84 and
human57 skeletal muscles. Because mast cells are generally
found near neurovascular elements, blood vessels, and the
Prevention and Attenuation of DOMS
connective tissue interstitium,85 they are ideally situated to To our knowledge, no treatment or manipulation can fully
influence nearby nociceptors. Overstretched connective tis- protect an untrained muscle from developing DOMS in el-
sue from myofiber rupture86 or disruption of the support- bow flexor muscles following a series of repeated lengthening
ing extracellular matrix (ECM)57 could provide a non- contractions even as little as two maximal lengthening
physiological stretch to some mast cells, causing a leakage contractions.41 However, attenuation of DOMS to a second
of granules and release of noxious agents. Mechanical bout of lengthening contractions produced by an initial
manipulation of certain tissues can produce mast cell bout of exercises has been referred to as the repeated bout
degranulation87 and mast cell degranulation can itself be effect50 and may last as long as 6 months.94 This repeated
injurious to muscle.88 bout effect was first observed as a stepwise marked reduction
in DOMS for elbow flexor muscles when high-force
lengthening contractions were repeated 2 weeks and 4 weeks
Connective Tissue following an initial bout.95 In contrast, force deficits were
In contrast to direct damage to myofibers, tissue swelling89 only slightly reduced with each successive bout, indicating
and disruption of the ECM57 following muscle injury may that the force-generating system was repeatedly disrupted.
be important in the cause of muscle soreness. It is well rec- Remarkably, no increase in plasma CK was measured follow-
ognized that extreme passive stretching can produce pain ing the second and third bout. This study supports the
because HTM receptors located in the connective tissues hypothesis that DOMS does not require myofiber disruption
around muscles are activated by excessive deformation. In of sufficient magnitude to allow the exit of intracellular
addition, myofibers appear swollen.30,90 Therefore, swelling proteins.
of cells and degradation of ECM could potentially result in Subsequently, many studies have verified this observation
soreness if the expansion of the muscle (swelling) exceeded that prior exposure to lengthening contractions attenuates
the threshold for mechanical activation of the receptors. the soreness following repeated exercise trials.96 For exam-
A disrupted and partially degraded matrix would serve as an ple, only 24 contractions were necessary to dramatically
excellent oncotic material promoting tissue water accumu- attenuate soreness produced 2 weeks later by 70 maximal
lation. Evidence for ECM breakdown was observed 2 days lengthening contractions.42 In contrast, some exercises may
after exercise by the presence of collagen breakdown prod- actually exacerbate the problem97 perhaps by producing
ucts in the urine.91 Expanded ECM can also be observed shorter muscles.98
around injured human myofibers.57 Thus the environment
around injured myofibers would favor the accumulation of
water resulting in a swollen muscle.
Treatment of DOMS
Evidence for muscle swelling following repeated length- Just as the exact mechanisms leading to DOMS are not
ening contractions has been reported using ultrasound completely understood, its treatment and the effects of those
imaging26 and magnetic resonance imaging.46,92 However, treatments on the condition are at present questionable
swelling alone is not sufficient to produce soreness unless (Figure 17-6).
the additional water was held in a closed compartment.30
The soreness increases as the limb is moved or the muscles
are palpated as if the tissue pressure within the muscle must Pharmacological Management of DOMS
exceed some threshold for activation of the HTM receptors. If the inflammatory response is a major contributor to
Therefore, sensitization of the receptors by chemical media- DOMS, then anti-inflammatory agents should be useful in
tors released in response to muscle injury would still appear the management of DOMS. However, anti-inflammatory
critical for DOMS. drugs have shown mixed results for treating DOMS. The
The connective tissue, in addition to containing HTM administration of 400 mg of ibuprofen given 4 hours before
receptors, also contains resident neutrophils and T cells.93 or 1200 mg given 24 hours after exercise was somewhat
After downhill running to produce muscle damage, more effective in decreasing perceived soreness and enhancing
T cells and neutrophils were found in the epimysium from recovery of muscle force at 24 to 48 hours after exercise-
those subjects who experienced DOMS compared with induced injury.21 In contrast, no significant effect of ibupro-
those who exercised but did not experience DOMS.93 The fen or other nonsteroidal anti-inflammatory drugs (NSAIDs)
430 SECTION III • Management of Sports Injury and Illness
DOMS
Exercise? Stretching?
produce a classic inflammatory response.108,110 Finally,
because the literature does not provide strong support for
using NSAIDs to treat or prevent DOMS and these drugs
Compression? Ice? are not benign, routine use of NSAIDs for DOMS cannot
be recommended.
Rest? Supplements?
Physical Modalities for DOMS
Figure 17-6 Cryotherapy
Schematic representation interventions commonly used for delayed Experimental evidence has been reported that cryotherapy
onset muscle soreness.
reduced the signs and symptoms of acute soft tissue
injury.111 The decrease in tissue temperature associated with
on DOMS has also been reported.99-103 Regardless of the cryotherapy is thought to limit the degree of injury by
type of NSAID, dosage, or time of delivery (e.g., before or stimulating cutaneous receptors to cause sympathetic vaso-
after exercise), NSAIDs produced little reduction in DOMS. constriction and by slowing the extravasation of blood
For example, no improvements in DOMS, muscle strength proteins to decrease swelling. In addition, a decrease in tis-
or endurance time were reported for 16 subjects receiving sue temperature would decrease cellular metabolism and
2400 mg of ibuprofen twice (24 hours before and 72 hours reduce the production of metabolites.112 Cold also dulls or
after) compared with placebo controls using a single bout diminishes the sensation of pain.112 Taken together, cryo-
of downhill running to produce muscle injury.100 Interest- therapy would be expected to reduce DOMS. Despite its
ingly, CK activity was actually higher in the ibuprofen widely accepted use among athletes, little or no benefit has
group.100 However, using repeated lengthening contrac- been reported using cryotherapy to treat DOMS.113-116
tions of the elbow flexor muscles, a reduction in CK activity Immersion in Cold. Subjects performed a total of
was observed in individuals treated with 2400 mg of ibu- 40 maximal lengthening contractions of the elbow flexor
profen for 5 days before and 10 days after exercise104—no muscles to produce injury and the injured arm was
measurements of DOMS were conducted. immersed in cold water (15°C [59°F]) for 15 minutes
Because diclofenac inhibits both the COX and LIPOX immediately after the exercise bout and every 12 hours for
pathways of arachidonic acid metabolism,105,106 it might be a total of seven sessions.113 Although the relaxed elbow
more effective in treating DOMS. Indeed, decreased muscle angle and CK activity were significantly lower for the cryo-
soreness and CK activity following elbow exercise has been therapy group, there was no effect on tenderness or loss of
reported for diclofenac.106 In addition, another NSAID that strength.113 A similar study, using 64 lengthening contrac-
alters both the COX and LIPOX pathways, ketoprofen, has tions, employed five repeated immersions of the injured arm
also been shown to decrease muscle soreness when 100 mg using colder water (5°C [41°F]) for 20 minutes each.114
was given 36 hours after the exercise.107 Each immersion was separated by 60 minutes. Again, no
Because prostaglandin E (PGE2) plays an important role beneficial reduction in DOMS was reported.114
in healing, inhibition of COX by NSAIDs could impair Lower-extremity muscles have also been subjected to
muscle healing by reducing PGE2 synthesis. Impaired lengthening contractions and followed with immersion in
recovery of muscle function after lengthening contractions cold (5°C [41°F]) or tepid water (24°C [75°F]).117 In
of the elbow flexor muscles resulted in NSAID-treated addition to measurement of perceived soreness, thigh cir-
subjects.108 Fifteen subjects were given either 300 mg of cumference, serum CK, and isometric strength, tests of
flurbiprofen or a placebo 24 hours before and for 14 days lower-extremity function were included, such as a hop test
after exercise protocol.108 Flurbiprofen did not reduce for distance and a sit-to-stand test. Surprisingly, the cold-
DOMS, swelling, or stiffness but did adversely lower the immersion treatment resulted in increased soreness during
maximal force, suggesting that additional weakness resulted the sit-to-stand test 24 hours after exercise.117
from NSAID administration. Furthermore, studies with In addition to treatments of the injured areas, whole-
animals have demonstrated that NSAIDs can have adverse body ice immersion has been recommended, but its effec-
effects on skeletal muscle healing following injury.109 tiveness to reduce DOMS remains unknown (see “Contrast
Delayed-Onset Muscle Soreness • CHAPTER 17 431
Baths” section). In addition, the discomfort of prolonged occasions, first starting at 18 hours after exercise and then
whole-body immersion in ice water and the risk of hypo- again at 32 hours after exercise. The cold pack intervention
thermia precludes its use. used a gel pack for 15 to 20 minutes every 4 hours between
Ice Massage. The effects of ice massage on DOMS 18 and 42 hours after exercise while lying prone or supine.
in the elbow flexor muscles was studied with 15- to Using self-reporting as a measure of function and pain, the
20-minute applications immediately, 24, or 48 hours heat wrap served as a preventive measure, starting 4 hours
following damaging exercise.115 No differences in ROM before the exercise bout, resulting in a substantial decrease
or soreness were observed between treated and untreated in low back pain and smaller deficits in function. Further-
arms. In fact, an increase in soreness was reported in sub- more, when subjects were tested 24 hours after exercise, the
jects following the 24-hour treatment.115 Similarly, when heat wrap again provided superior pain relief compared with
used immediately after exercise or 24 or 48 hours after the cold pack.123 Although the findings are interesting, no
exercise, ice massage was found to be ineffective in the objective measures of soreness and function were used. The
treatment of DOMS.118 results may also be unique to the muscles tested.
Ice massage was used in combination with exercise to
assess its role in the prevention and treatment of DOMS by Contrast Baths
comparing the intervention to ice massage and exercise Alternating heat and cold-water immersions have been
alone.116 Prior to an exercise protocol to induce DOMS, purported to assist with recovery after exercise.124 Based
ROM, strength, perceived soreness, and serum CK levels on anecdotal experience by athletes, warm spas with cold
were measured and again at 2, 4, 6, 24, 48, 72, 96, and plunges or contrast hot-cold baths have been recom-
120 hours after exercise. None of the treatments was able mended. Contrast baths are commonly used by physical
to significantly reduce DOMS. In fact, it appeared that the therapists and athletic trainers for a variety of conditions,
use of ice in the treatment of DOMS may actually be con- but little is known about the effectiveness of using such a
traindicated116 as the ice massage group had the highest modality for the prevention and treatment of DOMS. It has
peak soreness at rest, highest serum CK levels, and the been speculated that contrast baths create a pumping action
lowest peak total ROM of all the groups tested. through alternating vasodilation and vasoconstriction.124
In summary, it is possible that increasing the duration of Typical protocols consist of a warm to cold duration ratio
the application of cold or the number of cold applications of 3:1 or 4:1, with temperatures of 38°C to 44°C (100°F
may prove beneficial in reducing DOMS. However, because to 111°F) for warm water and 10°C to 18°C (50°F to
prolonged cryotherapy (greater than 20 minutes in dura- 64°F) for cold water. Treatment starts with 10 minutes of
tion) may actually cause nerve injury,119 prolonged applica- warm-water submersion followed by 1 minute of cold water
tions are not recommended. In contrast to its effectiveness and then 4 minutes of warm water. The cycle continues for
with acute soft tissue injury, cryotherapy (ice massage or ice 30 minutes, ending with warm water.125 However, for the
water immersion, single or multiple applications, before or injured athlete, the cycle should end with cold water to
after exercise) appears to have little or no effect on minimiz- promote vasoconstriction.124 As expected, many different
ing DOMS. This observation may result from the differ- protocols exist with differing warm/cold ratios, tempera-
ences in physiological processes that result in DOMS and tures, cycle times, and frequency of use.
perhaps also the inability of cryotherapy to markedly reduce Using whole-body immersion and 1 minute of cold
intramuscular temperatures.120 water (15°C [59°F]) immersion followed by 1 minute of
warm water (38°C [100°F]) for a total of 14 minutes fol-
Thermotherapy lowing lengthening contractions of the legs in a bilateral
Thermotherapy has been shown to increase tissue tempera- leg-press exercise, contrast baths resulted in reduction of
ture, local blood flow, muscle elasticity and metabolite perception of pain at 24, 48, and 72 hours after the exercise
production121—potentially important factors for reducing protocol compared with 14 minutes of continuous cold- or
DOMS if intramuscular temperature can actually be ele- hot-water immersion.122 However, immersion of only the
vated by thermotherapy. Typical hot water immersion lower extremity to the pelvis for contrast baths of 1 minute
(hydrotherapy) has been reported to have no effect on of cold water (8°C to 10°C [46°F to 50°F]) immersion
reducing DOMS in leg extensor muscles.122 However, followed by 2 minutes of warm water (40°C to 42°C
using a unique injury protocol to the back extensor muscles [104°F to 108°F)) for a total of 15 minutes did not reduce
and a commercially available heat wrap, the positive effects soreness compared with rest.126 If indeed valid, a pumping
of continuous low-level heat versus cold pack therapy action stimulated by alternating vasodilation and vasocon-
were reported.123 Approximately 8 hours of low-level heat striction of blood vessels122 should have resulted from both
(40°C [104°F]) was provided and the device allowed the protocols.122,126 No adequate explanation was provided to
subject to continue to be active while wearing the wrap. account for the different outcomes to contrast baths involv-
The heat wrap group used the device for 8 hours on two ing the whole body or injured limb.
432 SECTION III • Management of Sports Injury and Illness
in DOMS in volunteers subjected to exhausting exercise.142 can be used to enhance physical performance. A wide vari-
Using sensory-level electrical stimulation (TENS) and a ety of techniques are commonly used for massage. For clas-
high-voltage unit set at a frequency of 120 pps, soreness sic western massage or Swedish massage, the most common
perception was reduced during the treatment but did not form of massage used for athletes, five basic techniques
last long afterward.143 Similar findings of lack of prolonged are used: effleurage, pétrissage, tapotement, friction, and
effect were reported for repeated treatments over several vibration.151,152 The progression of the massage advances
days144 using high voltage to produce TENS.144 Thus, it was from distal to proximal and usually lasts between 10 and
possible for traditional TENS to be an effective treatment 30 minutes.152,153 A typical treatment begins and ends with
when the degree of muscle injury was small (e.g., three rep- light gliding strokes with the palm of the hand, known as
etitions) and the attenuation was planned to be temporary effleurage. The initial effleurage strokes then progress to
(e.g., during the treatment only). However, when the dam- deeper stroking known as pétrissage. Pétrissage involves a
age was large, such as is produced by exhaustive exercise, kneading motion or lifting, pressing, or rolling of the
TENS was ineffective. tissues. Tapotement, friction, and vibration can be added
Microcurrent electrical neuromuscular stimulation before the final effleurage strokes. Tapotement involves
(MENS) is a subsensory stimulation using electrical cur- stimulating the tissues either with repetitive percussion
rent amplitudes ( 1000 A) below the level necessary strokes or tapping and is commonly used before and during
for sensory nerve activation. None of the studies available competition.152 Friction techniques that involve circular
using MENS reported any reduction in DOMS. Both movements with the palm or fingertips purportedly can be
continuous stimulation for 48 hours145 and intermittent added for the specific purpose of reducing muscle spasm
treatments146-148 were conducted for varying times after following injury.152 Vibration or shaking is purportedly
muscle injury without effect. At present, MENS has no used for reduction in muscle tone.151
role in treating DOMS. Massage is considered to have a number of physiological
and psychological benefits that may contribute to pain
modulation and tissue repair aided in part by increased
Compression circulation and lymphatic flow.154 However, using exercise-
If exercise-induced muscle tissue injury leads to an influx of induced muscle damage to the quadriceps muscles, massage
fluid (edema) that results in an elevation of intramuscular did not alter blood flow to muscles, but did reduce soreness
pressure and this swelling contributes to the activation of to some degree.155 In contrast, light exercise alone im-
HTM receptors, then modalities that promote movement of proved blood flow and temporarily reduced soreness.155
fluid away from the muscle would be expected to result in less Although exercise might be expected to increase lymphatic
soreness and improved physical performance. Compression return in active muscles, massage was unable to increase
has been studied and results have been mixed depending on lymphatic flow or to reduce edema in humans.151 Despite
the type and duration of compression used. Intermittent com- these findings, a significant reduction in soreness was
pression can briefly reduce swelling and stiffness149 and would reported following a 30-minute massage using a distal
be expected to temporarily reduce the activation of HTM (hand) to proximal (shoulder) sequence with combinations
receptors in injured muscles. In contrast, if fluids could actu- of effleurage, pétrissage, and cross-fiber massage together
ally be squeezed out by external limb compression, constant with shaking.156
compression would be expected to have a more profound The effectiveness of a single massage technique, pétris-
effect. Constant compression using a compressive sleeve did sage, on the subjective reporting of soreness has been
reduce the perception of soreness and swelling following tested for its effectiveness on reducing DOMS.157 Pétris-
elbow flexor contractions.150 The compression garments used sage administered immediately following eccentric exercise
were made of raschel fabric with 25% elastic fabric and pro- did not alleviate DOMS examined 24 and 48 hours later.
vided a 10-mm Hg compressive force. The compression was In contrast, soreness was reduced in 48 hours by the com-
provided for 24 hours per day for 5 days after exercise. In bined effects of effleurage, tapotement, and pétrissage
addition to the decrease in soreness, recovery of muscle force given 2 hours after repeated lengthening contractions of
output and power were also hastened in this study. Although the knee flexor muscles.158 Standardized techniques of
this study shows promising results for the treatment of effleurage, pétrissage, and vibration composed the massage
DOMS, use of compression sleeves for all extremities may not treatment for a group of collegiate women volleyball and
be practical during an athlete’s training. basketball players who were subjected to unaccustomed,
intense training.159 Two days later, both reports of per-
ceived soreness and measurements of the pressure-pain
Massage threshold (algometry) revealed that DOMS was reduced
Massage, like compression, may also help move fluid away immediately after the 17-minute massage as well as provid-
from involved muscles. Massage has been touted as a ing some improvement in physical performance (shuttle
modality that facilitates recovery after intense exercise and run and vertical jump).159
434 SECTION III • Management of Sports Injury and Illness
In summary, some evidence is available to support the active contractions of muscles before a damaging bout of
use of massage to treat DOMS. Unfortunately, the attenu- lengthening contractions would not confer much protec-
ation of soreness is not profound and the mechanism of tion if any.
action is unknown. Because a wide variety of factors are
probably involved,156 additional well-controlled studies are
needed to provide a scientific basis for its action and further Exercise Immediately
insight into the best application. After DOMS-Producing Protocols
Mixed results have been obtained for exercises performed
immediately following protocols designed to produce
Stretching DOMS. For example, upper-arm ergometry was performed
Stretching prior to and after activity is thought to protect an for 8 minutes immediately following the injury protocol
individual from injury and soreness.160 However, a system- and again 24 hours later.146 The arm exercise did not
atic review using pooled data from five studies revealed that improve soreness measured at 24, 48, and 72 hours after
static stretching used before and after exercise produced the initial exercise bout.146 Repeating the same activity but
small but insignificant reductions in muscle soreness.160 using submaximal contractions (25) also did not reduce the
Stretching reduced soreness on average of less than 2 mm on soreness on the day following DOMS-inducing exercise.170
a 100-mm VAS.160 However, no objective recordings of In contrast, when light exercise (i.e., elbow flexion with a
soreness were used. Using an algometer in addition to sore- 5-pound dumbbell for two bouts of 25 repetitions) was
ness ratings (VAS), the effect of static stretching prior to repeated daily following a bout of lengthening contractions,
exercise was tested using hamstring muscle injury to pro- improvements in soreness ratings were reported.171
duce DOMS.161 Four 20-second static stretches prior to 100 Decreased soreness was also measured following high-
repetitions of resisted lengthening contractions of the knee velocity (300°/sec) isokinetic exercise using concentric
flexor muscles produced no preventive effect on DOMS muscle actions performed on the day following the injury
measured with either method in 10 female volunteers.161 protocol.172 Using maximal voluntary efforts and reciprocal
Using knee extensor muscles, passive static stretching (three knee flexion and extension movements, six bouts of 20 rep-
times for 30 seconds) was performed before and immedi- etitions with a rest of 3 minutes between bouts were per-
ately after intensive eccentric exercise and three times daily formed as a successful therapeutic intervention. It is difficult
for the following 7 days; passive stretching did not reduce to resolve these conflicting findings without knowledge of
muscle soreness at any point examined.162 However, both changes in intramuscular tissue pressure, inflammatory cell
static and ballistic stretching can independently produce infiltrates and algesic mediators.
muscle soreness, with the greatest soreness ratings resulting
from static stretching.163 Because stretching might actually
increase soreness, a control group using only the stretching Alternative Therapies and Nutritional Supplements
protocols should be required in future studies such as daily Hyperbaric Oxygen Therapy
stretching (training) prior to exercise. If chronic stretching Hyperbaric oxygen therapy (HBOT) has been used by elite
can actually result in longer muscles as limb distraction athletes as a means of hastening recovery following injury.
does,164 longer muscles would be less susceptible to injury Using 100% oxygen at a pressure of 2.5 atm, daily exposures
from lengthening contractions165 and thus DOMS might be for 60 minutes each were ineffective at reducing soreness
prevented by prior training with stretching. ratings for injured elbow flexor muscles.173,174 In contrast,
increased soreness has been reported to result from HBOT
at 48 and 72 hours following the exercise bout.175
Warmup
An active warmup of 100 shortening contractions per- Acupuncture
formed just before a damaging exercise bout was successful Acupuncture has been recognized as an effective modality for
at decreasing soreness and ROM associated with DOMS.166 pain management,176,177 yet little is known about the effects
However, using a similar warmup exercise did not result in of acupuncture on DOMS. However, following repeated
change.136 Furthermore, using an exhausting stepping lengthening contractions of the elbow flexor muscles to pro-
exercise, no effect of warmup on soreness was reported.167 duce DOMS, needling at traditional acupuncture points or at
Because the magnitude of the force during lengthening is a points identified as most tender by palpation did not reduce
major factor in producing muscle injury,168 fatiguing exer- pain (VAS) or soreness (algometry).178
cise could result in lower forces and thus lower injury
potential during certain activities but not others. However, Homeopathy
fatigue did not offer any protection in preventing muscle The homeopathic approach has been advocated by some
injury by repeated lengthening contractions under con- using Arnica, which is thought to have analgesic179 and
trolled conditions.169 Thus, warmup exercises consisting of anti-inflammatory properties.180 However, no benefit was
Delayed-Onset Muscle Soreness • CHAPTER 17 435
found for Arnica in the treatment of DOMS whether used DOMS.188 Perhaps antioxidant therapy might decrease
as a sublingual pellet181 or as a topical cream.182 DOMS if secondary free radical damage produced by inflam-
matory cells arriving in injured muscles were reduced.
Nutritional Supplements
Nutritional supplements have also been used to treat or pre-
vent DOMS. In a study using only six subjects, L-carnitine
Conclusion
(3 g/day for 3 weeks prior to exercise) decreased pain (VAS) This review has focused on many factors resulting from
and soreness (pain threshold) following knee extensor strain injury to skeletal muscles most likely to produce
exercise.183 DOMS and some that coexist with muscle injury (Figure
Although coenzyme Q10 (120 mg/day) reduced angina 17-7) as well as a wide variety of approaches for the pre-
pectoris following myocardial infarction,184 it may actually vention and treatment of DOMS. No attempt was made
be detrimental to skeletal muscle.185 Prior administration of to evaluate factors involved in perception of soreness
coenzyme Q10 resulted in an increase in markers of muscle including anticipatory fear of pain, anxiety, and catastro-
damage following cycle ergometry that was not seen in phizing.189 From the studies reviewed, only limited suc-
placebo controls.185 cess in reducing DOMS has been reported, providing
Other antioxidants such as vitamins C and E have been evidence that local algesic factors, once produced by
used without definitive results. The treatment of DOMS injured muscle (see Figure 17-7), will continue to sensi-
using vitamin C186 or E187 alone did not result in any measur- tize HTM receptors to encode pressure or movement as
able benefit, whereas an antioxidant mixture did reduce pain or tenderness until they are removed by the cessation
Blood vessel
Monocytes
PMN Plasma
Edema Bradykinin
p III PAIN
ending grou
p tive
e
cic
Leukotrienes Prostaglandins No
Lactate ATP
Arachidonic
Ca2+ K+ Creatine
acid
kinase
FORCE
FORCE
INJURY
of the inflammatory response. However, some limited 14. Christidis N, Nilsson A, Kopp S, Ernberg M: Intramuscular in-
success in reduction of DOMS was obtained by compres- jection of granisetron into the masseter muscle increases the
pressure pain threshold in healthy participants and patients with
sion, massage, and mild exercise perhaps by reducing tis-
localized myalgia, Clin J Pain 23(6):467–472, 2007.
sue pressure and hence the stimulus for HTM receptor 15. Clarkson PM, Hubal MJ: Exercise-induced muscle damage in
activation. Further advances may be forthcoming once humans, Am J Phys Med Rehabil 81(11 Suppl):S52–S69, 2002.
standardization of protocols and muscle groups such as 16. Fischer AA: Reliability of the pressure algometer as a measure of
using the elbow flexor muscles subjected to 50 lengthen- myofascial trigger point sensitivity, Pain 28(3):411–414, 1987.
17. Reeves JL, Jaeger B, Graff-Radford SB: Reliability of the pressure
ing contractions are tested between research groups for
algometer as a measure of myofascial trigger point sensitivity,
consistency. In addition, objective measurements of ten- Pain 24(3):313–321, 1986.
derness such as determination of a pressure-pain thresh- 18. Jaeger B, Reeves JL: Quantification of changes in myofascial trig-
old are required before interventions can be compared ger point sensitivity with the pressure algometer following passive
across studies. To date, DOMS appears to be an inevitable stretch, Pain 27(2):203–210, 1986.
19. Newham DJ, Mills KR, Quigley BM, Edwards RH: Pain and
part of life for active individuals and, although continual
fatigue after concentric and eccentric muscle contractions, Clin
training will prevent subsequent soreness during repeated Sci (Lond) 64(1):55–62, 1983.
exercises, vigorous unaccustomed activities will produce 20. Nussbaum EL, Gabison S: Rebox effect on exercise-induced
DOMS even in trained individuals. Because DOMS is acute inflammation in human muscle, Arch Phys Med Rehabil
transient, it will always resolve within a few days even 79(10):1258–1263, 1998.
21. Hasson SM, Daniels JC, Divine JG, et al: Effect of ibuprofen use
without intervention.
on muscle soreness, damage, and performance: A preliminary
investigation, Med Sci Sports Exerc 25(1):9–17, 1993.
References 22. Hasson SM, Wible CL, Reich M, et al: Dexamethasone
iontophoresis: Effect on delayed muscle soreness and muscle
1. Clarkson PM, Byrnes WC, McCormick KM, et al: Muscle soreness function, Can J Sport Sci 17(1):8–13, 1992.
and serum creatine kinase activity following isometric, eccentric, 23. Baker SJ, Kelly NM, Eston RG: Pressure pain tolerance at differ-
and concentric exercise, Int J Sports Med 7(3):152–155, 1986. ent sites on the quadriceps femoris prior to and following eccen-
2. Nosaka K, Newton M: Repeated eccentric exercise bouts do not tric exercise, Eur J Pain 1(3):229–233, 1996.
exacerbate muscle damage and repair, J Strength Cond Res 24. Chleboun GS, Howell JN, Conatser RR, Giesey JJ: Relationship
16(1):117–122, 2002. between muscle swelling and stiffness after eccentric exercise,
3. Clarkson PM, Nosaka K, Braun B: Muscle function after exercise- Med Sci Sports Exerc 30(4):529–535, 1998.
induced muscle damage and rapid adaptation, Med Sci Sports 25. Jones DA, Newham DJ, Clarkson PM: Skeletal muscle stiffness
Exerc 24(5):512–520, 1992. and pain following eccentric exercise of the elbow flexors, Pain
4. Nosaka K, Chapman D, Newton M, Sacco P: Is isometric 30(2):233–242, 1987.
strength loss immediately after eccentric exercise related to 26. Howell JN, Chleboun G, Conatser R: Muscle stiffness, strength
changes in indirect markers of muscle damage? Appl Physiol Nutr loss, swelling and soreness following exercise-induced injury in
Metab 31(3):313–319, 2006. humans, J Physiol 464:183–196, 1993.
5. Simons DG, Mense S: Understanding and measurement of muscle 27. Ebbeling CB, Clarkson PM: Exercise-induced muscle damage
tone as related to clinical muscle pain, Pain 75(1):1–17, 1998. and adaptation, Sports Med 7(4):207–234, 1989.
6. Graven-Nielsen T, Mense S: The peripheral apparatus of muscle 28. Sayers SP, Clarkson PM, Rouzier PA, Kamen G: Adverse events
pain: Evidence from animal and human studies, Clin J Pain associated with eccentric exercise protocols: Six case studies, Med
17(1):2–10, 2001. Sci Sports Exerc 31(12):1697–1702, 1999.
7. Philen RM, Eidson M, Kilbourne EM, et al: Eosinophilia-myal- 29. Birtles DB, Rayson MP, Jones DA, et al: Effect of eccentric exer-
gia syndrome. A clinical case series of 21 patients. New Mexico cise on patients with chronic exertional compartment syndrome,
Eosinophilia-Myalgia Syndrome Study Group, Arch Intern Med Eur J Appl Physiol 88(6):565–571, 2003.
151(3):533–537, 1991. 30. Friden J, Sfakianos PN, Hargens AR: Muscle soreness and intra-
8. Ali Z, Ranganathan P, Perry A, Gelbart M: Localized striated muscular fluid pressure: Comparison between eccentric and con-
muscle vasculitis in rheumatoid arthritis, J Clin Rheumatol centric load, J Appl Physiol 61(6):2175–2179, 1986.
13(1):35–37, 2007. 31. Gibala MJ, MacDougall JD, Tarnopolsky MA, et al: Changes in
9. Mense S, Meyer H: Bradykinin-induced modulation of the human skeletal muscle ultrastructure and force production after
response behaviour of different types of feline group III and IV acute resistance exercise, J Appl Physiol 78(2):702–708, 1995.
muscle receptors, J Physiol 398:49–63, 1988. 32. Peake JM, Nosaka K, Muthalib M, Suzuki K: Systemic inflamma-
10. Ernberg M, Lundeberg T, Kopp S: Pain and allodynia/hyperalgesia tory responses to maximal versus submaximal lengthening contrac-
induced by intramuscular injection of serotonin in patients with tions of the elbow flexors, Exerc Immunol Rev 12:72–85, 2006.
fibromyalgia and healthy individuals, Pain 85(1–2):31–39, 2000. 33. Nosaka K, Newton M, Sacco P: Responses of human elbow
11. Kumazawa T, Mizumura K: Thin-fibre receptors responding to flexor muscles to electrically stimulated forced lengthening exer-
mechanical, chemical, and thermal stimulation in the skeletal cise, Acta Physiol Scand 174(2):137–145, 2002.
muscle of the dog, J Physiol 273(1):179–194, 1977. 34. MacIntyre DL, Reid WD, Lyster DM, et al: Presence of WBC,
12. Jensen K, Tuxen C, Pedersen-Bjergaard U, et al: Pain and ten- decreased strength, and delayed soreness in muscle after eccentric
derness in human temporal muscle induced by bradykinin and exercise, J Appl Physiol 80(3):1006–1013, 1996.
5-hydroxytryptamine, Peptides 11(6):1127–1132, 1990. 35. Beaton LJ, Tarnopolsky MA, Phillips SM: Contraction-induced
13. Shah JP, Danoff JV, Desai MJ, et al: Biochemicals associated with muscle damage in humans following calcium channel blocker
pain and inflammation are elevated in sites near to and remote administration, J Physiol 544(Pt 3):849–859, 2002.
from active myofascial trigger points, Arch Phys Med Rehabil 36. Yu JG, Thornell LE: Desmin and actin alterations in human
89(1):16–23, 2008. muscles affected by delayed onset muscle soreness: A high resolu-
Delayed-Onset Muscle Soreness • CHAPTER 17 437
tion immunocytochemical study, Histochem Cell Biol 118(2): 58. Morgan DL, Allen DG: Early events in stretch-induced muscle
171–179, 2002. damage, J Appl Physiol 87(6):2007–2015, 1999.
37. Jones DA, Newham DJ, Torgan C: Mechanical influences 59. Warren GL, Ingalls CP, Lowe DA, Armstrong RB: Excitation-
on long-lasting human muscle fatigue and delayed-onset pain, contraction uncoupling: Major role in contraction-induced muscle
J Physiol 412:415–427, 1989. injury, Exerc Sport Sci Rev 29(2):82–87, 2001.
38. Nosaka K: Changes in serum enzyme activities after injection 60. Yeung EW, Balnave CD, Ballard HJ, et al: Development of
of bupivacaine into rat tibialis anterior, J Appl Physiol 81(2): T-tubular vacuoles in eccentrically damaged mouse muscle fibres,
876–884, 1996. J Physiol 540(Pt 2):581–592, 2002.
39. Evans GF, Haller RG, Wyrick PS, et al: Submaximal delayed- 61. Capetanaki Y, Bloch RJ, Kouloumenta A, et al: Muscle interme-
onset muscle soreness: Correlations between MR imaging findings diate filaments and their links to membranes and membranous
and clinical measures, Radiology 208(3):815–820, 1998. organelles, Exp Cell Res 313(10):2063–2076, 2007.
40. Nosaka K, Newton M: Difference in the magnitude of muscle 62. Nosaka K, Muthalib M, Lavender A, Laursen PB: Attenuation of
damage between maximal and submaximal eccentric loading, muscle damage by preconditioning with muscle hyperthermia
J Strength Cond Res 16(2):202–208, 2002. 1-day prior to eccentric exercise, Eur J Appl Physiol 99(2):
41. Nosaka K, Sakamoto K, Newton M, Sacco P: The repeated bout 183–192, 2007.
effect of reduced-load eccentric exercise on elbow flexor muscle 63. Warren GL, Lowe DA, Armstrong RB: Measurement tools used
damage, Eur J Appl Physiol 85(1–2):34–40, 2001. in the study of eccentric contraction-induced injury, Sports Med
42. Clarkson PM, Tremblay I: Exercise-induced muscle damage, 27(1):43–59, 1999.
repair, and adaptation in humans, J Appl Physiol 65(1):1–6, 1988. 64. Biral D, Jakubiec-Puka A, Ciechomska I, et al: Loss of dystrophin
43. Kulig K, Powers CM, Shellock FG, Terk M: The effects of and some dystrophin-associated proteins with concomitant signs
eccentric velocity on activation of elbow flexors: Evaluation of apoptosis in rat leg muscle overworked in extension, Acta
by magnetic resonance imaging, Med Sci Sports Exerc 33(2): Neuropathol 100(6):618–626, 2000.
196–200, 2001. 65. Stauber WT, Miller GR, Gibala MJ, MacDougall JD: Use of dou-
44. Chapman D, Newton M, Sacco P, Nosaka K: Greater muscle ble labeling and photo CD for morphometric analysis of injured
damage induced by fast versus slow velocity eccentric exercise, skeletal muscle, J Histochem Cytochem 43(11):1179–1184, 1995.
Int J Sports Med 27(8):591–598, 2006. 66. Komulainen J, Takala TE, Kuipers H, Hesselink MK: The disrup-
45. Newham DJ, Jones DA, Ghosh G, Aurora P: Muscle fatigue and tion of myofibre structures in rat skeletal muscle after forced
pain after eccentric contractions at long and short length, Clin lengthening contractions, Pflugers Arch 436(5):735–741, 1998.
Sci (Lond) 74(5):553–557, 1988. 67. Wrogemann K, Pena SDJ: Mitochondrial calcium overload: A
46. Mair J, Koller A, Artner-Dworzak E, et al: Effects of exercise on general mechanism for cell-necrosis in muscle diseases, Lancet
plasma myosin heavy chain fragments and MRI of skeletal muscle, 1:672–674, 1976.
J Appl Physiol 72(2):656–663, 1992. 68. Trump BF, Berezesky IK: Calcium-mediated cell injury and cell
47. Chapman DW, Newton MJ, Zainuddin Z, et al: Work and peak death, FASEB J 9(2):219–228, 1995.
torque during eccentric exercise do not predict changes in mark- 69. Lowe DA, Warren GL, Ingalls CP, et al: Muscle function and
ers of muscle damage, Br J Sports Med 242:585–591, 2008. protein metabolism after initiation of eccentric contraction-
48. Hough T: Ergographic studies in muscular soreness, Am J Physiol induced injury, J Appl Physiol 79(4):1260–1270, 1995.
7:76–92, 1902. 70. Crenshaw AG, Friden J, Hargens AR, et al: Increased technetium
49. Ebbeling CB, Clarkson PM: Muscle adaptation prior to recovery uptake is not equivalent to muscle necrosis: Scintigraphic, mor-
following eccentric exercise, Eur J Appl Physiol Occup Physiol phological and intramuscular pressure analyses of sore muscles
60(1):26–31, 1990. after exercise, Acta Physiol Scand 148(2):187–198, 1993.
50. Nosaka K, Clarkson PM: Muscle damage following repeated 71. Petrof BJ, Shrager JB, Stedman HH, et al: Dystrophin protects
bouts of high force eccentric exercise, Med Sci Sports Exerc the sarcolemma from stresses developed during muscle contrac-
27(9):1263–1269, 1995. tion, Proc Natl Acad Sci USA 90(8):3710–3714, 1993.
51. Warren GL, Ingalls CP, Lowe DA, Armstrong RB: What mecha- 72. McNeil PL, Khakee R: Disruptions of muscle fiber plasma mem-
nisms contribute to the strength loss that occurs during and in branes. Role in exercise-induced damage, Am J Pathol
the recovery from skeletal muscle injury? J Orthop Sports Phys 140(5):1097–1109, 1992.
Ther 32(2):58–64, 2002. 73. Sorichter S, Puschendorf B, Mair J: Skeletal muscle injury in-
52. Stauber WT, Willems ME: Prevention of histopathologic changes duced by eccentric muscle action: Muscle proteins as markers of
from 30 repeated stretches of active rat skeletal muscles by long muscle fiber injury, Exerc Immunol Rev 5:5–21, 1999.
inter-stretch rest times, Eur J Appl Physiol 88(1–2):94–99, 2002. 74. Simionescu N, Simionescu M, Palade GE: Permeability of muscle
53. Warren GL, Ingalls CP, Shah SJ, Armstrong RB: Uncoupling of capillaries to exogenous myoglobin, J Cell Biol 57(2):424–452,
in vivo torque production from EMG in mouse muscles injured 1973.
by eccentric contractions, J Physiol 515 (Pt 2):609–619, 1999. 75. Feola M, Glick G: Cardiac lymph flow and composition in acute
54. Hesselink MK, Kuipers H, Geurten P, Van Straaten H: Structural myocardial ischemia in dogs, Am J Physiol 229(1):44–48, 1975.
muscle damage and muscle strength after incremental number of 76. Malm C, Nyberg P, Engstrom M, et al: Immunological changes
isometric and forced lengthening contractions, J Muscle Res Cell in human skeletal muscle and blood after eccentric exercise and
Motil 17(3):335–341, 1996. multiple biopsies, J Physiol 529(Pt 1):243–62, 2000.
55. Lieber RL, Friden J: Muscle damage is not a function of muscle 77. Smith LL: Acute inflammation: The underlying mechanism in
force but active muscle strain, J Appl Physiol 74(2):520–526, delayed onset muscle soreness? Med Sci Sports Exerc 23(5):
1993. 542–551, 1991.
56. Friden J, Sjostrom M, Ekblom B: Myofibrillar damage following 78. MacIntyre DL, Sorichter S, Mair J, et al: Markers of inflamma-
intense eccentric exercise in man, Int J Sports Med 4(3):170–176, tion and myofibrillar proteins following eccentric exercise in hu-
1983. mans, Eur J Appl Physiol 84(3):180–186, 2001.
57. Stauber WT, Clarkson PM, Fritz VK, Evans WJ: Extracellular 79. Tidball JG, Berchenko E, Frenette J: Macrophage invasion does
matrix disruption and pain after eccentric muscle action, J Appl not contribute to muscle membrane injury during inflammation,
Physiol 69(3):868–874, 1990. J Leukoc Biol 65(4):492–498, 1999.
438 SECTION III • Management of Sports Injury and Illness
80. Armstrong RB: Initial events in exercise-induced muscular injury, 101. Grossman JM, Arnold BL, Perrin DH, Kahler DM: Effect of
Med Sci Sports Exerc 22(4):429–435, 1990. ibuprofen on delayed onset muscle soreness of the elbow flexors,
81. Duncan CJ, Jackson MJ: Different mechanisms mediate struc- J Sport Rehabil 4:253–263, 1995.
tural changes and intracellular enzyme efflux following damage 102. Barlas P, Craig JA, Robinson J, et al: Managing delayed-onset
to skeletal muscle, J Cell Sci 87(Pt 1):183–188, 1987. muscle soreness: Lack of effect of selected oral systemic analgesics,
82. Kozik A, Moore RB, Potempa J, et al: A novel mechanism for Arch Phys Med Rehabil 81(7):966–972, 2000.
bradykinin production at inflammatory sites. Diverse effects of a 103. Bourgeois J, MacDougall D, MacDonald J, Tarnopolsky M:
mixture of neutrophil elastase and mast cell tryptase versus tissue Naproxen does not alter indices of muscle damage in resistance-
and plasma kallikreins on native and oxidized kininogens, J Biol exercise trained men, Med Sci Sports Exerc 31(1):4–9, 1999.
Chem 273(50):33224–33229, 1998. 104. Pizza FX, Cavender D, Stockard A, et al: Anti-inflammatory
83. Kushnir-Sukhov NM, Brown JM, Wu Y, et al: Human mast cells doses of ibuprofen: Effect on neutrophils and exercise-induced
are capable of serotonin synthesis and release, J Allergy Clin muscle injury, Int J Sports Med 20(2):98–102, 1999.
Immunol 119(2):498–499, 2007. 105. Brooks PM, Day RO: Nonsteroidal antiinflammatory drugs—
84. Stauber WT, Fritz VK, Vogelbach DW, Dahlmann B: Character- Differences and similarities, N Engl J Med 324(24):1716–1725,
ization of muscles injured by forced lengthening. I. Cellular 1991.
infiltrates, Med Sci Sports Exerc 20(4):345–353, 1988. 106. Donnelly AE, McCormick K, Maughan RJ, et al: Effects of a
85. Nahirney PC, Dow PR, Ovalle WK: Quantitative morphology of non-steroidal anti-inflammatory drug on delayed onset muscle
mast cells in skeletal muscle of normal and genetically dystrophic soreness and indices of damage, Br J Sports Med 22(1):35–38,
mice, Anat Rec 247(3):341–349, 1997. 1988.
86. Ogilvie RW, Armstrong RB, Baird KE, Bottoms CL: Lesions in 107. Sayers SP, Knight CA, Clarkson PM, et al: Effect of ketoprofen
the rat soleus muscle following eccentrically biased exercise, Am on muscle function and sEMG activity after eccentric exercise,
J Anat 182(4):335–346, 1988. Med Sci Sports Exerc 33(5):702–710, 2001.
87. The FO, Bennink RJ, Ankum WM, et al: Intestinal handling- 108. Howell JN, Conaster RR, Chleboun GS, et al: The effect of
induced mast cell activation and inflammation in human postop- nonsteroidal anti-inflammatory drugs on recovery from exercise-
erative ileus, Gut 57(1):33–40, 2008. induced muscle injury. 2. Ibuprofen, J Musculoskeletal Pain
88. Lazarus B, Messina A, Barker JE, et al: The role of mast cells in 6:69–83, 1998.
ischaemia-reperfusion injury in murine skeletal muscle, J Pathol 109. Almekinders LC, Gilbert JA: Healing of experimental muscle
191(4):443–448, 2000. strains and the effects of nonsteroidal antiinflammatory medication,
89. Chleboun GS, Howell JN, Conatser RR, Giesey JJ: The relation- Am J Sports Med 14(4):303–308, 1986.
ship between elbow flexor volume and angular stiffness at the 110. Nosaka K, Clarkson PM: Changes in indicators of inflammation
elbow, Clin Biomech 12(6):383–392, 1997. after eccentric exercise of the elbow flexors, Med Sci Sports Exerc
90. Friden J, Sfakianos PN, Hargens AR, Akeson WH: Residual 28(8):953–961, 1996.
muscular swelling after repetitive eccentric contractions, J Orthop 111. Michlovitz S: Cold therapy modalities: Frozen peas and more. In
Res 6(4):493–498, 1988. Michlovitz S, Nolan T, editors: Modalities for therapeutic inter-
91. Brown SJ, Child RB, Day SH, Donnelly AE: Indices of skeletal vention, ed 4, Philadelphia, 2005, FA Davis Company.
muscle damage and connective tissue breakdown following eccen- 112. Enwemeka CS, Allen C, Avila P, et al: Soft tissue thermodynam-
tric muscle contractions, Eur J Appl Physiol Occup Physiol 75(4): ics before, during, and after cold pack therapy, Med Sci Sports
369–374, 1997. Exerc 34(1):45–50, 2002.
92. Foley JM, Jayaraman RC, Prior BM, et al: MR measurements of 113. Eston R, Peters D: Effects of cold water immersion on the
muscle damage and adaptation after eccentric exercise, J Appl symptoms of exercise-induced muscle damage, J Sports Sci
Physiol 87(6):2311–2318, 1999. 17(3):231–238, 1999.
93. Malm C, Sjodin TL, Sjoberg B, et al: Leukocytes, cytokines, 114. Paddon-Jones DJ, Quigley BM: Effect of cryotherapy on muscle
growth factors and hormones in human skeletal muscle and soreness and strength following eccentric exercise, Int J Sports
blood after uphill or downhill running, J Physiol 556(Pt 3): Med 18(8):588–593, 1997.
983–1000, 2004. 115. Yackzan L, Adams C, Francis KT: The effects of ice massage on
94. Nosaka K, Sakamoto K, Newton M, Sacco P: How long does the delayed muscle soreness, Am J Sports Med 12(2):159–165,
protective effect on eccentric exercise-induced muscle damage 1984.
last? Med Sci Sports Exerc 33(9):1490–1495, 2001. 116. Isabell WK, Durrant E, Myrer W, Anderson S: The effects of ice
95. Newham DJ, Jones DA, Clarkson PM: Repeated high-force massage, ice massage with exercise, and exercise on the prevention
eccentric exercise: Effects on muscle pain and damage, J Appl and treatment of delayed onset muscle soreness, J Athl Train
Physiol 63(4):1381–1386, 1987. 27(3):208–217, 1992.
96. Nosaka K, Newton MJ, Sacco P: Attenuation of protective effect 117. Sellwood KL, Brukner P, Williams D, et al: Ice-water immersion
against eccentric exercise-induced muscle damage, Can J Appl and delayed-onset muscle soreness: A randomised controlled
Physiol 30(5):529–542, 2005. trial, Br J Sports Med 41(6):392–397, 2007.
97. Whitehead NP, Allen TJ, Morgan DL, Proske U: Damage to 118. Howatson G, Gaze D, van Someren KA: The efficacy of ice mas-
human muscle from eccentric exercise after training with concentric sage in the treatment of exercise-induced muscle damage, Scand
exercise, J Physiol 512(Pt 2):615–620, 1998. J Med Sci Sports 15(6):416–422, 2005.
98. Butterfield TA, Leonard TR, Herzog W: Differential serial sarco- 119. Meeusen R, Lievens P: The use of cryotherapy in sports injuries,
mere number adaptations in knee extensor muscles of rats is con- Sports Med 3(6):398–414, 1986.
traction type dependent, J Appl Physiol 99(4):1352–1358, 2005. 120. Myrer JW, Measom G, Fellingham GW: Temperature changes
99. Kuipers H, Keizer HA, Verstappen FT, Costill DL: Influence of a in the human leg during and after two methods of cryotherapy,
prostaglandin-inhibiting drug on muscle soreness after eccentric J Athl Train 33(1):25–29, 1998.
work, Int J Sports Med 6(6):336–339, 1985. 121. Michlovitz S, Rennie S: Heat therapy modalities: Beyond fake
100. Donnelly AE, Maughan RJ, Whiting PH: Effects of ibuprofen on and bake. In Michlovitz S, Nolan T, editors: Modalities for thera-
exercise-induced muscle soreness and indices of muscle damage, peutic intervention, ed 4, Philadephia, 2005, FA Davis Com-
Br J Sports Med 24(3):191–195, 1990. pany.
Delayed-Onset Muscle Soreness • CHAPTER 17 439
122. Vaile J, Halson S, Gill N, Dawson B: Effect of hydrotherapy on onset muscle soreness, Clin Physiol Funct Imaging 22(5):
the signs and symptoms of delayed onset muscle soreness, Eur J 339–347, 2002.
Appl Physiol 102(4):447–455, 2008. 143. Butterfield DL, Draper DO, Ricard MD, et al: The effects of
123. Mayer JM, Mooney V, Matheson LN, et al: Continuous low-level high-volt pulsed current electrical stimulation on delayed-onset
heat wrap therapy for the prevention and early phase treatment of muscle soreness, J Athl Train 32(1):15–20, 1997.
delayed-onset muscle soreness of the low back: A randomized con- 144. Tourville TW, Connolly DA, Reed BV: Effects of sensory-level
trolled trial, Arch Phys Med Rehabil 87(10):1310–1317, 2006. high-volt pulsed electrical current on delayed-onset muscle
124. Cochrane DJ: Alternating hot and cold water immersion for soreness, J Sports Sci 24(9):941–949, 2006.
athlete recovery: A review, Phys Ther Sport 5(1):26–32, 2004. 145. Lambert MI, Marcus P, Burgess T, Noakes TD: Electro-membrane
125. Bukowski EL, Nolan TP. Hydrotherapy: The use of water as a microcurrent therapy reduces signs and symptoms of muscle
therapeutic agent. In Michlovitz S, Nolan T, editors: Modalities damage, Med Sci Sports Exerc 34(4):602–607, 2002.
for therapeutic intervention, ed 4, Philadelphia, 2005, FA Davis 146. Weber MD, Servedio FJ, Woodall WR: The effects of three
Company. modalities on delayed onset muscle soreness, J Orthop Sports Phys
126. Vaile JM, Gill ND, Blazevich AJ: The effect of contrast water Ther 20(5):236–242, 1994.
therapy on symptoms of delayed onset muscle soreness, J Strength 147. Allen JD, Mattacola CG, Perrin DH: Effect of microcurrent
Cond Res 21(3):697–702, 2007. stimulation on delayed-onset muscle soreness: A double-blind
127. Webster DF, Harvey W, Dyson M, Pond JB: The role of comparison, J Athl Train 34(4):334–337, 1999.
ultrasound-induced cavitation in the “in vitro” stimulation of 148. Denegar CR, Yoho AP, Borowicz AJ, Bifulco N: The effects of
collagen synthesis in human fibroblasts, Ultrasonics 18(1):33–37, low-volt, microamperage stimulation on delayed onset muscle
1980. soreness, J Sport Rehabil 1(2):95–102, 1992.
128. Byl NN, McKenzie AL, West JM, et al: Low-dose ultrasound 149. Chleboun GS, Howell JN, Baker HL, et al: Intermittent pneu-
effects on wound healing: A controlled study with Yucatan pigs, matic compression effect on eccentric exercise-induced swelling,
Arch Phys Med Rehabil 73(7):656–664, 1992. stiffness, and strength loss, Arch Phys Med Rehabil 76(8):
129. Young SR, Dyson M: Effect of therapeutic ultrasound on the 744–749, 1995.
healing of full-thickness excised skin lesions, Ultrasonics 150. Kraemer WJ, Bush JA, Wickham RB, et al: Influence of compres-
28(3):175–180, 1990. sion therapy on symptoms following soft tissue injury from
130. Francis CW, Onundarson PT, Carstensen EL, et al: Enhancement maximal eccentric exercise, J Orthop Sports Phys Ther 31(6):
of fibrinolysis in vitro by ultrasound, J Clin Invest 90(5): 282–290, 2001.
2063–2068, 1992. 151. Callaghan MJ: The role of massage in the management of the
131. Young SR, Dyson M: The effect of therapeutic ultrasound on athlete: A review, Br J Sports Med 27(1):28–33, 1993.
angiogenesis, Ultrasound Med Biol 16(3):261–269, 1990. 152. Weerapong P, Hume PA, Kolt GS: The mechanisms of massage
132. Speed CA: Therapeutic ultrasound in soft tissue lesions, and effects on performance, muscle recovery and injury preven-
Rheumatology (Oxford), 40(12):1331–1336, 2001. tion, Sports Med 35(3):235–256, 2005.
133. Hasson S, Mundorf R, Barnes W, et al: Effect of pulsed ultrasound 153. Cafarelli E, Flint F: The role of massage in preparation for and re-
versus placebo on muscle soreness perception and muscular perfor- covery from exercise, An overview, Sports Med 14(1):1–9, 1992.
mance, Scand J Rehabil Med 22(4):199–205, 1990. 154. Wright A, Sluka KA: Nonpharmacological treatments for muscu-
134. Craig JA, Bradley J, Walsh DM, et al: Delayed onset muscle loskeletal pain, Clin J Pain 17(1):33–46, 2001.
soreness: Lack of effect of therapeutic ultrasound in humans, Arch 155. Tiidus PM, Shoemaker JK: Effleurage massage, muscle blood
Phys Med Rehabil 80(3):318–323, 1999. flow and long-term post-exercise strength recovery, Int J Sports
135. Stay JC, Richard MD, Draper DO, et al: Pulsed ultrasound fails Med 16(7):478–483, 1995.
to diminish delayed-onset muscle soreness symptoms, J Athl 156. Smith LL, Keating MN, Holbert D, et al: The effects of athletic
Train 33(4):341–346, 1998. massage on delayed onset muscle soreness, creatine kinase, and
136. Evans RK, Knight KL, Draper DO, Parcell AC: Effects of warm- neutrophil count: A preliminary report, J Orthop Sports Phys Ther
up before eccentric exercise on indirect markers of muscle damage, 19(2):93–99, 1994.
Med Sci Sports Exerc 34(12):1892–1899, 2002. 157. Lightfoot JT, Char D, McDermott J, Goya C: Immediate postex-
137. Symons TB, Clasey JL, Gater DR, Yates JW: Effects of deep heat ercise massage does not attenuate delayed onset muscle soreness,
as a preventative mechanism on delayed onset muscle soreness, J Strength Cond Res 11:119–124, 1997.
J Strength Cond Res 18(1):155–161, 2004. 158. Hilbert JE, Sforzo GA, Swensen T: The effects of massage on de-
138. Ciccone CD, Leggin BG, Callamaro JJ: Effects of ultrasound layed onset muscle soreness, Br J Sports Med 37(1):72–75, 2003.
and trolamine salicylate phonophoresis on delayed-onset muscle 159. Mancinelli CA, Davis DS, Aboulhosn L, et al: The effects of mas-
soreness, Phys Ther 71(9):666–675, 1991. sage on delayed onset muscle soreness and physical performance
139. Rao VR, Wolf SL, Gersh MR: Examination of electrode place- in female collegiate athletes, Phys Ther Sport 7:5–13, 2006.
ments and stimulating parameters in treating chronic pain with 160. Herbert RD, Gabriel M: Effects of stretching before and after
conventional transcutaneous electrical nerve stimulation (TENS), exercising on muscle soreness and risk of injury: Systematic
Pain 11(1):37–47, 1981. review, BMJ 325(7362):468, 2002.
140. Denegar CR, Perrin DH: Effect of transcutaneous electrical 161. Johansson PH, Lindstrom L, Sundelin G, Lindstrom B: The
nerve stimulation, cold, and a combination treatment on pain, effects of preexercise stretching on muscular soreness, tenderness
decreased range of motion, and strength loss associated with and force loss following heavy eccentric exercise, Scand J Med Sci
delayed onset muscle soreness, J Athl Train 27(3):200–206, Sports 9(4):219–225, 1999.
1992. 162. Lund H, Vestergaard-Poulsen P, Kanstrup IL, Sejrsen P: The ef-
141. Craig JA, Cunningham MB, Walsh DM, et al: Lack of effect of fect of passive stretching on delayed onset muscle soreness, and
transcutaneous electrical nerve stimulation upon experimentally other detrimental effects following eccentric exercise, Scand J
induced delayed onset muscle soreness in humans, Pain 67 Med Sci Sports 8(4):216–221, 1998.
(2–3):285–289, 1996. 163. Smith LL, Brunetz MH, Chenier TC, et al: The effects of static
142. Minder PM, Noble JG, ves-Guerreiro J, et al: Interferential and ballistic stretching on delayed onset muscle soreness and
therapy: Lack of effect upon experimentally induced delayed creatine kinase, Res Q Exerc Sport 64(1):103–107, 1993.
440 SECTION III • Management of Sports Injury and Illness
164. Caiozzo VJ, Utkan A, Chou R, et al: Effects of distraction on 177. Pomeranz B: Scientific research into acupuncture for the relief of
muscle length: Mechanisms involved in sarcomerogenesis, Clin pain, J Altern Complement Med 2(1):53–60, 1996.
Orthop Relat Res 403:S133–S145, 2002. 178. Barlas P, Robinson J, Allen J, Baxter GD: Lack of effect of
165. Brockett CL, Morgan DL, Proske U: Human hamstring muscles acupuncture upon signs and symptoms of delayed onset muscle
adapt to eccentric exercise by changing optimum length, Med Sci soreness, Clin Physiol 20(6):449–456, 2000.
Sports Exerc 33(5):783–790, 2001. 179. Robertson A, Suryanarayanan R, Banerjee A: Homeopathic
166. Nosaka K, Clarkson PM: Influence of previous concentric exer- Arnica montana for post-tonsillectomy analgesia: A randomised
cise on eccentric exercise-induced muscle damage, J Sports Sci placebo control trial, Homeopathy 96(1):17–21, 2007.
15(5):477–483, 1997. 180. Cheung K, Hume P, Maxwell L: Delayed onset muscle soreness:
167. High DM, Howley ET, Franks BD: The effects of static stretching Treatment strategies and performance factors, Sports Med
and warm-up on prevention of delayed-onset muscle soreness, Res 33(2):145–164, 2003.
Q Exerc Sport 60(4):357–361, 1989. 181. Vickers AJ, Fisher P, Smith C, et al: Homoeopathy for delayed
168. Warren GL, Hayes DA, Lowe DA, Armstrong RB: Mechanical onset muscle soreness: A randomised double blind placebo
factors in the initiation of eccentric contraction-induced injury in controlled trial, Br J Sports Med 31(4):304–307, 1997.
rat soleus muscle, J Physiol 464:457–475, 1993. 182. Gulick DT, Kimura IF, Sitler M, et al: Various treatment
169. Morgan DL, Gregory JE, Proske U: The influence of fatigue on techniques on signs and symptoms of delayed onset muscle
damage from eccentric contractions in the gastrocnemius muscle soreness, J Athl Train 31(2):145–152, 1996.
of the cat, J Physiol 561(Pt 3):841–850, 2004. 183. Giamberardino MA, Dragani L, Valente R, et al: Effects of
170. Donnelly AE, Clarkson PM, Maughan RJ: Exercise-induced prolonged L-carnitine administration on delayed muscle pain
muscle damage: Effects of light exercise on damaged muscle, Eur and CK release after eccentric effort, Int J Sports Med 17(5):
J Appl Physiol Occup Physiol 64(4):350–353, 1992. 320–324, 1996.
171. Sayers SP, Clarkson PM, Lee J: Activity and immobilization after 184. Singh RB, Wander GS, Rastogi A, et al: Randomized, double-
eccentric exercise: I. Recovery of muscle function, Med Sci Sports blind placebo-controlled trial of coenzyme Q10 in patients with
Exerc 32(9):1587–1592, 2000. acute myocardial infarction, Cardiovasc Drugs Ther 12(4):
172. Hasson S, Barnes W, Hunter M, Williams J: Therapeutic effect of 347–353, 1998.
high speed voluntary muscle contractions on muscle soreness and 185. Malm C, Svensson M, Sjoberg B, et al: Supplementation with
muscle performance, J Orthop Sports Phys Ther 10:499–507, ubiquinone-10 causes cellular damage during intense exercise,
1989. Acta Physiol Scand 157(4):511–512, 1996.
173. Mekjavic IB, Exner JA, Tesch PA, Eiken O: Hyperbaric oxygen 186. Connolly DA, Lauzon C, Agnew J, et al: The effects of vitamin C
therapy does not affect recovery from delayed onset muscle sore- supplementation on symptoms of delayed onset muscle soreness,
ness, Med Sci Sports Exerc 32(3):558–563, 2000. J Sports Med Phys Fitness 46(3):462–467, 2006.
174. Harrison BC, Robinson D, Davison BJ, et al: Treatment of 187. Avery NG, Kaiser JL, Sharman MJ, et al: Effects of vitamin E
exercise-induced muscle injury via hyperbaric oxygen therapy, supplementation on recovery from repeated bouts of resistance
Med Sci Sports Exerc 33(1):36–42, 2001. exercise, J Strength Cond Res 17(4):801–809, 2003.
175. Bennett M, Best TM, Babul S, et al: Hyperbaric oxygen therapy 188. Bloomer RJ, Goldfarb AH, McKenzie MJ, et al: Effects of
for delayed onset muscle soreness and closed soft tissue injury, antioxidant therapy in women exposed to eccentric exercise,
Cochrane Database Syst Rev (4):CD004713, 2005. Int J Sport Nutr Exerc Metab 14(4):377–388, 2004.
176. Berman BM, Lao L, Langenberg P, et al: Effectiveness of 189. George SZ, Dover GC, Fillingim RB: Fear of pain influences
acupuncture as adjunctive therapy in osteoarthritis of the knee: outcomes after exercise-induced delayed onset muscle soreness at
A randomized, controlled trial, Ann Intern Med 141(12): the shoulder, Clin J Pain 23(1):76–84, 2007.
901–910, 2004.
18
CHAPTER
441
442 SECTION III • Management of Sports Injury and Illness
is in the cardiac muscle. The cardiac muscle is asymmetri- Blood pressure, in the hemodynamic sense, can be con-
cally hypertrophied and an associated nondilated left ven- ceptualized as a product of both cardiac output and periph-
tricle is present. The septal thickness is at least 15 mm thick eral vascular resistance.14 In young athletes, hypertensive
and the left ventricular (LV) cavity is less than 45 mm in changes in blood pressure are most commonly the result of
cases of HCM.9 Currently, echocardiography is the gold a significant increase in cardiac output, with minimal
standard for the detection of HCM. HCM is rare in the changes in peripheral vascular resistance. Heart rate, renal
setting of a normal electrocardiogram (ECG). ECG find- blood flow, plasma renin activity, and catecholamines are all
ings are relatively nonspecific, but include LV hypertrophy elevated in the young hypertensive athlete, and cardiac out-
and ST segment and T wave abnormalities. put is increased 10% to 20% more than that seen in normal
Currently, a diagnosis of HCM excludes participation in subjects. The hypertension of young athletes, therefore, has
competitive and noncompetitive sports, with the exception been characterized as a hyperadrenergic or hyperdynamic
of low-intensity sports. hypertension. On the other hand, in middle-aged or older
athletes, hypertensive blood pressure change is most likely a
reflection of significant increases in peripheral vascular resis-
Athletic Heart Syndrome tance with no change or a decrease in cardiac output.
In athletes, there is a well-accepted condition described as When clinically evaluating an athlete with hypertension,
athlete’s heart syndrome. This may be confused with HCM as the history should focus on behaviors that may affect blood
both conditions are characterized by an enlarged heart. pressure. These include a high intake of sodium and saturated
Isometric or endurance training trigger physiological adapta- fats (e.g., in processed and “fast” foods) and the use of
tions and structural cardiac remodeling, including increased alcohol, drugs (specifically stimulants taken before competi-
left ventricle wall thickness, enlarged ventricular and atrial tions or cocaine), tobacco, or anabolic steroids.15 Many
cavity dimensions, and increased cardiac mass.10 The athlete’s over-the-counter medications, including nonsteroidal anti-
heart has a septal thickness of less than 15 mm and the LV inflammatory drugs, caffeine, diet pills, and decongestants,
cavity is larger than 55 mm (Table 18-1).9 can also cause blood pressure to rise. In women, the estrogen
in oral contraceptive pills can also lead to hypertension.
Patients should also be questioned about the use of herbs
Hypertension and dietary supplements, with special attention given to sub-
Athletes and physically active people are thought to be free stances purported to increase energy or control weight. These
of high blood pressure (hypertension) because of their supplements often contain “natural” substances such as gua-
high level of fitness. In athletes, the overall presence of rana, ma huang, and ephedra, which are stimulants.
hypertension is approximately 50% less than the general
population.11
Certain populations of athletes are at increased risk of Risk Factors for Hypertension
hypertension. These include black athletes, elderly athletes,
• High sodium intake
obese athletes, diabetic athletes, those with renal disease, or • Excessive alcohol consumption
athletes with family history of hypertension. • Illicit drug use (e.g., cocaine)
Hypertension may occur in early adulthood. As people • Anabolic steroid use
age, the prevalence of hypertension increases. For example, • Stimulant use
5% to 10% of adults aged 20 to 30 are affected and 20% to • High stress
25% of adults aged 30 to 60 are affected.12 • Male gender
Interestingly, 80% of athletes who have blood pressure • Black race
higher than 142/92 at a preparticipation medical examina- • Family history of hypertension
tion eventually develop chronic elevated blood pressure.13 • Diabetes mellitus
• Smoking
• Obesity
Table 18-1
Heart Differences in Athletic Heart Syndrome
and Hypertrophic Cardiomyopathy The physical examination should include proper mea-
surement of blood pressure, which may include serial mea-
Athletic Heart Hypertrophic
surements. Laboratory tests that exclude other medical
Syndrome Cardiomyopathy
causes of hypertension may include an ECG; a complete
Septal thickness 15 mm 15 mm blood count; urinalysis; and measurements of sodium, po-
Left ventricular 55 mm 45 mm tassium, blood urea nitrogen, creatinine, fasting glucose,
cavity size total low-density lipoprotein, and high-density lipoprotein
cholesterol levels.
Medical Conditions in Sport • CHAPTER 18 443
Treatment includes both nonpharmacological and phar- Clinical characteristics include abnormalities of the ocu-
macological therapy. Nonpharmacological therapy includes lar, skeletal, and cardiovascular systems (Table 18-2).22-24
dietary changes aimed at restricting sodium intake. Intake The diagnosis is made if major criteria are present
of potatoes, bananas, and other foods high in potassium in two organ systems and a third is involved, or when
may provide some protection against high blood pressure.16 there is a family history of Marfan syndrome.22,23 The
A weight loss of 10 pounds can reduce blood pressure.17 skeletal abnormalities include arm span/height ratio of
Changes of lifestyle to include limiting alcohol intake to less greater than 1.05, tall stature, arachnodactyly (long,
than two beers per day.15 Regular aerobic exercise (moder- spiderlike fingers and toes), long and thin limbs, hyper-
ate level of exercise), muscle relaxation, meditation, and extensibility, scoliosis, and chest wall deformities. Lens
other stress management techniques can also be helpful.18 dislocations make up the ocular abnormality. Cardiovas-
From a pharmacological perspective, the ideal antihyper- cular abnormalities include progressive dilatation of the
tensive agent for use in competitive athletes should be free aortic or descending root, which is the ultimate cause of
of any depressant effect on the myocardium, have no ar- death. Mitral valve prolapse with mitral regurgitation
rhythmogenic potential, preserve the redistribution of blood and lateral ventricle systolic dysfunction may also
flow to exercising muscle, and not interfere with efficient predispose to life threatening arrhythmias. Clinically,
substrate use for energy demands.19 In the young athlete, symptoms are relatively nonspecific and may include
the agents that meet all these criteria are the angiotensin- fatigue, shortness of breath, syncope, or presyncopal-
converting enzyme (ACE) inhibitors. The use of beta block- type episodes. Aortic rupture usually results in sudden
ers should be discouraged because of their known ability death. It is generally recommended that athletes with
to impair LV function, their unfavorable effect on serum Marfan syndrome have regular cardiac evaluations and
lipids, and their negative influence on the mobilization not compete in high-intensity or contact sports. In cer-
of lipids during prolonged submaximal exercise. Likewise, tain situations, they may compete in low-intensity and
diuretics are unsuitable first-line agents for the athlete low-dynamic sports.
because of their unfavorable effect on serum lipids, their
potential to cause hypokalemia and hypomagnesemia, and
their negative influence on volume status. For the older Coronary Artery Abnormalities
patient, appropriate first-line agents include the calcium- Congenital coronary artery abnormalities are the second
channel blockers and the ACE inhibitors. A combination of most common cause of exercise-associated death in young
both these agents may be beneficial in treating the older patients. The most commonly reported coronary abnor-
athlete whose blood pressure is resistant to treatment with mality in the young athlete at autopsy is anomalous left
either agent used singly. The hypertensive black athlete coronary artery that originates from the right sinus of
deserves special mention because of the volume-dependent Valsalva and then makes an abrupt turn to travel between
nature of the hypertension. The patient may respond to the pulmonary artery and aorta.8 Anomalous right coro-
very small doses of diuretic such as 12.5 mg of hydrochloro- nary arteries and single coronary arteries have been
thiazide daily. Other options for this population include reported as well. It is next to impossible to screen for
antiadrenergic agents as well as the calcium-channel block- abnormalities for this condition on physical examination.
ers. For the athlete participating in events at which An athlete who presents with syncope, syncopal-type
drug testing will be done, special consideration must be episodes, or chest pain requires investigation and consul-
given to the choice of therapeutic agents, because beta tation by a cardiologist.
blockers (in some events) and diuretics are banned by both
the International Olympic Committee and the World
Anti-Doping Agency.
Table 18-2
Recommendations from the 26th Bethesda conference
for exercise in athletes with hypertension include no restric- Marfan Syndrome Abnormalities
tions if an athlete has high normal blood pressure or con- Skeletal Ocular Cardiovascular
trolled mild to moderate hypertension ( 140/90 mm Hg).
If hypertension is uncontrolled ( 140/90 mm Hg) or Arm span:height Lens Progressive dilatation
ratio of 1.05 dislocations of aortic root
there is any end organ damage present, then low-intensity
Tall stature Progressive dilatation
dynamic exercise is recommended.
Arachnodactyly of descending root
Long, thin limbs Mitral valve prolapse
Hyperextensibility Mitral regurgitation
Marfan Syndrome
Scoliosis Left ventricle systolic
Marfan syndrome is a genetic (autosomal dominant) dis- Chest wall dysfunction
order of connective tissue with an estimated prevalence deformities
of 1:5000 to 1:10,000 in the general population.20-23
444 SECTION III • Management of Sports Injury and Illness
athlete has developed influenza, it usually occurs in winter edema (HAPE) and high-altitude cerebral edema (HACE).
or early spring and is associated with a rapidly rising Both HAPE and HACE are life-threatening manifestations
fever, headache, and cough. Before treating with antiviral of altitude illness and fortunately only occur in 0.1% to 4.0%
medication (e.g., zanamivir, amantadine), a rapid enzyme of athletes traveling to high altitude.37
immunoassay should take place.
Pharyngitis (inflammation of the pharynx) is commonly
viral and presents with a sore throat. In a minority of cases, Upper Symptoms of Altitude Sickness
pharyngitis is due to a bacterial infection, specifically beta-
hemolytic streptococci. Typically, a fever of more than 38°C • Headache
(100.4°F) is present, along with tender enlarged cervical • Lightheadedness
• Confusion
lymph nodes, swelling of the tonsils, erythema, and exudate
• Weakness
in the setting of little or no cough or upper respiratory • Insomnia
symptoms. Before treating with antibiotics (e.g., penicillin • Gastrointestinal upset
[Pen V], amoxicillin [Amoxil]), a rapid enzyme immunoas- • Shortness of breath at rest
say should be done. • Coughing
• Balance difficulties
Asthma
Asthma is a chronic inflammatory disorder of the airways.
The inflammation causes airflow obstruction, which, in the Symptoms of high-altitude illness include headache,
presence of certain triggers, may cause acute bronchocon- lightheadedness, weakness, insomnia, and gastrointestinal
striction that may be life threatening if not treated. Clinical upset. More severe symptoms include shortness of breath at
features usually include wheezing; shortness of breath; chest rest, coughing, confusion, and balance difficulties.
tightness; and a dry, nonproductive cough. The best treatment for high-altitude illness is to descend to
a lower altitude. If symptoms are mild, athletes may be able to
stay at that altitude to allow their bodies to acclimatize. If
Common Triggers for Asthma and Airway symptoms are more severe, immediate descent of 1500 to
2000 feet (457 to 610 m) should occur. There may be a need
Bronchospasm
for further descent until the symptoms completely resolve.
• Cigarette smoke Pharmacological treatment for prevention and treatment
• Exercise of severe high-altitude illness include acetazolamide, nifedip-
• Molds ine, and dexamethasone.
• Dust High-altitude illness may be prevented by decreasing the
• Anxiety rate of ascent. Ascending slowly allows for gradual acclima-
• Stress
tization and leads to a lower likelihood of developing acute
• Cold weather
• Weather changes
mountain sickness.37 Guidelines for graded ascent include
• General pollution climbing from 1000 to 2000 feet per night (300 to 600 m)
when above 10,000 feet (3048 m).38,39 It is also recom-
mended to descend to a lower altitude to sleep. For exam-
ple, if skiing at an elevation of 10,000 feet (3048 m) during
Treatment of asthma includes the use of a medication, the day, an athlete should sleep the night before and the
such as an inhaled steroid, to work against the inflammation night after below an elevation of 8500 feet (2591 m).
component of the disease. A bronchodilator is used for the For more information on altitude disorders and other
relief of symptoms caused by the triggers. If symptoms environmental conditions, see Chapter 5.
worsen over time, pulmonary function tests should be con-
sidered along with further medications to act against the
inflammatory component of the condition.
Gastrointestinal System
Gastrointestinal problems can be part of a normal response
to intense exercise. In some surveys, up to 80% of runners
Altitude Sickness had gastrointestinal complaints.40 Lower gastrointestinal tract
Many activities, such as backpacking, mountain climbing, problems seem to be more common; however, upper gastro-
and downhill skiing involve traveling to extreme heights. If intestinal complaints do occur. Common upper gastrointesti-
activities include traveling to heights above 10,000 feet nal complaints include heartburn, reflux, nausea, vomiting,
(3048 m), the athlete may be at risk for altitude-related ill- bloating, and epigastric pain. Lower gastrointestinal tract
ness. There are three main types of high-altitude illness. They complaints include cramping, urge to defecate, diarrhea, rec-
include acute mountain sickness, high-altitude pulmonary tal bleeding, and flatulence.41
446 SECTION III • Management of Sports Injury and Illness
Runner’s Diarrhea
Runner’s diarrhea or “runner’s trots” is a common com- Lower Gastrointestinal Symptoms
plaint in long-distance running.43 Priebe studied runners
and, in 30% of the cases, this exercise-induced phenomenon • Abdominal cramping
• Urge to defecate
occurred.44 Symptoms included the passing of watery stools,
• Diarrhea
lower abdominal pain, and urgency of defecation, with • Rectal bleeding
some patients passing blood in the stool. The exact mecha- • Flatulence
nism is not entirely understood; however, anxiety, increased
intestinal motility, and possible hormonal influences may be
a few causes. A treating physician should take a good
history of supplements, including the use of caffeine, stimu- Hematology
lants, and electrolyte supplementation, which may contrib-
ute to the condition. Anemia
The treatment should include proper dietary intake prior Athletes may suffer from iron deficiency leading to symptoms
to exercise, the use of low-fiber and low-fat foods, as well as of fatigue and ultimately decreased performance. True anemia
ensuring an empty stomach prior to exercise. Occasionally, should not be confused with “sports anemia.” Sports anemia
medication such as loperamide may need to be used before is truly a dilutional pseudoanemia that is associated with exer-
competition. An antibiotic such as ciprofloxacin may be cise.45 In endurance athletes, reduction in both red blood cell
needed if there is an infectious cause for the diarrhea. mass and hemoglobin concentrations have been shown after
Medical Conditions in Sport • CHAPTER 18 447
a 20-day course of training.46 In addition, increased plasma blood cells are produced, which can lead to a sickling crisis
volume has been found in these athletes. The increased and can possibly be fatal. The incidence of sickle cell trait in
plasma volume combined with reduced red blood cell mass the National Football League has been found to be 6.7%.47
leads to the dilutional or pseudoanemia. Because of the remote chance of death resulting from a
sickling crisis, there is no policy or restrictions on athletes
competing. Early symptoms of a sickling crisis may include
bone, abdominal, and joint pain. Dehydration and high
Causes of Iron Deficiency Anemia
altitude are two factors that may precipitate a sickling crisis.
• Inadequate intake Medical attention should be sought if an athlete experiences
• Decreased absorption these symptoms.
• Increased loss
Infections
Infectious Mononucleosis
“True” iron deficiency anemia occurs from inadequate Infectious mononucleosis is commonly referred to as mono.
intake, decreased absorption, and increased loss of iron. It is caused by the Epstein-Barr virus. It occurs in up to 3%
Dietary intake varies for different populations. For example, of college-age students.48 Athletes usually present with fever,
the recommended daily intake for men is half of what is sore throat, fatigue, malaise, and enlarged lymph nodes.
required for premenopausal women.41 When increasing Physical examination findings include a fever of 39°C to 40°C
activity, dietary requirements may increase further. (102°F to 104°F), lymphadenopathy (swelling of the lymph
Inadequate absorption of iron may also contribute to nodes), an enlarged spleen, enlarged tonsils, and an erythem-
anemia. Iron from sources such as meat have different rates atous palate. Laboratory abnormalities include an elevated
of absorption than iron from vegetables. In some cases, as white blood cell count with an increase in neutrophils,
with endurance athletes, reduced blood flow to the intes- increased liver function tests, and positive serological findings.
tine may also decrease absorption rates. Complications occur in less than 1% of patients, and may
Athletes have many possible sites of blood loss. The gas- include splenic rupture, encephalitis (swelling of the brain),
trointestinal tract is the most likely location of loss, usually meningitis, and hemolytic anemia.48
occurring through the lower tract. Running may also cause
mechanical and subsequently ischemic damage to the bowel.
Blood loss from the urinary tract may stem from bladder Clinical Findings in Mononucleosis
wall damage secondary to mechanical trauma from running.
• Fever
Finally, red blood cell destruction in the foot and lower
• Sore throat
extremity muscles may also occur. Clinically, loss through • Fatigue
the lower gastrointestinal tract could present with dark • Malaise
stools, hematuria may present as frank blood in the urine • Enlarged lymph nodes
and bruising may be present in the lower extremities if me- • Enlarged spleen
chanical damage is the cause of red blood cell destruction. • Enlarged tonsils
Evaluation of the athlete who is anemic should include a • Erythematous oropharynx (inflamed oropharynx)
review of dietary intake as well as a complete blood cell
count and a peripheral blood smear. Also, a serum ferritin
level, as well as folate and vitamin B12 levels should be part
of a laboratory work up as these are all potential causes for Treatment of mononucleosis includes symptomatic treat-
anemia. ment to reduce fever and the pain of a sore throat. Isolation
Because iron deficiency may cause poor performance, is not necessary because the condition is not highly conta-
athletes should receive appropriate supplementation. This gious; it is usually spread through saliva contact between indi-
should be guided by the sport medicine team, which may viduals. Athletes should rest from sporting activities until all
include a nutritionist. See Chapter 4, “Nutrition Counseling acute symptoms have resolved, they are afebrile, laboratory
and Athletes,” for additional information. tests normalize, and when the spleen has returned to normal
size. Premature return risks the possibility of a ruptured
spleen, which can occur even while at rest with and without
Sickle Cell Trait contact. Despite the use of ultrasound, it is often difficult to
Sickle cell trait is a genetic abnormality carried by up to 10% assess whether a spleen is enlarged because of variability in
of the black population in the United States. People with spleen size. However, the majority of splenic ruptures occur
sickle cell trait have one copy of the sickle cell gene. If two within 21 days of the onset of symptoms; therefore, most
copies of the sickle cell gene are present, then abnormal red asymptomatic athletes can return to play after 4 weeks.
448 SECTION III • Management of Sports Injury and Illness
the groin and axillary area. When the lesions become wide-
HIV/AIDS and Hepatitis spread, antibiotic treatment should be initiated.
Human immunodeficiency virus (HIV) is the cause of
acquired immunodeficiency syndrome (AIDS). HIV infects
and seriously damages the body’s immune system. Without Methicillin-Resistant Staphylococcus Aureus
the protection of the immune system, people with AIDS Community-acquired methicillin-resistant Staphylococcus
suffer from fatal infections and cancers. People can be aureus (MRSA) is a variant of hospital-acquired MRSA,
infected with HIV for many years before becoming symp- which was first reported in 1963. MRSA infections are
tomatic. Other serious viral infections include hepatitis B becoming more common in athletes and active individuals.
(HBV) and hepatitis C (HCV). The hepatitis viruses infect The first reported cases were in a high school wrestling
the liver, causing serious illness, and may even be fatal. team in 1993 and a British rugby club in 1998. Because of
Transmission of HIV occurs through sexual activity with their resistance to standard beta-lactam antibiotics, these
the exchange of semen or vaginal and cervical secretions. conditions are concerning to athletes as well as the
Also, needle-stick injuries, blood transfusions, and blood public.52
into an open wound can result in HIV transmission. HBV Most MRSA infections initially manifest as folliculitis or
and HCV are also transmitted in similar ways to HIV. other skin findings such as pimples, pustules, or boils.
The risk of transmission of HIV in sport is exceedingly Typically, the athlete may describe his or her presentation as
low. Only 3 in 1000 health care workers have become an “infected pimple” or “insect bite.” Some MRSA infec-
infected after being stuck with a needle contaminated with tions may progress to abscess formation. In other cases, the
HIV-infected blood.47 Using known prevalence and expo- infection may manifest as a life-threatening illness, such as a
sure rates combined with conversion rates similar to those rapidly progressing sepsis or pneumonia.
of health care workers, the risk of being infected by HIV in The initial clinical examination usually reveals limited
the National Football League was much less than 1 in area of redness, warmth, and swelling, with and without pus
1,000,000 game exposures.49 drainage. Occasionally, the patient may have swelling and
Sport-specific prevention includes using protective pain in a joint. In more advanced cases, moderate to severe
equipment designed to prevent bloody injuries, dealing pain at the site of the infection may be reported; the pain
with bloody wounds immediately, and removing players may be due to soft tissue necrosis.
from participation if blood is visible. Stressing the impor- In severe cases of MRSA infection, endocarditis, septice-
tance of universal precautions for all athletes, coaches, and mia, necrotizing fasciitis, osteomyelitis, multisystem organ
training and medical staff is essential. failure, or death may occur. Severe cases may progress
A position statement from the Canadian Academy of extremely fast from the initial skin infection.
Sport Medicine states that an HIV-positive individual should The most common route of transmission of MRSA is
not be excluded from participating in sport exclusively on through an open wound, such as a superficial abrasion or from
the basis of his or her HIV infection.50 contact with an MRSA carrier. Other methods of transmission
include poor hand washing, poor personal hygiene (i.e., not
showering after workouts), sharing personal items (e.g., razors,
Staphylococcus Infections towels, clothing), or a failure to properly clean and disinfect
Staphylococcus aureus is a bacteria that can cause bother- exercise and training equipment.
some, contagious skin infections. Two common infections
are impetigo and folliculitis.51
Impetigo is a skin infection that is easily spread with Methicillin-Resistant Staphylococcus aureus
close contact with skin. It is commonly spread in wrestling. Prevention and Management Strategies
The lesions can be either larger, fluid-filled vesicles or
• Practice routine hand washing using soap and warm water or
smaller vesicles.
using an alcohol-based hand sanitizer
Active lesions preclude an athlete from participating in
• Immediately shower following activity
organized wrestling. Diagnosis is made clinically and may • Patients with open wounds, scrapes, or scratches should avoid
be confirmed with bacterial cultures. Treatment includes whirlpools
washing areas to keep the skin clean. When the lesions • Avoid sharing towels, razors, and daily athletic gear
become more widespread, antibiotic treatment should be • Properly wash athletic gear and towels after each use
initiated. • Maintain clean facilities and equipment
Folliculitis refers to an infected hair follicle. Lesions are • Refer to physician for active skin lesions that do not respond to
somewhat tender and are pustular in nature. If a deeper initial therapy
infection occurs, the lesions usually contain a large amount • Use bacterial cultures to establish proper diagnosis
of pus and are referred to as furunculosis. The lesions usu- • Care for and cover skin lesions appropriately before participation
ally occur on the buttock area, along the belt line, and in
Medical Conditions in Sport • CHAPTER 18 449
The first step to treating overtraining is to recognize it. myositis ossificans until proven otherwise. This may pro-
After recognition, the physical symptoms should first be long the treatment initially, but in the long term is more
treated. This usually involves decreasing or discontinuing likely to lead to an earlier resolution of the problem.
training for a time. An athlete logbook for self-analysis is an Provided the hematoma that forms in the muscle is given
important tool. The logbook should include training sufficient time to be reabsorbed and provided additional
details, comments on training (i.e., likes and dislikes), well- stresses are not applied to the injured tissue, normal recov-
being rating, causes of stress or dissatisfaction, and any ery with reabsorption of the hematoma and no develop-
injuries or illness that may occur.41 Addressing the psycho- ment of the myositis occurs. However, if the injury is
logical symptoms of overtraining is more difficult. In mild treated too vigorously or the injury site is continually trau-
cases, changes in workout and training regimens may be matized, mesenchymal cells derived from the fascial planes
helpful.62 However, in more severe cases, completely dis- and muscle sheaths that are part of the reparative granula-
continuing training and professional psychological and tion tissue may invade the hematoma site and mature into
psychiatric treatment may be needed. osteoblasts and proliferate to form immature or heterotopic
bone. Over time (6 weeks to 6 months), the amount of
bone formed maximizes, but can take up to 2 years to fully
Myositis Ossificans mature, with the immature bone being replaced by trabecu-
There are two types of myositis ossificans: myositis ossificans lar bone. Because of the strong possibility of developing
traumatica and myositis ossificans progressiva. Myositis ossi- myositis ossificans in the muscles mentioned previously, any
ficans progressiva, which is also called fibrous dysplasia ossifi- hematoma to these muscles must be treated with extreme
cans progressiva, is a rare progressive congenital condition care for at least 2 weeks, by which time a normal hematoma
in which multiple muscles ossify. The condition can be should begin to resolve.
lethal.63 The more common type of myositis ossificans Roentgenographic signs of injury are present in the fifth
is myositis ossificans traumatica, which is discussed in this or sixth weeks following injury. The initial appearance on
section. x-ray examination is that of a fluffy calcification with indis-
Myositis ossificans traumatica is a complication of a con- tinct margins lying in the soft tissue anterior to the bone
tusion combined with the formation of an intramuscular (Figure 18-1). As the lesion matures, it may enlarge, and
hematoma. This development of heterotopic (ectopic) bone margins become more distinct. It may coalesce with the
in soft tissue adjacent to bone is commonly associated with actual bone itself, at which stage the mass may become
trauma, surgery, or a disease such as heterotopic ossifica- smaller. Radionuclide bone scans may be used to assess the
tion. Most commonly, it is seen in the quadriceps, brachia- maturity of the lesion (they would be negative if the
lis, anterior hip muscles, and the soleus muscles.64-66 The bone is mature). However, bone scans can be confusing if
importance of this condition rests in the fact that contu- done prior to the typical radiographic changes becoming
sions are usually viewed as minor injuries by coaches and evident.
athletes and thus are not treated with much concern, Following the formation of a hematoma, risk factors that
although appropriate, carefully controlled management of should be avoided include continuing to play after injury,
the initial injury can prevent or lessen the possible develop- early massage, forceful passive stretching of the injured area,
ment of myositis ossificans. the application of heat to the area, too-rapid progression of
The most common cause of myositis ossificans traumat- rehabilitation, premature return to activity, reinjury to the
ica is trauma and occurs primarily in contact sports such as same area, and innate predisposition to the ectopic bone
football, rugby, ice hockey, and lacrosse.64-69 The signs and formation.
symptoms of developing myositis ossificans include a pal- Early treatment of myositis ossificans consists primarily
pable, often immobile mass that is increasingly tender or of relative rest and gentle range-of-motion exercises.68-71
painful and progressive loss of joint motion. Other possible The athlete should follow a regimen of protected weight-
indicators of the development of myositis ossificans include bearing with crutches for lower-limb injuries and avoid any
increase in pain or decrease in range of motion following heavy lifting in upper-limb injuries. Rest and immobiliza-
one or two treatment sessions, the persistent palpable tion should continue until pain and inflammation subside.
warmth at the injury site, or the palpation of increased Following the acute period (1 to 6 weeks), there may be
indurations in the hematoma. In some cases, the symptoms considerable loss of motion resulting from restricted muscle
and findings may be confused with a femoral stress fracture function. Early rehabilitation should be conservative and
or, more seriously, malignant bone tumors that are similar consists of careful active range-of-motion and strengthen-
both clinically and histopathologically to heterotopic bone. ing (pain-free and nonresisted) exercises. Forceful passive
Therefore, an extremely accurate history is essential. Early stretching should be avoided for at least 4 months. Until
diagnosis of myositis ossificans is extremely difficult, and, as there is a definitive decision that myositis ossificans is not
a precaution, hematomas that occur in the muscles listed occurring, any rehabilitation programs should not involve
previously or ones that are very painful should be treated as intense exercise. Any strengthening or range-of-motion
452 SECTION III • Management of Sports Injury and Illness
Conclusion
This chapter attempts to dispel the common belief that sports
medicine injuries are solely caused by insults to the musculo-
skeletal system. Although most athletes are healthy and an
active lifestyle should be encouraged, medical conditions that
preclude competition in sport should not be ignored. It is
very important for all health care practitioners involved with
sport to err on the side of caution and not simply assume that
symptoms are due to exercise. The importance of referring
these cases to physicians cannot be overstated.
References
1. Hirsh FJ: The generalist as a team physician, Phys Sports Med
7:89–95, 1979.
2. Maron BJ, Shirani J, Poliac LC, et al: Sudden death in young
competitive athletes: Clinical, demographic, and pathological
Figure 18-1 profiles, JAMA 276:199–204, 1996.
X-ray film of myositis ossificans. 3. Corrado D, Basso C, Schiavon M, Thiene G: Screening for hyper-
trophic cardiomyopathy in young athletes, N Engl J Med 339:
364–369, 1998.
4. Basso C, Maron BJ, Corrado D, Thiene G: Clinical profile of
exercises must be pain free. Anti-inflammatory agents such congenital coronary artery anomalies with origin from the wrong
as indomethacin may be given, and all activities are reduced. aortic sinus leading to sudden death in young competitive athletes,
The athlete should be re-evaluated frequently. If there is J Am Coll Cardiol 35:1493–1501, 2000.
5. Glover DW, Maron BJ: Profile of preparticipation cardiovascular
no progression of the condition, once pain subsides,
screening for high school athletes, JAMA 279:1817–1819, 1998.
gentle range-of-motion and strengthening exercises can be 6. Maron BJ, Araújo CG, Thompson PD, et al: Recommendations
initiated; however, exercise progression should be slow and for preparticipation screening and the assessment of cardiovascular
cautious. disease in masters athletes: An advisory for healthcare professionals
If there is no improvement of a hematoma injury after from the working groups of the World Heart Federation, the In-
ternational Federation of Sports Medicine, and the American
10 days, prednisone or a course of diphosphonates should
Heart Association Committee on Exercise, Cardiac Rehabilitation,
be administered. Return to activity can be considered when and Prevention, Circulation 103(2):327–334, 2001.
the bone mass show signs of stabilizing or maturing (which 7. Maron BJ, Thompson PD, Puffer JC, et al: Cardiovascular prepar-
may take several months). In some cases, full range of ticipation screening of competitive athletes: A statement for health
motion may not be possible and the criteria may need to be professionals from the Sudden Death Committee (clinical cardiol-
ogy) and Congenital Cardiac Defects Committee (cardiovascular
modified. However, even large ossific masses are compatible
disease in the young), American Heart Association, Circulation
with full range of motion and good function. 94:850–856, 1996.
Surgery is indicated only to reduce the mass effect of 8. Maron BJ: Sudden death in young athletes, N Engl J Med
the ectopic bone and should never be done until the 349:1064–1075, 2003.
Medical Conditions in Sport • CHAPTER 18 453
9. Huston TP, Puffer JC, Rodney WM: The athletic heart syndrome, 31. Kawabori I, Pierson WE, Conquest LL, Bierman CW: Incidence
N Engl J Med 313:24–32, 1985. of exercise-induced asthma in children, J Allergy Clin Immunol
10. Pluim BM, Zwingerman AH, van der Laarsed A, van der Wall EE: 58:447–455, 1976.
The athlete’s heart: A meta-analysis of cardiac structure and 32. Rupp NT, Guill MF, Brudno DS: Unrecognized exercise-induced
function, Circulation 101:336–344, 2000. bronchospasm in adolescent athletes, Am J Dis Child 146:941–944,
11. Lehmann M, Durr H, Merkelbach H, Schmid A: Hypertension 1992.
and sports activities: Institutional experience. Clin Cardiol 13: 33. Tan RA, Spector SL: Exercise-induced asthma, Sports Med 25:
197–208, 1990. 1–6, 1998.
12. Gifford RW Jr, Kirkendall W, O’Connor DT, Weidman W: Office 34. Bisgaard H: Long-acting beta(2)-agonists in management of
evaluation of hypertension. A statement for health professionals by childhood asthma: A critical review of the literature, Pediatr
a writing group of the Council for High Blood Pressure Research, Pulmonol 29:221–234, 2000.
American Heart Association, Circulation 79:721–731, 1989. 35. Cavallo A, Cassaniti C, Glogger A, Magrini H: Action of nedocro-
13. Tanji JL: Tracking of elevated blood pressure values in adolescent mil sodium in exercise-induced asthma in adolescents, J Investig
athletes at 1-year follow-up, Am J Dis Child 145:665–667, 1991. Allergol Clin Immunol 5:286–288, 1995.
14. Messerli FH, Garavaglia GE: Cardiodynamics of hypertension: A 36. Ilback NG, Fohlman J, Friman G: Exercise in coxsackie B3
guide to selection of therapy, J Clin Hypertens 3:100S–108S, myocarditis: Effects on heart lymphocyte subpopulations and the
1986. inflammatory reaction, Am Heart J 117(6):1298–1302, 1989.
15. The sixth report of the Joint National Committee on Prevention, 37. Schneider M, Bernasch D, Weymann J, et al: Acute mountain sick-
Detection, Evaluation, and Treatment of High Blood Pressure, ness: Influences of susceptibility, preexposure, and ascent rate, Med
Arch Intern Med 157:241–346, 1997. Sci Sports Exerc 34(12):1886–1891, 2002.
16. Whelton PK, He J, Cutler JA, et al: Effects of oral potassium on 38. Murdoch D: How fast is too fast? Attempts to define a recom-
blood pressure. Meta-analysis of randomized controlled clinical mended ascent rate to prevent acute mountain sickness, Int Soc
trials, JAMA 277:1624–1632, 1997. Mountain Med Newsletter 9(1):3–6, 1999.
17. The Trials of Hypertension Prevention Collaborative Research 39. Hackett P, Roach R: High-altitude medicine. In Auberbach P,
Group: Effects of weight loss and sodium reduction intervention editor: Wilderness medicine: Management of wilderness and
on blood pressure and hypertension incidence in overweight environmental emergencies, ed 4, St Louis, 2001, Mosby.
people with high-normal blood pressure, Arch Intern Med 40. Mellion MB, Walsh WM, Madden C, et al: Team physician’s hand-
157:657–667, 1997. book, ed 3, Philadelphia, 2002, Hanley & Belfus.
18. Petrella RJ: How effective is exercise training for the treatment of 41. Brukner P, Khan K: Clinical sports medicine, ed 3, Sydney, Australia,
hypertension? Clin J Sport Med 8:224–231, 1998. 2006, McGraw-Hill.
19. Chick TW, Halperin AK, Gacek EM: The effect of antihypertensive 42. Shawdon A: Gastro-oesophageal reflux and exercise. Important
medications on exercise performance: A review, Med Sci Sports pathology to consider in the athletic population, Sports Med
Exerc 20(5):447–454, 1988. 20(2):109–116, 1995.
20. Dietz HC, Cutting GR, Pyeritz RE, et al: Marfan syndrome 43. Rao SS, Beaty J, Chamberlain M, et al: Effects of acute graded
caused by a recurrent de novo missense mutation in the fibrillin exercise on human colonic motility, Am J Physiol 276(5 Pt 1):
gene, Nature 352:337–339, 1991. G1221–1226, 1999.
21. Robinson PN, Godfrey M: The molecular genetics of Marfan 44. Priebe M, Priebe J: Runners diarrhea—Prevalence and clinical
syndrome and related microfibrillopathies, J Med Genet 37:9–25, symptomatology, Am J Gastroenterol 73:872–878, 1984.
2000. 45. Fields KB: The athlete with anemia. In Fields KB, Fricker PA,
22. Pyeritz RE: Marfan syndrome and other disorders of fibrillin. In editors: Medical problems in athletes, Malden, MA, 1997, Blackwell
Rimoin DL, Connor JM, Pyeritz RE, Korf B, editors: Principles Scientific.
and practice of medical genetics, ed 4, Edinburgh, 2002, Churchill 46. Dressendorfer RH, Wade CE, Amsterdam EA: Development of
Livingstone. pseudo-anemia in marathon runners during a 20-day road race.
23. Dr Paepe A, Devereux RB, Dietz HC, et al: Revised diagnostic JAMA 246:1215–1218, 1981.
criteria for the Marfan syndrome, Am J Med Genet 62:417–426, 47. Murphy JR: Sickle cell hemoglobin (Hb AS) in black football
1996. players, JAMA 225:981–982, 1973.
24. Januzzi JL, Isselbacher EM, Fattori R, et al: Characterizing the 48. Ryan AJ, Evans AS Hoogland RJ, Seifert M: Infectious mononu-
young patient with aortic dissection: Results from the Interna- cleosis in athletes, Phys Sports Med 6:41–56, 1978.
tional Registry of Aortic Dissection (IRAD), J Am Coll Cardiol 49. Henderson DK, Feahey B, Wily M, et al: Risk of occupational
43:665–669, 2004. transmission of human immunodeficiency virus type 1 (HIV-1)
25. Thompson DD, Funk EJ, Carleton RA, Sturner WQ: Incidence of associated with clinical exposures, Ann Intern Med 113:740–746,
death during jogging in Rhode Island from 1975 through 1980, 1990.
JAMA 247:2535–2538, 1982. 50. Brown LS, Drotman P: What is the risk of HIV infection in ath-
26. American Heart Association website. Accessed 2008 from www. letic competition? 9th International Conference on AIDS, Berlin,
americanheart.org. June 1993.
27. Maron BJ, Gohman TE, Kyle SB, et al: Clinical profile and spec- 51. Robinson J: Canadian Academy of Sport Medicine: Position
trum of commotio cordis, Am J Cardiol 89:210–213, 2002. statement: HIV as it relates to sport. Updated 2007. Available at
28. Weinstock J, Maron BJ, Song C, et al: Commercially available chest http://www.casm-acms.org/pg_Statements.php.
wall protectors fail to prevent ventricular fibrillation induced by chest 52. Centers for Disease Control and Prevention: Community Associated-
wall impact (commotio cordis), Heart Rhythm 1:692, 2004. MRSA Information for the Public. Available at http://www.cdc.
29. Strasburger JF, Maron BJ: Images in clinical medicine: commotio gov/ncidod/dhqp/ar_mrsa_ca_public.html.
cordis, N Engl J Med 347:1248, 2002. 53. National Athletic Trainers’ Association: Official statement from the
30. Link MS, Maron BJ, Stickney RE, et al: Automated external defi- National Athletic Trainers’ Association on Community-Acquired
brillator arrhythmia detection in a model of cardiac arrest due to MRSA Infections (CA-MRSA), March 2005. Available at http://
commotio cordis, J Cardiovasc Electrophysiol 14:83–87, 2003. www.nata.org/statements/official/MRSA_Statement.pdf.
454 SECTION III • Management of Sports Injury and Illness
54. Canadian Diabetes Association: Canadian Diabetes Association 2008 64. Finerman GA, Shaporo MS: Sports-induced soft-tissue calcifica-
Clinical Practice Guidelines. Available at http://www.diabetes.ca/ tion. In Leadbetter WB, Buckwalter JA, Gordon SL, editors:
for-professionals/resources/2008-cpg/. Sports induced inflammation, Park Ridge, IL, 1989, American
55. Landry GL, Allen DB: Diabetes Mellitus and exercise, Clin Sports Academy of Orthopedic Surgeons.
Med 11(2):403–418, 1992. 65. Huss CD, Fuhl JJ: Myositis ossification of the upper arm, Am J
56. Smith LL, Burnet SP, McNeil JD: Musculoskeletal manifestations Sports Med 8:419–424, 1980.
of diabetes mellitus, Br J Sports Med 37(1):30–35, 2003. 66. Jackson DW, Feazin JA: Quadriceps contusions in young athletes.
57. Carroll MF, Tenite JL: Proteinuria in adults: A diagnostic J Bone Joint Surg Am 55:95–105, 1973.
approach. Am Fam Physician 62:1333–1340, 2000 67. Beiner J, Jokl P: Muscle contusion and myositis ossificans trau-
58. Abarbanel J, Benet AE, Lask D, Kimche D: Sports hematuria, J Urol matica, Clin Orthop Relat Res 403:S110–S119, 2002.
143:887–890. 1990. 68. Aronen JG, Garrick JG, Chronister RD, McDeritt ER: Quadriceps
59. Micheli L, Smith A, Bachl N, et al, editors: FIMS team physician contusions: Clinical results of immediate immobilization in
manual, ed 1, Hong Kong, 2001, Lippincott Williams & Wilkins 120 degrees of knee flexion, Clin J Sports Med 16:383–387, 2006.
Asia Ltd. 69. Wieder DL: Treatment of traumatic myositis ossificans with acetic
60. Ryan AJ, Burke ER, Falsetti HL, et al: Overtraining of athletes acid iontophoresis. Phys Ther 72:133–137, 1992.
(round table). Phys Sportsmed 11:92–110, 1983. 70. Jackson DW: Managing myositis ossificans in the young athlete,
61. Johnson MB, Thiese SM: A review of overtaining syndrome— Phys Sportsmed 3:56–61, 1975.
Recognizing the signs and symptoms, J Athl Train 27(4):352–354, 71. Lipscomb AB, Thomas ED, Johnson RK: Treatment of myositis
1992. ossificans traumatica, Am J Sports Med 4:111–120, 1976.
62. Henschen KP: Prevention and treatment of athletic staleness and 72. O’Donoghue DH, editor: Treatment of injuries to athletes, ed 4,
burnout, Sci Period Res Technol Sport 10:1–8, 1990. Philadelphia, 1984, WB Saunders.
63. Dixon TF, Mulligam L, Nassium R, Stevenson FH: Myositis 73. La Roux DA: Chondrosarcoma and myositis ossificans, J Manipula-
ossificans progressiva, J Bone Joint Surg Br 36:445–449, 1954. tive Physiol Ther 21:640–648, 1998.
19
CHAPTER
DERMATOLOGICAL CONSIDERATIONS
IN ATHLETICS
Donald W. Groot and Patricia A. Johnston
455
456 SECTION III • Management of Sports Injury and Illness
Figure 19-1
Elements of the skin.
The nails of the fingers and toes originate from the epider- The papillary dermis contains blood vessels that deliver
mis of the nail matrix, which is the moon-shaped structure at essential nutrients to and remove wastes from the skin. The
the proximal end of the nail (Figure 19-2). The cells of the complex system of nerves in the papillary dermis makes the
nail plate are not vital and consist of keratinized cells.1 skin one of the most sensitive organs of the body.
The dermis is the second layer of the skin. Divided into The glands of the skin are found in the papillary dermis,
two layers, the papillary dermis and the reticular dermis, it although they extend into the basal layer of the epidermis.
contains the building blocks of the skin. Collagen, a fibrous Sebaceous glands secrete lipids to lubricate the skin; eccrine
protein, is the most abundant fibroblast of the dermal con- glands release sweat to regulate fluctuations of body tem-
nective tissue. Collagen provides strength and structure to perature; and apocrine gland secretions are responsible for
the skin; it is most abundant in the deeper reticular layer of body odor. These glands vary in their location, size, and
the dermis but is also found in the papillary dermis. Elastins, distribution. For example, eccrine glands are most abun-
also a major component of the reticular dermis, are elastic dant in the palms of the hands and soles of the feet and are
proteins that give the skin tone and suppleness, so that it will nonexistent along the vermilion borders of the lips.
snap back into place when stretched. The breakdown of Although the hair follicle is an appendage of the epidermis,
fibrous and elastic proteins is responsible for many of the it extends into the papillary dermis, where it receives its blood
signs of aging, such as sagging skin and wrinkles. supply and surrounding network of nerves (Figure 19-3). The
hair follicle is alive and grows at an average rate of 1⁄2 to 1 inch
(1.3 to 2.5 cm) per month. The shaft or visible portion of the
hair consists of dead, keratinized cells.2
A layer of fat underlies the dermis. It plays an important
role in providing a protective pad between the skin and the
underlying skeletal and muscular structures. Subcutaneous fat
is also responsible for giving the skin a full, healthy look.2
In its role as an interface between the body and an often
hostile environment, the skin is subject to frequent and
often damaging abuse. This is particularly the case with
athletes. In mild cases, sports-related skin injuries may sim-
Figure 19-2 ply be annoying, yet in severe cases may impede an athlete’s
Elements of the nail. ability to perform.
Dermatological Considerations in Athletics • CHAPTER 19 457
The removal of dirt and debris from a wound is important escapes into the skin or the mucous membranes; it is
for proper healing. If debris is left behind, permanent discol- characterized by a purplish-red discoloration of the skin
oration in the form of a “dirt tattoo” may result. Running resulting from red cell extravasation.3
water through the wound may be adequate; however, if the Although the cause of red cell extravasation varies, in
wound is dirty, a more aggressive approach is required. Un- sports, bruising is largely the result of blunt trauma. The
der local anesthetic, the wound is scrubbed with a disposable, two types of bruises most commonly seen in athletes are
sterile, surgical brush that contains an antiseptic cleansing petechiae and ecchymoses. Petechiae are purpuric lesions,
solution. Any foreign material, such as glass or gravel, is which are less than 3 mm in diameter, and often occur in
carefully removed and necrosis of the tissue debrided. groups.4 An example of petechiae may be seen in a hockey
Once the wound is properly prepared, healing can take player who has been checked into the boards. His garment
place. Some areas of the body heal faster and better than oth- may leave a pattern of tiny vascular eruptions that match
ers depending largely on the blood supply to the region. For the weave of the cloth.3 This is known as “jersey bruise” or
example the face heals faster than the legs. The body lays patterned petechiae (Figure 19-4). Ecchymosis is a bruise
down a base of granulation tissue with a circular pattern of larger than 3 mm in diameter.
collagen fibers to fill in the missing dermis. This process
causes the wound to contract, drawing the epidermal edges
closer together. The skin loses its ability to retain water in the Types of Bruising
damaged area, contributing to the formation of a scab from
• Petechiae
the inflammatory deposits. Although the scab plays an
• Ecchymosis
important role in the control of infection, it can also slow the • Hematoma
healing process. To encourage more rapid epithelialization it
is best to keep a wound moist with an appropriate dressing.
A topical antibiotic, such as sodium fusidate or mupirocin
ointment under a semiocclusive (e.g., Mepore) dressing, will
reduce the risk of infection and will promote healing. An ice pack applied with pressure immediately after the
Scarring is inevitable with full-thickness wounds. The trauma will help stop the bleeding and control swelling.
cosmetic result may vary according to intrinsic and extrinsic With time, the macrophage cells of the body will clear away
factors. Intrinsic factors include a hereditary predisposition the blood cell particles, and the bruise will gradually fade
for scar formation or poor nutrition; extrinsic factors include from a deep purple or red discoloration to a green or yellow
poor surgical technique, infection, compromised blood sup- tone and finally disappear.
ply, use of topical or systemic steroids, and foreign materials A unique type of petechiae bruising found only in
in the wound. Scars may be categorized as normal, hypertro- athletes, adolescents in particular, is referred to as “black
phic, keloid, or atrophic. A normal scar, although never heel” or “black palm.” It is characterized by a grouping of
regaining the strength of tissue that has not been trauma- bluish black specks on the back of the heel or the padded
tized, is flat and similar in color to the surrounding skin. portion of the palm. It is due to the rupturing of the papil-
Hypertrophic and keloid scars are both overgrown, the lary capillaries in the skin. Athletes who participate in high-
difference lying in the mass of scar tissue deposited and the impact sports that involve jumping, twisting, and sudden
tendency for recurrence. Keloid scars tend to be extensively
overgrown and have a high rate of recurrence despite nu-
merous interventional therapies. Atrophic scars are deficient
in collagen and tend to be weak and depressed.
Types of Scars
• Normal
• Hypertrophic
• Keloid
• Atrophic
shearing movements or stops, such as basketball, football, debris has been incorporated into the skin during the heal-
lacrosse, tennis, and squash, are candidates for a black heel. ing process, no amount of cleansing will remove the result-
Black palm has been reported in athletes participating in ing discoloration.
sports involving friction and pressure to the palm of the The advent of laser technology has made it possible to
hand, such as weight lifting, tennis, mountain climbing, and remove dirt tattoos with a minimal risk of scarring. The type
golf.5,6 No intervention is required for this condition, as of laser selected for the surgery is important. Lasers that
there is no associated pain or functional disruption of the target the pigment in the skin, leaving the remaining tissue
foot or hand. Reassurance that these black skin lesions do relatively untouched, ensure the best results. Several lasers
not represent mole cancer is often sought by the athlete. have the color-specific selectivity to remove blue, black, and
Once the sport is stopped for the season, the condition brown discolorations in the skin, including the Q-switched
spontaneously disappears. Alexandrite and the single- or double-frequency Nd:YAG
Another type of ecchymotic condition unique to athletes lasers.
is known as “runner’s rump.” Postecchymotic hyperpig- The selective affinity of the laser light for certain discol-
mentation occurs in the cleft of the buttocks owing to the orations allows the laser surgeon to remove pigment from
constant repetitive contact between the cheeks of the but- the skin with minimal disruption to the surrounding tissue.
tocks. The condition is asymptomatic and subsides with a The energy emitted by the laser light when it hits the tar-
decrease in running.6 geted pigment causes a microscopic fragmentation of the
Hematomas may occur when the blood does not seep pigment particles. The macrophage cells of the immune
into the skin or mucous membranes but becomes trapped system then carry the minuscule waste particles away.2
and pools in a confined space, such as under the fingernail The methods of tattoo removal used in the past generally
or toenail (subungual hematoma). They may have to be left unsightly scars. Resurfacing techniques such as salabrasion
drained, especially in circumstances in which the pressure (salt scraping), dermabrasion (mechanical scraping), lasabra-
from the trapped blood is very painful, as is the case with sion (laser vaporization), and chemical peels as well as surgical
subungual hematomas. A needle into the collection of techniques such as skin grafting were the only available
blood may aspirate enough blood to relieve the pressure. options for the removal of tattoos. The new target-specific
Massage assists absorption of the loculated serous blood lasers have driven these techniques into obsolescence.
components of clear hematomas (seromas) that may be Decorative tattoos are popular among some athletes.
trapped in skeletal soft tissue. The trend is to tattoo a team logo or insignia into the skin.
These tattoos may be removed in a similar fashion to dirt
tattoos, although red and yellow pigments are more resis-
Dirt Tattoos tant to laser therapy.7
“Dirt tattoos” occur when dirt or other debris is embedded
in the skin from a traumatic injury, such as a fall on an
asphalt surface while cycling or running. This is sometimes Piezogenic Papules
referred to as “road rash” (Figure 19-5). Piezogenic papules have been reported in athletes partici-
If a wound is properly cleansed after an injury, dirt pating in prolonged endurance events such as marathons
tattoos are usually prevented. In instances in which the and triathlons (Figure 19-6).6 These skin-colored bumps
most commonly occur on the medial and lateral aspects of area innervated by a single nerve. It occurs on only one side
the heel and are due to a herniation of the subcutaneous fat of the body.10
into the dermis.4 The rash is characterized initially by painful red bumps
The athlete may experience pain only when the foot is (papules) that fill with a clear fluid, giving a blisterlike
weight-bearing. However, the pain can be such that it will appearance (vesicles). The vesicles then become infected
prevent the athlete from continuing with the sport. These (pustules). As the pustules dry up, a crust is formed that
papules have been reported, with no associated pain, in the falls off in the final stages of healing.11 Scars may result. The
general population. Therefore, there is some speculation as initial stages of the virus may be accompanied by a high
to why some individuals with this condition are prone to fever, headache, and general malaise. The entire cycle may
pain. Such factors as faulty weight bearing, bony spurs, and take 3 to 4 weeks.
secondary inflammatory changes to the deep dermis have When the initial signs of the virus are noted, oral acyclo-
been discussed.5 vir (Zovirax) or valacyclovir (Valtrex) has been found to be
Intralesional injections of the cortisone triamcinolone the most effective agent for aborting the disease cycle. It
acetonide (Kenalog) will shrink the fat, providing relief should be administered immediately. Once the virus has
to the individual who suffers pain. If there is no associated taken hold, the medication loses its effect. Because the drug
pain, intervention is not indicated except for cosmetic is of little value once the rash reaches the vesicular stage,
reasons.8 Orthotic support to the heel has been of benefit early diagnosis is crucial.
to some.6
Surfers rarely seek treatment, as the nodules tend to have and football, and in which taut, occlusive garments are
symbolic meaning for them.6 worn. Other sports in which there appears to be a relatively
high incidence of acne mechanica include cross-country
skiing, speed skating, competitive cycling, and aerobic
Conditions Caused by Equipment dancing. Golfers, hikers, and mountain climbers may expe-
Equipment-related skin problems are more common in rience acne mechanica along the strap lines of the equip-
some sports, such as hockey and football, than in others. ment that they carry on their back and over their shoulders.
Occlusive material, chemicals in cloth, and friction or pres- Weight lifters may notice that the problem is particularly
sure from the garments contribute to a wide variety of skin troublesome on their back because of contact with plastic-
conditions. Prevention plays an important role in the covered weight benches.6
management of equipment-related skin problems. Undergarments made of absorbent material specially
designed to wick moisture away from the skin, such as
Coolmax, Supplex, and Drylette, will help keep the skin dry
Skin Conditions Caused by Equipment and control the irritating friction caused by garments that
• Acne mechanica do not absorb moisture and breathe, such as nylon. A thin
• Folliculitis cotton lining between the skin and the garment is also help-
• Alopecia ful. Proper cleansing of the skin immediately after an activ-
• Subungual hemorrhages ity is important. Using a mild soap, the involved areas
• Ingrown toenails should be gently scrubbed with lukewarm water and a
• Blisters rough washcloth. Aggressive cleansing, particularly with
• Calluses and corns abrasive soaps, may cause further swelling of the pore open-
• Lichen simplex chronicus ings, compounding the problem.
• Chafing
Generally, over-the-counter preparations for the treatment
• Pseudobursitis
• Dermatitis
of acne mechanica have little effect, although preparations
containing benzoyl peroxide may be helpful in drying up
some lesions.
Application of a sulfur mixture, such as Sulfacet lotion,
Acne Mechanica may help open the pores to encourage better drainage of the
A combination of friction, pressure, and heat from occlusive oil from the glands and decrease inflammation from bacterial
clothing and equipment may cause swelling of the pore overgrowth. Sulfur lotions may be very drying, so they
openings of an athlete’s skin, preventing the oil glands from should be used sparingly. To further control inflammation,
draining properly. The trapped oil ferments, causing the 1% hydrocortisone powder may be added to the lotion.
gland to become irritated, inflamed, and in some cases Medications for acne are categorized as topical or
infected, resulting in acne (Figure 19-7). The problem is systemic. Tretinoin, a member of the retinoid (vitamin A)
common in the regions of the back, neck, shoulders, and family, is a topical antibacterial and pore-opening agent that
face because of the high concentration of oil glands in these has proved effective in controlling milder forms of acne
areas. It is particularly troublesome in sports that require mechanica. Unfortunately, the antibacterial drugs that are
heavy padding and protective equipment, such as hockey taken systemically for other forms of acne, such as tetracy-
cline, erythromycin, and minocycline, are not as effective
for acne mechanica. However, they may help prevent a
milder form of acne from becoming infected and cystic.
Isotretinoin (Accutane), which is the best medication cur-
rently available for pustulocystic acne, controls the secre-
tions of the sebaceous glands, preventing the build-up of
thick oils in the pores. Unfortunately, it can wreak havoc
with athletes, as the side effects may interfere with their
performance. Aching muscles and joints, lack of energy,
general lethargy, and dehydration are among the expected
side effects when isotretinoin is prescribed.
Folliculitis
Folliculitis, inflammation and infection of the hair follicles, is
Figure 19-7 a problem for some athletes, particularly on the scalp, when
Acne mechanica (football shoulder pad). helmets are required to protect the head from injury. It may
462 SECTION III • Management of Sports Injury and Illness
pledget of cotton wool to encourage the nail to grow above friction may be mild in areas of structural abnormality or
and beyond the inflamed skin. bony prominence, or it may be excessive in areas where the
The first step in prevention is to ensure properly fitting underlying structure is normal but the tissue is subjected to
footwear that has adequate anterior and vertical movement repeated stress (e.g., hands of a gymnast, heels of a runner).
in the toe box. Trimming the nails straight across with Architectural imbalance of the foot, poor walking or run-
V-shaped grooves notched into the nail edge will encourage ning habits, and poorly fitting footwear may all contribute
anterior, inward growth of the nail. Rubbing a glass slide to the formation of calluses and corns.16
across the middle of the nail will also stimulate the nail to Calluses commonly occur on the feet but may appear on
grow toward the center rather than peripherally into the any part of the body that is subject to repeated external
soft tissue of the skin.3 pressure and friction, as may be the case with athletic equip-
Persistent problems with ingrown toe nails may require ment or padding. For example, calluses commonly occur on
removal of a portion of the nail matrix to prevent growth of the hands of cyclists, oarsmen, gymnasts, golfers, and indi-
the problematic portion of the nail. viduals who play racket sports.6
Padded, well-ventilated gloves help prevent calluses of
the hands, and properly fitting footwear is the first step to
Blisters the management of calluses on the feet. Further interven-
Repetitive friction will cause a separation within the epider- tion may or may not be indicated. Some individuals view
mis or between the epidermis and the dermis. The resulting their calluses as a natural protection from blisters. Others
gap fills with fluid exudates and, in some cases, blood, find that calluses tend to contribute to the formation of
resulting in what is commonly referred to as a blister. blisters or eventually interfere functionally with perfor-
Footwear that fits properly is the first step in preventing mance. Soaking the feet in warm water will soften the
blisters. Absorbent socks are also important, as the tropical callus such that it is easy to pare down with an abrasive
environment of athletic footwear also contributes to the for- material such as pumice stone or a scalpel in cases of very
mation of blisters. Foot powders such as Zeasorb cellulose thick keratin. Regular applications of salicylic acid plasters,
powder are helpful in keeping the feet dry. Talcum is not which gradually eat away at the keratin, have also proved
recommended because it is essentially a powdered rock that, effective. Generally, once the offending source of friction
contrary to general belief, is not effective in absorbing mois- has been removed, the skin will return to normal without
ture and can be abrasive. In areas particularly prone to blister intervention.6
formation, a protective dressing such as Spenco 2nd Skin Corns are distinguished from calluses by a deep central
may be applied prophylactically or, once the blister has core of keratin. They tend to be exclusive to the feet and
formed, to protect the area from further trauma and to re- occur over the bony prominence of the toes and lateral edge
lieve discomfort. In those sports in which blisters may occur of the metatarsals. Keratoma is a medical term commonly
on the hands, such as cycling and gymnastics, protective used for cornlike formations on the bottom of the feet.
gloves should be worn. Because of the tenderness of corns they are particularly
The management of blisters is fairly straightforward. annoying to athletes.
Under sterile conditions, the blister should be drained; oth- Warts (verrucae) underlying calluses may sometimes be
erwise, pressure in the area can cause further peripheral misdiagnosed as corns. A simple test helps distinguish the
separation and a more extensive blister. Draining will also two. A corn is more painful under direct pressure than a
help relieve the pain. The epidermal covering should be left wart, whereas a wart is more painful when pinched.5
intact until underlying healing takes place, at which time the Correction of poorly fitting footwear and orthotics for
covering will dry up and slough on its own. This helps pre- architectural imbalances that contribute to the formation of
vent infection and promote rapid re-epithelialization. To hyperkeratosis are important to the prevention of repetitive
drain the blister, a sterile needle should be used to puncture formation of corns after treatment. To remove the core,
the epidermal covering. The excess fluid is aspirated or cantharidin (an extract from the blister beetle) is applied to
allowed to drain into a dressing. This procedure is repeated the lesion and kept under a salicylic acid plaster for three
several times over a 24-hour period, if necessary, to release days. A blister forms under the keratosis, separating it from
fluid build-up. A protective dressing is applied to discourage the underlying dermis. The resulting blister may be quite
further friction to the involved area.3 tender. It does, however, make the removal of the core and
the surrounding keratosis easier. Recurrence is common.6
Chafing
Chafing occurs in areas of prolonged friction and usually
involves coarse, sweaty garments. Erosion of the skin of the
areolae and nipples is particularly troublesome to male
long-distance runners wearing loose-fitting T-shirts. The
nipple may bleed and is very tender because of the chafing.
A popular solution is the application of petroleum jelly to
the nipple. Although helpful, it is not always effective. To Figure 19-10
avoid the problem, several options are available: snug, non- Skate or lace bite. Swelling over extensor tendons. (From Magee DJ:
occlusive, absorbent undergarments; no shirt at all; or a Orthopedic physical assessment, ed 5, St Louis, 2008, Saunders,
piece of circular adhesive tape applied over each of the p 850.)
nipples.6,17 Women are less prone to the problem because of
the soft exercise brassieres that are now available. Chafing
between the upper thighs is characterized by inflamed, is red, itchy, and scaly, and accompanied by vesicular pap-
tender skin, sometimes accompanied by a burning sensa- ules. Laymen’s terms abound for this condition and gener-
tion. To prevent the problem, long, close-fitting shorts or ally are sport-specific. For example, hockey players refer to
tights made of nonocclusive, absorbent material should be dermatitis as “gunk,” a term not found in any medical
worn. Loose-fitting shorts and pants should be avoided. dictionary.
A mild cortisone cream, such as HydroVal cream, A common cause of dermatitis and allergic reactions in
applied two to three times a day to chafed nipples or skin athletes is the chemicals in garments. Formaldehyde, which
will provide rapid relief and encourage healing in the area. is used in fabric to prevent mildew and wrinkling and to
preserve color, is very irritating to the skin when leached
out with sweat (Figure 19-11).
Pseudobursitis
Pseudobursitis is characterized by swelling, inflammation,
and tenderness in an area of chronic friction, causing a sub-
cutaneous pocket to form in which serous fluid gathers.
Hence the names pseudobursitis or “false bursitis” are used
because the fluid does not gather in an established bursa but
in a friction-induced sac.
This condition is common to hockey defensemen be-
cause the extra padding at the front of the skate rubs under
the pressure of the laces (Figure 19-10). Pseudobursitis
among hockey players is often referred to as “skate bite,”
reflecting the painful nature of the condition.
At one time, surgical removal of the lesion was the treat-
ment of choice. Today, however, potent topical cortisone
salves, such as Dermovate or Temovate ointment, applied
regularly to the area, controls the inflammation and
decreases the discomfort. Once the offending equipment is
no longer worn or proper protection is provided, the condi-
tion resolves on its own, and the cortisone treatments are
no longer necessary.
Dermatitis
Dermatitis and eczema are terms used synonymously to
describe conditions in which the skin is inflamed. The Figure 19-11
causes are many and varied, but characteristically the skin Contact dermatitis (elbow pad formaldehyde eczema).
Dermatological Considerations in Athletics • CHAPTER 19 465
Some individuals are hereditarily predisposed to irritable bind with milk caseins and are flushed away with the rinse
skin, a condition referred to as atopic dermatitis. Athletes cycle (Table 19-1).8
with this condition are particularly susceptible to equipment-
related irritation of the skin as well as environmental factors
such as chemicals in swimming pools.
Conditions Caused By Heat and Sweat
Cortisone salves such as HydroVal applied frequently The skin of the athlete is often immersed in a tropical-type
may be used to relieve the dermatitis, once present. How- environment because of the rise in body temperature through
ever, prevention is important in controlling the condition. exertion and the body’s natural cooling mechanism, sweat-
Careful washing of clothing will help prevent contact der- ing. Infectious organisms such as bacteria, viruses, and fungi
matitis. Detergent should be used sparingly in the wash, as thrive in this type of environment, and skin problems may
detergents and softeners are a source of skin irritation in result.
themselves. Bleach should be avoided, as it may activate The stratum corneum, or superficial layer of the epider-
rubber elastic, making it more allergenic. A cup of pow- mis, plays an important role in preventing the invasion of
dered milk added to the second rinse cycle will remove the infective micro-organisms. To serve this purpose well, the
formaldehyde in new clothing. The formaldehyde molecules stratum corneum must be dry and intact. The macerating
Table 19-1
Prophylactic Measures for Skin Conditions
Measure Rationale
Wear full or partial underclothing of Prevents dermatitis caused by sweat gland leaching of chemicals and dyes. Draws
soft, 100% cotton moisture away from the skin, preventing maceration of the stratum corneum and
avoiding the development of a breeding ground for bacterial and fungal infections
Use a minimal amount of detergent Detergents, bleach, and softeners are sources of irritation. Bleach can activate
(1⁄4 cup) when washing clothing. rubber and elastic, making them more allergenic. Formaldehyde in new clothing
Avoid bleach. Add powdered milk to will bind to caseins in the powdered milk. These will be flushed away with the
the second rinse cycle to wash away rinse water
formaldehyde in new garments
Use protective dressings such as Provides a buffer against trauma and friction and protects blisters from further
Spenco 2nd Skin on skin surfaces injury
exposed to trauma or friction
Use a moisturizer immediately after Controls dryness and reduces the likelihood of asteatotic eczema. This is
showering particularly important in cool, dry climates. Scaly, cracked skin is more susceptible
to contact dermatitis and infections
Use a protective wrap such as Adhesive tape can irritate the skin when next to the skin or when being removed
Pro-Wrap Foam underadhesive tape
Wear properly fitting equipment, Reduces friction. For example, individually casted skates and water molding of skate
especially footwear boots will immobilize the foot, reducing friction
Wear protective clothing Layer clothing in various ambient temperatures to allow for adjustment to changes
in body heat. Wet/dry suits, underwater boots and gloves, and bathing caps
provide protection in the water. Wide-brim hats, tightly woven cloth, and
sunglasses protect against the sun’s rays
Wear protective creams A broad-spectrum sunscreen with an SPF of 15 or more will protect against UVA
and UVB wavelengths of light. Apply when the skin is cool and dry. Oil-based
ointments, such as petroleum jelly, should be used on the lips and around the
nostrils to protect them from dehydration caused by cold and wind conditions
Postpone shaving and washing exposed The natural oils of the skin provide insulation from the wind and cold
skin surfaces when participating in
sports in cold temperatures
Adapted from Groot DW, Johnston PJ: A review of sports-related skin problems, Can J CME 2:19-27, 1990.
SPF, Sun protectant factor; UVA, ultraviolet A; UVB, ultraviolet B.
466 SECTION III • Management of Sports Injury and Illness
Intertrigo
Intertrigo is a condition in which the skin becomes inflamed Figure 19-12
because of moisture and constant friction in skin folds. It Miliaria rubra (prickly heat rash).
differs from chafing in that chafing is caused by friction
between two skin surfaces or the skin and a garment,
whereas intertrigo is caused by the maceration of the stra-
tum corneum in areas where moisture has difficulty escap- in individuals who wear occlusive exercise garments or who
ing, such as skin folds. In athletes, this commonly occurs in exercise in hot, humid environments. Crops of erythema-
the groin or axillary regions. The symptoms include burn- tous papules cause a very uncomfortable prickly sensation in
ing, itching, and redness of the skin. Secondary bacterial the skin. Because the sweat cannot escape through the
(candidiasis) or fungal (tinea) infections may accompany blocked pores, it leaks into the epidermis, resulting in a crop
intertrigo. In severe cases, the skin becomes eroded and of irritated, itchy papules and vesicles.18
weeping. Blockage of the sweat pores in these areas causes Miliaria profunda is the result of chronic miliaria rubra
small sweat gland cysts known as miliaria. Loose, absor- and involves more extensive damage to the sweat duct. This
bent, cotton underclothing is the first step in drawing condition is relatively uncommon except in the tropics; it is
moisture away from the skin. The area should be cleansed characterized by asymptomatic, pale, hard papules under
frequently, and, when thoroughly dry, a fine, absorbent the surface of the skin and may cause discomfort.18
dusting powder such as Zeasorb cellulose powder should be Generally speaking, there is no effective treatment for
applied. Talcum powders should be avoided, as they can be miliaria. It is best managed by avoiding those circumstances
abrasive and do not absorb moisture well. Underarm that promote the condition by causing an increase in body
deodorants and antiperspirants can be irritating to the temperature and profuse sweating. Unfortunately, for the
skin and should be avoided as long as the condition athlete this is more easily said than done. Occlusive clothing
persists. Emollients, such as silicone-based creams (e.g., that does not breathe, or excessive clothing in the case of
Prevex), may help reduce friction in more severe cases. If outdoor sports, should be avoided. Frequent changes to clean
antibacterial, antifungal, and mild cortisone preparations absorbent cotton or silk clothing that draws moisture away
are prescribed, the emollient should be applied on top of from the skin are important. Molecularly fine dusting powder,
these to maximize the absorption of the active therapeutic such as Zeasorb cellulose powder, may be helpful. Cool show-
agent into the skin. In cases in which the skin is actually ers or baths will offer some relief, followed by an application
eroded, wet medicated compresses, such as Buro Sol, may of calamine lotion. Because calamine lotion can be drying to
help in the healing process. the skin, a moisturizer applied over it may be required. How-
ever, moisturizers in themselves can create problems by plug-
ging the sweat pores and aggravating the condition. As a last
Miliaria resort, acetaminophen (e.g., Tylenol or Tempra) taken to
Miliaria refers to damage to the sweat gland, and, depending lower the body temperature may be helpful.
on the extent of damage, it may be classified as crystallina,
rubra, or profunda.
Miliaria crystallina refers to a superficial obstruction Acrochordons
of the sweat duct. It is found in individuals who sweat Acrochordons are frequently referred to as “skin tags.” They
profusely and is characterized by multiple groupings of thin, are small, benign polyps that are characteristically soft, pedun-
clear-walled vesicles.18 culated, and pigmented. Acrochordons generally appear in
Miliaria rubra, sometimes referred to as “prickly heat regions of chronic friction, such as the neck, the armpits, the
rash,” is caused by increased body temperature with associ- groin creases, and under the breasts. Skin, like muscle and
ated profuse sweating (Figure 19-12). It is commonly seen bone, tends to grow in the direction of physical stress and
Dermatological Considerations in Athletics • CHAPTER 19 467
Pitted Keratolysis
Maceration of the skin under conditions of sweat and heat
create the ideal environment for a condition known as
pitted keratolysis. A bacterial micro-organism infiltrates the
horny layer of the skin, causing a superficial infection on the
soles and under surfaces of the feet. These circular, pitted
lesions may blend to produce large irregular margins.
Because the condition is largely asymptomatic, individuals
may be unaware that they have it, although repetitive
trauma, such as running, may cause tenderness. The lesions
may take on a green or brown discoloration and may be
responsible for a foul odor of the feet (Figure 19-13).
Application of a topical antibiotic, such as sodium fusi-
date cream or mupirocin ointment, twice daily for 10 days
will rapidly resolve this problem in most cases. Soaking the
soles of the feet for 10 minutes a day in a mixture of 1 table-
spoon of formalin and 18 tablespoons of water will help
reduce sweat production and odor.
Figure 19-13
Pitted keratolysis (bacteria induced).
Conditions of Communal Contact
The interactive nature of sports places most athletes in an
environment of communal contact. Even the cleanest facili-
ties afford an opportunity for the transfer of bacteria, fungi, Dermatophytes
and viruses. Although any part of the body is susceptible, Dermatophyte is the medical term for ringworm, a fungus
the feet are most commonly involved. that causes keratin breakdown and inflammation of the skin.
The moist, hot conditions created when an individual
sweats during an athletic activity cause maceration of the
Conditions of Communal Contact stratum corneum, creating an ideal environment for fungal
growth.
• Dermatophytes (fungal infections)
There are many different species and strains of dermato-
- Tinea pedis
phytes, and the clinical features of the skin will vary some-
- Tinea unguium
- Tinea cruris what depending on the type and size of the dermatophyte
• Viral infections that is causing the problem. Variations in skin response also
- Herpes simplex (fever blisters, cold sores) depend on the area of the body that has been infected and
- Warts the immune response of the individual.18
- Molluscum contagiosum Common areas of the body for dermatophyte infection,
• Bacterial infections particularly among athletes, include the feet, the fingernails
- Impetigo and toenails, the axillae, and the groin. Tinea pedis, fungal
- Pseudomonas infection of the feet, is commonly referred to as “athlete’s
• Parasites foot.” If the nail plates of the feet or hands are involved,
the condition is called onychomycosis or tinea unguium.
468 SECTION III • Management of Sports Injury and Illness
“Jock itch” is the lay term for tinea cruris, or fungal infec- Fungal infection of the nail plate usually begins with a
tion of the groin. Ringworm may also be found in other single digit. The typical early warning sign is a small area of
areas of the body: tinea corporis involves the entire body; discoloration, white or yellow, at the lateral free edge of the
tinea capitis, the scalp; tinea barbae, the beard; tinea faciei, nail plate. It is at this point that treatment should be insti-
the face; and tinea manuum, the hands.19 gated to prevent damage to the nail plate and involvement
of the other digits. As the fungus spreads inward and to the
Tinea Pedis base of the nail, the discoloration may become darker and
Tinea pedis (athlete’s foot) generally begins in the toe clefts, the nail plate becomes thicker. Subungual hyperkeratosis
but may spread to other areas of the foot, particularly the (thick scale under the nail) will cause the nail plate to lift
sole. Scaling, peeling, and fissuring of the skin are clinical and crack. Discomfort may accompany gross involvement
features of tinea pedis. Itchiness and an unpleasant foot of the nail plate.
odor are common. The condition may be aggravated by Avoiding communal exposure by wearing protective
secondary bacterial infection (Figure 19-14). footwear in sports facilities is the first step in prevention.
Walking barefoot in communal areas such as locker The sharing of sports equipment such as gloves and foot-
rooms, showers, and along the sides of swimming pools is wear should also be avoided. Absorbent cotton socks, glove
one of the most common means of dermatophyte transfer. linings, and powders will help control the conditions that
Wearing protective footwear, such as thongs, in these areas support the growth of fungi.
is recommended. Keeping the foot dry, particularly between
the toes, to prevent maceration of the skin so that it does Tinea Cruris
not become a breeding ground for infection is important. Tinea cruris (“jock itch”) is more common among men
Towel drying after cleansing followed by blow drying than women. This is probably due to the fact that men
with cool air from a hair dryer is helpful. Absorbent socks perspire more than women. Furthermore, the skin is more
and foot powders, such as Zeasorb cellulose powder, are occluded in the groin area of men because the scrotum is
recommended. in contact with the skin of the thighs and because of the
type of undergarments that men wear.18 It is an interesting
Tinea Unguium fact that jock itch usually appears in the left groin crease
Onychomycosis refers to fungal infection of the nail plate, first, because the left testicle descends lower than the
whereas tinea unguium refers more specifically to the right. Raised erythematous (red) plaques with distinct
ringworm dermatophytes. In either case, fungal invasion margins characterize tinea cruris. These plaques appear in
of the nail plate presents a major therapeutic challenge. the groin, extending down the thigh and onto the scro-
The nails of athletes play an important protective role in tum, giving a butterfly-like appearance. The condition is
sports requiring either the hands or the feet. Yet trauma very itchy.
and the environmental conditions to which athletes The fungus may be transferred from the feet to the
are exposed—heat, sweat, occlusion, and communal groin, particularly when toweling off. Sharing of sports
exposure—make the nails of the athlete more susceptible equipment, clothing, or towels contributes to the transfer
to fungal infections. of dermatophytes from one individual to the next.
To prevent the spread of tinea cruris, sports equip-
ment, including towels, should not be shared (even
after towels have been laundered). Also, individuals
with athlete’s foot should be cautioned to dry the body
before drying the feet to avoid autoinfection of other
areas, particularly the groin. Loose-fitting, absorbent
undergarments are essential to the control of this con-
dition, as dermatophytes thrive in occlusive, tropical
environments.
The treatment of fungal infections including tinea
pedis, tinea unguium, and tinea cruris is very similar.
A topical antifungal cream, such as terbinafine (Lamisil),
miconazole (Micatin), ketoconazole (Nizoral), or clotrim-
azole (Canesten), is applied after thorough cleansing and
drying of the affected area, twice daily for 2 to 6 weeks.
In resistant cases, systemic medication, such as ketocon-
Figure 19-14 azole, griseofulvin (Fulvicin), or terbinafine, taken orally
Tinea pedis (athlete’s foot). may be required.
Dermatological Considerations in Athletics • CHAPTER 19 469
Molluscum Contagiosum
Molluscum contagiosum is a pox virus that is common in
children but can be transmitted sexually or through skin-
to-skin contact in adults. Wrestlers are an example of
athletes who might be susceptible to this condition. Small,
discrete, dome-shaped, smooth papules can appear on any
area of the body. They are translucent, flesh-colored lesions
that may or may not be erythematous at the base of the
dome. The papules have a core that, when expressed or
opened, removes the virus. Therefore the treatment of
choice usually involves curetting the lesions, although
imiquimod 5% cream or liquid nitrogen in some cases may
Figure 19-16 be recommended.
Plantar warts (outlined prior to laser removal).
Bacterial Infection
Infections of the skin are caused by a multiplicity of bacteria
Warts may spontaneously regress after a few weeks or that present with a variety of skin manifestations. This
may last for years. One school of thought is to leave the makes a definitive diagnosis challenging. Often they can
wart to follow its natural course. Owing to the contagious only be differentiated by culture. These organisms may
nature of warts and the social stigma attached to them, manifest in the skin as impetigo, folliculitis, furuncle (boil),
however, the authors advise seeking treatment as soon as carbuncle, or cellulitis. Of these, impetigo and folliculitis
possible. are most likely to appear in athletes and are due to the pres-
Various topical agents are available for the treatment of ence of the staphylococcus aureus or pseudomonas bacteria.
warts. These include preparations of salicylic acid and lactic Impetigo is a superficial bacterial infection that may
acid, formalin in water, glutaraldehyde in aqueous ethanol, appear in athletes who sustain abrasions or lacerations as
and podophyllin. These preparations are generally applied might be expected in contact sports. Folliculitis is an infec-
daily to the wart under an occlusive dressing. Patience and tion of the hair follicle that manifests as red, raised, pustules
determination are required. centered on the skin around the hair shaft.
If the warts are recalcitrant, more aggressive measures Infections of the skin may be treated with antibacterial
may be necessary to get rid of them. Cryotherapy, laser va- cleansers, topical antibiotics, or systemic antibiotics. The
porization, and surgical removal are common strategies. course of treatment is determined by the nature of the bacte-
Cryotherapy uses liquid nitrogen, which causes a localized rial infection.
frostbite that kills the virus. Alternatively, the liquid nitro- Of recent concern amongst athletes is the appearance of
gen may be applied less aggressively at 3-week intervals to resistant strains of bacteria such as methicillin-resistant
stimulate the immune system to eradicate the wart. Vascular Staphylococcus aureus (MRSA) in otherwise healthy popula-
removal lasers such as the flash pump dye laser may be used tions. As with other bacterial infections, athletes are particu-
to selectively compromise the supply of nutrients from the larly vulnerable because of skin-to-skin contact, the inherent
blood vessels and thereby cut off the wart’s lifeblood. risk of cuts and abrasions, and the use of communal
Another technique uses a vaporizing laser, such as the CO2 facilities.20 MRSA presents as sore, red bumps on the skin,
laser, to heat the individual cells of the wart to 100°C which are swollen, infused with pus, and warm to the touch.
(212°F), causing the lesion to disappear in a plume of steam They may give off a foul odor.21 Descriptive terms like
and tissue particles.1 The advantage of laser vaporization “pimples,” “spider bites,” or “boils” have been used when
versus surgical removal is that the laser light seals the blood identifying these lesions. If unattended, these lesions may
vessels, creating a better visual field for distinguishing the become abscessed, in which case surgical incision and drain-
root of the wart from normal tissue. In this manner, the age is necessary. In some cases the lesions may be accompa-
surgeon can be more certain that the entire wart has been nied by a fever. If such an infection goes unchecked, there
removed with minimal disturbance of the surrounding tis- is a risk that it could spread, resulting in life-threatening
sue. This decreases the time required for healing, minimizes consequences.21
Dermatological Considerations in Athletics • CHAPTER 19 471
Chemicals in swimming pools also contribute to hair The skin is dry, itchy, scaly, and irritated. This can be
shaft fragility, resulting in split ends and hair breakage. particularly annoying to the athlete. The best treatment
Thorough rinsing of the hair after shampooing helps con- option for eczema is prevention. A soap that contains a high
trol the problem. Conditioners contain proteins that help to concentration of fat (animal, glycerin, or resin) should be
temporarily mend damaged hair by binding hair shaft cells. used when bathing or washing the face. A deodorant or
Oils in conditioners also replenish the natural oils that have antiperspirant should be used separately. In severe cases,
been stripped from the hair by exposure to chemicals and Cetaphil lotion is a good soap substitute. The skin should
shampooing. They also contain quaternary compounds that be thoroughly rinsed and patted dry, and then a moisturizer
help to control “fly-away” hair, a common problem in dry, should be applied to slightly moist skin. Moisturizers with
cold climates and air-conditioned rooms.1 In the case of perfumes should be avoided, as they irritate the skin. The
severe damage, the only alternative is to cut the hair. To moisturizer does not replenish the natural oils but prevents
prevent the problem, a bathing cap should be worn. the oil and moisture in the skin from escaping. Chemically
enhanced moisturizers contain agents such as urea, glycolic
acid, and lactic acid that improve the entrapment of the
Asteatotic Eczema skin’s natural oils, for example, Uremol 10 and Lac-Hydrin
When dryness caused by lipid depletion results in irritated, lotions. Calmurid cream is particularly useful for cracked
inflamed skin, the condition is referred to as asteatotic eczema and fissured heels. Apply the cream before going to bed,
(Figure 19-17). This is a particularly common condition in wrap the feet in a plastic wrap, and cover them with socks
athletes who are exposed to environmental conditions that to maximize effectiveness.2 In severe cases, topical cortisone
strip the skin of its natural oils. Such environmental factors or a course of treatment with controlled ultraviolet light
may include wind, chemicals in swimming pools, and may be required.
deodorant soaps.
Scar Revision
Scar formation is inevitable when damage from an injury
enters the deeper layers of the skin. The causes of scar for-
mation are many and varied, and include external trauma
such as abrasions, cuts, or burns, and internal trauma from
disease entities such as acne, chicken pox, and shingles.
The appearance of a scar may vary according to intrinsic
and extrinsic factors. Heredity and nutrition are intrinsic
factors that may affect the way a wound heals. Infection,
compromised blood supply, use of a topical or systemic
steroid, foreign materials in the wound, and poor surgical
technique are examples of extrinsic factors that contribute
to the appearance of a scar.
injection of flesh-colored pigment into the scar with a tech- 11. Nagington J, Rook A, Highet AS: Virus and related infections.
nique known as microimplantation. The other option is simply In Rook A, Wilkinson DS, Ebling FJ, et al, editors: Textbook of
dermatology, Volume 1, Oxford, 1986, Blackwell Scientific.
to cover the scar with cosmetics such as Derma Color.
12. Evans JG: Recurrent aphthous stomatitis: Management of a
patient, Oral Health 8:27, 1993.
13. Basler RSW: Skin problems in winter sports. In Casey MJ, Foster C,
Conclusion Hixson EG, editors: Winter sports medicine, Philadelphia, 1989,
Throughout this chapter, the authors have touched on some FA Davis.
14. Resnick SS, Lewis LA, Cohen BH: The athlete’s foot, Cutis
of the common skin problems encountered by the athlete.
20:351–355, 1977.
The protective role the skin plays in maintaining one’s health 15. Sher RK: Jogger’s toe, Int J Dermatol 17:719–720, 1978.
cannot be overemphasized. As in any other area of medicine, 16. Gibbs RC, Boxer MC: Abnormal biomechanics of feet and their
some simple yet effective precautions may prevent skin dis- cause of hyperkeratosis, J Am Acad Dermatol 6:1061–1069,
eases that can interfere with training and performance. 1982.
17. Levit P: Jogger’s nipples, N Engl J Med 297:1127, 1977.
18. Champion RH: Disorders of the sweat glands. In Rook A,
Wilkinson DS, Ebling FJ, et al, editors: Textbook of dermatology,
Volume 3, Oxford, 1986, Blackwell Scientific.
References 19. Roberts SOB, Mackenzie DWR: Mycology. In Rook A, Wilkinson
1. Lever WF, Schaumburg-Lever G: Histopathology of the skin, DS, Ebling FJ, et al, editors: Textbook of dermatology, Volume 2,
Philadelphia, 1983, JB Lippincott. Oxford, 1986, Blackwell Scientific, 1986.
2. Groot DW, Johnston PA: Young as you look, Edmonton, Canada, 20. Centers for Disease Control and Prevention: Frequently asked
1993, InForum. questions about methicillin-resistant staphylococcus aureus (MRSA)
3. Groot DW, Johnston PA, Miller P, Sather G: Skin problems of a among athletes, November 2008. http://www.cdc.gov/ncidod/
professional hockey club: A season in review, Cont Derm 2:13–22, dhqp/ar_MRSA_AthletesFAQ.html
1988. 21. Mayo Clinic: MRSA: Understand your risk and how to prevent
4. Lynch PJ, Boyer JT: Clotting disorders in the skin (purpura). In infection. http://www.mayoclinic.com/health/mrsa/ID00049.
Fitzpatrick TB, Eisen AZ, Wolff K, et al, editors: Dermatology in 22. The Canadian Dermatology Association: “Dermatologists -
general medicine, New York, 1971, McGraw-Hill. Your Skin Experts,” Kingston, 2009, The Canadian Dermatol-
5. Wilkinson DS: Cutaneous reactions to mechanical and thermal ogy Association.
injury. In Rook A, Wilkinson DS, Ebling FJ, et al, editors: Textbook 23. McLean D: Dysplastic nevus: Precursor to melanoma, Med North
of dermatology, Volume 1, Oxford, 1986, Blackwell Scientific. Am 32:4460–4462, 1986.
6. Basler RSW: Skin injuries in sports medicine, J Am Acad Dermatol 24. Champion RH: Cutaneous reaction to cold. In Rook A, Wilkinson
21:1257–1262, 1989. DS, Ebling FJ, et al, editors: Textbook of dermatology, Volume 3,
7. Johnston PA, Groot DW: Tattoos: art or injury, Pulse 7(2):14–15, Oxford, 1986, Blackwell Scientific.
1993. 25. D’Ambrosia RD: Cold injuries encountered in winter sport, Cutis
8. Groot DW, Johnston PJ: A review of sports-related skin problems, 20:365–368, 1977.
Can J CME 2:19–27, 1990. 26. Washburn B: Frostbite, N Engl J Med 266:974–989, 1962.
9. Ryan TJ, Wilkinson DS: Diseases of the veins and arteries—Leg 27. Groot DW, Johnston PA: An approach to laser therapy, J Cutan
ulcers. In Rook A, Wilkinson DS, Ebling FJ, et al, editors: Textbook Med Surg 3(Suppl 4):S7–S13, 1999.
of dermatology, Volume 2, Oxford, 1986, Blackwell Scientific. 28. Groot DW, Johnston PA: Advances in cutaneous laser therapy,
10. Oxman MN: Varicella and herpes zoster. In Fitzpatrick TB, Eisen Can J Cl Med 4(8):4–8, 1997.
AZ, Wolff K, et al, editors: Dermatology in general medicine, 29. Yarborough JM: Ablation of facial scars by programmed
New York, 1971, McGraw-Hill. dermabrasion, J Derm Surg Oncol 14:292–294, 1988.
20
CHAPTER
478
Protective Equipment in Sports • CHAPTER 20 479
Custom-made items have definite advantages versus stock impact, absorb shock, or immobilize a body structure.
items in that they can be constructed and customized for a Lightweight plastics and foams can be combined to optimize
specific body part, injury, and athlete. Some problems with the products’ ability to absorb or deflect an impact. Most
off-the-shelf equipment can include proper fit and comfort.1 equipment companies combine materials, depending on the
A customized pad must fit exactly as intended and must function of the particular piece of gear. This provides com-
provide the protection or support specified for the injury or fort and cushion close to the body, and firmer, nonyielding
body part. The sports medicine clinician must be knowl- materials are placed on the outside to transfer the stresses
edgeable about the properties and uses of all of the materials over a broad area.7 Sports medicine clinicians should be
used in the construction of custom padding or supports. For familiar with various materials and how they react on impact
example, what materials have the ability to be heated and so that combinations of materials can be used effectively to
molded into a specific shape? These materials must also prevent injury or reinjury.
perform their purpose, and be safe for the athlete and
opponents. Also, what are the methods used in heating and
molding these materials? An example is the use of a hydro- Foam
collator to heat a thermomoldable plastic so it can be Foam is one of the most common products used in con-
shaped. The sports medicine clinician must also possess structing custom protective padding. It is available in an
some form of creativity or mechanical skill to create the pad array of types, thicknesses, and densities, depending on what
or support needed by the injured athlete. Mechanical skill is needed for the particular device. The primary consideration
includes the ability to use the tools necessary to shape the in choosing foam padding is the energy and shock-absorbing
materials, including scissors, flat knives, scalpels, or whatever capabilities of the material. These energy absorbing capabili-
the sports medicine clinician feels comfortable using.1 The ties depend on the thickness and density of the foam. The
most common purpose for a custom-made pad is to absorb foam should absorb shock and be light enough to be worn
shock and deflect forces away from the injured area. comfortably. The two main types of foam are open-cell and
closed-cell. Open-cell foams (Figure 20-1, A) are low-density
materials in which the cells are connected to allow air passage
Protective Materials from cell to cell. Similar to a sponge, these materials have the
Numerous materials are used in the manufacture of modern capacity to absorb fluids and are commonly used to pad bony
sports protective equipment. Every material of a given den- prominences or hard edges of protective equipment and cus-
sity, thickness, and temperature has certain properties that tom-fabricated pads. Open-cell foams generally do not have
help define that material’s use.5 Soft materials usually have good shock-absorbing qualities because they deform quickly
a lower density and are lightweight because air is incorpo- under stress. Closed-cell foam (Figure 20-1, B) is preferred
rated into the material. Soft materials protect optimally at because of its superior shock-absorbing abilities, and its resil-
low levels of impact intensity. ience to absorption of fluid such as perspiration.8 Closed-cell
Resilience or memory is another property of materials used foams should also rebound quickly after being compressed to
in protective equipment. Resilience is the ability of a material maintain protection.
to regain its shape quickly after impact. Highly resilient mate- Dual-density foam is also available. This consists of high-
rials are used when protection from repeated impacts is and low-density foam that has been glued together by the
required.5 Nonresilient materials can be used when one-time manufacturer. This can be useful when creating a pad
or occasional impact is expected, although the protective quickly on the field.
equipment may be ruined by that impact. These materials Some high-density foam is also thermomoldable. This
must be checked to ensure that the athlete does not continue means that when heated, it becomes flexible, allowing it to
to use the equipment if the material is crushed or compacted be shaped and modified as needed to a variety of shapes and
by repeated impacts. For example, the polystyrene foam inside sizes (Figure 20-2). After it has cooled it holds its final
bicycle helmets is lightweight and will crush on impact to shape until reheated. Cramer High Density Foam is an
protect the skull. When the material has been altered because example of foam that can be heated and molded into the
of impact, it no longer offers adequate protection and should shape needed.
be replaced. Nonresilient materials are tested by an indepen-
dent company to determine whether deformation and energy
absorption occurs below levels that would cause injury. Air Management Pads
Silicone, fiberglass, polyethylene foam, thermoplastic Air management pads are a relatively new type of protective
materials (e.g., Orthoplast, Aquaplast), neoprene, moleskin, padding and are often used when maximal shock absorption
felt, and adhesive foams are among the materials used in is required in lightweight gear. These pads are constructed
fabricating customized splints or equipment.6 Each has a of various open- and closed-cell foam pads encased in poly-
unique protective ability to conform to the body, deflect urethane or a nylon material.8 This encasement is airtight,
Protective Equipment in Sports • CHAPTER 20 481
A B
Figure 20-1
Demonstrating different densities of open-cell (A) and closed-cell foam (B).
Gel
Another material that is useful in absorbing shock is gel. Many
companies manufacture a variety of gels with different capa-
bilities. An example of a gel-based shock absorbing material is
Johnson and Johnson’s product Orthogel (Figure 20-3).
Orthogel comes in varying thicknesses and can be cut into
different shapes. Because of the consistency of the gel, it can
Figure 20-2 conform to bony areas of the body. Gel is useful for protecting
A custom-fabricated pad. A donut pad is cut from Thermoplast, and bony areas such as the foot, hand, and acromioclavicular (AC)
firmer Hexalite is molded and attached to the donut to give better joint of the shoulder. Another quality is that the gel can be cut
protection. This pad is used to protect the acromioclavicular joint.
and used as a horseshoe pad when treating an acute ankle
sprain. This horseshoe can be cooled and used for cryotherapy
as it provides compression and reduces and prevents swelling
in an acutely injured ankle. A drawback to using gel-based
which prevents quick deformation of the foam so that the materials is the lack of longevity associated with such prod-
energy is dissipated over a broad area. Air pads are fre- ucts. Gel has a tendency to absorb heat from the athlete’s
quently used in football shoulder pads, and various compa- body often resulting in the pad losing its shape. This reduces
nies incorporate different designs of foam placement within the ability of the material to provide protection over a long
the nylon encasement. These pads are more expensive than period. For gel-based pads to last, an athlete must care for the
traditional equipment, and the linings must be replaced or material properly (e.g., allow to dry in a cool place). This is a
patched if the nylon is torn because this allows too much air drawback because the sports medicine clinician should be able
to escape on impact. Nylon prevents fluids from entering to provide protection with minimal care. Because of the short
the pads, which helps avoid adding significant weight to lifespan of gel padding, the material should be reserved
the equipment. Body fluids such as sweat and blood are for protecting difficult bony areas. Gel is extremely useful in
482 SECTION III • Management of Sports Injury and Illness
Figure 20-4
Sheets of felt demonstrating different thicknesses.
Figure 20-3
Shock-absorbing gel.
Working
Temperature
(°F) Rigidity Shrinkage Stretch Drapability Moldability Bond Memory Comments
Plastic
NCM Clinic (Precision 160-170 3 1 3 3 3 3 2 Easy to work and contour
Splint/RS 3000) North
Coast/Polymed
Polyform/Kay Splint- 150-160 2 1 2⫹ 2⫹ 3 3 1 Easy to mold; do not overheat
Rolyan/Sammons
Ultraform (Sammons) 160 2 2 2 2 2 2 1 Nice feel/texture
Aquaplast, Blue-stripe 160-180 2 2 3⫹ 3⫹ 3 3 2 Better cut pattern when
(WFR/Aquaplast) translucent; highly moldable
Orthoplast II (Johnson 150-170 2 1 3 3 2 3 1 Looks, behaves like multiform
& Johnson)
Multiform I & II (AliMed) 150-180 3 2 3 3 2 3 1 Inexpensive; easy to mold
and work
Plastic and rubberlike
NCM Preferred/Custom 160-170 3 1 2 3 2 2 1 Versatile; skin rash with
Splint/JU1000 North perspiration
Coast/Polymed
Ultraform 294 (Sammons) 160 3 1 1 1 1 2 2 Difficult to form
Polyflex II/Kay Splint, 160 2 1 3 3 3 2 1 Good for small/large orthoses;
Isoprene scraps recyclable
483
(Sammons)
From Breger-Lee DE, Burford WL: Properties of thermoplastic splinting materials, J Hand Ther 4:202-211, 1992.
Range of scores is 1 (least) to 3 (most).
484 SECTION III • Management of Sports Injury and Illness
associated with some of the thermoplastic materials. is a heat-activated, lightweight, closed-cell foam that is heated
Shelf life also affects the quality of these materials. for 5 to 10 minutes in a convection oven at 285°F (140°C).
There are also high-temperature thermoplastics that This polyethylene material can be formed to the part to be
become malleable at temperatures of 325°F to 350°F protected and provides lightweight padding and support.11
(163°C to 177°C). These can be vacuum-molded or shaped These protective devices can be extremely useful in protecting
over plaster models. Heat guns can be used to make modi- a quadriceps contusion to prevent repeated blows and possible
fications. These materials can be transparent and are useful, subsequent development of myositis ossificans (see Chapter 18,
for instance, if a full-contact face mask is desired to allow “Medical Conditions in Sport”).
protection of a facial injury (e.g., W-Clear).
Plastics have come into their own in custom-made
padding. The most widely used is Johnson and Johnson’s Casting Material
Orthoplast. Orthoplast comes in sheets that are solid or per- Scotchcast fiberglass-polyurethane splints soften at room
forated. These sheets can be heated and molded to fit a spe- temperature (70°F to 75°F [21°C to 24°C]) and provide a
cific body part and form a hard protective shell (Figure 20-5). one-step, easily moldable splint that sets in 3 to 4 minutes.
The sports medicine clinician can use a hydrocollator to heat Functional strength in the material is attained in 20 minutes.
the material before molding. When the material cools it main- Scotchwrap has 25% of the fiberglass resin of Scotchcast,
tains its shape and remains rigid until it is reheated. Plastazote which causes it to be less rigid when dry. This could be an
alternative to RTV 11 rubber in high school athletes,
because it is easier to apply. However, a referee may require
the material to be covered with soft padding during partici-
pation to avoid injury to other players.
Hexcelite or X-Lite is a low-temperature thermoplastic
with an open-weave design that allows fabrication of light-
weight, highly ventilated splints. This material becomes mal-
leable with warm tap water and is self-bonding, so multiple
layers can be used to increase the rigidity of the device.
Silicone elastomer has been popular in fabricating soft
splints. This material is used when a more rigid material is
considered illegal in sporting competition. Silicone elasto-
mer casting is appropriate with certain types of hand or wrist
injuries or when a fracture has reached a healing state that
would not be compromised with less rigid protection. The
liquid-style elastomer is reinforced with layers of gauze ban-
daging when used for casting. The set-up time is controlled
by a separate catalyst that is added to the silicone when the
cast is made. Because the silicone cast is nonporous in its
finished form, it is typically worn only during competition.
Skin maceration can occur if the cast is worn for too long.
The athlete should wear a bivalved cast or splint at all other
A times until the injury has healed.
Another rigid form of protection is casting material such be used to hold foam onto a hard shell, and can
as Orthoglass (Figure 20-6). Orthoglass uses a fiberglass- be used to cover up sharp edges on customized hard
type resin that, when combined with tap water, becomes materials.
rigid. This material combined with foam and tape can make Heat Sources. The most common sources of heat
a resilient pad. This technology is extremely useful when to aid in the construction of protective padding include
one needs to make a protective shell or splint quickly hot pack machines (i.e., hydrocollator), hot air guns, or
and only the material and water is available, such as on the hair dryers, and a conventional oven with temperature
sideline of a football game. control.
Shaping Tools. The most commonly used tool used to
create custom pads are heavy-duty scissors. Other tools
Miscellaneous Items include sharp knives or scalpels and cast saws.
Off-the-shelf items can also be used in creating custom- Fastening Materials. Once created, custom pads are
made protection. The extremely durable plastic insert commonly held in place by tape adherent such as Tuff
can be cut out of a thigh pad and used to create a custom Skin and a simple wrap made of elastic and tape. Other
pad. These plastics are known to be durable and are methods include using hook-and-loop fastener straps,
also thermo-moldable. Care must be taken when using tensor bandages, and leather straps and buckles; even
these products especially if the sports medicine clinician laces can be slipped through eyelets that are drilled into
does not have experience working with these materials. whatever hard material is being used. This process can be
These materials should be researched to verify their used to create pads for different body parts using simple
safe use. modifications. For example, athletic tape can be used to
create a higher dome when constructing a pad for an AC
joint injury to provide greater protection (Figure 20-7).
Tools Used for Customizing Off-the-shelf items can also be used in conjunction with
Adhesives. A number of glues and adhesives can be used these custom-made pads to help provide proper fit and
to create custom padding by holding different materials comfort for the athlete. For example, shock pads, which
together to help form different shapes. are foam pads placed under standard football pads to
Adhesive Tape. Adhesive tape is one of the most absorb shock, can be used to keep a custom-made AC
commonly used tools in creating custom padding. Tape can pad in place. Also, a snug-fitting football girdle can
be used to help keep a custom-made thigh pad in place
comfortably.
Head Protection
Sports Requiring Helmets
• Amateur boxing
• Baseball
• Cycling
• Football
• Ice hockey
• Mens’ lacrosse
• Softball
• Whitewater sports (e.g., kayaking) A
Football Helmet
The football helmet has evolved from a simple leather cap to
a technological achievement in head injury prevention. Not
only are the materials used in creating the helmet important,
but the design itself is imperative in preventing head injuries.
These designs, NOCSAE standards, and rule changes have
dramatically reduced injury since its creation in 1896.2
A NOCSAE–approved helmet must resist against
B
concussive forces to the head that may injure the brain;
however, the helmet is not a guaranteed fail-safe against
injury.3 The athlete (and, in the case of student athletes, the
athlete’s parents) must be made aware of the proper fitting
and use of the helmet.
To make this clear to everyone involved in the use of helmet created by Riddell (Figure 20-8). Studies performed
football helmets, NOCSAE has adopted a warning label to in the laboratory setting have concluded that there has been
be placed on all helmets. A helmet is not legal for use if this a 20% reduction in concussion risk during simulated
label is not visible. The label must be placed on the helmet National Football League game collisions.12 In studies
by the manufacturer and the reconditioner.3 performed on the field using high school football players,
More recent technology has improved the effectiveness the Revolution helmet has also been shown to reduce
of the helmet. The most recent innovation is the Revolution the risk of concussion by as much as 31%.13 Figure 20-9
Protective Equipment in Sports • CHAPTER 20 487
B
Figure 20-9
Helmet linings. A, Baseball, lacrosse, and football air helmets (left to right). B, Various types of air hel-
mets; AHI (Athletic Helmets, Inc.) single-bladder, AHI double-bladder, and Riddell air helmets (left to
right).
A B
C D
E F
Figure 20-10
Fitting a football helmet (see box Helmet Fitting for explanation).
490 SECTION III • Management of Sports Injury and Illness
Figure 20-11
Different face mask configurations.
Table 20-2 rules mandate helmets and face masks with a NOCSAE
Face Mask Type by Position Played in Football standard. The strength of the steel wire is intermediate
compared with that required in football and ice hockey. The
Face Mask Playing Position
face mask is well off the face, but padding around the chin
Oral protection only Quarterback(s), running area protects the athlete if the face mask is driven backward
backs, defensive backs, in a collision.16 Four-point chin straps are used on all
kickers, wide receivers helmets (Figure 20-13).
Nose and oral protection Fullbacks, linebackers, Face masks are now available that protect the jaw area
tight ends and can be attached to baseball and softball batting helmets.
Jaw and oral protection (with Quarterbacks, linebackers, These devices can also be used for players on the field.
or without nose protection) linemen American Society for Testing and Materials (ASTM) stan-
dards have been developed, and progress is being made to
require face masks on batters in Little League baseball. The
Ice hockey face visors and masks have been shown to re- prototypes are a wire-cage or a clear, plastic guard that is
duce the number of facial injuries. Junior A hockey players attached to the batting helmet and shields the mouth and
wearing no face visor were 4.7 times more likely to suffer eye jaw area, with an opening at the mouth to prevent fogging.
and face injuries compared with players who wore a visor or The eyes are not covered, but are well protected from
cage. It has also been suggested that both full and partial face impact because the ball will not fit between the helmet’s
protection significantly reduces the incidence of eye and face visor and the jaw protector (see Figure 20-12, B).
injuries without increasing neck injuries and concussions.15
High school and NCAA ice hockey players are required to
wear face protection. Helmets must be equipped with wire Chin Straps
face masks. The openings in the wire guard must be small Chin straps help secure a helmet on the head. Certain sports
enough so that a hockey stick cannot fit through the holes such as cycling and kayaking use a single strap that is
and cause injury. Face guards used in hockey are approved by hooked under the chin. A single strap allows some rotation
multiple agencies such as the Hockey Equipment Certifica- of the helmet but is usually adequate in maintaining the
tion Council and the CSA. The National Federation of High appropriate position of the helmet on the top of the head.
School Athletic Associations and the NCAA require that goal- Football and lacrosse use four-point chin straps to prevent
keepers wear throat protection as well as face protection. They rotation of the helmet.
also require that all players wear full-face protection. Chin straps are connected to the helmet with metal
Lacrosse face masks protect the face from impact of grommets that must be replaced occasionally. There are
either the stick or the ball (Figure 20-12). Men’s lacrosse many companies that produce similar chin straps. Different
Protective Equipment in Sports • CHAPTER 20 491
A B
Figure 20-12
Face masks used in other sports. A, Plastic face mask used on baseball batting helmets. B, Lacrosse
face mask.
A B
Figure 20-13
Chin straps. A, Low-hookup chin strap (hard-cup). B, High-hookup chin strap.
styles include the hard shell lined with a vinyl-dipped foam found that the decreased angle of the low hookup means
or a soft cup made of leather or vinyl. The hard cup gives that there is less chance of the chin strap rotating off
the athlete added padding on the chin, whereas the soft cup the chin.
primarily functions to hold the helmet in place. Some chin
straps are available in different cup sizes.
In football, the four-point chin straps are secured by Eye Protection
either the high hookup or the low hookup (see Figure Special precautions must be taken to protect athletes’ eyes,
20-13). The Riddell helmets are drilled for low hookup, especially in projectile sports such as ice hockey, men’s and
and the AHI (Athletic Helmets, Inc.) helmets are drilled women’s lacrosse, and handball. Besides these obvious
for high hookup. Either helmet can be modified sports, racquet sports pose serious risk to the eye. Eye
by punching through a marked area on the helmet and guards should be made from polycarbonate to prevent
attaching a grommet. Some equipment managers have shattering (Figure 20-14).3
492 SECTION III • Management of Sports Injury and Illness
A B C
Figure 20-14
Examples of eye protectors. A, Plastic and lens are all one piece. B, Separate plastic lens. C, Polycarbonate
shield attached to football face mask.
protection. The decision to play is up to the athlete, the The majority of dental trauma can be prevented by using
athlete’s parents if he or she is a minor, and the physician. a correctly fitted mouthguard. Mouthguards should never
Legal counsel may be necessary if handicap discrimination be cut down or modified. This would void the manufactur-
is an issue. A signed waiver may be indicated, stating the er’s warranty and might create an obstructed airway. Mouth-
necessity of using protective eyewear and the possibility of guards have also been shown to reduce shock from blows to
injury to the good eye. Class I or II sports eye protectors the chin. Testing of the neurocognitive abilities of athletes
should be worn at all times during athletic endeavors, with who had suffered a concussion showed no difference be-
an additional face shield if there is a significant potential for tween athletes who used mouthguards and those who did
injury. not. This suggests that mouthguards do not prevent or re-
duce the incidence of concussions.25 Despite these findings,
some manufacturers of different types of mouthguards have
Mouthguard made claims that wearing their mouthguards can prevent
Many high school organizations and the NCAA require concussions. The Brain Pad, manufactured by WIPSS, is an
that participants in certain sports, such as football, wear example of one of these mouthguards. It has been shown
mouthguards, whereas the American Dental Association that there is no significant difference in the rate of concus-
recommends that all athletes wear mouthguards. sion among football and rugby players using standard
The most common types of mouthguards are the stock boil-and-bite mouthguards and the Brain Pad.26
variety often referred to as “boil and bite” (Figure 20-15).
These mouthguards are placed in hot water and then
molded to the athletes’ teeth by the athlete biting on the Ear Protectors
heated mouthguard. Another type is the custom-made The ears are protected from shearing forces and contusions
mouthguard that is fitted to the athlete’s maxillary arch by most helmets. Even though helmets are not used in box-
by a dentist. Custom-made mouthguards are produced ing, wrestling, and water polo, ear protection is required
from molds made of the athlete’s teeth. These devices are because of the high incidence of ear injury in these sports.
preferred by athletes because they make it easier to “Cauliflower ear,” a hematoma in the outer ear, may occur
breathe and talk during play and generally feel more com- without the use of appropriate equipment. This hematoma
fortable. However, cost may inhibit the use of custom often requires aspiration, and a splint is applied to maintain
mouthguards. Simple boil-and-bite mouthguards are as pressure and prevent the hematoma from returning. If
effective as custom pads and can be bought in bulk to fit adequate pressure is not maintained, the blood and exudate
an entire team. collect between the skin and cartilage and may solidify,
causing a permanent deformity. This type of injury is pre-
ventable with appropriate ear protection (Figure 20-16).6
Figure 20-15
Examples of mouthguards; custom (left) and heat-molded (right). Note
that the heat-molded mouthguard has a face-guard attachment to attach
the mouthguard to the face guard to prevent the mouthguard from Figure 20-16
being swallowed and to make it easier to remove. Example of ear protector: wrestling head gear.
494 SECTION III • Management of Sports Injury and Illness
A B
Figure 20-18
Examples of throat protectors. A, Throat protection for lacrosse goalie. B, Larynx extension for baseball
catcher.
A B
Figure 20-19
Examples of flat pads. A, Flat pad with belt attachment to help maintain an “air” pocket at the top of
the shoulder on impact. B, Channel system features wedges of hook-and-loop fasteners on the inside of
pads to protect the AC joint.
cups, and anterior and posterior pads. The arch around below the epaulets and should cover the deltoid. The
the cantilever is shaped to fit the contour of the upper posterior pads cover the trapezius and other posterior
body. The shoulder flaps (also called epaulets) extend muscles in addition to covering the scapula and spine.
from the edge of the arch over the shoulder caps. These The anterior pads cover the pectoral muscles as well as the
further protect the top of the entire shoulder area. The sternum and clavicle. Anterior pads may be slanted for-
shoulder cups also attach to the arch and are located just ward or even built up in pads made for linebackers and
496 SECTION III • Management of Sports Injury and Illness
A B
D
Figure 20-21
Standard extensions to football shoulder pads. A, Rib combination often used with football
quarterbacks. B, Posterior aspect of rib combination. C, Lateral arm protector, deltoid extension.
D, Back extension “kick plate.”
498 SECTION III • Management of Sports Injury and Illness
Figure 20-22
Shoulder pad components and common attachments.
Protective Equipment in Sports • CHAPTER 20 499
A B
Figure 20-23
Examples of hockey and lacrosse shoulder pads. A, Ice hockey shoulder pads. B, Lacrosse shoulder pads.
fitted to the athlete and is held in place by hook-and-loop before making custom-fabricated pads or splints to be used
fasteners. at the elbow or below.
A protective shell such as this can be created by modify- To prevent injury to the hand, gloves are often worn in
ing the process described previously (see box “Creating a addition to many types of foam or neoprene pads for the
Custom Hard-Shell Pad”). A role of tape can be used to distal aspect of the upper extremity. Gloves with silicone gel
create a high dome. Once created, the shell can be held in or foam padding are used in football, baseball, hockey, and
place by attaching it to a pair of shock pads or strapping it lacrosse (Figure 20-25).
to the athlete’s body. The elbow, wrist, and hand also require protection from
injury. Many of these injuries are from blunt trauma and
Shoulder Instability many off-the-shelf neoprene-type sleeves and pads are avail-
Many different types of shoulder harnesses are commer- able to provide protection.3 Injuries to these body parts are
cially available. They are popular among athletes in often trivialized, but can be debilitating. This is especially
collision-type sports. One example of a commercially avail- true for throwing and catching sports. In sports such as ice
able harness is the Sully Stabilizer. It has been shown that hockey and lacrosse, gloves are essential to preventing
shoulder harnesses can limit the shoulder’s range of injury to the wrist, hand, and fingers.
motion. These devices are designed to limit external rota- Custom-made protection can also be useful for protect-
tion and abduction.30 ing injuries to the hand. In the case of the ulnar collateral
ligament of the thumb, a hard splint can be constructed
using thermomoldable plastic to protect the injured liga-
Elbow, Wrist, and Hand Protection ment during play.
Injuries to the hands or fingers are among the most com-
mon injuries in sports—and the most neglected. These
injuries often cause minimal functional disability, and ade- Splint for Ulnar Collateral Ligament Sprain
quate protection with splinting materials may disqualify the • Cut thermomoldable plastic to desired size and heat for 60 seconds.
athlete. In collegiate and professional football, no rigid • Cut to desired shape .
material can be worn at the elbow or below unless it is • Mold plastic to hand using elastic wrap to hold in place.
adequately padded with closed-cell foam. Rules vary regard- • Add padding and moleskin to provide comfort and protect
ing the legality of protective equipment on the hand, usu- opponents.
ally depending on the sport and league. Clinicians should • Tape to athlete’s hand to provide protection to the thumb.
consult an authority about specific rules for individual cases
500 SECTION III • Management of Sports Injury and Illness
A B
C
Figure 20-24
Fitting of shoulder pads.
Figure 20-25
Examples of gloves for football and lacrosse. Varying amounts of dorsal and palmar padding are used,
depending on the amount of contact.
Chest protection is also very commonly used. Baseball (Figure 20-28). Protection can also be custom made to
catchers at every level of play are required to wear a chest protect an existing injury as described previously. A simple
protector (Figure 20-27, A). Lacrosse and ice hockey goalies donut can be added to a commercially available thigh pad
also wear a chest guard to absorb the shock of a lacrosse ball for extra protection. Muscle strains to the quadriceps,
or puck shot on goal (see Figure 20-27, B). Most of these groin, and hamstring are also common in sports. Neoprene
chest guards do nothing more than prevent mild contusions. sleeves are commercially available to help add extra support
It has been hypothesized that chest protectors can prevent to strained muscles.
sudden death; however, it has been shown in an animal model Properly fitting football pants are essential in maintain-
that commercially available baseball and lacrosse chest wall ing proper placement of thigh and knee pads. Thigh pads
protectors were ineffective in preventing ventricular fibrilla- should be centered over the quadriceps muscle group
tion triggered by blows to the chest.31 Improved technology approximately 6 to 7 inches (15 to 17 cm) above the knee-
and materials may improve the effectiveness of such devices. cap. When using asymmetrical thigh pads, the larger flare
should be placed on the lateral aspect of the thigh to avoid
injury to the genitalia.
Bras Deep quadriceps contusions are common in all contact
Sports bras are designed to restrict excessive movement of sports, although only football and hockey require thigh
the breasts during exercise, which can cause bruising and pads. Athletes in other sports may benefit from wearing
stretching of the suspensory ligaments. The bra should have football thigh pads in a girdle (see Figure 20-28, B) to pro-
wide elastic straps to prevent friction or binding, and all tect a healing contusion. Some athletic trainers suggest that
metal should be covered. There should be no seams in basketball players, especially those who frequently drive the
the cup area. Sports bras should be constructed of a firm, lane, wear thigh pads in practice. Stromgren has produced
compressive material and should allow for absorption of a girdle with thigh pads sewn in place; these are easily used
perspiration. with the equipment of any other sport.
A B
Figure 20-26
Rib protectors. A, “Flack jacket.” B, Body suit worn under the pants and shoulder pads to give protection
to the ribs and flanks.
A B
Figure 20-27
Examples of chest protectors. A, Chest protector for baseball catcher. B, Chest protector for lacrosse goalies.
A B
Figure 20-28
Examples of hip pads. A, Various types and sizes of hip pads for football. B, Girdle with pockets to hold
hip and thigh pads can be used in many sports such as basketball to protect an injury.
504 SECTION III • Management of Sports Injury and Illness
Clinical Note
The decision to wear braces should be made on an individual basis,
and lateral knee stabilizers should be available if they make the
athlete feel more confident.
A B
C
Figure 20-31
Examples of functional knee braces. A, CTi2 brace. B, Don Joy Defiance four-point brace. C, Lennox
Hill precision-fit brace.
nonweightbearing and weightbearing activity.37 However, do not wear a derotation brace after ACL reconstruction
during the transition from nonweightbearing to weight- are 2.74 times more likely to suffer a recurrent tear than
bearing, or during high-impact loading, bracing has not skiers who are braced. This positive effect of bracing recon-
been shown to stop anterior tibial translation.38 structed knees has not yet been shown to translate into
When dealing with the reconstructed knee, it is the au- other high-velocity or high-impact sports.
thors’ opinion that physicians seem to be prescribing braces Functional knee braces can be used during rehabilita-
to patients less often than in the past. Surveys given to phy- tion to give an athlete added security and stability with
sicians regarding whether to brace or not are varied. This early activity. It should be reiterated to the athlete that
suggests that there is a lack of consistency and scientific the brace can help control stability, but it does not replace
basis for bracing of the ACL-deficient or reconstructed strengthening of the limb, and the brace cannot prevent
knee.39 This being said, it has been shown that skiers who all injury.
506 SECTION III • Management of Sports Injury and Illness
A B
C D
Figure 20-33
Neoprene braces. A, Neoprene knee sleeve. B, Knee sleeve with opening at the patella. C, Knee sleeve
with patella stabilizers and felt buttresses sewed inside. D, Neoprene elbow sleeve with extra padding at
the olecranon.
508 SECTION III • Management of Sports Injury and Illness
Footwear
Appropriate footwear is one of the most important and
often intimidating pieces of athletic equipment. There are
numerous shoe manufacturers producing hundreds of mod-
els. The principal concern for sports medicine clinicians is
the possibility of an injury resulting from an improper selec-
tion. The shoes should be comfortable, prevent injury, and
Figure 20-34 not deter performance.
Shin guards. Baseball catcher’s shin guard (also incorporates a knee It is not necessary to have a sport-specific shoe for all
guard) (left); soccer or field hockey shin guard (right). activities. Individuals may benefit from wearing shoes spe-
cific to their activities if they perform their sports more than
three times a week.51 Sport-specific shoes attempt to pro-
hard, deflective outer layer and an inner layer of thin foam. vide extra protection for stresses particular to that activity or
Other shin guards are constructed with plastic stays sewn into to accommodate conditions unique to the surface on which
a felt material. This design gives the athlete a more comfort- the sport is played (Figure 20-36). Running shoes generally
able fit, because it conforms easily to the leg. Hook-and-loop have extra flexibility in the forefoot region to accommodate
straps and stirrups help stabilize the device inside the sock. the necessity for toe-off. Walking shoes have a more rigid
Shin guards can also incorporate padding or plastic shells over forefoot to prevent the bending stress placed through the
the ankle malleoli, which is also a site for contusions. forefoot and toes. Court shoes such as those for tennis,
racquetball, and basketball provide extra lateral support to
protect the ankle from excess side-to-side motion. Cross-
Ankle Support trainer shoes attempt to combine flexibility and lateral sta-
Ankle stabilizers, both rehabilitative and functional, are bility, but are not advisable for extensive running. Cleats are
extremely popular in athletics. There are many different produced for various field sports and are designed for
types of braces on the market and is usually chosen through different surfaces and field conditions, including artificial
personal preference (Figure 20-35). turf, natural grass, and wet conditions.
The effectiveness of ankle bracing is in question. Studies There are numerous manufacturers of football shoes that
have shown that taping and bracing of ankles has no effect have similar features. The shoe may be a low-top (come up
on ankle instability.45 Still other studies have shown that to the ankle) or a high-top (cover the ankle) with different
bracing can be effective in preventing ankle sprains.43,44,46,47 soles, depending on the type of playing surface. Low-top
Several laboratory studies have found that ankle bracing can shoes are typically used on the running-intensive positions
reduce the forces inflicted on the ankle during sudden (e.g., running backs, defensive backs, or quarterbacks). The
inversion and axial loading.46,47 These studies also find that use of low-top shoes is often discouraged because of the loss
Protective Equipment in Sports • CHAPTER 20 509
A B
E
Figure 20-35
Types of ankle braces. A, Air cast. B, Lace-up figure-8. C, Hinge type. D, Pro ankle brace. E, Rocketsoc
by Don Joy.
510 SECTION III • Management of Sports Injury and Illness
B C
Figure 20-36
Various types of shoes. A, left to right, Basketball shoes, low-top court shoes, metal cleats for baseball,
running shoes, flat soccer shoes, molded rubber cleats on soccer shoes. B, Dry-weather football shoes:
flat and “turf.” C, Football shoes for grass: seven screw-in studs for optimal traction (top); molded cleats
on outer sole (bottom).
of additional ankle support that high-top shoes provide. traction. Football players, especially linemen, wear this
The use of athletic tape over the shoe (i.e., spatting) to type of shoe on dry, artificial surfaces. Multi-cleated
provide additional support is discouraged because of the soles have 150 molded cleats (“turf shoes”) used for
difficulty in accessing the foot or ankle should an injury dry-weather activity. Molded cleats have a molded sole
occur. The types of soles available for different playing with cone-shaped cleats of varying heights for
surfaces include: increased traction in wet weather.
1. Artificial surfaces (see Figure 20-36, B). A basketball 2. Grass (see Figure 20-36, C). Seven-studded soles have
sole is a flat-bottom sole with small grooves to enhance seven removable, or “screw-in,” cleats on the bottom
Protective Equipment in Sports • CHAPTER 20 511
36. Colville MR, Lee CL, Ciullo JV: The Lenox Hill brace. An 44. Garrick JG, Requa RK: Prophylactic knee bracing, Am J Sports
evaluation of effectiveness in treating knee instability, Am J Sports Med 16(S1):118–123, 1988.
Med 14(4):257–261, 1986. 45. Tyler TF: Risk factors for noncontact ankle sprains in high school
37. Beynnon BD, Good L, Risberg MA: The effect of bracing on athletes: The role of hip strength and balance ability, Am J Sports
proprioception of knees with anterior cruciate ligament injury, Med 34(3):470–475, 2006.
J Orthop Sports Phys Ther 32(1):11–15, 2002. 46. Tohyama H: Stabilizing effects of ankle bracing under a combi-
38. Millet CW, Drez DJ: Principles of bracing for the anterior cruci- nation of inversion and axial compression loading, Knee Surg
ate ligament-deficient knee, Clin Sports Med 7(4):827–833, Sports Traumatol Arthrosc 14(4):373–378, 2006.
1988. 47. Cordova ML: Prophylactic ankle bracing reduces rearfoot
39. Decoster LC, Vailas JC: Functional anterior cruciate ligament motion during sudden inversion, Scand J Med Sci Sports 17(3):
bracing: A survey of current brace prescription patterns, Orthopedics 216–222, 2007.
26(7):701–706, 2003. 48. Gross MT, Liu HY: The role of ankle bracing for prevention of ankle
40. Sitler M, Ryan J, Hopkinson W, et al: The efficacy of a prophy- sprain injuries, J Orthop Sports Phys Ther 33(10):572–577, 2003.
lactic knee brace to reduce knee injuries in football. A prospec- 49. Pedowitz DI, Reddy S, Parekh SG, et al: Prophylactic bracing
tive, randomized study at West Point, Am J Sports Med decreases ankle injuries in collegiate female volleyball players,
18(3):310–315, 1990. Am J Sports Med 36(2):324–327, 2008.
41. Albright JP, Powell JW, Smith W, et al: Medial collateral ligament 50. Mickel TJ, Bottoni CR, Tsuji G, et al: Prophylactic bracing versus
knee sprains in college football. Effectiveness of preventive taping for the prevention of ankle sprains in high school athletes:
braces, Am J Sports Med 22(1):12–18, 1994. a prospective, randomized trial, J Foot Ankle Surg 45(6):
42. Najibi S, Albright JP: The use of knee braces, part 1: Prophylactic 360–365, 2006.
knee braces in contact sports, Am J Sports Med 33(4):602–611, 51. Gessel LM, Fields SK, Collins CL, et al: Concussions among
2005. United States high school and collegiate athletes, J Athl Train
43. Pietrosimone BG, Grogaard JB, Grindstaff TL, et al: A systematic 42(4):495–503, 2007.
review of prophylactic braces in the prevention of knee ligament 52. Adams J, Alder CM, Jarvis K, et al: Evidence of anterior temporal
injuries in collegiate football player, J Athl Train 43(4):409–415, atrophy in college-level soccer players, Clin J Sport Med
2008. 17(4):304–306, 2007.
21
CHAPTER
515
516 SECTION III • Management of Sports Injury and Illness
Table 21-1
Effect Size Comparing Interventions (Taping to No Taping)
Effect Sizes Inversion Eversion Dorsiflexion Plantar Flexion
Data from Cordova ML, Ingersoll CD, LeBlanc MJ: Influence of ankle support on joint range of motion before and after exercise:
A meta-analysis, J Orthop Sports Phys Ther 30(4):170-182, 2000.
sizes indicated a detriment in performance. Ankle taping had Ankle Bracing Compared with Ankle Taping
an effect size of 0.14 (90% confidence interval [CI] Martin and Harter7 used a treadmill tilted 8.5° to simulate
0.36–0.08) for sprint speed, 0.01 (90% CI 0.24–0.21) the inversion stress to the right ankle of 10 subjects. Active
for agility, and 0.14 (90% CI of 0.37–0.09) for vertical ROM was measured on all subjects prior to testing, followed
jump. The authors noted that effect sizes of 0.2 or greater by application of taping or bracing intervention. The bracing
were trivial and were equivalent to a 1% change in perfor- interventions used were the Swede-O Universal lace-up an-
mance for the three functional tasks. Taping in most cases kle brace and the Aircast sport stirrup orthosis (Figure 21-1
therefore has a small influence on increasing performance, and Figure 21-2). The preactivity ROM was then taken
and more likely inhibits it. before subjects walked and ran on the slanted treadmill
One of the earliest and most often referenced studies with video observation. Subjects performed 20 minutes of
regarding ankle taping was performed by Myburgh and exercise with movements simulating those of athletic com-
colleagues.6 Tape was used as a mechanical restraint to pas- petition. Postexercise motion was measured along with a
sive ROM measured before and after play in two squash final walk or run on the treadmill that was again videotaped
matches. Measurements were taken of 11 players before for analysis. Differences were found in walking and running
play began and at specific intervals during and after the two average inversion restraint provided the taping and bracing
matches. Ankle ROM was measured using a digital goniom- interventions. When walking on the treadmill, the sport
eter. Tape provided significant restrictions in ROM values stirrup provided the most restriction both before and after
before exercise and continuing until up to 10 minutes into exercise to inversion motion. While running on the tread-
match play. The authors noted that the ROM restrictions mill, the Swede-O lace-up brace and sport stirrup provided
prior to competition ranged between 30% and 50%. Restric- the most restriction to inversion motion. Taping was not
tion provided by the tape fell beyond 10 minutes of match as effective in limiting inversion active ROM as the two
play. It was also determined that nonelastic tape provided bracing interventions. The authors compared overall effec-
the most restriction among all types of ankle prophylaxis tiveness of the three interventions by averaging the restric-
tested at each time interval. tive properties of the interventions. Although the Swede-O
Garrick and Requa3 assessed the effects of ankle taping lace-up brace and Aircast sport stirrup had identical
and shoe (high top versus low top) on more than 2500 rankings, the authors noted that they believed the sport
intramural basketball players during the course of 2 years. stirrup provided the most restriction to motion. Taping
Results concluded that ankle taping is an effective inter- was found to be the least effective method of limiting
vention in the prevention of ankle injury and ankle inversion ROM.
reinjury. Players wearing high-topped basketball shoes Measurements were taken before and after activity in a
along with ankle taping had an ankle injury and sprain study by Paris and colleagues8 that evaluated 30 male subjects
incidence of 6.5 per 1000 player-games. When compared without a history of ankle instability. The subjects were
to the high topped shoe without taping, an increase of evaluated under three support conditions: the Swede-O lace-
almost five times was found at 30.4/1000 games. Low up ankle brace, the SubTalar Support brace, and taping.8
top shoes with ankle taping also found similar results in Preactivity measurements were taken without support inter-
17.6/1000 games versus 33.4/1000 games for the no ventions for all subjects. When compared with the control
tape condition. An interaction was noted between those group, preactivity values were significantly restricted for all
with a previous history of ankle sprain and a decreased four ankle motions (inversion, eversion, plantar, and dorsi-
rate of re-injury. In addition to using athletic tape, elastic flexion) under all conditions. Measurements were taken at
tape was found to have a positive effect on stability giving 15-minute intervals with the subjects repeating the exercise
an injury rate of 6.9/1000 player-games. The authors activity between measurements. After 15 minutes of activity,
also concluded that, given the rates of ankle injury among all three interventions had lost some effectiveness preventing
this group of athletes, ankle taping was effective in reduc- inversion. The SubTalar Support brace showed additional
ing the number of injuries. loosening between 15 and 30 minutes of activity. Eversion
Taping for Athletics and Rehabilitation • CHAPTER 21 517
Figure 21-1
Lace-up ankle braces comparable to the Swede-O ankle brace. (From Saliba E, Foreman S, Abadie RT:
Protective equipment considerations. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic inju-
ries and rehabilitation, p 928, Philadelphia, 1996, WB Saunders Company. Courtesy PRO Orthopedic
Devices Inc., Tucson, AZ.)
motion restriction was lost in the taping intervention after as well as for inversion and eversion ranges separately. The
15 minutes, whereas the Swede-O brace took 60 minutes to limitations provided by the Aircast brace were more signifi-
lose its effectiveness. The SubTalar brace did not lose its cant than those provided by the tape. Although the limita-
effectiveness at limiting this motion. Plantar flexion–limiting tions of ranges were significant, there was a significant loss
capabilities for the SubTalar brace and taping interventions of restriction for the taping intervention between the
were lost after the first 15 minutes of activity, and taping second and third bouts of exercise for total ROM. The
continued to lose effectiveness at 30, 45, and 60 minutes of same loss of restriction was not noted in the bracing
exercise. The Swede-O brace showed a significant increase in intervention.
plantar flexion at 30 minutes. Taping was the only condition Gross and colleagues assessed taping along with the
to lose dorsiflexion ROM limitations, which happened at Aircast sport stirrup and the Swede-O ankle brace on
45 minutes of activity. The authors concluded that the the ability to restrict eversion and inversion motions at the
Swede-O ankle brace and SubTalar brace were equally effec- ankle.10 In a design similar to the study by Gross and col-
tive at limiting plantar-flexion ROM. The Swede-O ankle leagues,9 measurements were taken for 16 subjects before
brace was seen to be more effective than taping and the application of tape, after application, and again after run-
SubTalar brace in limiting inversion ROM. ning on a figure-8 course for 10 minutes and performing
Passive inversion and eversion ROM was measured in a 20 unilateral toe raises. Each subject was positioned on a
study by Gross and colleagues9 using the Cybex II iso- Biodex dynamometer system to assess passive ROM. Each
kinetic dynamometer. Eleven subjects were tested before of the three conditions were effective in limiting eversion
ankle taping or bracing, after application of tape or a brace, range after application, each showed significant loss of
and following exercise with taping or bracing intervention. effectiveness at limiting eversion with exercise, and each was
A conventional form of taping was compared with the determined to provide significant restriction after exercise
Aircast air stirrup. Exercise consisted of 10 minutes running when compared with preapplication eversion range. The
a figure-8 course and 20 toe raises. Analysis revealed sig- taping and Swede-O brace interventions provided equal
nificant restrictions in ROM after tape and brace application restriction in preactivity eversion motion, whereas the
when compared with control measurements. After exercise, Aircast stirrup provided the most restriction. Inversion
the taping and bracing interventions still provided signifi- limitations were similar to eversion limits in that all three
cant restrictions in the total range of inversion and eversion, conditions provided for significant restriction following
518 SECTION III • Management of Sports Injury and Illness
Clinical Point
Ankle taping can reduce the number of ankle injuries but its effec-
tiveness decreases with activity.
activity for eversion and inversion ROM. The self- had a significantly shortened peroneal muscle reaction
adherent tape also restricted ROM after application for time when compared with those without tape. This short-
the same motions, and its restrictions of ROM lasted ened reaction time was not present in all subjects, how-
through the exercise bout. Both the white tape and self- ever; it appeared the ankles with the more stability did not
adherent tape provided significantly restricted motion show a significant difference in reaction time, whereas
after application and exercise for dorsiflexion and plantar ankles with more instability had lengthened reaction times.
flexion motions. There were significant differences found In addition to these findings, the authors also noted that
between the two taping materials. The self-adherent tape taped ankles reduced the reaction time, although this was
provided more restriction for longer periods than did the not noted in all cases, with the most significant reductions
white tape. The white tape lost 99% of its effectiveness for coming from the more unstable ankles.
inversion and eversion restriction after exercise, whereas
the self-adherent tape lost only 50%. Plantar flexion and Dynamic Testing
dorsiflexion ranges for both taping materials maintained Ankle taping along with the Swede-O ankle brace and the
65% of its pre-exercise ROM restriction. Kallassy brace were examined for their effects on four
The effect of ankle taping on mechanical stability and the dynamic events. Burkes and colleagues15 tested 30 sub-
influences on neuromuscular control of the ankle were jects twice on each of four events—vertical jump height,
studied by Alt and colleagues.14 Two taping methods were broad jump, 10-yard shuttle run, and 40-yard sprint—
tested using two different taping materials: Leukotape and without an ankle support and with the three support
Porotape. Twelve individuals without a history of ankle in- conditions. The results revealed that taping significantly
jury took part in five trials (control, standard or long-taping decreased performance values on all but one of the events.
method with the two materials, and short-taping method Vertical jump, shuttle run, and sprint performance were
with the two materials). Each trial was assessed for ankle all decreased by 4%, 1.6%, and 3.5%, respectively. The
inversion ROM, velocity of inversion, and the EMG activity Swede-O ankle brace showed similar trends that decreased
of selected muscles (anterior tibialis, peroneus longus, and performance of the vertical jump, broad jump, and sprint
medial head of gastrocnemius) before and after an exercise by 4.6%, 3.6%, and 3.2%, respectively. The Kallassy brace
bout. The exercise bout included injury simulations on a tilt reinforced the findings of the other conditions of the ver-
platform, jumping from height, and jumping on oblique tical jump, decreasing performance by 3.4%. In the shuttle
surfaces. Results for the mechanical stability of ankle taping run, the taping condition significantly impaired perfor-
revealed 42% and 41% decreases in inversion for the long- mance when compared with the Kallassy brace. A similar
taping techniques and 27% and 30% decreases for the short result was found for the broad jump when comparing the
methods before exercise, respectively, for both taping mate- Swede-O brace with the Kallassy brace, which signifi-
rials. After exercise, 38% and 37% decreases in inversion cantly limited distance. In addition, it must be noted that
were found with the long methods and 16% and 22% for the the application of any taping or bracing intervention
short methods. The only statistically significant difference decreased performance, although not all of the results
was found to be the short-taping method using Porotape were significant. The effectiveness of mechanical stability
when comparing scores before and after exercise. An overall provided by the tape and other braces was not evaluated
decrease of 35% inversion was found prior to exercise. As in this study; only the effect on performance was evalu-
reported in many studies, the loosening effect was also ated. Subjective assessments of the three conditions found
found in this study; however, it was not statistically signifi- that athletes felt most supported by tape, with the two
cant for Leukotape. Porotape did have a statistically signifi- braces lower but approximately equal. The Swede-O was
cant loss of ROM when applied in the short method. EMG found to be the least comfortable, with taping and
activity demonstrated no significant difference between tap- Kallassy braces equal in comfort.
ing method and material used. Overall, the taping interven- Future research on the effect taping has on ankle stability
tions decreased EMG activity approximately 18% across all should focus on measurements of ankle movements during
conditions prior to exercise. This reduction in activity was dynamic activities. The category of research may be more
also noted after exercise. helpful in determining the actual dynamic ranges of motion
As described earlier, Karlsson and Andreasson11 also involved with competitive movements in athletic competi-
examined the effect of taping on peroneal muscle reaction tion. Meana and colleagues16 examined the effect of taping
times. Twenty subjects, all of whom had a unilateral on restricting static and dynamic movements of the ankle
chronic lateral ankle injury, were tested with and without both before and after a 30-minute exercise bout on an agil-
a taping intervention, while the activity of the peroneus ity course. The course performed by the athletes required
longus and brevis were monitored. Testing was done on changes of direction, moving from a straight run to a defen-
an inversion platform that would simulate an inversion sive slide. These movements were chosen to mimic the
ankle sprain. Both ankles were tested (both stable and motions seen at the ankle during competitive sports compe-
unstable ankles) with and without tape. Unstable ankles tition. The researchers focused on two movements at the
520 SECTION III • Management of Sports Injury and Illness
ankle complex: supination and plantar flexion static ROMs. provide for increased effectiveness of the dynamic stabiliz-
Measurements were taken before applying tape, after apply- ers by increasing the amount of time available to react to
ing tape, before the agility course, and after the course had an inversion ankle sprain mechanism.
been run. High-speed cameras measured the dynamic
motions at a particular point in the exercise course. Static
ROM values for supination and plantar flexion were found
Clinical Point
to be restricted by 64.5% and 49.6% respectively. For dy- Taping may enhance the effectiveness of the dynamic stabilizers of
namic ROM values during the course, the effectiveness of the ankle.
the restriction was only significant for supination (13.5%)
during the braking phase. For all four ankle motions (plan-
tar flexion, dorsiflexion, supination, and pronation), there
was significant loss in the effectiveness of the tape. Supina- Ankle Taping and Placebo
tion and plantar flexion revealed 49.3% and 47.6% respec- The placebo effect of taping has recently been investigated
tively for static measurements, whereas the effectiveness by Sawkins and colleagues18 who tested 30 participants with
during dynamic movements were not significant for either a history of ankle injury. The subjects were tested under
movement. three conditions: true taping, placebo taping, and control
The effects of taping on inversion ROM was tested taping (no taping). The subjects were to perform two func-
dynamically by Ricard and colleagues.17 Dynamic inver- tional tests (hopping and modified star-excursion balance
sion was measured in three different groups before and test) in a random order, each being tested under all three
after exercise. Groups included taping (Figure 21-3) over tape applications, along with a practice trial that included
prewrap, taping to skin, and control (no taping). Four no taping intervention. Subjects were blinded to their
variables were measured using an electric goniometer and placement during and after tape application by a skirt that
an inversion trapdoor that simulated the effects of a was to cover the applied tape during functional testing. No
dynamic inversion ankle sprain mechanism. The four vari- significant difference in performance in either the hopping
ables included total inversion, time to maximal inversion, test or the modified star-excursion balance test for the three
average inversion velocity, and maximum inversion veloc- taping applications occurred. A secondary analysis of per-
ity. The analysis revealed no significant difference between ceptions held by the participants was completed to measure
taping-over-prewrap and taping-to-skin interventions. the stability, confidence, and reassurance of each taping
However, additional analysis revealed that the two taping application: 97% of those with the true taping felt more
interventions did provide significant differences on all four stability on the hopping test and 80% found the same on the
variables. Again, as echoed by previous research, taping modified star-excursion balance test. Placebo taping also
did provide for restriction in inversion ROM before and showed increases in the three perception categories, with
after exercise. Also interesting to note was the decrease in 17% of participants communicating improvements. A side
maximal inversion velocity and increase in time to maximal note to this study was that there did not appear to be any
inversion. The authors support the notion that taping in- functional deficits noted by the taping interventions when
terventions, whether accompanied by prewrap or not, may comparing the performance of taping with control taping.
Figure 21-3
The Gibney basketweave taping mehtod, as an example. (From Kennedy R: Mosby’s sport therapy taping
guide, p 16, St Louis, 1995, Mosby.)
Taping for Athletics and Rehabilitation • CHAPTER 21 521
The Ankle and Proprioception Refshauge and colleagues22 studied the effects of taping
Robbins and colleagues19 examined the effect of ankle tap- interventions on 16 subjects with a history of recurrent an-
ing and exercise on ankle proprioception. With the use of kle sprains. An inelastic tape was compared with no tape in
sloped blocks ranging from 0° to 25° in 2.5° increments, the ability of the subjects to detect passive movements of the
the researchers tested the effect of taping before and after ankle into eversion and inversion. Three different speeds
exercise on the ability of 24 subjects to determine the slope were used to test for movement perceptions. The results
of the blocks they were standing on. Ankle taping improved demonstrated that not only did the taping not provide for
proprioceptive capabilities when the slope of the block was enhanced proprioception, it actually decreased perception
great than 10°. Measurements were taken as a percentage of significantly.
absolute mean estimate error. Subjects in the taped group
had an average increase in error of 7% after exercise, whereas Ankle and Postural Control
those without tape averaged 39%. The effect of modern The effect of ankle taping on postural control was examined
athletic footwear on position sense was also evaluated, and by Bennel and Goldie23 using 24 subjects and a force plat-
it was determined that this footwear significantly impaired form plate system. Ankle taping, along with lace-up braces
the ability to distinguish foot position. The authors made and elastic bandages, were investigated for their influence
strong claims about the role of footwear in ankle injuries, on postural control. Each subject was tested under each
stating, “The inescapable conclusion is that footwear use is condition, along with the control. Subjects stood on the
ultimately responsible for ankle injury.”19 Citing statistics force platform with eyes closed and hands on hips. Mea-
from earlier work,20 the authors compared shoe wearing surements were taken for 5 seconds and data was analyzed
with barefoot position sense and taping. for mediolateral ground reaction forces along with nonsup-
Refshauge and colleagues21 investigated the effects of porting limb touchdowns. Tape, when compared with the
ankle taping on proprioceptive capabilities in subjects with control condition, was found to significantly inhibit pos-
recurrent ankle sprains and found no difference between tural control. The number of nonstance limb touchdowns
control and ankle-taping groups when examining motions was greatest for the ankle taping and bracing conditions,
of dorsiflexion and plantar flexion. They tested 43 subjects with taping having the most. It should be noted that the
at velocities of 0.1°, 0.5°, and 2.5° per second, none of subjects in this study did not actively exercise between the
which found a significant difference for the taped and application of the taping or bracing and the testing proce-
untaped groups. There was no proprioceptive benefit dures. This was done to rule out any variations that might
to taping in the sagittal plane of movement at the ankle be caused by loosening of the tape and braces, therefore
(Table 21-2). There was, however, an interaction between reducing their effect on the postural control.
increasing speeds of movement for taped and untaped In a similar study24 on the effect of ankle taping on
ankles. Expanding on this idea may show that increased postural steadiness, which was performed using a force
cutaneous stimulation of ankle taping combined with faster platform and taping, subjects with eyes open experienced no
movement may provide increased proprioceptive input, differences between taped and untaped ankle conditions.
thereby improving ankle control and a resultant decrease in However, when tested with eyes closed, there was a significant
ankle injury. difference in that taping adversely affected postural control.
Conclusions were that during single-leg stance with eyes
open, the visual inputs may have been able to counteract the
decreased postural awareness found with the taping. A synop-
Table 21-2 sis of all ankle studies can be seen in Table 21-3.
Proprioception and Movement Perception
Inversion Eversion The Foot
0.1 deg/sec Franettovich and colleagues25 studied five subjects on the
Untaped 4.71 0.78 4.92 0.80 effect of low-dye taping (Figure 21-4) on arch height and
Taped 5.18 0.67 5.09 0.55 muscle activity. The subjects were selected for the study
0.5 deg/sec because of the low medial longitudinal arch height with
Untaped 3.40 1.05 3.49 1.15 the stance phase of walking. The examiners took baseline
Taped 4.02 0.86 4.04 0.89 measurements of arch height in standing and EMG read-
2.5 deg/sec ings of the tibialis anterior, tibialis posterior, and pero-
Untaped 1.49 0.62 1.42 0.71
neus longus muscles while walking at the selected testing
Taped 1.65 0.81 1.42 0.76
speed on a treadmill for 10 minutes. The low-dye taping
Data from Refshauge KM, Kilbreath SL, Raymond J: The effect of
intervention was then applied and arch height was reas-
recurrent ankle inversion sprain and taping on proprioception at the sessed along with the muscle activity of the participants
ankle, Med Sci Sports Exerc 32:10-15, 2000. as they walked again on the treadmill for an additional
522 SECTION III • Management of Sports Injury and Illness
Table 21-3
Ankle Taping Article Synopsis
Article Population Description Results
Alt et al.14 12 subjects Two taping techniques/ Decreased EMG activity and loosening of tape
materials
Bennell and 24 subjects Postural control with tape Taping inhibited postural control
Goldie23
Burkes et al.15 30 subjects Functional performance Taping decreased functional performance
Cordova et al.4 Meta-analysis 19 studies Taping effective to limit ROM before and after exercise
Cordova et al.5 Meta-analysis 17 studies Taping most likely decreases physical performance
Garrick and 2500 basketball Taping and shoe height High-top shoes and taping provided best protection
Requa3 players against sprain
Gross et al.9 11 subjects Pre- and Tape had significant ROM restriction losses while
postmeasurements maintaining significant overall ROM restrictions
Gross et al.10 16 subjects Pre- and Total ROM restrictions significant
postmeasurements
Karlsson and 20 subjects EMG activity and taping Taping decreased reaction time of peroneals
Andreasson11
Martin and 10 subjects Running and walking with Taping provided inversion restraint that faded after
Harter7 inversion stress and tape exercise
Meana et al.16 15 athletes Static and dynamic ROM Taping decreased ROM values with loosening after exercise
Myburgh et al.6 11 squash players Pre- and Significant restriction before exercise until 10 minutes
postmeasurements into exercise
Paris et al.8 30 males Pre- and Tape had significant ROM restriction loss
postmeasurements
Refshauge et al.22 43 chronic ankle Proprioception with tape No benefit provided with tape
sprain subjects
Ricard et al.17 30 subjects Taping to skin No significant difference in inversion restriction
vs. prewrap
Robbins et al.19 24 subjects Proprioception with tape Enhanced proprioception with taping when inversion
slopes 20°
Sawkins et al.18 30 subjects Placebo taping More stability with real taping
Wilkerson12 30 football Two taping methods Modified method provided increased restrictions
players
EMG, Electromyography.
Figure 21-4
Medial longitudinal arch taping. (From Kennedy R: Mosby’s sport therapy taping guide, p 45, St Louis,
1995, Mosby.)
Taping for Athletics and Rehabilitation • CHAPTER 21 523
10 minutes. Analysis revealed that the arch taping in- vention to the wrist or fingers. Testing occurred in vary-
creased arch height by an average of 8 mm or 12.9% after ing combinations of dominant and nondominant hands,
tape application. Walking for 10 minutes reduced the along with wrist or finger taping. The dominant hand
average arch height to 5 mm or 8.5%. The taping inter- with fingers taped had strength differences that were not
vention significantly reduced the activity of the tibialis significant, as did the nondominant hand with and with-
anterior and tibialis posterior in both peak and average out tape. There was a significant finding in that the
activity. There was also an earlier onset of tibialis anterior untaped dominant hand was stronger that the dominant
activity with taping. There were no significant findings for hand with finger and wrist taping.
the peroneus longus muscle. The authors were not able to
identify the reason or relationship of the increased arch
height with taping and the decrease in EMG activity, only The Finger
that the changes were induced by the taping. Warme and Brooks29 studied the effect of taping on ten-
A study26 to examine the effects of four interventions don pulley failure. Nine pairs of freshly frozen cadaver
of subjective reports of pain and activity limitation in- hands were used in combination with a jig simulating the
cluded 42 individuals with a history of plantar fasciitis– “crimp grip” used in the sport of rock climbing. The A2
type foot pain. The four interventions included a control pulley (part of the flexor tendon sheath meant to anchor
group who received no intervention, a stretching group the flexor tendons of the fingers to the proximal phalanx
receiving triceps surae stretching, calcaneal taping to pull of each digit) of selected fingers was reinforced with three
the foot into inversion, and sham taping. The subjects wraps of cloth adhesive tape. Of the successful tests, the
received their interventions twice over the course of results revealed that the fingers reinforced with tape pro-
1 week. Significant differences were found for all groups vided no deterrence to the pulley failure, and did not
except for the control group in pre- and postintervention affect the order in which the other flexor pulleys failed.
reports of pain relief. Although there were significant Also, in 55% of the successful tests, the A2 pulley failed at
finding for reductions in pain for these three groups, the the same time as the A3 and A4 pulleys (A3 and A4 are
calcaneal taping proved to have significantly greater additional parts of the flexor tendon sheaths that are more
results in pain reduction. distal on the finger).
B C
Figure 21-5
Correction of posterior and lateral tilt of patella. A and B, To correct an inferior tilt, tape is placed on
the superior half of the patella. An anteroposterior force is exerted on the superior half of the patella to
lift the inferior pole away from the femur and infrapatellar fat pad. A and C, To correct a lateral tilt,
anteroposterior pressure is placed on the medial half of the patella to lift the lateral border away from
the femur. (From McConell J, Fulkerson J: The knee: Patellofemoral and soft tissue injuries.)
Taping for Athletics and Rehabilitation • CHAPTER 21 525
A B
Figure 21-6
Correction of patellar glide. A and B, Tape is placed just lateral to the lateral border of the patella and
is used to glide the patella medially on the femur. The thumb assists in gliding the patella medially, if
necessary, while the fingers pull the skin toward the patella, creating a “wrinkle.” Tape is anchored on
the posteromedial aspect of the medial femoral condyle. Tape is not brought into the popliteal fossa,
because this may irritate the skin in this area. (From McConnell J, Fulkerson J: The Knee: Patellofemo-
ral and soft tissues injuries.)
A B
Figure 21-7
Correction of patella lateral-external rotation. A and B, Tape is initially placed at the inferior patella
pole. The patella is grasped with the opposite hand and turned to decrease lateral-external rotation.
Tape is anchored as depicted. (From McConnell J, Fulkerson J: The Knee: Patellofemoral and soft
tissues injuries.)
outcome measures (visual analog scales, subjective forms, overload to the undersurface of the patella can be caused by
surface EMG, indwelling EMG, EMG of quadriceps mus- both intrinsic and extrinsic means. Intrinsic factors include a
cles, quadriceps muscle ratios) have all contributed to these patella alta or baja, deficiency of the lateral femoral condyle,
inconsistencies. and quadriceps muscle atrophy.36 Extrinsic factors include hip
retroversion or anteversion, hip muscle weakness, lateral tibial
torsion, or excessive pronation of the foot.36 It is purported
Altered Patellar Position that this strapping technique is critical for physical activity
McConnell first described her results of using a patellar taping to promote quadriceps strengthening.34 Several studies have
technique for the treatment of chondromalacia patella in attempted to assess patellar taping’s ability to actually cause
1986.34 The purpose of the taping technique was to correct patellar positional changes using various techniques including
abnormal patellar tracking to allow a patient to engage in radiographs, computed tomography (CT), and magnetic res-
pain-free exercise and physical therapy. Excessive mechanical onance imaging (MRI).
526 SECTION III • Management of Sports Injury and Illness
Subjects in this study did not demonstrate a change in VL ing mechanisms is still not available. This is in contrast to
EMG with the application of tape during either the stair the findings of Warden and colleagues,67 who used 13 in-
ascent or descent. vestigative trials to examine the effects of patellar taping or
bracing. Through a meta-analysis, the authors concluded
that on a 100-mm scale, tape applied to exert a medially
Proprioception directed force on the patella decreased chronic knee pain
Patellofemoral Joint compared with no tape by 16.1 mm (95% CI 22.2,
Callaghan and colleagues58 found that the application of 10.0; p 0.001). Coincidentally, sham taping applied to
patellar tape significantly improved the active and passive exert a medially directed force on the patella decreased
joint position sense in healthy subjects whose propriocep- chronic knee pain compared with no tape by 10.9 mm (95%
tive levels were graded as “poor,” whereas those with a CI 18.4, 3.4; p 0.001).
good proprioception grade saw no improvement in scores. Limitations of studies examining the effects of taping
This would lead one to believe that patellar taping may on patellofemoral pain appear to occur when evaluating
enhance proprioception in the patellofemoral joint. varying results. Variations in sample populations and
More recently, Callaghan and colleagues59 assessed the sample sizes reduce the ability to determine differences.
ability to increase joint position sense through patellar Most studies are underpowered and the ability to
taping in those with patellofemoral pain. The study tested detect statistical power is hampered. In addition, a lack of
32 subjects with a history of patellofemoral pain before and long-term follow up potentially limits generalizations of
after the introduction of patellar taping. Their study at first taping.68
glance did not seem to show an enhancement of joint posi- A synopsis of all patellar taping articles can be seen in
tion sense following patellar taping. But, when the authors Table 21-4.
placed the subjects into a proprioception status according
to their error, the “poor” proprioception cohort scores
were enhanced at all angles tested; however, when looking Patellofemoral Taping Clinical Prediction Rule
at absolute error, scores were enhanced only to a significant Lesher and colleagues69 described a clinical prediction rule
level at 20° of knee flexion. developed to determine which patients would respond
favorably to patellar taping. Their study involved 50 volun-
teers with patellofemoral pain who received treatment with
Decreased Patellar Pain a medial-glide taping technique. Of these patients, 26 had
An obvious reason for patellar taping is that of reducing immediate pain relief with patellar taping. Two of their
anterior knee pain. Despite conflicting evidence regarding examination items, (1) positive patellar tilt greater than 5°
various aspects of patellar taping, a large number of articles or (2) tibial varum greater than 5°, composed the clinical
have emphatically found that patellar taping reduces ante- prediction rule for success. Application of these two items
rior knee pain. Many authors have reported decreases in improved the probability of a successful outcome from 52%
pain following patellar taping48-50,53,55,60-65 and report that to 83%. This clinical prediction rule is useful in identifying
using both the medial glide and a placebo technique characteristics of patients with PFPS who may benefit from
reduced perceived patellofemoral pain by 70% to 80% in taping. This was not a randomized controlled clinical trial,
those with symptoms. however, so they were unable to determine if the patient’s
response was solely the result of the taping technique.
Although there appears to be consensus that taping
Clinical Point does relieve patellar pain in the short term, it is still pres-
In most patellofemoral pain syndrome patients, medial taping ently unknown how or why this occurs. There continues
decreases pain. to be inconsistencies regarding patellar taping and its
ability to alter patellar mechanics, vasti inhibition, vasti
muscle recruitment, and recruitment timing of vasti mus-
cles. Further study is warranted in these inconsistent areas
Systematic Reviews and Meta-Analysis of knowledge.
Recent reviews and meta-analysis have reported conflicting
findings regarding the use of tape for those with PFPS.
Aminaka and Gribble66 identified and reviewed 16 studies
Taping for the Shoulder
with an average Physiotherapy Evidence Database (PEDro) Although a multitude of studies exist for taping of the knee,
score of 4.25 out of 10 and determined that although patel- the scientific literature is limited in regard to tape for shoul-
lar taping appeared to reduce pain and improve function in der conditions. Shoulder taping may be useful for some of
patients with PFPS during activities of daily living and reha- the same reasons that knee taping is thought to benefit pa-
bilitation exercise, strong evidence to identify the underly- tient populations, such as stimulating greater proprioceptive
Taping for Athletics and Rehabilitation • CHAPTER 21 529
Table 21-4
Patellofemoral Taping Article Synopsis
Article Population Description Results
Pain
Bockrath et al.60 PFPS—12 subjects Assessment of congruence angle No change in congruence; 50% reduction
radiographically with isometric quad- in pain
riceps contraction; VAS pain during
step down (1) taped (2) untaped
Christou50 PFPS—15 women Pain, force production, and EMG of In PFPS, medial glide and placebo reduced
Normal—15 women VMO and VL—(1) taped medial pain; PFPS and tape did not alter leg
glide, (2) taped lateral glide, press force; PFPS increased VMO,
(3) placebo during leg press decreased VL; opposite in normal
Clark et al.61 PFPS—81 subjects Pain, patient satisfaction, quadriceps Taping was not associated with discharge;
strength, subjective scale scores all exercise groups showed decrease in
(1) exercise, tape, and education; pain
(2) exercise and education; (3) tape
and education; (4) education alone
Cowan et al.51 PFPS—10 subjects EMG of VMO and VL during stair PFPS with taping changed temporal char-
Normal—12 ascent and descent acteristics of VMO and VL; no increased
subjects EMG onset in asymptomatic patients.
Harrison et al.62 PFPS—113 subjects Pain via VAS; subjective scores; PFPS with taping (group 3) showed
step test (1) home exercise alone; significant improvement at 1 month.
(2) physical therapist monitored Groups 2 and 3 showed more
exercises program; (3) patellar improvement than group 1, but
taping, exercise, and biofeedback not at a significant level.
Herrington63 PFPS—14 subjects Pain via VAS; concentric and eccentric PFPS taping decreased pain and increased
quadriceps peak torque (1) taped, peak torque.
(2) un-taped
Kowall et al.64 PFPS—25 subjects Pain via VAS; EMG activity; isokinetic Both groups had decreased pain, taping
strength testing (1) standard physical was not significantly more than untaped
therapy, (2) standard physical therapy subjects; both groups had greater
plus patellar taping strength and EMG activity.
Ng and Cheng55 PFPS—15 subjects Pain and EMG VMO/VL ratio during Taping significantly decreased pain and
single-legged semisquat (1) tape, VMO/VL EMG ratio during single-
(2) untaped legged semisquat.
Powers et al.52 PFPS—15 women Stride characteristics and sagittal plane 78% pain reduction with tape; only
motion (1) taped; (2) untaped; free significant change was stride length
walking, fast walking, ascending and increased during ramp ascent.
descending ramp and stairs
Salsich et al.57 PFPS—10 subjects: PFPS kinematics, ground reaction 92.6% reduction in pain with taped
5 women, 5 men forces and EMG ascending and condition; improved cadence, knee
descending stairs (1) taped, flexion angles, and moments with tape;
(2) untaped no change in vastus EMG with tape.
Whittingham PFPS—30 subjects: VAS for pain; functional scores Improvements in pain and function for all
et al.65 24 men, 6 women (1) patellar taping and exercise, groups; tape and exercise demonstrate
(2) placebo tape and exercise, better pain function scores.
(3) exercise alone
Bennell et al.54 Normal—12 with Kinematics and EMG—stair stepping, Neither ther tape or control tape had an
history of PFPS normal gait, fast gait—(1) no tape, effect on EMG onset timing; ther tape
(2) control tape, (3) ther tape increased stance knee flexion angles; initial
ground reaction force decreased with tape.
Christou50 PFPS—15 women Pain, force production and EMG In PFPS medial glide and placebo reduced
Normal—15 women of VMO and VL—(1) taped pain; PFPS and tape did not alter leg
medial glide, (2) taped lateral glide, press force; PFPS increased VMO and
(3) placebo during leg press decreased VL; opposite in normal.
Continued
530 SECTION III • Management of Sports Injury and Illness
Table 21-4
Patellofemoral Taping Article Synopsis—cont’d
Article Population Description Results
Neuromuscular Control, Muscle Recruitment, and Knee Joint Kinematics
Cowan et al51 PFPS—10 EMG of VMO and VL during stair PFPS with taping changed temporal char-
Normal—12 ascent and descent acteristics of VMO and VL; no change in
EMG onset in asymptomatic.
Ernst et al.53 PFPS—14 women Lower extremity kinetics during Taping provided greater extensor moment
lateral step up and vertical jump— and power than no tape and placebo;
(1) taped, (2) untaped; (3) placebo vertical jump was greater in uninvolved
tape, (4) uninvolved knee than taped, placebo or no tape; no differ-
ence in vertical jump height with tape.
Herrington36 Normal—10 women Normals will see suboptimal firing Taping significantly decreased VMO and
with patellar taping; EMG and kine- VL EMG; taping significantly decreased
matics two conditions: (1) taping, peak stance knee flexion, knee flexion
(2) control angular velocity.
Ng and Cheng55 PFPS—15 subjects Pain and EMG VMO/VL ratio Taping significantly decreased pain and
during single-legged semisquat VMO/VL EMG ratio during single-
(1) tape, (2) untaped legged semisquat
Powers et al.52 PFPS—15 women Stride characteristics and sagittal plane 78% pain reduction with tape; only signifi-
motion (1) taped, (2) untaped; free cant change was increased stride length
walking, fast walking, ascending and during ramp ascent.
descending ramp and stairs
Ryan and Normal—25 Normal patients’ EMG during perfor- Lateral taping caused a small but signifi-
Rowe49 students mance of four single-leg squats with cant increase in VM/VL ratios versus
17 female, 8 male four taping conditions: (1) medial, medial, but not no tape; no difference in
(2) lateral, (3) neutral, (4) control medial taping.
Salsich et al.57 PFPS—10 subjects: PFPS kinematics, ground reaction 92.6% reduction in pain with taped
5 women; 5 men forces and EMG ascending and condition. Improved cadence, knee
descending stairs (1) taped, flexion angles, and moments with tape;
(2) untaped no change in VL EMG with tape.
Patellar Position
Gigante et al.42 PFPS—16 women PFPS CT: (1) taping; (2) control; Taping did not affect PF lateralization or
assess PF congruence angle; muscles tilt; findings do not support use of taping
relaxed, muscles contracted for passive correction of incongruence.
Herrington37 PFPS—8 subjects: PFPS MRI taken at 0°, 10°, 20° of Taping resulted in significant reduction of
5 women; 3 men knee flexion lateral patellar distance at all angles.
Larsen et al.45 20 asymptomatic Radiographs of modified Merchant Taping resulted in medial glide, but was
men view (1) pretape, (2) taped, (3) after ineffective after exercise.
exercise
Pfeiffer et al.40 18 asymptomatic MRI (1) taping, (2) no taping, Significant difference in lateral displace-
women (3) after exercise measured at 0°, ment at all angles (taped and untaped
12°, 24°, and 36° condition). Significant differences in tape
before and after exercise.
Somes et al.41 PFPS—9 subjects: Radiographs in open kinetic and closed Increased lateral PF angle with tape in
7 women; 2 men kinetic chains at 45° knee flexion: CKC; no change in PF congruence
(1) tape, (2) untapped conditions angle; pain reduced 45% with tape.
Worrell et al.44 PFPS—12 subjects PFPS MRI: (1) taping, (2) bracing, Taping and bracing significantly decrease
(3) control at eight different angles PF congruence at an angle of 10° only.
Joint Proprioception
Callaghan et al.59 PFPS—32 subjects Normal subjects performed active- No statistically significant differences
angle reproduction, passive-angle between taped or untaped conditions.
reproduction, and threshold to
detect passive movement
CKC, Closed kinetic chain; CT, computed tomography; EMG, electromyography; MRI, magnetic resonance imaging; PF, patellofemoral; PFPS,
patellofemoral pain syndrome; ther, therapeutic; VAS, visual analog scale; VL, vastus lateralis; VMO, vastus medialis oblique.
Taping for Athletics and Rehabilitation • CHAPTER 21 531
feedback, improving scapulohumeral rhythm, improving without tape. Scapular taping decreased upper trapezius and
joint position, and muscle length-tension relationships. increased lower trapezius activity in people with suspected
Ackerman and colleagues70 looked at upper trapezius shoulder impingement during an overhead reaching task.
EMG activity in professional violinists. This is one of the Taping also decreased upper trapezius activity during lifting
few shoulder taping studies that actually assessed EMG dur- into shoulder abduction in the scapular plane. The authors
ing a true functional activity, in this case playing the violin. speculate the load used may not have been enough to affect
The authors used a taping technique to move the scapula the other muscles assessed because their EMG activity was
away from excessive protraction in an effort to enhance not altered with the tape or no-tape procedures.
muscular length-tension relationships. In addition, the vio-
linist’s music quality was independently assessed between
taped and untaped conditions. Compared with the no-tape Joint Position Sense
condition, scapular taping actually increased upper trapezius Zanella and colleagues77 quantified the effects of scapular
muscle activity by 49%. The raters, who were blinded to taping on shoulder joint repositioning during motions of
performance and taping condition, rated the musical pieces shoulder flexion and abduction. Assessing 30 subjects
of the taped condition as of lower quality. It was believed with no pathological conditions of the shoulder, they
that the mechanical restriction to movement during the determined absolute error in joint reposition and scapular
taped condition and the violinist straining against this was position via lateral scapular slide testing using a plumb
the reason for the deterioration in musical performance line and winging. The authors found no difference for
quality. taped or untaped conditions in joint position sense or
Host71 described a case study of a 40-year-old male winging of the scapula.
patient with an 8-month history of anterior subacromial
impingement who was able to return to full overhead sports
activity following scapular taping. By using a scapular taping Stabilization After Stroke
technique, the patient was able to return to full activities, Hanger and colleauges78 performed shoulder strapping
including tennis and racquet ball, without symptoms after with patients who had experienced a stroke. It was hoped
approximately 10 physical therapy visits. that strapping in the hemiplegic shoulder would reduce
Morrissey has reported that taping under tension in the pain, preserve ROM, and improve functional outcomes. In
line of a muscle’s fiber direction facilitates muscle recruit- their study, Hanger and colleagues78 randomized shoulder
ment.72 This has since been disputed, at least for muscle strapping with standard physical therapy for 6 weeks com-
activity of the lower trapezius. Alexander and colleagues73 pared with standardized physical therapy alone. Interven-
were able to dispute that taping the lower portion of the tion with strapping showed no differences for pain, ROM,
trapezius would facilitate motor activity. In assessing the or functional outcome after the intervention phase. It
Hoffman reflex to determine motoneuron pool excitability, appeared that the presence of neglect or sensory loss, but
they found that using the application of cover tape inhibited not subluxation, at baseline was independently associated
the upper trapezius by 4%, and applying more pressure via with a poor outcome.
a top tape layer inhibited the muscle by 22%. In addition,
Cools and colleagues,74 following a taping procedure across
the muscle belly of the upper trapezius and parallel to the Posture
direction of the lower trapezius, were unable to find Lewis and colleagues79 objectively assessed postural changes
changes in EMG activity in any of the scapular muscles. and symptoms of those with subacromial impingement
In direct contrast to these studies, Morin and colleagues75 before and following scapular taping, and placebo scapular
found significant alterations in the upper trapezius and taping. Postural taping produced significant effects for all
middle trapezius with taping procedures. In their study, the postural measures, including measurements for forward
upper trapezius was taped across the belly and resulted in head, kyphosis, scapular displacements, and pain-free ROM.
muscle inhibition during an isometric contraction, whereas Visual analog pain scores for shoulder flexion and scapular
the middle and lower trapezius demonstrated an increase in plane abduction were not altered. These authors concluded
EMG activity. Morin and colleagues studied the proposed that changing one or more components of posture may
effect on normal patients without pathological conditions. have a positive effect on those with subacromial impinge-
They recommended future studies be performed to see if ment syndrome.
the same effects would occur for those with pathological Although there is limited evidence to support taping
conditions of the shoulder. More recently, Selkowitz and for posture and muscle recruitment in the shoulder, it
colleagues76 attempted to determine if upper trapezius EMG does appear that this form of treatment may be useful as
activity could be decreased with an upper trapezius inhibi- an adjunctive therapy. As such, several precautions are
tory taping technique. Surface EMG of the shoulder advised. The taping procedure used should not restrict
girdle muscles was assessed while lifting overhead with and the athlete’s ROM. When taped, the athlete should be
532 SECTION III • Management of Sports Injury and Illness
able to move the shoulder through motions that were sensory stimulation to assist or limit motion, and (5) assist
previously more painful. The amount of pain relief is in the removal of edema by directing exudates toward a
generally variable, with the best outcome occurring with lymph duct. None of these claims, however, have been
total or near-total relief of symptoms. It must also be shown to be true. KT differs from traditional white athletic
stressed that this is generally not an isolated technique tape in that it is elastic and can be stretched to 140% of its
used all by itself. This is most often an intervening modal- original length before being applied to the skin.82 In addi-
ity to allow athletes to perform their given activities. tion, KT is latex-free and the adhesive is 100% acrylic and
Once the athlete can perform normal activities, the taping heat-activated.81 Because the tape is 100% cotton, it can be
should slowly be diminished. worn in the pool or shower and has a single-application
At the present time, there continues to be ample wear time of approximately 3 to 4 days.83
evidence that a clear consensus cannot be met regarding Thelen and partners83 assessed the clinical efficacy of KT
recommendation of shoulder taping procedures. Differ- compared with sham KT when applied for 2 days to college-
ences in studies include surface versus indwelling EMG age students with shoulder pain and diagnosis of shoulder
recordings, injured versus uninjured populations, dominant impingement. The therapeutic KT group demonstrated
versus nondominant arm, isometric versus isotonic muscle immediate improvements in pain-free shoulder abduction,
contractions, and the use of various forms of tape and but were unable to show any differences between the sham
taping procedures. treatment KT with regard to ROM, pain, or disability
scores at any time interval.
Yoshida and Kahavov84 were able to find an increase in
Kinesio Tape trunk flexion ROM when compared with a group that was
Kinesio tape (KT) procedures and techniques have been not taped. They were not able to find any differences for
purported to improve a variety of physiological problems, trunk extension and lateral flexion motions when evaluating
including ROM and strength (Figure 21-9).80 Kase and taped versus untaped conditions.
colleagues81 proposed several benefits, depending on the Application of KT in an effort to increase reproduction
amount of stretch applied to the tape during application: of joint position sense of the ankle demonstrated no change
(1) provide positional stimulus through the skin, (2) align in constant or absolute error as compared with no taping in
fascial tissue, (3) create space by lifting fascia and soft tissue a healthy, uninjured population.82
above the area of pain and inflammation, (4) provide Finally, Fu and colleagues83 looked at the immediate and
delayed effects of KT on muscle strength in the quadriceps
and hamstrings when tape was applied to the anterior thigh
of healthy, young athletes. Their results revealed no signifi-
cant difference in muscle power via isokinetic testing com-
pared with no tape, immediately after taping, and 12 hours
after taping.
At the present time, the studies on the effects of KT
have been mostly empirically based rather than evidence-
based, and come from case series, case studies, and small
pilot studies. Unfortunately, these forms of evidence are at
the lower end of the evidence-based hierarchy. At the pres-
ent time, there is limited evidence regarding benefits for
the use of KT techniques in athletic or general populations.
Future studies are greatly needed to ultimately decide if
this form of taping has a place in sports and orthopedic
rehabilitation.
Conclusion
After a thorough review of the literature, one still wonders
about the effects of taping in efforts to prevent injury or
Figure 21-9 stabilize injured joints of the body. Conflicting or limited
Shoulder Kinesio tape procedure. This is the anterior view of the tape evidence seems to predominate. Clearly high level I and II
application used to assist a member of the 2000 U.S. Olympic Team
after she dislocated her shoulder on the floor exercise mat. (From
randomized controlled clinical trials should be undertaken
Andrews JR, Wilk KE, Reinold MM: The athlete’s shoulder, ed 2, to determine efficacy of these procedures. There appears to
Philadelphia, 2009, Churchill Livingstone.) be limited clinical evidence that ankle taping can be used to
Taping for Athletics and Rehabilitation • CHAPTER 21 533
limit abnormal motion for brief periods. It has been consis- 19. Robbins S, Waked E, Rappel R: Ankle taping improves proprio-
tently shown that patellar taping does provide a mechanism ception before and after exercise in young men, Br J Sports Med
29:242–247, 1995.
for pain relief in most studies, although it is still unclear 20. Gregory JE, Morgan DL, Proske U: Changes in size of the stretch
exactly what mediates this favorable response. Newer tech- reflex of can and man attributed to after effects in muscle spindles,
niques such as KT have yet to be scientifically proven J Neurophysiol 58:628–640, 1987.
effective. In this era of cost containment, clinicians should 21. Refshauge KM, Kilbreath SL, Raymond J: The effect of recurrent
critically look at the use of taping for athletic musculoskel- ankle inversion sprain and taping on proprioception at the ankle,
Med Sci Sports Exerc 32:10–15, 2000.
etal injury prevention and treatment approaches. 22. Refshauge KM, Raymond J, Kilbreath SL, et al: The effect of ankle
taping on detection of inversion-eversion movements in partici-
pants with recurrent ankle sprain, Am J Sports Med 37:371–375,
References 2009.
23. Bennell KL, Goldie PA: The differential effects of external ankle
1. Perrin DH: Athletic taping and bracing, ed 2, Champaign, IL, support on postural control, J Orthop Sports Phys Ther 20:287–295,
2005, Human Kinetics. 1994.
2. Prentice W: Modern principles of athletic training, St Louis, 1989, 24. Watson L, Bennel KL: The effect of ankle taping on postural
Mosby. steadiness, Proceedings of the 10th International Congress of the
3. Garrick JG, Requa RK: Role of external support in the prevention World Confederation for Physical Therapy, Sydney, Australia,
of ankle sprains, Med Sci Sports Exerc 5:200–203, 1973. 1987.
4. Cordova ML, Ingersoll CD, LeBlanc MJ: Influence of ankle sup- 25. Franettovich M, Chapman A, Vincenzino B: Tape that increases
port on joint range of motion before and after exercise: A meta- medial longitudinal arch height also reduces leg muscles activity:
analysis, J Orthop Sports Phys Ther 30(4):170–182, 2000. A preliminary study, Med Sci Sport Exerc 40:593–600, 2008.
5. Cordova ML, Scott D, Ingersoll CD, LeBlanc M: Effects of ankle 26. Hyland MR, Webber-Gaffney A, Cohen L, Lichtman PT: Ran-
support on lower-extremity functional performance: A meta- domized controlled trial of calcaneal taping, sham taping, and
analysis, Med Sci Sports Exerc 37:635–641, 2005. plantar fascia stretching for the short-term management of plantar
6. Myburgh KH, Vaughan CL, Isaacs SK: The effects of ankle guards heel pain, J Orthop Sports Phys Ther 36(6):364–371, 2006.
and taping on joint motion before, during, and after a squash 27. Vincenzino B, Brooksbank J, Minto J, et al: Initial effects of elbow
match, Am J Sports Med 12:441–446, 1984. taping on pain-free grip strength and pressure pain threshold,
7. Martin N, Harter RA: Comparison of inversion restraint provided J Orthop Sports Phys Ther 33:400–407, 2003.
by ankle prophylactic devices before and after exercise, J Athl 28. Rettig AC, Stube KS, Shelbourne DK: Effects of finger and wrist
Train 28:324–329, 1993. taping on grip strength, Am J Sports Med 25:96–98, 1997.
8. Paris DL, Kokkaliaris J, Vardaxis V: Ankle ranges of motion during 29. Warme WJ, Brooks D: The effect of circumferential taping on
extended activity periods while taped and braced, J Athl Train flexor tendon pulley failure in rock climbers, Am J Sports Med
30:223–228, 1995. 28:674–678, 2000.
9. Gross MT, Bradshaw MK, Ventry LC, Weller KH: Comparison of 30. Olmsted LC, Vela LI, Denegar CR, Hertel J: Prophylactic ankle
support provided by ankle taping and semirigid orthosis, J Orthop taping and bracing: A numbers-needed-to-treat and cost-benefit
Sports Phys Ther 9:33–39, 1987. analysis, J Athl Train 39:95–100, 2004.
10. Gross MT, Lapp AK, Davis M: Comparison of Swede-O-Universal 31. Sitler M, Ryan J, Wheeler B, et al: The efficacy of a semirigid ankle
ankle support and Aircast Sport-Stirrup orthoses and ankle tape in stabilizer to reduce acute ankle injuries in basketball: A random-
restricting eversion-inversion before and after exercise, J Orthop ized clinical study at West Point, Am J Sports Med 22:454–461,
Sports Phys Ther 13:11–19, 1991. 1994.
11. Karlsson J, Andreasson GO: The effect of external ankle support 32. Surve I, Schwellnus MP, Noakes T, Lombard C: A fivefold reduc-
in chronic lateral ankle joint instability. An electromyographic tion in the incidence of recurrent ankle sprains in soccer players
study, Am J Sports Med 20:257–261, 1992. using the Sport-Stirrup orthoses, Am J Sports Med 22:601–606,
12. Wilkerson GB: Comparative biomechanical effects of the standard 1994.
method of ankle taping and a taping method designed to enhance 33. Manske RC, Davies GJ: A nonsurgical approach to examination
subtalar stability, Am J Sports Med 19:588–595, 1991. and treatment of the patellofemoral joint, Part 1: Examination and
13. Purcell SB, Schuckman BE, Docherty CL, et al: Differences in treatment of the patellofemoral joint, Crit Rev Phys Rehabil Med
ankle range of motion before and after exercise in 2 tape condi- 15:141–166, 2003.
tions, Am J Sports Med 37:383–389, 2009. 34. McConnell J: The management of chondromalacia patellae:
14. Alt W, Loher H, Gollhofer A: Functional properties of adhesive A long-term solution, Aust J Physio 32:215–223, 1986.
ankle taping: Neuromuscular and mechanical effects before and 35. McConnell J, Fulkerson J:: The Knee: Patellofemoral and soft tissue
after exercise, Foot Ankle Int 20:238–245, 1999. injuries. In Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic
15. Burkes RT, Bean BG, Marcus R, Barker HB: Analysis of athletic Injuries and Rehabilitation, Philadelphia, 1996, WB Saunders.
performance with prophylactic ankle devices, Am J Sports Med 36. Herrington L: The effect of patellofemoral joint taping, Crit Rev
19:104–106, 1991. Phys Rehabil Med 12:271–276, 2000.
16. Meana M, Alegre LM, Elvira JL, Aguado X: Kinematics of ankle 37. Herrington L: The effect of corrective taping of the patella on
taping after a training session, Int J Sports Med 29:70–76, 2008. patella position as defined by MRI, Res Sports Med 14:215–223,
17. Ricard MD, Sherwood SM, Schulthies SS, Knight KL: Effects of 2006.
tape and exercise on dynamic ankle inversion, J Athl Train 35: 38. Dye S: The pathophysiology of patellofemoral pain, Clin Orthop
31–37, 2000. 436:100–110, 2005.
18. Sawkins K, Refshauge K, Kilbreath S, Raymond J: The placebo 39. Dye S, Staubli H, Biedert R, Vaupel G: The mosaic of patho-
effect of ankle taping in ankle instability, Med Sci Sports Exerc physiology causing patellofemoral pain: Therapeutic implications,
39:781–787, 2007. Op Tech Sports Med 7:46–54, 1999.
534 SECTION III • Management of Sports Injury and Illness
40. Pfeiffer RP, DeBeliso M, Shea KG, et al: Kinematic MRI assess- 59. Callaghan MJ, Selfe J, McHenry A, Oldham JA: Effects of patellar
ment of McConnell taping before and after exercise, Am J Sports taping on knee joint proprioception in patients with patellofemoral
Med 32:621–628, 2004. pain syndrome, Man Ther 13:192–199, 2008.
41. Somes S, Worrell TW, Corey B, Ingersol CD: Effects of patellar 60. Bockrath K, Wooden C, Worrell T, et al: Effects of patellar taping
taping on patellar position in the open and closed kinetic chain: a on patella position and perceived pain, Med Sci Sports Exerc
preliminary study, J Sport Rehabil 6:299–308, 1997. 25:989–992, 1993.
42. Gigante A, Pasquinelli F, Paladini P, et al: The effects of patella 61. Clark DI, Downing N, Mitchell J, et al: Physiotherapy for anterior
taping on patellofemoral incongruence, Am J Sports Med 29: knee pain: a randomized controlled trial, Ann Rheum Dis 59:
88–92, 2001. 700–704, 2000.
43. Worrell T, Ingersoll C, Farr J: Effects of patellar taping and brac- 62. Harrison EL, Sheppard MS, McQuarrie AM: A randomized con-
ing on patellar position: An MRI case study, J Sports Rehabil trolled trial of physical therapy treatment program in patellofemoral
3:146–153, 1994. pain syndrome, Physiother Canada 51:93–106, 1999.
44. Worrell T, Ingersoll C, Bockrath-Pugliese K, Minis P: Effect of 63. Herrington L: The effect of patellar taping on quadriceps peak
patellar taping and bracing on patellar position as determined by torque and perceived pain: A preliminary study, Phys Ther Sport
MRI in patients with patellofemoral pain, J Athl Train 33:16–20, 2:23–28, 2001.
1998. 64. Kowall MG, Kolk G, Nuber GW, et al: Patellar taping in the treat-
45. Larsen B, Andreasen E, Urfer A, et al: Patellar taping: A radio- ment of patellofemoral pain: A prospective randomized study, Am
graphic examination of the medial glide technique, Am J Sports J Sports Med 24:61–66, 1996.
Med 23:465–471, 1995. 65. Whittingham M, Palmer S, Macmillan R: Effect of taping on pain
46. Merchant AC, Mercer RL, Jacobsen RH, Cool CR: Roentgeno- and function in patellofemoral pain syndrome: A randomized con-
graphic analysis of patellofemoral congruence, J Bone Joint Surg trolled trail, J Orthop Sports Phys Ther 34:504–510, 2004.
Am 56:1391–1396, 1974. 66. Aminaka N, Gribble PA: A systematic review of the effects of
47. Manske RC, Davies GJ: A nonsurgical approach to examination therapeutic taping on patellofemoral pain syndrome, J Athl Train
and treatment of the patellofemoral joint, Part 2: Pathology and 40:341–351, 2005.
nonsurgical management of the patellofemoral joint, Crit Rev Phys 67. Warden SJ, Hinman RS, Watson MA, et al: Patellar taping and
Rehabil Med 15:253–293, 2003. bracing for the treatment of chronic knee pain: A systematic review
48. Davies GJ, Manske RC, Slamma K, et al: Selective activation of the and meta-analysis, Arthritis Rheum 59:73–83, 2008.
vastus medialis oblique: What does the literature really tell us? 68. Fagen V, Delahunt E: Patellofemoral pain syndrome: a review
Physiotherapy Canada 53:136–151, 2001. on the associated neuromuscular deficits and current treatment
49. Ryan CG, Rowe PJ: An electromyographical study to investigate options, Br J Sports Med 42:489–495, 2008.
the effects of patellar taping on the vastus medialis/vastus lateralis 69. Lesher JD, Sutlive TG, Miller GA, et al: Development of a clinical
ratio in asymptomatic participants, Physiother Theory Pract 22: prediction rule for classifying patients with patellofemoral pain
309–315, 2005. syndrome who respond to patellar taping, J Orthop Sports Phys
50. Christou EA: Patellar taping increases vastus medialis oblique Ther 36(11):854–866, 2006.
activity in the presence of patellofemoral pain, J Electromyography 70. Ackerman B, Adams R, Marshall E: The effect of scapula taping on
Kines 14:495–504, 2004. electromyographic activity and musical performance in profes-
51. Cowan SM, Bennell SL, Hodges PW: Therapeutic patellar taping sional violinists, Aust J Physio 48:197–203, 2002.
changes the timing of vasti muscle activation in people with 71. Host HH: Scapular taping in the treatment of anterior shoulder
patellofemoral pain syndrome, Clin J Sports Med 12:339–347, impingement, Phys Ther 75:803–812, 1995.
2002. 72. Morrissey D: Proprioceptive shoulder taping, J Bodywork Mov Ther
52. Powers CM, Landel R, Sosnick T, et al: The effects of patellar taping 4:189–194, 2000.
on stride characteristics and joint motion in subjects with patello- 73. Alexander CM, Stynes S, Thomas A, et al: Does tape facilitate
femoral pain, J Orthop Sports Phys Ther 26:286–667, 1997. or inhibit the lower fibres of trapezius? Man Ther 8:37–41,
53. Ernst GP, Kawaguchi J, Saliba E: Effect of patellar taping on knee 2003.
kinetics of patients with patellofemoral pain syndrome, J Orthop 74. Cools AM, Witvrouw LA, Danneels LA, Cambier DC: Does
Sports Phys Ther 29:661–667, 1999. taping influence electromyographic muscle activity in the
54. Bennell K, Duncan M, Cowan S: Effect of patellar taping on vasti scapular rotators in healthy shoulders? Man Ther 7:154–162,
onset timing, knee kinematics, and kinetics in asymptomatic indi- 2002.
viduals with a delayed onset of vastus medialis oblique, J Orthop 75. Morin GE, Tiberio D, Austin G: The effect of upper trapezius
Res 24(9):1854–60, 2006. taping on electromyographic activity in the upper and middle
55. Ng GYF, Cheng JM: The effects of patellar taping on pain and trapezius region, J Sports Rehabil 6:309–319, 1997.
neuromuscular performance in subjects with patellofemoral pain 76. Selkowitz DM, Chaney C, Stuckey SJ, Vlad G: The effects of
syndrome. Clin Rehabil 16:821–827, 2002. scapular taping on the surface electromyographic signal amplitude
56. Mungovan SF, Henley EC, Renton AL, Turner GR: The effect of of shoulder girdle muscles during upper extremity elevation
patellofemoral taping on EMG activity and torques produced in individuals with suspected shoulder impingement syndrome,
about the knee joint during standing up from a seated position. J Orthop Sports Phys Ther 37:694–702, 2007.
Proceedings of World Confederation of Physical Therapy, London, 77. Zanella PW, Willey SM, Seibel SL, Hughes CJ: The effect of
1991. scapular taping on shoulder joint reposition, J Sport Rehabil
57. Salsich GB, Brechter JH, Farwell D, Powers CM: The effects of 10:113–123, 2001.
patellar taping on knee kinetics, kinematics, and vastus lateralis 78. Hanger HC, Whitewood P, Brown G, et al: A randomized con-
muscle activity during stair ambulation in individuals with patel- trolled trial of strapping to prevent post-stroke shoulder pain, Clin
lofemoral pain, J Orthop Sports Phys Ther 32:3–10, 2002. Rehabil 14:370–380, 2000.
58. Callaghan MJ, Selfe J, Bagley P, Oldham JA: The effect of patellar 79. Lewis JS, Wright C, Green A: Subacromial impingement syn-
taping on knee joint proprioception, J Athl Train 37:19–24, drome: The effect of changing posture on shoulder range of
2002. movement, J Orthop Sports Phys Ther 35:72–87, 2005.
Taping for Athletics and Rehabilitation • CHAPTER 21 535
80. Yoshida A, Kahavov L: The effect of kinesio taping on lower trunk blinded, clinical trial, J Orthop Sports Phys Ther 38:389–395,
range of motion, Res Sports Med 15:103–112, 2007. 2008.
81. Kase K, Wallis J, Kase T: Clinical therapeutic applications of the 84. Yoshida A, Kahavov L: The effect of kinesio taping on lower trunk
kinesio taping method, Tokyo, Japan, 2003, Ken Ikai Co Ltd. range of motion, Res Sports Med 15:103–112, 2007.
82. Halseth T, McChesney JW, DeBeliso M, et al: The effects of 85. Fu TC, Wong AMK, Pei YC, et al: Effect of kinesio taping
kinesio taping on proprioception at the ankle, J Sports Sci Med on muscle strength in athletes—a pilot study, J Sci Med Sport 11:
3:1–7, 2004. 198–201, 2008.
83. Thelen MD, Dauber JA, Stoneman PD: The clinical efficacy
of kinesio tape for shoulder pain: A randomized, double-
22
CHAPTER
SPORTS-RELATED CONCUSSION
Alex M. Taylor and Michael W. Collins
536
Sports-Related Concussion • CHAPTER 22 537
were observed in a sample of concussed athletes involved in pre-existing disorders including anxiety, depression, learning
a motor control and coordination task.27 disabilities, or anemia that complicate accurate diagnosis.36,37
More recently, researchers have started to examine brain Athletes should be educated to a thorough knowledge of all
functioning with variants of traditional EEG: evoked poten- potential signs and symptoms.
tials and event-related potentials (ERPs). The latter is pre-
sumed to be associated with cognitive rather than sensory
processing.28 Recent findings suggest that these techniques
may be of considerable benefit for the assessment of a single Symptoms of Concussion Reported by Athlete
concussive event and research has shown significantly • Headache
decreased signal intensities in concussed athletes that are • Change in sleep pattern
associated with severity of postconcussive symptoms.29 • Feeling fatigued
Investigations focusing on the P300 response, which is a • Feeling “foggy” or groggy
specific component of a ERP in which positive or negative • Nausea
amplitudes are associated with different cognitive processes, • Balance problems or dizziness
have shown attenuated signal amplitudes and longer reac- • Double vision or fuzzy or blurry vision
• Sensitivity to light or noise
tion time in symptomatic concussed athletes when com-
• Feeling sluggish or slowed down
pared with an asymptomatic group and nonconcussed
• Concentration or memory problems
controls.29,30 In addition, longer visual P300 peak latencies
Data from University of Pittsburgh Medical Center’s Sideline Concussion Card.
have been correlated with self-reported attention and mem-
ory deficits in athletes with three or more concussions.29,30
However, two separate investigations of boxers found no
unusual P300 latencies.31,32 The discrepancy argues for con-
tinued research in this area to further explore the sensitivity It is helpful, although not always possible, to gain in-
of electrophysiological techniques to detect brain function- formation from multiple informants (e.g., athlete, team-
ing abnormalities in concussed athletes. mates, athletic trainer, parents, and coach) across multiple
time points (e.g., immediately following injury, a few
hours later, at 24 hours after injury, 48 hours after
Assessment of Concussion injury) to determine the severity of the injury and track
There is evidence to suggest that many athletes do not recovery.
regularly report concussive injuries to team physicians,
sports physical therapists, certified athletic trainers, family
members, or others.33,34 In a study of Canadian Football Sideline Assessment
League players, only 19% of those diagnosed with concus- As with any serious injury, assessment begins with the
sion realized they had sustained an injury.35 Injuries also go athlete’s level of consciousness, and airway, breathing, and
unreported because athletes may not understand the seri- circulation. The attending medical staff must always be pre-
ousness of their injury or purposely deny symptoms to pared with an emergency action plan in the event that the
continue playing.34 evacuation of a critically head- or neck-injured athlete is
necessary. This plan should be familiar to all staff, be well
delineated, and frequently rehearsed.
Clinical Point
Loss of Consciousness
Up to 90% of concussions are undetected and most are not reported Although the dramatic on-field presentation of LOC can
to health care practitioners. make concussion easy to detect and calls for the immediate
removal from play, it is relatively uncommon in sports-
related injury. In most studies, it is identified in less than
10% of all patients.5-7 In addition, research has shown that
In addition to under-reporting, the variable presentation the brief LOC ( 1 minute) typically associated with
and severity of mTBI makes it a difficult injury to recognize sports-related concussion may not reliably predict recovery
and assess. Athletes may present with only one or several time or neuropsychological outcome.38-41 Despite these
symptoms, any and all of which are important from a diag- findings, most grading scales rely on the presence and dura-
nostic and management standpoint. There may be neither a tion of LOC to determine the severity of injury and make
direct trauma to the head nor LOC. Clumsiness, confusion, return-to-play decisions. Regardless of its prognostic value,
or obvious amnesia may not be evident. Many symptoms a patient experiencing extended LOC (typically defined as
can reflect other causal factors, including dehydration, lack greater than 1 minute) requires immediate neurological
of sleep, or overtraining. There may also be concomitant or evaluation. Most practitioners agree that athletes who lose
Sports-Related Concussion • CHAPTER 22 539
or depression, nervousness or anxiety, and less commonly, management. Moreover, concussive injuries in well-known
silliness or euphoria. Affect may be described by the athlete professional athletes raised awareness and resulted in man-
or parent as flattened or labile. Emotional changes may be dated implementation of baseline computerized neuropsy-
very brief or may be prolonged in the case of a more sig- chological testing by the National Football League (NFL).
nificant injury such as when an athlete reports persistent Similarly, after career-ending concussive injuries in the
depression. National Hockey League (NHL), the NHL mandated base-
line neuropsychological testing for all athletes. In addition,
Sleep Disturbances several large-scale studies of professional, collegiate, and
Hypersomnia has been reported in athletes following high-school athletes have continued to demonstrate neuro-
sports-related concussion. Normal sleep-wake patterns can cognitive sequelae of concussion, and some have demon-
become dysregulated and some athletes experience difficul- strated longer recovery times than previously recorded. For
ties initiating or maintaining sleep. These difficulties may example, in a 3-year prospective study of high school and
contribute to daytime fatigue and decreased levels of college athletes, concussed high school athletes demon-
energy. Proper sleep hygiene is advocated, including going strated more prolonged memory impairment than college
to bed and waking at the same time, limiting caffeine in- athletes, and worse performance than age matched controls
take, reducing naps, and eliminating reading or watching 7 days after injury. Neuropsychological functioning in the
television in bed. sample of injured college athletes was equal to age-matched
controls by 3 days after injury.55 In addition, a study of
2141 high school athletes found that a percentage of the
Neuropsychological Outcomes concussed athletes continued to demonstrate difficulties on
In addition to reported symptoms, previous investigations cognitive tasks 3 weeks after injury.56 These results were in
have shown that concussed athletes perform worse on objec- contrast to the findings of a 6-year prospective study involv-
tive measures of neurocognitive functioning when compared ing the NFL. The latter investigation comprised a total of
with their own baseline (preinjury) scores or nonconcussed 887 concussions recorded in 650 players.57 Recovery, as
controls. With group data, most findings suggest that recov- determined by return to play, was as follows: 56% recovered
ery occurs within 2 to 14 days, but some patients demon- on the day of injury, 35.9% recovered 1 to 6 days after
strate significantly longer recovery.7,37,41,42,50,51 In addition, injury, 6.5% recovered 7 to 14 days after injury, and 1.6%
studies have shown that injured athletes who report no recovered more than 14 days after injury. Those athletes
symptoms demonstrate worse performance than uninjured who returned to play in the same game had fewer and
controls, suggesting that subtle neurocognitive sequelae briefer signs and symptoms of concussion, and they did not
may linger beyond reported symptoms.52,53 appear to have significantly increased risk for a second
The benefits of neuropsychological testing within the injury either in the same game or during the remainder of
context of sports medicine were first recognized in the the season. In a subset of the concussed NFL players who
mid-1980s when employed as part of a 4-year prospective underwent baseline neuropsychological evaluations and
study of mTBI in college athletes.54 Aiming to estimate then completed a second evaluation within a few days fol-
the incidence of head injuries in football and to determine lowing their concussion, there was no statistically significant
the neuropsychological sequelae of mTBI, recovery time, decline on any traditional paper and pencil measures of
risk factors for injury, and potential for longer-term neuropsychological functioning.58 That these data contrast
effects, results demonstrated the presence of acute deficits findings of studies examining younger athletes suggests that
for up to 10 days in injured athletes and provided a frame- age and developmental factors may play a role in recovery
work for the future study of sports-related concussion. from concussion.
Subsequent studies have replicated initial findings in this
area. For example, one investigation examined 1631 uni-
versity football players. In addition to assessment of
Clinical Point
symptoms and postural stability, participants were evalu-
ated before and after injury on traditional paper-and- Neurocognitive assessment should be performed prior to the start
pencil measures of neuropsychological functioning. Con- of the season to determine “normal” or baseline level of cognitive
cussed athletes’ balance problems resolved within 3 to functioning.
5 days, self-reported postconcussion symptoms gradually
resolved by day 7, and neuropsychological functioning
improved within 5 to 7 days.5
The utility of neuropsychological measures in docu- Variable findings in research investigating neuropsycho-
menting cognitive recovery following concussion in sports, logical recovery following concussion have lead to more
even in the absence of reported symptoms, has prompted individualized management of concussion regardless of
more widespread use as a clinical tool in concussion age. Initially, testing was mostly composed of traditional
542 SECTION III • Management of Sports Injury and Illness
(e.g., paper-and-pencil measures) to assess baseline and neuropsychological testing also provides practitioners with
postinjury levels of cognitive functioning. However, as an objective evidence to support their treatment plans.
increasing number of sports organizations have recognized
the utility of these measures, many limitations to traditional
testing emerged, including the cost and availability of
Cumulative Effects
trained neuropsychologists to administer and interpret Although data concerning the longer-term effects of repeti-
the data, leading to the development and increased use of tive concussion vary, there is some evidence that a history of
computer-based neurocognitive testing. concussion is associated with changes in neurophysiology,
Computer-based testing procedures have a number of subjective symptoms, and neuropsychological test perfor-
advantages. First, the use of computers allows a large num- mance.65,66 However, the number or severity of previous inju-
ber of athletes to be tested with fewer resources. An entire ries has not been shown to conclusively predict longer-term
football team may be baseline tested in one or two sessions. sequelae or increased vulnerability. In general, studies of
The data can easily be saved and accessed remotely, and athletes with three or more concussions suggest an increased
with some systems data are summed into a clinical report risk of sustaining additional concussive injuries, worse on-field
that can be interpreted by an appropriately trained sports presentations with subsequent concussion, slowed recovery,
concussion specialist. The use of computers may provide a and greater acute changes in memory performance.66-68
more accurate measurement of cognitive processes such as Research examining athletes who have sustained one or two
reaction time and information processing speed. This previous concussions have mixed results.37,69-71
increased accuracy may increase the validity of test results in In contrast with most studies of repetitive injuries,
detecting subtle changes in neurocognitive processes. In research evaluating the pathophysiology and neuropsycho-
addition, computerized testing allows for the randomiza- logical functioning of boxers reveals the potential for
tion of test stimuli, which should improve reliability across significant longer-term sequelae.72-78 At their worst, the
multiple administration periods by minimizing practice neurological deficits affecting boxers may potentially re-
effects. semble Parkinson disease and include a progressive pattern
Several computer-based tests currently exist, including of difficulties characterized by confusion, loss of coordina-
Immediate Post-Concussion Assessment and Cognitive tion, problems with speech, and upper-body tremors. Often
Testing (ImPACT), CogState, Headminders, and Auto- referred to as dementia pugilistica or chronic boxer’s
mated Neurocognitive Assessment Matrices (ANAM).59-62 encephalopathy, the neurological changes observed in boxers
Most have published manuals describing their psychometric are associated with cerebral atrophy, cortical and subcortical
properties, and studies have demonstrated their reliability, neurofibrillary tangles, and cellular loss in the cerebellum.79-81
validity, sensitivity, specificity, and added value when com- Research has shown that genetic protein apolipoprotein E
pared with self-reported symptoms alone.52,63,64 However, (APOE) with the 4 allele may be a risk factor for develop-
none should be used as a standalone measure and instead ment of neurological dysfunction and progressive disease in
should be part of comprehensive assessment that includes a this population.82,83
clinical interview, evaluation of symptoms, and overall There is also evidence demonstrating a relationship
medical history. between boxing and neurocognitive impairment. Although
In ideal situations and as recommended by current the results have varied depending on the level of participa-
guidelines, baseline neuropsychological assessment should tion (e.g., amateur or professional), findings suggest that
be administered prior to the start of the season to determine the extent of neuropsychological impairments may be
“normal” individual cognitive functioning. Following associated with the number of bouts fought.84,85
injury and to assess the severity of injury as well as other
management considerations, including return to school and
exertion, the first evaluation is often performed while the
Recovery and Return to Play
athlete remains symptomatic. Subsequent testing is per- Although significant individual variability exists in recovery
formed 7 to 10 days after injury and then as recommended from concussion, previous group studies have indicated that
by the treating clinician. A score significantly lower than a single concussion typically resolves in less than 2 weeks.
baseline, defined by statistical reliable change, or premorbid More recent studies, however, have suggested even longer
estimates of functioning reflects ongoing sequelae and recovery times, especially at the high school level of partici-
precludes return to play. pation.43,55,56 Most sports medicine researchers and profes-
In summary, neuropsychological deficits associated with sionals agree that returning an athlete to contact sport
concussion are reported in the literature, and cognitive test- participation prior to complete recovery might increase the
ing appears to be a highly valuable tool in documenting im- risk of poor outcome. Authors have also indicated that
pairment and tracking recovery from concussive injury. As retirement from sport should be considered when less bio-
the diagnosis of concussion can be a difficult process and mechanical impact or indirect blows result in symptoms of
athletes at all levels of competition may minimize symptoms, concussion or when duration of symptoms is significantly
Sports-Related Concussion • CHAPTER 22 543
increased with successive injuries.86 Thus, the most impor- management and implementation of postinjury neuropsy-
tant step a practitioner can take toward a positive prognosis chological testing as a “cornerstone” of proper postinjury
is proper assessment and management of concussion in the management and decisions regarding return to play.10
acute and follow-up stages of injury.
6. Guskiewicz KM, Weaver NL, Padua DA, Garrett WE Jr: Epide- 25. Tysvaer AT, Storli OV: Soccer injuries to the brain. A neurologic
miology of concussion in collegiate and high school football and electroencephalographic study of active football players, Am
players, Am J Sports Med 28(5):643–650, 2000. J Sports Med 17(4):573–578, 1989.
7. Macciocchi SN, Barth JT, Alves W, et al: Neuropsychological 26. Thompson J, Sebastianelli W, Slobounov S: EEG and postural
functioning and recovery after mild head injury in collegiate correlates of mild traumatic brain injury in athletes, Neurosci Lett
athletes, Neurosurg 39(3):510–514, 1996. 377(3):158–163, 2005.
8. Congress of Neurological Surgeons: Committee on head injury 27. Slobounov S, Sebastianelli W, Simon R: Neurophysiological
nomenclature: Glossary of head injury, Clin Neurosurg 12: and behavioral concomitants of mild brain injury in collegiate
386–394, 1966. athletes, Clin Neurophysiol 113(2):185–193, 2002.
9. American Academy of Neurology: Practice parameter: The man- 28. Mendez CV, Hurley RA, Lassonde M, et al: Mild traumatic
agement of concussion in sports (summary statement). Report of brain injury: Neuroimaging of sports-related concussion,
the Quality Standards Subcommittee, Neurology 48(3):581–585, J Neuropsychiatry Clin Neurosci 17(3):297–303, 2005.
1997. 29. Dupuis F, Johnston KM, Lavoie ME, et al: Concussion in
10. Aubry M, Cantu R, Dvorak J, et al: Summary and agreement athletes produce brain dysfunction as revealed by event-related
statement of the First International Conference on Concussion in potentials, NeuroReport 11(18):4087–4092, 2000.
Sport, Vienna 2001. Recommendations for the improvement of 30. Lavoie ME, Dupuis F, Johnston KM, et al: Visual p300 effects
safety and health of athletes who may suffer concussive injuries, beyond symptoms in concussed college athletes, J Clin Exp
Br J Sports Med 36(1):6–10, 2002. Neuropsychol 26(1):55–73, 2004.
11. Ommaya AK, Gennarelli TA: Cerebral concussion and traumatic 31. Breton F, Pincemaille Y, Tarriere C, Renault B: Event-related
unconsciousness. Correlation of experimental and clinical obser- potential assessment of attention and the orienting reaction in
vations of blunt head injuries, Brain 97(4):633–654, 1974. boxers before and after a fight, Biol Psychol 31(1):57–71,
12. Gaetz M: The neurophysiology of brain injury, Clin Neurophysiol 1991.
115(1):4–18, 2004. 32. Murelius O, Haglund Y: Does Swedish amateur boxing lead to
13. Katayama Y, Becker DP, Tamura T, Hovda DA: Massive increases chronic brain damage? 4. A retrospective neuropsychological
in extracellular potassium and indiscriminate release of glutamate study, Acta Neurologica Scandinavica 83(1):9–13, 1991.
following concussive brain injury, J Neurosurg 73:889–900, 33. Erlanger DM, Kutner KC, Barth JT, Barnes R: Neuropsychology
1990. of sports-related concussion: Dementia pugilistica to post
14. Giza CC, Hovda DA: The neurometabolic cascade of concussion, concussion syndrome, Clin Neuropsychol 13:193–209, 1999.
J Athl Train 36:228–235, 2001. 34. McCrea M, Hammeke T, Olsen G, et al: Unreported concussion
15. Giza CC, Hovda DA: The pathophysiology of traumatic brain in high school football players: Implications for prevention, Clin
injury. In Lovell MR, Echemendia RJ, Barth JT, Collins MW, J Sports Med 14(1):13–17, 2004.
Editors: Traumatic brain injury in sports, Lisse, Netherlands, 35. Delaney JS, Lacroix VJ, Leclerc S, Johnston KM: Concussions
2004, Swets & Zeitlinger. during the 1997 Canadian Football season, Clin J Sports Med
16. McCrory P, Johnston K, Meeuwisse W, et al: Summary and 10:9–14, 2000.
agreement statement of the 2nd International Conference on 36. Iverson GL, Brooks BL, Collins MW, Lovell MR: Tracking
Concussion in Sport, Prague 2004, Br J Sports Med 39(4): neuropsychological recovery following concussion in sport,
196–204, 2005. Brain Inj 20:245–252, 2006.
17. Chen SHA, Kareken DA, Fastenau PS, et al: A study of persistent 37. Collins MW, Grindel SH, Lovell MR, et al: Relationship between
post-concussion symptoms in mild head trauma using positron concussion and neuropsychological performance in college foot-
emission tomography, J Neurol Neurosurg Psychiatry 74: ball players, JAMA 282(10):964–970, 1999.
326–332, 2003. 38. Iverson GL, Lovell MR, Smith SS: Does brief loss of conscious-
18. Umile EM, Sandel ME, Alavi A, Plotkin RC: Dynamic imaging ness affect cognitive functioning after mild head injury? Arch
in mild traumatic brain injury: Support for the theory of medial Clin Neuropsychol 15(7):643–648, 2000.
temporal vulnerability, Arch Phys Med Rehabil 83:1506–1513, 39. Lovell MR, Iverson GL, Collins MW, et al: Does loss of conscious-
2002. ness predict neuropsychological decrements after concussion? Clin
19. Chen JK, Johnston KM, Frey S, et al: Functional abnormalities J Sports Med 9(4):193–198, 1999.
in symptomatic concussed athletes: An fMRI study, Neuroimage 40. Collins MW, Iverson GL, Lovell MR, et al: On-field predictors of
22(1):68–82, 2004. neuropsychological and symptom deficit following sports-related
20. Jantzen KJ, Anderson B, Steinberg FL, Kelso JA: A prospective concussion, Clin J Sports Med 13(4):222–229, 2003.
functional MR imaging study of mild traumatic brain injury in 41. Guskiewicz KM, Ross SE, Marshall SW: Postural stability and
college football players, Am J Neuroradiol 25(5):738–745, neuropsychological deficits after concussion in collegiate athletes,
2004. J Athl Train 36(3):263–273, 2001.
21. Chen JK, Johnston KM, Collie A, et al: A validation of the post 42. McCrea M, Kelly JP, Randolph C, et al: Immediate neurocognitive
concussion symptom scale in the assessment of complex concus- effects of concussion, Neurosurg 50(5):1032–1040, discussion
sion using cognitive testing and functional MRI, J Neurol 1040–1042, 2002.
Neurosurg Psychiatry 78:1231–1238, 2007. 43. Lovell MR, Collins MW, Iverson GL, et al: Recovery from mild
22. Lovell MR, Pardini JE, Welling JS, et al: Functional brain abnor- concussion in high school athletes, J Neurosurg 98(2):296–301,
malities are related to clinical recovery and time to return to play 2003.
in athletes, Neurosurg 61:352–360, 2007. 44. Pellman EJ, Powell JW, Viano DC, et al: Concussion in profes-
23. Kaplan HA, Browder J: Observations on the clinical and brain sional football: Epidemiological features of game injuries and re-
wave patterns of professional boxers, JAMA 156(12):1138–1144, view of the literature—Part 3, Neurosurg 54(1):81–94, discussion
1954. 94–96, 2004.
24. Kross R, Ohler K, Barolin GS: Cerebral trauma due to heading— 45. Asplund CA, McKeag DB, Olsen CH: Sport-related concussion:
Computerized EEG analysis of football players, EEG-EMG 14: Factors associated with prolonged return to play, Clin J Sports
209–212, 1983. Med 14(6):339–343, 2004.
Sports-Related Concussion • CHAPTER 22 547
46. Collins MW, Field M, Lovell MR, et al: Relationship between 66. Iverson GL, Gaetz M, Lovell MR, Collins MW: Cumulative
postconcussion headache and neuropsychological test perfor- effects of concussion in amateur athletes, Brain Inj 18(5):
mance in high school athletes, Am J Sports Med 31(2):168–173, 433–443, 2004.
2003. 66. Collins MW, Lovell MR, Iverson GL, et al: Cumulative effects of
47. Mihalik JP, Stump JE, Collins MW, et al: Posttraumatic migraine concussion in high school athletes, Neurosurg 51(5):1175–1179,
characteristics in athletes following sports-related concussion, discussion 1171–1180, 2002.
J Neurosurg 102(5):850–855, 2005. 67. Guskiewicz KM, McCrea M, Marshall SW, et al: Cumulative
48. Erlanger D, Kaushik T, Cantu R, et al: Symptom-based assess- effects associated with recurrent concussion in collegiate football
ment of the severity of a concussion, J Neurosurg 98:477–484, players: The NCAA Concussion Study, JAMA 290(19):
2003. 2549–2555, 2003.
49. Iverson GL, Gaetz M, Lovell MR, Collins MW: Relation 68. Moser RS, Schatz P, Jordan BD: Prolonged effects of concussion
between subjective fogginess and neuropsychological testing in high school athletes, Neurosurg 57(2):300–306; discussion
following concussion, J Int Neuropsychol Society 10:904–906, 300–306, 2005.
2004. 69. Moser RS, Schatz P: Enduring effects of concussion in youth
50. Barr WB, McCrea M: Sensitivity and specificity of standardized athletes, Arch Clin Neuropsychol 17(1):91–100, 2002.
neurocognitive testing immediately following sports concussion, 70. Macciocchi SN, Barth JT, Littlefield L, Cantu RC: Multiple
J Int Neuropsychol Society 7:693–702, 2001. concussions and neuropsychological functioning in collegiate
51. Warden DL, Bleiberg J, Cameron KL, et al: Persistent prolonga- football players, J Athl Training 36(3):303–306, 2001.
tion of simple reaction time in sports concussion, Neurology 71. Iverson GL, Brooks BL, Lovell MR, Collins MW: No cumulative
57(3):524–526, 2001. effects for one or two previous concussions, Br J Sports Med
52. Fazio VC, Lovell MR, Pardini JE, Collins MW: The relation 40(9):802–805, 2006.
between post concussion symptoms and neurocognitive per- 72. Jordan BD, Zimmerman RD: Computed tomography and mag-
formance in concussed athletes, NeuroRehabil 22:207–216, netic resonance imaging comparisons in boxers, JAMA 263(12):
2007. 1670–1674, 1990.
53. Erlanger D, Saliba E, Barth J, et al: Monitoring resolution of 73. Zhang L, Ravdin LD, Relkin N, et al: Increased diffusion in the
postconcussion symptoms in athletes: Preliminary results of a brain of professional boxers: A preclinical sign of traumatic brain
web-based neuropsychological test protocol, J Athl Training injury? Am J Neuroradiol 24(1):52–57, 2003.
36(3):280–287, 2001. 74. Rabadi MH, Jordan BD: The cumulative effect of repetitive
54. Barth JT, Alves WM, Ryan T, et al: Mild head injury in sports: concussion in sports, Clin J Sports Med 11(3):194–198, 2001.
Neuropsychological sequelae and recovery of function. In Levin 75. Dale GE, Leigh PN, Luthert P, et al: Neurofibrillary tangles
HS, Eisenberg HM, Benton AL, Editors: Mild head injury, in dementia pugilistica are ubiquitinated, J Neurol Neurosurg
New York, 1989, Oxford. Psychiatry 54(2):116–118, 1991.
55. Field M, Collins MW, Lovell MR, Maroon J: Does age play a role 76. Roberts GW, Allsop D, Bruton C: The occult aftermath of
in recovery from sports-related concussion? A comparison of boxing, J Neurol Neurosurg Psychiatry 53(5):373–378, 1990.
high school and collegiate athletes, J Pediatrics 142(5):546–553, 77. Miele VJ, Carson L, Carr A, Bailes JE: Acute on chronic subdural
2003. hematoma in a female boxer: A case report, Med Sci Sports Exerc
56. Collins MW, Lovell MR, Iverson GL, et al: Examining concussion 36(11):1852–1855, 2004.
rates and return to play in high school football players wearing 78. Lampert PW, Hardman JM: Morphological changes in brains of
newer helmet technology: A three-year prospective cohort study, boxers, JAMA 251:2676–2679, 1984.
Neurosurg 58(10):275–286, 2006. 79. Serel J, Jaros O: The mechanisms of cerebral concussion in boxing
57. Pellman EJ, Viano DC, Casson IR, et al: Concussion in profes- and their consequences, World Neurol 3:351–358, 1962.
sional football: Injuries involving 7 or more days out—Part 5, 80. Corsellis JA, Bruton CJ, Freeman-Browne D: The aftermath of
Neurosurg 55(5):1100–1119, 2004. boxing, Psychol Med 3(3):270–303, 1973.
58. Pellman EJ, Viano DC, Casson IR, et al: Concussion in profes- 81. Jordan BD: Neurologic aspects of boxing, Arch Neurol 44:
sional football: Repeat injuries—Part 4, Neurosurg 55(4):860–873, 453–459, 1987.
discussion 873–876, 2004. 82. Jordan BD, Relkin NR, Ravdin LD, et al: Apolipoprotein E
59. Lovell MR, Collins MW: ImPACT: Immediate post-concussion epsilon4 associated with chronic traumatic brain injury in boxing,
assessment and cognitive testing, Pittsburgh, PA, 1998. JAMA 278(2):136–140, 1997.
60. CogSport, accessed January 26, 2008, from http://cogstate. 83. Stewart WF, Gordon B, Selnes O, et al: Prospective study
com/go/sport. of central nervous system function in amateur boxers in the
61. Erlanger DM, Feldman DJ, Kutner K: Concussion resolution United States, Am J Epidemiol 139(6):573–588, 1994.
index. New York, 1999, Headminder, Inc. 84. Kemp P, Houston A, Macleod M, Pethybridge RJ: Cerebral per-
62. Reeves D, Thorne R, Winter S, Hegge F: The united tri-service fusion and psychometric testing in military amateur boxers and
cognitive performance assessment battery, (UTC-PAB), Report control, J Neurol Neurosurg Psychiatry 59:368–374, 1995.
89–1, San Diego, 1989, US Naval Aerospace Medical Research 85. Heilbronner RL, Bush SS, Ravdin LD, et al: Neuropsychological
Laboratory and Walter Reed Army Institute of Research. consequences of boxing and recommendations to improve safety:
63. Schatz P, Pardini JE, Lovell MR, et al: Sensitivity and specificity A National Academy of Neuropsychology education paper, Arch
of the ImPACT test battery for concussion in athletes, Arch Clin Clin Neuropsychol 24(1):11–19, 2009.
Neuropsychol 21:91–99, 2006. 86. Echemendia RJ, Cantu R: Return to play following cerebral head
64. Van Kampen D, Lovell MR, Pardini JE, et al: The “value added” injury. In Lovell MR, Echemendia RJ, Barth JT, Collins MW,
of neurocognitive testing in managing sports concussion in Editors: Traumatic brain injury in sports: A neuropsychological
athletes, Am J Sports Med 34(10):1630–1635, 2006. and international perspective, Netherlands, 2004, Swets &
65. Gaetz M, Goodman D, Weinberg H: Electrophysiological Zeitlinger.
evidence for the cumulative effects of concussion, Brain Inj 87. Cantu RC: Second-impact syndrome, Clin Sports Med 17(1):
14(12):1077–1088, 2000. 37–44, 1998.
548 SECTION III • Management of Sports Injury and Illness
88. McQuillen JB, McQuillen EN, Morrow P: Trauma, sport, and normative data for the post-concussion scale, Appl Neuropsychol
malignant cerebral edema, Am J Forensic Med Pathol 9(1):12–15, 13(3):166–174, 2006.
1988. 97. Farace E, Alves W: Do women fare worse: A meta-analysis of
89. Lovell MR, Collins MW, Iverson GL, et al: Grade 1 or “ding” gender differences in traumatic brain injury outcome, J Neurosurg
concussions in high school athletes, Am J Sports Med 32(1): 93:539–545, 1998.
47–54, 2004. 98. Roof RL, Duvdevani R, Stein DG: Gender influences outcome of
90. Bruce DA, Alavi A, Bilaniuk L, et al: Diffuse cerebral swelling brain injury: Progesterone plays a protective role, Brain Res
following head injuries in children: The syndrome of “malignant 607:333–336, 1993.
brain edema.” J Neurosurg 54(2):170–178, 1981. 99. Roof RL, Hall ED: Estrogen-related gender differences in survival
91. Pickles W: Acute general edema of the brain in children with rate and cortical blood flow after impact acceleration head injury in
head injuries, New Engl J Med 242(16):607–611, 1950. rats, J Neurotrauma 17:367–388, 2007.
92. Barnes BC, Cooper L, Kirkendall DT, et al: Concussion history 100. Rogers E, Wagner AW: Gender, sex steroids, and neuroprotec-
in elite male and female soccer players, Am J Sports Med tion following traumatic brain injury, J Head Trauma Rehabil
26(3):433–438, 1998. 21(3):279–281, 2006.
93. Covassin T, Schatz P, Swanik CB: Sex differences in the neuropsy- 101. Stein DG, Hoffman SW: Estrogen and progesterone as neuro-
chological function and post-concussion symptoms of concussed protective agents in the treatment of acute brain injuries, Pediatr
collegiate athletes, Neurosurg 61:345–350, 2007. Rehabil 6(1):13–22, 2003.
94. Broshek DK, Kaushik T, Freeman JR, et al: Sex differences in 102. Emerson CS, Hadrick JP, Vink R: Estrogen improves biochemi-
outcome following sports-related concussion, J Neurosurg 102: cal and neurologic outcome following traumatic brain injury in
856–863, 2005. male rats, but not females, Brain Res 8:95–100, 1993.
95. Covassin T, Swanik CB, Sachs M, et al: Sex differences in baseline 103. Teasdale G, Nicole J, Murray G: Association of apolipoprotein E
neuropsychological functioning and concussion symptoms of polymorphism with outcome after brain injury, Lancet 350:
collegiate athletes, Br J Sports Med 40:923–927, 2006. 1069–1071, 1997.
96. Lovell MR, Iverson GL, Collins MW, et al: Measurement of 104. Gross R: APOE epsilon 4 allele and chronic traumatic brain
symptoms following sports-related concussion: Reliability and injury, JAMA 278:2143, 1997.
23
CHAPTER
Introduction high risk for spinal cord trauma, such as football and hockey.
Millions of people participate each year in organized and rec- The change in the incidence of injury attributable to sports
reational sports, placing themselves at risk for possible injury. may speak to how clinicians involved in sports medicine may
The majority of individuals participate without suffering from be in a position to influence the prevention, management, and
significant injury or disability. Most injuries that do occur are outcome of these injuries. The role that providers play differs
relatively minor, allowing the participants to return to their depending on the level of organization of the sport (i.e.,
desired recreational activities and lifestyle without incident. youth league, interscholastic, intercollegiate, or professional),
Unfortunately, catastrophic injuries do sometimes occur from and the clinician’s level of involvement with the team or
participation in organized or recreational athletic activity. athlete.
Such catastrophic, and potentially fatal, injuries involve frac- The makeup of the sports medicine team varies depend-
tures and fracture-dislocations of the cervical spine. ing on the situation. In organized sports, physicians, ath-
Current epidemiological data from the National Spinal letic trainers, physical therapists, paramedics, and emergency
Cord Injury Information Network1 reveals that approximately medical technicians (EMTs) specifically trained in the man-
12,000 new traumatic spinal cord–injured patients each year agement of acute cervical injuries are often present when an
require medical intervention (or 40 cases/million in the U.S. injury occurs and are available to assist. However, in recre-
population). Involvement in athletic activity has accounted for ational sports, a paramedic or EMT is often called on to
7.4% of all spinal cord injuries yearly since 2005. This recent manage an acute cervical injury after it has occurred.
data demonstrates a decrease in incidence caused by athletic
competition compared with data from Keenen and Benson,2
published in 1992, who reported that 15% of spinal cord Clinical Point
injuries were a result of sports (Figure 23-1).
Sports medicine clinicians of all disciplines have always In organized sports, the overall responsibility of the sports medicine
team is to establish and practice an effective emergency plan. This
been actively involved in seeking improvements to athletic
includes any policies and procedures necessary for the emergency
equipment, strength and conditioning programs, rules
management of catastrophic injuries prior to the occurrence of any
changes, coaching standards, and techniques that could affect injury.3,4 All personnel must be appropriately trained and aware of
injury rates in a positive manner. Advocacy of clinicians for their role and must practice to maintain proficiency. Communication
these changes have focused on sports that place participants at links and an agreed-on chain of command within the sports medicine
team and with all other appropriate medical personnel, such as
paramedics and emergency medical technicians are pivotal to the
Note: This chapter includes content from previous contributions by successful management of any emergency. If catastrophic injury
James E. Zachazewski, MS, PT, SCS, ATC, Gary Geissler, MS, PT,
occurs, an effective emergency management plan can successfully
SCS, ATC, and Donald Hangen, MD, as it appeared in the predecessor
be implemented in an efficient, expedient manner.
of this book—Zachazewski JE, Magee DJ, Quillen WS, editors: Athletic
injuries and rehabilitation, Philadelphia, 1996, WB Saunders.
549
550 SECTION III • Management of Sports Injury and Illness
Figure 23-3
Catastrophic football injuries by year, 1977-2007. (Data from Mueller FO, Cantu RC: Annual survey of
catastrophic football injuries, National Center for Catastrophic Sport Injury Research, University of North
Carolina, Chapel Hill, NC; available at http://www.unc.edu/depts/nccsi/.)
incidence per participant. When Table 23-1 and Table 23-2 are usually unilateral and transient in nature, lasting seconds
are reviewed, it can be seen that, although a greater number to minutes. Pain and paresthesia may radiate into the upper
of high school football players have suffered catastrophic extremity. Shoulder or arm weakness may be present as
cervical spine injuries, the incidence is much higher in the an additional symptom. Signs and symptoms are usually
collegiate athlete. This data has been fully reviewed and unilateral. If significant neck pain exists, if these symptoms
reported by Boden et al.10 include two or more extremities, or if any of the symptoms
Tracking of these devastating injuries should continue to mentioned previously last beyond a few minutes, clinicians
allow the sports medicine community to continue to recog- should consider the possibility of a more significant injury
nize patterns of injury and advocate for appropriate rules, and initiate cervical spine injury precautions.
technique, and equipment changes to minimize their effect. Statistically these injuries are infrequent in sports, with
the exception of American football.11,12 The burner or stinger
Epidemiology is the most common neural injury sustained by football play-
ers. Burners or stingers most commonly affect defensive
Types of Injury backs, linebackers, and lineman because of the most common
Brachial Plexus Injuries mechanism of injury, tackling.13 Clancy and colleagues,14
Brachial plexus injuries, often termed burners or stingers, are Clancy,15 Markey and colleagues,16 and Sallis and colleagues17
most commonly incurred in collision sports such as football have reported that up to 65% of collegiate football players
(Figure 23-4). The football rules change instituted in 1976 have sustained at least one burner during their collegiate ca-
as a result of the efforts of the NFHNIR required a return reers. These injuries and other nerve peripheral nerve injuries
to shoulder blocking and tackling. Because of this change, about the shoulder and cervical spine have been thoroughly
an increase in the frequency of brachial plexus injuries reviewed and discussed by Safran in 2004.18,19
might have been anticipated, because a common mecha-
nism causing these injuries in football is shoulder depression Sprains and Strains
during blocking and tackling. However, a review of data Minor injuries to the cervical spine that are a result of
collected on collegiate athletes from 1975 through 1978 by trauma are usually termed sprains (collagen tissue) or
the National Athletic Injury Reporting System did not strains (contractile tissue). Trauma is imposed by some
demonstrate this to be the case. means of acceleration, deceleration, or contact with an
The signs and symptoms of all types of brachial plexus object such as the ground, an opponent, or the ball. This is
injuries usually sustained in sports include sharp, burning probably the most common type of injury to the cervical
pain in the shoulder that may shoot down toward the hand. spine in sports, although no reports are available in the
Complaints of neck pain are infrequent. These symptoms literature detailing the specific incidence of this injury.
552 SECTION III • Management of Sports Injury and Illness
Table 23-2
Epidemiological Summary
High School College Combined
Annual Average: 1998-2002 Mean SD Mean SD Mean SD
Direct catastrophic football cervical spine injuries 11.54 4.24 3.54 1.61 15.08 4.7
Data from Boden BP, Tacchetti RL, Cantu RC et al: Catastrophic cervical spine injuries in high school and college football players, Am J Sports
Med 34:1223-1232, 2006.
CI, Confidence interval; SD, standard deviation.
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 553
Traction
Compression
(pinching)
Figure 23-4
Mechanism of injury for brachial plexus (burner or stinger) pathological conditions. (From Magee DJ:
Orthopedic physical assessment, ed 5, p 139, St Louis, 2007, Saunders.)
resulted in a fracture, subluxation, or dislocation. of these, Banerjee and colleagues provide an excellent summary
25, or 2.4%, involved the C3-C4 level.24 of unstable fractures and dislocations of the lower cervical
Lower Cervical Spine (C5-C7). Injuries at the spine.28 The axial force that most often causes these cata-
lower cervical spine account for most of the fractures and strophic injuries is a result of the cervical spine being
dislocations seen in sports. The most common level of compressed between the mass of the oncoming body ver-
injury is C5-C6.25 Again, axial loading is the most com- sus the instant deceleration of the head. The position of
mon mechanism of injury, although six common patterns the head and cervical spine often dictate the effect of this
of injury have been reported in the literature.26 These compressive force. Neutral alignment or slight lordosis
patterns are compressive flexion, vertical compression, of the cervical spine allows compressive forces to be
distractive flexion, compressive extension, distractive ex- dissipated by paravertebral musculature and vertebral
tension, and lateral flexion. Each of these patterns may be ligaments (Figure 23-6, A). Slight head and neck flexion
further subdivided into stages based on the degree of liga- result in an elimination of cervical lordosis (Figure 23-6, B).
mentous injury and osseous damage. These stages and The spine now behaves like a column, energy from com-
their medical and surgical management have been fully pressive forces is now transferred directly to the vertebrae
reviewed by Leventhal.27 as opposed to the soft tissues, causing buckling of
the column and potentially catastrophic injury (Figure
23-6, C). Most commonly, slight flexion occurs with this
Mechanism of Injury to the Cervical Spine compressive force. The compressive failure of the verte-
• Vertical (axial) compression (upper, middle, and lower) bral body, in conjunction with lengthening of the poste-
• Compressive flexion (upper and lower) rior column often results in a “flexion teardrop” injury
• Distractive flexion (lower) (Figure 23-7, A). This injury is highly unstable and often
• Compressive extension (upper and lower) associated with spinal cord injury.29 Pure compressive
• Distractive extension (lower) force results in a burst type fracture with retropulsion
• Lateral flexion (lower) of osseous material into the spinal canal causing cord
compromise (Figure 23-7, B).
A B C
Figure 23-6
Response of the cervical spine to applied axial load. A, With the neck in neutral alignment, the vertebral
column is extended. The compressive force can be dissipated by the spinal musculature and ligaments.
B, With the neck in a flexed posture, the spine straightens out and becomes collinear with the axial
force. C, At the time of impact, the straightened cervical spine undergoes a rapid deformation and
buckles under the compressive load. (From Banerjee R, Palumbo MA, Fadale PD: Catastrophic cervical
spine injuries in the collision sport athlete, Part I—Epidemiology, functional anatomy and diagnosis,
Am J Sports Med 32:1081, 2004.)
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 555
A B
Figure 23-7
Compression injuries of the lower cervical spine. A, Compressive-flexion pattern. The “teardrop”
fracture variant is characterized by compressive failure of the anterior column with a coronal plane
fracture extending through the vertebral body. Tensile forces cause the disruption of the posterior spinal
ligaments. B, Vertical compression pattern. In the “burst” fracture variant comminution of the vertebral
body can be associated with retropulsion of osseous fragments into the spinal canal. (From Banerjee R,
Palumbo MA, Fadale PD: Catastrophic cervical spine injuries in the collision sport athlete, Part I—
Epidemiology, functional anatomy and diagnosis, Am J Sports Med 32:1082, 2004.)
Cervical Spine Stenosis with Cord Neurapraxia as an isolated finding or associated with congenital fusion,
and Transient Quadriplegia disc disease, or ligamentous instability.30
This syndrome was originally reported by Torg and colleagues The diagnosis of cervical spinal stenosis is based on the
in 198630 and reviewed by Torg and Fay in 1991.31 Torg and size of the vertebral canal relative to the vertebral body, as
colleagues estimate the incidence rate for transient quadriple- originally described in 1986 by Torg and colleagues.30 For
gia to be 7.3 per 10,000 exposures in football,30,32 and the this initial study, a group of 24 football players with tran-
rate for paresthesia associated with transient quadriplegia was sient quadriplegia attributed to neurapraxia of the cervical
1.3 per 10,000 exposures in the survey of a single season.30 spinal cord was studied. All demonstrated vertebral canal/
Athletes with cervical stenosis, whether acquired or develop- vertebral body ratios of less than 0.80 (Figure 23-8). This
mental, appear to be predisposed to this condition.33 Neck ratio was thought to indicate significant spinal stenosis, as
pain is usually not present and cervical range of motion is un- the ratio in a group of controls was 0.98.35
compromised. Symptoms of transient paresthesia (“tingling”) Since the original description and the development of
or loss of sensation) may be associated with motor deficits the Torg “ratio,” other conflicting studies have questioned
ranging from no motor deficit to mild quadriparesis or the use of this ratio as an absolute value to be used as
complete quadriplegia involving both arms, both legs, all four criteria for significant spinal stenosis.36,37 Odor and col-
extremities, or an ipsilateral arm and leg. Signs and symptoms leagues demonstrated that 74 of 224 asymptomatic pro-
are temporary and function returns during a wide time frame fessional and rookie football players (33%) demonstrated a
ranging from 15 minutes to 48 hours.34 Torg ratio of less than 0.80 at one or more levels between
This very acute, transient neurologic episode is of C3 and C6,36 whereas Herzog and colleagues examined
cervical spinal cord origin. This diagnosis should not be 80 symptomatic professional football players and reported
confused with nerve root or brachial plexus injuries, which an abnormal Torg ratio in 49%.37 Although demonstrated
are unilateral. This syndrome may follow forced hyperflex- to be highly sensitive at 93%, unfortunately the Torg ratio
ion, hyperextension, or axial loading of the spine. Routine demonstrates a positive predictive value of only 0.2%.38
radiographs are negative for fracture or dislocation. Devel- Thus, the Torg ratio may be abnormal in individuals
opmental cervical spine narrowing is often apparent, either with and without a transient quadriplegic episode. These
556 SECTION III • Management of Sports Injury and Illness
A B C
Figure 23-8
A, The spinal canal/vertebral body ratio is the distance from the midpoint of the posterior aspect of the
vertebral body to the nearest point on the corresponding spinolaminar line (a) divided by the antero-
posterior width of the vertebral body (b). B and C, Comparison between the spinal canal/vertebral
body ratio in a “normal” control subject with that in a stenotic patient demonstrated on lateral radio-
graphs of the cervical spine. The ratio is 1:1 (1) in the control subject (B) compared with 1:2 (0.50) in
the stenotic patient (C). (From Torg JS, Pavlov H, Genuario S et al: Neurapraxia of the cervical spinal
cord with transient quadriplegia, J Bone Joint Surg Am 68:1354-1370, 1986.)
factors make the use of this ratio a poor screening tool for
sports participation. Clinical Caution
Ratios and tools such as these, however, are of assis- The presence of a canal/vertebral body ratio of 0.8 or less (see Figure
tance in return to play decisions that the medical team 23-8) is not a contraindication to participation in contact sports for
must make if injury with cervical cord neurapraxia has oc- asymptomatic individuals. However, for individuals with a ratio of less
curred. The recurrence of cervical cord neurapraxia, and than 0.8 who do experience a cervical cord neuropraxia, there is a
the sensory and motor symptoms that occur with it, are relative contraindication to return. The risk of recurrence is strongly
more predictable. Based on logistic regression analysis by and inversely correlated with the sagittal diameter of the canal. In
Torg and colleagues,34 there is a strong inverse correlation this case, the diameter is useful in the prediction of future episodes
between the risk of recurrence and the disk-level canal of neuropraxia (p 0.001) (see Figure 23-9).34
diameter and the ratio of the spinal canal to the vertebral
body (Figure 23-9). Using this graph, it can be seen that
the risk of recurrence is predictable and the clinician can
accurately counsel athletes, coaches, and parents regarding dislocations of the cervical vertebrae increased 204% to 4.14
return to play. per 100,000 exposures, and the rate of cervical injuries
The Torg ratio and other factors may have to be consid- associated with quadriplegia increased 116% to 1.58 per
ered prior to diagnosing a significant spinal stenosis and 100,000 exposures compared with data reported by
determining whether an athlete may continue to play. It Schneider and Kahn for the years 1959 through 1963.40
is important, however, that each case is evaluated on an During this same period, a decrease in the rate of intracranial
individual basis. hemorrhages (66%) and craniocerebral deaths (42%) was
noted (Figure 23-10).39 This shift in injury patterns—a
Sport-Specific Incidence of Cervical Trauma decrease in significant head injuries and an increase in cervi-
Football cal spine injuries—is probably attributable to changes in
Trauma to the cervical spine in football that produces sig- protective equipment used from the early 1960s to the early
nificant injuries is infrequent but often catastrophic. Torg, 1970s. During this period, better protection of the face and
in a retrospective review of the years 1971 through 1975,39 head were afforded by a change in face mask designs and
demonstrated that the rate of fractures, subluxations, or helmet technology. The protection provided by improved
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 557
.9
.8
.7
Probability of
Recurrence
.6
.5
.4
.3
.2
.1
0
6 7 8 9 10 11 12 13 14 15
MRI Disc Level Canal
Diameter (mm)
.9 Figure 23-10
.8 Intracranial and cervical spine injury fatalities, 1945-1988. (From
.7 Clarke KS: An epidemiologic view. In Torg JS, editor: Athletic injuries
Probability of
Recurrence
.6
to the head, neck and face, ed 2, St Louis, 1991, Mosby.)
.5
.4
.3
.2
.1
0
.3 .4 .5 .6 .7 .8 .9 1 1.1 1.2 1.3
X-ray Spinal Canal/Vertebral
Body Ratio
Figure 23-9
Graphs developed using logistic regression analysis in which the risk
of recurrence can be plotted as a function of the disc-level diameter
measured on magnetic resonance imaging (upper) and the spinal
canal/vertebral body ratio calculated on the basis of x-ray films
(lower). The construction of these plots is based on the result that
increased risk of recurrence is inversely correlated with the canal
diameter. Future cervical cord neurapraxia patients can be counseled
regarding their individual risk of recurrence based on the particular
size of their spinal canal. (From Torg JS, Corcoran AT, Thibault LE
et al: Cervical cord neurapraxia: Classification, pathomechanics,
morbidity and management guidelines, J Neurosurg 87:847, 1997.)
striking the word intentionally so that now all contact which have decreased the incidence of facial injuries, has
with the head as the initial point of contact is illegal for increased the incidence of cervical spine injury.
high school and college football.8 In addition, it was
made a “point of emphasis” by the American Football Winter Sports
Coaches Association in 2007 that game officials should Considering the number of individuals who participate in
call a foul when such incidences occur. winter sports, the incidence of injury is surprisingly low.
Traumatic cervical spine fractures, subluxations, and Reid and Saboe have reviewed spine injuries specific to
dislocations have continued to progressively decrease sports in Canada. Of 202 injuries reviewed, 25% (n 48)
since the 1976 rule change. Between 1976 and 1987, occurred from participation in winter sports.45 In their
the rate of severe cervical spine injuries decreased 70% at study, done in 1991, snowmobiling accounted for 10%,
the high school level and 65% at the collegiate level. The tobogganing for 6%, alpine skiing for 6%, and ice hockey for
largest rate change took place in 1977 and 1978, the 3% of the cervical spine injuries.
2 years after the rule change took effect. Injuries contin- Cervical spine injuries account for approximately 25% of
ued to decline until approximately 1984 and remained all spine fractures that occur in relation to snowmobiling.
the same during the next 3 years.41 Data for subsequent Injuries are often related to driving a snowmobile at night;
years, available through the National Center for being under the influence of alcohol; being unfamiliar with
Catastrophic Sports Injury Research, can be viewed in the terrain; or various operator errors, such as becoming air-
Figure 23-3.8 borne, colliding with objects, or tipping over. Toboggan
injuries frequently involve younger individuals. Approximately
Ice Hockey one third of the cervical spine fractures in tobogganing occur
In Canada, spinal cord injuries incurred as a result of playing in individuals younger than the age of 15. Collisions with
ice hockey were rare until approximately 1980. Prior to 1980, objects, becoming airborne, and demonstrating poor judg-
there was an average of two to three injuries per year. From ment account for most mechanisms of injury.
1982 to 1987, approximately 15 injuries per year were re- It has been estimated that spinal injuries account for
ported. Tator reviewed the literature available and docu- between 4% and 17% of all injuries to alpine skiers and snow-
mented a total of 117 cervical spine and spinal cord injuries boarders. Although this is low in comparison with other
between 1966 and 1987 in Canada.42 In a subsequent publi- orthopedic trauma, the catastrophic factor can be much
cation encompassing a longer period, reviewing the years higher. The incidence of significant spinal injury (lumbar and
1966 to 1993, Tator and colleagues43 reported a total of 241 cervical) is reported to be 1 for every 100,000 skier days for
spinal fractures and dislocations, 90% involving C1 to T1. skiing and 4 for every 100,000 snowboarder days.46,47 During
Between the years 1982 and 1993, an increased rate of spinal the course of two seasons (1994-1996), Tarazi and colleagues
column injury occurred equal to 16.8 per year. A total of 207 detailed 14 fractures associated with the cervical spine out of
players had good medical documentation. Based on this a total of 56 skier or snowboarders with spinal related injuries.
documentation, it has been reported that 8 players died, 108 A total of eight fractures were reported in skiers and six in
sustained permanent spinal cord injury, and the cord lesion snowboarders, with jumping being attributed as the major
was complete in 52 players. It has been reported that the cause of injury.46 In a longer-term retrospective review during
incidence of spinal cord damage and paralysis is three times 11 ski seasons, Floyd reported a total of 12 cervical fractures
greater in Canadian ice hockey than American football.8,43 or dislocations out of a total of 57 significant spinal injuries.47
Of these injuries, 70% occurred when a checked player col- The most common mechanisms of injury include attempting
lided headfirst with the boards; 73% of these injuries occurred a jump and landing poorly or losing control and hitting a tree.
during games, when the intensity of competition and check- Other factors are collisions with other skiers or objects. All of
ing from behind were the highest. Tator also attributed the these factors are related directly or indirectly to errors in judg-
increase in incidence since 1980 to better reporting mecha- ment and control, which often cannot be influenced by the
nisms, physical factors related to players (e.g., increased health care professional.
weight and speed of skating), social and psychological factors
among young hockey players (e.g., increased aggression and Water Sports
willingness to take risks), coaching attitudes and techniques Between 1964 and 1974, 152 of 1600 patients (9.5%)
(e.g., insufficient emphasis on conditioning, the risks of admitted to the Spinal Cord Injury Service at Rancho Los
hockey, and methods of protecting the spine from injury; Amigos Hospital were injured during recreational activities.
overemphasis on body contact), and small rinks with rigid Of these patients, 82 (54%) had been injured while diving.
boards. In an effort to prevent these injuries, rule changes The average depth of water into which these individuals
have been instituted prohibiting checking from behind and were diving was 5 feet (1.5 m). Surfing accounted for
checking an opponent who does not have control of the 29 injuries, and water skiing for seven.48 All of these indi-
puck.44 Unlike in football, Tator has stated that he has found viduals were injured by striking the head on the bottom of
no evidence that the increased use of helmets and face masks, the pool, lake, river, or ocean. As the head struck, the body
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 559
continued to progress forward, resulting in an axial loading gymnastic injuries and, more specifically, in injuries resulting
or compressive flexion injury. A typical vertical compression from the use of trampolines and mini-trampolines.55
load may result, although opinions vary.49 Cheerleading injuries have risen significantly since 1980 as
this activity has become more popular in the United States
Rugby and has increased in complexity and danger. The Consumer
Rugby is gaining popularity in North America, as evidenced Product Safety Commission reported an estimated 4954 hos-
by club- and varsity-level competition for men and women at pital emergency room visits in 1980 caused by cheerleading
universities and numerous recreational leagues. Injury data injuries. By 1986 the number had increased to 6911, to
must be drawn from the British Commonwealth countries, approximately 16,000 in 1994, to 21,906 in 1999, and to
where it is played on a large scale. 28,414 in 2004.8 Data from the National Center from
Retrospective data available for Australia and England Catastrophic Sports Injury Research between 1982 and 2002
between the years 1960 and 1985 demonstrates that 107 report 1.95 catastrophic injuries (0.6/100,000 participants).
injured patients were admitted to spinal cord centers in Of the 39 catastrophic injuries reported, 8 involved cervical
Australia50 and 82 injuries occurred in England from 1959 fractures or major ligament injuries and 3 involved spinal cord
through 1987.51 Injuries usually occurred from a collapsing contusions. Injury rates for college versus high school cheer-
scrum or from tackling. Hookers were the most often leaders demonstrate a 5:1 ratio.8
injured players in amateur play because of their position and Recent rule changes by the American Association of
its requirements during play. A rule change was initiated in Cheerleading Coaches and Administrators (AACCA) were
England in 1983 that reduced injuries from 10 the previous put in place in an effort to reduce the number of injuries.
season to 5 between 1986 and 1987. This change kept play- In 2006, the AACCA College Rules Committee restricted
ers on their feet and in a more upright position in the scrum 21⁄2-high pyramids, basket tosses, and other select skills
and the maul. Silver and Gill described the mechanisms of to be performed only on grass or matted surfaces. High
injury during rugby as the head being driven into the school teams, which were already restricted from perform-
ground or a blow to the head.51 Retrospective data pub- ing 21⁄2-high pyramids at all, were also restricted from per-
lished in the United States details similar results. Wetzler and forming basket tosses without a mat by the AACCA and
colleagues52 report that between 1970 and 1996 of the 62 National Federation of High Schools. In addition, The
significant cervical spine injuries that occurred in U.S. rugby, NCAA introduced legislation in 2006 requiring all colle-
36 (58%) happened during the scrum. During this portion giate cheerleading coaches to be safety-certified for their
of the rugby match, the head and neck of a player involved teams to qualify for the NCAA’s catastrophic insurance
in the scrum is in a flexed position and may have a compres- plan. Additional rules were added in 2008 to both the
sive load imposed upon it. Wetzler and colleagues52 provide AACCA College and National Federation of High School
great detail regarding the method of injury and possible Rules Committees standardizing basketball court rules
explanation of the mechanism of failure in their review. for these age levels, prohibiting released twisting skills and
inverted skills on this surface.
Gymnastics, Trampoline, and Cheerleading
Significant cervical spine injuries associated with gymnastics Mechanics and Pathomechanics
are predominantly associated with the use of the trampoline
as a training device. Of permanent spinal cord injuries to Mechanism of Injury
female gymnasts from 1973 through 1975, 70% were associ- Multiple mechanisms of injury may be responsible for cervi-
ated with the trampoline. Other pieces of apparatus may be cal fractures, subluxations, or dislocations. Numerous theo-
involved, however. During the same period, 33% of men’s ries have been proposed regarding the mechanism of injury
injuries were associated with the trampoline, 22% with the that is usually associated with sports. Purported mecha-
floor exercise and high bar, and 11% with the rings and mini- nisms of injury must withstand the scrutiny of research and
trampoline.53 More than 114 catastrophic injuries have been critical review. Although mechanisms such as hyperflexion
attributed to the use of a trampoline since the initial report and hyperextension are feasible, they have not withstood
by Ellis in 1960.54 These injuries are usually associated with such scrutiny. Even though injury may be possible from
a somersault and an uncontrolled landing.55 hyperflexion, hyperextension, or lateral bending and rota-
The incidence of injury led to a position paper by the tion, most of the force of these energies is absorbed by the
American Academy of Pediatrics in 1977.56 This paper cervical spine range of motion, strength of the musculature,
caused the American Alliance for Health, Physical Education intervertebral discs, and, to a lesser extent, the ligaments.
and Recreation and the NCAA Committee on Competitive Injuries that occur from these forces are most often sprains,
Safeguards and Medical Aspects of Sports to issue guidelines strains, or brachial plexus injuries, generally not fractures,
making use of the trampoline optional and voluntary, and subluxations, or dislocations.
specifically detailing safety and maintenance standards. Since Attempts have been made to associate equipment spe-
1978, a distinct decrease has been observed in all catastrophic cific to football with these mechanisms. It has been stated
560 SECTION III • Management of Sports Injury and Illness
that the face mask may cause hyperflexion with the ground felt. A member of the medical team often becomes the tar-
or an opponent; however, this was not reported to be the get of this shift. Any time members of the team are in a
factor in the more than 200 injuries that occurred between position to manage a catastrophic and potentially fatal
1971 and 1975.57 Various authors and researchers have also injury, they may be at risk of being accused of incompetence
demonstrated that the so-called guillotine effect of the hel- or negligence. Patterson60 and Heck and colleagues61 pro-
met (the posterior rim of the helmet impacts the cervical vide an excellent, concise discussion of the legal aspects of
spine during tackling or contact with another player) is not athletic injuries to the cervical spine.
implicated in football-related cervical spine fractures and General claims against the athletic or sports medicine
dislocations.22,23,58,59 staff usually concern instruction in proper technique, the
condition and appropriateness of equipment, the match-
ing of participants based on size and skill, supervision, or
Clinical Point postinjury care. Defensive responses to these claims in-
Current theory and evidence demonstrate that the most commonly
clude the assumption of risk by the competitor, statutory
acknowledged mechanism responsible for fracture-dislocation of the immunity, a release or waiver signed by the participant or
cervical spine in sports is that of axial loading in flexion. The factor parents, and the standard of reckless disregard.61 Whether
of axial loading is a common thread presented earlier in this chapter such defenses are successful in exonerating the medical
concerning the sport-specific incidence of injury. team of legal liability depends on the facts of each
particular case and the law of the state in which the legal
action is brought.
To be better positioned to both avoid and defend such
When the cervical spine is placed in a position of slight legal claims, the medical team must take reasonably pru-
flexion, there is a reduction of cervical lordosis, and the dent precautions to minimize the risk of injury for the
cervical spine is straightened (Figure 23-12). When an axial participant during practice or competition and to mini-
load is applied in this position (as may be the case with mize their own risk should catastrophic injury and the
spearing in football or diving into a shallow pool) (Figure possibility of litigation occurs. To minimize the athlete’s
23-13), the energy-absorbing and energy-dissipating mech- risk, all equipment should be in good repair, comply with
anisms afforded to the cervical spine through flexion, exten- standards set by the National Operating Committee on
sion, and lateral bending and rotation are reduced. Load Standards for Athletic Equipment, and be fit by appropri-
thus occurs on a segmented vertical column. When this ately trained personnel only (e.g., athletic trainer, equip-
load exceeds the energy-absorbing capacity of the vertebral ment manager, coach). All athletes should undergo a
bodies, intervertebral discs, posterior elements or liga- preseason physical examination that specifically includes
ments, failure and injury result. Injuries incurred may be questions relevant to previous cervical spine injuries and
crush fractures of the cervical vertebrae, buckling (which examination and screening of the cervical spine if the ath-
produces an acute flexion dislocation at one level), or a lete is involved in a collision sport. The medical staff must
combination of these two modes. The numerous anatomic make sure that a well-defined and well-communicated
and analytical modeling studies confirming this mechanism emergency plan is in place. Education, training, continu-
of injury have been reviewed by Otis and colleagues.57 ing practice and preparation are key elements to the
Because of the mechanics just described, it should be successful management of a true emergency situation.
obvious that the majority of cervical spine injuries in sports Recognized policies and procedures should be in place
that produce cervical fracture or fracture-dislocation, with and agreed on by all medical personnel, athletic adminis-
or without neurological involvement, are caused by cervical trators, coaches, and outside emergency medical person-
flexion with axial loading. Proper technique is critical in the nel such as EMTs or paramedics who will assist the sports
prevention of injury. Tackling or contact with the head in medicine staff. The appropriate equipment must be avail-
any collision sport (e.g., football, rugby, ice hockey) or div- able, readily positioned, and in good repair to allow for
ing into shallow water and striking the crown of the head appropriate management of catastrophic cervical spine
may produce catastrophic injury. These injuries are pre- injuries.3,62 Practice and competition venues should be
vented not by equipment, but by adherence to appropriate easily accessible to all emergency personnel.
technique, following the rules, and common sense.
A B
Figure 23-12
When the neck is flexed approximately 30° (A), the cervical spine becomes straight from the standpoint
of force, energy absorption, and effect on tissue deformation and failure. The straightened cervical spine,
when axially loaded, acts as a segmented column (B). (From Torg J: National Football Head and Neck
Injuries Registry: Report on the cervical quadriplegia from 1971-1975, Am J Sports Med 7:127, 1979.)
A B C D E F
Figure 23-13
Axial load applied to a segmented column initially results in deformation by compression. If the axial
load is large enough, more marked deformation occurs. Absorption of excessive amounts of energy
during this axially applied load may result in buckling, with resultant fracture or dislocation of the
segmented column.
562 SECTION III • Management of Sports Injury and Illness
Box 23-3 National Collegiate Athletic Association Sports Medicine Handbook—Guidelines to Use During
a Serious On-Field Player Injury
These guidelines have been recommended for National Football League officials and have been shared with National Collegiate Athletic Association
championships staff.
• Players and coaches should go to and remain in the bench area once medical assistance arrives. Adequate lines of vision between the
medical staffs and all available emergency personnel should be established and maintained.
• Players, parents, and nonauthorized personnel should be kept a significant distance away from the seriously injured player or players.
• Players or nonmedical personnel should not touch, move, or roll an injured player.
• Players should not try to assist a teammate who is lying on the field (i.e., removing the helmet or chin strap or attempting to assist breathing
by elevating the waist).
• Players should not pull an injured teammate or opponent from a pile-up.
• Once the medical staff begins to work on an injured player, they should be allowed to perform services without interruption or interference.
• Players and coaches should avoid dictating medical services to the athletic trainers or team physicians or taking up their time to perform such
services.
From National Collegiate Athletic Association: 2007–08 NCAA Sports Medicine Handbook 2007-08, p 11, Indianapolis, IN, 2007, National Collegiate Athletic Association.
immobilization, and transport of the athlete who has suffered situations. Hypothetical injury situations should be used so
a cervical spine injury—the physician, the athletic trainer, or that techniques of immobilization and transport may be
EMS personnel. Scenarios should be put in place in regard to practiced and everyone knows his or her role. Ensuring
who is going to assume emergency responsibilities if one proper training of staff and communication among all per-
member of the medical team mentioned previously is not in sonnel involved is the best way to guarantee appropriate
attendance. If responsibilities cannot be predetermined, management of this type of injury. On-the-job training at
trauma triage guidelines and legal regulations must be the time of the emergency is inappropriate.
followed regarding lines of authority. On-field management consists of injury recognition and
triage, situation management and immobilization of the cer-
vical spine, and transport.62 Only a small percentage of
sports-induced cervical spine injuries are significant and result
Clinical Point in permanent neurological deficit. Figure 23-14 and Figure
In any emergency situation, communication is the key factor. All 23-15 summarize and present algorithm-based action plans
professionals involved in this situation have the same primary goal: for significant cervical spine injury.
the safe, efficient management of a traumatic situation.
Clinical Caution
Prior to the start of the season, all protective equipment A cervical lesion without neurological deficit can easily become one
and emergency care equipment must be checked to make with a neurological deficit if it is improperly handled.28,67
sure that it is in good operational condition. Some members
of the team may be uncomfortable with the evaluation and
management of the cervical spine owing to the severity of
the consequences of significant injury or the potential for Suspicion of cervical spine injury may occur through
further damage if mishandled. Training sessions should be observation of the position of the head and neck at the
scheduled with all members of the sports medicine staff, time of the injury. If the mechanism of injury was not ob-
and local EMS personnel if possible. These training sessions served, observing whether the athlete is moving immediately
should assist in easing lack of confidence in handling specific following the injury will provide significant information
Algorithm – On-Field Evaluation of Cervical Spinal Injury: Neck Pain vs. Extremity Symptoms
Does athlete have neck pain? Does athlete have extremity symptoms?
No Yes Yes No
No Unilateral Bilateral
No
Figure 23-14
Algorithm for on-field evaluation of cervical spine injury: neck pain versus extremity symptoms. (From
Banerjee R, Palumbo MA, Fadale PD: Catastrophic cervical spine injuries in the collision sport athlete,
Part I—Epidemiology, functional anatomy and diagnosis, Am J Sports Med 32:1077-1087, 2004.)
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 565
Figure 23-15
Algorithm for suspicion of cervical spine injury.
about the severity of the injury. Most athletes will move after responsiveness. Responsiveness and consciousness determine
injury if they are able. An athlete lying completely still fol- the next sequence of events (see Chapter 18 in Orthopedic
lowing injury is an indication that a potentially significant Physical Assessment, 5th edition, another book in this series).
injury has occurred. Teammates of the injured athlete
should be instructed not to move or touch the athlete until Clinical Note
the clinician has determined exactly what is wrong.
The clinician’s initial duty is to establish the responsiveness On reaching the injured athlete, responsiveness, airway, breathing,
of the athlete while stabilizing the athlete’s cervical spine. It is and circulation must be always be established.
imperative that the athlete not be moved while checking for
566 SECTION III • Management of Sports Injury and Illness
Figure 23-16
Plastic pieces that hold face masks in place may be cut with a razor knife or other commercially available
products, or may require the use of an electric screwdriver to allow the face mask to swing out of the
way, enabling access to the athlete’s airway without removal of the helmet.
Continued
568 SECTION III • Management of Sports Injury and Illness
Clinical Caution
When dealing with spinal injury, the sports medicine team should
always err on the side of caution. If any doubt exists, immobilize the
athlete on a spine board.
Figure 23-17
Plastic backboard and scoop stretcher.
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 569
A B
Figure 23-18
A, Appropriate grasp and immobilization of the athlete’s head and neck. The member of the team
immobilizing the head and neck must make sure that when the athlete is rolled into a supine position,
the hands are not crossed and the team member is able to maintain appropriate support for the duration
of the time required to fully immobilize the athlete. B, Appropriate logrolling technique. Sufficient
support of the entire body with assistance in placing the backboard in the best position is needed to
prevent moving the athlete a second time to place him or her in the center of the board.
same side of the injured player. The team leader is still athlete’s neck and the ends are brought together and
responsible for immobilization and control of the head and secured. After some type of cervical support is applied as
neck. A fourth assistant is responsible for repositioning the described earlier, the athlete’s torso is secured to the spine
board under the athlete. The athlete is lifted and lowered board prior to securing the head.72 Areas around the ath-
on command of the leader to a height sufficient to allow the lete’s legs and in the lumbar area are padded to remove
spine board or vacuum mattress to be repositioned under any room between the athlete and strapping system when
the athlete. using a spine board. This minimizes any movement of the
athlete’s torso relative to the board. After the athlete’s
torso is secured, the head and neck are secured. A foam
Clinical Caution block, a rolled-up blanket, or towels are placed around the
The spine board or vacuum mattress is moved relative to the head when securing the athlete to a spine board to assist
athlete. The athlete is not moved in any direction other than verti- in immobilization (Figure 23-20).
cally. This minimizes movement of the athlete and the potential for If a vacuum splint or mattress system is being used, the
complications. head may be sufficiently immobilized without use of
the towel or blanket roll. This additional padding is not
necessary when using the vacuum mattress system and
vacuum cervical collar, as they may be brought in close
proximity to the athlete prior to removing the air from
The athlete’s vital signs, level of consciousness, and the system. Together these create a rigid support (Figure
neurological status are monitored by the team leader 23-21). As with any system of spine immobilization, suffi-
throughout the procedure of positioning the athlete on cient personnel are required to carry out the task, minimiz-
the spine board. At this time, extrication or other type of ing the chances of further injury to the athlete. Care is
rigid collar should be applied to assist in immobilization of taken to maintain appropriate access to the athlete’s airway,
the head and neck if the athlete is not wearing a helmet should it be required.
(Figure 23-19).72 Commercially available cervical collars Throughout the procedure of applying an extrication
may not fit if an athlete is wearing a helmet or shoulder collar, blanket roll, or vacuum immobilization system,
pads. In this situation the head is blocked with foam longitudinal support and control of the head are main-
blocks that may be incorporated as part of the backboard tained by the team leader. Only after the athlete’s head
immobilization. If these are not available, a towel or blan- and neck are secured to the immobilization device does
ket roll should be substituted when immobilized on the the team leader relinquish control of the head and neck.
spine board.68 The towel roll or blanket is slid under the Once the athlete has been secured, he or she is lifted
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 571
Figure 23-19
Application of an extrication collar with the athlete in a supine position. This type of collar cannot
usually be used if the athlete is wearing a helmet.
using the immobilization device and transported to athlete to seek medical attention. Other reasons included
the appropriate emergency medical facility for further polytrauma and altered levels of consciousness. The inci-
management. dence of a delay in diagnosis of trauma in the cervical spine
is estimated to be approximately 30%. It should also be
noted that approximately 50% to 60% of spine-injured pa-
Emergency Department Management tients have an associated nonspinal injury.83
The goals of emergency department management of ath- It has been estimated that 5% to 10% of spinal cord
letes with suspected cervical spine trauma are to (1) avoid, injuries occur in the immediate postinjury period.84
if present, further damage to the spinal cord; (2) prevent Extreme care must be exercised when moving and trans-
injury to uninjured tissues; (3) assess the athlete for neuro- porting athletes with possible cervical trauma. Immobili-
logical injury; and (4) image the cervical spine for the pres- zation of the cervical spine must be maintained during
ence of fractures, dislocations, instability, or disc hernia- examination and imaging until an unstable cervical spine
tions. The dictum of “do no harm” certainly applies. Early injury is ruled out. This immobilization includes a spine
pharmacological treatment can be instituted and the appro- board, cervical collar, or other appropriate stabilization
priate neurosurgical and orthopaedic consultations obtained devices. If a helmet is in place, it should remain on during
for definitive treatment and stabilization. transport; however, the face mask must be removed as
It is important to maintain a high suspicion for cervical previously discussed. The helmet can be useful in assisting
spine injury and obtain a prompt diagnosis. In one series,82 with stabilization of the cervical spine during transport.
a delay in diagnosis of spine trauma led to a 10% incidence In addition, removal of the helmet requires significant
of secondary neurological deficits. Patients with a spine in- motion of the cervical spine. Therefore, it is best to
jury diagnosed on initial evaluation had a much lower exclude unstable fractures prior to removal, if possible. In
(1.5%) incidence of secondary neurological injury. Reasons the presence of cervical spine injury, the helmet should be
for a delay in diagnosis included failure to obtain a radio- removed only in the emergency department setting by
graph, missing a fracture on a radiograph, or failure of the personnel trained in the care of such injuries.
572 SECTION III • Management of Sports Injury and Illness
Figure 23-20
A, Athlete secured to backboard with a foam block incorporated into the backboard system. B, A towel or
blanket roll appropriately placed around the head and neck for immobilization if other types of material for
securing the head and neck are not available.
Figure 23-21
Athlete immobilized in a vacuum cervical collar and mattress.
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 573
or exclude grossly unstable cervical spine fractures and to of the player’s head and neck should be reapplied as the
check for the presence of prevertebral soft tissue swelling. head is released from the spine board. This is accomplished
Cervical spine alignment is determined by four parallel lines by having an assistant place his or her fingers on each side
running along the anterior surface of the vertebral bodies, of the mandible around the helmet. At this time the head
the posterior border of the vertebral bodies, the posterior and neck are stabilized by placing one hand behind the
surface of the facet joints, and the spinolaminar interfaces.88 athlete’s neck and exerting pressure along the occiput, and
The lateral view is also used to assess vertebral body height placing the other hand along the mandible. The helmet is
and disc spaces, as well as the spinal canal diameter and the removed by unsnapping the cheek pads and expanding it
atlas-dens interval. laterally to clear the ears. After it is removed, longitudinal
The open-mouth view is used specifically to examine the manual stabilization should be maintained by placing one
atlantoaxial vertebrae for fractures or abnormal relationships hand on each side of the head with the fingers under the
that may indicate rotary subluxation. The other anteroposte- angle of the mandible and in the proximity of the mastoid
rior view is used to visualize from C3 to C7. This view dem- process (Figure 23-22). The shoulder pads may then be
onstrates the tracheal air shadow (which should be in midline) removed by cutting all straps and slipping them off the ath-
and the alignment of the pedicles, spinous processes, and lete, being careful not to disturb the position of the head
articular masses. Oblique projections are used to give addi- and neck. Cervical spine films are repeated if appropriate
tional information about the facet joints and to image neural visualization was not obtained with the helmet and shoul-
foramen. Readers are referred to the text by Harris for a com- der pads in place.
plete description of evaluation cervical spine films, which is
beyond the scope of this chapter.89 Intervention
Other imaging studies include tomograms, which can be When spinal cord injury is present, prompt consideration
used to look for subtle fractures in areas of super-imposed should be given to early pharmacological treatment.3
bony structures. Computed tomography (CT) provides Although there has been much controversy about the safety
axial images that can be used to better evaluate subtle and efficacy of various treatments, animal studies and clinical
fractures and to image areas not well visualized on plain trials have demonstrated the value of some agents. A random-
radiographs. In addition to axial images, three-dimensional ized controlled clinical trial of methylprednisolone, a cortico-
reconstructions can be done to image complex fractures. steroid, demonstrated some efficacy of this agent following
Myelography alone or in combination with CT scans can be acute spinal cord injury.91 Patients in this study were given a
used to evaluate for any cord or nerve root compression. 30-mg/kg dose of methylprednisolone, followed by 5.4 mg/
Magnetic resonance imaging techniques can be used to kg/hr given by continuous drip for a total of 23 hours. Theo-
obtain sagittal, axial, and coronal views of bony elements, retically, steroids will reduce the degree of edema in injured
intervertebral discs, the spinal cord, cerebrospinal fluid, spinal cord tissues. Other drugs that may be of possible ben-
ligaments, and other anatomical structures. efit to spinal cord–injured patients include opiate antagonists
Flexion and extension lateral views of the cervical spine such as thyrotropin-releasing hormone and opiate receptor
can be obtained to look for ligamentous instability. These antagonists such as naloxone.
views should be obtained only after an unstable fracture Once an unstable cervical spine injury is detected, prompt
pattern has been excluded and should be done with volun- involvement of specialists trained in definitive management of
tary motion. They are contraindicated in patients with such injuries is instituted. Although the individuals involved
neurological injury and those with altered states of con- vary among institutions, generally an orthopaedic surgeon
sciousness. These views are useful in assessing not only manages further stabilization and a neurosurgeon is involved
acute ligamentous instability, but also late cervical spine if significant neurological injury is present. Stabilization pro-
instability following traumatic injury. White and Punjabi cedures completed in the emergency department include ap-
have defined stability of the lower cervical spine as “the abil- plying traction through either a halo ring or the more rapidly
ity of the spine to limit the patterns of displacement under applied Gardner-Wells tongs. In some cases traction may be
physiologic stress so as not to damage or irritate the spinal the definitive treatment, or it may be preliminary to surgical
cord or nerve roots.”90 Radiographically, this displacement stabilization. The halo ring can also be connected to a vest
has been defined as angular displacements of 11° more than apparatus for long-term immobilization.
visualized in adjacent vertebral segments, or sagittal plane
displacements of one segment in relationship to another of Return-to-Play Considerations
greater than 3.5 mm.
and Contraindications
Helmet and Shoulder Pad Removal Following a cervical spine injury the sports medicine staff
Helmet and shoulder pad removal is often required to is often asked by the athlete “When can I return to play?”
obtain full radiographic evaluation and has been well- Whether or not an athlete can return to play and assume
summarized by Denegar and Saliba.68 Manual stabilization the risk of potential recurrence of what could be a
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 575
Figure 23-22
Helmet removal. Care is taken to manually support and immobilize the head and cervical spine. The
cheek pads are carefully removed and the helmet is spread laterally prior to removal.
catastrophic injury is not an easy question to answer. The on less than unequivocally substantiated data regarding risk
over-riding factor relative to return to play following cer- as documented in the literature or by anecdotal evidence,
vical spine injury has been that the individual is neuro- and absolute contraindication as a condition in which recog-
logically intact, asymptomatic, pain free, and has full nized factors are documented in the literature or known
strength and range of motion. Although these physical on the basis of experience. However, clinicians should keep
examination factors may be present, there may continue to in mind at all times Torg’s statement: “The criteria for
be an underlying risk for recurrence. Providing the best return to contact activities in the presence of cervical spine
advice for the indications and contraindications relative to abnormalities or post injury are intended as guidelines only.
return to play based on evidence has been, and continues Owing to the lack of credible scientific evidence, they are for
to be, difficult. the most part predicated on anecdotal experience at best.” 92
Until recently, the literature concerning cervical spine Tables 23-3 to 23-8 provided by Torg, a leading authority
injuries has centered around diagnosis and treatment. Com- in the area of cervical spine trauma in athletics, provide a
prehensive guidelines regarding the return to sports that valuable resource for sports medicine clinicians who must
place an athlete at risk for a potentially catastrophic cervical provide advice to athletes regarding to play.
spine injury have been lacking. Torg has recently published
a report to describe the developmental and post-traumatic
conditions of the cervical spine that might present as no
Conclusion
contraindication, a relative contraindication, or an absolute Injuries to the cervical spine associated with sports have the
contraindication to continued participation.92 Torg defines potential to cause severe spinal cord trauma or quadriplegia;
no contraindication as a condition in which no recognized they may even prove to be fatal. It is therefore imperative
risk factors are documented in the literature or known on that the sports medicine team be well skilled in on-field
the basis of anecdotal evidence, relative contraindication as emergent care management, immobilization, transporta-
a condition in which permitting return to play is predicated tion, and emergency department management of these
576 SECTION III • Management of Sports Injury and Illness
Table 23-3
Congenital Conditions: Contraindications to Return to Athletic Activity
Contraindication
Congenital Condition None Relative Absolute
Odontoid agenesis X
Odontoid hypoplasia X
Os odontoideum X
Spina bifida occulta X
Atlanto-occipital fusion X
Klippel-Feil anomaly
Type I: X
Mass fusion of the cervical and upper thoracic vertebrae
Type II: X
Fusion of only one or two interspaces at C3 and below with full cervical range of motion
and not occipitocervical abnormalities, instability, disc disease, or degenerative changes
From Torg JS: Cervical spine injuries and return to football, Sports Health 1:376-383, 2009.
Table 23-4
Developmental Conditions: Contraindications to Return to Athletic Activity
Contraindication
Developmental Condition None Relative Absolute
Stenosis of the cervical spine (i.e., one or more vertebrae with a canal-vertebral ratio of 0.8)
Spinal Stenosis of the cervical spine and no other symptoms X
Spinal Stenosis of the cervical spine and motor or sensory manifestations of cervical cord neurapraxia X
Spinal Stenosis of the cervical spine and documented episode of cervical cord neurapraxia X
associated with ligamentous instability, magnetic resonance imaging evidence of neurological
damage lasting longer than 36 hours, or multiple recurrence
Spear-tacklers spine: Developmental stenosis of the cervical canal; persistent straightening or X
reversal of the normal cervical lordotic curve; pre-existing post-traumatic roentgenographic
abnormalities of the cervical spine; a history of prior root or cord neurapraxia and
documentation of the patient’s using the spear-tackling technique
From Torg JS: Cervical spine injuries and return to football, Sports Health 1:376-383, 2009.
Table 23-5
Traumatic and Ligamentous Injuries of the Upper and Middle/Lower Cervical Spine: Contraindications to Return to Athletic Activity
Contraindication
Upper Cervical Spine: Traumatic Injuries None Relative Absolute
From Torg JS: Cervical spine injuries and return to football, Sports Health 1:376-383, 2009.
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 577
Table 23-6
Fractures: Contraindications to Return to Athletic Activity
Contraindications
Fractures None Relative Absolute
Healed, stable compression fractures of the vertebral body in an asymptomatic patient with no X
evidence of neurologic-injury and full, pain-free range of cervical motion: These fractures can
settle and cause increased deformity. Patients with this type of fracture should be carefully
observed.
Healed, stable end plate fractures without involvement of the ligamentous or posterior bony X
structures in asymptomatic patients with no evidence of neurologic-injury and full, pain-free
range of cervical motion
Healed, stable spinous process “clay shoveler” fractures in an asymptomatic patient with no X
evidence of neurologic-injury and full, pain-free range of cervical motion
Healed, stable fractures involving the elements of the posterior neural ring in asymptomatic X
patients with no evidence of neurologic-injury and full, pain-free range of cervical motion:
Because a rigid ring cannot break in one location, healing of paired fractures of the ring must
be evident on x-ray and imaging studies
Acute fractures of the vertebral body or posterior bony structures with or without associated X
ligamentous laxity
Vertebral body fractures with evidence of a sagittal component on anteroposterior radiographs X
Vertebral body fractures with or without displacement associated with posterior arch fractures X
or ligamentous laxity
Comminuted vertebral body fractures with displacement into the spinal canal X
Any healed fracture of the vertebral body or the posterior bony structures; in patient with X
associated pain, evidence of neurologic injury and limitation of cervical motion
Healed, displaced fractures involving the lateral masses with resulting facet incongruity X
From Torg JS: Cervical spine injuries and return to football, Sports Health 1:376-383, 2009.
Table 23-7
Intervertebral Disc Injuries: Contraindications to Return to Athletic Activity
Contraindication
Injury None Relative Absolute
Healed anterior or lateral disc herniation that is treated conservatively in patients who are X
asymptomatic; have no evidence of neurological injury; and have full, pain-free range of
cervical motion
Lateral or central disc herniation that has been treated with intervertebral diskectomy and X
interbody fusion in patients who have a solid fusion; are asymptomatic; have no evidence of
neurological injury; and have full, pain-free range of cervical motion
Acute or chronic cervical disc herniation in patients with associated neurological findings, pain, X
or significant limitation of cervical motion
From Torg JS: Cervical spine injuries and return to football, Sports Health 1:376-383, 2009.
578 SECTION III • Management of Sports Injury and Illness
Table 23-8
Status Following Cervical Fusion: Contraindications to Return to Athletic Activity
Contraindication
Status None Relative Absolute
Stable single-level anterior or posterior fusion in patients who are asymptomatic; have no X
evidence of neurological injury; and have full, pain-free range of cervical motion
Stable two- or three-level fusion in patients who are asymptomatic; have no evidence of X
neurological injury; and have full, pain-free range of cervical motion
Anterior or posterior fusion of four or more levels; because of the increased stresses on the X
articulations of the adjacent vertebrae and the propensity for the development of degenerative
changes at these levels, these patients (with only rare exception) should not be permitted to
return to athletic activity
Any fusion for instability of C1 regardless of roentgenographic evidence of successful fusion X
From Torg JS: Cervical spine injuries and return to football, Sports Health 1:376-383, 2009.
injuries. Management of the injury by the sports medicine 11. Hirasawa Y, Sakakida K: Sports and peripheral nerve injury, Am J
team, in whom the injured athlete is placing his or her trust, Sports Med 11:420–426, 1983.
must be efficient and flawless to minimize the consequences 12. Takazawa H, Sudo N, Akoi K, et al: Statistical observation of nerve
of traumatic cervical spine injuries. Policies, procedures, and injuries in athletes (in Japanese), Brain Nerve Injury 3:11–17, 1971.
13. Hershman EB: Brachial plexus injuries, Clin Sports Med 9:311–329,
protocols for the management of these injuries should be in 1990.
place for all organized athletic teams and organizations. The 14. Clancy WG, Brand RL, Bergfeld JA: Upper trunk brachial plexus
sports medicine team should practice techniques involved in injuries in contact sports, Am J Sports Med 5:209–214, 1977.
on-field emergent care, immobilization, and transportation 15. Clancy WG: Brachial plexus and upper extremity peripheral nerve
at least once each year. injuries. In Torg JS, editor: Athletic injuries to the head, neck and
face, Philadelphia, 1982, Lea & Febiger.
16. Markey KL, Di Bennedetto M, Curl WW: Upper trunk brachial
plexopathy: The stinger syndrome, Am J Sports Med 21:650–655,
References 1993.
1. National Spinal Cord Injury Statistical Center: Spinal cord informa- 17. Sallis FE, Jones K, Knopp W: Burners: Offensive strategy for an
tion network: Facts and figures at a glance—Update January 2008, under-reported injury, Phys Sports Med 20:47–55, 1997.
University of Alabama Birmingham; accessed at www.spinalcord. 18. Safran MR: Nerve injury about the shoulder in athletes, Part I—
uab.edu. suprascapular nerve and axillary nerve, Am J Sports Med 32:
2. Keenen TL, Benson DR: Initial evaluation of the spine injured 803–819, 2004.
patient. In Browner BD, Juputer JB, Levine AM, Tafton PG, 19. Safran MR: Nerve injury about the shoulder in athletes, Part II—
editors: Skeletal trauma, Philadelphia, 1992, WB Saunders. Long thoracic nerve, spinal accessory nerve, burners/stingers,
3. Kleiner DM, Almquist JL, Bailes J, et al: Prehospital care of the thoracic outlet syndrome, Am J Sports Med 32:1063–1076, 2004.
spine-injured athlete: A document from the Inter-Association Task 20. Glasgow SG: Upper cervical spine injuries (C1–C2). In Torg J, editor:
Force for Appropriate Care of the Spine Injured Athlete, Dallas, TX, Athletic injuries to the head, neck and face, St Louis, 1991, Mosby.
2001, National Athletic Trainers Association. 21. Torg JS, Treux R, Quedenfeld TC, et al: The National Football
4. Banerjee R, Palumbo MA, Fadale PD: Catastrophic cervical spine Head and Neck Injury Registry: Report and conclusions 1978,
injuries in the collision sport athlete—Part 2, Am J Sports Med JAMA 241:1477–1479, 1979.
32:1760–1764, 2004. 22. Torg JS, Vegso JJ, Sennett B, et al: The National Football Head
5. Torg JS, Quedenfeld TC, Bustein A, et al: National Football and Neck Injury Registry: 14 year report on cervical quadriplegia,
Head and Neck Injury Registry: Report on cervical quadriplegia 1971–1984, JAMA 254:3439–3443, 1986.
1971–1975, Am J Sports Med 7:127–132, 1979. 23. Torg JS, Treux RC, Marshall J, et al: Spinal injury at the third and
6. Schneider RC: Serious and fatal neurosurgical football injuries, fourth cervical vertebrae from football, J Bone Joint Surg Am
Clin Neurosurg 12:226–236, 1966. 59:1015–1019, 1977.
7. Schneider RC: Head and neck injuries in football, Baltimore, 24. Torg JS, Pavlov H: Middle cervical spine injuries (C3 and C4). In
1973, Williams & Wilkins. Torg JS, editor: Athletic injuries to the head, neck and face,
8. Mueller FO, Cantu RC: Annual survey of catastrophic football St Louis, 1991, Mosby.
injuries, National Center for Catastrophic Sport Injury Research, 25. Shields CL, Fox JN, Stauffer ES: Cervical cord injuries in sports,
University of North Carolina, Chapel Hill, NC; accessed at Phys Sports Med 6:71–76, 1978.
http://www.unc.edu/depts/nccsi/). 26. Allen BL, Ferguson RL, Lehmann TR, et al: A mechanistic classi-
9. Clarke KS: An epidemiologic view. In Torg J, editor: Athletic fication of closed, indirect fractures and dislocations of the lower
injuries to the head, neck and face, St Louis, 1991, Mosby. cervical spine, Spine 7:1–5, 1982.
10. Boden BP, Tacchetti RL, Cantu RC, et al: Catastrophic cervical 27. Leventhal MR: Management of lower cervical spine injuries.
spine injuries in high school and college football players, Am J In Torg J, editor: Athletic injuries to the head, neck and face,
Sports Med 34:1223–1232, 2006. St Louis, 1991, Mosby.
Traumatic Sports Injuries to the Cervical Spine • CHAPTER 23 579
28. Banerjee R, Palumbo MA, Fadale PD: Catastrophic cervical spine 51. Silver JR, Gill G: Injuries of the spine sustained during rugby,
injuries in the collision sport athlete, Part I—Epidemiology, func- Sports Med 5:328–334, 1988.
tional anatomy and diagnosis, Am J Sports Med 32:1077–1087, 52. Wetzler MJ, Akpta T, Laughlin W, et al: Occurrence of cervical
2004. spine injuries during the rugby scrum, Am J Sports Med 26:
29. Torg JS, Pavlov H, O’Neil MJ, et al: The axial load teardrop frac- 177–180, 1998.
ture: A biomechanical, clinical and roentgenographic analysis, Am 53. Clarke K: Survey of spinal cord injuries in schools and college
J Sports Med 19:355–364, 1991. sports, 1973–1975, J Safety Res 9:140, 1977.
30. Torg JS, Pavlov H, Genuario SE, et al: Neurapraxia of the cervical 54. Ellis WG, Green D, Holzaepfel NR, Sahs AL: The trampoline and
spinal cord with transient quadriplegia. J Bone Joint Surg Am serious neurological injuries: A report of five cases, JAMA 174(13):
68:1354–1370, 1986. 1673-1676, 1960.
31. Torg JS, Fay CM: Cervical stenosis with cord neurapraxia and 55. Torg JS: Trampoline induced cervical quadriplegia. In Torg J, editor:
transient quadriplegia. In Torg J, editor: Athletic injuries to the Athletic injuries to the head, neck and face, St Louis, 1991, Mosby.
head, neck and face, St Louis, 1991, Mosby. 56. American Academy of Pediatrics, Committee on Accident and
32. Torg JS, Guille JT, Jaffe S: Injuries to the cervical sine in American Poison Prevention: Trampolines, Evanston, IL, 1977, American
football players, J Bone Joint Surg Am 84:112–122, 2002. Academy of Pediatrics.
33. Torg JS, Pavlov H: Cervical spinal stenosis with cord neurapraxia 57. Otis JC, Burstein AH, Torg JS: Mechanisms and pathomechanics
and transient quadriplegia, Clin Sports Med 6:115–133, 1987. of athletic injuries to the cervical spine. In Torg J, editors: Athletic
34. Torg JS, Corcoran AT, Thibault LE, et al: Cervical cord neurapraxia: injuries to the head, neck and face, St Louis, 1991, Mosby.
Classification, pathomechanics, morbidity and management guide- 58. Virgin H: Cineradiographic study of football helmets and the
lines, J Neurosurg 87:843–850, 1997. cervical spine, Am J Sports Med 8:310–317, 1980.
35. Pavlov H, Torg JS, Robie B, et al: Cervical spinal stenosis: Deter- 59. Carter DR, Frankel VH: Biomechanics of hyperextension injuries
mination with vertebral body ratio method, Radiology 164: to the cervical spine in football, Am J Sports Med 8(5):302–319,
771–774, 1987. 1980.
36. Odor JM, Watkins RG, Dillin WH, et al: Incidence of cervical 60. Patterson D: Legal aspects of athletic injuries to the head and
spinal stenosis in professional and rookie football players, Am J cervical spine. In Torg J, editor: Athletic injuries to the head, neck
Sports Med 18:507–509, 1990. and face, St Louis, 1991, Mosby.
37. Herzog RG, Wiens JJ, Dillingham MF, et al: Normal cervical 61. Heck FJ, Weiss MP, Gartland JM, et al: Minimizing liability risks
spine morphometry and cervical spinal stenosis in asymptomatic of head and neck injuries in football, J Athl Training 29:128–139,
professional football players, Spine 16:178–186, 1991. 1994.
38. Torg JS, Naranja RJ, Pavlov H, et al: The relationship of develop- 62. Bailes JE, Petschauer M, Guskiewicz KM, et al: Management of
mental narrowing of the cervical spinal canal to reversible and cervical spine injuries in athletes. J Athl Training 42:126–134,
irreversible injury of the cervical spinal cord in football players, 2007.
J Bone Joint Surg Am 78:1308–1314, 1996. 63. National Collegiate Athletic Association: 2007-08 NCAA Sports
39. Torg JS: Epidemiology, biomechanics and prevention of cervical Medicine Handbook 2007–08, Indianapolis, IN, 2007, National
spine trauma resulting from athletics and recreational activities, Collegiate Athletic Association.
Oper Tech Sports Med 1:159–168, 1993. 64. National Football League: Guidelines for game officials to use
40. Schneider RC, Kahn EA: Serious and fatal neurosurgical football during a serious on-field player injury, New York, 1999, National
injuries, Clin Neurosurg 12:226–236, 1966. Football League.
41. Torg JS, Vegso JJ, O’Neill J, et al: The epidemiologic, pathologic, 65. Banerjee R, Palumbo MA, Fadale PD: Catastrophic cervical spine
biomechanical and cinematographic analysis of football induced injuries in the collision sport athlete, Am J Sports Med 32:
cervical spine trauma, Am J Sports Med 18:50–57, 1990. 1760–1764, 2004.
42. Tator CH: Injuries to the cervical spine and spinal cork resulting 66. Feld F: Management of the critically injured football player, J Athl
from ice hockey. In Torg J, editor: Athletic injuries to the head, Training 28:206–212, 1993.
neck and face, St Louis, 1991, Mosby. 67. Vegso JJ, Torg JS: Field evaluation and management of cervical
43. Tator CH, Carson JD, Edmonds VE: Spinal injuries in ice hockey, spine injuries. In Torg J, editor: Athletic injuries to the head, neck
Clin Sports Med 17:183–194, 1998. and face, St Louis, 1991, Mosby.
44. Tator CH, Edmonds VE, Lapczak L. Spinal injuries in ice hockey: 68. Denegar C, Saliba E: On field management of the potentially
A review of 182 North American cases and analysis of etiologic cervical spine injured athlete, J Athl Training 24:108–111,
factors. In Castalki CR, Bishop PJ, Hoerner ER, editors: Safety 1989.
in ice hockey, Vol 2, Philadelphia, 1993, American Society for Test- 69 Feld F, Blanc R: Immobilizing the spine injured football player,
ing and Materials. J Emerg Med Serv 12:38–40, 1987.
45. Reid DC, Saboe LA: Spine injuries resulting from winter sports. 70. Feld F: Management of the critically injured football player, J Athl
In Torg J, editor: Athletic injuries to the head, neck and face, Training 28:206–212, 1993.
St Louis, 1991, Mosby. 71. Segan RD, Cassidy C, Bentkowski J: A discussion of the issue of
46. Tarazi F, Dvorak MF, Wing PC: Spinal injuries in skiers and snow- football helmet removal in suspected cervical spine injuries, J Athl
boarders, Am J Sports Med 27:177–180, 1999. Training 28:294–305, 1993.
47. Floyd T: Alpine skiing, snowboarding and spinal trauma, Arch 72. Heckman JD: Emergency care and transportation of the sick and
Orthop Trauma Surg 121:433–436, 2001. injured, ed 5, Rosemont, IL, 1993, American Academy of Ortho-
48. Shields CW, Fox JM, Stouffer ES: Cervical cord injuries in sports. paedic Surgeons.
Phys Sports Med 6:71–76, 1978. 73. DeLorenzo RA, Olson JE, Boska M, et al: Optimal positioning
49. Torg JS: Injuries to the cervical spine and cork resulting from for cervical immobilization, Ann Emerg Med 28:301–308,
water sports. In Torg J, editor: Athletic injuries to the head, neck 1996.
and face, St Louis, 1991, Mosby. 74. Tierney RT, Mattacola CG, Sitler MR, et al: Head position and
50. Taylor TKF, Coolican MRJ: Spinal cord injuries in Australia foot- football equipment influence cervical spinal-cord space during
ball, 1960–1985, Med J Aust 147:112–118, 1987. immobilization, J Athl Training 37:185–189, 2002.
580 SECTION III • Management of Sports Injury and Illness
75. La Prade RF, Schentzler KA, Broxterman JR, et al: Cervical spine 83. Benson DR, Keenen TL, Antony J: Unsuspected associated lesions
alignment in the immobilized hockey player: A computed tomo- in the fractured spine, Presented at the Orthopaedic Trauma
graphic analysis of the effects of helmet removal, Am J Sports Med Association Meeting, Dallas, TX, October 1988.
28:800–803, 2000. 84. Castelano V, Bocconi FL: Injuries of the cervical spine with spinal
76. Metz CM, Kuhn JE, Greenfield ML: Cervical spine alignment in cord involvement (myelic fractures): Statistical considerations, Bull
immobilized hockey players: Radiographic analysis with and without Hosp Joint Dis 31:188–194, 1970.
helmets and shoulder pads, Clin J Sports Med 8:92–95, 1998. 85. Davidson RM, Burton JH, Snowise M, et al: Football protective
77. Donaldson WF, Laureman WC Heil B, et al: Helmet and shoulder gear and cervical spine imaging, Ann Emerg Med 38:26–30,
pad removal from a player with suspected cervical spine injury, 2001.
Spine 23:1729–1733, 1998. 86. Hollengerg GM, Beitia AO, Tan RK, et al: Imaging of the cervi-
78. Prinzen RK, Syrotuik DG, Reid DC: Position of the cervical ver- cal spine in sports medicine, Curr Sports Med Rep 2:33–40,
tebrae during helmet removal and cervical collar application in 2003.
football and hockey, Clin J Sports Med 5:155–161, 1995. 87. Waeckerle FJ, Kleiner DM: Protective athletic equipment and
79. Swenson TM, Lauerman WF, Donaldson WF, et al: Cervical spine cervical spine imaging, Ann Emerg Med 38:26–30, 2001.
position in the immobilized football player—radiographic analysis 88. Pavlov H, Potter HG: Imaging techniques applicable to athleti-
before and after helmet removal, Med Sci Sports Exerc cally induced cervical spine trauma, Oper Tech Sports Med 1:
26(suppl):S148, 1994. 169–182, 1993.
80. Hulstyn MS, Palumbo MA, Fadale PD, et al: The effect of protec- 89. Harris JH: The radiology of acute cervical spine trauma, ed 2,
tive football equipment on alignment of the injured cervical spine: Baltimore, 1987, Williams & Wilkins.
Radiographic analysis in a cadaveric model. Presented at American 90. White AA, Punjabi MM: Clinical biomechanics of the spine,
Orthopaedic Society of Sports Medicine, Toronto, Canada, July Philadelphia, 1978, JB Lippincott.
1995, Abstracts, p 27. 91. Bracken MB, Shepard MJ, Collins WF, et al: A randomized
81. Shriger DK: Immobilizing the cervical spine in trauma: Should we controlled trial of methylprednisolone or naloxone in the treat-
seek an optimal position or an adequate one? Ann Emerg Med ment of spinal cord injury, N Engl J Med 322:1405–1411,
28:351–353, 1996. 1990.
82. Reid DC, Henderson R, Saboe L, et al: Etiology and 92. Torg JS: Cervical spine injuries and return to football, Sports
clinical course of missed spine fractures, J Trauma 27:980–986, Health 1:376–383, 2009.
1987.
24
CHAPTER
MAXILLOFACIAL INJURIES
John P. Kelly
581
582 SECTION III • Management of Sports Injury and Illness
Table 24-1
Prophylaxis Against Tetanus: 2008 CDC Recommendations
History of Previous Tetanus
Immunization Clean, Minor Wounds All Other Wounds
Uncertain or fewer than three doses Give vaccine (⬍ 7 years old: DTaP; Give vaccine and tetanus
10-64 years old: Tdap) immune globulin
Three or more previous doses No need to vaccinate (unless ⬎ 10 years since Give vaccine if ⬎ 5 years since
last dose) last dose
Data from Centers for Disease Control and Prevention: Prevention of specific infectious diseases. In CDC Travelers’ Health, Atlanta, GA,
Centers for Disease Control and Prevention. Accessed at http://wwwn.cdc.gov/travel/yellowBookCh4-Tetanus.aspx.
CDC, Centers for Disease Control and Prevention; DTaP, diphtheria, tetanus, and acellular pertussis; Tdap, tetanus, diphtheria, and acellular
pertussis.
Lacerations
Types
Simple linear lacerations result from contact of the skin
with sharp objects such as skates or sticks. Stellate lacera-
tions have the appearance of a bursting of the skin and usu-
ally result from a blunt object striking skin that overlies
bone (Figure 24-3). In either case, it is not uncommon for
large lacerations to give the appearance of tissue loss owing
to retraction of the wound edges along the lines of skin ten-
sion; however, careful inspection and reapproximation of
the wound edges will frequently reveal no loss of tissue.
Avulsive wounds actually do result in loss of tissue and
require more complex methods of repair.
B
Figure 24-1
A, External trauma to larynx over prominence of thyroid cartilage Types of Lacerations
(“Adam’s apple”). B, Fracture of the larynx, as seen on the lateral
view, produces narrowing of airway and disruption of the vocal cords. • Linear
Airway compromise is worsened as tissues become edematous. • Stellate
• Avulsion
epinephrine is injected into the hematoma, and the area is Cleansing and Debridement
gently massaged. The lidocaine and hematoma are then The most favorable repair of lacerations occurs when early
removed. A form-fitting compression dressing is applied cleansing is carried out and debridement of all foreign
after the procedure and left in place for 48 to 72 hours. material is accomplished. This is particularly important for
Return to activity is strictly a matter of the athlete’s wounds that are grossly contaminated with dirt, grass,
comfort. gravel, and the like, as foreign material may promote subse-
Abrasions occur when the integrity of the skin surface is quent wound infection. Effective cleansing, debridement of
lost as a result of falls or collisions with hard or rough sur- foreign material, and prompt skin closure are the most
faces. Careful, gentle cleansing of the abraded surface effective means of promoting good healing in the absence
should be carried out, and particular attention must be paid of infection, making antibiotic use rarely necessary for
to any embedded foreign bodies, such as dirt or asphalt; simple facial lacerations.
584 SECTION III • Management of Sports Injury and Illness
A B
C D
Figure 24-2
“Cauliflower ear.” A, Hematoma (H) of the auricle caused by a wrestling injury. B, Hematoma being
aspirated. C, Contoured head dressing to force perichondrium back against auricular cartilage. D, Good
result 4 weeks after injury. (From Handler SD: Diagnosis and management of maxillofacial injuries. In
Torg J, editor: Athletic injuries to the head, neck and face, pp 611–634, St Louis, 1991, Mosby.)
Inspection of the wound prior to closure is essential contraindicated, both because a vital landmark for align-
for identification of devitalized tissue whose retention ment of the laceration is lost and because regrowth of the
will contribute to the promotion of later wound infec- eyebrow cannot be ensured. Other specific anatomical
tion. However, the excellent blood supply of this region landmarks for the alignment of lacerations are the gray
allows the physician to be very conservative in the de- line of the eyelid and the vermillion border of the lip
bridement of tissue. Compromised tissue, whether it is (Figure 24-4).
contused or jagged, can and should be preserved in most
facial wounds; only skin that is definitively necrotic Anesthesia
should be sacrificed at the time of initial repair. It is not For all but the most extensive lacerations, local anesthesia is
necessary to shave hair at the site of a laceration on the preferred method of management. Although regional
the scalp or face. In fact, shaving of the eyebrows is nerve blocks of the supraorbital, infraorbital, or mental
Maxillofacial Injuries • CHAPTER 24 585
A B
Figure 24-3
Linear and stellate type lacerations before (A) and after (B) skin closure.
nerves may be employed, infiltration of the wound edges Facial Nerve. Deep lacerations of the cheek, posterior to
with a solution of 2% lidocaine containing 1:100,000 epi- a vertical line from the lateral canthus of the eye, place
nephrine will provide excellent anesthesia and aid in hemo- the main branches of the facial nerve at risk (Figure 24-5).
stasis of the wound. However, care must be taken not to Examination of a patient with such an injury requires that
distort the wound by excessive infiltration, as vital clues to attention be paid to the patient’s ability to raise the eye-
perfect alignment of the skin edges can be lost. brow, furrow the forehead, close the eyes tightly, and smile
and pucker the lips. Any deficit in these facial animations in
Special Structures the presence of a laceration in the described location sug-
The specialized anatomy of facial structures requires careful gests an injury to a branch of the facial nerve, which can and
attention in the course of treatment of lacerations. Both must be repaired primarily. For lacerations occurring ante-
deep and surface structures must be taken into account. rior to that line, facial nerve reanastomosis is not necessary,
because the nerve has branched sufficiently that animation
of the involved muscles can be anticipated to return without
surgical intervention. Facial nerve repair generally requires
Structures Requiring Special Care that the athlete be transferred to a hospital where an operat-
and Consideration when Suturing ing microscope is available.
• Facial nerve Parotid Duct. The salivary duct from the parotid gland,
• Parotid duct which opens into the mouth through the buccal mucosa
• Eyebrows adjacent to the upper molar teeth, runs along a course exter-
• Eyelids nally identified by a line from the tragus of the ear to the alar
• Ears base of the nose. Any deep laceration of the posterior cheek
• Nose that traverses this line must be inspected carefully for identi-
• Lips fication of the duct. If the duct is severed, it will require
• Tongue direct suture repair along with placement of a plastic catheter
within its lumen for a period of 7 to 10 days.
586 SECTION III • Management of Sports Injury and Illness
A B C
Figure 24-4
Anatomical landmarks for alignment of lacerations. A, Eyebrow. B, Gray line of eyelid. C, Vermillion
border of lip.
the tarsal plate) and the surface anatomy (the lashes and the
“gray line” of the lid edge) (see Figure 24-4, B). Both
cosmetic and functional impairment can be the result of
inattention to the anatomical details in this area.
Ears and Nose. Deep lacerations of the ear and nose
share the common problem of laceration of underlying car-
tilage, which must be repaired or debrided prior to skin
closure, lest the cosmetic result be unfavorable.
Lips. Like the eyelid, the lips must be carefully
repaired after lacerations to preserve function and appear-
ance. Through-and-through lacerations of the lips, which
are frequently the result of external blows that drive the
teeth through the lip, must be inspected for the presence
of any tooth fragments that may have been dislodged
by the external blow. The circumferential muscle of the
lip, the orbicularis oris, must be repaired with sutures
prior to closure of the skin or the mucosa. Any laceration
that crosses the vermilion border of the lip, where the
mucosa meets the skin, requires precise alignment of
the vermilion border before any other sutures are placed
(Figure 24-6).
Figure 24-5 Tongue. Most lacerations of the tongue result from
Landmarks for identification of critical area for facial nerve injury external force that causes the patient’s teeth to bite the
(A) and parotid duct laceration (B). tongue. Most tongue lacerations are minor and do not ne-
cessitate suture closure. However, if there is persistent
bleeding or there is a large flap defect of the tongue, sutur-
Eyebrows. As mentioned earlier, the eyebrows provide ing is recommended and will allow for prompt return to full
an excellent cue to proper alignment of lacerations in that activity.
area. Failure to repair the wound with excellent alignment
of the eyebrow will result in a very noticeable cosmetic Suturing
deformity that is difficult to repair at a later date. Although many minor facial lacerations might be managed
Eyelids. As will be discussed shortly, a through-and- successfully by approximating the wound edges with adhe-
through laceration of the eyelid requires careful examina- sive strips, such indirect measures may not be adequate for
tion to rule out injury to the globe itself. Repair of the the athlete seeking a quick return to activity. Suture repair
eyelid must be carried out with attention to alignment and of even small lacerations provides hemostasis and skin integ-
repair of the deep structures (the orbicularis oculi muscle, rity to allow the athlete to return to competition immedi-
the levator muscle of the upper lid, the orbital septum, and ately. A dressing of collodion is often more effective than
Maxillofacial Injuries • CHAPTER 24 587
Figure 24-6
Laceration of the lip that involves the orbicularis oris. This structure must be repaired prior to closure of
the skin. Note how the vermillion border of the lip is precisely aligned following repair.
Examination
In the absence of effective prevention of eye injury, the
priorities for those with initial responsibility for manage-
ment involve recognition of the injury, limitation of pro-
gression of the injury’s severity, and arranging for prompt
referral for specialized care.3
Figure 24-7
Landmarks of surface anatomy of the globe.
Priorities in Management of Eye Injuries
• Recognize degree of injury, especially visual acuity
• Limit the injury’s severity
• Arrange, as appropriate, prompt specialized care
indicate bleeding into the vitreous fluid or detachment of of a minor blow to the eye. In the absence of other symp-
the retina. In either case, ophthalmological consultation is toms or signs, no treatment is required, and the individual
essential for full examination of the retina with dilation of can return to full activity immediately, with the expectation
the pupils. that the bloody discoloration will resolve in a week or two.
By asking the patient to move the eye in all directions, Chemosis, or edema of the conjunctiva, which is seen in
assessment of the functions of the extraocular muscles can association with subconjunctival hemorrhage, mandates a
be readily carried out. Impairment in motion may be the thorough investigation for more significant injury either to
result of direct injury to the muscles or injury to the cranial the orbit or to the globe itself. Diffuse chemosis and sub-
nerves supplying the muscles. conjunctival hemorrhage may indicate actual corneal lacera-
tion or perforation of the globe; such serious injury may
have no other signs or symptoms initially but must be sus-
Anterior Eye Segment Injuries pected. Should these findings be made after trauma, a plas-
tic or metal shield should be placed over the eye while
prompt referral for ophthalmological care is made.
Anterior Eye Injuries Hyphema. Bleeding into the anterior chamber of the eyes,
• Foreign bodies ranging from small streaks visible beneath the cornea to com-
• Corneal abrasion plete filling of the anterior chamber that obliterates the view
• Subconjunctival hemorrhage of the iris and pupil, is known as hyphema. This type of injury
• Hyphema is vision threatening, even with the smallest amount of blood,
not only because of the high risk of rebleeding within 3 or
4 days and the significant risk of developing post-traumatic
glaucoma (i.e., increased intraocular pressure), but also be-
Foreign Bodies. Foreign bodies, including displaced cause one third of patients with hyphema have other signifi-
contact lenses, are probably the most common and the cant eye injuries that must be diagnosed and treated. Such
most benign of the emergency problems that athletes en- injuries may occur readily in sports such as squash and hockey
counter. Care must be taken not to allow the athlete to rub in which small, hard projectiles or sticks can injure the unpro-
the eye, because this may cause a corneal abrasion. The tected eye. Suspicion or evidence of this injury demands
simple sensation of a foreign body, occasionally accompa- prompt referral, with the eye protected by a shield in the
nied by tearing and scleral redness in the area of the foreign interim. Patients with sickle cell disease are at higher risk for
object, requires that the lids be everted to search for the the secondary complications of hyphema.
object. Copious irrigation with normal saline is usually suf-
ficient to remove the offending agent, and the athlete can
return to activity immediately. If the article is embedded Posterior Eye Segment Injuries
such that it cannot be flushed away, referral for ophthalmo- Even in the absence of grossly visible injury to the anterior
logical consultation is preferable to attempted instrumenta- portions of the eye, blunt trauma can result in severe
tion and risk of corneal abrasion. If the athlete must be damage to the posterior segments of the eye. Such injuries
transported for consultation, both eyes should be covered to include lens dislocation, retinal edema, retinal tears or de-
minimize any movement of the injured eye. tachment, vitreous hemorrhage, choroidal rupture, and
Corneal Abrasion. When there has been a glancing optic nerve injury. Various degrees of alteration of vision,
blow to the eye, a scratch, or a persistent foreign body, the ranging from minor blurring to loss of visual fields to com-
likelihood of corneal abrasion is high. The patient usually plete loss of vision, signify the presence of such injuries after
has exquisite pain; photophobia and tearing are common trauma. The absence of a red reflex when a light is shone
accompaniments. A fluorescein-impregnated strip can be through the pupil may be noted with such injuries, but the
moistened and touched to the conjunctival fold between symptoms of visual loss alone are sufficient to warrant that
the sclera and the lower lid. Examination with a blue light the athlete be withdrawn from activity and referred for spe-
will then demonstrate the corneal defect as a green stain or cialized examination and treatment. Again, a shield that
streak. Once the diagnosis is made, the eyelid should be protects the eye from pressure should be placed while the
closed and patched and the patient sent for ophthalmologi- patient is in transit.
cal referral. Definitive care usually includes cycloplegic eye-
drops, topical antibiotics, and patching for several days. In
the absence of other accompanying injury, the athlete can Clinical Point
return to full competition as soon as the patch is removed.
Subconjunctival Hemorrhage. Bright red blood over- Alteration in vision suggests injury to the posterior eye segment
lying the sclera in the plane beneath the conjunctiva may following trauma.
occur spontaneously (often in scuba divers) or as the result
590 SECTION III • Management of Sports Injury and Illness
Figure 24-10
LeFort classification for midface fractures. LeFort I, A horizontal maxillary fracture at the level of the
nasal floor. LeFort II, A pyramidal fracture, with the base of the pyramid being the palate and upper
teeth and the apex of the pyramid at the nasal bone. LeFort III, Complete separation of the midface
from the base of the skull.
592 SECTION III • Management of Sports Injury and Illness
Figure 24-11
Zygomatic fractures. Inspection from above with palpation of the cheek demonstrates asymmetry and
depression of the fractured zygoma.
Maxillofacial Injuries • CHAPTER 24 593
A B C
Figure 24-12
Mandibular fractures. A, Malocclusion. B, Palpation of the inferior border of the mandible. C, Palpation
of the mandibular condyle.
patient unable to close. Palpation of the condyles will show lower jaw can be treated successfully with closed reduction,
an absence of condyles in the usual position immediately such treatment requires immobilization of the jaw by wiring
anterior to the tragus of the ear and the presence of a bony the upper and lower teeth to one another for a period of
prominence 1 to 2 cm (0.4 to 0.8 inches) anterior to the 4 or more weeks. This treatment clearly compromises the
normal position of the joint. athlete’s ability to compete, both because of nutritional dif-
Early reduction of the dislocated jaw is most effective, as ficulties and because of the inability to engage in mouth
delayed reduction is complicated by the development of breathing during exertion. An alternative to closed reduc-
pain and muscle spasm, which may necessitate pharmaco- tion is surgical repair with rigid plating of the fractured
logical muscle relaxation or anesthesia. In the acute phase, bone (Figure 24-13). Although this is more complex surgi-
the jaw is relocated as follows: cally, the patient’s jaw can be mobilized early, nutrition and
1. The clinician faces the patient, who is seated in a breathing are greatly improved, and early return to compe-
sturdy chair. tition (based on resolution of pain and swelling and the use
2. The clinician’s thumbs are placed in the mouth of protective headgear) can be anticipated.
lateral to the posterior teeth (never on the teeth),
with the fingers grasping the lower border of the jaw
externally.
3. A rotational force is applied to bring the posterior jaw
downward while the chin is brought forward.
4. When the condyle is rotated sufficiently to clear the
anterior margin of the joint, the jaw will passively re-
trude, and the teeth can gently be brought together.
The athlete must be cautioned to limit jaw-opening
width for several days, and anti-inflammatory medication is
recommended to reduce the joint effusion that follows such
an injury.
When a jaw fracture is diagnosed, referral for specialty
care is required. Treatment ranges from a soft diet and an-
algesics for patients with undisplaced or incomplete frac-
tures to surgical reduction and fixation for patients with Figure 24-13
more significant injuries. Although many fractures of the Rigid plating of a mandibular fracture.
594 SECTION III • Management of Sports Injury and Illness
Figure 24-14
Anatomical classification of dental injuries. 1, Enamel fracture. 2, Fracture Figure 24-15
exposing the dentin. 3, Fracture exposing the pulp. 4, Fracture extending Multiple teeth loosened as an independent segment as a result of
below the gingiva. 5, Root fracture. blunt trauma.
Maxillofacial Injuries • CHAPTER 24 595
Conclusion
Prevention of maxillofacial injuries in athletics remains the
Box 24-2 Guidelines for Initial Treatment
best treatment. Wearing of protective eyewear, mouth-
of an Avulsed Tooth guards, and effective face masks and enforcement of the
Extraoral Time rules of play will reduce even further the incidence of inju-
1. Extraoral time is one of the most critical factors affecting ries. Effective treatment and prompt rehabilitation of the
prognosis. facially injured athlete are a function of effective initial diag-
2. If possible, replant the tooth immediately at the time of injury. If nosis and treatment, as outlined here, and prompt referral
contaminated, rinse with water before replanting. for consultation with the appropriate maxillofacial, ophthal-
• If notified by telephone, instruct patient, parent, or involved mological, or dental specialist.
party on replantation technique.
• Stress importance of seeing a dentist immediately for follow-up
splinting and treatment.
References
Transport Media
1. Schaefer SD: The treatment of acute external laryngeal injuries:
When immediate replantation is not possible, place tooth in the best State of the art, Arch Otolaryngol Head Neck Surg 117:35–39,
transport medium possible. 1991.
1. Buccal vestibule (in saliva between cheek and gum, but patient 2. Stock JG, Cornell FM: Prevention of sports-related eye injury, Am
must be conscious because of the possibility of aspiration or Fam Physician 44:515–520, 1991.
swallowing, especially if a small child) 3. Shingleton BJ: Eye injuries, N Engl J Med 325:408–413, 1991.
2. Hanks’ Balanced Salt Solution 4. Zagelbaum BM, Hersh PS, Donnenfeld ED, et al: Ocular trauma in
3. Milk major league baseball players, N Engl J Med 330:1021–1023,
4. Saline 1994.
5. If none of these are readily available, water 5. DeYoung AK, Robinson E, Godwin WC: Comparing comfort and
wearability: Custom-made vs. self-adapted mouthguards, J Am
Dent Assoc 125:1112–1118, 1994.
25
CHAPTER
596
Abdominal and Thoracic Injuries • CHAPTER 25 597
consideration of concurrent injury to the lower floating lack of circumferential protection to the abdomen, the
ribs (Figure 25-1). sports medicine clinician must be aware of the possibility of
Blow to the Solar Plexus. The condition commonly intra-abdominal injury in the patient who has had a blow to
known as “having the wind knocked out of you” is caused the solar plexus. Table 25-1 helps to differentiate among
by a traumatic blow to the abdomen of an athlete whose the signs and symptoms of a blow to the solar plexus, an
abdominal muscles are not tensed. The athlete will normally abdominal wall injury, and an intra-abdominal injury.
report an inability to catch his or her breath. The initial
management includes ruling out airway obstruction by Abdominal Muscle Strain
objects such as the mouth guard, tongue, or turf from the Strains of the abdominal muscles are extremely common
field. If symptoms persist once a clear airway is confirmed, athletic injuries. Symptoms depend on the size and location
the hip belt should be loosened and an attempt to relax the of injury. The most commonly injured abdominal muscle,
athlete made by placing the athlete in the supine crook lying the rectus abdominis, may be damaged at the musculoten-
(the knees and hips flexed with feet on ground). Having the dinous junction adjacent to the lower anterior rib origin, at
athlete take a repeated deep breath and hold it often the pubic insertion, or at the horizontal fibrous bands
restores the athlete’s breath more quickly. A cold towel within the muscle itself.
may be applied to the forehead, and the athlete should be The potential mechanisms of injury include a sudden,
assured that symptoms will be short-lived. Because of the violent muscular contraction or recurrent microtrauma
Figure 25-1
Superficial anatomy of the abdominal and thoracic wall.
598 SECTION III • Management of Sports Injury and Illness
Table 25-1
Differentiation of Intra-Abdominal Injury from Abdominal Wall Injury from Blow to the Solar Plexus
Intra-Abdominal Injury Abdominal Wall Injury Blow to Solar Plexus
Mechanism Blunt or penetrating trauma Direct trauma Blow to untensed abdominal muscle
Pain location Initially localized, often Localized Minimal pain
becomes diffuse
Symptoms Pain that increases Steady pain Inability to catch breath
Duration Prolonged Moderate to prolonged Brief
Pain with tensing muscles Often Yes No
Referred pain Often No No
Physical examination Guarding, rebound, rigidity, Localized tenderness Minimal to no tenderness
quiet bowel sounds
Laboratory studies Abnormal Normal Normal
from overuse, such as commonly occurs in soccer or other The onset of symptoms is generally abrupt, with local-
sports requiring repetitive abdominal contractions. Physical ized pain, muscle guarding, nausea, and vomiting. Pain
examination reveals localized tenderness and muscle spasm may be provoked by straight-leg raising or hyperextension
at the site of injury and pain during active muscle contrac- of the back. A palpable mass, which becomes fixed when
tion or stretching. It is vital that this injury be differentiated the muscle is contracted, is often identifiable. A bluish dis-
from damage to the intra-abdominal organs. coloration of the periumbilical area, known as the Cullen
Certain forms of abdominal muscle strain, especially sign, may appear. Computed tomography (CT) helps to
those that occur at the ribs, pubis, or the iliac crest, may confirm the diagnosis and outline the extent of hematoma
result in chronic symptoms. Initial treatment should formation.7
include relative rest and protection of the injured muscle. Most cases of rectus abdominis hematoma may be
Activity should be limited by pain. An avulsed fragment of treated nonoperatively. Treatment includes application of
iliac crest is often reattached surgically, although surgery ice during the first 48 hours after injury, followed by heat.
has little role in the treatment of proximal or midsub- Strengthening of the abdominal muscles should be insti-
stance tears. Rectus abdominis muscle strains have been tuted with isometric exercises and should progress to sit-
identified as an extremely common occurrence in com- ups, crunches, and other exercises as pain permits. If
petitive tennis players. The injury mechanism was felt to active bleeding persists, surgical ligation of the inferior
be eccentric overload, followed by forced contraction of epigastric artery and hematoma evacuation may be re-
the nondominant rectus during the cocking phase of the quired. Because a relatively small approach that spares the
service motion. A tennis-specific rehabilitation program abdominal fascia can be used for this drainage, surgery
stressing eccentrics and plyometric strengthening of the may actually speed up return to sport. High-speed and
abdominal wall muscles was introduced to prevent recur- contact sports may be resumed as soon as the area is pain
rences.5,6 A different study identified a group of soccer free, usually in 1 to 2 weeks.4 Percutaneous drainage of
players with chronic groin pain and the absence of preop- the hematoma is rarely successful because of early clot
eratively identifiable inguinal hernias, who at the time of organization.
surgical exploration were found to have various irregu-
larities of the abdominal wall, including inguinal hernias, Hernia
and microscopic tears or avulsions of the internal oblique A hernia is a protrusion of an anatomical structure via a
muscle. These individuals were successfully treated with passageway or weakened area of the body wall. Approxi-
herniorrhaphy and were able to return to play within mately 1.5% of Americans are estimated to have hernias.8
3 months.6 Table 25-2 lists the relative occurrence rates of various
Rectus Abdominis Intramuscular Hematoma. The forms of hernias.9 The groin is the location of 81% of
rectus abdominis muscle receives its blood supply from hernias, with 86% of these occurring in men. Although
branches of the underlying inferior epigastric arteries. Sud- 84% of all femoral hernias affect women, inguinal hernias
den severe motions, such as an abrupt twisting of the trunk, still occur more commonly than femoral hernias in
a sudden contraction of the abdominal muscles, or a sudden women.9
extension of the spine, may produce a tear in the rectus It seems unlikely that hernias are ever exclusively caused by
abdominis muscle. The resultant shearing forces may athletic participation, although they may be aggravated by ac-
rupture the supplying epigastric artery or vein, resulting in tivities that increase intra-abdominal pressure such as weight-
intramuscular hematoma formation. lifting and rowing. Hernias should always be considered in the
Abdominal and Thoracic Injuries • CHAPTER 25 599
Ultrasound has been suggested as a less expensive alter- small and close spontaneously by the age of 2 years, thus
native to MRI in the diagnosis of athletic pubalgia. Some requiring no specific treatment. If surgical repair is neces-
authors have shown a strong correlation between ultra- sary, the procedure is relatively simple in children, but is
sound findings of posterior abdominal wall insufficiency and more complicated in adults. In adults, the surrounding
intraoperative findings.36 Herniography involves plain ra- walls of the linea alba are rigid and thus predispose patients
diographs that are obtained after injection of a radio-opaque to strangulation and incarceration of intra-abdominal struc-
dye into the peritoneal cavity. It is commonly employed in tures that may protrude.14
Europe to determine if a patient with chronic groin pain Epigastric hernias are located in the linea alba, or ab-
will benefit from a herniorrhaphy. Limitations of herniogra- dominal midline, superior to the umbilicus, and generally
phy include a high false-positive rate,37 as well as the possi- contain only a small amount of preperitoneal fat. Epigastric
bility of hollow viscus perforation, vasovagal reactions, hernias are often asymptomatic and not recognized;
allergic reactions to contrast dye, and infections.38-40 The autopsy studies reveal their presence in 5% of normal
high complication rate of 3% to 6% has made herniography adults.9 Surgery is indicated only if enlargement or pain
a rarely used diagnostic tool in the United States. develops, in which case repair is relatively simple.
The treatment of athletic pubalgia is normally surgical be- Ventral hernias, which are typically complications of
cause nonoperative treatment with rest, anti-inflammatories, previous midline abdominal surgery, are uncommon in
massage, and heat or ice is rarely successful.6,21,23 Physical athletes. Repair of ventral hernias may be quite difficult,
therapy with a focus on core strengthening may actually especially when they are of large size, occur in obese indi-
resolve the imbalance between the hip and pelvic muscle viduals, or are associated with vertical incisions. The recur-
stabilizers.21 If all other sources of groin pain have been ruled rence rate is high at 15%.13 Table 25-4 provides useful
out and 6 to 12 weeks of nonsurgical management have guidelines for the timing of return to activity after the sur-
failed, surgical repair should be considered.6,11,20 Laparoscopic gical repair of various hernia types and other abdominal
or open surgical repair of the weakened posterior inguinal wall surgical procedures.
has been shown to have excellent results with an 80% to 97% Obturator Nerve Entrapment. A frequently recog-
success rate.11,20,21,24,26 Meyers has been a proponent of pelvic nized cause of chronic groin pain in athletes is entrapment
floor repair with reattachment of the inferolateral edge of the of the obturator nerve as it enters the thigh within the fascia
rectus abdominis to the pubic bone with or without adductor of the short adductor muscle. Obturator nerve entrapment
longus release.18 Regardless of the type of repair that is done, pain is insidious in nature and characteristically noted
laparoscopic repair has shown a more rapid return to sport around the pubic bone, where the adductor muscle has its
with an average of 2 to 6 weeks in comparison with 1 to origin. Pain may be referred to the anterosuperior iliac spine
6 months with open repair.41 Laparoscopic repair also has the on the same side as the nerve entrapment and often radiates
benefit of better visualization of the involved structures and down the medial thigh toward the knee.44 Exercise com-
ability to perform repair of bilateral hernias through the same monly exacerbates the pain and it is relieved by rest. Incom-
incision.42 plete adductor muscle weakness or spasm in the affected leg
Another common cause of groin pain is a pathological may occur after exercise along with numbness or paresthesia
condition of the intra-articular hip such as from a labral tear if the entrapment is long-standing. On physical examina-
or cartilage defect. The history and physical findings of the tion, the patient will have reproduction of his or her pain
patient with a labral tear is often very similar to that of the with resisted internal hip rotation or by passively externally
patient with sports hernia and thus should always be in- rotating and abducting the affected hip while standing.44
cluded in the differential diagnosis. Pain is typically activity- Imaging studies are rarely useful in the diagnosis of
related and exacerbated by passive rotation of the hip. MRI obturator nerve entrapment, although MRI may show atro-
and magnetic resonance arthrogram are excellent diagnostic phy of the short and long adductor muscles as well as the
tools to rule out pathological conditions of the hip in the gracilis muscle. Electromyography (EMG) studies are com-
patient with chronic groin pain. Intra-articular corticoste- monly used in the workup of neuropathy and often reveal
roids into the hip can be used as both a diagnostic and chronic denervation in the short and long adductor mus-
therapeutic modality.43 cles. When trying to determine the diagnosis and the need
Other Abdominal Hernias. Femoral hernias, which for surgical intervention, a selective anesthetic block of the
occur far more commonly in women, are often difficult to obturator nerve may be performed. A successful nerve
detect. The hernia protrudes through the femoral ring, block will alleviate pain brought on by provocative maneu-
beneath the inguinal ligament, just medial to the femoral vers and reproduce any postexercise weakness.44
vein at the fossa ovalis. Surgical repair should be carried out Treatment of obturator nerve entrapment is initially con-
as early as possible so as to avoid incarceration or strangula- servative with rest, nonsteroidal anti-inflammatory drugs
tion, which are common sequelae of this hernia type. (NSAIDs), physical therapy involving adductor muscle
Umbilical hernias are common in infants and children. and pelvic strengthening exercises, and groin stretches.
Of white newborns, 10% are born with umbilical hernias, as Conservative therapy is more effective in patients without
are 40% to 90% of black newborns. The great majority are EMG evidence of denervation or with a short duration of
Abdominal and Thoracic Injuries • CHAPTER 25 603
Table 25-4
Hernia Repair and Abdominal Surgery: Return-to-Activity Guidelines
Procedure Return to Classes PRE* and Conditioning Noncontact Full Activity
Inguinal hernia
Indirect (children) 1 wk 2 wk 3 wk 4 wk
Indirect (adult) 1 wk 3 wk 7 wk 8-10 wk
Direct 1 wk 3 wk 8 wk 12 wk
Femoral hernia 1 wk 3 wk 8 wk 12 wk
Umbilical hernia
Children 1 wk 2 wk 3 wk 3 wk
Adults 1 wk 2 wk 4-6 wk 8 wk
Epigastric hernia 1 wk 2 wk 3-4 wk 6 wk
Ventral hernia 2 wk 8 wk 3-6 mo ?avoid
Appendectomy 1 wk 3 wk 4 wk 6 wk
Other uncomplicated 2 wk 4 wk 8 wk 12 wk
abdominal operations
object. Removal of the object should take place only after Prior to the advent of faster and more precise
large-bore needle intravenous access has been obtained and CT scans, diagnostic peritoneal lavage (DPL) was a useful
blood is available for emergent transfusion in the case of major test in the initial evaluation of an individual with multiple
exsanguination (blood loss) at the time of removal. system injuries or an impaired level of consciousness.
The procedure involves paracentesis with abdominal cav-
ity saline lavage. DPL has fallen out of favor because of
Clinical Caution its inability to specify the location or extent of intra-
Large, penetrating foreign objects should only be removed in a surgical abdominal injury, high sensitivity which overpredicts the
operating room except when the airway is compromised. need for surgery,4 poor results in the detection of retro-
peritoneal bleeding, risk associated with its invasiveness,
and controversy over the management of intermediate
Blunt trauma is by far the most common type of athletic results. CT has gained widespread acceptance in the initial
abdominal injury. The same blows that produce abdominal evaluation of intra-abdominal trauma. It is noninvasive
muscle contusions and rectus sheath hematomas may lead to and extremely accurate in the identification of the loca-
severe intra-abdominal trauma.4 At the onset of the traumatic tion and extent of significant intra-abdominal injury,
event, the unprotected abdomen is struck by an opposing including liver, spleen, and kidney lacerations, as well as
force, and the abdominal organs are compressed against the retroperitoneal hematomas.50 CT is also particularly valu-
vertebral column. The severity of symptoms resulting from able in avoiding unnecessary exploratory laparotomies
blunt abdominal trauma varies widely, ranging from severe and potential organ removal,4 which may have previously
pain in the presence of significant bleeding and peritoneal been performed on the basis of equivocal DPL results.
irritation to only mild tenderness. Peritoneal irritation may Overall, CT has increased the nonoperative management
occur after injury to the stomach, gallbladder, pancreas, small of blunt abdominal trauma.51 Shortcomings of CT in-
intestine, or colon as a result of bacterial or chemical con- clude its limited ability to detect hollow viscus injuries,
tamination. Initially the only symptom that may be present is and the expertise required to accurately interpret subtle
localized tenderness, but soon the peritoneal signs, including findings.
abdominal rigidity, guarding, referred pain, and loss of bowel The initial treatment decision in the presence of intra-
sounds, may ensue. Diaphragmatic irritation caused by an abdominal injury is whether to operate. The presence of
injury to the liver or spleen, or a subdiaphragmatic fluid col- obvious intra-abdominal bleeding, penetrating trauma to
lection may produce pain that is referred to the correspond- the abdomen or the thorax, or a mechanism and physical
ing shoulder. Table 25-1 helps to differentiate the signs and findings in an injury that is strongly suggestive of a “surgical
symptoms of intra-abdominal visceral injury from abdominal abdomen” indicates the need for urgent laparotomy. Such
wall injury and a solar plexus blow. individuals should not be observed for an extensive period,
The initial evaluation of an awake and alert individual because these injuries may result in sudden and rapid
who has sustained acute, blunt abdominal injury begins deterioration.
with a careful history of injury and complete physical ex- An approach to the initial evaluation of the acutely
amination, including abdominal palpation, auscultation, injured abdomen begins with observation of the entire
and hemodynamic evaluation.4 Figure 25-6 illustrates the exposed anterior and posterior abdomen, flanks (side of
major organs of the abdominal cavity. Depending on the individual between rib and hip), lower chest, buttocks,
findings, it is often possible to avoid extensive laboratory, and perineum for evidence of contusions, abrasions, lac-
radiographic, and invasive procedures. Suspicion must be erations, and penetrating wounds. Contusions may not
maintained, because up to 43% of individuals who have a appear for several hours after trauma has occurred. The
significant intra-abdominal injury initially present with a abdomen should then be auscultated to assess the fre-
negative findings on physical examination (Table 25-5).46,48 quency and quality of bowel sounds. The presence of
Moreover, it has been reported that 20% of subjects with a bacteria, blood, or chemical irritants in the abdomen may
retroperitoneal hematoma appear to have an initially benign result in an ileus, or paralysis of the intestines, manifested
abdominal examination.49 by absent or reduced bowel sounds. This finding, how-
ever, is extremely nonspecific and should prompt further
evaluation. The abdomen should then be examined for
Clinical Caution
physical signs of peritoneal irritation, including rebound
With abdominal injuries, the presence of pain out of proportion to the tenderness, muscle guarding, tenderness with percussion,
injury, peritoneal pain, referred pain to the back and shoulder, tachy- or pain with coughing.
cardia, hypotension, multiple body system injuries, or an impaired The complete examination of the abdomen must
ability to respond to painful stimuli should prompt the clinician to include careful evaluation of the three regions of the
perform additional diagnostic studies. abdomen: the intrathoracic abdomen, the “true” abdo-
men, and the retroperitoneal abdomen. The organs
Abdominal and Thoracic Injuries • CHAPTER 25 605
Figure 25-6
Anatomy of the abdominal cavity.
Table 25-5
Physical Examination of the Abdomen After Blunt Trauma Frequently is Misleading
Signs of Visceral Injury on Initial Incidence of Significant Intra-Abdominal
Abdominal Examination Percent of Patients Injury (%)
Obvious 22 80
Equivocal 46 35
Negative 12 43
Unreliable because of head or spine injury 19 35
From Olsen WR: Abdominal trauma in the athlete. In Schneider RL, Kennedy JC, Plant ML, editors: Sports injuries — mechanisms, prevention,
and treatment, pp 809-817, Baltimore, 1985, Williams & Wilkins.
located in each region are listed in Table 25-6. The intra- abdomen is often extremely difficult to evaluate by physi-
thoracic abdomen, which is difficult to palpate because it cal examination. Hematomas are a common finding in
lies protected by the bony thorax, is susceptible to injury the retroperitoneal space, and CT is often required for a
from blows to the lower or middle abdomen, which direct diagnosis. Table 25-7 summarizes the usefulness of the
forces upward. The true abdomen is more accessible to various diagnostic modalities in the evaluation of each
examination by palpation, whereas the retroperitoneal abdominal region.
606 SECTION III • Management of Sports Injury and Illness
Table 25-6
Organs of the Three Abdominal Regions
Intrathoracic “True” Retroperitoneal
Abdomen Abdomen Abdomen
Table 25-7
Usefulness of Diagnostic Evaluation Methods
by Abdominal Region
Region Palpation DPL CT
Intrathoracic 1 2 3
“True” 3 2 3
Retroperitoneal 1 1 3
A B
C D
E
Figure 25-8
Computed tomography–based classification of splenic injury:
Class 1, Subcapsular hematoma or localized capsular disruption without significant parenchymal injury.
Class 2, Single or multiple capsular and parenchymal disruptions, transverse or longitudinal, that do not
extend into the hilum or involve major blood vessels. Intraparenchymatous hematoma may or may not
coexist.
Class 3, Deep fractures, single or multiple, transverse or longitudinal, extending into the hilum and
involving the major blood vessels.
Class 4, Completely shattered or fragmented spleen, or separated from its normal blood supply at the
pedicle (may or may not have associated intra- or extra-abdominal injury). (Text from Buntain WL,
Gould HR, Maull KI: Predictability of splenic salvage by computed tomography, J Trauma 28(1):24-34,
1988. Illustrations from Afflect TP: Severe sports-related spleen injury, Phys Sports Med 20:109-123, 1992.)
608 SECTION III • Management of Sports Injury and Illness
The spleen was once considered an expendable organ that firmed. Endurance training for 2 to 3 weeks is advised, fol-
played little physiological role in adults. The treatment of lowed by return to noncontact sports and ultimately to con-
splenic injuries has now taken a major shift toward the pres- tact sports; however, this is not always followed. A recent
ervation of splenic tissue. Splenectomy results in the loss of journal article reported on the case of a competitive college
an invaluable reticuloendothelial filter of the blood, reduced football player who suffered a grade 3 splenic injury that re-
immune function with lowered levels of immunoglobulin G quired surgery. A laparoscopic splenectomy was performed on
and immunoglobulin M and T-cells, and an increased risk the patient and he was discharged from the hospital 20 hours
of overwhelming bacterial infection. The encapsulated or- later. He was able to play football 12 days later. The authors
ganisms Streptococcus pneumoniae, Haemophilus influenzae stressed that although most consider minimally invasive sur-
type B, and Neisseria meningitides are particularly virulent for gery for the treatment of splenic injuries contraindicated,
splenectomized individuals and are often the cause of post- there may be a role in select patients.56
splenectomy sepsis.4
The criteria for nonoperative management of splenic
injuries include hemodynamic stability with an adequate Clinical Point
hematocrit, a nonenlarging splenic defect, no evidence of
head injury, and stable peritoneal findings. All nonoperative Generally, return-to-play criteria following intra-abdominal injuries
should include:
patients should be treated in the hospital with observation,
• Time for organ healing (6 to 8 weeks)
serial examinations, and hematocrit levels to detect any he- • Endurance training before noncontact sports (2 weeks)
modynamic instability. Strict bedrest is necessary. Up to • Radiographic evidence organ has healed
90% of class 1 and 2 injuries can be treated nonoperatively, • Normal laboratory results for that organ
without blood transfusions, and can be ready for discharge
in less than 7 days.53 Hospitalization is particularly impor-
tant, given the risk of delayed rupture or hemorrhage.
Failure of nonoperative management is normally noted at Infectious Mononucleosis and Splenic Damage.
48 to 72 hours, but there may be ruptures as late as Infectious mononucleosis, a viral infection caused by the
2 months after injury.4 A repeat CT should be performed Epstein-Barr virus, commonly affects adolescents and young
5 to 7 days after the initial scan to look for stabilization or adults and is found in 3% of all college students.57 Clinical
improvement. If the injury to the spleen seems to be worse manifestations include sore throat, fever, cervical adenopathy
at this point, then operative management is needed. Non- (enlarged cervical glands), splenomegaly (enlarged spleen),
operative management has been shown to be effective in and hepatomegaly (enlarged liver). Splenic enlargement oc-
90% of children and 70% of adults.4 curs in up to 70% of individuals with infectious mononucleo-
Surgical exploration and treatment are indicated in cases in sis between days 4 and 21 of the illness. This period coincides
which conservative management fails or is deemed inappro- with the time of maximal risk for splenic rupture, which com-
priate. After surgery, the athlete generally spends 5 to 7 days plicates 0.1% to 0.2% of cases. Individuals with splenomegaly
in the hospital. Strenuous activity should be avoided for 6 to who participate in contact sports are at increased risk for
8 weeks and contact sports returned to in 3 months.4 splenic rupture. Vigorous physical activity should be curtailed
Return-to-play decisions after splenic injury require great until splenomegaly resolves. A spleen that is palpable during
prudence. Class 1 and 2 injuries (see Figure 25-8) may heal abdominal physical examination is at least two to three times
completely within 6 to 8 weeks without surgery.53 Two weeks its normal size. It may take as long as 3 weeks from the time
of endurance training should be instituted before return to that the splenic tip is no longer palpable for splenomegaly to
even noncontact sports. Return to contact sports should be completely resolve. There have been no reports in the litera-
delayed for another 2 to 3 weeks following the healing period ture of splenic rupture in mononucleosis after 3 weeks.57
and may take more than 4 months total. If the athlete is trying
for an earlier return to contact sports, a careful evaluation of
radiographic evidence via CT must be performed to assess the Clinical Caution
spleen and liver score. There is no single parameter to predict
In individuals with infectious mononucleosis, the spleen is at
safe return to sport. In general, the patient must be evaluated maximum risk for rupture between days 4 and 21 of the illness, so
at the 1-month mark to make sure that he or she is afebrile high-impact activity and contact sports should be avoided.
(no fever), well hydrated, and asymptomatic without any evi-
dence of a palpable liver or spleen. Even when all of these
conditions are met, there is no guarantee that the spleen may
not rupture with trauma.55 It is important that each athlete The management of mononucleosis-induced spleno-
treated nonoperatively be taken on a case-by-case basis look- megaly includes examinations of the abdomen on at least a
ing at both physical and radiographic criteria.4 Severe injuries weekly basis. Radiographs, ultrasonograms, and CT scans
may be followed with serial CT scans or ultrasonograms on a may also be helpful to confirm resolution of splenomegaly
monthly or bimonthly basis until complete healing is con- before allowing the athlete to return to activity. Low-impact
Abdominal and Thoracic Injuries • CHAPTER 25 609
endurance training should be resumed initially, whereas the symptoms or appearance are worsened then operative
high-impact activity and contact sports should be avoided intervention is necessary. Surgical management is indi-
for an additional 2 to 3 weeks.58,59 Corticosteroids may be cated if hemodynamics are unstable, the abdomen dis-
useful in the treatment of upper airway obstruction, which tends, and the hematocrit continues to fall or fails to re-
is often associated with infectious mononucleosis, although spond to blood transfusions. After surgery, the patient
they have not been shown to reduce the prevalence or may require a long hospital stay. Clinical recovery is best
severity of splenomegaly. assessed by the use of serial CT scans, which will demon-
strate early healing within 2 to 4 weeks. Complete healing
Liver Injury must be confirmed before permitting an athlete to return
With the advent of the CT scan, the ability of the clinician to full activity under careful monitoring. The process of
to diagnose minor liver injuries has been greatly increased.4 complete healing usually takes 3 to 6 months.64
The liver now accounts for 4.4% to 4.9% of athletic
injuries.1 It is especially at risk because of its large size and Intestinal Tract Injury
unprotected position. Athletes with hepatomegaly should Ruptured Hollow Viscus. Rupture of a hollow viscus
not engage in contact sports until the liver has returned to is an uncommon injury, but has been reported in athletes
normal size.4 The most common mechanism of injury is a who have sustained blunt abdominal trauma.60,65,66 The
blunt blow to the right abdomen or lower chest, but liver specific segments of bowel that are fixed to the abdomi-
injuries can also occur by a sudden deceleration or displace- nal wall appear to be most susceptible to rupture. These
ment of a lower right rib fracture. A case report has also include the duodenum, proximal jejunum, terminal il-
described liver injury after a blow to the left abdomen.60 eum, and any areas attached by adhesions. The mecha-
Symptoms of liver injury vary with the severity of damage nism of injury is not known, although it is suspected that
but may include right upper quadrant pain, diffuse ab- the bowel is crushed against the spine, resulting in rup-
dominal pain, or peritoneal irritation signs, if heavy bleed- ture or hematoma formation.66 The duodenum seems to
ing is present. Liver injuries, unlike splenic injuries, rarely be particularly vulnerable to injury where it crosses the
progress to serious hemorrhage. spine.
Hepatic contusions result in mild right upper quad- The symptoms of bowel rupture include severe abdomi-
rant abdominal pain, occasional nausea and vomiting, nal pain, nausea, vomiting, and muscle spasm. The quality
hemodynamic stability, and an absence of peritoneal of abdominal pain is typically diffuse, and “gripping” or
signs. Treatment includes bed rest with observation and “crampy” in nature. Injury to various portions of the intes-
avoidance of athletic activities for at least 2 to 3 weeks, tinal tract may refer pain to other locations in the abdomen
at which time endurance activities may be gradually as follows: stomach or duodenum to the epigastrium, small
reintroduced.61 bowel to the umbilical area, and colon to the suprapubic
Hepatic lacerations range from minor tears producing region. The physical examination may reveal rebound ten-
little bleeding, to more severe, deeper parenchymal bleed- derness consistent with peritoneal irritation, an absence of
ing. Hemodynamic instability caused by parenchymal bowel sounds, and abdominal rigidity.
bleeding will require surgical intervention and repair. Of The diagnosis of bowel rupture may be suspected by the
all liver injuries, 80% involve the right hepatic lobe be- presence of free air under the diaphragm on an upright
cause of its larger volume, proximity to the lower ribs, abdominal radiograph and may be confirmed by CT with
and the location of the falciform ligament.61 Most liver contrast, MRI scan, or exploratory laparotomy. The treat-
lacerations result in subcapsular hematoma formation or ment of a ruptured hollow viscus is surgical, with immediate
intraparenchymal tears. Associated hemorrhage is typi- repair of damage, irrigation of the abdominal cavity, and
cally minimal, with 70% having stopped bleeding by the appropriate treatment of peritonitis.
time of laparotomy.62,63 The American Association for the Intramural Hematoma. Intestinal intramural hema-
Surgery of Trauma organ injury scale is used to classify toma has been reported as a result of contact in an adolescent
hepatic injuries on as scale from I to VI. Unfortunately football player.65 The duodenum is particularly susceptible to
this grading system does not have applicability to guiding injury, given the presence of a transitional area between the
thereapy.4 The amount of hemoperitoneum detected by portion that is tightly anchored to the abdominal wall and
CT scan, rather than the degree of liver damage, corre- the loosely tethered segment attached to mesentery. This
lates well with the need for operative intervention.60 Liver area becomes particularly stressed during sudden decelera-
trauma may be managed nonoperatively in the presence tion, which commonly occurs in football, bicycling, and
of hemodynamic stability and the absence of peritoneal equestrian sports. The resultant forces may cause the submu-
signs or significant extrahepatic injury. Nonoperative cosal vessels to be sheared against the muscularis mucosa,
management consists of bedrest, careful hemodynamic with bleeding into the duodenal wall, between the muscularis
monitoring and frequent physical and laboratory evalua- and submucosal layers. Partial to complete luminal obstruc-
tion.4 If the patient remains stable, then a CT should be tion may ensue. The mechanism of this injury is severe decel-
repeated 5 to 7 days after the injury. If, at this time, eration rather than blunt trauma.65
610 SECTION III • Management of Sports Injury and Illness
Intestinal Ischemia. Ischemic bowel disease can occur Kidney damage must be suspected when an athlete has
in the athlete and the team physician should be aware of the sustained a blow to the flank, abdomen, or lower chest. The
symptoms as well as the proper methods of diagnosis and most common sign of renal injury is hematuria, but kidney
management. Abdominal pain and diarrhea may actually be damage may be present without it in 25% of cases.72,73 Other
early symptoms of ischemia. The range of ischemic bowel signs and symptoms of renal damage include flank pain,
disease is varied in severity and treatment. Gastritis caused tenderness, and ecchymosis. The quantity of hematuria
by ischemia may be treated with acid blockade, whereas (blood in the urine) correlates poorly with the degree of
colitis may require volume repletion with intravenous fluids renal injury, but if it persists longer than 48 to 72 hours, a
or even transfusion with blood products. Resection is rarely more comprehensive workup for renal trauma must be
necessary. Severe infarctions caused by intestinal ischemia performed.73 An example of a susceptible body position for
are rare but sometimes fatal.67 renal injury occurs when the body is extended, and the
abdominal muscles are relaxed, as when a football player is
Kidney Injury leaping for a pass.74 Hematuria may also occur secondary to
The kidney is the second most commonly injured intra- repeated microtrauma from exercise, resulting in cumulative
abdominal organ in sports participants after the spleen.52 damage to the urinary tract. The source of exercise-induced
Glenn and Harvard found that renal trauma was the cause of hematuria may be the kidney, bladder, urethra, or prostate.73
hospitalization in 19% of all injured athletes who required Long-distance runners are particularly prone to this condi-
hospitalization for sports trauma.68 Two 2003 reviews of pe- tion as a result of shock transmission from repeated
diatric trauma registries revealed that although renal injuries footstrikes, as are boxers who sustain recurrent punches to
do occur in sports, they happen at a much lower rate than the torso.
from other causes. McAleer showed that out of 113 injuries Types of kidney injuries include contusion, subcapsular
incurred from team sports, only 6 sustained renal injuries.69 hematoma, parenchymal rupture into the renal pelvis, rup-
Wan and colleagues performed a retrospective review of ture across the capsule, and laceration (Figure 25-9).3 Renal
81,923 cases, of which 5439 were sports-related.52 Of the 42 contusion, the most common type of kidney injury, typically
total kidney injuries found in this review, 26 were associated
with football. A recent study looking at renal injuries in pro-
fessional football players showed an average of 2.7 renal inju-
A B
ries per season.70 Most injuries are renal contusions that result
from blunt blows to the flank or abdomen. The upper one
third of the right kidney and the upper one half of the left
kidney lie above the twelfth rib, within the thorax. Three lay-
ers of anterior abdominal muscles, retroperitoneal fat, the
psoas muscles, and the paravertebral muscles provide further
renal protection, particularly when the muscles are tensed. C
Kidney injury may be severely painful, particularly if damage
has occurred within the substance of the kidney with resultant
bleeding into the collecting system. Occult hematuria (blood
in the urine) without radiographic evidence of injury is a com-
mon finding in boxers, football players, basketball players, and
long-distance runners. A 1993 study looked at the urine of 45
male and female athletes after completing a long-distance
race. On lab analysis, 24.4% were found to have red blood
cells in their urine. The source of the blood was found to be
the lower urinary tract and after 7 days, there was no sign of
blood in the athletes’ urine.71
Clinical Note
D E
Children may be at increased risk of renal damage because of the
absence of fatty anatomical padding, decreased rigidity of the rib
cage, and the larger size of the pediatric kidney. A recent study Figure 25-9
Common kidney injuries. A, Subcapsular hematoma. B, Contusion.
showed that the size and maturity of the child may play a role in his
C, Parenchymal rupture into renal pelvis. D, Rupture across capsule.
or her potential for renal injury.52
E, Laceration. (From Diamond DL: Sports-related abdominal
trauma, Clin Sports Med 1:91, 1989.)
Abdominal and Thoracic Injuries • CHAPTER 25 611
results from a shock transmitted to the kidney after a blow well as loss of the psoas muscle and renal outlines, if retro-
to the torso. These injuries are usually self-limited, although peritoneal bleeding is present. Contrast-enhanced CT scan,
extravasated blood under the capsule may be problematic if if available, is generally preferable to IVP, because it is
it becomes infected. Increasing forces may produce more quicker to perform, noninvasive, and has greater accuracy in
serious kidney damage, such as capsular rupture, perirenal diagnosing a renal hilar injury, renal contusion or lacera-
hematoma formation, and subcapsular hemorrhage with tion, extravasation of urine, and possible retroperitoneal
progression to kidney necrosis. The severity and clinical bleeding.4 CT has the additional advantage of assessing
manifestations of renal rupture depend on the extent and damage to other organs.78 IVP has a lower specificity, and
area of injury. Extrinsic hemorrhage may trigger symptoms is inadequate in the diagnosis of vascular injuries such as
of localized pain, back and flank muscle spasm, and painful renal artery thrombosis, which may necessitate the use of
muscle functioning. arteriography.
The issue of the athlete with only one functioning kidney
is one that has arisen in the literature during the last few
years. In 1986, Dorsen recommended that young patients
with solitary kidneys only participate in noncontact sports Differential Diagnosis of Hematuria
to avoid the possibility of renal injury. Older patients with • Trauma
financial incentive or exceptional skill were taken on a case- • Infection
by-case basis if they were able to give informed consent and • Urinary tract stones
sign a waiver if they wished to participate.75 A 1994 survey • “Runner’s hematuria”
to members of the American Medical Society for Sports • Neoplasms (benign and malignant)
Medicine revealed that 54.1% of those polled allowed ath- • Prostatitis (inflamed prostate)
letes with a solitary kidney to participate in collision or • Glomerulonephritis (inflamed glomerulus of kidney)
contact sports as long as protective equipment was used, a • Analgesic nephropathy (kidney disorder)
waiver signed, and consultation with a urologist obtained.76 • Sickle cell anemia
In the pediatric patient, it is imperative that parents be • Disorders of coagulation
• Thrombocytopenia (reduced number of platelets)
counseled about the risk of renal injury caused by sporting
injuries, especially in the child with a solitary kidney. Protec-
tive equipment should be offered and the parent made
aware that modifications to the child’s participation in high-
risk sporting activities be made to decrease the risk of injury The absence of red blood cells on a single urinalysis does
to the solitary kidney.77 In a 2008 poll of National Football not exclude the possibility of renal damage. If the clinical
League (NFL) physicians and trainers, 61% of respondents presentation and mechanism of injury provide a strong sus-
would allow a professional athlete with one kidney to play, picion of renal damage, successive urine specimens should
50% would not allow a college athlete with one functioning be collected. If continued concern exists, contrast CT or
kidney to play, and 60% would advise against a high school IVP should be performed.
player with one kidney from participating in football.70 The treatment of renal injuries depends on the type and
extent of damage. The great majority of cases without
hemodynamic instability and a stable hematocrit will heal
without complications when treated with monitoring and
Clinical Caution complete bed rest until hematuria clears. This approach has
Athletes with one kidney should only be allowed to compete in had the added benefit of decreasing the number of nephrec-
collision sports if they understand the risk, wear extra protective tomies done when renal injuries are explored at the time of
padding over the kidney, sign a waiver, and consult a urologist. injury. Hospitalization is indicated to monitor for contin-
ued bleeding, development of shock, hematoma expansion,
or continued free extravasation of urine on IVP or contrast
CT scan. These conditions warrant surgical intervention.
The medical evaluation of an athlete with hematuria who Prior to discharge, the renal injury should be documented
has sustained trauma to the abdomen, back, or lower chest by a repeat CT to determine stabilization and healing. The
should include a complete history and physical examina- patient should also be told that microscopic hematuria may
tion, urinalysis, complete blood count, and a plain-film persist for 2 to 4 weeks after the injury. If hematuria persists
radiograph of the abdomen. Patients with gross hematuria, longer than 4 weeks or reappears at a later point in time,
microscopic hematuria, hypotension, or a flank mass may re-evaluation is necessary.4
require further evaluation with a CT scan or intravenous The athlete who has sustained a relatively minor renal
pyelogram (IVP).4 Plain x-ray films may disclose associated injury should avoid strenuous sports activity for at least
injuries, such as lower rib or lumbar vertebral fractures, as 4 weeks. This reduces the risk of rebleeding, because it
612 SECTION III • Management of Sports Injury and Illness
takes 15 to 21 days for clots to dissolve. The recovery “Runner’s hematuria” must be considered in the evalua-
phase of more significant renal trauma should include tion of an athlete with hematuria. Macrohematuria or
serial monitoring of the blood pressure, urinalysis, and CT microhematuria, often with dysuria (painful urination) and
or IVP every 3 months for 1 year. These measures will help suprapubic pain, has been reported in up to 18% of runners
identify the late-developing complications of urinoma, at the conclusion of a marathon race.80 Cystoscopic studies
hydronephrosis, transient hypertension, reduced renal have identified the presence of a mucosal contusion at the
function, infection, and renal calcification. The athlete bladder base that involves the trigone, from the internal
who has sustained extensive renal laceration or contusion meatus to the interureteric ridge, and a mirror image contu-
should be allowed to return to contact sports only after sion lesion on the posterior bladder wall.81 It is suspected
contrast CT confirms complete healing, which often takes that the repetitive impacts of running result in the bladder
6 or more months.79 mucosal contusion, especially if the bladder is empty.
Hematuria typically resolves rapidly with rest.
Ureteral Injury
The ureter is the least commonly injured portion of the Pancreatic Injury
urinary tract. Avulsion of the ureter has been reported after Sports-related injury to the pancreas is uncommon be-
a severe blow to a hyperextended back, which may occur cause of its relatively protected anatomical location, deep
during a fall from a horse or during a motor vehicle acci- in the retroperitoneum. Injuries can result from atrau-
dent. The most common symptom of ureteral rupture is matic methods as well as blunt abdominal trauma.82 An
nondescript back pain, often in conjunction with signs of extremely forceful abdominal blow that compresses the
severe abdominal injuries and peritoneal irritation. The organ against the spine is usually necessary to produce
diagnosis may be confirmed by contrast CT or IVP, and the pancreatic damage. Because of the vital physiological na-
treatment is surgical. ture of the pancreas, the severity of trauma necessary to
induce damage to the pancreas, and the corrosive nature
Bladder Injury of pancreatic contents, injuries to the pancreas are often
The urinary bladder is infrequently injured in sports life-threatening. For this reason, pancreatic injury should
because of its location deep to the pubic bones within the always be included in the differential diagnosis of the ath-
protective pelvic ring. The empty bladder’s collapsed con- lete with abdominal pain.82
figuration also reduces its susceptibility to injury. The signs and symptoms of pancreatic injury include
mild to severe midabdominal pain that often radiates to the
back, nausea and vomiting, signs of peritoneal irritation,
and shock. Damage to the pancreas may occur in the form
Clinical Caution of a contusion with pseudocyst development, traumatic
pancreatitis, laceration, or transection. Incidental pancre-
As a preventive measure for bladder injuries, it is wise to have
atitis, such as that occurring with excessive alcohol intake
contact-sport athletes use the bathroom to void prior to competition
or cholelithiasis, must also be considered in the differential
so the bladder is under less tension.
diagnosis of pancreatic abnormalities. The diagnosis is
made by CT or MRI scan. Serum amylase determination
may serve as a useful screening test, but a level in the nor-
mal range does not exclude the possibility of pancreatic
Bladder contusion, the most common bladder injury, damage. Atraumatic pancreas injury is treated via limitation
typically results from abdominal or pelvic trauma. The pre- of gastric stimulation, fluid replacement, analgesia, and
sentation is hematuria with indefinite suprapubic tenderness metabolical stabilization. Traumatic injury to the pancre-
and an absence of peritoneal signs, such as abdominal rigid- atic duct has been found in the recent literature to be the
ity and rebound tenderness. Bladder rupture is a rare but primary source of morbidity and mortality. Any treatment
extremely serious condition that necessitates prompt recog- plan, whether nonoperative or surgical, should focus on
nition and surgical treatment. The symptoms of bladder serial clinical examinations, measuring pancreatic enzyme
rupture include severe suprapubic pain, which often pro- levels, and magnetic resonance cholangiopancreatography
gresses rapidly to peritoneal signs and shock. An individual (MRCP) or endoscopic retrograde cholangiopancreatogra-
who is unable to void after abdominal or pelvic trauma phy (ERCP) to rule out ductal injury.82 The treatment of a
should undergo a cystogram. Any extravasation of contrast sports-related traumatic pancreatic injury is determined by
on cystography accurately depicts the site of injury. If ure- the severity of the injury. Conservative care includes bed
thral damage is suspected, retrograde urethrography should rest, bowel rest, and fluid replacement, whereas severe
precede blind catheterization to avoid inducing further injury may require surgical intervention, including distal
damage to the urethra. pancreatectomy.
Abdominal and Thoracic Injuries • CHAPTER 25 613
Injuries to the Genitalia and Perineum preservation of the injured testicle. Scrotal trauma can
displace the testicles into the perineum, suprapubic area, or
inguinal region.4
Testicular rupture, the most serious groin injury, is
Genitalia and Perineum Structures uncommon because of the mobility of the testes. Rupture
That Could Be Injured in Sports usually results from high-velocity sports, such as bicycling,
• Testicles when a testis is compressed between the bicycle saddle and
• Scrotum the pubic bones or when hit by a puck in ice hockey. The
• Penis tunica vaginalis, which covers the tubular and vascular com-
• Urethra ponents of the testis, ruptures after impact. The symptoms
• Perineum include pain and bleeding into the scrotum with massive
swelling. The treatment is emergent surgical testicular
repair and drainage of the scrotum.
Blunt groin trauma may cause a rapid accumulation of
blood in the scrotum, known as a hematocele, which is
Testicular and Scrotal Injury caused by rupture of the pampiniform plexus venous net-
Groin trauma is relatively common in sports that use hard work of the spermatic cord. Treatment for a hematocele
implements, such as ice hockey, baseball, softball, and involves bed rest, application of ice, and elevation of the
lacrosse. Many of these sports use hard, protective cups to scrotum with the possibility of surgical ligation of bleed-
safeguard this area, and thus serious injury occurs only ing vessels in case the hematoma continues to accumulate
rarely. Interestingly, football players seldom, if ever, wear rapidly. Individuals with varicoceles, a condition charac-
such protection. Testicular injury was actually found to have terized by chronic engorgement of the pampiniform
a relatively low incidence in a recent review of the National plexus, seem to be at increased risk of developing a
Pediatric Trauma Registry, with only 1 case out of 459 hematocele.
sports-related injuries reported.52 The symptoms of testicu- Contusions of the testicle or scrotum are the most com-
lar or scrotal injury, which include localized pain, scrotal mon groin injuries. They are most accurately evaluated in
swelling, and ecchymosis, are relatively nonspecific (Figure the period immediately following the injury, before swelling
25-10). The early identification of serious injuries, such as develops. Initial treatment should include bed rest, the ap-
testicular rupture or torsion, however, is essential for the plication of ice packs, scrotal elevation, and oral analgesics.
Figure 25-10
Anatomy of the male genitalia.
614 SECTION III • Management of Sports Injury and Illness
Ambulation is permitted once pain has resolved and swell- testicular rupture must be considered, and urgent uro-
ing has stabilized. A scrotal support should then be worn logical consultation should be sought.
for several days.83 Based on recent studies, testicle injuries are a relatively
Torsion of the spermatic cord may occur spontaneously, rare phenomenon in American sports, but do occur.52,69
after a blow to the scrotum, or as a result of forceful con- The athlete with a single testicle must be counseled as to the
traction of the cremasteric muscle, which draws the testis risk for a catastrophic injury should the remaining testicle
superiorly over the pubis and twists the cord. Torsion is be damaged. Protective equipment should always be used
unlikely if a supporter is worn. This injury must be sus- and appropriate activity modifications made to provide the
pected, particularly in the young athlete who experiences best level of groin protection to the athlete.
sudden or slowly progressive abdominal or groin pain with
no history of trauma. The physical examination may reveal Penile and Urethral Injury
poor definition of the scrotal structures. The diagnosis is The penis is rarely injured when the athlete wears an
suggested further by a radionuclide scan that shows reduced athletic supporter. Bicycle racers commonly experience a
uptake in the involved testicle, an indication for prompt traumatic irritation of the pudendal nerve as a result
surgical intervention. of prolonged episodes of direct pressure from the
Other conditions that must be considered in the evalua- hard bicycle saddle on the pudendal nerve. Symptoms,
tion of an athlete with groin pain include epididymitis and which may include localized penile numbness, priapism
neoplasms. Epididymitis (inflammation of elongated, cord- (erection of penis), and ischemic neuropathy, typically
like structure along the posterior border of the testis) typi- resolve after the bicycle race. The condition is usually
cally manifests with a gradual onset of scrotal pain in young preventable by using a longitudinally furrowed saddle
males. A soft, nontender testis adjacent to a discretely ten- and by the athlete avoiding squeezing the saddle during
der, swollen epididymis, is noted on physical examination. hill-climbing.
Pyuria (pus in urine) may be apparent on urinalysis. Testicu- The urethra is rarely injured in athletics. Men are
lar carcinomas are relatively common neoplasms in young generally affected more commonly than women. The
men and must be considered in the evaluation of any scrotal mechanism of injury is often a straddle injury, which most
masses. frequently occurs in bicycling, gymnastics, or equestrian
The workup and evaluation of scrotal and testicular events. The bulbous portion of the urethra is most often
injuries always should begin with a thorough history of involved, because the penile urethra is usually protected
injury. The physical examination may be best performed by the supporter, and the posterior urethra by the pubic
with the individual in the supine position so as to help bones. A serious blow to the perineum, pelvic diastasis, or
relieve discomfort and reduce the tug of gravity on the the presence of blood at the urethral meatus should
testicle. The anatomical structures should be palpated prompt further diagnostic investigation with retrograde
systematically with an attempt to identify each testis, epi- urethrography. Other symptoms of urethral injury may
didymis, and spermatic cord. The presence of scrotal include penile or perineal hematoma, and an absent or
swelling or fullness should prompt the use of transillumi- high-riding prostate on rectal examination.4 If urethral
nation to help differentiate between a hydrocele, which injury is suspected, retrograde urethrography should
does transilluminate and produces a testicular shadow, always be performed before passing a urethral catheter.
and a hematocele or testicular mass that does not transil- Extravasation of contrast during the retrograde urethro-
luminate. A Doppler probe evaluation is useful if one gram accurately delineates the location and extent of
suspects torsion of the cord, and the presence of a sper- urethral damage. The treatment is surgical repair, with a
matic artery pulse at the hilum of the testis helps to rule suprapubic cystostomy placed for urinary diversion. Cath-
out torsion. Ultrasonography provides the most useful eterized stenting or cystostomy may be used for 8 to
noninvasive imaging assessment of the scrotal contents. It 10 days without further surgery depending on the extent
helps to identify hematoceles, testicular masses, epididy- of the injury to the urethra.4 Urethral stricture is a com-
mal swelling, and testicular integrity. Ultrasonography mon complication.
may be limited, however, by available equipment and the
expertise of the individual ultrasonographer. Diagnostic Perineum Injuries
percutaneous needle aspiration of scrotal fluid should Hematoma. Women athletes occasionally sustain sports-
generally be avoided to reduce the risk of introducing related trauma (e.g., straddle injury, fall in water
infection and because of the technical difficulty of the skiing) to the vulva and labia, resulting in edema and hema-
procedure. Aspiration may be appropriate, however, in toma formation. Appropriate treatment includes ice applica-
the presence of a tensely swollen scrotum.83 As a general tion, oral analgesics, and protection. Vulvar hematomas
rule, if groin trauma results in a nonpalpable testicle rarely require surgical intervention and athletes may return
and a scrotum in which transillumination is ineffective, to sport once the pain and swelling have resolved.4 Vaginal
Abdominal and Thoracic Injuries • CHAPTER 25 615
lacerations rarely accompany such injuries, but their prompt and most circular in the superior thorax and becomes
recognition and treatment are necessary to avoid infection progressively larger and more oval in shape inferior to the
or long-term dysfunction. seventh rib. The orientation of the ribs is nearly horizon-
Vaginal Water Injection Injuries. The female re- tal at the top, gradually becomes increasingly oblique
productive organs are fortunately well protected by the lower in the thorax, and approaches verticality at the
pubis and thus not very frequently injured. Water skiing, inferior end. The upper seven “true” ribs articulate
however, may result in “water injection” damage to the anteriorly with the sternum by costochondral cartilage.
vagina, uterus, and fallopian tubes. A novice skier may The costochondral cartilage of the so-called false eighth
have difficulty standing and consequently assumes a squat- through tenth ribs does not attach immediately to the
ting position, which may enable water to enter the vagina. sternum, but instead joins the costocartilage of the adja-
Vaginal damage, incomplete abortions, and salpingitis cent rib above. The eleventh and twelfth ribs, known
(inflammation of the uterine tube) may occur. Salpingitis as the floating ribs, are engulfed by abdominal muscula-
manifests with signs of an acute abdomen and sepsis. ture anteriorly, with no bony attachment. The undersur-
However, symptoms do not generally appear clinically face of each rib has a groove through which traverse the
until after 3 days, at which time the athlete may not intercostal neurovascular structures. The intercostal
associate the injury with the infection. Vaginal injection nerves may refer pain to the chest and directly innervate
of water injuries may be avoided by wearing neoprene the thoracic wall.
shorts or wetsuits. The ribs lie subcutaneously in the anterior chest. This
places them at greater risk for damage from direct trauma
than the deeper-positioned posterior aspects of the ribs,
which are better protected by the heavy musculature of
Thoracic Injuries
the back and paraspinal muscles. The ribs are elevated
by the intercostal and other accessory muscles during
Thoracic Structures that Could Be Injured in Sport inspiration, with a resultant increase in the anterior-
• Ribs posterior diameter of the lower thorax. Adjacent ribs are
• Thoracic muscles further secured by fascial extensions from the external
• Sternum intercostal muscles between ribs. The abdominal muscles
• Pectoralis major stretch from the lower anterior ribs to the pelvic brim,
• Breast providing the anterior connection between the thorax and
• Vascular tissue the pelvis.
• Lungs Contusion. A direct blow to the anterior chest often
• Heart leads to contusion of the subcutaneously located ribs,
• Esophagus whereas a similar blow to the posterior chest is more likely
to cause paraspinal muscular injury. The most common
symptom of a rib contusion occurring from direct trauma is
localized pain during deep inspiration. The physical exami-
Injuries of the Chest Wall nation reveals localized tenderness over the injury without
Rib Injuries the crepitation that is sometimes noted with a rib fracture.
Twelve pairs of ribs articulate with the twelve correspond- In addition, manipulation of the affected rib at a site distant
ing thoracic vertebrae. Strong ligaments firmly attach each to the injury should not induce injury site pain. A rib contu-
rib to its analogous vertebra and to those located immedi- sion should be treated symptomatically. Once the possibility
ately above and below. Ribs one, eleven, and twelve articu- of an occult fracture has been eliminated, the athlete may be
late with only one vertebra, and ribs two through ten allowed to return to participation with padding over the
articulate posteriorly via the costovertebral and costotrans- injury site.
verse joints with the two adjacent vertebrae. Additional
capsular ligaments hold each rib tightly against the vertebral
body and transverse process at each level, whereas other
ligaments extend vertically from the transverse process of
Clinical Note
the vertebrae above, to the upper aspect of the rib below.
The strength of these ligamentous attachments makes The clinical differentiation of a rib fracture from a contusion is difficult,
sprains uncommon. The anatomy of the ribcage is pre- but injury site (localized) pain being elicited when the examiner com-
sented in Figure 25-11. presses the chest by placing one hand on the back of the hemithorax
Each rib-costocartilage pair, the corresponding verte- and the other on the front is usually indicative of fracture.
bra, and the sternum form a ring structure that is smallest
616 SECTION III • Management of Sports Injury and Illness
Figure 25-11
Anatomy of the ribcage, sternum, and costochondral joints.
have spontaneously reduced by the time a physician is con- Chronic Costochondral Injuries. Costochondral
sulted. The diagnosis of a rib-vertebral subluxation or reduced subluxation becomes chronic when an athlete fails to seek
dislocation is made by the identification of a localized tender medical evaluation until after multiple episodes of sublux-
spot that corresponds to the site of injury and the complete ation have occurred. The treatment of this condition is
resolution of symptoms when local anesthetic is injected into determined by the amounts of instability and pain. In the
the joint. If the subluxation has reduced, the athlete may presence of joint stability, when pain is the major complaint,
return to sports participation in 7 to 10 days with lower chest local injections with anesthetics and corticosteroids may be
strapping. employed. If some degree of pain relief is not achieved after
Occasionally, dislocations remain unreduced at the time repeated injections during the first 3 to 4 days, it is unlikely
of evaluation. Pain is typically more severe, and physical that further injections will be effective. If pain is severe and
findings reveal localized tenderness, muscle spasm, and disabling with or without instability, surgery may be consid-
joint motion. Associated damage to the neurovascular ered. Surgery involves the resection of adequate opposing
bundle often causes neuritis symptoms in the distribution of joint surfaces so that they no longer rub together. Given the
the costal nerve. Unreduced dislocations should be manu- inherent stability of the rib even after resection of the cos-
ally reduced to prevent complications of long-term degen- tochondral junction and the difficulty in fusing rib to carti-
erative joint disease. Reduction may be accomplished by lage, the rib end is generally not internally fixated. Chronic
hyperextending the spine and allowing the shoulders and instability or dislocation alone does not justify surgery, but
arms to fall backward, and then applying direct pressure if localized pain, swelling, and muscle spasm occur, surgery
to the posterior dislocated segment while simultaneously may become necessary. Surgery in such cases involves the
applying pressure against the anterior chest. resection of a portion of chondral cartilage or the rib end to
Acute Costochondral Injuries. The anterior attach- avoid painful impingement.
ment of the rib is far more frequently injured than the ver- Fortunately, given the common occurrence of costo-
tebral junction. Direct sternal trauma or lateral compression chondral injuries, few are severe enough to require the
of the chest may produce costochondral joint sprain, sub- discontinuation of sports. It is important, however, to
luxation, or dislocation. The diagnosis is made based on the treat acute injuries with reduction, pad application, and
presence of tenderness at the costochondral junctions, strapping to avoid chronic symptoms. Union of a separated
which are located one to two finger-breadths lateral to the costochondral junction takes 8 weeks, during which time
costosternal junctions. Occasionally a popping sensation or contact sports should be avoided.
palpable step-off is felt with twisting of the torso. The sever- Costochondritis. It is important to recognize costo-
ity of the injury is determined by the amount of tenderness, chondritis (inflammation of the costal cartilage) as a source
localized anterior chest wall swelling, and hematoma forma- of chest pain in the athlete. Often, it presents as pain and
tion over the injury site. The patient will have full range of tenderness over the second to fifth costochondral or chon-
motion of the shoulder but active abduction may cause the drosternal joints. Swelling, heat, and erythema are normally
swelling to become more prominent.85 More severe sprains absent. Inflammation has been suggested as the source of
are associated with pain during deep inspiration. Persistent costochondritis because some patients show an elevated
joint dislocation is readily apparent clinically as a step-off at erythrocyte sedimentation rate (ESR) and morning
the joint site, which may reduce with an audible click, as stiffness.86 Symptoms are often provoked by shoulder
direct pressure is applied over the rib end. Radiographs are adduction with rotation of the arm to the same side. Radio-
of little use in diagnosing costochondral separations, be- graphs are usually negative but can potentially show mild
cause the costocartilage is radiolucent. MRI may be used if soft tissue swelling. CT and bone scan may also be used to
there is significant clinical concern for the injury. make the diagnosis.85 The treatment of costochondritis
Acute costochondral separation without displacement or is with analgesia and reassurance, and symptoms usually
a palpable click involves an at least partially intact ligamen- resolve within 1 year.
tous complex. The treatment is to prevent further injury Fracture. In both the athlete and nonathlete, a simple,
and relieve discomfort with injection of a long-acting local nondisplaced rib fracture is the most common result of
anesthetic. In the presence of a palpable step-off or audible blunt thoracic trauma.4 The first through third ribs are well
click, the treatment should be directed toward preventing protected by the shoulder girdles, making superior rib frac-
recurrence. A direct pressure pad should be applied over the tures rare. First and second rib fractures usually only occur
anterior end of the rib rather than over the costochondral from significant direct force or from deceleration. There-
joint. A rib belt or strapping may be used to hold the pad fore, the presence of these injuries should suggest the pos-
in place. Union of acute costochondral separation occurs sibility of coexisting injuries to the aorta, great vessels, and
slowly (often longer than a rib fracture), typically taking airways. Arteriography may be considered if clinically ap-
6 to 8 weeks. Participation in contact sports should be propriate. A special type of stress fracture of the first rib has
withheld for 3 to 4 weeks. also been reported (discussed later).
618 SECTION III • Management of Sports Injury and Illness
attached to the scapula, a sling may be worn to promote possible. Closed reduction, under general anesthesia, may
rest and recovery. Similarly, if an abdominal muscle has initially be attempted, although open reduction with wire
been injured, bed rest, with the head of the bed and the loop internal fixation may be required. As with any severe
knees elevated to completely relax the abdominal muscles, chest injury, the presence of subluxation or dislocation
may be prescribed. should alert the clinician to the possibility of underlying
visceral injury.
Sternum Sprains are uncommon at the junction of the sternal
The sternum, which protects the vital anatomical structures body and xiphoid as a result of the free anterior-posterior
of the mediastinum, is made up of three bones: the upper movement of this joint. Sternal body–xiphoid dislocations
manubrium, the middle body, and the lower xiphoid (see are rare.
Figure 25-11). The first rib and the upper portion of the Sternoclavicular Dislocation. Dislocation of the ster-
second rib usually inserts onto the manubrium. The lower noclavicular joint is a relatively rare occurrence with an
portion of the second rib and the third through sixth (and incidence of only 1% of all dislocations. Regardless of its low
sometimes seventh) ribs insert on the sternal body. The incidence, the sports medicine clinician should be wary of
seventh rib usually inserts on the xiphoid. The newborn has the potential complications of mediastinal hemorrhage,
six unfused sternal segments, which gradually fuse through tracheal rupture, and esophageal perforation, which may be
the late teenage years to form the three-bone adult ster- associated with this injury.95-97
num. Persistent perfusion lines should not be mistaken Sternoclavicular dislocations have been found in athletes
for fractures when radiographically evaluating children and engaged in contact sports such as football and rugby.
adolescents. Patients tend to be males younger than 25 years old.98
Contusion. The subcutaneous location of the sternum Anterior dislocations are seen much more commonly than
makes it susceptible to contusions. Participants in contact posterior dislocations because of the weakness of the ante-
sports that do not require the use of protective sternal rior sternoclavicular ligaments.99
pads or that involve high-velocity objects are particularly
vulnerable to sternal injury. A direct blow to the sternum
typically produces superficial edema, ecchymosis, periosteal Clinical Caution
reaction, and a severe “shock reaction,” in which the athlete
transiently senses difficulty with respiration. Deep inspira- Posterior dislocations of the sternoclavicular joint are much more
dangerous because of the risk of injury to the great vessels and
tion will not typically aggravate pain in the absence of
airway that lie directly beneath the sternoclavicular joint.
complications.
Mild and moderate sternal contusions are treated
with ice, followed by heat application. If pain is severe,
however, the area of injury may be injected with local A thorough history and physical examination is normally
anesthetics. A protective pad should be applied before all that is needed to make the diagnosis of sternoclavicular
permitting the athlete to return to contact sports. Foot- dislocation. The patient will have pain in the area of the
ball shoulder pads generally provide excellent sternal sternoclavicular joint, which is exacerbated by motion of the
protection. arm. If the diagnosis is not obvious, an x-ray examination
Sprain, Subluxation, and Dislocation. A direct ster- can be performed with a 40° cephalic tilt or a CT scan may
nal blow may also result in sternal joint sprain, subluxation, be done.100 CT has the added benefit of being able to diag-
or dislocation. The ligaments between the manubrium and nose injury to the retrosternal structures.101
body are quite firm and thus are rarely damaged. When Treatment of acute sternoclavicular dislocations depends
joint subluxation or dislocation does occur, however, reduc- on the direction of the dislocation. Anterior dislocations
tion is usually spontaneous. Clinical symptoms include pain may be reduced acutely, whereas posterior dislocations must
and tenderness at the manubrium-body junction without be reduced emergently in the operating room because of
pain during ordinary breathing. But severe pain is produced the possibility of compression of the mediastinal structures.
when direct compressive pressure is placed on the manu- A thoracic surgeon may be needed to assist with surgery in
brium or sternal body. the case of vascular injury. Postreduction management is
The treatment of a sprain or spontaneously reduced with sling immobilization for 4 to 6 weeks until healing is
subluxation entails avoidance of sports participation for a complete.96,98 If the joint remains unstable, it may need to
minimum of 7 to 10 days, followed by usage of a hollowed be repaired surgically. Athletes should avoid returning to
plastic sternal pad. If chronic pain symptoms persist, play until they have pain-free range of motion with a stable
injections of local anesthetics with corticosteroids may be sternoclavicular joint.
considered. Fracture. Sternal fractures may also result from direct
On rare occasions, sternal injury produces a complete trauma. Most fractures occur in the upper portion of the
dislocation. These injuries should be reduced as soon as sternal body, caused by direct pressure driving the body
Abdominal and Thoracic Injuries • CHAPTER 25 621
by uncoordinated eccentric contraction occur at the muscu- recommends an accelerated rehabilitation protocol for
lotendinous junction, or as an avulsion of the tendon from pectoralis major rupture starting with elbow range of
the humerus.74 Wolfe et al108 and Kakwani and Matthews111 motion from day 1. At 2 weeks, passive external rotation
demonstrated that the relatively short muscle fibers of the is introduced along with isometric strengthening exercises
inferior portion of the sternocostal head of the pectoralis for the rotator cuff and pectoralis muscles with the shoul-
muscles must lengthen disproportionately during the final der in neutral rotation. It is imperative that the physical
30° of humeral abduction, external rotation, and extension therapist be in contact with the surgeon so as to ascertain
as the weight is lowered during the bench press. These the proper “safe arc” for external rotation exercises as
inferior fibers are placed at a mechanical disadvantage, determined on intraoperative testing of the repaired pec-
which, in conjunction with the high-load eccentric forces of toralis tendon.111 The “safe arc” is determined by the
the lift, causes rupture.108 surgeon after reattachment of the distal end of the pecto-
The symptoms of acute pectoralis major muscle rupture ralis tendon in the operating room. By testing the stability
are a tearing sensation into the axilla; severe anterior chest of the fixation and determining a range of motion in
pain, which may radiate to the shoulder or upper arm; a which the repair is sound, the physical therapist can be
“snapping” or “popping” sound; ecchymosis; and swell- given parameters within which he or she can successfully
ing. The diagnosis may be difficult to confirm unless the rehabilitate the patient without fear of rupturing the
injury is seen immediately after rupture, because of non- newly repaired tendon.
specific swelling and extreme pain. Repeated physical ex- MRI is an excellent early diagnostic tool to assist in the
aminations are often necessary. Characteristic physical diagnosis and management of pectoralis major ruptures and
findings include bruising and local tenderness accompa- will allow for the identification of the exact location and
nied by weakness of upper arm adduction, flexion, internal extent of the rupture.107,111 To help prevent ruptures, it
rotation and bulging of the torn pectoralis muscle during seems sensible to change the arc of the bench press exercise
forced adduction. In addition, if the tear occurs with an to limit hyperextension of the arm and the resultant passive
avulsion of the tendon, a palpable defect may be noted in stretch of the muscle fibers. In addition, despite denials of
the anterior axillary fold. A tear localized at the musculo- anabolic steroid usage in weight lifters who had sustained
tendinous junction may be inapparent to palpation and pectoralis major ruptures, the possibility of an association
inspection because of the integrity of the fascial covering. must be considered.107
A clue to the diagnosis is an absent pectoralis major
shadow and a loss of the normal anterior axillary fold on Breast Injury
the frontal chest radiograph.111 Athletic female breast injury has become an increasingly
The treatment of complete pectoralis major rupture is common occurrence as the number of women participating
generally nonsurgical for elderly or sedentary individuals. in sports at all levels has increased. Breast injury may occur
Incomplete tears are also typically treated nonoperatively. as a result of direct trauma or repetitive microtrauma from
Injuries that go unrepaired will leave the individual with inadequate breast support. One report revealed that 56% of
a significant strength deficit compared with the unin- physically active female subjects had experienced previous
volved side. Immediate surgical repair is the treatment of sports-related breast discomfort or pain.113
choice for young or athletic individuals.109 Pectoralis Direct trauma to the breast may produce fat necrosis or
major ruptures that are repaired surgically result in com- hematoma formation, both of which are painful and may
parable muscular torques and work measurements relative result in the formation of a focal breast mass. Mammo-
to the uninvolved side.108 Immediate surgical repair is graphic appearance of these lesions is often indistinguish-
optimal, because this reduces the development of adhe- able from that of malignancy. The treatment of direct breast
sions, muscle retractions, atrophy, and any delays in trauma is oral analgesics, cold application, followed by heat
return to athletic competition. A success rate of 90% good application, breast support, and protection with padding.
to excellent results for acute repair has been reported NSAIDs are contraindicated because of the risk of increased
in the literature compared with 70% for nonoperative bleeding.4 Sports participation should be limited until
treatment.110,112 Individuals with chronic tears, who may inflammation has subsided.
be identified by serial examinations, strength testing, and Running causes the female breasts to bounce vertically
MRI scan, have undergone successful operative repair. and slap against the chest wall, producing breast contusions
The common surgical procedure involves a deltopectoral and soreness. Women with large breasts are especially at risk
incision, evacuation of hematoma, and reattachment of for running-induced breast injury. Inadequate breast sup-
the tendon to bone with a variety of techniques including port may also result in stretching of the Cooper ligaments,
direct suture to the periosteum, suture to the remaining the structures that attach the breast to the chest wall. This
tendon, drill holes, and suture anchors. A sling is gener- has been called runner’s breast and often results in pain.
ally used for 2 to 4 weeks postoperatively. Kakwani now Chronic lack of breast support may exacerbate ptosis, or
Abdominal and Thoracic Injuries • CHAPTER 25 623
tracheal deviation contralaterally. Cardiac tamponade pro- Severe pulmonary contusions often occur in conjunc-
duces a narrowed pulse pressure and distended neck tion with extrathoracic injuries, which may detract from
veins. the danger of the pulmonary damage. Children are
prone to pulmonary contusions in the absence of rib frac-
Pulmonary Injuries tures because the compressive nature of their rib cages
Contusion. Most cases of pulmonary contusion result allows the force of the impact to be primarily transmitted
from motor vehicle accidents, although athletes may experi- to the lungs.117 A severe contusion results in an increased
ence blunt chest trauma of sufficient force to cause the alveolar-to-arterial oxygen gradient and reduced arterial
condition. Trauma-induced alveolar capillary damage with oxygen pressure while breathing 100% oxygen, in addition
interstitial and intra-alveolar hemorrhage leads to pulmo- to the presence of frankly bloody tracheobronchial secre-
nary parenchymal edema and hemorrhage, atelectasis, and tions and progressive respiratory failure. Despite aggres-
copious tracheobronchial secretions, which may impair sive treatment with mechanical ventilation, tracheobron-
pulmonary function. Hypoxemia ensues because of the chial suctioning, bronchodilators, and diuretics to reduce
ventilation-perfusion mismatch that is created.14 pulmonary edema, this condition may prove fatal.
Initial chest radiographs are often normal, but unilat- Pneumothorax. Pneumothorax is the most common
eral or bilateral, patchy, ill-defined pulmonary infiltrates complication of rib fractures and the most common intra-
may develop within 1 to 6 hours of injury.14 Thus, if a thoracic injury following blunt thoracic trauma.117 A fractured
pulmonary contusion is suspected, the athlete should be rib edge may puncture the pleura and lung to cause a leakage
admitted to the hospital, and serial chest x-ray films of air into the intrapleural space (i.e., a pneumothorax). A
should be obtained. CT scan has recently gained favor simple pneumothorax may also occur in the absence of rib
because of its high diagnostic sensitivity in the early stages fractures. Mechanisms of injury include sudden compres-
of contusion.116 sion of the chest while the glottis is closed with resultant
alveolar blowout and spontaneous bleb rupture. Most epi-
sodes of simple pneumothorax are self-limited in that the
apposition of the lung and pleural surfaces tends to seal the
Clinical Caution air leak. The findings of dyspnea, cyanosis, and progressive
Patients with pulmonary contusions may have normal initial chest respiratory collapse are consistent with severe cases. Signs of
radiographs, but pulmonary infiltrates can develop within 1 to 6 hours pulmonary insufficiency may be absent, however, in young,
of injury.14 If the mechanism of injury is indicative of a pulmonary athletic individuals because of their large functional cardio-
contusion, the athlete should be admitted to the hospital for serial pulmonary reserve.
chest x-ray examinations or a computed tomography scan.
Clinical Caution
A young athletic individual who has suffered a thoracic injury resulting
The symptoms of a mild contusion include tachypnea, in a pneumothorax may not show the signs of pulmonary insufficiency
tachycardia, the presence of rales on auscultation of the lung such as dyspnea, cyanosis, and progressive respiratory collapse
fields, and a cough with abundant blood-tinged secretions because of their large functional cardiopulmonary reserve.
(hemoptysis). Hemoptysis is present in 50% of all patients
with pulmonary contusion.90 The treatment of mild pulmo-
nary contusion incorporates pulmonary physical therapy, The physical examination may reveal tachypnea, de-
nasotracheal suctioning, analgesics, humidified oxygen sup- creased breath sounds to auscultation, and hyperresonance
plementation, bronchodilators as needed, and appropriate to percussion. Chest radiography often confirms the pres-
antibiotic therapy or prophylaxis. In general, mild pulmo- ence of a pneumothorax, and the sensitivity is improved
nary contusions are self-limited and the athlete may begin further by obtaining upright inspiration and expiration films
gradual training as soon as the symptoms resolve and there (Figure 25-15).
is radiographic resolution with the knowledge that both The treatment of a simple pneumothorax depends on the
exercise tolerance and reserve will be greatly lowered.14,117 percentage of lung volume that is lost, the severity of pulmo-
nary compromise, and the need for general anesthesia to
address associated injuries. The size of a pneumothorax is
Clinical Note estimated as a percentage of volume loss within a hemitho-
rax, by viewing the chest radiograph. Generally, a pneumo-
The athlete who has suffered a mild pulmonary contusion may return thorax of 15% to 25% without respiratory distress or the
to gradual training as soon as the symptoms resolve and there is need for general anesthesia may be treated without a chest
radiographic resolution. tube.117 Serial chest radiographs should be obtained to
confirm improvement. A pneumothorax should resorb by
Abdominal and Thoracic Injuries • CHAPTER 25 625
Clinical Caution
Although the majority of subcutaneous emphysema caused by rib
fractures resolves spontaneously, occasionally cardiac decompensa-
tion may occur as a result of pressurized mediastinal air, forcing
collapse of the great veins and restricting blood return to the right
side of the heart.
resulting in thrombosis that may lead to myocardial infarc- vulnerable time in the cardiac cycle.123,124 Ultimately, com-
tion. Additional potential complications of cardiac contusion motio cordis may lead to sudden cardiac death. The auto-
are right-sided heart failure, hypotension, arrhythmia, and mated external defibrillator (AED) should be used if an
rupture of the intraventricular septum, with a resultant acute episode of commotio cordis occurs. If an AED is not avail-
left-to-right shunt.14 able, a precordial “thump” can be given to start the
Cardiac contusion is diagnosed by maintaining suspicion heart.123 Commotio cordis has been seen in such sports as
based on the mechanism of injury and by the characteristic youth baseball, lacrosse, hockey, cricket, and soccer.
electrocardiographic changes that are consistent with myo-
cardial damage. Of all patients with cardiac contusion, 70%
show sinus tachycardia on electrocardiogram (ECG).90
Clinical Note
Other ECG findings include premature atrial and ventricu-
lar complexes. In addition to an ECG, the athlete suspected An automated external defibrillator should be kept with the trainer’s
of having a myocardial contusion should have serial cardiac equipment at athletic activities. In the unlikely event that one is not
enzymes and an echocardiogram. Unfortunately, the avail- available or malfunctioning, a precordial thump may be used in the
able diagnostic tools are not specific for cardiac contusion event of a witnessed episode of commotio cordis.
and are unable to predict the risk of complications.
Clinical Caution
Dysrhythmias are most likely to develop in the first twelve hours after Physical Signs of Pericardial Tamponade
suffering a cardiac contusion. • Neck vein distension
• Shock
• Cyanosis
• Pulsus paradoxus (an abnormal decrease [ 10 mm Hg] in
The presence of arrhythmia, heart failure, elevated cre- systolic pressure and pulse wave amplitude during inspiration)
atine kinase myocardial band, or wall motion abnormalities
requires a longer inpatient observation period. Decisions
on return to play after cardiac contusion depend on the
extent of the injury and the presence of associated injuries. Rupture of the Aorta. Rupture of the aorta is a rare
Consultation with a cardiologist is recommended.91 complication of blunt chest trauma in which the descending
Commotio Cordis. Commotio cordis is the commonly aorta undergoes torsion, and the aortic wall is disrupted at
used term for ventricular fibrillation resulting from a sud- the ligamentum arteriosum. Occasionally, damage occurs to
den blow to the anterior chest wall during an extremely the ascending aorta at the root of the heart. Most victims of
628 SECTION III • Management of Sports Injury and Illness
aortic rupture die immediately from massive exsanguina- 4. Amaral JF: Thoracoabdominal injuries in the athlete, Clin Sports
tion, but a few survive as a result of the formation of a “false Med 16(4):739–753, 1997.
5. Maquirriain J, Ghisi JP, Kokalj AM: Rectus abdominis muscle
aneurysm” between the periaortic tissues and the pleura.
strains in tennis players. Br J Sports Med 41(11):842–848, 2007.
The diagnosis may be suspected on the basis of widening of 6. Taylor DC, Meyers WC, Moylan JA, et al: Abdominal muscula-
the cardiac silhouette on chest radiograph. CT scan, MRI ture abnormalities as a cause of groin pain in athletes, Am J Sports
scan, or retrograde aortography is confirmatory. The treat- Med 19:239–242, 1991.
ment is immediate surgical repair. 7. De Shazo WF: Hematoma of the rectus abdominis in football,
Phys Sports Med 12:73–75, 1984.
8. US Department of Health, Education, and Welfare: National
Esophageal Injury health survey of hernias, Series B, No. 25, Dec 1960.
Most injuries to the esophagus are the result of penetrating 9. Nyhus LM, Bombeck CT: Hernias. In Sabiston DC, editor: Text-
trauma rather than blunt injury. Esophageal perforation book of surgery—The biological basis of modern surgical practice,
may manifest as extreme chest pain followed by the gradual ed 13, Philadelphia, 1986, WB Saunders.
10. Smedberg SGG, Broome AEA, Gullmo A, Roos H: Herniogra-
onset of fever over several hours. Regurgitation of blood,
phy in athletes with groin pain, Am J Surg 140:378–382, 1985
hoarseness, dysphagia, and respiratory distress may also be 11. Kluin J, den Hoed PT, van Linschoten R, et al: Endoscopic
present. The chest radiograph may show mediastinal air, evaluation and treatment of groin pain in the athlete, Am J Sports
widening, and a pleural effusion. The diagnosis is confirmed Med 32(4):944–949, 2004.
by water-soluble contrast radiography or esophagoscopy. 12. De Paulis F, Cacchio A, Michelini O, et al: Sports injuries in the
pelvis and hip: Diagnostic imaging, Eur J Radiol 27 Suppl
The treatment is immediate surgical debridement, suture
1:S49–59, 1998.
closure of damaged tissues, and drainage. 13. Haycock CE: How I manage hernias in the athlete, Phys Sports
Med 11:77–79, 1983.
14. Lawrence PF, Bell RM, Dayton MT, Ahmed MI: Essentials of
Conclusion general surgery, ed 3, Philadelphia, 2000, Lippincott Williams &
Wilkins.
The abdominal cavity, by nature of its relative lack of bony
15. Stoker DL, Spiegelhalter DJ, Singh R, Wellwood JM: Laparo-
protection, is quite susceptible to blunt trauma injury dur- scopic versus open inguinal hernia repair: Randomized prospective
ing athletics. The structures of the abdominal wall are often trial. Lancet 343:1243–1245, 1994.
injured by direct compression forces, whereas the intra- 16. Renstrom P, Peterson L: Groin injuries in athletes, Br J Sports
abdominal organs are often damaged by compression Med 14:30–36, 1980.
17. Ekstrand J, Hilding J: The incidence and differential diagnosis of
against the spine. Injuries to the abdomen may become life-
acute groin injuries in male soccer players, Scand J Med Sci Sports
threatening, particularly if significant time passes without 9:98–103, 1999.
treatment. A major exsanguination from a ruptured blood 18. Meyers WC, McKechnie A, Philippon MJ, et al: Experience
vessel may rapidly progress to shock and death without with “sports hernia” spanning two decades, Ann Surg 248(4):
prompt, appropriate treatment. 656–665, 2008.
19. Lovell G: The diagnosis of chronic groin pain in athletes: A review
Thoracic injuries are more likely to be life-threatening
of 189 cases, Aust J Sci Med Sport 27:76–79, 1995.
because of a disruption of the cardiopulmonary systems. 20. Malycha P, Lovell G: Inguinal surgery in athletes with chronic
Most serious intrathoracic injuries result from shearing groin pain: The “sportsman’s” hernia, Aust N Z J Surg 62:
forces of deceleration that may disrupt vital structures. Pen- 123–125, 1992.
etrating trauma from objects such as a displaced rib fracture 21. Ahumada LA, Ashruf S, Espinosa-de-los-Monteros A, et al: Ath-
letic pubalgia: Definition and surgical treatment, Ann Plast Surg
must also be considered as causes of thoracic injury. Injuries
55:393–396, 2005.
to the surface of the thorax typically manifest as muscle 22. Polglase AL, Frydman GM, Farmer KC: Inguinal surgery for
strains or ruptures, contusions, or bony fractures. The ath- debilitating chronic groin pain in athletes, Med J Aust 155:
letic health care professional must be well trained and 674–677, 1991.
knowledgeable in the early assessment, stabilization, and 23. Larson CM, Lohnes JH: Surgical management of athletic pubalgia,
Oper Tech Sports Med 10:228–232, 2002.
management of the various types of traumatic injuries that
24. Meyers WC, Foley DP, Garrett WE, et al: Management of severe
may involve the abdomen and chest. lower abdominal or inguinal pain in high performance athletes:
PAIN (Performing athletes with Abdominal or Inguinal Neuro-
muscular Pain Study Group), Am J Sports Med 28:2–8, 2000.
References 25. Leblanc KE, Leblanc KA: Groin pain in athletes, Hernia 7:
68–71, 2003.
1. Johnson R: Abdominal wall injuries: Rectus abdominis strains, 26. Hackney RG: The sports hernia: A cause of chronic groin pain,
oblique strains, rectus sheath hematoma, Curr Sports Med Rep Br J Sports Med 27:58–62, 1993.
5(2):99–103, 2006. 27. Renstrom P: Tendon and muscle injuries in the groin area, Clin
2. Bergqvist D, Hedelin H, Karlsson G, et al: Abdominal injury Sports Med 11:815–830, 1992.
from sporting activities, Br J Sports Med 16:76–79, 1982. 28. Steele P, Annear P, Grove JR: Surgery for posterior wall inguinal
3. Diamond DL: Sports-related abdominal trauma. In Ray RL, deficiency in athletes, J Sci Med Sport 7:415–421, 2004.
editor: Clinics in sports medicine—Emergency treatment of the 29. Gentisaris M, Goulimaris I, Sikas N: Laparoscopic repair of groin
injured athlete, Philadelphia, 1989, WB Saunders. pain in athletes, Am J Sports Med 32:1238–1242, 2004.
Abdominal and Thoracic Injuries • CHAPTER 25 629
30. Farber AJ, Wilckens JH: Sports hernia: Diagnosis and therapeutic 54. Buntain WL, Gould HR, Maull KI: Predictability of splenic
approach, J Am Acad Orthop Surg 15(8):507–514, 2007. salvage by computed tomography. J Trauma 28:24–34, 1988.
31. Verrall GM, Slavotinek JP, Fon GT: Incidence of pubic bone 55. Waninger KN, Harcke HT: Determination of safe return to play
marrow edema in Australian rules football players: Relation to for athletes recovering from infectious mononucleosis: A review
groin pain, Br J Sports Med 35:28–33, 2001. of the literature. Clin J Sports Med 15(6):410–416, 2005.
32. Albers SL, Spritzer CE, Garrett WE, Meyers WC: MR findings in 56. Mostafa G, Matthews BD, Sing RF, et al: Elective laparoscopic
athletes with pubalgia, Skeletal Radiol 30: 270–277, 2001. splenectomy for grade III splenic injury in an athlete. Surg
33. Shortt CP, Zoga AC, Kavanagh EC, Meyers WC: Anatomy, Laparosc Endosc Percutan Tech 12(4):283–286; discussion 286–288,
pathology, and MRI findings in the sports hernia, Semin 2002.
Musculoskelet Radiol 12(1):54–61, 2008. 57. Kinderknecht JJ: Infectious mononucleosis and the spleen, Curr
34. Zajick DC, Zoga AC, Omar IM, Meyers WC: Spectrum of MRI Sports Med Rep 1(2):116–120, 2002.
findings in the sports hernia, Semin Musculoskelet Radiol 12(1): 58. Maki DG, Reich RM: Infectious mononucleosis in the athlete:
3–12, 2008. Diagnosis, complications, and management, Am J Sports Med
35. Zoga AC, Kavanagh EC, Omar IM, et al: Athletic pubalgia and 10:162–173, 1982.
the “sports hernia”: MR imaging findings, Radiology 247(3): 59. Rutkow IM: Rupture of the spleen in infectious mononucleosis,
797–807, 2008. Arch Surg 113:718–720, 1978.
36. Orchard JW, Read JW, Neophyton J, Garlick D: Groin pain 60. Stricker PR, Hardin BH, Puffer JC: An unusual presentation of
associated with ultrasound finding of inguinal canal posterior wall liver laceration in a 13-yr-old football player, Med Sci Sports Exerc
deficiency in Australian rules footballers, Br J Sports Med 32: 25:667–672, 1993.
134–139, 1998. 61. Mustalich AC, Quash ET: Sports injuries to the chest and abdo-
37. Joesting DR: Diagnosis and treatment of sportman’s hernia, men. In Scott WN, Nisonson B, Nicholas JA, editors: Principles
Curr Sports Med Reports 1:121–124, 2002. of sports medicine, Baltimore, 1984, Williams & Wilkins.
38. Sutcliffe JR, Taylor OM, Ambrose NS, Chapman AH: The use, 62. Hiatt JR, Harrier D, Koenig BV, Ransom KJ: Nonoperative
value and safety of herniography, Clin Radiol 54:468–472, management of major blunt liver injury with hemoperitoneum,
1999. Arch Surg 125:101–103, 1990.
39. Hamlin JA, Kahn AM: Herniography: A review of 333 hernio- 63. Moon KL, Federele MP: CT in hepatic trauma, Am J Radiol
grams, Am Surg 64:965–969, 1998. 141:309–314, 1983.
40. Ekberg O: Complications after herniography in adults, Am J 64. Cywes S, Rode H: Blunt liver trauma in children—Non-operative
Roentgenol 140:491–495, 1983. management, J Pediatr Surg 20:14–18, 1985.
41. Unverzagt CA, Schuemann T, Mathisen J: Differential diagnosis 65. Henderson JM, Puffer JC: Abdominal pain in a football player,
of a sports hernia in a high school athlete, J Orthop Sports Phys Phys Sports Med 17:47–52, 1989.
Ther 38(2):63–70, 2008. 66. Murphy CP, Drez D: Jejunal rupture in a football player, Am J
42. Liem M, van der Graaf Y, van Steensel CJ, et al: Comparison Sports Med 15:184–185, 1987.
of conventional anterior surgery and laparoscopic surgery for 67. Moses FM: Exercise-associated intestinal ischemia, Curr Sports
inguinal hernia repair, N Engl J Med 336:1541–1547, 1997. Med Reports 4(2):91–95, 2005 Apr.
43. Swan KG, Wolcott M: The athletic hernia, Clin Orthop Relat Res 68. Glenn JF, Harvard BM: The injured kidney, JAMA 173:1189,
455:78–87, 2007. 1960.
44. Bradshaw C, McCrory P, Bell S, Brukner P: Obturator nerve 69. McAleer IM, Kaplan GW, LoSasso BE: Renal and testis injuries
entrapment: A cause of groin pain in athletes, Am J Sports Med in team sports, J Urol 168:1805–1807, 2002.
25(3):403–409, 1997. 70. Brophy RH, Gamradt SC, Barnes RP, et al: Kidney injuries in
45. Douglas DM: The healing of aponeurotic incisions, Br J Surg professional American football: Implications for management of
40:79, 1952. an athlete with 1 functioning kidney, Am J Sports Med 36(1):
46. Olsen WR: Abdominal trauma in the athlete. In Schneider RC, 85–90, 2008.
Kennedy JC, Plant ML, editors: Sports injuries—Mechanisms, 71. Kallmeyer JC, Miller NM: Urinary changes in ultra long-distance
prevention, and treatment, Baltimore, 1985, Williams & marathon runners, Nephron 64(1):119–121, 1993.
Wilkins. 72. Peterson NE: Genitourinary trauma. In Feliciano DV, Moore
47. Higgins GL: Penetrating trauma—Managing and preventing EE, Mattox KL, editors: Trauma, ed 3, Stamford, CT, 1996,
javelin wounds, Phys Sports Med 22:88–94, 1994. Appleton & Lange.
48. Green GA: Gastrointestinal disorders in the athlete, Sports Med 73. Holmes FC, Hunt JJ, Sevier TL: Renal injury in sport, Curr
11:453–470, 1992. Sports Med Reports 2(2):103–109, 2003.
49. American College of Surgeons: Abdominal trauma. In Advanced 74. Kulund DN: The injured athlete, Philadelphia, 1982, JB
trauma life support student manual, Chicago, 1989, American Lippincott.
College of Surgeons. 75. Dorsen PJ: Should athletes with one eye, kidney, or testicle play
50. Coant PN, Kornberg AE, Brody AS, Edwards-Holmes K: Markers contact sports? Phys Sportsmed 14:130, 1986.
for occult liver injury in cases of physical abuse in children, Pediatrics 76. Anderson CR: Solitary kidney and sports participation, Arch Fam
89:274–278, 1992. Med 4:886, 1994.
51. Fabian TC, Croce MA: Abdominal trauma, including indications 77. Psooy K: Sports and the solitary kidney: How to counsel parents,
for celiotomy. In Feliciano DV, Moore EE, Mattox KL, editors: Can J Urol 13(3):3120–3126, 2006.
Trauma, ed 3, Stamford, CT, 1996, Appleton & Lange. 78. Kenney P: Abdominal pain in athletes, Clin Sports Med 6:
52. Wan J, Corvino TF, Greenfield SP, DiScala C: Kidney and 885–904, 1987.
testicle injuries in team and individual sports: Data from the 79. Stricker PR, Puffer JC: Case report: Renal laceration—A skate-
national pediatric trauma registry, J Urol 170:1528–1532, boarder’s symptoms are delayed, Phys Sports Med 21:59–68,
2003. 1993.
53. Affleck TP: Severe sports-related spleen injury, Phys Sports Med 80. Siegel AJ, Hennekens CH, Soloman HS, Van Boeckel B: Exercise-
20:109–123, 1992. related hematuria, JAMA 241:391–392, 1979.
630 SECTION III • Management of Sports Injury and Illness
81. Blalock NJ: Bladder trauma in long-distance runners, Am J Sports 103. Wright SW: Myth of the dangerous sternal fracture, Ann Emerg
Med 7:239–241, 1979. Med 22:1589–1592, 1993.
82. Echlin PS, Klein WB: Pancreatic injury in the athlete, Curr Sports 104. Jones HK, McBride GG, Mumby RC: Sternal fractures associ-
Med Reports 4(2):96–101, 2005. ated with spinal injury, J Trauma 29:360–364, 1989.
83. Hoover DL: How I manage testicular injury, Phys Sports Med 105. Hills MW, Delprado AM, Deane SA: Sternal fractures: Associated
14:127–129, 1986. injuries and management, J Trauma 35:55–60, 1993.
84. Thomas PL: Thoracic back pain in rowers and butterfly 106. Sturm JT, Luxenberg MG, Moudry BM, et al: Does sternal
swimmers: Costo vertebral subluxation, Br J Sports Med 2(2):81, fracture increase the risk for aortic rupture? Ann Thorac Surg 48:
1988. 697–698, 1989.
85. Gregory PL, Biswas AC, Batt ME: Musculoskeletal problems of 107. Miller MD, Johnson DL, Fu FH: Rupture of the pectoralis major
the chest wall in athletes, Sports Med 32(4):235–250, 2002. muscle in a collegiate football player: Use of magnetic resonance
86. Disla E, Rhim HR, Reddy A, et al: Costochondritis: A prospec- imaging in early diagnosis, Am J Sports Med 21:475–477, 1993.
tive analysis in an emergency department setting, Arch Int Med 108. Wolfe SW, Wickiewicz TL, Cavanaugh JT: Ruptures of the
154(21):2466–2469, 1994. pectoralis major muscle, Am J Sports Med 20:587–593, 1992.
87. Thompson BM, Finger W, Tonsfeldt D: Rib radiographs for 109. Zeman SC, Rosenfeld RT, Lipscomb PR: Tears of the pectoralis
trauma: Useful or wasteful? Ann Emerg Med 15:261–265, major muscle, Am J Sports Med 7:343–347, 1979.
1986. 110. McEntire JE, Hess WE, Coleman SS: Rupture of the pectoralis
88. DeLuca SA, Rhea JT, O’Malley T: Radiographic evaluation of rib major muscle, J Bone Joint Surg Am 54:1040–1046, 1972.
fractures, Am J Roentgenol 138:91–92, 1982. 111. Kakwani RG, Matthews JJ: Rupture of the pectoralis major muscle:
89. De Lacey G: Clinical and economic aspects of the use of x-rays Surgical treatment in athletes, Int Orthop 31:159–163, 2007.
in accident and emergency departments, Proc R Soc Med 69: 112. Park JY, Espinella JL: Rupture of the pectoralis major muscle:
758–759, 1976. A case report and review of the literature, J Bone Joint Surg Am
90. Eckstein M, Henderson S, Markovchick V: Thoracic trauma. In 52:577–581, 1970.
Marx JA, Hockberger RS, Walls RM, editors: Rosen’s emergency 113. Lorentzen D, Lawson L: Selected sports bras: A biomechanical
medicine, ed 5, St Louis, 2002, Mosby. analysis of breast motion while jogging, Phys Sports Med 15:
91. Perron AD: Chest pain in athletes, Clin Sports Med 22:37–50, 128–139, 1987.
2003. 114. Gehlsen G, Albohm M: Evaluation of sports bras, Phys Sports Med
92. Sullivan JA: In Grana WA, Kalenak A, editors: Clinical sports 8:89–98, 1980.
medicine, Philadelphia, 1991, WB Saunders. 115. O’Donoghue DH: Treatment of injuries to athletes, Philadelphia,
93. Karlson KA: Rib stress fractures in elite rowers: A case series and 1984, WB Saunders.
proposed mechanism, Am J Sports Med 26(4):516–519, 1998. 116. Brooks AP, Olson LK: Computed tomography of the chest in the
94. Mithofer K, Giza E: Pseudoarthrosis of the first rib in the over- trauma patient, Clin Radiol 40:127–132, 1989.
head athlete, Br J Sports Med 38(2):221–222, 2004. 117. Richardson M: Injury to the lung and pleura. In Feliciano DV,
95. Cope R: Dislocations of the sternoclavicular joint, Skeletal Radiol Moore EE, Mattox KL, editors: Trauma, ed 3, Stamford, CT,
22:233–238, 1993. 1996, Appleton & Lange.
96. Ferrera PC, Wheeling HM: Sternoclavicular joint injuries, Am J 118. Curtin SM, Tucker AM, Gens DR: Pneumothorax in sports, Phys
Emerg Med 18:58–61, 2000. Sportsmed 28:23–32, 2000.
97. Jougon JB, Lepront DJ, Dromer CEH: Posterior dislocation of 119. Partridge RA, Coley A, Bowie R, et al: Sports-related pneumo-
the sternoclavicular joint leading to mediastinal compression, thorax, Ann Emerg Med 30:539–541, 1997.
Ann Thorac Surg 61:711–713, 1996. 120. Schramel FM, Postmus PE, Vanderschueren RG: Current aspects
98. Fererra PC, Williams CC: Posterior sternoclavicular joint of spontaneous pneumothorax, Eur Respir J 10(6):1372–1379,
dislocation, Phys Sportsmed 27:105–113, 1999. 1997.
99. Djerf K, Tropp H, Asberg B: Case report: Retrosternal clavicular 121. Abolnik IZ, Lossos IS, Gillis D, et al: Primary spontaneous pneu-
dislocation in the sternoclavicular joint, Clin Radiol 53:75–76, mothorax in men, Am J Med Sci 305:297–303, 1993.
1998. 122. Fabian TC, Kram HB, Appel PL, Shoemaker WL: Increased
100. Lee FA, Gwinn JL: Retrosternal dislocation of the clavicle, incidence of cardiac contusion in patients with traumatic thoracic
Radiology 110:631–634, 1974. aortic rupture, Ann Surg 208:615–618, 1988.
101. Destout JM, Gilula LA, Murphy WA, et al: Computed tomogra- 123. Geddes LA, Roeder RA: Evolution of our knowledge of sudden
phy of the sternoclavicular joint and sternum, Radiology death due to commotio cordis, Am J Emerg Med 23:67–75,
138:123–128, 1981. 2005.
102. Chiu WC, D’Amelio LF, Hammond JS: Sternal fracture in blunt 124. Fuchs T: Commotio Cordis in an athlete, Heart Rhythm
chest trauma: A practical algorithm for management, Am J 2(9):991–993, 2005.
Emerg Med 15:252–255, 1997.
26
CHAPTER
631
632 SECTION IV • Special Populations and Epidemiology
Table 26-1
Physiological Differences between Adult Males ACL and result in rupture.4 Noncontact ACL injuries also
and Females may occur when landing from a jump with the body
positioned in minimal hip and knee flexion. DeMorat and
Variable Difference colleagues10 have shown that excessive quadriceps force
relative to the hamstring muscles can cause excessive tibial
Upper extremity strength Males are 40% to 50% stronger
Lower extremity strength Males are 20% to 30% stronger forward translation, especially with the knee positioned in
VO2 max (untrained) Males are 15% to 30% higher minimal flexion.
VO2 max (trained) Males are 10% to 15% higher Following the passage of Title IX, researchers have re-
ported a higher relative incidence of ACL injury in females
VO2 max; Maximum oxygen consumption. who participate in basketball and soccer.8,11-13 Prodromos
and colleagues14 recently examined the incidence of ACL
injury across gender and sport. They reported that female
The purpose of the following sections is to provide the best basketball and soccer players were generally three times
available evidence to guide clinical decision making when more likely to sustain an ACL injury than males.
treating the female athlete. During the past 25 years, researchers have identified
both intrinsic and extrinsic risk factors that may account for
the ACL injury gender bias (Table 26-2). Intrinsic factors
Anterior Cruciate Ligament Injury include anatomical or physiological factors such as intercon-
ACL injury is one of the most serious knee injuries experi- dylar notch width, ACL size, posterior tibial slope, physio-
enced by physically active individuals. The average esti- logical laxity, and hormonal influences.45 Extrinsic influ-
mated annual cost associated with treatment (e.g., diagnos- ences include biomechanical or neuromuscular factors such
tic testing, surgical reconstruction, and rehabilitation) in as in nature. They are modifiable to change and are the
the United States has been estimated to exceed $2 billion.4 basis for many injury prevention programs.46-48
Despite progressive treatment, a risk remains for the devel-
opment of knee osteoarthritis.5,6 These findings have led to Intrinsic Risk Factors
the identification of risk factors and the development of ACL injury is thought to occur when the ligament is
ACL-injury prevention programs.7 stretched excessively over the femoral condyles. This mech-
Nearly 70% of ACL injuries occur from a noncontact anism may occur with the abutment of the ACL within the
mechanism during sports such as basketball and soccer.8 intercondylar notch when the knee is positioned close to
A common mechanism of injury involves deceleration or a full extension.49 Therefore, individuals with a decreased
sudden change in direction such as a cutting movement.9 intercondylar notch size may be more prone to an ACL
This maneuver may apply excessive torsional force onto the injury. Based on this theory, many investigators15-17 have
Wider Narrower
pelvis pelvis
More-musclular
Less-musclular thigh development
thigh development Femoral
Less-developed anteversion VMO
VMO hypertrophy
Narrow Wider
Increased Less femoral
flexibility/ femoral notch
flexibility notch
hyperextension Lateral
Genu tibial Genu Medial or
valgum torsion varum neutral
tibial torsion
A
B
Figure 26-1
Musculoskeletal differences between the sexes. A, Female lower-extremity posture. B, Male lower-
extremity posture. (From Griffin LY, editor: Rehabilitation of the injured knee, pp 298-299, St Louis,
1995, Mosby.)
The Female Athlete • CHAPTER 26 633
Figure 26-2
The position-of-no-return mechanism for anterior cruciate ligament injury in the female athlete.
(© 2000 Mary Lloyd ML Ireland, MD. Reproduced with permission.)
cutting maneuvers following a fatiguing protocol. More- female is more likely to incur an ACL injury during the
over, these differences were more pronounced during the preovulatory phase (follicular and ovulatory phases). This
unanticipated task. Together, results from these studies sup- conclusion contradicts the previous premise regarding
port the need for additional work that better depicts field increased estrogen and ACL laxity. Hewett and colleagues58
conditions. suggested that reduced dynamic knee stability (e.g., de-
creased neuromuscular control) might contribute to ACL
Menstrual Cycle and Anterior Cruciate injury during earlier phases of the menstrual cycle based
Ligament Injury on earlier work by Sarwar and colleagues.59 However,
Some believe that hormonal differences may contribute to more recent works29,30 have not found a relationship be-
the increased risk of ACL rupture in female athletes. This tween fluctuating estrogen levels and knee neuromuscular
line of research is based on the premise that fluctuation in control.
estrogen levels may contribute to ACL injury. Oral contraceptives (OCs) increase and stabilize either
Beginning with the onset of menses, the menstrual cycle levels of estrogen and progesterone, or just those of proges-
can be divided into the following phases: follicular, ovula- terone, and prevent the luteinizing hormone surge and
tory, and luteal. Within this cycle, estrogen levels are lower resultant ovulation. Some believe that controlling fluctua-
during the follicular phase and rise dramatically during the tions in estrogen levels may minimize the risk of ACL
ovulatory phase and throughout the luteal phase. Research- injury. Hewett and Myer60 reported increased passive and
ers24,25 believe that increased estrogen levels may contribute dynamic knee stability in females who took OCs compared
to ACL laxity, thus predisposing the female athlete to with those who did not take OCs. Although OC use may
injury. Although investigators25-28 have examined the rela- reduce female ACL injury rates,61-63 further studies are
tionship between menstrual cycle and ligamentous laxity, needed to establish this association.
conflicting results exist. Criticisms include small sample size
and the reliance on subjective history for identifying the Prevention Programs
phase of menstrual cycle at the time of injury.45 As described previously, extrinsic factors are modifiable and
Hewett and colleagues58 recently conducted a systematic correction of these factors has been the focus on many ACL-
review of the literature regarding menstrual cycle and ACL injury prevention programs. Most programs7,46,48,64 have
injury risk. Based on this review, they concluded that a included a combination of strengthening, neuromuscular
The Female Athlete • CHAPTER 26 635
training, and instruction in proper landing and cutting tech- of lateral patella tracking and consider a Q-angle greater
niques. Although findings from these studies support than 20° as excessive.67 Although females generally appear
the use of prevention programs, it remains elusive as to the to exhibit higher Q-angles than males, studies have not sup-
most important element of each. Lephart and colleagues65 ported the relationship between a higher Q-angle and
reported favorable changes in neuromuscular and biome- PFPS.68 A reason for this finding is that the Q-angle is a
chanical parameters in healthy high school female athletes static measure that may not adequately depict patella move-
who completed an 8-week intervention of either plyometric ment during dynamic activities. Powers69 has theorized that
or resistance exercise. increased hip adduction and internal rotation can increase
More recent studies7,46 have prospectively followed the Q-angle by moving the patella medial to the anterior
female soccer players who have participated in the Prevent superior iliac spine (referred to as an increase in the
Injury and Enhance Performance (PEP) injury prevention “dynamic” Q-angle). Based on this premise, a female with
program (www.aclprevent.com). This program is a combi- a “normal” static Q-angle may perform dynamic activities
nation of strengthening, stretching, plyometrics, agilities, such as running, jumping, and stair descent with increased
and instruction in proper technique as part of a warm-up to hip adduction and internal rotation. Prior works31,70 have
play. Gilchrist and colleagues7 recently reported that female shown that females perform athletic maneuvers with greater
soccer players who participated in the PEP program were hip adduction and internal rotation than males; these find-
3.3 times less likely to sustain an ACL injury. ings may support a relatively higher incidence of PFPS in
Grindstaff and colleagues66 conducted a systematic females. Therefore, assessment of changes in the Q-angle
review and support the use of ACL-injury prevention pro- during dynamic tasks might provide conclusive information
grams. Important aspects of a program include dynamic regarding the relationship between PFPS and the Q-angle.
balance activities, agility skills, plyometrics with an emphasis
on proper knee position (i.e., minimizing a knee valgus Hip Influences and Patellofemoral Pain Syndrome
or varus alignment), and core and hip strengthening. Per- An emerging body of work has focused on the influence of
haps the most important aspect of a prevention program is the hip on PFPS. To date, many researchers71-75 have exam-
attention to proper technique. Female athletes should be ined hip strength and consistently found hip abductor,
encouraged to land softly using a greater degree of hip and external rotator, and extensor weakness in females with
knee flexion to minimize external moments applied to the PFPS. Because these muscles primarily control hip adduc-
knee. They also should be instructed to avoid pivoting on a tion and internal rotation during dynamic activities, weak-
fixed foot and taught to decelerate using a multiple-step ness or faulty timing could cause altered hip kinematics and
technique. possibly contribute to abnormal lateral patella tracking at
Although much attention has been focused on the causal the knee. Table 26-3 summarizes reference force values and
factors and prevention of ACL injury, additional studies are test positions that clinicians may use for identifying hip
needed to understand this enigma. Future investigations weakness in females with PFPS.
should be directed toward examining mechanisms of injury A few studies have simultaneously examined the interrela-
in an on-field setting and identifying the critical compo- tionship between hip weakness and altered lower extremity
nents of prevention programs. Furthermore, Prodromos kinematics in females with PFPS. Bolgla and colleagues73 were
and colleagues14 recently found that injury prevention the first to examine hip strength and hip and knee kinematics
programs were more effective at preventing ACL injury in in this patient population. Although subjects with PFPS dem-
female soccer players than in those playing basketball. These onstrated significant hip abductor and external rotator weak-
findings infer the need for the development of prevention ness, they did not exhibit increased hip adduction, hip internal
programs specific to a particular sport.
Table 26-3
Patellofemoral Pain Syndrome
A Summary of Force Values (Expressed as a Percentage
Patellofemoral pain syndrome (PFPS) is one of the most of Body Mass) for Females Diagnosed with Patellofemoral
common pathological conditions of the knee. Unlike re- Pain Syndrome
search regarding the incidence of ACL injury, limited data
exist regarding the incidence and causes of PFPS in females. Hip Hip
However, clinicians have anecdotally concluded a gender Abductors External Rotators
bias regarding causal factors of PFPS. Ireland et al.71 23.3 ⫾ 6.9 10.8 ⫾ 4.0
Robinson and Nee72 16.0 ⫾ 8.0 16.0 ⫾ 6.0
Causal Factors Cichanowski et al.74 29.0 ⫾ 8.0 17.0 ⫾ 4.0
PFPS may result from abnormal patella tracking that causes Bolgla et al.73 22.5 ⫾ 5.9 11.1 ⫾ 3.1
excessive compressive stress to the lateral patella facet. Clini- Willson and Davis75 21.1 ⫾ 6.0 9.1 ⫾ 2.6
cians routinely measure the Q-angle to quantify the degree
636 SECTION IV • Special Populations and Epidemiology
rotation, or knee valgus during stair descent. Although this foot function that impeded shock attenuation (e.g., gait
task was representative of one that elicits patellofemoral patterns of greater pressure on the lateral aspect of the foot
joint pain, subjects might have used compensatory patterns and running patterns of greater vertical peak force under
to minimize knee pain when performing this lower demand- the lateral heel) developed PFPS. It is important to note
ing task.76 that few studies have examined the relationship between
Others have examined hip and knee kinematics during foot function and PFPS; additional studies are needed to
more demanding activities such as running, single-leg better understand this interrelationship.
squats, and single-leg jumping. Findings from Willson and
colleagues77 and Willson and Davis78 showed that females Interventions
with PFPS exhibited greater hip adduction, but less hip Unlike ACL-prevention programs specifically aimed at
internal rotation, compared with controls during running, reducing injury in the female athlete, the best treatment
single-leg squatting, and repetitive single-leg jumping. They approach for females with PFPS remains elusive. However,
concluded that decreased hip internal rotation might have more recent works84 support the use of hip strengthening
represented a means for reducing lateral patella stress. for the treatment of PFPS. Mascal and colleagues85 reported
Dierks and colleagues79 reported a strong correlation (r ⫽ positive outcomes for two female subjects who participated
⫺0.74) between hip abductor weakness and peak hip ad- in a 14-week intervention that targeted the hip, pelvis, and
duction following prolonged running. These results implied trunk muscles. Tyler and colleagues86 and Boling and col-
that patients with PFPS might not demonstrate altered ki- leagues87 also reported improvements in pain and function
nematics until they achieve a certain threshold of weakness. in subjects with PFPS who participated in a program target-
In summary, females with PFPS commonly demonstrate hip ing the hip musculature. Limitations for these studies
weakness and use altered lower-extremity mechanics com- included use of a case report format,85 inclusion of male and
pared with controls. It remains elusive whether hip weak- female subjects,86,87 and use of hip exercise that also affect
ness was the cause of or the result from PFPS. Prospective the quadriceps. Future works should examine the effects
studies are needed to understand associations between hip of isolated hip strengthening on improving impairments
strength and lower extremity kinematics. associated with PFPS.
Prior works88,89 have supported the use of quadriceps
Foot and Ankle Influences and Patellofemoral strengthening for the treatment of PFPS. Although many
Pain Syndrome clinicians prefer weightbearing (closed kinetic chain)
Tiberio80 has theorized that excessive subtalar pronation exercise, studies have not supported the preferential use
may contribute to PFPS. From a biomechanical standpoint, of weightbearing exercise over nonweightbearing (open
increased subtalar joint pronation results in obligatory tibial kinetic chain) exercise.84,90 Rather, quadriceps exercise
internal rotation. Interestingly, tibial internal rotation brings performed in a pain-free manner appears to be the critical
the patella toward the tibial tubercle and decreases the consideration.
Q-angle. However, during gait, the knee must extend dur- Herrington and Al-Sherhi91 recently conducted a con-
ing the latter phases of stance to propel the limb to the trolled trial of weightbearing and nonweightbearing quad-
swing phase. To achieve knee extension, the tibia must be riceps exercises for a group of males with PFPS. Regardless
in an externally rotated position relative to the femur, a of exercise group, males demonstrated significant improve-
position accomplished via increased femoral internal rota- ments with knee pain, strength, and function. These find-
tion. As described previously, increased femoral internal ings support the primary use of quadriceps strengthening
rotation will cause an increase in the dynamic Q-angle and for males; however, it is unclear if females with PFPS will
may contribute to PFPS. respond similarly. Although females with PFPS may respond
Powers and colleagues76 examined foot and lower- well to quadriceps strengthening,90 they may receive addi-
extremity rotation in subjects diagnosed with and without tional benefit from hip strengthening. Future works should
PFPS during gait. They did not find any between-group focus on developing a clinical prediction rule for identifying
differences regarding the amount or timing of peak foot a patient cohort that may respond more favorably to a com-
pronation or tibial internal rotation. However, subjects with bination of hip and knee strengthening exercise.
PFPS exhibited significantly less hip internal rotation than Evidence92,93 supports orthosis use for the treatment of
controls. These authors concluded that subjects with PFPS PFPS. Sutlive and colleagues50 identified aspects of a physi-
might have reduced the Q-angle using this compensatory cal examination to determine a cohort of subjects with
hip strategy. PFPS that may benefit from orthosis prescription in combi-
Recently, researchers81-83 have prospectively examined nation with activity modification. They found that subjects
the influence of increased foot pronation on PFPS causes. with PFPS who exhibited a forefoot valgus greater than or
Results from these studies have not supported an associa- equal to 2°, passive great toe extension less than or equal to
tion between increased pronation and PFPS. Instead, data 78°, and a navicular drop less than or equal to 3 mm
from these studies suggested that subjects who exhibited responded favorably. These results inferred that subjects
The Female Athlete • CHAPTER 26 637
with a more rigid foot type received greater benefit from the Bennett and colleagues107 measured tibiofibular varum,
orthosis intervention and suggested that shock attenuation weightbearing resting calcaneal position, and gastrocnemius
may have reduced PFPS symptoms. These findings also are length in 125 high school cross-country runners prior to
consistent with prospective etiological studies81,82 that re- their competitive season. All athletes were monitored for
ported the development of PFPS in subjects who exhibited symptoms of MTSS. After 8 weeks, 15 runners (25 limbs)
less pronation during gait. presented with MTSS compared with a randomly select
In summary, PFPS is a multifactor problem with no clear 25 limbs. Navicular drop test (NDT) was compared in these
cause or recommended best practice pattern. Prospective 50 limbs. A T-test showed a significant difference in NDT
studies are needed to better understand the influences of the between injured and uninjured limbs, with the injured limb
hip, knee, and foot-ankle complex on the cause of PFPS. having greater navicular drop (6.8 mm vs. 3.6 mm). Plisky
Researchers also should strive to establish both classification and colleagues108 examined bilateral NDT, foot length,
systems and clinical guidelines94,95 to further improve the height, body mass index, previous running injury, running
management of patients with PFPS. More information on experience, and use of orthoses or tape in a group of high
this topic can be found in Chapter 18, “Patellofemoral school cross-country runners. Runners were followed
Joint” in Pathology and Intervention in Musculoskeletal during the season to determine athletic exposure and occur-
Rehabilitation, volume III in this series. rence of MTSS. Overall injury rate was higher in females.
Only gender and body mass index were significantly associ-
ated with the occurrence of MTSS. In addition, those
Medial Tibial Stress Syndrome (MTSS) runners with a previous running injury were more than two
MTSS is one of the most common causes of exercise-related times as likely to develop MTSS.
leg pain.96 The term sometimes referred to as shin splints Other contributing factors are repetitive overload, run-
describes a specific overuse injury producing pain along the ning on an unyielding surface, and shoe error (wrong type
posteromedial aspect of the distal two thirds of the tibia. or wearing too long [i.e., shoe worn out]). It is also specu-
The sports in which athletes are most commonly afflicted lated that increasing training volume and hills contribute
are cross-country, track, basketball, and volleyball. The to MTSS.
incidence of MTSS in long-distance runners can be as high Treatment should focus on relative rest in the acute
as 16.8% and is more prevalent in the female runner.97,98 phase. The athlete’s biomechanics should be examined and
The pathogeneses of MTSS is controversial. Some an off-the-shelf orthotic device prescribed for the athlete
authors characterize the condition as a periostitis (inflam- with pes planus to minimize the amount of pronation. In
mation of the periosteum) caused by strain of the medial those athletes who present with a rigid foot, shock absorb-
tibial fascia. Others describe it as a tearing at the muscle- ing shoes should be worn. Gastrocnemius and soleus length
bone interface. Muscles that have been identified as possible needs to be assessed and flexibility exercises given if the
culprits include the posterior tibialis,99,100 soleus,101,102 and complex is tight. Strengthening of the hip musculature such
flexor digitorum longus.103 However, in a review of litera- as the gluteus medius is also advocated.
ture, Tweed and colleagues104 concluded that MTSS “is not
an inflammatory process of the periosteum but instead a
stress reaction of the bone that has become painful.” It is a
condition that has the potential of developing into a stress Suggested Parameters for Safe Return-to-Running
fracture if not cared for properly. Program
The diagnosis of MTSS is based on clinical history and
• Start at 50% of the preinjury state (intensity and duration)
symptoms. Pain and tenderness is usually diffuse and • Level surface
located along the medial-distal two thirds of the tibia. Com- • Appropriate warmup
monly, athletes will complain of pain at the beginning of a • Increase 10% per week
run. The pain may subside during the middle of the run but • Progress duration prior to intensity
recurs at the end of the run. Provocative tests to rule in
MTSS include pain with passive ankle dorsiflexion, resisted
plantar flexion, toe raises, or single-leg hops. If the clinician
suspects a tibial stress fracture, then a bone scan should be The last resort for treatment of MTSS is a fasciotomy.
sought. The decision for surgery is based on the failure of
Potential biomechanical risk factors for MTSS include conservative measures. The literature presents positive
excessive foot pronation,98,105 increased velocity of prona- outcomes following fasciotomy.109 For more information
tion, and increased compensated rear- and forefoot varus on repetitive stress injuries see Chapters 21 and 22 on
alignment.106 Theoretically, the antipronation muscles fatigu- repetitive stress pathological conditions in Pathology and
ing over time may increase the amount of force attenuated by Intervention in Musculoskeletal Rehabilitation, volume III
the bone and periosteal tissue. in this series.
638 SECTION IV • Special Populations and Epidemiology
sensation, reflexes, or myotomes. A radiograph using an squeeze, isometric hip external rotation (Figure 26-4), and
oblique view may identify a Scottie Dog sign (fracture repetitive prone knee curls are helpful. An SI belt helps
through the pars). Stress fractures may not show-up initially with instability and can be worn until muscle strength is
with radiographs; therefore, a bone scan or magnetic reso- adequate to stabilize the joint. Joint mobilization to hypo-
nance imaging (MRI) scan is recommended. mobile joints in the lumbar spine also may be indicated.
Spondylolysis and grade I spondylolisthesis are treated Biomechanical analysis of running and sport techniques is
with training modifications to correct hyperextension during appropriate.
techniques.119 The athlete should be trained to maintain a
neutral spine with static and dynamic activities. Muscle im- Intervertebral Disc Lesion
balances, such as tight hip flexors, should be restored around The intervertebral disc has limited vascularity and therefore
the hip joint. An athlete with a grade II spondylolisthesis depends on mechanical pumping and movement for health
or higher should be cautioned about aggressive sporting and repair. Most disc lesions come on gradually and affect
activities that require hyperextension. Radiographs should the levels of L4-L5 and L5-S1.122 A woman who is older
be performed annually to check for a progression in the than 25 years old is more prone to disc lesions than the
anterior slippage. External supports may provide stability younger athlete, although the incidence in adolescents
and proprioceptive cuing. Joint mobilization of stiff seg- appears to be increasing.123 The mechanism of injury usu-
ments above the fractured level is beneficial. Prognosis for a ally involves some combination of lumbar hyperflexion, axial
grade I and II spondylolisthesis is good. Surgical interven- compression, and rotation. The disc injury may occur from
tion may be required in a low percentage of athletes if neu- a single episode or repetitive trauma. Repeated minor
rological signs progress. Low grade slips can be addressed by trauma, such as sustained compression in flexion and rota-
direct fusion with return to noncontact sports.120 tion, gives rise to circumferential fissures usually located
along the inner portion of the annulus.124 Weakening of the
Pathological Conditions of the Sacroiliac Joint annular layers reduces the ability of the annulus to contain
The SI joint is inherently a stable joint with little motion.121 the nucleus, which can lead to disc protrusion. Disc injuries
However, injury can occur to this joint from excessive load- are found in athletes who participate in sports that require
ing or from a fall onto the buttock. The female athlete may excessive torsion such as golf, racquetball, or tennis. In the
be particularly vulnerable to SI injury secondary to monthly event that the disc material impinges on the nerve root,
cycling of hormones or increased ligamentous laxity during neurological signs will be present. Sciatica has a high sensi-
pregnancy. According to Marymont and colleagues,122 most tivity (95%) for disc herniation.125
SI problems typically affect the young, skeletally immature
female athlete. A sacral stress fracture also should be ruled
out, especially in distance runners who report pain in the
sacral region.
Symptoms associated with SI-related pathological condi-
tions include joint pain that may refer to the groin. Pain is
worse with extension and rotation to the side of dysfunc-
tion, compression or distraction of the SI joint, and loading
activities such as hopping. Hip and trunk motion may be
painful and should be evaluated. Special tests such as the
flexion, abduction, and external rotation test (FABER
or Patrick test) and specific joint techniques (i.e., shear,
compression, distraction) should also be performed.
A thorough clinical examination may reveal SI joint,
pelvic asymmetry, and leg length discrepancy. X-ray exami-
nations of the pelvis and SI joint may be normal. An MRI
can be helpful in detecting both soft tissue and stress
fracture, although MRI for a typical SI joint dysfunction has
low specificity. The gold standard is a diagnostic injection
under fluoroscopic guidance to confirm a pathological con-
dition of the joint. Blood work (HLA B27) will help to
differentiate between sacroiliitis or ankylosing spondylitis.
Exercises to help stabilize the SI joint should include the
hip rotators, especially the posterior fibers of the gluteus
medius and the single-joint hip extensors. Exercises such as Figure 26-4
wall sits with gluteal squeeze, lateral step-ups with gluteal Gluteal strengthening exercises.
640 SECTION IV • Special Populations and Epidemiology
Cobb angle), compromise of the cardiopulmonary system is health: energy availability, menstrual function, and bone
probable. There appears to be an association between health. Therefore, alterations in one or more of these areas
scoliosis and participation in sports such as gymnastics, ice may adversely affect the health of the female athlete.136
skating, and dance. Smith and Micheli116 found the preva-
lence of scoliosis to be 33% in female skaters compared with
the general population. Energy Availability
In mild cases, the athlete may be asymptomatic. In other Bonci and colleagues137 have stated that low energy avail-
cases, the athlete will complain of back pain that may be ability is the hallmark factor contributing to the other
aggravated by prolonged positioning or intense exercise. aspects (amenorrhea and osteoporosis) of the triad. Energy
Radiographic evidence will reveal a scoliotic curve. Clinical availability is defined as the energy intake minus the exer-
signs include a lateral curvature of the spine, lateral shift, leg cise energy expenditure per kilogram of lean body mass.136
length discrepancy, and rib hump (structural scoliosis). An athlete may lessen energy availability by either decreas-
The key to managing scoliosis is early diagnosis and ing intake (e.g., disordered eating or eating disorder) or
intervention. As well, the clinician must counsel the young increasing expenditure (e.g., excessive exercise).
athlete on sport participation. Although sports are not con- Disordered eating refers to an entire spectrum of abnor-
traindicated, the athlete needs to alert the health profes- mal behavior such as fasting, restrictive consumption, or the
sional of spine pain during activity. Rehabilitation focuses use of laxatives or diuretics.137 In contrast, eating disorders,
on maintaining trunk mobility, muscle balance, soft tissue such as anorexia and bulimia nervosa, represent clinical
techniques, and breathing exercises. In moderate cases, syndromes defined by strict diagnostic criteria.137 However,
bracing may be appropriate. In contact sports, the brace both represent a means of reducing the available energy by
must be padded to prevent lacerations and contusions. reducing intake. Conversely, an athlete can reduce energy
Surgery is indicated for severe progressive curves. availability by increasing energy expenditure through exces-
sive exercise. Therefore, an athlete need not necessarily
Costochondral Joint present with disordered eating to be at risk for detrimental
The costochondral joint may be injured from direct impact effects caused by low energy availability.
or overuse.132 Possible joint separation may occur when a When energy availability decreases, the body attempts
force is applied to the chest, causing the costal cartilage to maintain energy balance by disrupting reproduction,
to separate from the sternum. The athlete complains of cellular maintenance, thermoregulation, and growth.138
pain and tenderness in one of the costochondral joints. Decreased energy availability associated with disordered
A snapping sensation may also be present. Symptoms will be eating may further lead to an increased risk of depression
made worse by sudden movements, strain, and coughing. It and anxiety and adversely affect the cardiac, gastrointestinal,
appears that this condition is more common in young endocrine, reproductive, skeletal, renal, and central nervous
adults; is related to exercise; and is more common in sports systems.139
such as golf, rowing, and throwing sports.133 Radiological
examination is normal. Effective treatment includes cortico-
steroid injections into the region and nonsteroidal anti- Menstrual Dysfunction
inflammatory drugs (NSAIDs). Modalities such as phono- Menstrual function may be described as eumenorrhea
phoresis and electrical stimulation may be used initially for (menstrual cycle at a 28-day median interval), oligomenor-
pain, followed by a progressive exercise program focusing rhea (menstrual cycle at a 35-day or longer median inter-
on the pectoralis and serratus muscles. Joint mobilization val), or amenorrhea (absence of a menstrual cycle),136
and manipulation may be indicated for associated hypomo- with dysfunction resulting from altered hypothalamic reg-
bile joints in the thoracic spine or costal articulations.134 ulation. Specifically, decreased secretion of gonadotropin-
Strapping or taping may help with pain or instability. releasing hormone by the hypothalamus reduces the
Taping can be applied over the affected joint in a criss-cross pulsatility of the luteinizing hormone produced by
or L-shaped manner to help stabilize the joint. Differential the pituitary.140 Loucks and Thuma141 and Loucks and
diagnosis includes cardiac involvement because Tietze dis- colleagues142 have reported a reduction in luteinizing hor-
ease is a condition involving the same area of the anterior mone pulsatility when decreasing energy availability in
chest, but is associated with swelling. Polyarthritis is charac- females who have a regular menstrual cycle. These findings
terized by inflammation of five or more joints. suggest that a loss in energy availability may contribute to
amenorrhea.
Amenorrhea associated with a decrease in estrogen143
Female Athlete Triad may lead to anovulation (failure to ovulate), infertility, and
The female athlete triad was first described in 1992 as decreased bone density. Although infertility is generally
a combination of disordered eating, amenorrhea, and reversible with the restoration of menses, it is important to
osteoporosis in female athletes.135 Each of these areas rep- note that ovulation may return prior to menses restoration.
resents a spectrum of three interrelated aspects of women’s Therefore, an athlete may become pregnant should she not
642 SECTION IV • Special Populations and Epidemiology
use an adequate form of birth control during this time. have recommended the use of self-report questionnaires to
Unfortunately, bone density loss may remain even after the facilitate the detection of disordered eating as athletes are
restoration of menses.144,145 commonly less apt to disclose these behaviors. More impor-
Other adverse effects associated with lack of estrogen tant, health care providers and coaches should observe and
include decreased oxidative metabolism in skeletal muscle, monitor athletes for behavior changes such as excessive
increased low-density lipoprotein (LDL) cholesterol lev- weight loss, fatigue, excessive exercise, and decreased
els,146,147 and vaginal dryness.148 Decreased oxidative me- performance.137
tabolism translates to decreases in performance. Increased The medical history should focus on diet and energy
LDL levels may increase the risk of cardiac disease. Vaginal intake, exercise, weight changes, menstrual history, fracture
dryness can increase the prevalence of candidal infection history, and the patient’s satisfaction with current weight.
and dyspareunia (abnormal pain during sexual intercourse). Mental health practitioners should be consulted if disor-
In summary, although reduced estrogen is commonly dered eating is discovered. Because early intervention is
manifested with menstrual dysfunction, it adversely affects preferred, Diagnostic and Statistical Manual criteria need
other systems. not be strictly observed.154
The physical examination should address signs of eating
disorders, such as lanugo (fine soft hair covering body),
Bone Mineral Density bradycardia, and hypercarotenemia (high levels of carotene
Reduced bone mineral density (BMD) has important impli- in blood giving the skin a yellow appearance). The practi-
cations for the female athlete as it may lead to osteoporosis tioner also should assess height and weight. Fingernails
as well as the incidence of stress fracture. When associated should be examined for brittleness; the backs of the hands
with amenorrhea, the risk of incurring a stress fracture should be examined for signs of callus or abrasion from
increases twofold to fourfold.149 induced vomiting.137 A pelvic examination may reveal vagi-
In females, BMD normally increases until approxi- nal atrophy. An electrocardiogram may show a prolonged
mately age 30 and significantly tapers after menopause. QT interval.
Reduced BMD occurs when bone resorption exceeds bone
formation. Risk factors associated with reduced BMD
Clinical Signs and Symptoms Associated
include female sex, low weight, and decreased estrogen.136
Estrogen is needed to facilitate bone remodeling as it has
with the Female Triad
an inhibitory effect on osteoclast activity in studies exam- • Lanugo (a soft, fine hair covering all parts of the body)
ining osteoporosis and decreased estrogen in postmeno- • Bradycardia (decreased heart rate)
pausal females.150 • Hypercarotenemia (excessive carotene in blood—abnormal yellow
Evidence has suggested a similar decrease in estrogen skin)
in response to low energy availability.122,130 Ihle and • Low body weight
Louks151 have quantified a dose-response relationship • Fingernail discoloration
• Vaginal atrophy
between energy availability and bone turnover in young
• Abnormal electrocardiogram (prolonged QT interval)
exercising females. They found that reduced energy avail-
ability suppressed estradiol and altered selected bone
marker concentrations indicative of increased bone re-
sorption. These findings suggest that low energy avail- Laboratory tests should include a complete blood cell
ability can adversely affect hypothalamic function, as count with differential blood chemistries and electrolytes,
manifested by reduced estrogen secretion, and lead to thyroid stimulating hormone, erythrocyte sedimentation
decreased BMD. rate, and urinalysis to identify abnormalities indicative of
malnutrition or its sequelae. Secondary amenorrhea should
be evaluated by a pregnancy test, follicle stimulating hor-
Evaluation mone, leuteinizing hormone, prolactin, and cortisol levels.
Up to 84% of athletes with disordered eating are asymp- If these are normal, the physician should perform a proges-
tomatic.152 This is particularly concerning given that the terone challenge. In the presence of estrogen, withdrawal
incidence of eating disorders in athletes may be as much as bleeding will occur in 7 to 10 days. Possible diagnoses will
20 to 30 times higher than age-matched peers.153 Because then include progesterone deficiency, polycystic ovarian
of this, practitioners must be aware of the various aspects of syndrome, some medications and normogonadotropic hy-
the spectrum and be vigilant for clues to its presence when pogonadism. If the challenge fails, test for androgen excess
working with the female athletes. Interaction with the caused by tumors, adrenal hyperplasia, or certain genetic
female athlete may occur during a preparticipation evalua- disorders such as Turner syndrome should be performed.
tion, an annual health visit, and or a health visit associated If all of the testing is normal, functional hypothalamic
with one or more areas of the triad. Bonci and colleagues137 amenorrhea is diagnosed by exclusion. One exception is
The Female Athlete • CHAPTER 26 643
that an athlete in recovery may respond to the progesterone postmenopausal women, their benefit is unproven in pre-
challenge. menopausal women. Evidence160 suggests that use in a
BMD testing should be performed on any individual premenopausal female may adversely affect the growth and
with a 6-month history of disordered eating or amenorrhea development of a fetus should she become pregnant. There-
or after suffering multiple stress fractures.155 The World fore, bisphosphonates are contraindicated in athletes of
Health Organization (WHO)156 has established criteria childbearing age because of possible detrimental effects on
based on BMD, as measured using techniques such as dual- a fetus. Given the time these drugs stay in human bone and
energy x-ray absorptiometry, for diagnosing osteoporosis. their slow release, the detrimental effects are not assuaged
The diagnosis is based on a T-score, which represents the by simply stopping when trying to become pregnant.160
number of SDs above or below the average BMD for
young, healthy, white women.157 The WHO156 considers a
person with a T-score more than 2.5 SD below the average
Pregnancy and Exercise
BMD as having osteoporosis. A limitation of this classifica- The recommendations for exercising while pregnant have
tion system is that the WHO has based these criteria on become clearer in the last decade. Most research has shown
studies using postmenopausal women.158 that females will benefit from aerobic exercise.161-163 The
The International Society for Clinical Densitometry level at which they exercise depends on prepregnancy fitness
(ISCD) recommends comparing young individuals’ bone level and should be guided by their physicians. The Ameri-
density with that of age- and sex-matched controls to deter- can College of Obstetricians and Gynecologists (ACOG)
mine those with low bone density (defined as a Z-score).158 has led the way in setting guidelines for exercising while
The ISCD defines osteoporosis as a Z-score below ⫺2, pregnant, first with a statement in 1985 and subsequent
meaning that the BMD is less than that expected for a updates in 1994 and 2002 (available at www.acog.org/
specified age range. This system may be more advantageous publications/patient_education/bp119.cfm).164
than that used by the WHO osteoporosis scale as it ac- Many physiological changes occur during pregnancy that
counts for differences in age and sex. Refer to the National have an effect on exercise. With regard to the cardiovascular
Athletic Trainers’ Association Position Statement: Prevent- system, there is a 50% increase in cardiac output, blood
ing, Detecting, and Managing Disordered Eating in volume increases by 45%, and resting heart rate can increase
Athletes137 for comprehensive guidelines for additional up to 15 beats per minute.165 The respiratory system
information. responds to pregnancy with an increase in minute ventila-
tion and breathing effort.166 The required energy intake
increases to approximately 3000 kcal/day and carbohy-
Treatment drates are the preferred fuel source. Related to the muscu-
Because bone density loss may not be fully recoverable, loskeletal system, there is an increase in joint laxity, weight
prevention is paramount. Prevention programs should gain ranges from 20 to 40 pounds (9 to 18 kg), and there
include nutrition and exercise counseling and education. is an increase in lumbar lordosis.163 All these factors will
Once diagnosed, treatment of the triad should be compre- affect the intensity and mode in which the pregnant woman
hensive and include a variety of players. The primary team can exercise.
should include a physician, dietitian, and coach. When avail- The benefits of exercising while pregnant can be both
able, family members; an athletic trainer or sports physical physical and psychological. It has been shown that exercis-
therapist; an exercise physiologist; and a psychologist, psy- ing women have improved strength and posture and there
chiatrist, or clinical social worker also should be consulted. is a prevention of excessive maternal weight gain.167 These
The initial intervention should focus on increasing energy factors undoubtedly help with a reduction in low back
availability to greater than 45 kcal/kg per day. Simply pain.167 Related directly to birthing, Clapp168 found that
increasing body weight will promote bone density and re- women who take part in some form of exercise on the aver-
store normal menstruation for an athlete with low body age had a shorter active labor during vaginal births. Plasma
weight.136 Athletes with disordered eating also should enter glucose has been shown to be significantly reduced by
into a contract with the treatment team and be allowed to 45 minutes of exercise a day at least three times per week,
participate only if they adhere to the treatment plan and and it may help to control or prevent gestational diabe-
show signs of improved health. tes.169 Some of the psychological benefits of exercise include
Antidepressants may assist in the treatment of eating a reduction of depression170 and improved self-esteem.171
disorders; however, medications have not been effective for The exercise prescription should be designed in conjunc-
improving bone density in young athletes. Prior research159 tion with the woman’s physician. Guidelines have been
has shown that hormone replacement therapy (HRT) and defined by both the American College of Sports Medicine
OCs are ineffective in individuals with eating disorders. (available at www.acsm.org/AM/Template.cfm?Section⫽
In those without eating disorders, data are inconclusive. current_comments1&Template⫽/CM/ContentDisplay.
Although bisphosphonates are a mainstay of treatment in cfm&ContentID⫽8638)172 and the ACOG (available at
644 SECTION IV • Special Populations and Epidemiology
Table 26-4
Benefits of Exercising While Pregnant
Exercise Prescription During Pregnancy
Physical Benefits
• Improves posture Sedentary
• Improves strength
Frequency 3 times per week
• Improves endurance
Intensity Perceived exertion: moderately hard;
• Prevention of excessive weight gain
HR: 65% to 75% max
• Reduces low back pain
Type Low impact (walking, bicycling,
• Shorter active labor
swimming, aerobics)
• Controls blood glucose levels
Time/duration 30 minutes
Psychological Benefits
• Improves self-image Recreational Athlete
• Reduces depression
Frequency 3 to 5 times per week
Intensity Perceived exertion: moderately hard
to hard, HR: 65% to 80% max
Type Low impact (running, tennis,
www.acog.org/publications/patient_education/bp119. cross-country skiing)
cfm).164 Both groups recommend aerobic exercise such as Time/duration 30 to 60 minutes
walking or swimming at moderate intensity (3-4 metabolic
equivalent tasks). Running is appropriate only if the indi- Elite Athlete
vidual was running prior to her pregnancy. In general, peak
Frequency Minimum 4 to 6 times per week
heart rate should not exceed 140 beats per minute. Regard-
Intensity Perceived exertion: hard, HR:
ing duration and frequency of exercise, the 2002 position
75% to 80% max
statement from the ACOG states that “in absence of either Type As with recreational athlete, can
medical or obstetric complications, 30 minutes or more of include competitive activities
moderate exercise a day on most, if not all days of the Time/duration 60 to 90 minutes
week is recommended for pregnant women.”173 For more
specific guidelines based on prepregnancy training level see Adapted from Joy EA: Exercise and pregnancy. In Ratcliffe SD:
Table 26-4. Family practice obstetrics, ed 2, Philadelphia, 2001, Hanley & Befus.
The effect of high-volume exercise during pregnancy HR, Heart rate.
in elite female athletes has been published in the
literature.162,172 The investigations found no detrimental
results to the mother or fetus with the exercise program. In addition, with aging, there is a decline in strength that
Beilock and colleagues found that highly trained women can lead to injury and stress urinary incontinence (SUI).
who limited their aerobic and strength training during
pregnancy did not significantly affect their postpartum
training program.175 Hormonal Changes
Further recommendations and warning signs are found For women in their late 40s and early 50s, cessation of men-
in Table 26-5. There are few absolute and relative contrain- struation (menopause) will occur. Problems associated with
dications to aerobic exercise in pregnancy and these are menopause include an increase incidence of osteoporosis
found in Table 26-6. In conclusion, it appears that healthy and a decline in cardiovascular health caused by diminishing
females with uncomplicated pregnancy can continue to estrogen levels.145 In addition, after approximately age 30,
exercise at moderate levels without harm to themselves or women begin to lose muscle mass and strength. Age-related
their child. decline in lean body mass correlates with several alterations,
including a decrease in endogenous growth hormone, a
decrease in pituitary responsiveness to growth hormone–
Older Female Athlete releasing hormone, and neuromuscular alteration.
It has been reported that one of the fastest growing groups Many of these detriments that occur with aging can be
of exercisers is the middle-aged and older woman. Benefits prevented or minimized with a consistent routine of aerobic
of choosing a physically active lifestyle include a lower inci- exercise and strength training. Researchers have found that
dence of chronic degenerative disease, lower age-specific exercise along with proper calcium-rich diet can enhance
mortality rate, and the ability to live independently. The bone density and reduce bone loss.176 The increased me-
older athletic woman has unique challenges that may affect chanical stress associated with weightbearing exercise can
her ability to be active, including hormonal changes increase bone mineralization. In addition, upper-extremity
that influence tissue health and the cardiovascular system. bone mass can be improved with strengthening exercise.
The Female Athlete • CHAPTER 26 645
Table 26-5
Recommendations and Warning Signs Related to Exercise and Pregnancy164,172
Warning Signs to Stop Exercise
Recommendations and Seek Medical Evaluation
Drink plenty of water before, during, and after exercise Vaginal bleeding
Eat small, frequent meals throughout the day Dyspnea prior to exertion
Avoid exercises that require bouncing, jarring, leaping, risk of abdominal injury Dizziness
such as contact sports, downhill skiing, scuba diving, horseback riding Headache
Do not exercise on the back as this may reduce blood flow to the heart Chest pain
Avoid heavy weightlifting and any activities that require straining Muscle weakness
Avoid exposures to extremes of air pressure as in high altitude (unless you are Calf pain or swelling
accustomed) or scuba diving Preterm labor
Do not increase intensity of your workout beyond prepregnancy levels Decreased fetal movement
Amniotic fluid leakage
Table 26-6
Absolute and Relative Contraindications to Exercise during Pregnancy
Absolute Contraindications to Exercise during Pregnancy Relative Contraindications to Exercise during Pregnancy
Regarding the risk of cardiovascular disease, exercise increased risk of breast cancer. Natural hormones made
along with a low-fat diet may reduce this risk. Higher levels from soy or yams are becoming more popular.
of physical activity are associated with lower blood pressure,
heart rate, serum cholesterol, LDLs, body mass index, fast-
ing insulin, and fasting insulin/glucose ratios. Stress Urinary Incontinence
Training-induced improvements in strength and balance As more women engage in regular exercise, the issue of
may provide an added benefit by preventing the falls that bladder leakage has surfaced.177-179 Nygaard and col-
cause a great number of fractures among the elderly.177 Help- leagues178 reported 47% of women who exercise regularly
ing young women learn how to strength train (i.e., proper have some degree of urinary incontinence. Complaints of
technique, proper loading) during the years when they are SUI during physical activity have prompted greater atten-
able to increase bone mass may help to prevent osteoporosis tion to conservative management techniques that support a
and related fractures. woman’s goal of fitness and establishment of healthy pelvic
HRT is a choice for some women following menopause. muscles simultaneously, especially those of the pelvic floor.
HRT will help to decrease vasomotor symptoms, urogenital Pelvic floor muscles form a hammock of muscular tissue
atrophy, cardiovascular disease risk, and bone loss. Unfortu- that provides support for the pelvic organs in addition to
nately, accompanying these benefits are side effects such as sphincter control. These muscles are sensitive to hormonal
weight gain, headaches, leg cramps, and a potential status and are rich in estrogen receptor sites. High-impact
646 SECTION IV • Special Populations and Epidemiology
physical activities, estrogen depletion,180 and pelvic muscle 7. Gilchrist J, Mandelbaum BR, Melancon H, et al: A randomized
weakness are among the risk factors associated with SUI. controlled trial to prevent noncontact anterior cruciate ligament
injury in female collegiate soccer players, Am J Sports Med
Conservative treatment for SUI includes a pre-exercise
36(8):1476–1483, 2008.
routine of voiding prior to exercise and avoiding beverages 8. Griffin LY, Agel J, Albohm MJ, et al: Noncontact anterior cruciate
that include caffeine and alcohol. It may be necessary to ligament injuries: Risk factors and prevention strategies, J Am
restrict fluids, although not to the point of dehydration, Acad Orthop Surg 8:141–150, 2000.
during the exercise session. While exercising, the athlete 9. Renstrom P, Ljungqvist A, Arendt EA, et al: Non-contact ACL
injuries in female athletes: An International Olympic Committee
may need to wear a minipad or, in some cases, an intravagi-
current concepts statement, Br J Sports Med 42:394–412,
nal support such as a pessary or bladder neck support pros- 2008.
thesis. Strengthening exercises and muscle re-education 10. DeMorat G, Weinhold P, Blackburn T, et al: Aggressive quadri-
should be a component of the woman’s fitness routine. ceps loading can induce noncontact anterior cruciate ligament
Physical therapists and other health care providers can ask injury, Am J Sports Med 32(2):477–483, 2004.
11. Roush MB, Sevier TL, Wilson JK, et al: Anterior knee pain: A
women more questions about pelvic floor function, encour-
clinical comparison of rehabilitation methods, Clin J Sport Med
age women to exercise these muscles, and seek medical care 10:22–28, 2000.
when they exhibit problems such as SUI. Health care pro- 12. Arendt EA, Dick RW: Knee injury patterns among men
viders should promote preventative pelvic muscle exercises and women in collegiate basketball and soccer. NCAA data and
rather than restorative. review of the literature, Am J Sports Med 23:694–701, 1995.
13. Hootman JM, Dick RW, Agel J: Epidemiology of collegiate
injuries for 15 sports: Summary and recommendations for injury
Conclusion prevention initiatives, J Athl Train 42(2):311–319, 2007.
14. Prodromos CC, Han Y, Rogowski J, et al: A meta-analysis of the
During the last 25 years, the opportunities for females incidence of anterior cruciate ligament tears as a function of
in sports have grown tremendously. The high number gender, sport, and a knee-injury-reduction regimen, Arthroscopy
23(12):1320–1325, 2007.
of females participating in sports has been associated with
15. Ireland ML, Ballantyne BT, Little K, McClay IS: A radiographic
an increase in a number of musculoskeletal injuries and analysis of the relationship between size and shape of the inter-
other high-level activity problems. In some circumstances, condylar notch and anterior cruciate ligament study, Knee Surg
there appears to be a predisposition of the female to Sports Traumatol Arthrosc 9:200–205, 2001.
injury. This chapter presented the most common muscu- 16. Chandrashekar N, Slauterbeck J, Hashemi J: Sex-based differ-
ences in the anthropometric characteristics of the anterior cruciate
loskeletal injuries, including ACL injury, PFPS, MTSS,
ligament and its relation to intercondylar notch geometry, Am J
and other problems common to the female athlete. Sports Med 33(10):1492–1498, 2005.
Strategies and programs to prevent injury are also 17. Shelbourne KD, Davis TJ, Klootwyk TE: The relationship
discussed. Along with musculoskeletal injuries, the exist- between intercondylar notch width of the femur and the inci-
ing knowledge on the female triad is summarized with dence of anterior cruciate ligament tears, Am J Sports Med
26(3):402–408, 1998.
information given on the symptoms, diagnosis, and treat-
18. Hashemi J, Chandrashekar N, Mansouri H, et al: The human
ment. The chapter concludes with unique issues facing anterior cruciate ligament: Sex differences in ultrastructure and
the older woman athlete. correlation with biomechanical properties, J Orthop Res 26
(945–950), 2008.
19. DeJour H, Bonnin M: Tibial translation after anterior cruciate
References ligament rupture. Two radiological tests compared, J Bone Joint
Surg Br 76:745–749, 1994.
1. National Collegiate Athletics Association: Gender equity in 20. Brandon ML, Haynes PT, Bonamo JR, et al: The association
intercollegiate athletics. A practical guide for colleges and univer- between posterior-inferior tibial slope and anterior cruciate liga-
sities, Indianapolis, IN, 2008, National Collegiate Athletics ment insufficiency, Arthroscopy 22(8):894–899, 2006.
Association. 21. Stijak L, Herzog RF, Schai P: Is there an influence of the tibial
2. Griffin LY: Better understanding of ACL injury prevention, The slope of the lateral condyle on the ACL lesion? A case-control study,
NCAA News, October 9, 2000, http://www.ncaa.org/wps/ Knee Surg Sports Traumatol Arthrosc 16(2):112–117, 2008.
ncaa?ContentID⫽26659. 22. Rosene JM, Fogarty TD: Anterior tibial translation in collegiate
3. McArdle WD, Katch FI, Katch VL: Exercise physiology: Energy, athletes with normal anterior cruciate ligament integrity, J Athl
nutrition, and human performance, ed 6, Philadelphia, 2007, Train 34:93–98, 1999.
Lippincott Williams & Wilkins. 23. Uhorchak JM, Scoville CR, Williams GN, et al: Risk factors
4. Silvers HJ, Mandelbaum BR: Prevention of anterior cruciate liga- associated with noncontact injury of the anterior cruciate
ment injury in the female athlete, Br J Sports Med 41(Suppl I): ligament: A prospective four-year evaluation of 859 West Point
i52–i59, 2007. cadets, Am J Sports Med 31:831–842, 2003.
5. van der Hart CP, van den Bekerom MPJ, Patt TW: The occurrence 24. Wojtys EM, Huston LJ, Lindenfeld TN, et al: Association
of osteoarthritis at a minimum of ten years after reconstruction of between the menstrual cycle and anterior cruciate ligament inju-
the anterior cruciate ligament, J Orthop Surg 3:24, 2008. ries in female athletes, Am J Sports Med 26(5):614–619, 1998.
6. Lohmander LS, Ostenberg A, Englund M, Roos H: High preva- 25. Romani W, Patrie J, Curl LA, Flaws JA: The correlations between
lence of knee osteoarthritis, pain, and functional limitations in estradiol, estrone, estriol, progesterone, and sex hormone-
female soccer players twelve years after anterior cruciate ligament binding globulin and anterior cruciate ligament stiffness,
injury, Arthritis Rheum 50(10):3145–3152, 2004. J Women’s Health 12:287–298, 2003.
The Female Athlete • CHAPTER 26 647
26. Belanger MJ, Moore DC, Crisco III JJ, et al: Knee laxity does 46. Mandelbaum BR, Silvers HJ, Watanabe DS, et al: Effectiveness
not vary with the menstrual cycle before or after exercise, Am J of a neuromuscular training program in preventing anterior cru-
Sports Med 32(5):1150–1157, 2004. ciate ligament injuries in female athletes, Am J Sports Med
27. Shultz SJ, Kirk SE, Johnson MJ, et al: Relationship between sex 33:1003–1010, 2005.
hormones and anterior knee laxity across the menstrual cycle, 47. Hewett TE, Lindenfeld TN, Riccobene JV, Noyes FR: The effect
Med Sci Sports Exerc 36(7):1165–1174, 2004. of neuromuscular training on the incidence of knee injury in
28. Beynnon BD, Bernstein IM, Belisle A, et al.: The effect of estra- female athletes, Am J Sports Med 27(6):699–705, 1999.
diol and progesterone on knee and ankle joint laxity, Am J Sports 48. Pollard CD, Sigward SM, Ota S, et al: The influence of in-season
Med 33(9):1298–1304, 2005. injury prevention training on lower-extremity kinematics during
29. Abt JP, Sell TC, Laudner KG, et al: Neuromuscular and biome- landing in female soccer players, Clin J Sport Med 16:223–227,
chanical characteristics do not vary across the menstrual cycle, 2006.
Knee Surg Sports Traumatol Arthrosc 15:901–907, 2007. 49. Cleland JA, Fritz JM, Whitman JM, et al: The use of a lumbar
30. Chaudhari AMW, Lindenfeld TN, Andriacchi TP, et al: Knee and spine manipulation technique by physical therapists in patients
hip loading patterns at different phases in the menstrual cycle. who satisfy a clinical prediction rule: A case series, J Orthop Sports
Implications for the gender difference in anterior cruciate liga- Phys Ther 36:209–214, 2006.
ment injury rates, Am J Sports Med 35(5):793–800, 2007. 50. Sutlive TG, Mitchell SD, Maxfield SN, et al: Identification of indi-
31. Ferber R, Davis IM, Williams DSI: Gender differences in lower viduals with patellofemoral pain whose symptoms improved after
extremity mechanics during running, Clin Biomech 18:350–357, a combined program of foot orthosis use and modified activity:
2003. A preliminary investigation. Phys Ther 84(1):49–61, 2004.
32. Ford KR, Myer GD, Toms H, Hewett TE: Gender differences in 51. Schmitz RJ, Riemann BL, Thompson T: Gluteus medius activity
the kinematics of unanticipated cutting in young athletes, Med during isometric closed-chain hip rotation, J Sport Rehabil 11(3):
Sci Sports Excer 37(1):124–129, 2005. 179–188, 2002.
33. Landry SC, McKean KA, Hubley-Kozey CL, et al: Neuromuscu- 52. Ireland ML: The female ACL: Why is it more prone to injury?
lar control and lower limb biomechanical differences exist be- Orthop Clin North Am 33:637–651, 2002.
tween male and female elite adolescent soccer players during an 53. Fung DT, Zhang LQ: Modeling of ACL impingement against
unanticipated run and crosscut maneuver, Am J Sports Med the intercondylar notch, Clin Biomech 18:933–941, 2003.
35(11):1901–1911, 2007. 54. Fleming BC, Renstrom PA, Ohlen G, et al.: The gastrocnemius
34. Ford KR, Myer GD, Hewett TE: Valgus knee motion during muscle is an antagonist of the anterior cruciate ligament, J Orthop
landing in high school female and male basketball players, Med Res 19:1178–1184, 2001.
Sci Sports Exer 35:1745–1750, 2003. 55. Hewett TE, Myer GD, Ford KR: Decrease in neuromuscular
35. Lephart SM, Ferris CM, Riemann BL, et al: Gender differences control about the knee with maturation in female athletes, J Bone
in strength and lower extremity kinematics during landing, Clin Joint Surg Am 86(8):1601–1608, 2004.
Orthop 401:162–169, 2002. 56. Leetun DT, Ireland ML, Willson JD, et al: Core stability mea-
36. McLean SG, Huang X, Su A, van den Bogert AJ: Sagittal plane sures as risk factors for lower extremity injury in athletes, Med Sci
biomechanics cannot injure the ACL during sidestep cutting, Sports Exer 36(6):926–934, 2004.
Clin Biomech 19:828–838, 2004. 57. McLean CL: The ACL injury enigma: We can’t prevent what we
37. Nagano Y, Ida H, Akai M, Fukubayashi T: Gender differences in don’t understand, J Athl Train 43(5):538–540, 2008.
knee kinematics and muscle activity during single limb drop land- 58. Hewett TE, Zazulak BT, Myer GD: Effects of the menstrual
ing, The Knee 14:218–223, 2007. cycle on anterior cruciate ligament injury risk: A systematic
38. Schmitz RJ, Kulas AS, Perrin DH, et al: Sex differences in lower review, Am J Sports Med 35(4):659–668, 2007.
extremity biomechanics during single leg landings, Clin Biomech 59. Sarwar R, Niclos BB, Rutherford OM: Changes in muscle
22:681–688, 2007. strength, relaxation rate and fatigability during the human men-
39. Wojtys EM, Ashton-Miller JA, Huston LJ: A gender-related strual cycle, J Physiol 493:267–272, 1996.
difference in the contribution of the knee musculature to sagittal- 60. Hewett TE, Myer GD: The effects of oral contraceptives on knee
plane shear stiffness in subjects with similar knee laxity, J Bone stability and neuromuscular performance in female athletes, Med
Joint Surg Am 84:10–16, 2002. Sci Sports Exerc 32:S207, 2000.
40. Decker MJ, Torry MR, Wyland DJ, et al: Gender differences in 61. Moller-Nielsen J, Hammar M: Women’s soccer injuries in relation
lower extremity kinematics, kinetics, and energy absorption to the menstrual cycle and oral contraceptive use, Med Sci Sports
during landing, Clin Biomech 18:662–669, 2003. Exerc 21:126–129, 1989.
41. Jacobs CA, Uhl TL, Mattacola CG, et al: Hip abductor function 62. Moller-Nielsen J, Hammar M: Sports injuries and oral contra-
and lower extremity landing kinematics: Sex differences, J Athl ceptive use. Is there a relationship? Sports Med 12:152–160,
Train 42(1):76–83, 2007. 1991.
42. Lawrence III RK, Kernozek TW, Miller EJ, et al: Influences of 63. Myklebust G, Engebretsen L, Braekken IH, et al: Prevention of
hip external rotation strength on knee mechanics during single- anterior cruciate ligament injuries in female team handball play-
leg drop landings in females, Clin Biomech 23:806–813, 2008. ers: A prospective intervention study over three seasons, Clin J
43. Kernozek TW, Torry MR, Iwaski M: Gender differences in lower Sports Med 13:71–78, 2003.
extremity landing mechanics caused by neuromuscular fatigue, 64. Zebis MK, Bencke J, Andersen LL, et al: The effects of neuro-
Am J Sports Med 36(3):554–565, 2008. muscular training on knee joint motor control during sidecutting
44. Borotikar BS, Newcomer R, Koppes R, McLean SL: Combined in female elite soccer and handball players, Clin J Sport Med
effects of fatigue and decision making on female lower limb land- 18:329–337, 2008.
ing postures: Central and peripheral contributions to ACL injury 65. Lephart S, Abt JP, Ferris CM, et al: Neuromuscular and biome-
risk, Clin Biomech 23:81–92, 2008. chanical characteristic changes in high school athletes: A plyomet-
45. Counts J, Bolgla LA, Ireland ML. Female issues in sport: Risk ric versus basis resistance program, Br J Sports Med 39:932–938,
factors and prevention of ACL injuries. In: Johnson D, Pedowitz 2005.
R, editors, Practical orthopaedic sports medicine and arthroscopy, 66. Grindstaff TL, Hammill RR, Tuzson AE, Hertel J: Neuromuscular
Philadelphia, 2006, Lippincott Williams & Wilkins. control training programs and noncontact anterior cruciate ligament
648 SECTION IV • Special Populations and Epidemiology
injury rates in female athletes: A numbers-needed-to-treat analysis, 86. Tyler TF, Nicholas SJ, Mullaney MJ, McHugh MP: The role of
J Athl Train 41(4):450–456, 2006. hip muscle function in the treatment of patellofemoral pain syn-
67. Livingston LA: The quadriceps angle: A review of the literature, drome, Am J Sports Med 34(4):630–636, 2006.
J Orthop Sports Phys Ther 28:105–109, 1998. 87. Boling MC, Bolgla LA, Mattacola CG, et al: Outcomes of a
68. Caylor D, Fites R, Worrell TW: The relationship between quad- weight-bearing rehabilitation program for patients diagnosed
riceps angle and anterior knee pain syndrome, J Orthop Sports with patellofemoral pain syndrome, Arch Phys Med Rehabil
Phys Ther 17(1):11–16, 1993. 87(11):1428–1435, 2006.
69. Powers CM: The influence of altered lower-extremity kinematics 88. Natri A, Kannus P, Jarvinen M: Which factors predict the long-
on patellofemoral joint dysfunction: A theoretical perspective, term outcome in chronic patellofemoral pain syndrome? A 7-yr
J Orthop Sports Phys Ther 33(11):639–646, 2003. prospective follow-up study, Med Sci Sports Exerc 30:1572–1577,
70. Lephart SM, Ferris CM, Riemann BL, et al: Gender differences 1998.
in strength and lower extremity kinematics during landing, Clin 89. Bolgla LA, Malone TR: Exercise prescription and patellofemoral
Orthop 401:162–169, 2002. pain: Evidence for rehabilitation, J Sport Rehabil 14(1):72–88,
71. Ireland ML, Willson JD, Ballantyne BT, Davis IM: Hip strength 2005.
in females with and without patellofemoral pain, J Orthop Sports 90. Witvrouw E, Danneels L, van Tiggelen D, et al: Open versus
Phys Ther 33(11):671–676, 2003. closed kinetic chain exercise in patellofemoral pain. A 5-year pro-
72. Robinson RL, Nee RJ: Analysis of hip strength in females seek- spective randomized study, Am J Sports Med 32(5):1122–1129,
ing physical therapy treatment for unilateral patellofemoral 2004.
pain syndrome, J Orthop Sports Phys Ther 37(5):232–238, 91. Herrington L, Al-Sherhi A: A controlled trial of weight-bearing
2007. versus non-weight-bearing exercises for patellofemoral pain,
73. Bolgla LA, Malone TR, Umberger BR, Uhl TL: Hip strength J Orthop Sports Phys Ther 37(4):155–160, 2007.
and hip and knee kinematics during stair descent in females with 92. Eng JJ, Pierrynowski MR: Evaluation of soft foot orthotics in the
and without patellofemoral pain syndrome, J Orthop Sports Phys treatment of patellofemoral pain syndrome, Phys Ther 73(5):
Ther 38(1):12–18, 2008. 62–68, 1993.
74. Cichanowski HR, Schmitt JS, Johnson RJ, Niemuth PE: Hip 93. Johnston LB, Gross MT: Effects of foot orthoses on quality of
strength in collegiate female athletes with patellofemoral pain, life for individuals with patellofemoral pain syndrome, J Orthop
Med Sci Sports Exer 39(8):1227–1232, 2007. Sports Phys Ther 34(8):440–448, 2004.
75. Willson JD, Davis I: Lower extremity strength and mechanics 94. Wilk KE, Davies GJ, Mangine RE, Malone TR: Patellofemoral
during jumping in women with patellofemoral pain, J Sport disorders: A classification system and clinical guidelines for
Rehabil 18(1):75–89, 2009. nonoperative rehabilitation, J Orthop Sports Phys Ther 28(5):
76. Powers CM, Chen PY, Reischl SF, Perry J: Comparison of foot 307–322, 1998.
rotation and lower extremity rotation in persons with and with- 95. Witvrouw E, Werner S, Mikkelsen C, et al: Clinical classification
out patellofemoral pain, Foot Ankle Intern 23(7):634–640, of patellofemoral pain syndrome: Guidelines for non-operative
2002. treatment, Knee Surg Sports Traumatol Arthrosc 13:122–130,
77. Willson JD, Binder-Macleod S, Davis IS: Lower extremity 2005.
jumping mechanics of female athletes with and without patello- 96. Andrish JT: Leg pain. In DeLee JC, Drez D, editors: Orthopedic
femoral pain before and after exertion, Am J Sports Med 36(8): sports medicine, Philadelphia, 1994, WB Saunders.
1587–1596, 2008. 97. Clement DB, Taunton JE, Smart GW, McNicol KL: A survey of
78. Willson JD, Davis I: Lower extremity mechanics of females overuse running injuries, Phys Sportsmed 9:47–58, 1981.
with and without patellofemoral pain across activities with 98. Yates B, White S: The incidence of risk factors in the develop-
progressively greater task demands, Clin Biomech 23:203–211, ment of medial tibial stress syndrome among naval recruits, Am
2008. J Sports Med 32:772–780, 2004.
79. Dierks TA, Manal KT, Hamill J, Davis IS: Proximal and distal 99. Saxena A, O’Brien T, Bunce D: Anatomic dissection of the tibi-
influences on hip and knee kinematics in runners with patello- alis posterior muscle and its correlation to medial tibial stress
femoral pain during a prolonged run, J Orthop Sports Phys Ther syndrome, J Foot Surg 29:105–108, 1990.
38(8):448–456, 2008. 100. D’Ambrosia RD, Zelis RF, Chuinard RG, Wilmore J: Interstitial
80. Tiberio D: The effect of excessive subtalar joint pronation on pressure measurements in the anterior and posterior compart-
patellofemoral mechanics: A theoretical model, J Orthop Sports ments in athletes with shin splints, Am J Sports Med 5:127–131,
Phys Ther 9(4):160–165, 1987. 1977.
81. Thijs Y, Van Tiggelen D, Roosen P, et al: A prospective study on 101. Beck BR, Osternig LR: Medical tibial stress syndrome. The loca-
gait-related intrinsic risk factors for patellofemoral pain, Clin J tion of muscles in the leg in relation to symptoms, J Bone Joint
Sport Med 17(6):437–445, 2007. Surg Am 76:1057–1061, 1994.
82. Hetsroni I, Finestone A, Milgrom C, et al: A prospective biome- 102. Detmer D: Chronic shin splints: Classification and manage-
chanical study of the association between foot pronation and the ment of medial tibial stress syndrome, Sports Med 3:436–446,
incidence of anterior knee pain among military recruits, J Bone 1986.
Joint Surg Br 88(7):905–908, 2006. 103. Beck BR, Osternig LR: Medial tibial stress syndrome. The loca-
83. Thijs Y, De Clercq D, Roosen P, Witvrouw E: Gait-related intrinsic tion of muscles in the leg in relation to symptoms, J Bone Joint
risk factors for patellofemoral pain in novice recreational runners, Surg Am 76:1057–1061, 1994.
Br J Sports Med 42(6):466–471, 2008. 104. Tweed JL, Avil SJ, Campbell JA, Barners MR: Etiologic factors in
84. Fagan V, Delahunt E: Patellofemoral pain syndrome: A review the development of medial tibial stress syndrome, J Am Podiatric
on the associated neuromuscular deficits and current treatment Med Assoc 98:107–111, 2008.
options, Br J Sports Med 42:489–495, 2008. 105. Ilahi OA, Kohl HW: Lower extremity morphology and align-
85. Mascal CL, Landel R, Powers CM: Management of patello- ment and risk of overuse injury, Clin J Sports Med 8:38–42,
femoral pain targeting hip, pelvis, and trunk muscle function: 1998.
2 case reports, J Orthop Sports Phys Ther 33(11):647–660, 106. Messier SP, Pittala KA: Etiologic factors associated with selected
2003. running injuries, Med Sci Sports Exerc 20:501–505, 1988.
The Female Athlete • CHAPTER 26 649
107. Bennett JE, Reinking MF, Pluemer B, et al: Factors contributing 131. Jull GA: Examination of the lumbar spine. In Grieve GP, editor:
to the development of medial tibial stress syndrome in high Modern manual therapy of the vertebral column, Edinburgh,
school runners, J Orthop Sports Phys Ther 31(9):504–510, 1986, Churchill Livingstone.
2001. 132. Gregory PL, Biswas AC, Batt ME: Musculoskeletal problems of
108. Plisky MS, Rauh MJ, Heiderscheit B, et al: Medial tibial stress the chest wall in athletes, Sports Med 32(4):235–250, 2002.
syndrome in high school cross-country runners: Incidence and 133. Rumball JS, Lebrun CM, Di Ciacca SR, Orlando K: Rowing
risk factors, J Orthop Sports Phys Ther 37(2):40–47, 2007. injuries, Sports Med 35(6):537–555, 2005.
109. Slimmon D, Bennell K, Brukner P, et al: Long term outcome of 134. Aspegren D, Hyde T, Miller M: Conservative treatment of a female
fasciotomy with partial fasciectomy for chronic exertional collegiate volleyball player with costochondritis, J Manipulative
compartment syndrome of the lower leg, Am J Sports Med 30: Physiol Ther 30(4):321–325, 2007.
581–588, 2005. 135. Nattiv A, Agostini R, Drinkwater B, Yeager KK: The female
110. Jackson DW, Mannarino F: Lumbar spine injuries in athletes. In athlete triad. The inter-relatedness of disordered eating, amen-
Scott WN, Nisonson B, Nicholas JA, editors: Principles of sports orrhea, and osteoporosis, Clin J Sports Med 13:405–418,
medicine, Baltimore, 1984, Williams & Wilkins. 1994.
111. Hall SJ: Mechanical contribution to lumbar stress injuries in 136. Nattiv A, Loucks AB, Manroe MM, et al: Position stand: The
female gymnasts, Med Sci Sports Exerc 18:599–602, 1986. female athlete triad, Med Sci Sports Exerc 39(10):1867–1882,
112. Reid DC: Sports injury assessment and rehabilitation, New York, 2007.
1992, Churchill Livingstone. 137. Bonci CM, Bonci LJ, Granger LR, et al: National Athletic Trainers’
113. Micheli LJ, Wood R: Back pain in young athletes: Significant Association position statement: Preventing, detecting, and managing
differences from adults in causes and patterns, Arch Pediatr disordered eating in athletes, J Athl Train 43(1):80–108, 2008.
Adolesc Med 149(1):15–18, 1995. 138. Wade GN, Schneider JE, Li HY: Control of fertility by metabolic
114. Barash HL, Galante J, Lambert C, Ray R: Spondylolisthesis and cues, Am J Physiol 270:E1–E19, 1996.
tight hamstrings, J Bone Joint Surg Am 52(7):1319–1328, 139. Romes ES, Ammerman S, Rosen DS, et al: Children and adoles-
1970. cents with eating disorders: The state of the art, Pediatrics
115. Corrigan B, Maitland GD: Practical orthopedic medicine, 111:e98–e108, 2003.
London, 1983, Butterworth-Heinemann Ltd. 140. Loucks AB, Mortola JF, Girton L, Yen SSC: Alterations in the
116. Smith AD, Micheli LJ: Injuries in competitive figure skaters, Phys hypothalamic-pituitary-ovarian and the hypothalamic-pituitary-
Sportsmed 10:36–47 1982. adrenal axes in athletic women, J Endocrinol Metab 68:402–411,
117. Congeni J, McCulloch J, Swanson K: Lumbar spondylolysis: A 1989.
study of natural progression in athletes, Am J Sports Med 141. Loucks AB, Thuma JR: Luteinizing hormone pulsatility is dis-
25(2):248–253, 1997. rupted at a threshold of energy availability in regularly menstruating
118. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K, Reilly J: Pathology women, J Clin Endocrinol Metab 88(1):297–311, 2003.
and pathogenesis of lumbar spondylosis and stenosis, Spine 3: 142. Loucks AB, Verdun M, Heath EM: Low energy availability, not
319–328, 1978. stress of exercise, alters LH pulsatility in exercising women,
119. Porterfield JA, DeRosa C: Mechanical low back pain: Perspectives J Appl Physiol 84(1):37–46, 1998.
in functional anatomy, Philadelphia, 1991, WB Saunders Co. 143. Zanker CL, Swaine IL: Relation between bone turnover, oestra-
120. Debnath UK, Freeman BJ, Gregory P, et al: Clinical outcome diol, and energy balance in women distance runners, Br J Sports
and return to sport after the surgical treatment of spondylolysis Med 32:167–171, 1998.
in young athletes, J Bone Joint Surg Br 85:244–249, 2003. 144. Keen AD, Drinkwater BL: Irreversible bone loss in former amen-
121. Lee D: Manual therapy for the thorax, Delta, Canada, 1994, orrheic athletes, Osteoporos Int 7:311–315, 1997.
DOPC. 145. Warren MP, Brooks-Gunn J, Fox RP, et al: Osteopenia in exercise
122. Marymont JV, Lynch MA, Henning CE: Exercise-related stress associated amenorrhea using ballet dancers as a model: a longitu-
reaction of the sacroiliac joint, Am J Sports Med 14:320–323, dinal study, J Clin Endocrinol Metab 87:3162–3168, 2002.
1986. 146. Friday KE, Drinkwater BL, Bruemmer B, et al: Elevated plasma
123. Gerbino II PG, Micheli LJ: Back injuries in the young athlete, low-density lipoprotein and high density lipoprotein cholesterol
Clin Sports Med 14:571–590, 1995. levels in amenorrheic athletes: Effects of endogenous hormone
124. Adams MA, Hutton WC: The mechanical function of the lumbar status and nutrient intake, J Clin Endocrinol Metab 77:
apophyseal joints, Spine 8:327–330, 1983. 1605–1609, 1993.
125. Deyo RA, Diehl AK, Rosenthal M: How many days of bed rest 147. O’Donnel E, De Souza MJ: The cardiovascular effects of chronic
for acute low back pain? A randomized clinical trial, N Engl J hypoestrogenism in amenorrheic athletes: A critical review, Sports
Med 315:1064–1070, 1986. Med 34:601–627, 2004.
126. Saunders HD, Saunders R: Evaluation, treatment, and preven- 148. Hammar ML, Hammar-Henriksson MB, Frisk J, et al: Few oligo-
tion of musculoskeletal disorders, Chaska, MN, 1993, Saunders amenorrheic athletes have vasomotor symptoms, Maturitas
Group. 34:219–225, 2000.
127. Boden SD, Davis DO, Dina TS, et al: Abnormal magnetic- 149. Bennell K, Matheson G, Meeuwisse W, Brikner P: Risk factors for
resonance scans of the lumbar spine in asymptomatic subjects: stress fractures, Sports Med 28:91–122, 1999.
A prospective investigation, J Bone Joint Surg Am 72:403–408, 150. Hassager C, Colwell A, Assiri AMA: Effect of menopause
1990. and hormone replacement therapy on urinary excretion of pyri-
128. Maitland GD: Vertebral manipulation, ed 5, London, 1986, dinium cross-links: A longitudinal and cross-sectional study, Clin
Butterworth-Heinemann Ltd. Endocrinol 37(1):45–50, 1992.
129. Childs JD, Fritz JM, Flynn TW, et al: A clinical prediction rule 151. Ihle R, Loucks AB: Dose-response relationships between energy
for classifying patients with low back pain most likely to benefit availability and bone turnover in young exercising women, J Bone
from spinal manipulation: A validation study, Ann Intern Med Miner Res 19:1231–1240, 2004.
141(12):920–928, 2004. 152. Hinton PS, Kubas KL: Psychosocial correlates of disordered eat-
130. Grieve GP: Common vertebral joint problems, Edinburgh, 1981, ing in female collegiate athletes: Validation of the ATHLETE
Churchill Livingstone. questionnaire, J Am Coll Health 54(3):149–156, 2005.
650 SECTION IV • Special Populations and Epidemiology
153. Brownell KD, Rodin J, Wilmore JH: Eating, body weight and 167. Dewey KG, McCrory MA: Effects of dieting and physical activity
performance in athletes: Disorders of modern society, Philadelphia, on pregnancy and lactation, Am J Clin Nutrition 59:446S–453S,
1992, Lea and Febiger. 1994.
154. American Academy of Pediatrics Committee on Adolescence: 168. Clapp JF: The course of labour after endurance exercise, Am J
Identifying and treating eating disorders, Pediatrics 111: Obstet Gynecol 163:1799–1805, 1990.
204–211, 2003. 169. Dye TD, Knox KL, Artal R, et al: Physical activity, obesity, and
155. Khan AA, Hanley DA, Bilezikian JP, et al: Standards for perform- diabetes in pregnancy, Am J Epidemiol 146:961–965, 1997.
ing DXA in individuals with secondary causes of osteoporosis, 170. Clarke PE, Gross H: Women’s behavior, beliefs and information
J Clin Densitom 9:47–57, 2006. sources about physical exercise in pregnancy, Midwifery 20:
156. World Health Organization: Assessment of fracture risk and its 133–141, 2004.
application to screening for postmenopausal osteoporosis, WHO 171. Wallace AM, Boyer DB, Dan A: Aerobic exercise, maternal
Tech Report Ser 843:1–129, 1994. self-esteem and physical discomforts during pregnancy, J Nurse-
157. NIH Consensus Development Panel: Osteoporosis prevention, Midwife 31:255–262, 1986.
diagnosis, and therapy, JAMA 285(6):785–795, 2001. 172. Artal R, Clapp JF, Vigil DV: ACSM Current Comment: Exercise
158. International Society for Clinical Densitometry Writing Group during pregnancy. American College of Sports Medicine. Acessed
for the ISCD Position Development Conference: Diagnosis of at www.acsm.org/AM/Template.cfm?section=current_comments18
osteoporosis in men, women, and children, J Clin Densitom Template=/CM/ContentDisplay.cfm8contentID=8638.
7:17–26, 2004. 173. American College of Obstetricians and Gynecologists: Exercise
159. Falsetti L, Gambera A, Barbetti L, Specchia C: Long-term during pregnancy and the postpartum period. American College
follow-up of functional hypothalamic amenorrhea and prognostic of Obstetricians and Gynecologists Committee Opinion No. 267,
factors, J Clin Endocrinol Metab 87:500–505, 2002. Obstet Gynecol 99:171–173, 2002.
160. Patlas N, Golomb G, Yaffe P, et al: Transplacental effects of 174. Kardel KR, Kase T: Training in pregnant women: Effects on fetal
bisphosphonates on fetal skeletal ossification and mineralization development and birth, Am J Obstet Gynecol 178:280–286, 1998.
in rats, Teratology 60:68–73, 1999. 175. Beilock SL, Feltz DL, Pivarnik JM: Training patterns of athletes
161. Artal R, Sherman C: Exercise during pregnancy: Safe and benefi- during pregnancy and postpartum, Res Quart Ex Sport 72:
cial for most, Phys Sportsmed 27:51–58, 1999. 39–46, 2001.
162. Kardel KR: Effects of intense training during and after pregnancy 176. Krolner B, Toft B, Nielson SP, Tondevold E: Physical exercise as
in top-level athletes, Scand J Med Sci Sports 15:79–86, 2005. prophylaxis against involutional vertebral bone loss: a controlled
163. Paisley TS, Joy EA, Price RJ: Exercise during pregnancy: A prac- trial, Clin Sci 64:541–546, 1983.
tical approach, Current Sports Med Reports 2:325–330, 2003. 177. Elia G: Stress urinary incontinence: Removing barriers to exer-
164. Comittee on Patient Education of the American College of Obste- cise, Phys Sportsmed 27(1):39–52, 1999.
tricians and Gynecologists: Excersise during pregnancy. American 178. Nygaard IE, DeLancey JO, Arnsdorf L, Murphy E: Exercise and
Congress of Obstetricians and Gynecologists, 2003. Accessed at incontinence, Obstet Gynecol 75(5):848–851, 1990.
www.acog.org/publications/patient-education/bp119.cfm. 179. Wallace K: Female pelvic floor functions, dysfunctions, and
165. Veille JC: Maternal and fetal cardiovascular response to exercise behavioral approaches to treatment, Clin Sports Med 13(2):
during pregnancy, Semin Perinatol 20:250–262, 1996. 459–481, 1994.
166. Jaque-Fortunato SV, Wiswell RA, Khodiguian N, Artal R: A com- 180. Griebling TL, Nygaard IE: The role of estrogen replacement
parison of the ventilatory responses to exercise in pregnant, post- therapy in the management of urinary incontinence and urinary
partum, and nonpregnant women, Semin Perinatol 20:263–276, tract infection in postmenopausal women, Endocrinol Metab Clin
1996. North Am 26(2):347–360, 1997.
27
CHAPTER
651
652 SECTION IV • Special Populations and Epidemiology
and performance of dancers by cultivating educational, casual review of the Medline and the Cumulative Index to
medical, and scientific excellence.”4 Worldwide, several other Nursing and Allied Health Literature (CINAHL) databases
professional associations are either totally devoted to dance reveals that the number of articles therein containing either
medicine and science or embrace this specialty as part of the the word dance or the word ballet in their titles and that are
broader performing arts medicine field. In addition, some devoted to some aspect of dance medicine and science has
national dance associations maintain subgroups focused on increased substantially in the last five decades; there were no
dance medicine and science. Table 27-1 identifies many of such articles in 1959. This point, of course, excludes
these organizations. publications not indexed in those two databases, conference
The relative newness of dance medicine and science com- presentations, and similar dissemination avenues. Clearly,
pared with sports medicine and science, combined with the the discipline’s breadth is increasing.
complex technical intricacies of dance means that there are
many fertile areas for research to advance the field. Some of
the demands of dance on the musculoskeletal system are Dance as an Athletic Endeavor
inferred by supposition or anecdote rather than by scientific Anyone who spends time in a dance teaching, rehearsal, or
inquiry. However, an increasing number of researchers performance venue will have little doubt about the vigor and
are accelerating the field’s knowledge base. For example, a athleticism of dancers. Stretanski has called classical ballet a
“full contact sport”5 because of its potential for injury. Others
Table 27-1 corroborate the view that dancers as artists certainly possess
characteristics associated with traditional athletes.6-11 Any
Representative Professional Organizations Wholly
dissenting opinion is likely based solely in one’s unwillingness
or Partially Devoted to Dance Medicine and Science*
to understand the extent to which aerobic and anaerobic
Country Organization power; flexibility; muscular strength, endurance, and power;
Organizations Primarily Focused on Dance proprioceptive function; coordination; agility; and other
(or Performing Arts) Medicine and Science parameters commonly associated with sports participation
are required for success in dance. Although typical dance
France Médecine des Arts (Arts Medicine) training—without ancillary physical conditioning workouts—
Germany Tanz Medizin Deutschland e.V. (TaMeD, does not improve maximum oxygen consumption and other
Dance Medicine Germany)
physiological variables to the same degree that sports training
Monaco Association Danse Médecine Recherche
does,7,12-17 dancers’ bodies must withstand high physical
(Dance Medicine Research Association)
The Netherlands Nederlandse Vereniging voor Dans–en stresses like those of their sports counterparts.18 The daily
Muziek Geneeskunde (Dutch regimen of training that is common in dance creates a level of
Performing Arts Medicine Association) exposure and movement repetition that increases susceptibil-
New Zealand Arts Medicine Aotearoa New Zealand ity to injury when compared with nondancers.19
Spain Asociación Española de Medicina de la
Danza (Spanish Association of Dance
Medicine) Differences in Working with Dancers
United Kingdom British Association for Performing Arts versus Traditional Athletes
Medicine It is not required that the health care professional have
United States International Association for Dance
dance experience to administer care to dancers, although it
Medicine and Science
Performing Arts Medicine Association
is helpful. Experience in sports medicine is generally useful
National Athletic Trainers’ Association, for the clinician working with dancers, but there is not an
Clinical & Emerging Practices Athletic automatic knowledge transfer. Understanding these points
Trainers’ Committee, Performing Arts and motivating oneself to understand dancers in the context
Medicine Workgroup of their sphere of physical activity will prevent many misun-
American Physical Therapy Association, derstandings and grievances.
Performing Arts Special Interest Group
through” injuries is typical,47 especially in dancers with practitioners has been shown to reduce both time loss from
more experience48 or in those who believe that engaging in dancing and medical expenses.31
a treatment regimen will interfere with their ability to par-
ticipate in dance.49 Regardless of dancers’ general propen- Limitations Imposed by Wardrobe and Performance
sity to tolerate pain, injuries create psychological stress that One of the most noticeable differences between dancers
can adversely affect their ability to dance.20,54,55 Further- and traditional athletes is the amount of taping and bracing
more, the psyche of the dancer that allows him or her that is possible. While these prophylactic and protective
to achieve excellence may be a contributor to injury measures are taken for granted as part and parcel of sports,
incidence,53 particularly in classical ballet.22 the appearance requirements for dancers on stage and the
range of motion necessary for their successful performance
restrict some of the clinician’s options. The aesthetic faux
pas of a tutu-clad ballerina wearing a knee-stabilizing brace
Dance Health Care over her tights is obvious. Another common example is
ankle taping; most dancers likely will reject taping such as
• Dancers are extremely diligent in their work ethic and they that used for basketball or football players because it is too
typically take dance classes and rehearse for many hours daily restrictive of plantar flexion and they do not wear socks plus
• Dancers tend to “dance through” injuries rather than seek health sneakers or cleats that would hide the tape. When a dancer
care advice
does permit taping, a reduced volume will be used; flesh-
• Although a sports medicine model is helpful in working with
colored tape is preferable, or the dancer will apply makeup
dancers, these athletic artists must be respected for their unique
talents and abilities that require adaptation of sports medicine cream or powder to blend white tape into the skin. Modern
methods dancers pose even greater challenges with their bare feet
• “Stop dancing” is injury care advice that is universally deplored by because foot pads, supports, and orthotics are not easily
dancers affixed, they detach easily, they change how the dancer
senses the interface between the foot and the floor, and they
may be evident to the audience.
Environmental Differences
The Panoply of Injuries in Dance
Athletes in typical sports environments are usually accus- Dance participation is associated with a high frequency of
tomed to the cadre of professionals who surround them: injury.20,21,27,29,31,46,51,59-72 The percentage of participants
physicians, athletic trainers, physical therapists, and a variety affected is high; 95% is not unheard of in a professional
of other specialists. In fact, it is unlikely in professional and ballet company.27,51 Table 27-2 provides overall injury rates
Olympic sports and extremely unusual at the university reported by various authors. Although epidemiological
level, and even at most large- to medium-sized high schools, correction is not made for the variety of possible definitions
for there to be no sports medicine provision whatsoever. In of “injury” that would aid comparisons among studies73-78
addition, American sports receive unprecedented public and in spite of the fact that vast numbers of dancers lie
attention and they usually enjoy a financial state in which outside the medical profession’s sphere of data collection
health care for their participants is both possible and pre- ability, it is clear that dancers sustain substantial numbers of
sumptive. Virtually the opposite is true of most dance injuries. The data on dance injuries are less sophisticated
programs below the top echelon of professional companies; simply because dancers as a subpopulation have not
furthermore, many dancers are medically uninsured or un- enjoyed the same level of access to injury evaluation and
derinsured.56,57 This problem is particularly exacerbated for recording processes compared with those available in a
dancers in small professional companies or who dance part- typical sports medicine setting; consequently, more system-
time.56 Ambegaonkar and Caswell58 found that university- atic research is required.
level dance students in the United States are woefully Several reasons for such a high injury incidence are
underserved by the medical profession. A discussion about apparent. Chief among these, especially for amateur danc-
the relative merits of funding either sports or dance is not ers, is their lack of the body structure (e.g., tissue strength,
the place of this chapter, but it seems indisputable that flexibility) and biomechanical capability that allows them to
financial disparity exists between sports and the arts and one succeed in dance.79 This is particularly true in ballet, in
effect of this is a negative effect on dancers’ access to health which the requirements are very regimented and can be
care. Moreover, because they have not progressed through unforgiving to the musculoskeletal system. Injurious techni-
systems in which specialized health care providers were cal errors may develop from inadequate dance training,
readily available, dancers tend to be more independent maladaptation to choreography that is beyond the dancer’s
when confronted by injuries. In light of this, it is important skill level, or neuromuscular compensation because of
to note that management of injuries by qualified health care injury. If such errors are not corrected they may be carried
Musculoskeletal Dance Medicine and Science • CHAPTER 27 655
Table 27-2
Injury Data for Dancers Reported by Various Authors
Duration of
Authors Type of Dancer Injury Data Data Collection
Arendt and Professional ballet 7.4 injuries per dancer (567 injuries in 77 dancers) 5 years
Kerschbaumer67
Bowling62 Professional ballet and 84% of dancers injured (118 of 140) Career
modern 12% had 5 or more injuries
Byhring and Professional ballet 75% of dancers injured (31 of 41) 5 months
Bø20 3.2 injuries per dancer
Gamboa et al.86 Elite preprofessional 42% of dancers injured (151 of 359) 5 years
ballet 1.3 injuries per dancer (198 injuries in 151 dancers)
Garrick279 Female 64% of dancers injured (38 of 59) 20 months
preprofessional ballet 5.1 injuries per dancer (194 injuries in 38 dancers)
Garrick and Professional ballet 2.97 injuries per dancer (309 injuries in 104 dancers) 3 years
Requa21 23% of dancers accounted for more than 50% of all injuries
Kerr et al.61 Female university 97% of dancers injured (38 of 39) 8 months
dance students 2.4 injuries per dancer
Laws63 Student and professional 80% of all dancers injured 1 year
dancers, all genres more injuries in ballet than modern
Liederbach Professional ballet and 2.5 injuries per dancer per year (3721 injuries in 5 years
et al.29 modern dancers 298 dancers)
Luke et al.102 Preprofessional 112 self-reported injuries in 39 dancers 1 season
dancers 71 injuries in 39 dancers reported to and identified by a
physical therapist
95% of dancers reported at least 1 injury during their careers
Nilsson et al.27 Professional ballet 95% of dancers injured (93 of 98) 5 years
3.8 injuries per dancer (390 injuries in 98 dancers)
Rovere et al.65 Dance students, 85% of dancers 1 year
all theatrical genres 1.9 injuries per dancer (352 injuries in 185 dancers)
Solomon et al.28 Professional ballet average of 84% of dancers injured per year 5 years
560 total injuries in 5 years in a company with an average
size of 62 dancers per year
Thomas and Professional and 90% of 204 dancers injured at least once Career
Tarr280 student dancers, no dancer older than age 35 had not been injured
all genres in dancers younger than age 35, the number of uninjured
dancers decreased with increasing age
Note: Reported data is not the same for all authors because of differences in how the studies were done.
throughout a dancer’s career, thus compounding their Injuries to the lower extremity account for the vast pro-
deleterious effects. portion of all dance injuries,20,27,29,46,62,65,68,70,86 with most
The inherent nature of dance requires countless repeti- of these occurring in the ankle and foot. One factor report-
tions of movements in the quest to perfect choreography to edly contributing to this is low thigh torque and power.87
the satisfaction of the artistic director, teacher, and audi- A number of studies report that trunk or spine injuries com-
ence. Dancers usually spend far more hours daily in the pose 20% or more of all injuries in dancers.21,51,61-63 Overuse
studio than traditional athletes spend on the field, court, or injuries generally are more common than traumatic injuries
track, and the lack of the well-defined season and off-season simply because of the repetitive nature of dance rehearsal.
periods characteristic of most sports requires dancers to stay Nilsson27 found that incidences in overuse versus traumatic
at peak performance continuously.59 This creates not only injuries were related to gender. In their study of profes-
increased exposure time in which injuries can occur, but it sional ballet dancers, men suffered more lower-extremity
induces fatigue, a known contributor to injury.80-83 Other traumatic injuries, whereas women suffered more overuse
factors associated with the high injury rate include poor injuries in this region. Men also experienced more upper-
training,51 suboptimal lower body muscular power,84 and extremity injuries than women because of the partner-lifting
low aerobic fitness.85 that is integral to their role in classical ballet. However, this
656 SECTION IV • Special Populations and Epidemiology
Satin
Heavy Muslin
Burlap
Insole
B
Figure 27-3
A, A side view of a cutaway shank of a pointe shoe showing the layers
of fabric and leather construction. B, A view directly into the toe box
Figure 27-2 of a pointe shoe after the rest of the shoe has been cut away. The
Typical pointe shoes, including a close-up of three different styles of several layers of materials used in constructing pointe shoes are
the platform on which the dancer stands when en pointe. Ballet danc- shown, as well. These are typically impregnated with glue to form
ers select their shoes with specific features they prefer and then pre- and harden the toe box.
pare the shoes for use by a customized conditioning process accord-
ing to their personal taste.
ballet—may use one, two, or even three different pairs of From an injury-prevention perspective, a properly fitting
pointe shoes in a single performance. pointe shoe provides key support to the dancer; the shoe is
The anatomy of a pointe shoe has been well described especially important for stability of the midfoot as it aug-
elsewhere,89,93,94 and it is illustrated in Figure 27-4. Knowl- ments the ligaments of the Lisfranc joints,95 which include
edge about the shoes is important when consulting with a the dorsal tarsometatarsal, plantar tarsometatarsal, and
dancer about foot injuries, or with parents about their interosseous ligaments.96,97 Additional dependable informa-
youngsters beginning pointe work. Pointe shoes do not tion about pointe shoes is available from sources for both
come in right and left; neither are their sizes related to health care providers93 and performers and teachers.89
women’s street shoe sizes, although conversion charts
are available.89 Dancers and teachers have very particular
preferences from both fitting and aesthetic perspectives. In The Ankle and Foot in Demi-plié, Demi-pointe,
general the shoes should fit closely about the foot and not and en Pointe
unduly compress the sides of the forefoot. Subungual Of all athletic activities, only classical ballet requires its
hematoma, hallux valgus, Morton’s neuroma and other participants to repeatedly move from full forced dorsiflexion
forefoot problems may result from poorly fitting shoes. (in the demi-plié position) to full forced plantar flexion (the
658 SECTION IV • Special Populations and Epidemiology
B B
C
Table 27-3
Ankle Range of Motion in Female Dancers Reported by Various Authors
Mean Age Mean ⫾ SD Mean ⫾ SD
Authors Measurement Method of Participants Dorsiflexion Plantar Flexion
CFL
ATFL
ATFL ATFL
CFL CFL
Figure 27-7
Orientations of the anterior talofibular (ATFL) and calcaneofibular ligaments (CFL) in different ankle
positions. The ligament positions are based on investigations performed in nondancers108,113,114,274-278
because these ligaments have not previously been studied in situ in a dancer population. The fibula is
outlined for ease of visualization. (From Russell JA, McEwan IM, Koutedakis Y et al: Clinical anatomy
and biomechanics of the ankle in dance, J Dance Med Sci 12(3):77, 2008. Reprinted with permission of
J. Michael Ryan Publishing.)
the heel inverts. Figure 27-8, B-D compare proper foot this does not serve the dancer well. Ages most often pro-
alignment with sickling and winging. Sickling and winging posed are 11 to 14. One study of ballet dancers with flexor
can be problematic whether a dancer is en pointe or en hallucis longus (FHL) tendinopathy found the range of ages
demi-pointe, so strong feet and ankles and proper instruc- at initial training en pointe to be 4 to 16 years old, with a
tion will help alleviate these technical faults, both of which mean of 10.130 Meck and colleagues131 discovered that age
can lead to stress injuries. was the most common parameter used by ballet schools
to determine a student’s ability to begin pointe; 96% of
Appropriate Age at Which to Start Pointe Work the schools studied incorporated age into their pointe readi-
Few questions are as common among parents and teachers of ness evaluation programs and the mean age when pointe was
girls in ballet than, “At what age can she start pointe work?” initiated was 11.2 years. Nonetheless, chronological age must
Although it may seem desirable to answer with a definite age, not be the most heavily weighted variable informing the
Medial Lateral
B C D
Figure 27-8
A, A ballet dancer standing en pointe with a winged foot, an alignment that places stress on the hallux
and midfoot. Notice the angular difference between the hindfoot/ankle (solid lines) and the midfoot/
forefoot (dotted lines). The tailed bracket marks the lift of the lateral toe box off the floor and the
arrowhead identifies where this dancer’s weight is being borne. B, Proper alignment of the ankle and
foot. C, A sickled foot. Compared with B, notice the angle between the distal leg and ankle and the
midfoot/forefoot. D, A winged foot, where the angle between the leg/ankle and the midfoot/forefoot
is in the opposite direction as that in a sickled foot.
662 SECTION IV • Special Populations and Epidemiology
decision to allow a young dancer to commence pointe work. literature include 127° for university dancers135 and 128°
The consequences of starting too early are far greater than for preprofessional dancers.70
those of starting too late. The ability to succeed technically is Turnout is not a simple movement of hip external rota-
improved and the risk of injury is reduced if the youngster tion, even though that is its primary component. A ratio
waits until the skeleton and musculature are strong of 60% of turnout motion occurring above the knee and
enough.11,132-134 40% of the motion occurring below the knee has been
Balance and coordination are additional important proposed as an appropriate guideline.69,101 If the ideal
factors.129 Strength in the ankles and feet are not the only 90° of turnout in one limb can be performed, this is
important components; strong and well-controlled muscu- accumulated from 60° to 70° of hip external rotation and
lature in the trunk, hips, and thighs are equally important 20° to 30° spread across the natural positioning of the
to dancing en pointe, and are even more critical for dancers knee, ankle, and foot.136 Actual external rotation range of
with hypermobile feet and ankles.132 motion may be less of a limiting factor compared with the
The attributes outlined in the following textbox offer a lack of experience and technical ability that prevents danc-
guideline that, although seemingly a “rule-of-thumb,” ers from maximizing their turnout when dancing. In fact,
must not be applied without careful evaluation of the indi- improved neuromuscular coordination and strengthening
vidual dancer. If the student began serious ballet training at the hip’s external rotators can yield an additional 15° to
age 8 or later, participates in ballet class at least twice a 30° of turnout.137
week, and possesses adequate maturity in the areas listed Femoral neck version plays a role in a dancer’s ability
previously, then pointe work is usually appropriate begin- to attain turnout. An anteverted femoral neck may me-
ning in the fourth year of ballet training. Dancers taking chanically limit a dancer’s potential for turnout, whereas a
instruction only once per week, who are not intending to retroverted femoral neck allows greater turnout (Figure
engage in preprofessional ballet training, or who lack the 27-11).126,136,138,139 It has been postulated that dancers who
necessary skeletal maturity and muscular strength must be begin their training early in life experience a “molding”
discouraged from pointe work.133 For further information, of the femoral neck that accommodates to the turned out
the reader is referred to a detailed history and physical position by the time the skeleton solidifies. Some reports
examination for young dancers that is offered by Shah.134 have indicated that those who started dance training by
age 5 or 6 exhibit more clinical turnout than dancers
who started later,26 and after age 11, increases in turnout
motion can only occur via hip capsule extensibility.140
Factors for Deciding When to Begin Training In another study, however, students who participated in at
En Pointe133 least 6 hours of ballet training per week between the ages
• Stage of physical development of 11 and 14 showed less femoral neck anteversion
• Quality of trunk, abdominal, and pelvic control (i.e., core stability) than students who trained less than 6 hours per week.141
• Hip-knee-ankle-foot alignment Counterintuitively, these authors did not find an association
• Strength and flexibility of the feet and ankles between age of starting ballet training and femoral
• Frequency and duration of the student’s ballet training neck version, passive hip external rotation, nor functional
• Age turnout. Neither were these variables related to the number
of years of training.
A “normal” version angle is between 8° and 15°.142
Bauman and colleagues143 calculated an average neck version
The Lower Extremity and Turnout angle of 11.4° using data from five studies containing a total
Ballet is the dance genre in which turnout (i.e., the ability of 1436 subjects; the range of measurements in these
to laterally rotate the entire lower extremity) is exceedingly studies was 20° of retroversion to 50° of anteversion. Then
important and in which it receives the most attention (often Bauman’s group compared this value with version angles in a
excessively so, to the point of injury). The ideal ballet turn- contingent of professional ballerinas. The dancers exhibited a
out is 180°; that is, in a fully turned-out position a dancer mean femoral version angle similar to the general population:
wishes to set his or her calcanei back-to-back with the lon- 11.9° of anteversion (range ⫽ 4° to 24°). Practically speak-
gitudinal axes of the feet along a straight line. This is termed ing, the more a dancer tends toward femoral neck antever-
first position, one of six fundamental stances in ballet (Figure sion, the more potential turnout limitation he or she will
27-9 and Figure 27-10). Functional turnout is the amount have. Conversely, the more he or she tends toward retrover-
of turnout motion attained by a dancer in his or her usual sion, the easier it will be to achieve turnout. Longitudinal
studio setting. The vast majority of dancers are unable to studies that periodically measure femoral version in a cohort
achieve the desired 180°, although they try various of dancers from age of initiating ballet training (often age 4)
methods to squeeze a few more degrees from their lower through to adulthood are the only way to confirm the effect
extremities. First-position turnout values reported in the of ballet training on the femoral neck.
Musculoskeletal Dance Medicine and Science • CHAPTER 27 663
A B
Figure 27-9
A, A dancer standing in first position. B, The close-up of turnout. The white dotted line indicates the
180° ideal, whereas the black dotted lines bisect the foot and represent this dancer’s functional turnout.
First
Turnout
• In turnout, 60% should occur above the knee (60° to 70° of hip
external rotation) and 40% below the knee (20° to 30° at the knee,
ankle, and foot)
Second
• Strengthening the hip external rotators and improving neuromuscular
coordination can add 15° to 30° to turnout
• Both bony and soft tissue limitations can restrict a dancer’s ability
to achieve his or her desired turnout
Third Fifth • Forcing one’s turnout can lead to foot pronation, knee valgus
stress, anterior pelvic tilt, and lumbar lordosis
12o
Anteversion Impingement
(typical)
25o Impingement
Anteversion
15o
Impingement
Retroversion
Figure 27-12
Pronation of the feet that is a consequence of forcing turnout. (From
Kadel NJ: Foot and ankle injuries in dance, Phys Med Rehabil Clin
Figure 27-11
North Am 17(4):815, 2006.)
Schematic diagram showing the superior view of a transverse section
through the right hip joint and indicating the relationship between
femoral neck version angle and turnout. The light gray shape repre-
sents the position of the femoral condyles. Notice the differences in
foot position among the neck version angles following external pathological finding of posterior ankle impingement in a
rotation to the point at which the femoral neck impacts the posterior
lip of the acetabulum (dark shaded circles). Dancers with greater
soccer player is not appreciably different from that of the
anteversion will be more limited in their turnout ability, whereas same injury in a dancer even though the mechanism of on-
retroverted femoral necks are favorable to attaining turnout. set and the kinesiology of the activities causing the problem
are different. The same is true of ankle sprains, Achilles
tendinopathy, and many other injuries. The following is not
dancers who were injured versus dancers who were not in- intended to be an exhaustive monograph describing all
jured (25.4° vs. 4.7°), suggesting that forcing one’s turnout common dance injuries. A few injuries are highlighted here
is related to incidence of injury.148 In a group of 28 elite because of their prevalence in the dance population or
professional ballet dancers101 and another group of 29 because the circumstances surrounding their occurrence in
preprofessional dancers,70 those with less functional turnout dancers are particularly unique and interesting.
experienced more injuries. It is speculated that the dancers
with lower turnout were accustomed to forcing their
turnout motion, which led to increased injury rates. Ankle Impingement Syndromes
The requirement that dancers repeatedly plantar flex and
Selected Musculoskeletal Injuries dorsiflex the ankle in weightbearing can give rise to impinge-
ment syndromes on both the posterior and anterior aspects
in Dancers of the ankle. These types of injuries often are related to ana-
Injuries in dancers are, in general, pathologically similar to tomical variations in the foot (e.g., os trigonum)149-153 in
injuries sustained by traditional athletes even though the addition to the pathomechanics of executing dance skills
exact mechanisms of injury may differ. That is to say, the such as demi-plié, demi-pointe, and pointe.150-152,154,155
Musculoskeletal Dance Medicine and Science • CHAPTER 27 665
Posterior Ankle Impingement under the tibia during relevé, or rising on the toes. In this
The cause of posterior impingement most familiar to clini- scenario, the talus slides anteriorly in the ankle mortise and the
cians is os trigonum, an anatomical variation that appears in superior calcaneus similarly moves forward, impinging against
5% to 25% of adults.156-162 Closely related to this is a pro- the posterior edge of the tibial plafond and causing pain.
truding lateral talar tubercle, or Stieda process.132,163-166 Regardless of the exact pathogenesis, any space-
Figure 27-13 illustrates three anatomical variations of the occupying structure in the posterior compartment of the
talus. Some debate exists about whether what appears to be ankle can create symptoms when the calcaneus and talus
an os trigonum in certain individuals may in fact be a Stieda approach the posterior distal tibia during plantar flexion.
process separated from the body of the talus by a compres- Pain associated with posterior impingement, especially an
sion fracture secondary to forced plantar flexion.167-169 Soft os trigonum or Stieda process, most often occurs postero-
tissue structures, including the FHL tendon,149,170-175 deep laterally, thus differentiating these problems from FHL
posteromedial deltoid ligament,176 posterior intermalleolar tendinopathy, a syndrome that produces pain at the pos-
ligament,177,178 and posterior tibiotalar ligament,179 also can teromedial ankle.180,184 Dancers with posterior impinge-
produce posterior impingement symptoms. ment syndrome complain of posterior ankle pain and
Peace and colleagues153 used magnetic resonance imag- describe a limitation of motion in their demi-pointe or
ing (MRI) scans to study ballet dancers with posterior en pointe positions. During a clinical examination, forced
impingement symptoms; 30% of the subjects exhibited os plantar flexion of the ankle reproduces these symptoms. In
trigonum. This is higher than the prevalence reported in cases of failed conservative measures, operative treatment
the general population, perhaps because of the forced plan- has been shown successful.168,173,182,185,186
tar flexion of ballet during the years when the secondary
ossification center of the lateral talar tubercle is adjoining Anterior Ankle Impingement
the tubercle and the talar body. An os trigonum might be As in the posterior ankle, impingement syndrome in the
quiet for years until it becomes symptomatic following a anterior region of the ankle can arise from bone or soft tis-
sprained ankle or other traumatic episode.149,180,181 This sue. Symptoms originating in bone can be initiated by
may be related to force created by the posterior talofibular repetitive impact of the anterior edge of the tibial plafond
ligament during ankle trauma because the ligament attaches and the dorsal talus that causes exostoses to form on either
to the lateral talar tubercle. or both bones.139,151,155,187-194 Although contact between
Additional anatomical variations have been shown to pre- the tibia and talus does not usually occur, dancers may
dispose dancers to pathological conditions of the ankle, espe- experience impingement when they repeatedly force their
cially posterior impingement syndrome.149,153,154,167,168,182,183 ankles into maximum dorsiflexion during demi-plié.151,155
Greater than 5 mm of downward protrusion of the posterior Because of this required repetition, exostosis formation
lip of the tibial plafond (posterior malleolus) and greater than occurs more frequently in dancers than nondancers,155,195
5 mm of upward protrusion of the superior calcaneal tuberos- and both pes cavus79,151 and limited subtalar motion145 can
ity both have been cited as contributory to pathological increase the likelihood that a dancer will develop exostoses.
conditions resulting in posterior impingement.153 These are Another possible result of repeated forced dorsiflexion in
depicted in Figure 27-14. demi-plié is a deepened sulcus on the dorsal talar neck.196
One other mechanism of posterior impingement bears
mentioning. Lateral ankle sprains that lead to ankle instability
also can produce a posterior impingement syndrome.79,180 In
a dancer with an unstable ankle, the foot moves forward from Tibia
Fibula
PM
Talar dome
Talus
Lateral
process
Medial
FH FH
Anterior
tubercle
FH Lateral tubercle Os trigonum Stieda’s process CT
A B C Calcaneus
Figure 27-13
Superior view of three right tali, with posterior being toward the
bottom of the diagram. Three different variations of the lateral talar Figure 27-14
tubercle are illustrated and the position of the tendon of flexor Lateral view of ankle anatomy showing a protruding posterior malleolus
hallucis longus is indicated by the circle marked FH. A, A typical (PM) and calcaneal tuberosity (CT), either of which increases the likeli-
talus. B, A talus with an os trigonum. C, A talus with a Stieda process. hood of posterior ankle impingement in dancers.
666 SECTION IV • Special Populations and Epidemiology
Achilles Tendinopathy
Tendinopathy217 or tendinosis218 are the terms currently
Figure 27-15
employed to describe tendon overuse injury because the T1-weighted magnetic resonance images of ballet dancers standing
classic signs of inflammation—denoted by the suffix in the en pointe. In the larger image, the black arrows indicate the band of
word tendinitis—are generally not present in this type of hypointense signal of the Achilles tendon. The white arrow indicates
condition.217,219 The distinguishing difference between the indentation made by the posterior lip of the pointe shoe and the
these two terms is the presence of intratendinous degenera- gray arrows indicate the impressions of the shoe’s ribbon. The inset
image is a different dancer exhibiting an even more pronounced
tion in tendinosis218,220; tendinopathy refers to any abnormal curve in the tendon substance, as indicated by the open arrows. To
state of a tendon. The Achilles tendon is prone to injury in understand the components of the overlaying shoe, compare these
any genre of dance in which repeated dorsiflexion and plan- images with the photo of the ankle and foot en pointe in Figure 27-5
tar flexion are required; however, classical ballet presents a and the en pointe x-ray image in Figure 27-7.
Musculoskeletal Dance Medicine and Science • CHAPTER 27 667
With very few exceptions (e.g., the men’s ballet troupe the first distal phalanx. In particular, the bend in the tendon
Les Ballets Trockaderos de Monte Carlo), pointe dancers are just before it enters the fibro-osseous tunnel under the
women. Following exercise-induced collagen degradation, sustentaculum tali (Figure 27-16) heightens the chance of
the rate of collagen synthesis is reduced in women com- injury from a nonhomogeneous force distribution through
pared with men,223 a phenomenon possibly related to circu- the tendon221 during rising to and lowering from the toes,
lating estradiol levels,224,225 but apparently independent and when jumping. In an advanced stage, the FHL tendon
of menstrual phase.223,226 If a hormonal mediation of rela- and its synovial sheath may swell and develop adhesions, or
tive collagen strength exists, it may intimate a greater inci- the tendon may develop areas of degeneration. Any or all of
dence of Achilles tendinopathy in women dancers, especially these can cause a hallux saltans (“trigger toe”) tenosynovitis
in conjunction with the potential for added insult to the when the tendon does not slide smoothly through its
morphological structure of the tendon that is elicited by the tunnel.139,180,228,229
en pointe position as just described. Further insight into FHL tendinopathy may be precipitated by the presence
pathological changes in tendon can be found in “Tendon of an unstable os trigonum171 because the trigonal bone is
Pathology and Injuries: Pathophysiology, Healing, and a nonunited protrusion of the lateral tubercle that creates
Treatment Considerations,” which is Chapter 3 in Scientific the lateral border of the groove for the tendon. Several
Foundations and Principles of Practice in Musculoskeletal authors corroborate a strong, direct relationship between
Rehabilitation, another book in this series. symptoms in these two structures149,170,171,173-175,230,231
because of their proximity to one another.
Aream of
common
pathology
Retinaculum
(gray)
Figure 27-16
Medial view of the foot showing the path of the flexor hallucis longus tendon as it changes direction around
the posterior talus and under the sustentaculum tali. The grey arrow indicates the usual position of pathological
conditions of the tendon just proximal to the retinacular tunnel that can cause a triggering injury.223
668 SECTION IV • Special Populations and Epidemiology
the rotational force that results in this fracture’s characteris- such areas is not unusual in response to arduous schedules
tic appearance (Figure 27-17). of dance rehearsal and performance (Figure 27-19). Perios-
A Jones fracture (Figure 27-18) occurs at the junction teal elevation indicates the presence of the reparative callus
of the diaphysis and proximal metaphysis of the fifth associated with stress fractures.238 The second metatarsal
metatarsal.232,234,235 Named for the author who first can also exhibit a stress fracture at its base, an injury that is
described it in 1902, Jones236 reported that this injury rare in nondancers because it is induced by the repetitive
occurred in his own foot—recounting that he sustained it longitudinal forces through the foot that are sustained
while dancing—and in patients seen in his practice. This during dance.239-242 Other common sites for stress fractures
particular fracture must be cared for surgically because of in dancers are the tibia (often related to later stages of shin
its propensity to proceed to malunion or nonunion, often splints), fibula, and lumbar spine.232,237,243,244
because of a poor or disrupted blood supply.235 Further- The rigors of dance training combined with intervals of
more, those who participate in sports and dance are amenorrhea have been suggested as risk factors for stress
unlikely to accept an extended period of immobilization fractures in dancers.237,243,245 Dancers may ignore the early
and the risk of nonunion that can complicate treatment of symptoms of stress reactions and stress fractures because of
a Jones fracture. the tenacity they possess for continuing their dance activity.
However, this can be disastrous if the pathological condi-
tion proceeds through the cortex of the involved bone,
Stress Fractures particularly in a weightbearing bone like the tibia.246 For
Stress fractures are a common overuse injury in dance, more information on stress fractures, see “Repetitive Stress
especially in the foot.237 The second metatarsal shaft is the Pathology—Bone,” Chapter 21, in Pathology and Interven-
most frequently affected; because of its length, it bears tion in Musculoskeletal Rehabilitation, another book in this
more force than the other metatarsals when a dancer stands series.
in demi-pointe.232 Cortical hypertrophy of the diaphyses in
Figure 27-18
Figure 27-17 Jones fracture (arrow) of the proximal fifth metatarsal diaphysis.
Spiral “dancer’s fracture” of the fifth metatarsal shaft. (From Kadel (From Kennedy JG, Hodgkins CW, Columbier J-A et al: Foot and
NJ: Foot and ankle injuries in dance, Phys Med Rehabil Clin North ankle injuries in dancers. In Porter DA, Schon LC, editors: Baxter’s
Am 17(4):818, 2006.) the foot and ankle in sport, ed 2, p 474, Philadelphia, 2008, Mosby.)
Musculoskeletal Dance Medicine and Science • CHAPTER 27 669
dancing days, or 3.2 per 100,000 dancing days when con- plete rupture of the ligament confirmed by clinical and
sidering classical ballet dancers only. In fact, in their 10-year radiological examination”29).
study, the modern dancers experienced no ACL tears Substantial evidence exists that women athletes who
whereas the classical dancers sustained six. The left knee was participate in sports that elicit rotational forces across the
involved in every case and, of these, four occurred in men knee—such as those requiring cutting and jumping—
and two occurred in women. All were treated operatively, are much more likely than men to sustain an ACL
but three dancers had to retire from dance because of post- injury.215,248-250 Jump landings have been proposed as one
surgical symptoms. These authors calculated the risk of mechanism for such injury.251 Both studies of ACL inju-
a dancer suffering an ACL rupture of the left knee in a ries in dance outlined previously reported virtually identi-
10-year classical ballet career to be 7%. cal injury mechanisms in their samples of dancers: knee
In another study, Liederbach and colleagues29 prospec- valgus and external rotation forces upon landing from a
tively studied 298 professional ballet and modern dancers jump (Figure 27-20). One set of investigators proposed
for 5 years. In this cohort, 12 ACL sprains occurred, 10 of this landing style as the single most important risk factor
which were in women. Contrasting with the data of for ACL tear in dancers.30 With the large proportion of
Meuffels and Verhaar, in this study, modern dancers experi- dancers being women and the heavy emphasis on jumping
enced a higher risk than did classical ballet dancers: 9 of the in many dance genres, it is perhaps surprising that more
12 injuries were in modern dancers. The ACL injury rate ACL injuries are not reported. Although it does not
in ballet was 0.005 injuries per 1000 exposures and for appear that male and female dancers differ in their jump
modern dance, it was 0.012 injuries per 1000 exposures landing biomechanics,252 several parameters about dance
(an exposure was a single class, rehearsal, or performance in and dancers may account for the contrast of these results
which a dancer participated). Overall, the injury rate of with ACL injuries in a sports environment. These include
ACL injury in all dancers was 0.009 per 1000 exposures. more forgiving shoe-to-floor or foot-to-floor interfaces,
It is important to note that Meuffels and Verhaar studied more controlled (i.e., choreographed) movements, and
ACL rupture, whereas Liederbach and colleagues recorded generally greater flexibility among dancers. Consistent
ACL injuries (an injury being “a first-time partial or com- exposure to balance training and jump training may also
Figure 27-19
Anterior-posterior and oblique x-ray examinations of the left foot
of a ballet dancer who presented with a clinical history of relentless Figure 27-20
rehearsals en pointe over several weeks, extreme midfoot pain, and Characteristic landing pattern of a dancer that is associated with
exquisite point tenderness on the second and third metatarsals. anterior cruciate ligament injury. Note the externally rotated hip and
Dotted boxes highlight second, third, and fourth metatarsal shafts pronated foot with resulting valgus stress to the left knee. (From
with cortical thickening. Arrowheads indicate areas of periosteal Meuffels DE, Verhaar JAN: Anterior cruciate ligament injury in
elevation suggesting stress fractures of second and third metatarsals. professional dancers, Acta Orthop 79(4):516, 2008.)
670 SECTION IV • Special Populations and Epidemiology
play a role.29,252 One more crucial factor to contemplate posterior iliotibial band or anterior edge of the gluteus
was identified by Liederbach and colleagues’ study. As maximus muscle sliding across the greater trochanter.254 On
shown in Table 27-4, most ACL injuries occurred in the the other hand, the internal type may result—among several
evening, at the end of a season, and during performances, causes—from the iliopsoas tendon rubbing over the ante-
suggesting that fatigue may play a role in these dance rior ridge on the femoral head,140 the iliopectineal ridge,11
injuries. or a portion of the iliacus muscle belly.253,255 Jacobs and
Young256 found certain kinesiological characteristics in
dancers with a snapping hip compared with dancers without
Knee Ligament Injuries in Dancers a snapping hip: narrow width between the pelvic ilia,
• Anterior cruciate ligament (ACL) rupture is not a common occurrence increased hip abduction range of motion, decreased hip
in dancers, but the nature of dance likely precludes participation by external rotation range of motion, and increased external
a dancer with a torn ACL rotation strength.
• Occurrence of ACL injuries in dancers seems to be associated with The iliopsoas is the most frequently involved anatomical
fatigue and related factors because research shows that most of structure in snapping hip.253 This complex is a combination
the injuries occur late in the day, at the end of the season, and of the iliacus and psoas major muscles with their distal
during performances tendinous portions forming a common tendon that inserts
at the lesser trochanter of the femur. Figure 27-21 illus-
trates the femoropelvic anatomy deep to the iliopsoas
Psoas
one customary way of categorizing the condition is as either Il
external or internal snapping hip. The nature of hip motion i
ac
in dance requires as large a range of motion in this joint as
us
pronate and, thus, load the medial foot (see Figure 27-12)
and because a common mechanism of ACL injury involves Dancing and Osteoarthritis
landing from a jump with substantial medial loading (see • Osteoarthritic changes seen on x-ray examinations are a typical
Figure 27-20). Whether hypermobile dancers are more prone finding in dancers
to injury because they also exhibit a proclivity to medially load • The first metatarsophalangeal joint is the most common site for
the lower extremity warrants study. osteoarthritis in dancers
• Even among older, retired dancers, physical symptoms usually
do not correlate with x-ray examination manifestations of
Osteoarthritis osteoarthritis
Based on the demanding activities and schedules of most
dancers, it is often presumed that development of osteoarthri-
tis is an inevitable consequence of participating in dance. As
summarized in Table 27-6, this seems to be generally
true,196,269-272 but the extent of the symptoms associated with
Case Studies
arthritic changes in dancers’ joints is widely variable. The find- The following two case studies illustrate the importance
ing of degenerative joint disease is not, by itself, necessarily of careful diagnostics in dance medicine. In both of these
adverse to dancing.271-273 Teitz and Kocoyne271 found that cases, the dancers involved sought care for recalcitrant
radiographically confirmed hip capsule calcifications and knee, injuries, but sadly that care was not helpful and the danc-
ankle, and first metatarsophalangeal joint changes occurred in ers became frustrated with their injuries and their caregiv-
young (late 20s to early 40s) retired dancers, yet did not cor- ers. However, once a dance medicine specialist established
relate with the dancers’ symptoms. Neither was the x-ray evi- a correct diagnosis, the dancers were able to proceed
dence associated with dancers’ retirement from dance. Van toward recovery. Both of these are fairly recent cases. The
Dijk and colleagues272 studied retired dancers between 50 and intent is not to show the clinical progression to a success-
66 years old and found no clinical complaints among them in ful resumption of activity, but, rather, to focus on how a
spite of a plethora of hip, ankle, subtalar, and first metatarso- health care provider’s familiarity with the demands of
phalangeal arthroses on x-ray examination. Andersson and dance and special attention to a dancer-patient’s com-
colleagues269 studied the same joints in a cohort of former plaints can yield an appropriate diagnosis and treatment
dancers ranging in age from 44 to 80 years and, although the regimen.
prevalence of joint degeneration was greater in dancers than
nondancers, only in the hips and knees were frequent symp-
toms reported. Only one study could be found that evaluated Case Study 1: Posterior Ankle Pain
dancers with backgrounds other than just classical ballet. The A 19-year-old female ballet and modern dancer presented
long-term effect of other dance genres on joint degeneration to a dance medicine clinician complaining of persistent pos-
represents a fertile field for research. terior left ankle pain. She reported a history of symptoms in
Table 27-6
Radiographic Findings of Arthroses in Dancers Reported by Various Authors
General Presence of Degenerative
Author(s) No. Subjects Age of Subjects Genre Hip Knee Ankle Subtalar First MTP
relatively hard and stiff sole. The dancer denied paresthesia was thought that, apart from trauma, a turf-toe type of
in her toes and swelling was unremarkable in any part of injury that was so painful and persistent was unlikely.
the forefoot. As a result of the history and examination— Furthermore, the intense focal pressure on the sesamoids
and considering the concentration of symptoms at the during demi-pointe—especially considering how a pointe
lateral sesamoid—the dance medicine clinician’s clinical shoe’s sole could amplify this—was deemed important
impression was bipartite lateral sesamoid. Lateral sesa- and, in fact, this is what elicited the greatest pain. Point
moiditis was a differential impression. The dancer was tenderness over the lateral sesamoid added further to the
referred to her orthopaedic surgeon again, and radio- suspicion of bipartite sesamoid or sesamoiditis. Once
graphs confirmed a bipartite lateral sesamoid (Figure again, careful attention to the injury history and to the
27-23). The surgeon advised against surgery (surgery is dancer’s equipment and regimen provided vital assistance
contraindicated in the first metatarsophalangeal joint of to caring for her. Moreover, it is not a minor point that
dancers because of the likelihood that the joint’s crucial this case is saddled with the added emotional challenge of
hyperextension range will be compromised), but acknowl- a very talented dancer requiring an extended period of
edged a lack of expertise for working with dancers and discontinuance from dance.
referred the dancer back to the dance medicine clinician
who consulted with a podiatrist specializing in injuries of
elite dancers. MRI examination was undertaken to discern
Conclusion
the extent of bone and soft tissue involvement. The MRI Dancers certainly are athletes and dance injuries are com-
examination confirmed the diagnosis, demonstrating bone monplace. Unquestionably, working with dancers presents
marrow edema and soft tissue inflammation, so the dancer many challenges to the musculoskeletal health care provider;
was removed from participation to allow the greatest but the challenges are also what make the task enjoyable.
chance for healing. Following 6 months of rest, the dancer Health care providers will find in dancers an extremely
began to test her injured foot in a very controlled fashion, creative, interesting, and grateful group of patients. A tradi-
but relevé remained painful. Because the load on the sesa- tional sports medicine model is helpful in working with
moids during ballet is substantial, she continued pursuing dancers, yet it is not an ideal match because of several unique
the conservative course of rest in the hope of being able to characteristics of a dance environment. These include the
return to dance later. After a complete year of rest, she dancer’s intense psyche, limitations imposed by wardrobe
undertook a very gradual and methodical resumption of requirements, and unrelenting training regimens.
her dance activity, with hopefulness that her symptoms will The majority of dance injuries are of the overuse variety. It
not recur. is highly unlikely that a dancer will escape injury during his or
Significant to this case was the need to listen to the her career; most musculoskeletal conditions are exacerbated
dancer’s history to establish the probable mechanism. It by the very nature of dance training, and many of them are
endemic to dance. Careful assessment and well-considered
care plans are helpful, whereas advice to “stop dancing” as a
categorical solution to injuries is quite the opposite and will
only frustrate the dancer-patient, as it would any athlete.
Dancers respond well to practitioners who show genuine
interest in dance and at least a basic understanding of what
dance entails as a physical and artistic activity.
Acknowledgments
I am grateful for three of my students at the University of
California–Irvine who served as models for some of my
figures: Ashley McConnell, Laura Obler, and Amy Quanbeck.
Also, I deeply appreciate my former faculty colleagues and
students in the Dance Department at Belhaven College and
my current faculty colleagues and students in the Dance
Department at UC-Irvine. They have taught me much more
about dance and dance medicine than they realize. Two of my
Figure 27-23 current colleagues, Dr. Lisa Naugle and Dr. Nancy Ruyter,
X-ray examination of the forefoot of a 14-year-old ballet dancer with
pain and exquisite point tenderness over the lateral hallux sesamoid.
provided invaluable reviews of portions of this chapter. Finally,
Arrowhead points to the bipartite sesamoid that was the source of the my wife, Ruth, deserves a special accolade for the encourage-
dancer’s symptoms. ment she gave me to undertake this writing project.
Musculoskeletal Dance Medicine and Science • CHAPTER 27 675
25. Milan KR: Injury in ballet: A review of relevant topics for the
References physical therapist, J Orthop Sports Phys Ther 19(2):121–129,
1. Snook GA: The history of sports medicine. Part I, Am J Sports 1994.
Med 12(4):252–254, 1984. 26. Miller EH, Schneider HJ, Bronson JL, et al.: A new consider-
2. Welch JE: Pioneering in health education and services at Amherst ation in athletic injuries: The classical ballet dancer, Clin Orthop
College, J Am Coll Health 30(6):289–295, 1982. 111:181–191, 1975.
3. Sparger C: Physiotherapy at the Sadler’s Wells School of Ballet, 27. Nilsson C, Leanderson J, Wykman A, et al: The injury panorama
Physiotherapy 38(1):8–13, 1952. in a Swedish professional ballet company, Knee Surg Sports
4. International Association for Dance Medicine and Science: Traumatol Arthrosc 9(4):242–246, 2001.
About IADMS, 2009. Available at: http://www.iadms.org/ 28. Solomon R, Solomon J, Micheli LJ, et al: The “cost” of injuries
displaycommon.cfm?an⫽8. Accessed November 21, 2009. in a professional ballet company, Med Prob Performing Artists
5. Stretanski MF: Classical ballet: The full contact sport, Am J Phys 14:164–169, 1999.
Med Rehabil 81(5):392–393, 2002. 29. Liederbach M, Dilgen FE, Rose DJ: Incidence of anterior cruci-
6. Fitt SS: Dance kinesiology, ed 2, New York, 1996, Schirmer ate ligament injuries among elite ballet and modern dancers:
Books. A 5-year prospective study, Am J Sports Med 36(9):1779–1788,
7. Koutedakis Y, Jamurtas A: The dancer as a performing athlete, 2008.
Sports Med 34(10):651–661, 2004. 30. Meuffels DE, Verhaar JAN: Anterior cruciate ligament injury in
8. Koutedakis Y, Pacy PJ, Carson RJ, et al: Health and fitness in professional dancers, Acta Orthop 79(4):515–518, 2008.
professional dancers, Med Prob Performing Artists 12(1):23–27, 31. Bronner S, Ojofeitimi S, Rose D: Injuries in a modern dance
1997. company: Effect of comprehensive management on injury inci-
9. Stretanski MF: Medical and rehabilitation issues in classical ballet, dence and time loss, Am J Sports Med 31(3):365–373, 2003.
Am J Phys Med Rehabil 81(5):383–391, 2002. 32. Sides SN, Ambegaonkar JP, Caswell SV: High incidence of shoul-
10. Council of Arts Accrediting Associations: Briefing paper: An der injuries in collegiate modern dance students, Athl Ther Today
overview of health issues for performing and visual arts students, 14(4):43–46, 2009.
Reston, VA, 1991, Council of Arts Accrediting Associations. 33. Shybut TB, Rose DJ, Strongwater AM: Second metatarsal physeal
11. Toledo SD, Akuthota V, Drake DF, et al: Sports and performing arrest in an adolescent flamenco dancer: A case report, Foot Ankle
arts medicine. 6. Issues relating to dancers, Arch Phys Med Reha- Int 29(8):859–862, 2008.
bil 85(Suppl 1):75–78, 2004. 34. Cromie S, Greenwood JG, McCullagh JF: Does Irish-dance
12. Baillie Y, Wyon M, Head A: Highland dance: Heart-rate and training influence lower-limb asymmetry? Laterality 12(6):
blood lactate differences between competition and class, Int J 500–506, 2007.
Sports Physiol Perf 2(4):371–376, 2007. 35. Bejjani FJ: Occupational biomechanics of athletes and dancers: A
13. Koutedakis Y, Hukam H, Metsios G, et al: The effects of three comparative approach, Clin Podiatr Med Surg 4(3):671–711,
months of aerobic and strength training on selected performance- 1987.
and fitness-related parameters in modern dance students, J Strength 36. Bejjani FJ, Halpern N, Pio A, et al: Musculoskeletal demands on
Cond Res 21(3):808–812, 2007. flamenco dancers: A clinical and biomechanical study, Foot Ankle
14. Redding E, Wyon M: Strengths and weaknesses of current meth- 8(5):254–263, 1988.
ods for evaluating the aerobic power of dancers, J Dance Med Sci 37. Kauther MD, Wedemeyer C, Kauther KM, et al: Breakdancer’s
7(1):10–16, 2003. “Headspin Hole”: First description of a common overuse
15. Wyon MA, Abt G, Redding E, et al: Oxygen uptake during mod- syndrome, Sportverletz Sportschaden 23(1):52–53, 2009.
ern dance class, rehearsal, and performance, J Strength Cond Res 38. Kauther MD, Wedemeyer C, Wegner A, et al: Breakdance
18(3):646–649, 2004. injuries and overuse syndromes in amateurs and professionals,
16. Wyon MA, Deighan MA, Nevill AM, et al: The cardiorespira- Am J Sports Med 37(4):797–802, 2009.
tory, anthropometric, and performance characteristics of an 39. Winkler AR, Barnes JC, Ogden JA: Break dance hip: Chronic
international/national touring ballet company, J Strength Cond avulsion of the anterior superior iliac spine, Pediatr Radiol
Res 21(2):389–393, 2007. 17(6):501–502, 1987.
17. Wyon MA, Redding E: Physiological monitoring of cardiorespi- 40. Cho CH, Song KS, Min BW, et al: Scaphoid nonunion in break-
ratory adaptations during rehearsal and performance of dancers: A report of 3 cases, Orthopedics 32(7):526, 2009.
contemporary dance, J Strength Cond Res 19(3):611–614, 41. Cho CH, Song KS, Min BW, et al: Musculoskeletal injuries in
2005. break-dancers, Injury 40(11):1207–1211, 2009.
18. Conti SF, Wong YS: Foot and ankle injuries in the dancer, 42. McCauley A, Lamb KL: An assessment of the prevalence and
J Dance Med Sci 5(2):43–50, 2001. correlates of injuries in Irish dancers [Abstract], J Sports Sci
19. Solomon R, Brown T, Gerbino PG, et al: The young dancer, 22(3):251, 2004.
Clin Sports Med 19(4):717–739, 2000. 43. Henderson J, MacIntyre D: A descriptive survey of injury
20. Byhring S, Bø K: Musculoskeletal injuries in the Norwegian patterns in Canadian Premier Highland dancers, Physiother Can
National Ballet: A prospective cohort study, Scand J Med Sci 58(1):61–73, 2006.
Sports 12(6):365–370, 2002. 44. Pedersen ME, Wilmerding MV: Injury profiles of student and
21. Garrick JG, Requa R: Ballet injuries: An analysis of epidemiol- professional flamenco dancers, J Dance Med Sci 2(3):108–114,
ogy and financial outcome, Am J Sports Med 21(4):586–590, 1998.
1993. 45. Walls RJ, Brennan SA, Hodnett P,, et al.: Overuse ankle injuries
22. Hamilton LH, Hamilton WG, Meltzer JD, et al: Personality, in professional Irish dancers, Foot Ankle Surg 16(1):45–49,
stress, and injuries in professional ballet dancers, Am J Sports Med 2010.
17(2):263–267, 1989. 46. Washington EL: Musculoskeletal injuries in theatrical dancers:
23. Hardaker WT Jr.: Foot and ankle injuries in classical ballet Site, frequency, and severity, Am J Sports Med 6(2):75–98,
dancers, Orthop Clin North Am 20(4):621–627, 1989. 1978.
24. Khan K, Brown J, Way S, et al: Overuse injuries in classical ballet, 47. Leavesley RGE, Borthwick AM: Foot and lower-limb injury in
Sports Med 19(5):341–357, 1995. ballet: Dancers’ perspectives, Br J Podiatry 6(3):73–79, 2003.
676 SECTION IV • Special Populations and Epidemiology
48. Air M: Health care seeking behavior and perceptions of the 74. Ekstrand J, Karlsson J: The risk for injury in football. There is a
medical profession among pre- and post-retirement age Dutch need for a consensus about definition of the injury and the design
dancers, J Dance Med Sci 13(2):42–50, 2009. of studies, Scand J Med Sci Sports 13(3):147–149, 2003.
49. Lai RYJ, Krasnow D, Thomas M: Communication between 75. Brooks JHM, Fuller CW: The influence of methodological issues
medical practitioners and dancers, J Dance Med Sci 12(2):47–53, on the results and conclusions from epidemiological studies of
2008. sports injuries: Illustrative examples, Sports Med 36(6):459–472,
50. Tajet-Foxell B, Rose FD: Pain and pain tolerance in professional 2006.
ballet dancers, Br J Sports Med 29(1):31–34, 1995. 76. Hodgson L, Gissane C, Gabbett TJ, et al: For debate: Consensus
51. Ramel E, Moritz U: Self-reported musculoskeletal pain and dis- injury definitions in team sports should focus on encompassing
comfort in professional ballet dancers in Sweden, Scand J Rehabil all injuries, Clin J Sport Med 17(3):188–191, 2007.
Med 26(1):11–16, 1994. 77. Garrick JG: The frequency of injury, mechanism of injury, and
52. Anderson R, Hanrahan SJ: Dancing in pain: Pain appraisal and epidemiology of ankle sprains, Am J Sports Med 5(6):241–242,
coping in dancers, J Dance Med Sci 12(1):9–16, 2008. 1977.
53. Rip B, Fortin S, Vallerand RJ: The relationship between passion 78. Bronner S, Ojofeitimi S, Mayers L: Comprehensive surveillance
and injury in dance students, J Dance Med Sci 10(1–2):14–20, of dance injuries: A proposal for uniform reporting guidelines for
2006. professional companies, J Dance Med Sci 10(3–4):69–80, 2006.
54. Macchi R, Crossman J: After the fall: Reflections on injured 79. Hamilton WG: Foot and ankle injuries in dancers, Clin Sports
classical ballet dancers, J Sport Behav 19(3):221–234, 1996. Med 7(1):143–173, 1988.
55. Adam MU, Brassington GS, Matheson GO: Psychological factors 80. McLean SG, Samorezov JE: Fatigue-induced ACL injury risk
associated with performance-limiting injuries in professional stems from a degradation in central control, Med Sci Sports Exerc
ballet dancers, J Dance Med Sci 8(2):43–46, 2004. 41(8):1661–1672, 2009.
56. Requa RK, Garrick JG: Do professional dancers have medical 81. McLean SG, Fellin RE, Suedekum N, et al: Impact of fatigue
insurance? Company-provided medical insurance for professional on gender-based high-risk landing strategies, Med Sci Sports Exerc
dancers, J Dance Med Sci 9(3–4):81–83, 2005. 39 (3):502–514, 2007.
57. Weiss DS, Shah S, Burchette RJ: A profile of the demographics 82. Chappell JD, Herman DC, Knight BS, et al: Effect of fatigue on
and training characteristics of professional modern dancers, knee kinetics and kinematics in stop-jump tasks, Am J Sports Med
J Dance Med Sci 12(2):41–46, 2008. 33(7):1022–1029, 2005.
58. Ambegaonkar JP, Caswell SV: Dance program administrators’ 83. Gefen A: Biomechanical analysis of fatigue-related foot injury
perceptions of athletic training services, Athl Ther Today mechanisms in athletes and recruits during intensive marching,
14(3):17–19, 2009. Med Biol Eng Comput 40(3):302–310, 2002.
59. Bronner S, Ojofeitimi S, Spriggs J: Occupational musculoskeletal 84. Angioi M, Metsios GS, Koutedakis Y, et al: Physical fitness and
disorders in dancers, Phys Ther Rev 8:57–68, 2003. severity of injuries in contemporary dance, Med Prob Performing
60. Askling C, Lund H, Saartok T, et al: Self-reported hamstring Artists 24:26–29, 2009.
injuries in student-dancers, Scand J Med Sci Sports 12:230–235, 85. Twitchett E, Brodrick A, Nevill AM, et al: Does physical fitness
2002. affect injury occurrence and time loss due to injury in elite voca-
61. Kerr G, Krasnow D, Mainswaring L: The nature of dance tional ballet students? J Dance Med Sci 14(1):26–31, 2010.
injuries, Med Prob Performing Artists 7:25–29, 1992. 86. Gamboa JM, Roberts LA, Maring J, et al: Injury patterns in elite
62. Bowling A: Injuries to dancers: Prevalence, treatment and preprofessional ballet dancers and the utility of screening pro-
perception of causes, BMJ 298:731–734, 1989. grams to identify risk characteristics, J Orthop Sports Phys Ther
63. Laws H: Fit to dance 2, London, 2005, Dance UK. 38(3):126–136, 2008.
64. Sohl P, Bowling A: Injuries to dancers: Prevalence, treatment and 87. Koutedakis Y, Khaloula M, Pacy PJ, et al: Thigh peak torques and
prevention, Sports Med 9(5):17–22, 1990. lower-body injuries in dancers, J Dance Med Sci 1(1):12–15, 1997.
65. Rovere GD, Webb LX, Gristina AG, et al: Musculoskeletal 88. Grant G: Technical manual and dictionary of classical ballet,
injuries in theatrical dance students, Am J Sports Med 11(4): ed 3, New York, 1982, Dover Publications.
195–198, 1983. 89. Barringer J, Schlesinger S: The pointe book: Shoes, training and tech-
66. Olsson I: A 2-year study of 77 dancers: Almost 90 per cent needed nique, ed 2, Hightstown, NJ, 2004, Princeton Book Company.
help because of injury, Lakartidningen 95(15):1689, 1998. 90. Lee C: Ballet in Western culture: A history of its origins and
67. Arendt YD, Kerschbaumer F: Injury and overuse pattern in pro- evolution, New York, 2002, Routledge.
fessional ballet dancers, Z Orthop Ihre Grenzgeb 141(3):349–356, 91. Gaynor Minden Inc: 10 Ergonomic Secrets, 2009. Available at http://
2003. gaynorminden.com/tensecrets.php. Accessed August 5, 2009.
68. Ambegaonkar JP: Dance medicine: At the university level, Dance 92. Bloch International: thermoMorphtechnology, 2009. Available at
Res J 37(2):113–119, 2005. http://www.bloch-tmt.com/. Accessed August 5, 2009.
69. Schon LC, Weinfeld SB: Lower extremity musculoskeletal prob- 93. Novella TM: Pointe shoes: Fitting and selection criteria, J Dance
lems in dancers, Curr Opin Rheumatol 8(2):130–142, 1996. Med Sci 4(2):73–77, 2000.
70. Negus V, Hopper D, Briffa NK: Associations between turnout 94. Teitz CC, Harrington RM, Wiley H: Pressures on the foot in
and lower extremity injuries in classical ballet dancers, J Orthop pointe shoes, Foot Ankle 5(5):216–221, 1985.
Sports Phys Ther 35(5):307–318, 2005. 95. Kadel N, Boenisch M, Teitz CC, et al: Stability of Lisfranc joints
71. Hincapié CA, Morton EJ, Cassidy JD: Musculoskeletal injuries in ballet pointe position, Foot Ankle Int 26(5):394–400, 2005.
and pain in dancers: A systematic review, Arch Phys Med Rehabil 96. Solan MC, Moorman CT III, Miyamoto RG, et al: Ligamentous
89:1819–1829, 2008. restraints of the second tarsometatarsal joint: a biomechanical
72. Baker J, Scott D, Watkins K, et al: Self-reported and reported evaluation, Foot Ankle Int 22(8):637–641, 2001.
injury patterns in contemporary dance students, Med Probl 97. Johnson A, Hill K, Ward J, et al: Anatomy of the Lisfranc
Perform Art 25(1):10–15, 2010. ligament, Foot Ankle Spec 1(1):19–23, 2008.
73. Van Mechelen W, Hlobil H, Kemper HC: Incidence, severity, 98. American Academy of Orthopaedic Surgeons: Joint motion:
aetiology and prevention of sports injuries: A review of concepts, Method of measuring and recording, Chicago, 1965, American
Sports Med 14(2):82–99, 1996. Academy of Orthopaedic Surgeons.
Musculoskeletal Dance Medicine and Science • CHAPTER 27 677
99. Gerhardt JJ: Documentation of joint motion, ed 4, Portland, 123. Macintyre J, Joy EA: Foot and ankle injuries in dance, Clin Sports
1994, ISOMED. Med 19(2):351–368, 2000.
100. Reese NB, Bandy WD: Joint range of motion and muscle length 124. Shah S, Luftman J, Vigil DV: Stress injury of the talar dome and
testing, ed 2, St Louis, 2010, Saunders Elsevier. body in a ballerina: A case report, J Dance Med Sci 9(3):91–95,
101. Hamilton WG, Hamilton LH, Marshall P, et al: A profile of the 2005.
musculoskeletal characteristics of elite professional ballet dancers, 125. O’Loughlin PF, Hodgkins CW, Kennedy JG: Ankle sprains and
Am J Sports Med 20(3):267–273, 1992. instability in dancers, Clin Sports Med 27(2):247–262, 2008.
102. Luke AC, Kinney SA, D’Hemecourt PA, et al: Determinants of 126. Clippinger K: Dance anatomy and kinesiology, Champaign, IL,
injuries in young dancers, Med Prob Performing Artists 2007, Human Kinetics.
17(3):105–112, 2002. 127. Oztekin HH, Boya H, Nalcakan M, et al: Second-toe length and
103. Novella TM: Simple techniques for quantifying choreographi- forefoot disorders in ballet and folk dancers, J Am Podiatr Med
cally essential foot and ankle extents of motion, J Dance Med Sci Assoc 97(5):385–388, 2007.
8(4):118–122, 2004. 128. Tuckman AS, Werner FW, Bayley JC: Analysis of the forefoot on
104. Steinberg N, Hershkovitz I, Peleg S, et al: Range of joint move- pointe in the ballet dancer, Foot Ankle 12(3):144–148, 1991.
ment in female dancers and nondancers aged 8 to 16 years, Am 129. Kravitz SR, Huber S, Murgia CJ, et al: Biomechanical study of
J Sports Med 34(5):814–823, 2006. bunion deformity and stress produced in classical ballet, J Am
105. Wiesler ER, Hunter DM, Martin DF, et al: Ankle flexibility and Podiatr Med Assoc 75(7):338–345, 1985.
injury patterns in dancers, Am J Sports Med 24(6):754–757, 130. Sammarco GJ, Cooper PS: Flexor hallucis longus tendon injury
1996. in dancers and nondancers, Foot Ankle Int 19(6):356–362,
106. Sammarco GJ, Burstein AH, Frankel VH: Biomechanics of the 1998.
ankle: A kinematic study, Orthop Clin North Am 4(1):75–96, 131. Meck C, Hess RA, Helldobler R, et al: Pre-pointe evaluation
1973. components used by dance schools, J Dance Med Sci 8(2):37–42,
107. Lundberg A, Goldie I, Kalin B, et al: Kinematics of the ankle/ 2004.
foot complex: Plantarflexion and dorsiflexion, Foot Ankle 132. Howse AJG: Dance technique and injury prevention, ed 3,
9(4):194–200, 1989. London, 2000, A & C Black.
108. Bonnin JG: Injuries to the ankle (facsimile of the 1950 edition), 133. Weiss DS, Rist RA, Grossman G: When can I start pointe work?
Darien, CT, 1970, Hafner Publishing Co. Guidelines for initiating pointe training, J Dance Med Sci
109. Kitaoka HB, Patzer GL: Clinical results of the Mayo total ankle 13(3):90–92, 2009.
arthroplasty, J Bone Joint Surg Am 78(11):1658–1664, 1996. 134. Shah S: Determining a young dancer’s readiness for dancing on
110. Kitaoka HB, Alexander IJ, Adelaar RS, et al: Clinical rating sys- pointe, Curr Sports Med Rep 8(6):295–299, 2009.
tems for the ankle-hindfoot, midfoot, hallux, and lesser toes, Foot 135. Welsh TM, Rodriguez M, Beare LW, et al: Assessing turnout in
Ankle Int 15(7):349–353, 1994. university dancers, J Dance Med Sci 12(4):136–141, 2008.
111. Lundberg A: Kinematics of the ankle and foot: In vivo roentgen 136. Hardaker WT Jr., Erickson L: The pathogenesis of dance injury.
stereophotogrammetry, Acta Orthop Scand 60(Suppl 233):1–24, In Shell CG, editor: The dancer as athlete, Champaign, IL, 1986,
1989. Human Kinetics Publishers.
112. Russell JA, Shave RM: Tri-color superimposition x-rays for evalua- 137. Clippinger-Robertson K: A unique challenge: Biomechanical
tion of extreme ankle and foot motion in ballet dancers, American considerations in turnout, JOPERD 58(5):37–40, 1987.
Orthopaedic Society for Sports Medicine Annual Conference, 138. Hamilton WG: Physical prerequisites for ballet dancers,
Keystone, Colorado, 2009. J Musculoskel Med 3:61–66, 1986.
113. Anderson KJ, LeCocq JF: Operative treatment of injury to the 139. Thomasen E: Diseases and injuries of ballet dancers, Århus,
fibular collateral ligament of the ankle, J Bone Joint Surg Am Denmark, 1982, Universitetsforlaget I Århus.
36(4):825–832, 1954. 140. Sammarco GJ: The dancer’s hip, Clin Sports Med 2(3):485–498,
114. Ferran NA, Maffulli N: Epidemiology of sprains of the lateral 1983.
ankle ligament complex, Foot Ankle Clin North Am 11(3): 141. Hamilton D, Aronsen P, Løken JH, et al: Dance training inten-
659–662, 2006. sity at 11-14 years is associated with femoral torsion in classical
115. Foetisch CA, Ferkel RD: Deltoid ligament injuries: Anatomy, ballet dancers, Br J Sports Med 40(4):299–303, 2006.
diagnosis, and treatment, Sports Med Arthrosc 8:326–335, 142. Magee DJ: Orthopedic physical assessment, ed 5, Philadelphia,
2000. 2008, Saunders Elsevier.
116. Russell JA, McEwan IM, Koutedakis Y, et al: Clinical anatomy 143. Bauman PA, Singson R, Hamilton WG: Femoral neck antever-
and biomechanics of the ankle in dance, J Dance Med Sci sion in ballerinas, Clin Orthop 302:57–63, 1994.
12(3):75–82, 2008. 144. Grossman G, Waninger KN, Voloshin A, et al: Reliability and
117. Nigg BM, Skarvan G, Frank CB, et al: Elongation and forces of validity of goniometric turnout measurements compared with
ankle ligaments in a physiological range of motion, Foot Ankle MRI and retro-reflective markers, J Dance Med Sci 12(4):
11(1):30–40, 1990. 142–152, 2008.
118. Siegler S, Block J, Schneck CD: The mechanical characteristics of 145. Grossman G: Measuring dancer’s active and passive turnout,
the collateral ligaments of the human ankle joint, Foot Ankle J Dance Med Sci 7(2):49–55, 2003.
8(5):234–242, 1988. 146. Kadel NJ: Foot and ankle injuries in dance, Phys Med Rehabil
119. Renstrom P, Wertz M, Incavo S, et al: Strain in the lateral liga- Clin N Am 17 (4):813–826, 2006.
ments of the ankle, Foot Ankle 9(2):59–63, 1988. 147. Micheli L: Back injuries in dancers, Clin Sports Med 2(3):
120. Bahr R, Pena F, Shine J, et al: Ligament force and joint motion 473–484, 1983.
in the intact ankle: A cadaveric study, Knee Surg Sports Traumatol 148. Coplan JA: Ballet dancer’s turnout and its relationship to self-
Arthrosc 6:115–121, 1998. reported injury, J Orthop Sports Phys Ther 32(11):579–584,
121. Colville MR, Marder RA, Boyle JJ, et al: Strain measurement in 2002.
lateral ankle ligaments, Am J Sports Med 18(2):196–200, 1990. 149. Hamilton WG: Stenosing tenosynovitis of the flexor hallucis
122. Hamilton WG: Sprained ankles in ballet dancers, Foot Ankle longus tendon and posterior impingement upon the os trigonum
3(2):99–102, 1982. in ballet dancers, Foot Ankle 3(2):74–80, 1982.
678 SECTION IV • Special Populations and Epidemiology
150. Kadel NJ, Micheli LJ, Solomon R: Os trigonum impingement 176. Paterson RS, Brown JN, Roberts SNJ: The posteromedial
syndrome in dancers, J Dance Med Sci 4(3):99–102, 2000. impingement lesion of the ankle: A series of six cases, Am J Sports
151. Kleiger B: Anterior tibiotalar impingement syndromes in dancers, Med 29(5):550–557, 2001.
Foot Ankle 3(2):69–73, 1982. 177. Fiorella D, Helms CA, Nunley JAI: The MR imaging features of
152. Kleiger B: The posterior tibiotalar impingement syndrome in the posterior intermalleolar ligament in patients with posterior
dancers, Bull Hosp Jt Dis Orthop Inst 47(2):203–210, 1987. impingement syndrome of the ankle, Skeletal Radiol 28:
153. Peace KAL, Hillier JC, Hulme A, et al: MRI features of posterior 573–576, 1999.
ankle impingement syndrome in ballet dancers: A review of 178. Rosenberg ZS, Cheung YY, Beltran J, et al: Posterior intermal-
25 cases, Clin Radiol 59:1025–1033, 2004. leolar ligament of the ankle: Normal anatomy and MR imaging
154. O’Kane JW, Kadel N: Anterior impingement syndrome in features, Am J Roentgenol 165:387–390, 1995.
dancers, Curr Rev Musculoskel Med 1(1):12–16, 2008. 179. Koulouris G, Connell D, Schneider T, et al: Posterior tibiotalar
155. Stoller SM, Hekmat F, Kleiger B: A comparative study of the ligament injury resulting in posteromedial impingement, Foot
frequency of anterior impingement exostoses of the ankle in Ankle Int 24(8):575–583, 2003.
dancers and nondancers, Foot Ankle 4(4):201–203, 1984. 180. Hamilton WG: Posterior ankle pain in dancers, Clin Sports Med
156. Tsuruta T, Shiokawa Y, Kato A, et al: Radiological study of the 27(2):263–277, 2008.
accessory skeletal elements in the foot and ankle, Nippon Seikeigeka 181. Ihle CL, Cochran RM: Fracture of the fused os trigonum, Am J
Gakkai Zasshi 55(4):357–370, 1981. Sports Med 10(1):47–50, 1982.
157. Lawson JP: Symptomatic radiographic variants in extremities, 182. Labs K, Leutloff D, Perka C: Posterior ankle impingement
Radiology 157:625–631, 1985. syndrome in dancers: A short-term follow-up after operative
158. Kleinberg S: Supernumerary bones of the foot, Ann Surg treatment, Foot Ankle Surg 8:33–39, 2002.
65(4):499–509, 1917. 183. Macquirriain J: Posterior ankle impingement syndrome, J Am
159. Shands AR, Jr.: The accessory bones of the foot: An x-ray study Acad Orthop Surg 13(6):365–371, 2005.
of the feet of 1,054 patients, South Med Surg 93:326–336, 184. Hamilton WG, Patel MM, Sibel RA: Impingement syndromes of
1931. the foot and ankle. In Porter DA, Schon LC, editors: Baxter’s the
160. Geist ES: Supernumerary bones of the foot—A röntgen study of foot and ankle in sport, ed 2, Philadelphia, 2008, Mosby.
the feet of one hundred normal individuals, J Bone Joint Surg Am 185. Abramowitz Y, Wollstein R, Barzilay Y, et al: Outcome of resection
s2-12(3):403–414, 1915. of a symptomatic os trigonum, J Bone Joint Surg Am 85(6):
161. O’Rahilly R: A survey of carpal and tarsal anomalies, J Bone Joint 1051–1057, 2003.
Surg Am 35(3):626–642, 1953. 186. Kadel NJ: Excision of os trigonum, Oper Tech Orthop 14(1):1–5,
162. Gottlieb A: Post-traumatic os trigonum, J Int Coll Surg 26(1): 2004.
80–82, 1956. 187. O’Donoghue DH: Impingement exostoses of the talus and tibia,
163. Stieda L: Ueber secundäre fusswerzelknochen, Archiv für Anato- J Bone Joint Surg Am 39(4):835–852, 1957.
mie, Physiologie und Wissenschaftliche Medizin 36:108–111, 1869. 188. Berberian WS, Hecht PJ, Wapner KL, et al: Morphology of
164. Hedrick MR, McBryde AM: Posterior ankle impingement, Foot tibiotalar osteophytes in anterior ankle impingement, Foot Ankle
Ankle 15(1):2–8, 1994. Int 22(4):313–317, 2001.
165. Howse AJG: Posterior block of the ankle joint in dancers, Foot 189. Tol JL, Verheyan CPPM, van Dijk CN: Arthroscopic treatment
Ankle 3(2):81–84, 1982. of anterior impingement in the ankle: A prospective study with a
166. Brodsky AE, Khalil MA: Talar compression syndrome, Am J five- to eight-year follow-up, J Bone Joint Surg Br 83(1):9–13,
Sports Med 14(6):472–476, 1986. 2001.
167. Bureau NJ, Cardinal E, Hobden R, et al: Posterior ankle 190. Tol JL, van Dijk CN: Etiology of the anterior ankle impingement
impingement syndrome: MR imaging findings in seven patients, syndrome: A descriptive anatomical study, Foot Ankle Int
Radiology 215:497–503, 2000. 25(6):382–386, 2004.
168. Jourdel F, Tourne Y, Saragaglia D: Posterior ankle impinge- 191. Tol JL, Verhagen RAW, Krips R, et al: The anterior ankle impinge-
ment syndrome: A retrospective study in 21 cases treated ment syndrome: Diagnostic value of oblique radiographs, Foot
surgically, Rev Chir Orthop Reparatrice Appar Mot 91(3): Ankle Int 25(2):63–68, 2004.
239–247, 2005. 192. Tol JL, van Dijk CN: Anterior ankle impingement, Foot Ankle
169. GolanÓ P, Vega J, Pérez-Carro L, et al: Ankle anatomy for the Clin N Am 11:297–310, 2006.
arthroscopist. Part II: Role of the ankle ligaments in soft tissue 193. Van Dijk CN: Anterior and posterior ankle impingement, Foot
impingement, Foot Ankle Clin N Am 11:275–296, 2006. Ankle Clin N Am 11:663–683, 2006.
170. Hamilton WG, Geppert MJ, Thompson FM: Pain in the posterior 194. Nihal A, Rose DJ, Trepman E: Arthroscopic treatment of ante-
aspect of the ankle in dancers: Differential diagnosis and operative rior ankle impingement syndrome in dancers, Foot Ankle Int
treatment, J Bone Joint Surg Am 78(10):1491–1500, 1996. 26(11):908–912, 2005.
171. Lohrer H: Flexor hallucis longus tendon rupture as an impinge- 195. Liebler WA: Injuries of the foot in dancers. In Bateman JE,
ment lesion induced by os trigonum instability, Sportverletz editor: Foot Science, Philadelphia, 1976, WB Saunders.
Sportschaden 20(1):31–35, 2006. 196. Schneider HJ, King AY, Bronson JL, et al: Stress injuries and
172. Karasick D, Schweitzer ME: The os trigonum syndrome: Imag- developmental change of lower extremities in ballet dancers,
ing features, Am J Roentgenol 166:125–129, 1996. Radiology 113:627–632, 1974.
173. Tey M, Monllau J, Centenera J, et al: Benefits of arthroscopic 197. Umans HR: Ankle impingement syndromes, Semin Musculoskel
tuberculoplasty in posterior ankle impingement syndrome, Knee Radiol 6(2):133–139, 2002.
Surg Sports Traumatol Arthrosc 15(10):1235–1239, 2007. 198. Umans HR, Cerezal L: Anterior ankle impingement syndromes,
174. Van Dijk CN: A 2-portal endoscopic approach for diagnosis Semin Musculoskel Radiol 12(2):146–153, 2008.
and treatment of posterior ankle pathology, Arthroscopy 16(8): 199. Van Dijk CN, Tol JL, Verheyen CCPM: A prospective study
871–876, 2000. of prognostic factors concerning the outcome of arthroscopic
175. Hillier JC, Peace K, Hulme A, et al: MRI features of foot and surgery for anterior ankle impingement, Am J Sports Med 25(6):
ankle injuries in ballet dancers, Br J Radiol 77:532–537, 2004. 737–745, 1997.
Musculoskeletal Dance Medicine and Science • CHAPTER 27 679
200. Sanders TG, Rathur SK: Impingement syndromes of the ankle, 223. Miller BF, Hansen M, Olesen JL, et al: Tendon collagen synthesis
Magn Reson Imaging Clin North Am 16(1):29–38, 2008. at rest and after exercise in women, J Appl Physiol 102(2):
201. Akseki D, Pinar H, Bozkurt M, et al: The distal fascicle of the 541–546, 2007.
anterior inferior tibiofibular ligament as a cause of anterolateral 224. Hansen M, Koskinen SO, Petersen SG, et al: Ethinyl oestradiol
ankle impingement: Results of arthroscopic resection, Acta administration in women suppresses synthesis of collagen in
Orthop Scand 70(5):478–482, 1999. tendon in response to exercise, J Physiol (Lond) 586(12):
202. Akseki D, Pinar H, Yaldiz K, et al: The anterior inferior tibio- 3005–3016, 2008.
fibular ligament and talar impingement: a cadaveric study, Knee 225. Hansen M, Miller BF, Holm L, et al: Effect of administration of
Surg Sports Traumatol Arthrosc 10:321–326, 2002. oral contraceptives in vivo on collagen synthesis in tendon and
203. Haller J, Bernt R, Seeger T, et al: MR-imaging of anterior tibiota- muscle connective tissue in young women, J Appl Physiol
lar impingement syndrome: Agreement, sensitivity and specificity 106(4):1435–1443, 2009.
of MR-imaging and indirect MR-arthrography, Eur J Radiol 58: 226. Miller BF, Hansen M, Olesen JL, et al: No effect of menstrual
450–460, 2006. cycle on myofibrillar and connective tissue protein synthesis in
204. Van den Bekerom MPJ, Raven EEJ: The distal fascicle of the contracting skeletal muscle, Am J Physiol Endocrinol Metab
anterior inferior tibiofibular ligament as a cause of tibiotalar 290(1):E163–168, 2006.
impingement syndrome: A current concepts review, Knee Surg 227. Hamilton WG: Tendonitis about the ankle joint in classical ballet
Sports Traumatol Arthrosc 15:465–471, 2007. dancers, Am J Sports Med 5(2):84–88, 1977.
205. Wolin I, Glassman F, Sideman S, et al: Internal derangement of 228. Shybut G, Miller C: “Trigger toe” in a ballet dancer, Med Prob
the talofibular component of the ankle, Surg Gynecol Obstet Performing Artists 20(2):99–102, 2005.
91(2):193–200, 1950. 229. Kolettis GJ, Micheli LJ, Klein JD: Release of the flexor hallucis
206. Ferkel RD, Karzel RP, Del Pizzo W, et al: Arthroscopic treatment longus tendon in ballet dancers, J Bone Joint Surg Am 78(9):
of anterolateral impingement of the ankle, Am J Sports Med 1386–1390, 1996.
19(5):440–446, 1991. 230. Tamburrini O, Porpiglia H, Barresi D, et al: The role of magnetic
207. Cerezal L, Abascal F, Canga A, et al: MR imaging of ankle resonance imaging in the diagnosis of the os trigonum syndrome,
impingement syndromes, Am J Roentgenol 181:551–559, 2003. Radiol Med (Torino) 98(6):462–467, 1999.
208. Kim S-H, Ha K-I: Arthroscopic treatment for impingement of 231. Wredmark T, Carlstedt CA, Bauer H, et al: Os trigonum
the the anterolateral soft tissues of the ankle, J Bone Joint Surg Br syndrome: A clinical entity in ballet dancers, Foot Ankle
82(7):1019–1021, 2000. 11(6):404–406, 1991.
209. Liu SH, Raskin A, Osti L, et al: Arthroscopic treatment of antero- 232. Goulart M, O’Malley MJ, Hodgkins CW, et al: Foot and ankle
lateral ankle impingement, Arthroscopy 10(2):215–218, 1994. fractures in dancers, Clin Sports Med 27(2):295–304, 2008.
210. Meislin RJ, Rose DJ, Parisien S, et al: Arthroscopic treatment 233. O’Malley MJ, Hamilton WG, Munyak J: Fractures of the distal
of synovial impingement of the ankle, Am J Sports Med 21(2): shaft of the fifth metatarsal: Dancer’s fracture, Am J Sports Med
186–189, 1993. 24(2):240–243, 1996.
211. Jordan LK, III, Helms CA, Cooperman AE, et al: Magnetic 234. Evans A: “Dancer’s fracture” —A clinical perspective, Australas
resonance imaging findings in anterolateral impingement of the J Podiatr Med 32(1):13–19, 1998.
ankle, Skeletal Radiol 29:34–39, 2000. 235. Nunley JA: Fractures of the base of the fifth metatarsal: The
212. Liu SH, Nuccion SL, Finerman G: Diagnosis of anterolateral Jones fracture, Orthop Clin N Am 32(1):171–180, 2001.
ankle impingement: Comparison between magnetic resonance 236. Jones R: Fracture of the base of the fifth metatarsal bone by
imaging and clinical examination, Am J Sports Med 25(3): indirect violence, Ann Surg 35(6):697–700.692, 1902.
389–393, 1997. 237. Kadel NJ, Teitz CC, Kronmal RA: Stress fractures in ballet
213. Rubin DA, Tishkoff NW, Britton CA, et al: Anterolateral soft- dancers, Am J Sports Med 20(4):445–449, 1992.
tissue impingement in the ankle: diagnosis using MR imaging, 238. Warden SJ, Burr DB, Brukner PD: Repetitive stress pathology:
Am J Roentgenol 169:829–835, 1997. Bone, In Magee DJ, Zachazewski JE, Quillen WS, editors:
214. Fong DT-P, Hong Y, Chan L-K, et al: A systematic review on Pathology and intervention in musculoskeletal rehabilitation,
ankle injury and ankle sprain in sports, Sports Med 37(1):73–94, St Louis, 2009, Saunders.
2007. 239. Micheli LJ, Sohn RS, Solomon R: Stress fractures of the second
215. Hootman JM, Dick R, Agel J: Epidemiology of collegiate injuries metatarsal involving Lisfranc’s joint in ballet dancers: A new overuse
for 15 sports: Summary and recommendations for injury preven- injury of the foot, J Bone Joint Surg Am 67(9):1372–1375, 1985.
tion initiatives, J Athl Train 42(2):311–319, 2007. 240. O’Malley MJ, Hamilton WG, Munyak J, et al: Stress fractures at
216. Yeung MS, Chan KM, So CH, et al: An epidemiological survey the base of the second metatarsal in ballet dancers, Foot Ankle Int
on ankle sprain, Br J Sports Med 28(2):112–116, 1994. 17(2):89–94, 1996.
217. Sharma P, Maffulli N: Tendon injury and tendinopathy: Healing 241. Muscolo L, Migues A, Slullitel G, et al: Stress fracture nonunion
and repair, J Bone Joint Surg Am 87(1):187–202, 2005. at the base of the second metatarsal in a ballet dancer, Am J
218. Kaeding C, Best TM: Tendinosis: Pathophysiology and nonop- Sports Med 32(6):1535–1537, 2004.
erative treatment, Sports Health 1(4):284–292, 2009. 242. Albisetti W, Perugia D, De Bartolomeo O, et al: Stress fractures
219. Kjær M, Langberg H, Heinemeier K, et al: From mechanical of the base of the metatarsal bones in young trainee ballet dancers,
loading to collagen synthesis, structural changes and function in Int Orthop 34(1):51–55, 2010.
human tendon, Scand J Med Sci Sports 19(4):500–510, 2009. 243. Lundon K, Melcher L, Bray K: Stress fractures in ballet: A
220. Hodgkins CW, Kennedy JG, O’Loughlin PF: Tendon injuries in twenty-five year review, J Dance Med Sci 3(3):101–107, 1999.
dance, Clin Sports Med 27(2):279–288, 2008. 244. Nussbaum AR, Treves ST, Micheli LJ: Bone stress lesions in ballet
221. Arndt AN, Komi PV, Brüggemann G-P, et al: Individual muscle dancers: Scintigraphic assessment, Am J Roentgenol 150(4):
contributions to the in vivo achilles tendon force, Clin Biomech 851–855, 1988.
13:532–541, 1998. 245. Molnar M: Stress fracture of the second metatarsal: A case report,
222. Clement DB, Taunton JE, Smart GW: Achilles tendinitis and J Dance Med Sci 1(1):22–24, 1997.
peritendinitis: Etiology and treatment, Am J Sports Med 12(3): 246. Martinez SF, Murphy GA: Tibial stress fracture in a male ballet
179–184, 1984. dancer: A case report, Am J Sports Med 33(1):124–130, 2005.
680 SECTION IV • Special Populations and Epidemiology
247. Ambegaonkar JP, Shultz SJ, Schulz MR: Anterior cruciate 266. Mishra MB, Ryan P, Atkinson P, et al: Extra-articular features of
ligament injury in collegiate female dancers, Athl Ther Today benign joint hypermobility syndrome, Rheumatology (Oxford)
14(4):13–16, 2009. 35(9):861–866, 1996.
248. Agel J, Arendt EA, Bershadsky B: Anterior cruciate ligament 267. Klemp P, Chalton D: Articular mobility in ballet dancers:
injury in National Collegiate Athletic Association basketball and A follow-up study after four years, Am J Sports Med 17(1):
soccer: A 13-year review, Am J Sports Med 33(4):524–531, 72–75, 1989.
2005. 268. Briggs J, McCormack M, Hakim AJ, et al: Injury and joint
249. Gwinn DE, Wilckens JH, McDevitt ER, et al: The relative hypermobility syndrome in ballet dancers—A 5-year follow-up,
incidence of anterior cruciate ligament injury in men and women Rheumatology (Oxford) 48(12):1613–1614, 2009.
at the United States Naval Academy, Am J Sports Med 28(1): 269. Andersson S, Nilsson B, Hessel T, et al: Degenerative joint
98–102, 2000. disease in ballet dancers, Clin Orthop 238:233–236, 1989.
250. Arendt EA, Agel J, Dick R: Anterior cruciate ligament injury 270. Brodelius Å´: Osteoarthrosis of the talar joints in footballers and
patterns among collegiate men and women, J Athl Train ballet dancers, Acta Orthop Scand 30:309–314, 1961.
34(2):86–92, 1999. 271. Teitz CC, Kocoyne RF: Premature osteoarthrosis in professional
251. Chappell JD, Creighton RA, Giuliani C, et al: Kinematics and dancers, Clin J Sport Med 8(4):255–259, 1998.
electromyography of landing preparation in vertical stop-jump: 272. Van Dijk CN, Lim LSL, Poortman A, et al: Degenerative joint
Risks for noncontact anterior cruciate ligament injury, Am J disease in female ballet dancers, Am J Sports Med 23(3):295–300,
Sports Med 35(2):235–241, 2007. 1995.
252. Orishimo KF, Kremenic IJ, Pappas E, et al: Comparison of land- 273. Ambré T, Nilsson BE: Degenerative changes in the first
ing biomechanics between male and female professional dancers, metatarso-phalangeal joint of ballet dancers, Acta Orthop Scand
Am J Sports Med 37(11):2187–2193, 2009. 49:317–319, 1978.
253. Winston P, Awan R, Cassidy JD, et al: Clinical examination and 274. Makhani JS: Lacerations of the lateral ligaments of the ankle,
ultrasound of self-reported snapping hip syndrome in elite ballet J Int Coll Surg 38(5):454–466, 1962.
dancers, Am J Sports Med 35(1):118–126, 2007. 275. Sarrafian SK: Anatomy of the foot and ankle: Descriptive, topographic,
254. Wahl CJ, Warren RF, Adler RS, et al: Internal coxa saltans functional, ed 2, Philadelphia, 1993, JB Lippincott Company.
(snapping hip) as a result of overtraining, Am J Sports Med 276. Stiehl JB: Biomechanics of the ankle joint. In Stiehl JB, editor,
32(5):1302–1309, 2004. Inman’s joints of the ankle, ed 2, Baltimore, 1991, Williams and
255. Déslandes M, Guillin R, Cardinal É, et al: The snapping iliopsoas Wilkins.
tendon: New mechanisms using dynamic sonography, Am J 277. Logan BM, Singh D, Hutchings RT: McMinn’s color atlas of foot
Roentgenol 190(3):576–581, 2008. and ankle anatomy, ed 3, Philadelphia, 2004, Mosby.
256. Jacobs M, Young R: Snapping hip phenomenon among dancers, 278. Christman RA: The normal foot and ankle. In Christman RA,
Am Correct Ther J 32(3):92–98, 1978. editor: Foot and ankle radiology, St Louis, 2003, Churchill
257. Blankenbaker DG, Tuite MJ: Iliopsoas musculotendinous unit, Livingstone.
Semin Musculoskel Radiol 12(1):13–27, 2008. 279. Garrick JG: Early identification of musculoskeletal complaints
258. Allen WC, Cope R: Coxa saltans: The snapping hip revisited, and injuries among female ballet students, J Dance Med Sci
J Am Acad Orthop Surg 3(5):303–308, 1995. 3(2):80–83, 1999.
259. Reid DC, Burnham RS, Saboe LA, et al: Lower extremity flexi- 280. Thomas H, Tarr J: Dancers’ perceptions of pain and injury:
bility patterns in classical ballet dancers and their correlation to Positive and negative effects, J Dance Med Sci 13(2):51–59,
lateral hip and knee injuries, Am J Sports Med 15(4):347–352, 2009.
1987. 281. Bennell KL, Khan KM, Matthews B, et al: Hip and ankle
260. Da Silva AH, Bonorino KC: BMI and flexibility in ballerinas of range of motion and hip muscle strength in young novice
contemporary dance and classical ballet, Fitness Perf J 7(1): female ballet dancers and controls, Br J Sports Med 33:
48–51, 2008. 340–346, 1999.
261. Beighton P, Horan F: Orthopaedic aspects of the Ehlers-Danlos 282. Bennell KL, Khan KM, Matthews BL, et al: Changes in hip and
syndrome, J Bone Joint Surg Br 51(3):444–453, 1969. ankle range of motion and hip muscle strength in 8-11 year old
262. Klemp P, Stevens JE, Isaacs S: A hypermobility study in ballet novice female ballet dancers and controls: A 12 month follow up
dancers, J Rheumatol 11(5):692–696, 1984. study, Br J Sports Med 35:54–59, 2001.
263. McCormack M, Briggs J, Hakim A, et al: Joint laxity and the 283. Khan K, Roberts P, Nattrass C, et al: Hip and ankle range of
benign joint hypermobility syndrome in student and professional motion in elite classical ballet dancers and controls, Clin J Sport
ballet dancers, J Rheumatol 31(1):173–178, 2003. Med 7(3):174–179, 1997.
264. Foss KDB, Ford KR, Myer GD, et al: Generalized joint laxity 284. Lin C-F, Su F-C, Wu H-W: Ankle biomechanics of ballet dancers
associated with increased medial foot loading in female athletes, in relevé en pointé dance, Res Sports Med 13:23–35, 2005.
J Athl Train 44(4):356–362, 2009. 285. Novella TM: An easy way to quantify plantarflexion in the ankle,
265. Grahame R: Joint hypermobility and genetic collagen disorders: J Back Musculoskel Rehabil 5:191–199, 1995.
Are they related? Arch Dis Child 80(2):188–191, 1999.
28
CHAPTER
681
682 SECTION IV • Special Populations and Epidemiology
Table 28-1
Competitive Sports and Recreation Activities Offered by US Disabled Sports Organizations
Organization
Sport AAAD DAAA DSUSA WSUSA USABA USCPAA USLASA SOI
Alpine skiing x x x x
Archery x x x
Basketball x x x x
Bocce x x
Bowling x x x
Canoeing x x
Cross country x x x
Cycling x x x x x
Diving x x
Equestrian x x
Figure skating x
Floor hockey x
Goal ball x
Gymnastics x x
Handball x
Ice hockey x
Judo x
Nordic skiing x x x x
Poly hockey x
Powerlifting x x x x x x x
Racquetball x
Road racing x x x x
Roller skating x
Shooting x x x x x x
Slalom x x x x
Soccer x x x
Softball x x x
Speed skating x x x
Swimming x x x x x x x x
Table tennis x x x x x x x
Team handball x x x
Tennis x x x x
Track and field x x x x x x x x
Volleyball x x x
Weight lifting x x
Wrestling x x
From Curtis KA, Gailey RS Jr: The athlete with a disability. Adapted from Paciorek MJ, Jones JA: Sports and recreation for the disabled: A resource
manual, Indianapolis, 1989, Benchmark Press.
AAAD, American Athletic Association of the Deaf; DAAA, Dwarf Athletic Association of America; DSUSA, Disabled Sports USA (amputees);
SOI, Special Olympics International (developmentally disabled); USABA, United States Association of Blind Athletes; USCPAA, United States
Cerebral Palsy Athletic Association; USLASA, United States Les Autres Sports Association (other disabilities); WSUSA, Wheelchair Sports USA.
sports are weighing the advantages and disadvantages and governing bodies. The parallel organization for the
of such a change. The evolution of disabled sports has disabled is the International Paralympic Committee (IPC).
been rapid and appears to be gaining momentum. The The IPC’s primary responsibility is to sanction disabled
organizational structure presented in this text will change sporting events and act as a coordinating committee among
to some degree in the future, as will some of the organiza- the host city of the Paralympic Games and the six interna-
tions’ names, but the basic format will probably remain tional DSOs (IDSOs), which are the Comite International
the same. des Sports des Soudes, Cerebral Palsy International Sports
The International Olympic Committee (IOC) presides and Recreational Association, International Blind Sport
over all international Olympic-sanctioned sporting events Association, International Stoke-Mandeville Wheelchair
The Athlete with Disability • CHAPTER 28 683
Sports Federation, International Sports Organization for the Cerebral Palsy Athletic Association, United States Associa-
Disabled, and International Sport Federation for Persons tion for Blind Athletes, Wheelchair Sports USA (WSUSA),
with Mental Handicaps. Representation to the IDSOs is and Disabled Sports USA. The United States Les Autres
granted to DSOs from all countries that meet the criteria for Sports Association is currently not recognized by the USOC,
membership. The IDSOs process information from partici- but the organization contributes significantly to the disabled
pating countries and communicate directly to the IPC or the sports movement. Each of the US DSOs has representation
hosting Paralympic Games city. Policy and international to its respective international DSO as a voting member.
rules for competition are governed by the IDSOs (Figure
28-1). The IOC works with member countries, which are
represented by their individual national organizing commit-
Classification of Athletes with Disabilities
tees (NOCs) and international sports federations. The Classification systems have existed almost as long as sports
United States Olympic Committee (USOC) is the NOC for for persons with disabilities. The systems are intended to
the United States and is the coordinating body for amateur provide a means to ensure equitable competition, in which
sports, with the primary purpose of preparing Olympic and ability and skills, not degree of physical disability, are the
Pan American Games teams. The five membership categories variables among competitors. Accordingly, athletes of similar
within the USOC are group A, Olympic/Pan American levels of disability are grouped together in a “class” desig-
sports organizations, which includes the 42 NGBs for nated for competition. Individuals in the same class compete
each sport; group B, community-based multisport organiza- against each other in individual sports, such as track and field
tions, armed forces, and education-based multisport organi- or swimming. In team sports, athletes in various classes are
zations; group C, affiliated sport organizations; group D, allowed to compete as a team only in prescribed combina-
state Olympic organizations; and group E, organizations of tions, which serve to ensure that the most severely disabled
sport for the disabled (Figure 28-2). players will not be excluded from the sport.
The Committee on Sports for the Disabled currently
recognizes six DSOs: American Athletic Association for the
Deaf, Dwarf Athletic Association of America, United States Classification Systems
Classification systems in disabled sports provide equitable competition
when ability and skills are the variables for competition.
Figure 28-2
Organizational chart for the National Organization Committees. The United States Olympic Committee
coordinates the five organizations identified and reports to the International Olympic Committee.
For some of these reasons, athletes within a DSO were direct relationship. In 2009, the International Paralympic
prevented from competing against athletes from other DSOs, Committee issued a position statement mandating the devel-
as each DSO developed separate meets for its national cham- opment of evidence-based classification systems related to
pionships. At the world championship events, at which mul- health and functioning as advocated by the International
tiple DSOs represented various countries, amputees compet- Classification of Functioning, Disability and Health (ICF),
ing in wheelchairs had a different competition from paraplegics and the use of selective sport classification.6 To describe each
in wheelchairs for each distance of a track meet. In the 1988 classification system currently used goes beyond the scope of
Seoul Paralympics, this division by classification and by dis- this chapter. Table 28-2 summarizes the various systems used
ability group resulted in more than 40 different 100-meter in some competitive sports.
races being run. This was confusing and nonproductive for Rehabilitation professionals and physicians have tradition-
meet organizers, athletes, and spectators. ally been involved as classifiers in most DSOs, because tradi-
Dissatisfaction with classification systems has been the tional classification involved physical examination and disabil-
norm, rather than the exception, throughout the history of ity assessment. These traditional observations still play a
sports for the disabled. In the mid-1980s, Horst Strohkendl part in some functional classification systems, but more
developed the first classification system that was based on important now is the observation of athletic performance in
observation of an athlete’s function during actual wheelchair the sport. Thus the role of the classifier in the era of functional
basketball competition rather than the athlete’s neurological classification is to observe performance in sports competition.
level.3 Other sports have followed, in an effort to consolidate Classification is frequently carried out by a team of classifiers,
athletes by classification in their sports rather than by their including medical personnel, sports technical experts, ath-
disabilities. Sport-specific functional classification systems have letes, and coaches. Physical therapists are particularly well
now been developed for track and field, swimming, table ten- suited for this role because of their strengths in the observa-
nis, and shooting.4 For example, between the 1988 and 1992 tion of normal and abnormal movement.
Paralympics, a 10-class function classification system for swim-
ming was implemented. This system combines cerebral palsy,
amputee, and wheelchair athletes who would have competed Clinical Point
in 25 classes in the 1992 Paralympic Games. The 10-class
system is intended to reduce the time and organizational An ability of the classifier to observe movement carefully during
effort required to hold the competition. Despite the benefits functional performance is critical to the classification process.
of simplifying an athletic event, Richter and colleagues5 argue
that this system lacks reliability and validity by integrating
disability groups and applying arbitrary criteria that disadvan-
tage certain disability groups. Classification systems are cur-
Technical Assessment
rently in flux and are expected to evolve further as a result Traditionally, a coach is responsible for the training of an ath-
of the experiences in sport-specific functional classification. lete, and the medical team plays a supportive role, responding
Performance and degree of disability do not always show a to injuries or implementing injury prevention programs.
The Athlete with Disability • CHAPTER 28 685
Table 28-2
Classification Systems for Athletes with Disabilities
Organization Sport Classification System
DAAA, DSUSA, WSUSA, USABA, USABA, Alpine skiing 10 classifications, based on type of ski equipment
USCPAA, USLASA used
DSUSA, WSUSA, USLASA Basketball (wheelchair) 3-class US system based on neurological function;
4-class international system based on functional
trunk movement in wheelchair; combined
classification points of players on court limited
by rules
DSUSA Cycling 3-class system, based on limb involvement
DAAA, DSUSA, WSUSA, USABA, USLASA Powerlifting Competition by weight classes
DAAA, DSUSA, WSUSA, USLASA Swimming 10-class integrated system, with different
classification for breast-stroke, backstroke, and
freestyle
DSUSA, USLASA Table tennis (standing) 5-class system for standing athletes
DSUSA, WSUSA, USLASA Table tennis 5 seated classes based on upper extremity and trunk
(wheelchair) function
DSUSA Track and field 9-class system based on upper- vs. lower-extremity
(amputees, standing)* involvement and level of amputation
DSUSA, WSUSA, USLASA Track and field (wheel- 4 classes for track events; 7 seated classes for field
chair) events; 1 standing class for field events
DSUSA, USLASA Volleyball (sitting) All players must sit
DSUSA Volleyball (standing) 8-class system; uses combined classification points
of players on court
AAAD All sports for AAAD Must have hearing loss greater than 55 db in best
ear
DAAA All sports for DAAA Eligibility based on height less than 50
USABA All sports for USABA† 3-class system, based on visual field and acuity
USCPAA All sports for 8-class system, based on level of function of
USCPAA‡ extremities and ambulatory status
USLASA All sports for 6-class system, based on extremity and trunk
USLASA§ function in sitting and standing competition
SOI All Participants compete in classes by age, gender, and
ability level
AAAD, American Athletic Association of the Deaf; DAAA, Dwarf Athletic Association of America; DSUSA, Disabled Sports USA (amputees);
SOI, Special Olympics International (developmentally disabled); USABA, United States Association of Blind Athletes; USCPAA, United States
Cerebral Palsy Athletic Association; USLASA, United States Les Autres Sports Association (other disabilities); WSUSA, Wheelchair Sports USA.
*
Bilateral above-knee amputees can compete in a wheelchair or standing.
†
In cycling, athletes ride tandem.
‡
In international swimming competition, an integrated system is used.
§
Most athletes compete under specific functional classifications for wheelchair or ambulatory athletes.
Two approaches to the analysis of biomechanical events process can be either complex or general. In many cases, an
may be employed to study human movement. The first is educated coach can visually observe the majority of biome-
the quantitative approach, which applies numerical values to chanical constraints that may hinder an athlete’s perfor-
describe all movements. This method is the most explicit, mance. Often an in-depth quantitative analysis only confirms
but it is complex, expensive, time consuming, and, for the what the coach has observed. The following is a brief outline
average athlete, unnecessary. In contrast, the qualitative ap- suggesting the major topic areas that should be considered
proach describes movement in non-numerical terms using when performing a movement analysis:
observation, qualitative data, and applied physical principles
as the foundation for interpretations made by the observer. The Physiological Laws That Relate
Qualitative analysis is more easily employed than quantita- to the Neuromuscular and Musculoskeletal Systems
tive analysis. Qualitative analysis can be performed simply The athlete’s body size and weight, strength, range of
by general observation, memory of a performance, or use of motion, muscular tone, limb length, sensation, balance,
videotape. Obviously, videotaped recordings provide a more coordination, agility, vision, hearing, endurance, and other
accurate account of the movement being analyzed and can physiological considerations that may be inherent to the
be reviewed to verify the impressions of the observer.7 type of disability or to the athlete’s current physical condi-
The disability of the athlete adds another factor to the tion must be analyzed. For example, athletes with quadri-
equation when attempting to enhance athletic performance plegia or paraplegia are able to maximize their performance
and prevent injury. Each athlete presents with some form of using different wheelchair strokes and trunk position as a
biomechanical restriction: either a physical limitation, such as result of the level of disability and the motor function avail-
increased tone, weakened muscles, loss of range of motion, able. Likewise, many swimmers with various disabilities find
or vision loss, or the need for an additional mechanical device the backstroke to be faster for them than the crawl stroke
such as a wheelchair or prosthesis. A systematic assessment of and therefore choose the backstroke when competing in
each component of the athlete’s sport must be made, as with freestyle events.
able-bodied athletes, yet the therapist or coach must now
take into consideration how each component of the skill be- The Mechanical Laws Based on Newton’s Laws
ing learned can be mastered by either physical or mechanical of Motion
compensation. This is the challenge put before all those who The effects of physical laws such as gravity, friction, inertia,
work with disabled athletes, and that is what makes this work and momentum should be examined, especially as they relate
so exciting and gratifying. to any physical compensation by an athlete. Likewise, me-
Regardless of the approach—quantitative, qualitative, or chanical advantages and disadvantages with regard to adaptive
a combination of the two—movement analysis must be devices should be explored to determine the best modification
performed in a systematic manner. The following is provided for a particular athlete participating in a specific sport. Dis-
to give some insight into the performance enhancement abled athletics has been the catalyst for numerous technical
process and the role that the medical professional can play. advances as a result of modifications developed by athletes.
Figure 28-3
A model of the components of sprinting, divided into three phases: start, mid-distance, and finish.
HTAL, Head, trunk, arm, and leg. (From Curtis KA, Gailey RS Jr: The athlete with a disability.
Courtesy of Advanced Rehabilitation Therapy, Inc., Miami, FL.)
Therefore, if a cerebral palsy athlete has increased tone in the introduced in recent years. Despite these achievements, there
throwing arm (or anywhere throughout the body), one if is still considerable room for improvement in this area.
not all of the throwing phases may be affected to some
degree. As a result, alternative solutions that promote mo-
tion away from the limitations may enhance a throwing Identify Performance-Enhancement Methods
performance. Throwing the implement backward over the Finally, after each of the component skills has been identi-
shoulder or sideways over the head may help increase the arc fied and the athlete’s current level of performance has been
of motion during the acceleration or deceleration phase. evaluated, a program designed to improve the performance
must be outlined. For a disabled athlete, training, equip-
The Mechanical Efficiency of Adaptive Equipment ment, and motivation are paramount when designing a
Once all the aspects of movement analysis have been com- strategy to prepare for competition. Performance enhance-
pleted, the evaluation team must ask how an adaptive device ment in itself is a major topic of discussion. The following
can provide a mechanical advantage to overcome a given limi- is a brief overview of some considerations for planning a
tation. Historically, the majority of innovative adaptive devices training program for a disabled athlete:
for disabled athletics have arisen through the efforts of dis-
abled athletes themselves. One of the most significant advances Training Methods
in recent years has benefited lower-extremity amputees. Pros- Today there are as many different training programs for
thetic designs have been developed to maximize athletic per- athletes as there are successful athletes who would like to
formance rather than just to facilitate walking. Contemporary share their secret to success. Many of these training meth-
socket designs take muscular efficiency into account, prosthetic ods are sound and well worth taking under advisement.
knees meet the superior cadence demands placed on them, and Coaches and medical professionals must consider the nature
newer foot materials and configurations optimize athletic of the athlete’s disability and what, if any, limitations must
performance. The same can be said about wheelchairs, or- be placed on the athlete to prevent injury or unnecessary
thotic devices, and other adaptive innovations that have been medical complications. Although few disabled athletes have
688 SECTION IV • Special Populations and Epidemiology
activity restrictions, there are many athletes who will benefit selecting a strengthening, endurance, agility, speed, or any
from preventive measures when participating in sports or other type of program. Often a brief biomechanical analysis
training as outlined in Table 28-3. must be performed when creating a training program. If the
Once any precautions are identified, the disabled athlete athlete cannot use a traditional weight-training apparatus
must begin a physical training program comparable to that of because of physical limitations, such as an inability to use
any able-bodied athlete. Similar training principles apply when the hands to grip, alternative methods, such as securing the
Table 28-3
Injuries and Disability-Specific Medical Conditions of Athletes with Disabilities
Problem Prevention Treatment
Chronic overuse syndromes Taping, splinting, protective padding, Rest; apply injury-specific principles of
(shoulder impingement, proper wheelchair positioning, good care; selective strengthening, muscle
tendonitis, bursitis, carpal technique balancing, flexibility; analysis of
tunnel syndrome) technique
Overexertion (muscle strains) Warm-up and stretching; proper Rest; gradual progression of exercise
conditioning and equipment program
Falls, physical contact (sprains, Equipment safety; appropriate padding Apply injury-specific principles of care;
contusions) for sport; appropriate sport-specific check for signs of fracture in athletes
spotting; qualified assistance/guides for without movement or sensation
athletes
Blisters Encourage callus formation; protective Apply injury-specific principles of care; be
taping, gloves, padding, cushioning; aware of areas that lack sensation; make
adequate clothing prosthetic adjustments
Abrasions/lacerations Check equipment for sharp or abrasive Apply injury-specific principles of care; be
surfaces; wear protective clothing; use aware of areas that lack sensation
cushions or towels in all transfers; use
mats on hard surfaces; camber
wheelchair wheels
Decubitus ulcers and burns Adequate cushioning; proper weight Bed rest if necessary to remove all pres-
shifting; dry clothing; special precautions sure from a weight-bearing surface;
for areas without sensation; skin open wound care as necessary; check
inspection; good nutrition and hygiene equipment
Hyperthermia Minimize exposure to direct sun; provide Remove from ambient conditions; cool
shade; wear adequate clothing for immediately; seek medical assistance
insulation and maintain hydration; spray
externally with water; avoid hot and
humid conditions
Hypothermia Minimize exposure; wear adequate Cover and seek medical assistance
clothing, keeping head covered;
maintain hydration; avoid exposure to
cold and wet conditions
Autonomic dysreflexia Encourage regular bowel and bladder Lift to sitting position; search for source
habits in competitive situations of stimulus, usually full bladder or bowel;
attempt to relieve condition; this is a
medical emergency
Orthostatic hypotension Wear elastic stockings or corset supports; Recline in wheelchair or on ground/bed;
avoid heat encourage deep breathing
Seizures Avoid stress, dehydration, extremes of Protect head and keep airway open by jaw
temperatures, and fatigue thrust; avoid putting objects in the
mouth
Unexplained fever (often Drink fluids; practice good hygiene for Seek medical treatment
urinary tract infections) self-catheterization
Allergies (bee sting, drug) Notify medical personnel at competition Seek medical treatment
site of potential problem; be prepared
Eye injuries Protective eyewear, goggles, safety glasses Apply injury-specific principles of care
The Athlete with Disability • CHAPTER 28 689
hand to the handle, may have to be employed. If environmen- system. However, there is considerable evidence in the lit-
tal conditions such as poor weather prohibit a wheelchair erature to support the premise that sports involvement
athlete from performing the necessary road work for cardio- among adults with disabilities promotes improved self-
vascular endurance, a roller trainer may be used. In short, the concepts and psychological well-being.10
problem-solving process must continue with training as
it does with competition, placing as few limitations on the
athlete as possible.
Clinical Point
It is very important to assess the individual athlete’s goals and pre-
Considerations for Planning a Training Program injury performance level and design realistic programs accordingly
for Disabled Athletes whether he or she is an able bodied or disabled athlete.
• Training method
• Equipment enhancement
Motivation
The motivation of a disabled athlete is no different from the Clinical Point
motivation of an able-bodied athlete. As with all athletes,
the intrinsic desires that compel an individual to succeed Injured disabled athletes should be seen as athletes with injuries who
may vary, but the positive methods of motivation available also happen to have permanent disabilities rather than disabled
to coaches remain the same. A discussion of the various persons with injuries.
motivational techniques that may be employed is beyond
the scope of this chapter. Supportive personnel must
develop a working relationship, and each must learn how to
maintain the quest to strive for mutual goals and continued Some athletes with disabilities self-treat serious injuries
success. It is important to keep in mind that success is not rather than seeking medical assistance.11,12 This may result
always defined by winning. in reinjury and the progression to chronic disability. Their
training programs may also lack sufficient attention to
flexibility and conditioning.13 The sports rehabilitation
Psychosocial Considerations team’s ability to intervene and prevent chronic soft tissue
Sports involvement has been reported to have positive changes, which increase further risk of injury, is of critical
effects on the physical conditioning and self-image of adults importance.
with disabilities.8 In fact, elite wheelchair athletes have psy- The active socialization and actual physical activity
chological profiles that are similar to those of elite able- involved with sports participation may provide benefits for
bodied athletes.9 An athlete with a disability is likely to an individual with a disability. Active individuals with dis-
present similar challenges to medical professionals as an abilities have been reported to have fewer problems with
able-bodied athlete, with a few exceptions. body image, a higher degree of physical function, and fewer
Depending on the age at the onset of the disability and medical complications than members of the inactive
the time since its onset, an athlete with a disability may still disabled population.8,14,15
be actively engaged in the various stages of the coping pro- It is also important to look at the skills developed
cess, such as denial, anger, or depression. Frustrations en- through athletic participation. Athletics is an acceptable
countered in athletic competition or following an athletic way to reintegrate with the community. Through athletic
injury may compound already existing feelings of loss or participation, there is a de-emphasis on the disability and
anger. An individual’s ability to cope with outside stresses a focus on goal-oriented objectives and resources. Ath-
may vary widely, depending on the nature of the disability letic participation encourages the development of net-
and the person’s internal resources and social support working skills and interpersonal relationships that may be
690 SECTION IV • Special Populations and Epidemiology
useful in work settings as well. An individual who partici- professionals should not address a companion or coach
pates in athletics becomes less dependent on society instead of the athlete.
and makes more contributions to society. Athletes are
motivated to raise funds for equipment and travel and
are responsible for themselves during travel. This disci- Common Injuries and Disability-Specific
pline often carries over to educational and employment Medical Problems of Athletes
endeavors.16
Like their able-bodied counterparts, some individuals
with Disabilities
with disabilities who participate in sports have substance Preventive practices for disabled athletes are becoming a
abuse problems with alcohol or drugs. Many athletes with growing concern among coaches and medical staff alike.
spinal cord injuries were initially injured in an alcohol- or Coaches and athletes must be educated in proper warmup
drug-related incident.17 Sports medicine professionals who techniques, including stretching, elevating core body tem-
work with athletes with disabilities need to be aware of the perature, and sport-specific drills. Moreover, all athletes
signs and symptoms of substance abuse and know the should be required to wear or use the recommended safety
appropriate referrals to make. gear for every sport. Coaches and event organizers should
Another segment of the population of athletes with dis- also be obligated to provide certified or skilled spotters,
abilities has various cognitive and sensory disorders. Ath- sighted guides, or assistive personnel to ensure every
letes who have sustained brain injuries sometimes exhibit athlete’s safety during competition.
behavior that is difficult to understand. Any athlete who The health professional providing care to athletes with
becomes combative, abusive, or a danger to himself or her- disabilities needs to be aware of common injuries and con-
self or to other athletes should be removed to an area where ditions that are inherent to certain disability groups. Table
he or she can refocus and calm down, away from any over- 28-3 provides information concerning prevention and treat-
stimulation that might add to the problem. Athletes who ment of common injuries and medical problems of athletes
are unable to communicate verbally may use sign language with disabilities. Table 28-4 presents the type and frequency
or communication boards. Although not all athletes of commonly reported injuries sustained by wheelchair
with disabilities are able to understand instructions, health athletes.
Table 28-4
Common Injuries of Wheelchair Athletes
128 Adult Athletes, 90 Adult Athletes,
All Sports11 (% of All Sports18 (% of 69 Pediatric Track 19 Elite Adult
291 Reported 346 Reported Athletes29 (% of Athletes12 (% of 50
Injuries) Injuries) Athletes Reporting) Reported Injuries)
hand; they can crack and result in painful fissures, open to unnoticed because of the lack of sensation that would nor-
infection. mally accompany a bony fracture. Therefore, following any
Hands should be cleaned frequently and calluses filed injury, one must be aware of signs and symptoms such as
with a pumice stone. Open cracks or fissures, blisters, and abnormal body position, bruising, edema, or grinding sen-
other abrasions should be managed with antibiotic creams sations with movement. The athlete should be evaluated by
and covered with bandages or dressings, as appropriate. x-ray examination to rule out a fracture, as movement
Wheelchair athletes often develop symptoms of carpal tun- of bony fragments may interfere with healing and cause
nel syndrome from the repetitive trauma of wheelchair further damage to muscles and blood vessels.
propulsion, causing compression in the carpal tunnel By using such simple preventive techniques, athletes
area.11,30 Gloves are recommended for training and compe- who compete in wheelchairs can have safe and productive
tition, but recent evidence questions their efficacy in competitive careers.
preventing carpal tunnel syndrome.30 Any athlete with
symptoms of hand tingling or numbness should be referred
for evaluation for carpal tunnel syndrome. Injuries of Athletes Who Compete Standing
Leather batting gloves or handball gloves are most easily Athletes with disabilities who compete while standing rep-
adapted and reinforced for wheelchair pushing, with layers resent a variety of physical disabilities and sports interests.
of tape applied to the areas of highest pressure. Custom- They often compete with disabilities such as upper and
designed leather mitts with reinforced neoprene use hook- lower extremity amputations, visual deficits, and cerebral
and-loop fasteners to keep the hand in a closed position, palsy. These athletes do not appear to be at greater risk for
creating a fist, and are widely used in road racing. This the common musculoskeletal problems associated with
innovative glove design incorporates high-friction materials sports participation in the general population.13 Although
and maximizes the force generated during contact with the musculoskeletal problems may be no more frequent for
push rim. Because of the enhanced power available to the athletes with disabilities, disability-related problems are seen
athlete, stroke dynamics have changed, and wrist and elbow among athletes who wear prostheses for running and ath-
injuries may decrease in frequency. letes who sustain falls and other accidental injuries second-
ary to their disabilities or the use of assistive devices.
Lack of Protective Sensation
Spinal cord injury, multiple sclerosis, and other neurological Abrasions and Blisters to Bony Prominences
disorders interfere with the normal protection that pressure, Within Prosthetic Socket
temperature, and pain sensation provide. Pressure points, Many lower-extremity amputees run wearing prostheses.
especially under sitting areas, may lead to skin breakdown, Common problems are skin breakdown, bruising, abrasion,
ulceration, and infection. Insensitive skin must be inspected blistering, skin rashes, and swelling on the residual limb,
frequently. within the prosthetic socket, after or during exercise. These
Any time there is persistent redness of the skin, that area problems can sometimes be prevented by proper adjust-
should have all pressure from sitting, clothes, or equipment ment of prosthetic fit and alignment and prompt manage-
relieved until the redness resolves and normal skin color ment of developing skin lesions.
returns. Otherwise, these areas may go on to ulcerate and Common sites for these problems in below-knee ampu-
may progress to serious infections. Athletes with open pres- tees are the fibula head, distal anterior end of the tibia,
sure sores should not participate in competition. Training distal end of the fibula, medial and lateral femoral condyles,
should cease, and the athlete should avoid sitting or any over the patella, and over scar tissue and poorly healed skin.
position that may place him or her at risk for additional Above-knee amputees may experience similar problems
pressure damage, until the area is completely healed. over the pubic or ischial rami, over the ischial tuberosities,
Athletes with chronic pressure sore problems may need at the distal lateral femur, over the greater trochanter, or
customized seating systems that alleviate areas of pressure. over sites of scar tissue or poor healing.
Wheelchair cushions can be modified to accommodate an Depending on the nature of the injury or trauma sus-
athlete’s individual needs. If an athlete has chronic prob- tained, it may be appropriate to use a number of different
lems caused by positioning in the sports wheelchair, he management strategies. For bruising and blisters, the athlete
or she should be referred to a physical or occupational can relieve friction by wearing additional (dry) stump socks
therapist for evaluation and recommendations for possible or foam pads, or by applying abrasion protection products
adaptations. (e.g., Second Skin, Bioclusive, DuoDerm, Tegaderm, Ampu-
Fractures account for less than 5% of all injuries sustained Balm) over soft tissue areas that commonly break down as
by wheelchair athletes.11 However, osteoporosis is fre- a result of continual friction. Unfortunately, in most cases
quently associated with lower-extremity paralysis. As a the application of foam or leather padding may cause total-
result, athletes may be susceptible to lower-extremity frac- contact suction sockets to lose suction, and pistoning may
tures from relatively minor injuries. These fractures may go result.
The Athlete with Disability • CHAPTER 28 693
Ideally, the pads are used prophylactically prior to the running defensively when there are cars or bicycles present,
event. However, often they are applied after a blister has carrying identification that includes pertinent medical infor-
formed to permit continued participation. Use of these mation, and dressing appropriately for a workout will help
protective pads must be monitored regularly, especially dur- improve safety margins.
ing long-distance events, because once the inner silicone gel It is strongly recommended that athletes with disabilities
dries out, the outer covering material can become a source train with other athletes or groups who can provide com-
of irritation. panionship, support, and an extra measure of safety. Volun-
It may be appropriate to use rest, ice, and compression teers who run with blind athletes especially must be able to
and to decrease additional trauma to the limb through sup- concentrate on obstacles and sudden environmental changes,
ported ambulation with crutches or a cane. as well as individual athletic needs and performance.
Falls
Accidental falls are likely to occur in runners with disabili-
ties, as a result of uneven ground surfaces and environmen-
tal conditions. Falling is the most common cause of hand
abrasions. Ambulatory athletes with disabilities may use
special equipment such as prostheses, crutches, and canes,
which are subject to fatigue and sudden breakdown, espe-
cially in the face of the uncommon stress associated with
athletics. Blind runners present an obvious problem in that
they lack the visual acuity to detect environmental hazards
in their path. Sighted guides are critical to their optimal and
safe performance.
Some athletes with disabilities wear bicycle helmets when
running to provide an extra measure of safety, if they have
problems with footing or balance. Athletes who use assistive
devices such as crutches or canes should check for cracks or
fissures in metal shafts or rubber tips prior to use.
All athletes with disabilities should take the same precau-
tions recommended to athletes in the general population to Figure 28-5
help prevent accidents. Wearing reflective clothing at night, Above-knee amputee sprinter.
694 SECTION IV • Special Populations and Epidemiology
Clinical Point
Clinical Caution Thermal injuries and temperature regulation are common problems
For disabled athletes with neurological lesions above T4, diminished in all athletes with disabilities.
sympathetic response limits heart rate and blood pressure use as
effective indications of exercise intensity.
Equipment and surfaces such as asphalt or metal may
heat up in the sun and cause burns to a person without
sensation. Similarly, individuals with paralyzed limbs often
It is also important to note that an athlete with a dis- have impaired circulation, with a tendency to develop swell-
ability is often unable to rest an injury completely because ing of their feet, because their muscles do not assist in ve-
of the demands for continued daily function. For exam- nous return. There is also a relatively lower blood flow to
ple, a wheelchair athlete who sustains a shoulder injury is the skin and deep tissues. This makes the limb more suscep-
unable to rest because demands of everyday mobility tible to sunburn or frostbite, and even lesser degrees of heat
require the use of the shoulder joint. An amputee who or cold may cause serious deep tissue damage.
injures the sound limb will have increased difficulty with In addition, in spinal cord injury and in multiple sclero-
ambulation if the prosthetic limb becomes the dominant sis, there are problems with regulation of core body tem-
limb. To regain the ability to perform everyday tasks, the perature caused by a loss of normal blood flow regulation
temptation to increase the use of the injured extremity via the central nervous system. Athletes with quadriplegia
prematurely may increase recovery time and the risk of often report heat and cold intolerance.11 This is com-
injury. Alternatives to daily activities, rehabilitation, and pounded by an inability to sweat below the level of a spinal
training methods designed to reduce the risk of insult to cord injury. Many medications used for pain, depression,
the injured limb should be explored by the physical allergy, bladder dysfunction, high blood pressure, and other
therapist and athlete. problems also interfere with normal sweating.
696 SECTION IV • Special Populations and Epidemiology
antibiotics. Athletes should refrain from competition and Autonomic dysreflexia is a medical emergency. The
training for at least 8 hours after the initiation of antibiotic individual should assume or remain in a sitting position if
treatment and should be without a fever for at least possible to minimize blood pressure changes. The bladder
24 hours before resuming participation. should be emptied and the bowel evacuated; the condi-
To prevent recurrent bladder infection, athletes should tion should then be re-evaluated. Immediate medical
ensure adequate fluid intake to flush the bladder regularly. intervention should follow if the hypertension has not
They must also have access to clean areas to allow good resolved.
technique to avoid contamination during the handling and Recent studies have revealed that many elite wheelchair
use of catheters and connecting tubing and bags. athletes with quadriplegia routinely self-induce autonomic
If catheter tubing becomes blocked, the athlete may dysreflexia to increase sympathetic outflow and improve
develop a bladder obstruction and be unable to urinate. performance during competition.52,53 With autonomic dys-
Bladder obstruction can obstruct blood flow back to the reflexia, the athlete experiences uncontrollably high hyper-
heart by pressure on the inferior vena cava, or cause abnor- tension, which may lead to cerebral hemorrhage and death.
mally high blood pressure by stimulation of reflex activity. “Boosting” via clamping a catheter or inducing a painful
If bladder obstruction precipitates autonomic dysreflexia, stimulus is a dangerous and foolhardy practice and should
blood pressure can rise dangerously high and even cause a be discouraged among all athletes.
cerebral hemorrhage. Also, rapid relief of an obstruction
may cause a precipitous drop in blood pressure and result in
shock damage to the heart or kidneys. Exercise may exacer- Blood Flow
bate these problems. Some muscle and joint diseases have associated problems
with spasm of the arteries of the hands and feet that may be
induced by cold. Edema or swelling in paralyzed limbs may
Hypotension be increased by generalized increased blood flow with exer-
Wheelchair athletes with multiple sclerosis and spinal cord cise or prolonged sitting with straps around the legs or
injury may experience hypotension with rapid position trunk. If blood flow is obstructed, there may be problems
changes, caused by the inability of the sympathetic nervous with venous return and development of thrombophlebitis.
system to accommodate for a rapidly shifting blood volume. Persistent swelling in a leg that does not get better with
Infections from pressure sores may also cause pressure drop. elevation may indicate thrombophlebitis, although symp-
Pain, antispasticity, antiseizure, and bladder and bowel toms usually occur without warning. Fragments of the
medications may all affect blood pressure regulation. This thrombus may break off, resulting in pulmonary embolus,
may cause problems in endurance activities and even lead to often a life-threatening complication.
lightheadedness or fainting. Edema should resolve with elevation of the extremities.
If an athlete in a wheelchair experiences lightheadedness Redness or heat in the area can signify a serious problem.
caused by hypotension, the individual should be helped into Edema of the lower extremities should be treated by re-
a recumbent position or the wheelchair should be tipped moving obstructive straps and reclining and elevating the
back. These maneuvers will help increase venous return. limbs above the heart. Individuals with persistent edema
Gentle pressure on the abdomen with deep breathing may with signs of inflammation should be properly evaluated
also be helpful. If problems with lightheadedness continue, for infectious processes or thrombophlebitis and treated
the athlete should be referred to a physician for evaluation appropriately.
of the problem.
Dysphagia
Hypertension Athletes with cerebral palsy sometimes present with dyspha-
Autonomic dysreflexia is a serious problem of spinal gia or difficulty swallowing. An athlete with dysphagia may
cord–injured athletes whose lesions are above the midtho- drool saliva from the mouth, which can cause a great deal
racic level. This reflexive process, causing massive sympa- of fluid loss. In addition, an athlete who has difficulty swal-
thetic outflow, often begins from an obstruction of bowel lowing may choke on water or soft drinks.
or bladder. Because an athlete with dysphagia is at risk for losing
fluids by drooling, coaches and supportive personnel should
ensure that the athlete has access to fluids that are easy to
Clinical Caution swallow and that straws are available. Generally, athletes
with dysphagia are able to swallow frequent small amounts
Any spinal cord–injured athlete with sudden hypertension or pounding of thicker liquids, such as juices, more easily than water.
headache should be suspected of having autonomic dysreflexia. Because dehydration may be a problem, avoiding exposure
to the sun is also important.
The Athlete with Disability • CHAPTER 28 699
be substituted. Athletes with disabilities must be especially essential to drink bottled water and to be cautious about
careful, because even traces of prescription medications such food choices. Food from street vendors in any country
as sympathomimetics, antihypertensives, diuretics, cortico- should be avoided. Ice made from contaminated water is
steroids, or pain medications routinely prescribed in the often overlooked and may cause serious gastrointestinal
management of their chronic medical conditions may problems when added to bottled water.
result in a positive drug test. It is critical that alternative non- Athlete nutrition may suffer from changes in diet. With
banned medications be prescribed well in advance of the decreased protein intake, immune system function may be
competition, as some banned medications can be detected in compromised.54 It is a good idea to advise athletes to bring
the urine as long as several months after the last dose was a supply of high-protein food sources from home for emer-
taken. It is also important to remember that all over-the- gencies and for supplementation of the local diet. Choices
counter medications and prescription medications that the such as nuts, trail mix, peanut butter, cans of tuna fish, and
medical team brings should meet the USOC or SMSCC small packages of cereal may provide protein to supplement
guidelines as well. the diet at the competition site.
14. Curtis KA, McClanahan S, Hall KM, et al: Health, vocational, and 34. Pagliarulo MA, Waters R, Hislop HJ: Energy cost of walking of
functional status in spinal cord injured athletes and nonathletes, below-knee amputees having no vascular disease, Phys Ther
Arch Phys Med Rehabil 67:862–865, 1986. 59:538–542, 1979.
15. Stotts KM: Health maintenance: Paraplegic athletes and nonath- 35. Torburn L, Perry J, Ayyappa E, Shanfield SL: Below-knee amputee
letes, Arch Phys Med Rehabil 67:109–114, 1986. gait with dynamic elastic response prosthetic feet: A pilot study,
16. Shephard RJ: Benefits of sport and physical activity for the J Rehabil Res Dev 27:369–384, 1990.
disabled: Implications for the individual and for society, Scand J 36. Waters RL, Perry J, Antonelli EE, et al: Energy cost of walking of
Rehabil Med 23:51–59, 1991. amputees: The influence of level of amputation, J Bone Joint Surg
17. Sweeney FF, Foote JE: Treatment of drug and alcohol abuse in Am 58:42–46, 1976.
spinal cord injured veterans, Int J Addict 17:897–904, 1982. 37. Waters RL, Yakura JS: The energy expenditure of normal and
18. McCormack DAR, Reid DC, Steadward RD, Syrotuik DG: Injury pathological gait, Crit Rev Phys Med 1:183, 1989.
profiles in wheelchair athletes: Results of a retrospective survey, 38. Fisher SV, Gullickson G: Energy cost of ambulation in health and
Clin J Sport Med 1:35–40, 1991. disability: A literature review, Arch Phys Med Rehabil 59:121–132,
19. Aljure J, Eltorai I, Bradley WE, et al: Carpal tunnel syndrome in 1978.
paraplegic patients, Paraplegia 23:182–186, 1985. 39. Huang CT, Jackson JR, Moore NB, et al: Amputation: Energy
20. Gellman H, Sie I, Waters RL: Late complications of the weight- cost of ambulation, Arch Phys Med Rehabil 60:18–24, 1979.
bearing upper extremity in the paraplegic patient, Clin Orthop Rel 40. James U: Oxygen uptake and heart rate during prosthetic walking
Res 233:132–135, 1988. in healthy male unilateral above-knee amputees, Scand J Rehabil
21. Burnham R, Newell E, Steadward R: Sports medicine for the Med 5:71–80, 1973.
physically disabled: The Canadian team experience at the 1988 41. Traugh GH, Corcoran PJ, Rudolpho LR: Energy expenditure of
Seoul Paralympic Games, Clin J Sport Med 1:193–196, 1991. ambulation in patients with above-knee amputations, Arch Phys
22. Sie I, Waters RL, Adkins RH, Gellman H: Upper extremity pain Med Rehabil 56:67–71, 1975.
in the post rehabilitation spinal cord injured patient, Arch Phys 42. Flandry E, Beskin J, Chambers R, et al: The effects of the
Med Rehabil 73:44–48, 1992. CAT-CAM above-knee prosthesis on functional rehabilitation,
23. Burnham RS, Steadward RD: Upper extremity peripheral nerve Clin Orthop 239:249–262, 1989.
entrapments among wheelchair athletes: Prevalence, location and 43. Gailey RS, Lawrence D, Burditt C, et al: The CAT-CAM socket
risk factors, Arch Phys Med Rehabil 75:519–524, 1994. and quadrilateral socket: A comparison of energy cost during
24. Bayley JC, Cochran TP, Sledge CB: The weightbearing shoulder- ambulation, Prosthet Orthot Int 17:95–100, 1993.
impingement syndrome in paraplegics, J Bone Joint Surg Am 44. DiAngelo DJ, Winter DA, Dhanjoo N, Newcombe WR: Perfor-
69:676–678, 1987. mance assessment of the Terry Fox jogging prosthesis for above-
25. Burnham RS, May L, Nelson E, Steadward R: Shoulder pain in knee amputees, J Biomech 22:543–558, 1989.
wheelchair athletes—The role of muscle imbalance, Am J Sports 45. Enoka RM, Miller DI, Burgess EM: Below-knee amputee running
Med 21:238–242, 1993. gait, Am J Phys Med 61:68–84, 1982.
26. Robinson MD, Hussey RW, Ha CY: Surgical decompression of 46. Winter DA, Sienko SE: Biomechanics of below-knee amputee gait,
impingement syndrome in the weight-bearing shoulder, Arch Phys J Biomech 21:361–367, 1988.
Med Rehabil 74:324–332, 1993. 47. Smith AW: A biomechanical analysis of amputee athlete gait, Int J
27. Neer CS: Anterior acromioplasty for the chronic impingement Sports Biomech 6:262–282, 1990.
syndrome in the shoulder, J Bone Joint Surg Am 54:41–50, 48. Czerniecki JM, Gitter A, Munro C: Joint moment and muscle
1972. power output characteristics of below knee amputees during run-
28. Barber DB, Gall NG: Osteonecrosis: An overuse injury of the ning: The influence of energy storing prosthetic feet, J Biomech
shoulder in paraplegia: Case report, Paraplegia 29:423–426, 24:63–75, 1991.
1991. 49. Corcoran PJ: Sports medicine and the physiology of wheelchair
29. Wilson PE, Washington RL: Pediatric wheelchair athletics: Sports marathon racing, Orthop Clin North Am 11:697–716, 1980.
injuries and prevention, Paraplegia 31:330–337, 1993. 50. Arnheim DD: Modern principles of athletic training, ed 6,
30. Burnham RS, Chan M, Hazlett C, et al: Acute median nerve dys- St Louis, 1985, Times Mirror/Mosby College Publishing.
function from wheelchair propulsion: The development of a 51. Roy S, Irvin R: Sports medicine: Prevention, evaluation,
model and study of the effect of hand protection, Arch Phys Med management and rehabilitation, Englewood Cliffs, NJ, 1983,
Rehabil 75:513–518, 1994. Prentice-Hall.
31. Ganguli S, Datta SR, Chatterjee BB: Metabolic cost of walking at 52. Burnham R: Boosting self-induced autonomic dysreflexia in wheel-
different speeds with patellar tendon bearing prosthesis, J Appl chair athletes, Paper presented at Vista ’93 Conference, Jasper,
Physiol 36:440–443, 1974. Alberta, Canada, May 19, 1993.
32. Gonzalez EG, Corcoran PJ, Reyes RL: Energy expenditure in 53. Raymond S: Using dysreflexia to enhance athletic performance: An
below-knee amputees: Correlation with stump length, Arch Phys athlete’s opinion, Paper presented at Vista ’93 Conference, Jasper,
Med Rehabil 55:111–119, 1974. Alberta, Canada, May 19, 1993.
33. Molen NH: Energy/speed relation of below-knee amputees walking 54. Good RA, Lorenz BA: Nutrition, immunity, aging, and cancer,
on motor-driven treadmill, Int Z Angew Physiol 31:173–185, 1973. Nutr Rev 46:62–67, 1988.
29
CHAPTER
704
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 705
Table 29-2
World Masters Outdoor Track and Field World Records at 100 Meters
Age Group Marks Athlete Name Country Age Meet Date
In April, 2010, a team physician consensus statement was allows masters athletes to have a slower increase in body fat
published in Medicine and Science in Sports and Exercise and preserve lean mass to a greater extent than the general
entitled “Selected Issues for the Masters Athlete and the population.
Team Physician: A Consensus Statement” that provides a
guide to the care and treatment of these athletes for selected
conditions.12 Changes in Muscle Structure
and Function in the Masters Athlete
Physiological Effects of Aging The primary function of skeletal muscle is for movement
and generation of force. This function occurs at both the
on the Masters Athlete macroscopic and microscopic level. Muscle fibers are classi-
Progressive loss of muscle strength and endurance resulting fied as type I, type IIa, and type IIb fibers. Type I fibers, also
in a loss of athletic performance and function has tradition- known as “slow-twitch” fibers, are more resistant to fatigue
ally been accepted as a consequence of aging. However, than types IIa or IIb, also known as “fast-twitch” fibers.
several studies have shown that a significant portion of these In comparison with slow-twitch fibers, fast-twitch fibers
losses in function may be musculoskeletal adaptations to fatigue faster and are mainly anaerobic. It is generally
physical inactivity.13-19 These studies have shown that high- accepted that slow-twitch fibers are mainly used for endur-
intensity training in the frail elderly can lead to a significant ance, whereas fast-twitch fibers are used for speed and
increase in their ability to resume activities of daily living power. In regard to hypertrophy (muscle growth), fast-
(ADLs). Masters athletes continue to challenge this concept twitch fibers grow faster and larger than slow-twitch fibers.
of age-related decline and may serve as a model from whom Sarcopenia is of profound importance for the mainte-
a better understanding may be gained of the inevitable nance of posture, locomotion, and the ability to perform
senescent changes that occur. ADLs.24 Arm, leg, and back strength decline at an overall
rate of 8% per decade, starting in the third decade of life. It
is important to note that the rate of decline is not linear, but
Changes in Body Composition is slightly slower early in the decline and accelerates late in
in the Masters Athlete life. Healthy men and women in their seventh and eighth
Body composition comprises body fat and fat free mass, decades of life demonstrate average reductions of 20% to
which includes skin, bone, internal organs, and muscle 40% in maximal isometric strength.24,25 From a functional
mass.20 In our relatively sedentary society, it is typical to perspective, the age-associated reduction of quadriceps
gain approximately 1 pound (0.5 kg) a year between the muscle strength is such that the average 80-year-old is at or
ages of 25 and 65 years. This increase in girth is attributable near the minimum level of strength required to rise from a
to fat mass and generally occurs in the peritoneum, which chair.26,27
puts older adults at greater risk for diabetes and heart dis-
ease. Occurring concomitantly with the expansion of the
waistline, a reduction in lean mass begins in middle age,
primarily of skeletal muscle and bone. Even in men and Clinical Point
women who are rigorously active throughout the course of
a lifetime (e.g., masters athletes), there is a change in body Sarcopenia is the progressive decline of muscle mass, force generation,
composition reflecting the expected increase in fat mass and and quality associated with aging.
the related loss of lean mass.15 A cross-sectional comparison
of sedentary women indicates that percentage body fat is
higher in 50- to 60-year-old women (42.1%) compared
with women in their twenties (27.1%) and seventies (36.7%).
The absolute quantity of body fat of masters athletes is This age-associated decline in muscular force genera-
similar to that of young, active women and lower than that tion also negatively affects the performance capacity of the
of sedentary 50- to 60-year-old women. Cross-sectional masters athlete. The loss in muscle mass and subsequent
data indicate that the percentage of body fat for masters loss of muscle force is the consequence of an actual decline
athletes is relatively constant at approximately 28% between in the number of muscle fibers present and the atrophy of
the ages of 35 and 75.21 In masters athletes, the percentage many of the remaining fibers, particularly among the fast-
of body fat varies by sport. Those participating in long- twitch or type II fibers. This preferential decline in type II
distance track events have a lower percentage body fat fiber area also affects the ability to recruit muscles quickly,
(23.5%) than those participating in short-distance track which makes athletic activities requiring explosive power
events (28.8%).21 For the same age span, masters athletes (e.g., sprinting, jumping) more difficult. Despite these
have a lower rate of decline (7.5%) in lean muscle mass than senescent changes in muscle tissue, masters athletes con-
the general population (25%-30%).21-23 Thus, maintenance tinue to perform at a level much higher than their seden-
of a high level of physical activity throughout the lifespan tary counterparts.
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 707
endurance exercise–trained men and women demonstrate of athletic activity. A result of these age-related tissue
greater “absolute” (1 mL/kg per 1 min) rates of decline changes is a decrease in the passive viscoelastic properties or
in VO2 max with age than healthy sedentary adults.40,42,44,45 “flexibility” of the connective tissue elements.
It is suspected that this is a result of these athletes having Connective tissue tends to increase with age in propor-
greater baseline levels of VO2 max as young adults and a tion to muscle mass, to become less hydrated, and to
proportionally greater loss of exercise with aging com- change its relative composition of collagen and elastin, all of
pared with sedentary adults.44,45 Based on current scien- which contribute to its increased density and rigidity. Aging
tific research, a progressive reduction in VO2 max appears results in a decrease in the amount of insoluble collagen and
to be the primary physiological mechanism associated with total collagen. Both of these have been correlated with
declines in endurance performance in the masters athlete. decreases in the tensile strength of tendons and increases in
the stiffness of tendons.46 The result of this change is an
increase in passive mechanical resistive torque in response
to stretching of the connective tissues in and around an
Age-Related Structural Changes involved joint complex, a condition that contributes to joint
in the Cardiovascular System stiffness resulting in range of motion (ROM) loss. Clini-
cally, flexibility is defined as the ROM around a joint.
Heart Research suggests that flexibility decreases with age
• Myocardium
(approximately 20% to 30% between 30 to 70 years of
• Increased wall thickness
age).46 This may make it harder for the masters athlete to
• Accumulation of lipofuscin
• Increased elastin, fat, and collagen adequately move easily into ranges required for his or her
• Endocardium desired sports activity.
• Thickened areas composed of elastic, collagen, and muscle
fibers
• Fragmentation and disorganization of elastic, collagen, and
muscle fibers Clinical Point
• Conduction system
• Atrophy and fibrosis of left bundle branches Flexibility decreases approximately 20% to 30% between 30 and
• Decreased number of sinoatrial node pacemaker cells 70 years of age.
• Valves
• Thickening and calcification
Vasculature
• Increased size (primarily of proximal vessels) In summary, the sports medicine professional needs
• Increased wall thickness (primarily of distal vessels) to have a basic understanding of the senescent changes
• Increased connective tissue and lipids in subendothelial layer that occur in the injured masters athlete. The challenge to
• Atrophy of elastic fibers in medial layer
the clinician is to determine how these changes may influ-
• Disorganization and degeneration of elastin and collagen
ence clinical decision making. A general understanding of
From Irwin S: Cardiopulmonary physical therapy: A guide to practice, ed 4,
St Louis, 2004, Mosby. the age-related physiological changes that occur in the
masters athlete is necessary for the design and implemen-
tation of effective therapeutic interventions in this special
population.
OA is categorized as either primary or secondary. Primary varsity sports by today’s boys and girls, it is commonplace for
OA has an unknown cause and is thought to lead to joint several athletes each year to have a significant ligament injury
destruction caused by an articular cartilage defect, whereas requiring surgery. Although many of these athletes are able
secondary OA is thought to occur as a result of previous to return to their sports, few clinicians take into consider-
trauma, hemarthrosis, infection, osteonecrosis, or some ation the future risk of OA in these athletes.
other condition.51 The pathological process of OA generally
results in the following characteristics: (1) erosion of hyaline Imaging of Knee Osteoarthritis
articular cartilage covering long bones; (2) sclerosis, or The primary means of evaluation of OA is plain-film radiog-
thickening, of bone under articular cartilage in an attempt raphy. However, a strong correlation between radiographic
at a reparative process, (3) formation of bone spurs or severity and loss of function has not been shown. According
osteophytes (Figure 29-2).28,52 to Moskowitz,62 arthritis is demonstrated in 90% of the
population by the age of 40 when viewing weightbearing
joints such as knees, hips, and ankles. What complicates this
Knee Osteoarthritis picture is that many of these individuals may show evidence
OA of the knee is known to cause more symptoms and dis- of OA on a radiograph, but have absolutely minimal or no
ability than OA affecting any other joint in the body.53,54 symptoms. Often there is a poor correlation between pain
Approximately 80% of those with knee OA will develop a and actual structural damage.63 Some of this disparity may
varus deformity caused by medial joint compartment narrow- be due to the fact that radiographs do not image synovitis
ing, with the remaining patients demonstrating a valgus knee or bone marrow edema.64 Bedson and Croft65 reported
angulation (~5% to 10%) or no angulation (~5% to 10%).55 several other reasons for this disparity between radiograph
Many masters athletes have secondary knee OA because of evidence and function, including (1) insufficient radio-
ligamentous, cartilage or bone injuries received when par- graphic views to estimate the association between degenera-
ticipating in sports at a younger age. Several studies have tion and pain, (2) the wide variation in definitions of
shown a substantial increased risk of knee OA in individuals pain that may result in discrepancy between the score and
with a history of anterior cruciate ligament rupture, meniscal the amount of evidence of OA, and (3) the nature of the
tears, and fractures.56-61 Given the increased participation in study population. Therefore, the prevalence of OA, when
NORMAL JOINT
Bone Muscle
Bursa
Synovial
membrane
Tendon
Synovial
fluid
Joint capsule
(ligaments) Cartilage
Figure 29-2
Typical osteoarthritic changes that may occur with advancing age. Severe erosion of articular cartilage
results in bone on bone, altered biomechanics at the joint, an increase in joint friction or resistance to
movement, and frequently pain and swelling. (From Brown M: Effects of aging-growth changes and
lifespan concerns (40). In Magee DJ, Zachazewski JE, Quillen WS, editors: Scientific Foundations and
Principles of Practice in Musculoskeletal Rehabilitation, p 307, St. Louis, 2007, Saunders.)
710 SECTION IV • Special Populations and Epidemiology
assessed by radiographs, may be much higher than those exercises are a crucial part of any program for those with
actually experiencing pain and disability.66 Knee-specific OA OA. Although joints should never be passively forced
has been shown to be present more often when both patel- through a range, gentle ROM, joint mobilizations, and
lofemoral and tibiofemoral joints are affected, creating stretching exercises should be performed with each exercise
more pain.67 session.79-81
One of the major diagnostic criteria for arthritis is the Both loss of knee flexion and extension can be affected
symptom of joint pain. Articular cartilage itself is not in knee OA, although knee flexion is usually limited to a
innervated, so where is the pain coming from? The general greater degree. The restoration of full extension is critical
consensus is that the pain is a result of inflammation of the for the establishment of a normal gait pattern and an
synovium, medullary hypertension, microfractures of the adequate of flexion is needed for sport-specific activities.
underlying subchondral bone, stretching of periosteal nerve Although the masters athlete with knee OA may only com-
endings caused by sclerosis, osteophyte formation, or exces- plain about knee pain and loss of motion, the clinician
sive stretching of ligaments and spasm of muscles surround- needs to consider loss of mobility of the entire trunk and
ing the affected joint.68 Symptoms of OA include pain and lower extremity. Examining mobility of the lumbar spine,
stiffness in and around the joint, osteophyte formation, hip, ankle, and foot is an important part of the physical
cartilage degeneration, joint malalignment, weightbearing examination of a masters athlete with knee pain. Limitations
difficulty, muscle spasm, weakness, and ROM loss. in the lumbopelvic or lower-extremity kinetic chain may
need to be addressed.80,81
Mobilization techniques specific to the knee include
dorsal and anterior glides of the tibia on the femur; medial
Radiographic Evidence of Osteoarthritis68 and lateral rotation of the tibia on the femur; and superior,
inferior, and lateral patellofemoral glides. For masters ath-
• Decreased joint space (cartilage degeneration)
• Sclerosis of subchondral bone
letes with restricted motion at the knee or hip, combining a
• Osteophyte formation at joint margins home exercise program with skilled manual therapy appears
• Subchondral cyst formation to work best. Deyle and colleagues79,82 determined that
• Genu varum or valgum joint deformity providing a home program in addition to manual therapy
was more effective in increasing overall function, decreasing
pain and stiffness, and requiring less medication use at
a 1-year follow-up. In this study, clinicians were encouraged
to evaluate and treat any ROM limitations in the lumbar
Rehabilitation Exercises for Knee Osteoarthritis spine, hip, ankle or foot if it was believed that this
Rehabilitation for those with lower-extremity OA should would improve knee function.79,82 A more recent study has
include all facets of training including flexibility, mobility, shown that the pain-pressure threshold was significantly
muscle strengthening, endurance training, and cardiovascu- increased following anterior and posterior glide tibiofemo-
lar training. Consideration of each of these training aspects ral joint mobilizations as compared with manual contact
is critical when designing a rehabilitation plan of care for the or no contact.83 For more information on this topic, see
aging athlete. Chapter 27, “Physical Rehabilitation After Total Knee
The goals of any specific rehabilitation program should Arthroplasty,” in Pathology and Interventions in Musculo-
depend on the individual athlete’s specific needs. For the skeletal Rehabilitation, Volume 3 of this series.
aging athlete, this includes ROM, strengthening, and en-
durance training. Lower-extremity strength training allows Unloading Braces and Insoles
the muscular system to work to attenuate impact loads, for Knee Osteoarthritis
provide needed joint stability, and support independent The majority of knee OA affects the medial compartment of
function.69 The American College of Sports Medicine has the knee, which bears greater than 60% of the load during
determined several specific muscle groups that should be weightbearing.84-86 As the medial joint compartment
emphasized with a strengthening program for older adults becomes more arthritic, a loss of medial joint space is
to maintain independence in ADLs. These muscle groups observed on radiographs and eventually visually, with the
include the hip extensors, knee extensors, ankle plantar patient exhibiting a varus or bowlegged knee deformity. To
flexors, and ankle dorsiflexors.9 Exercises for these muscle offset or “unload” the medial compartment, especially dur-
groups should be done at functional speeds and using func- ing physical activity, two biomechanical interventions have
tional patterns specific to the athlete’s needs.70-72 been suggested.
There appears to be significant consensus with respect to A specialized “counterforce” knee brace may be custom
the efficacy of exercise in the case of knee OA.73-78 Because fit to the patient. Typically, the athlete is measured and then
ROM of affected joints may be limited due to pain, muscle the brace is made with an intrinsic valgus correction of 2°
spasm, or soft tissue contractures, motion and flexibility to 3°. Often, via a small hex wrench or key, the athlete can
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 711
increase the valgus force by several additional degrees. This 2 or 3 because of dehydration and dilution.99 Recom-
allows some individual customization of the brace during mended injection schedules depend on preparations used.
different physical activities. Biomechanical analysis has For Hylan G-F 20, an injection weekly for 3 weeks is rec-
shown that wearing a valgus unloading brace can alter pain, ommended, whereas for sodium hyaluronan, the recom-
joint position sense, strength, and function in the older mended dosage is an injection weekly for 3 to 5 weeks.99
athlete.87-90 The hypothesis surrounding the brace effective- Most of the clinical studies on the use of injectable hyal-
ness has been the fact that if a brace can place the knee with uronic acid are inconsistent. Early studies demonstrated
medial joint space narrowing in neutral or a slight valgus relief of symptoms and benefit from this form of treat-
alignment, normal biomechanical loading may be restored. ment,100-103 although others did not.104,105 Problems abound
In addition, recent evidence appears to illustrate that with these early studies including heterogenicity of patient
pain relief may also be a result from diminished muscle co- populations, different formulations of injected preparations,
contractions rather than from so-called medial compart- and different treatment regimens.99
ment unloading.91 Using a knee unloading brace is not Despite these problems in research methodology, several
always feasible in the older athlete with knee OA. Custom meta-analyses indicate that viscosupplementation has a
unloading braces are very expensive and often are not fully therapeutic effect on pain, function, and patient global
covered by insurance. Other comorbidities, body size, and assessment.106-108 A limitation of these multiple studies is
body shape may also prohibit the success of an unloading that, to date, the effect of a placebo response on study par-
brace. In addition, prolonged brace wear can cause skin ticipants has not been fully analyzed and that adverse effects
breakdown and leg pain. Empirically, it appears the unload- of the injections have been reported.109
ing brace works best for the athlete who can wear the brace One of the problems with use of injectable viscosupple-
for his or her desired athletic activity, but does not necessar- mentation is the accurate placement of intra-articular needle.
ily need it for ADLs. Jackson and colleagues,110 using fluoroscopic confirmation
As an adjunct or as an alternative, the clinician may con- of needle position, found that accurate placement was very
sider the use of a laterally wedged insole for the masters difficult. When using an anterolateral approach, only 71% of
athlete with medial compartment knee OA. For this to be injections were performed in the correct position. Injection
effective, the athlete cannot have significant ankle instabil- site pain and discomfort is another common complication
ity. Too much ankle laxity will result in any changes made at seen with injectable hyaluronate. Although hyaluronate
the rearfoot not being transmitted up the kinetic chain. Are injections are used frequently when treating symptoms of
lateral insoles effective? Using insoles to statically alter the OA, the potentially high placebo effect with the use of hyal-
knee in a more upright position by placing the calcaneus uronate injections warrants further study before the true
in a position of valgus, Sasaki84,85 and Yasuda reduced the efficacy of this intervention can be determined.
mechanical load on the medial joint surface. These two
studies and others illustrate that a laterally wedged insole
may be effective in reducing pain and improving function in Hip Osteoarthritis
individuals with medial compartment OA.92-97 This insole The most common predisposing factor for hip OA is
research has yielded some interesting findings. At present, it age.111-113 Hip arthritis is common and occurs in up to 4%
appears that a laterally wedged, full-length orthotic is more to 6% of the population.114 Risk factors for hip OA include
effective than a heel wedge alone,92-94 that the wedged systemic issues such as ethnicity, age, gender, hormonal
insole should not be used with heeled footwear,98 and that status, genetics, bone density, and nutrition. Local biome-
having the patient self-select wedge size based on numeric chanical risk factors include joint injury, obesity, occupa-
pain ratings before and after wedge use is best.97 An addi- tion, sports participation, physical activity, altered joint
tional benefit of using a wedged insole is that it is signifi- biomechanics, and muscle weakness.115 Hip OA is more
cantly less expensive than a custom unloading brace. Fur- common in laborers than those with sedentary jobs. This
ther research is needed to identify which individuals would probably is accounted for by stress caused by heavy lifting
benefit from an unloading brace and a wedged insole. and carrying in those occupations.114,116-118 Previous hip
injury is also associated with hip OA.110,118 Cooper and
Viscosupplementation Therapy colleagues119 reported that the odds ratio for hip OA when
in Knee Osteoarthritis having a previous hip injury as 4.3 (95%, confidence interval
Many palliative treatments in the form of viscosupplementa- 2.2-8.4). In addition, patients with OA of one hip are at
tion have become available to help reduce symptoms associ- increased risk of developing OA in the opposite hip.120 A
ated with articular cartilage degradation. These come in the masters athlete’s previous occupation may determine his or
form of intra-articular injections with hyaluronic acid. her risk of hip OA. Numerous studies in Europe and the
Hyaluronic acid is a normal component of synovial fluid, United States have found a higher prevalence of hip OA in
which bathes the articular surfaces of the normal knee. men whose occupation involves repetitive lifting of heavy
In an arthritic knee, this molecule is depleted by a factor of loads.121-124 Suspected occupational risk factors for hip OA
712 SECTION IV • Special Populations and Epidemiology
have been suggested, including regular heavy lifting, oper- are simply from disuse and are from muscle-tendon unit
ating machinery, and walking on uneven ground.124-131 shortening, passive stretching should suffice. This is likely
One of the problems in diagnosing hip OA is that symp- not the case in the masters athlete. If, however, these limita-
toms can be vague and not localized solely to the hip tions are from hip capsular attenuation, joint mobilizations
region. As other areas afflicted with OA, the severity of OA may be more beneficial. Joint mobilization techniques may
in the hip may not exactly correlate with the degree of dam- be required in all planes, but most commonly will involve
age seen radiographically. Pain and symptoms associated increasing hip flexion and hip medial rotation in those with
with hip OA tend to be of much greater degree than radio- hip OA.
graphic evidence seems to justify, whereas symptoms may Although evidence for the use of manual therapy for hip
also be moderate in the presence of severe radiographic OA is limited, there are several studies that do support its
changes. use. Hoeksma and colleagues demonstrated the superiority
In hip OA, the entire joint structure and function is af- of manual therapy plus exercise over exercise in isolation for
fected with joint capsular changes (shortening and lengthen- hip OA.141 Furthermore, a case series from MacDonald and
ing) along with subsequent articular cartilage degeneration.132 coauthors described outcomes of individual patients treated
Later in the disease process, osteophytes or bone spurs may with manual physical therapy and exercise for hip OA.144
develop from excessive tensile force on the hip joint capsule This case series reported reductions in pain and an increase
or from abnormal pressure on the articular cartilage.132,133 in hip ROM in subjects with hip OA.
Other changes also develop, including sclerosis of the sub- Proximal stability of the hip is required for almost all
chondral bone from increased focal pressure, and in some weightbearing activities. Studies indicate that patients with
cases, cyst formation.134 Muscle weakness often develops hip OA have decreased strength compared with nonarthritic
around the hip joint with OA,135 specifically the abductor control subjects.137,145 Initial exercises can begin in the
muscles in the hip.136 The hip abductor weakness progres- hook lying position because of the effects of gravity
sively weakens in the later stages of hip OA, which may create and pain that could occur with full weightbearing. Once
a Trendelenburg gait pattern.137 exercises are tolerated in hook lying, advancement to pro-
Recently, several studies have found an association be- gressive resistive exercises via machine weights or isotonic
tween acetabular labral tears and the early onset of hip exercises may commence.
OA.138-140 This is important to understand as the aging
athlete may have had previous injuries or lower-level symp- Does Running Increase the Risk of Hip
toms of hip discomfort that may have gone on for years or Knee Osteoarthritis in the Masters Athlete?
without formal treatment. Many have questioned if running can increase the risk of hip
and knee OA. Multiple studies have attempted to answer
Rehabilitation of Hip Osteoarthritis this question. Some studies have reported that running,
Rehabilitation for hip OA includes therapeutic exercise and especially in excess, does increase the risk of OA.146,147
manual therapy. Manual therapy techniques may be benefi- Other investigations have shown no influence of distance
cial for those with restricted hip capsular mobility. Hoeksma running on OA.148-150 In several studies, moderate distance
and colleagues141 performed a clinical trial assessing the running has been reported to perhaps have a protective
effectiveness of manual therapy compared with exercise effect in preventing the development of hip OA.151,152 At
therapy in those with hip OA. Successful outcomes were present, the preponderance of data seems to indicate that
found in 81% of those receiving manual therapy compared long-distance running in moderation does not appear to
with only 50% in the exercise group. Positive effects related increase the risk of hip or knee OA in healthy individuals
to improvements of pain, hip function, and ROM lasted up and that running may even have a protective effect on the
to 29 weeks. risk of OA. Previous trauma to the hip or knee, whether
Evidence shows that those with hip OA have limitation in the result of injury or overuse, excessive running above
strength of the hip musculature and limitations in ROM as the individual’s physical threshold, and intrinsic anatomical
compared with those with no hip problems.137,142 One of instability in the joints may accelerate the onset of OA. The
the earliest signs of hip OA is restriction of hip ROM. clinician should weigh the risks of running against the
Altman and colleagues have described hip flexion of 115° or cardiovascular and musculoskeletal benefits of running.
less and medial rotation less than 15° to be prevalent in pa-
tients with hip OA.112 Birrell and colleagues have noted that Surgical Treatment for Hip Osteoarthritis
an increased number of restricted planes of ROM increases Surgical treatment for hip OA includes but is not limited to
the specificity of ruling in hip OA as the actual diagnosis.143 arthroscopic or open procedures. Arthroscopic surgery is
Therefore, the mainstay of conservative treatment must in- less invasive and is indicated for pathological conditions of
clude increasing limited motion and strength. Limitations in the hip such as symptomatic tears of the labrum, ligamen-
rotation can be restored by use of joint mobilization and tum teres injuries, snapping hip syndrome, and removal
passive stretching of the hip musculature. If these limitations of loose bodies. Open procedures commonly performed
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 713
include a variety of total hip arthroplasty (THA) treatments. cartilage of the humeral head and glenoid fossa. Depending
With advances in surgical techniques and high-performance on the mechanism of injury, the result may be either a clas-
prosthetic components, many aging athletes are able to sical Hill-Sachs lesion or, if dislocated posteriorly, a reverse
return to an acceptable level of sports both recreational and Hill-Sachs lesion. These injuries can cause articular cartilage
competitive following THA. For more information on this to disrupt from bone or cause an osteochondral compres-
topic see Chapter 26, “Physical Rehabilitation After Total sion defect. Recent evidence concludes that arthritic changes
Hip Arthroplasty,” in Pathology and Intervention in Muscu- after a dislocation are due to the age of the patient, the time
loskeletal Rehabilitation, Volume 3 in this series. of insult, and the span of time between insult and treatment
after injury.163,164 Primary OA of the shoulder is generally
due to more chronic causes such as rotator cuff disease. Up
Glenohumeral Osteoarthritis to 76% of patients with cartilage lesions of the shoulder
In addition to weightbearing joints, OA affects the shoulder have associated rotator cuff degeneration or tears, whereas
in an estimated 20% of the elder population.153 This rate is only 19% of subjects without cartilage problems experience
well below that of other locations in the body, but its effects rotator cuff degeneration or tears.157 This is probably
appear to be just as debilitating and are a common cause of caused by progressive wear and the fact that the rotator cuff
depression, anxiety, activity limitations, and job perfor- tendons have areas of reduced blood supply, making them
mance decrements.154 Treating glenohumeral arthritis in more vulnerable to degeneration with increased age.165 As
the masters athlete requires providing adequate pain relief with treatment of knee and hip OA, there are several medi-
and restoration of ROM and function. Full-thickness artic- cal treatment options, including rehabilitation, supplemen-
ular cartilage defects in the shoulder have limited capacity tation, medicine, and surgery. At present, there is no way in
to heal.155 Multiple causes of articular cartilage abnormali- which the natural progression of OA can be altered.
ties in the glenohumeral joint occur and include avascular
necrosis, chondrolysis, idiopathic focal defects, OA, osteo- Rehabilitation Interventions for Shoulder
chondritis dissecans, postsurgical cartilage abnormalities Osteoarthritis
(iatrogenic injuries and post-traumatic defects).155-157 Nu- Rehabilitation depends on whether the OA is treated con-
merous risk factors abound for shoulder OA and include servatively or following surgical procedures. Conservative
age, genetics, sex, weight, joint infection, history of shoul- treatment of shoulder OA begins with activity modification
der dislocation, previous injury, overhead sports, or heavy and pain control, followed by progressive ROM and
labor.158 Similar to the knee, OA of the shoulder can occur strengthening exercises. Pain reduction can be attempted
as either a primary or secondary process. Although primary through the use of numerous modalities. Limited evidence
OA of the shoulder occurs as a gradual onset of pain, ath- exists regarding the best modality for glenohumeral OA.
letes may remember an inciting event or injury that created Moist heat and electrical stimulation may help alleviate
symptoms. Secondary OA occurs as the result of some symptoms, but is generally not long lasting. Use of these
trauma or damage to the glenohumeral joint. Degeneration modalities may allow soft tissue relaxation, allowing more
of the glenohumeral joint is a difficult condition for the ease with obtaining or regaining valuable shoulder ROM.
masters athlete. This is especially true of athletes who Although ROM of the shoulder is important, clinicians must
participate in overhead sports such as baseball, tennis, remember that the patient’s arthritic glenohumeral joint
swimming, or volleyball. However, competitors in cycling, surfaces may not be congruent. Aggressive attempts at in-
football, basketball, and soccer may also find themselves creasing ROM may exacerbate an already irritated condition.
with severe post-traumatic, postreconstruction, or primary Therefore, working within a pain-free motion may be more
cartilage loss in their shoulders. Unfortunately, this may beneficial.166 Because shoulder joint stiffness is a poor prog-
lead to impeded performance in these elder athletes. nostic indicator for surgical outcomes, its avoidance should
Shoulder OA presents as a gradual onset of pain, crepitus be adequately addressed in conservative rehabilitation.160
with decreased motion in those older than 50 years of age Strengthening within the nonpainful range of shoulder
who may have a history of previous shoulder surgery.159 motion is beneficial as some physiological overflow may
Classic signs and symptoms include pain, weakness, and occur. Particular emphasis on the rotator cuff muscles and
limited shoulder lateral rotation secondary to anterior soft scapular stabilizers is important because these muscles pro-
tissue contracture.160 Rotator cuff integrity may be difficult vide a strong foundation on which upper-extremity move-
to determine in the presence of pain, and this can make ment can occur. Because some of these patients may have
an exact diagnosis difficult. Diagnostic imaging reveals chronic rotator cuff arthropathy, strength gains may be
joint space narrowing, humeral osteophytes, and posterior minimal or slow at best. Conservative treatments should be
subluxation of the humeral head.161,162 exhausted before attempts at surgery are considered. For
Secondary OA from trauma in the shoulder is often due more information on this topic, see Chapter 25, “Shoulder
to history of dislocation or subluxation. During a sublux- Arthroplasty,” in Pathology and Intervention in Musculoskel-
ation or dislocation, excessive forces may be imparted to the etal Rehabilitation, Volume 3 in this series.
714 SECTION IV • Special Populations and Epidemiology
Tendon Pain
Tendinopathy in the Masters Athlete A significant challenge in providing intervention to patients
Primary disorders of tendons are common and constitute a with tendinopathy or fasciopathy is in understanding the
high proportion of referrals of the sports medicine clinician. potential sources of pain. In the traditional histopathologi-
Certain tendons are particularly vulnerable to degenerative cal model, tendon pain was considered an inflammatory
pathological conditions; these include the Achilles,170 problem, hence the term tendinitis. However, as previously
patella,171 proximal or high hamstring,172 gluteus medius,173 discussed, there is a lack of inflammatory cells in chronically
rotator cuff,174 and common wrist flexor and extensor painful tendons; this observation applies not only to the
tendons.175 It is important to note that both high hamstring Achilles tendon, but to other problematic tendons includ-
and gluteus medius tendinopathy are often misdiagnosed as ing the patellar, rotator cuff, and wrist extensor tendons.180
piriformis syndrome or trochanteric bursitis respectively.172,173 There is some evidence that there may be a neurochemical
The sports medicine–trained clinician should be aware of aspect of tendinopathy pain. Alfredson and Lorentzon177
this as misdiagnosis can prevent the masters athlete from found higher concentrations of glutamate in painful ten-
receiving the appropriate treatment in a timely manner. dons, including Achilles tendon, extensor carpi radialis
Tendon pain is a common condition in the masters ath- brevis tendon, and patellar tendon, and reported the pres-
lete and can cause lasting disability. Significant advances have ence of glutamate receptor sites in nerve endings associated
been made in understanding the pathophysiological charac- with painful tendons. Using immunohistochemical analyses
teristics of these conditions. Histopathological evidence, of painful Achilles tendons, Schubert and colleagues182
together with advances in imaging techniques, has made found sprouting of substance P–positive nerve fibers, which
clinicians more appreciative of the degenerative nature of may explain the transmission of the tendon pain.
these conditions. Traditionally, treatments have placed a Historically, the mechanical model of tendon pain has
heavy emphasis on anti-inflammatory strategies, which are implicated that pain is a consequence of repetitive loading
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 715
of the tendon, resulting in collagen disruption.183 In the affected tendon. However, studies in this area are lacking
past decade, several imaging studies have seriously ques- and currently no high-quality evidence exists for or against
tioned this model. First, studies on patellar tendons184-187 the use of these two manual therapy interventions for treat-
and Achilles tendons170 have shown that the tendon can be ment of tendinopathy.
partially disrupted without pain, or painful without disrup-
tion.188,189 Other research on pathological conditions of the Eccentric Training for Tendinopathy
tendon at the shoulder and ankle has found the location of One of the most exciting outcomes of tendinopathy
a pathological tendon condition is not in the region sub- research has been the positive findings of eccentric exercise
jected to the highest tensile forces, but rather in a region of as a treatment for chronic tendinopathy. Eccentric loading
relative stress shielding where tensile forces are lower.190,191 exercises involve active lengthening of the muscle tendon
These findings are inconsistent with a model that describes unit. Eccentric training as a treatment for chronic tendi-
excessive tensile forces as a primary stimulus for pathologi- nopathy is not a new concept.197,198 The original Achilles
cal conditions of the tendon. To explore new avenues of tendinopathy eccentric exercise protocol published by
examination and intervention for tendinopathy, clinicians Stanish and colleagues198 in 1986 has been expanded and
must recognize that research findings are contrary to a improved. In the protocol by Alfredson and colleagues,199
traditional view of pathological conditions of the tendon as the patient groups were required to perform three sets of 15
inflammatory conditions caused by repetitive tensile stress repetitions of eccentric heel lowering at a slow speed with
on the tendon. If we continue to allow such a traditional the knee straight and bent, twice per day for 12 weeks. The
view to persist, attempts to relieve tensile stress or reduce control group was required to perform concentric
inflammation will continue to result in frustration for exercises (active shortening of the muscle tendon unit). As
clinicians and patients alike. opposed to performing pain-free eccentric heel lowering per
the original Stanish protocol,198 in the Alfredson protocol,
resistance was increased to the point at which performance
Treatment of Tendinopathy in the Masters Athlete of the exercise became painful but not disabling. The sub-
Management of tendinopathy should address both intrinsic jects were instructed to increase the resistance used once the
and extrinsic factors identified in the physical examination. exercise became pain-free. High levels of patient satisfaction
Correction of training errors, cross-training, and active rest were seen in the eccentric loading groups (82%) and all
are common recommendations made in the early stages of 12 participants returned to their sports activities. In subse-
rehabilitation. A multitude of treatment interventions exist quent long-term follow-up (mean 3.8 years) Alfredson and
for treating tendinopathy, although more research is neces- co-workers have confirmed both the initial good results and
sary to determine their efficacy and effectiveness. a statistically significant reduction of tendon thickening
and resolved neovasculation.200,201 One problem with the
Manual Therapy for Tendinopathy Alfredson protocol was that it was less successful for patients
There are several manual therapies popular in the treatment with insertional Achilles tendinopathy.202 Initially, it was
of tendon disorders, the two most common being friction thought that this was because of differences in pathological
massage and augmented soft tissue mobilization (ASTM). conditions; however, this appears to be untrue.203 Jonsson
Made popular by Cyriax, deep transverse friction massage and colleagues have reported that modifying the Alfredson
(DTFM) is a part of many clinical tendinopathy programs. protocol by performing the eccentric Achilles exercises on
A Cochrane review in 2002192 examined the available evi- the floor instead of off a step improves success in those with
dence for DTFM. There were only two randomized con- insertional Achilles tendinopathy.204 These researchers
trolled trials of sufficient quality to be included: one on the hypothesize that the avoidance of excessive passive dorsiflex-
treatment of lateral epicondylalgia and the other on the ion in weightbearing prevents soft tissue impingement be-
iliotibial band syndrome. Neither of these two trials demon- tween tendon, bursa, and bone at the calcaneal tendon. In
strated a lasting benefit versus the control group for either addition, investigators have determined that the need to
pain or functional status.192 Therefore, at present, no con- avoid sports activity during eccentric training for Achilles
clusions can be drawn concerning the use or nonuse of tendinopathy is not necessary. Silbernagel and colleagues
DTFM for the treatment of tendinopathy. A second popular investigated whether any difference in outcomes could be
technique is that of ASTM.193,194 This is an intervention found between those subjects who rested and those who
that involves the use of ergonomically designed instruments continued their sports activity.205 The exercise training
that theoretically assist clinicians in treatment of areas group was allowed, with the use of a pain-monitoring
exhibiting excessive soft tissue fibrosis.195,196 Following each model, to continue Achilles tendon–loading activity, such as
ASTM treatment, the patient completes a stretching and running and jumping, whereas the active rest group had to
strengthening program. Both DTFM and ASTM are stop such activities during the first 6 weeks. No negative
thought to stimulate blood supply in the vicinity of the effects could be demonstrated from continuing Achilles
tendinopathy and this is thought to promote healing of the tendon–loading activity, with the use of a pain-monitoring
716 SECTION IV • Special Populations and Epidemiology
model, during treatment.205 This is important as it allows athlete) who are also willing to perform multiple repeti-
the clinician, with some confidence, to permit loading activ- tions, twice daily, 7 days a week for 12 weeks, and this will
ity during rehabilitation. This may allow better adherence to not suit all patients. Although results appear promising,
the rehabilitation program by the athlete if he or she does future research is still needed to support the use of eccentric
not feel that the health professional is taking away the exercise in the management of tendinopathy.
desired activity. The eccentric training program described by
Silbernagel and colleagues is shown in Box 29-1.205 Injection Therapy for Tendinopathy
The success of eccentric training for Achilles tendinopa- A systematic review of corticosteroid injection for lateral
thy has fostered efforts to determine whether eccentric epicondylalgia found a total of 12 trials suitable for analysis.
training will work for other tendinopathies. Two small stud- The review authors concluded that corticosteroid injection
ies on the use of eccentric exercises on a decline board for was effective in the short term (2 to 6 weeks) but that in the
treatment of patella tendinopathy have shown positive long term, there was no difference in outcome when com-
results.206,207 A pilot study has also been performed showing pared with those not receiving injections.210,211 There are
some positive results using eccentric exercises in patients several case reports of tendon rupture following corticoste-
with supraspinatus tendinopathy.208 Despite these promis- roid injection,212-215 particularly involving the Achilles ten-
ing results, questions remain.209 Why eccentric training don.214,215 Because of the concerns surrounding tendon
appears to work is uncertain. The eccentric programs also integrity following steroid injection, the mounting evidence
seem to be of more benefit for active individuals.200 These shows that the use of intratendinous injections is contrain-
programs require highly motivated people (e.g., the masters dicated. In contrast, evidence surrounding peritendinous
themselves at risk for implant failure and subsequent revi- Patients who have been active and athletically skilled
sion. It appears that activity level is the most variable prior to THA will have the greatest chance for returning to
patient-related factor and may explain why some implants a high level of skilled activity postoperatively. Individuals
last longer.238 Joint load must be considered when dis- with increased athletic ability typically display less joint
cussing postarthroplasty activity levels with patients. If forces than those who are less skilled. Attempting to learn a
patients resume activities that place high loads on the new athletic skill is unlikely to be successful and may put the
joint, wear and tear may increase exponentially.239,240 Be- patient at risk for injury after surgery.
cause cardiovascular fitness is an important preventative What specific recommendations exist for returning to
measure, it is important to determine at what level exercise and sports activities following total joint arthro-
masters athletes can return to activities that promote this. plasty? Most literature reviews are based on personal opinion
Speed walking appears to be a good alternative to run- rather than prospective studies. In general, low-impact
ning, while still providing for cardiovascular fitness. Com- activities are tolerated well by patients given that forces and
pressive loads at the hip joint are 4 to 4.5 times the wear will be lower relative to high-impact exercise and sport.
athlete’s body weight when power walking.239 Jogging or As impact and torsional loading increase during high-impact
running will increase hip joint compressive forces to sports and exercise, relative risk associated with activity
greater than 5 times the athlete’s body weight. Unfortu- increases as well.239,241 Surgeons and residents at the Mayo
nately, there are many activities without documented Clinic242 surveyed themselves and reviewed the literature
evidence on joint forces and loads. Kuster239 suggests the regarding return to athletics following THA. They deter-
following guidelines: during daily activities, loads of 3 to mined that orthopedic surgeons should suggest the follow-
4 times the athlete’s body weight may apply; while in ing low-impact sports to their patients who are interested in
sporting activities, loads of 5 to 10 times the athlete’s returning to sports: sailing, swimming, scuba diving, cycling,
body weight may occur. Other considerations include golf, and bowling. They advise against high-impact activities
weight training, which will increase loads, and endurance such as running, water skiing, football, baseball, basketball,
activities in which load depends on speed. hockey, handball, karate, soccer, and racquetball. In 1999,
Healy and colleagues243 conducted a survey of 54 members
of The Hip Society to determine their recommendations for
Clinical Points athletics and sport participation following hip arthroplasty
surgery. The survey was completed by Society members and
Activity level, and type and amount of joint loading are better parame- they were asked to rate 42 different sports as either recom-
ters than age when determining implant longevity following total joint mended or allowed, allowed with experience, no opinion,
arthroplasty. and not recommended. See Table 29-3 for a list of these
activities and recommendations.243
Table 29-3
Activities Following Total Hip Arthroplasty—1999 Hip Society Survey
Recommended/Allowed Allowed with Experience Not Recommended No Conclusions Made
Modified from Healy WL, Iorio R, Lemos MJ: Athletic activity after joint replacement, Am J Sports Med 29(3):382, 2001.
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 719
Golf has been widely studied and the majority of sur- Regarding physical activity, patients should be moti-
geons permit or do not discourage patients to return to golf vated to maintain appropriate cardiovascular fitness levels.
after THA, but it is recommended that patients use a cart Cardiovascular exercise is beneficial for the THA patient
while playing. Mallon and colleagues244-247 determined that for many other reasons including general health, preven-
surgeons allow patients to return to golf 19.5 weeks after tion of cardiac problems, and for improvement of bone
surgery. Golfers surveyed stated that their driving distance quality and implant fixation. Low-impact aerobic exercise
decreased 3.3 yards and their handicap increased by suggestions that allow for increased heart rate are the most
1.1 strokes after THA. These golfers played an average of appropriate. Aerobics are completed 3 to 4 days per week
3.7 times per week and were followed for 3 or more years. for 30- to 40-minute sessions. Whether the patient wants
At an average follow-up time of 61 months, hybrid and to return to recreational or competitive sports is ultimately
uncemented total hip arthroplasties were associated with up to him or her, although prudent guidance from the
less loosening as determined by radiograph when compared surgeon and rehabilitation clinician physical therapist is
with cemented total hip arthroplasties. No differences in essential. For these individuals, skiing, tennis, and hiking
pain during or after golf were noted.244-247 can be suggested, along with consideration of their previ-
Mont and colleagues235 evaluated tennis following THA. ous athletic participation. Recommendations that help
For 58 tennis players who had 75 THA surgeries, only 14% reduce joint forces are essential to reducing hip joint load-
of the patients stated that their physician approved of their ing. These include using ski poles when hiking; skiing on
return to tennis. Of these patients, 21% specifically had the flat, groomed runs; and cross-country skiing techniques.
surgery to return to tennis and they did so after approxi- Many of these masters athletes will push the durability and
mately 7 months. These individuals played three times per longevity of arthroplasty implants by engaging in high-
week and maintained their presurgical national tennis rank- demand sports and activities that repetitively cycle the im-
ing. Revision was necessary for 4% of these patients at a plant with and without excessive loads. Health care
mean of 8 years after their initial hip arthroplasty. professionals must learn from these situations as well as
Healy and colleagues243 suggest that patient education is engage in further research to assist in determining what
crucial when addressing treatment options and expectations activities are appropriate and possible for the aging athlete
regarding return to activity and sport. Emphasizing the im- following THA.
portance of previous activity and athletic skill, preoperative
rehabilitation, proper choice of components and procedure,
adherence to precautions, and surgeon skill and experience Total Knee Arthroplasty
on THA outcomes are essential. Setting realistic expectations As with masters athletes with a THA, considerations to the
for return to sport and emphasizing the risks and benefits of prosthetic wear and joint-loading forces during sports activ-
specific activities is also important. For the active patient, ity following TKA is important. Normal and fast walking
Healy and his colleagues243 recommend a cementless acetab- speeds have joint loads estimated at 2.8 and 4.3 times body
ular component, a hemispheric titanium porous-coated im- weight, respectively. Power walking results in tibiofemoral
plant inserted with an under-ream press-fit technique and compressive joint forces of 4 to 4.5 times the athlete’s
supplemental screw fixation, with a minimum polyethylene bodyweight.240 An estimated load during slow jogging is
thickness of 6 mm. Femoral components for active patients 7.5 to 8 times the athlete’s body weight for male patients
may be cemented or cementless. For cemented techniques and 8.5 to 9 times the athlete’s body weight for women.
they recommend cobalt-chrome implants with the proper Knee joint moments increase with increasing speed, result-
femoral offset for restoration of abductor biomechanics. ing in knee joint loads of 10 or more times the athlete’s
Second-generation cementing techniques with vacuum mix- body weight with jogging.240 Cycling has demonstrated
ing are also used. For cementless techniques, a cobalt-chrome increasing compressive forces with increasing workload.
tapered wedge stem with porous coating is inserted with the Saddle height can also influence joint load; the higher the
appropriate offset. A 28-mm ball is used to balance wear and saddle, the lower the compressive force. Cycling demon-
stability factors.243 strates a tibiofemoral joint load of 1.2 times the athlete’s
bodyweight.240 Hiking is another activity patients may want
to participate in after TKA. Downhill walking places large
Patient Education Following Total Joint Arthroplasty loads on the knee joint. Fast downhill walking has demon-
is Essential and Should Include: strated loads up to 8 times the athlete’s body weight. The
• Treatment options use of ski poles is recommended to reduce these joint load-
• Treatment expectations regarding return to activity and sport ing forces by as much as 20%. Unfortunately, there are
• Pre- and postoperative rehabilitation many activities without documented evidence on joint
• Adherence to precautions forces and loads. Kuster and Stachowiak240 report that dur-
• Risks and benefits of specific activities ing daily activities, loads of 3 to 4 times the athlete’s body
• Maintenance of cardiovascular fitness weight may apply, whereas in sporting activities, loads of
5 to 10 times the athlete’s body weight may occur. Other
720 SECTION IV • Special Populations and Epidemiology
considerations include weight training, which will increase More than half of these surgeons also suggested that
loads, and endurance activities, in which load depends on patients use a golf cart after knee arthroplasty. The golfers
speed. evaluated played an average of almost four rounds of golf a
week. At a 3-year follow-up, the golfers noted that their
handicap increased an average of 4.6 strokes and their driv-
ing distance decreased an average of 12 yards. The majority
Clinical Point of these golfers did use golf carts and 84% did not have pain
Use of ski poles or walking sticks can reduce lower limb joint loading when playing golf, but did complain of mild ache after play-
forces by up to 20%. ing. Right-handed golfers with left TKA experienced more
discomfort associated with playing golf than those follow-
ing a right TKA. This was likely due to the rotational
stresses required on the left knee during a right-handed golf
swing.
Recommendations for Return to Sport Diduch and colleagues248 evaluated outcomes of TKA in
after Total Knee Arthroplasty young, active patients. The mean age of patients was
Bradbury and colleagues234 evaluated participation in sports 51 years and 24% regularly participated in strenuous activi-
after TKA. They demonstrated that 65% of their patients ties such as tennis, skiing, bicycling, farm, or construction
who participated in regular exercise before TKA returned to work. All but two of the 88 patients experienced increased
sports after the procedure. The majority of these patients activity levels postoperatively. The average survivorship of
returned to low-impact sports (91%), although some (20%) the prosthesis for this group was 94% at 18-year follow-up.
returned to higher-impact activities such as tennis. Of Despite the active lifestyles of these patients, loosening was
42 patients who underwent simultaneous bilateral TKA, not a problem. Healy and colleagues243 recommend an an-
20 participated in sports prior to surgery. Of those 20 pa- teromedial arthrotomy with a cemented and minimally
tients, 15 (75%) returned to sports following completion constrained PCL-sacrificing or PCL-substituting condylar
of their rehabilitation program. Healy and colleagues243 knee implant for active patients requiring a TKA. They use
surveyed members of The Knee Society regarding recom- intramedullary femoral instrumentation and extramedullary
mendations for athletics and sports participation following tibial instrumentation to achieve the correct tibiofemoral
TKA. Table 29-4 illustrates the results of this survey. alignment of 5° to 7.0°. The femoral component should be
Mallon and Callaghan246 investigated members of The made of cobalt-chrome with a rounded condylar geometry
Knee Society and active golfers who had a TKA. Of the and conforming patellofemoral joint. The tibial implant is
surveyed surgeons, 92% did not discourage patients from modular and made of titanium with a high-molecular-
playing golf after knee arthroplasty, nor did they note in- weight polyethylene insert at least six to eight mm thick.
creased complications in those patients returning to golf. It is recommended that patients avoid recreational and
Table 29-4
Activities Following Total Knee Arthroplasty—1999 Knee Society Survey
Recommended/Allowed Allowed with Experience Not Recommended No Conclusions Made
Modified from Healy WL, Iorio R, Lemos MJ: Athletic activity after joint replacement, Am J Sports Med 29(3):384, 2001.
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 721
athletic activity until their quadriceps and hamstrings are Mitchell and colleagues251 examined the mechanics of
sufficiently rehabilitated in physical therapy.243 Masters ath- the shoulder during the golf swing for amateur senior golf-
letes are counseled to maintain cardiovascular fitness with ers and established normative data characterizing shoulder
activities such as swimming and cycling. If a masters athlete motion. Key components of the golf swing required 119°
wishes to participate in more aggressive activities, the horizontal adduction, 94° of vertical elevation during the
patient should be assisted in making reasonable choices. backswing, and 59° lateral rotation during the follow-
through for the nondominant arm. The dominant shoulder
required 48° of lateral rotation during the backswing and
Total Shoulder Arthroplasty 103° elevation with 108° horizontal adduction during the
Although hip and knee total joint arthroplasty remain com- follow-through. The expectation of a patient wishing to
mon procedures in orthopedics, total shoulder arthroplasty return to golf would require that he or she be able to
(TSA) is less prevalent. The total number of hip and knee achieve these ranges of motion against gravity and hold
joint arthroplasties performed annually is nearly 20 times these positions against resistance. Table 29-6 compares the
that of TSA.249 Trends in pain relief and patient satisfaction normal ROM after TSA to the normal ROM needed for a
tend to mirror those found in joint arthroplasty of the golf swing in an older amateur golfer. These expectations
hip and knee. Subjectively, 92% of patients describe their may be less attainable in patients having a TSA because of
shoulder as “much better” or “better” following TSA.250 rotator cuff deficiency and more realistic in patients with
isolated OA.252
Recommendation for Return to Sport Jensen and Rockwood253 studied 24 golfers following
after Total Shoulder Arthroplasty TSA. Of the 24 golfers, 23 were able to return to golf. The
To assess the appropriateness of athletic activity, one must average return to golf took 4.5 months. No radiographic
consider the sport being pursued following TSA. A survey of evidence of component loosening was noted compared
the American Society of Shoulder and Elbow Surgeons re- with nongolfers at follow-up evaluations ranging between 2
ported by Healy and colleagues243 revealed recommenda- to 10 years postoperatively. Handicap scores of these patients
tions of appropriate sports activity following TSA. These were reported to improve on average by five strokes. Mem-
results are illustrated in Table 29-5. None of the recom- bers of the American Society of Shoulder and Elbow Surgeons
mended sports were classified as contact sports and were were surveyed regarding the risks involved with playing golf
relatively low-impact with respect to the upper extremity. after a TSA. Of those surveyed, 91% recommended patients
Most activities also involved primarily a uniplanar movement return to golf and believed there was no increased risk of
of the shoulder. Bowling, horseshoes, and cross-country postoperative complications by playing golf.243
skiing are all sports that require primarily sagittal plane In regard to tennis, the survey demonstrated an interest-
movement of the shoulder. In addition, the stress to the ing contradiction. Doubles tennis was recommended, but
dynamic stabilizers during the deceleration phase of these no conclusion was made about singles tennis.243 Ground
activities is partially negated by gravitational forces. strokes would appear to be appropriate if adequate strength
Table 29-5
Activities Following Total Shoulder Arthroplasty—1999 American Shoulder and Elbow Society Survey
Recommended/Allowed Allowed with Experience Not Recommended No Conclusions Made
Modified from Healy WL, Iorio R, Lemos MJ: Athletic activity after joint replacement, Am J Sports Med 29(3):386, 2001.
722 SECTION IV • Special Populations and Epidemiology
Table 29-6 strength and mobility of the lumbar and thoracic spine may
Comparison of Shoulder Range of Motion During the Golf become an important factor in making an appropriate rec-
Swing with Range of Motion Following Total Shoulder ommendation on postoperative throwing. Other muscles of
Arthroplasty the legs and arms may compensate for shoulder weakness.
The patient may also alter throwing mechanics with a push-
Horizontal Lateral
ing motion similar to throwing a shot put. This requires less
Shoulder ROM Adduction Elevation Rotation
rotation of the shoulder and uses more of the triceps and
Dominant shoulder 108° 103° 48° pectoralis major musculature to propel the ball. For those
ROM during the masters athletes wishing to pursue throwing sports, it is
golf swing recommended that they have pain free anti-gravity control
Non-dominant 119° 94° 59° of the arm in elevated and laterally rotated position and that
shoulder ROM they demonstrate dynamic control of not only the shoulder,
during the golf swing but of the trunk and lower body as well.
Shoulder ROM Not 90° 47°
following total available
shoulder arthroplasty Total Ankle Arthroplasty
Data from Mitchell K, Banks S, Morgan D, Sugaya H: Shoulder In the past, athletic activity following total ankle arthro-
motions during the golf swing in male amateur golfers, J Orthop plasty (TAA) has been strongly discouraged.256 In 1994,
Sports Phys Ther 33(4):196-203, 2003; and Wilcox RB, Arslanian LE, Kitaoka and colleagues257 reported an overall prosthetic
Millett P: Rehabilitation following total shoulder arthroplasty, survivorship of 65% at 10 years postoperatively, but only a
J Orthop Sports Phys Ther 35(12):821-836, 2005.
42% prosthetic survivorship in a subgroup of patients
ROM, Range of motion.
younger than 57 years old. Prosthetic loosening caused by
the shearing forces during athletic activity is of most con-
cern regardless of cement or uncemented fixation.258 Pivot-
and dynamic control was demonstrated in the affected ing and cutting maneuvers risk dislocation and malleoli
shoulder below shoulder height. Traditional serving me- fractures caused by the lack of ligamentous integrity and
chanics may have to be altered secondary to predictable dynamic strength that is often compromised with ankle
elevation and rotational motion loss following TSA. This surgery. Normal postoperative ROM of combined dorsi-
may require even more involvement of the muscles of the flexion and plantar flexion is often significantly less than
legs and torso to generate power needed to perform an ef- what is considered normal. The limited ROM would
fective tennis stroke. As a result, a complete evaluation of likely hinder and dramatically change the mechanics of the
the patient’s trunk and lower extremities with regard to entire lower limb, including the foot, ankle, knee, and hips.
strength, mobility, and proprioception is critical in making Ankle stability, functional ROM, strength, and balance
an appropriate recommendation for the return to sport. require careful assessment before returning to any sport
Overhead sports pose interesting challenges. It is well activity. Low-impact activities with primarily movement in
known that athletes involved in throwing and racquet the sagittal plane logically put the patient at lower risk for
sports tend to have differences in rotational ROM, specifi- complications.
cally with significant increases in lateral rotation of the The emergence of newer surgical techniques is promis-
dominant side.254,255 Optimal lateral rotation as reported in ing. Wood and Deakin259 reported a revision rate at 5 years
the literature following TSA averages only 60°.252 This is far to be approximately 7% in a sample of 200 ankles. Anderson
below averages seen in overhead athletes. In addition, limi- and colleagues260 retrospectively followed patients with
tations in rotator cuff strength may further hinder the TAA using the Scandinavian total ankle replacement pros-
ability to attain sport-specific positions and stabilize the thesis between the years 1993 and 1999, and reported 30%
shoulder in such positions. Follow-through and decelera- of the patients required a revision for their TAA, but noted
tion phases of overhead throwing require significant force the patients who underwent surgery later had much greater
from the rotator cuff. Inadequate eccentric strength of success. Valderrabano and colleagues261 examined 147 pa-
these muscles increases the risk of injury and the inherent tients (28 to 86 years of age) 2 to 4 years following TAA.
stability of the shoulder.255 Patient satisfaction, ROM, American Orthopaedic Foot and
Because of the factors listed previously, it seems unlikely Ankle Society hindfoot score, radiological assessment, rate,
that many patients having TSA of their throwing arm would level, and type of sports activity were recorded and com-
be physically able to perform such tasks. The sports medi- pared with the patient’s preoperative results. At follow-up,
cine team should consider that loss of functional lateral excellent and good outcomes were reported in 83% of cases
rotation ROM may manifest itself in other biomechanical and 69% of patients were pain free. The mean ROM preop-
compensations. Trunk rotation may become excessive to eratively was 21° and after TAA, it was 35°. Before surgery,
counteract the lack of shoulder rotation. In this instance, 36% of the patients were active in sports; after surgery, this
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 723
percentage rose significantly to 56%. Overall, sports-active individuals well into their golden years. Because of the
patients with a TAA showed better functional results than physiological changes associated with aging, the masters
did inactive ones.261 athlete requires a knowledgeable health professional who
can balance patient safety with return to sport. These mas-
ters athletes require greater counseling, closer follow-up,
Timing of Return to Sport and scrutiny of the physiological demands and musculosk-
After Total Joint Arthroplasty eletal stresses of their desired sport. Ultimately, clinicians
Determining when a total joint arthroplasty patient is and masters athletes must find a balance between a return
ready to return to sport is essential. Whether it is directly to participation, safety, and a lifelong enjoyment of their
determined by the treating clinician or physician or self- sport.
initiation, a conservative approach is prudent. Functional
and acceptable ROM that allows for athletic or exercise
movements is necessary, as is well-balanced muscle strength References
across the joints involved. Ensuring that the older athlete 1. United Nations: Report of the second world assembly on aging,
has good balance in bilateral and unilateral stance is very Madrid, Spain, 2002.
important for those returning to sports. If balance and pos- 2. Kinsella K, Velkoff V: An aging world, US Census Bureau, Editor,
Washington, DC, 2001, US Governement Printing Office.
tural stability are compromised, risk of injury during sport
3. US Census Bureau: International database. Table 094. Midyear
may increase. Sport-specific rehabilitation exercises should population, by age and sex. Available from: http://www.census.
be added to the plan of care when the athlete has passed gov/population/www/projections/natdet-D1A.html.
specific examination- and performance-based criteria. Even- 4. Physical Activity Guidelines Advisory Committee: Physical Activity
tually, it is necessary to put the masters athlete through Guidelines Advisory Committee Report, Washington, DC, 2008,
US Department of Health and Human Services.
more rigorous testing to ensure he or she is ready to return
5. Warburton DE, Katzmarzyk PT, Rhodes RE, Shephard RJ:
to sport. Evidence-informed physical activity guidelines for Canadian
As the world of sports medicine has evolved, so has the adults, Can J Public Health 98(Suppl 2): S16–68, 2007.
context in which athletes are defined. Athletes span the 6. Kushi LH, Byers T, Doyle C, et al: American Cancer Society
entire life cycle, and the traditional age-related boundaries Guidelines on Nutrition and physical activity for cancer
prevention: reducing the risk of cancer with healthy food
by which athletes are confined have expanded. Athletic
choices and physical activity, CA Cancer J Clin 56(5):254–281;
careers and recreation in sports may not be terminated by a quiz 313–314, 2006.
joint arthroplasty procedure. Although there appears to be 7. Williams PT: Vigorous exercise, fitness and incident hypertension,
some inherent risk to performing sports following arthro- high cholesterol, and diabetes, Med Sci Sports Exerc 40(6):
plasty, low-impact and noncontact sports are usually appro- 998–1006, 2008.
8. Lee IM, Skerrett PJ: Physical activity and all-cause mortality:
priate and generally are encouraged by physicians. Newer
What is the dose-response relation? Med Sci Sports Exerc 33
surgical techniques and prosthetic materials have shown (6 Suppl):S459–471; discussion S93–94, 2001.
greater durability and have decreased postoperative compli- 9. Mazzeo RS, Cavanagh P, Evans WJ, et al: American College of
cations. Overall survivorship of arthroplasty procedures Sports Medicine Position Stand. Exercise and physical activity for
demonstrates satisfactory results between 15 to 20 years in older adults. Med Sci Sports Exerc 30(6):992–1008, 1998.
10. Spiduso WW, Francis KL, MacRae PG: Physical dimensions of
the literature. In many procedures, press fit or uncemented
aging, ed 2, Champaign, IL, 2005, Human Kinetics.
fixation is recommended for younger, active patients. Press 11. National Senior Games Association, 2009 01/06/2009 [cited
fit or uncemented fixation provides less initial fixation, but 2009 January 7]; Welcome page NSGA. Available from: http://
allows bone ingrowth for a strong, long-term fixation and www.nsga.com/DesktopDefault.aspx.
preserves greater bone integrity in cases in which a future 12. Team Physician Consensus Statement: Selected issues for the
master athlete and the team physician: A consensus statement.
revision is needed.
Med Sci Sports Exerc 42(4):820–833, 2010.
As medical science advances to provide individuals with 13. Chin APMJ, van Uffelen JG, Riphagen I, van Mechelen W: The
greater longevity, expectations of function and recreation functional effects of physical exercise training in frail older people:
will continue to grow as well. Patients who undergo total A systematic review, Sports Med 38(9):781–793, 2008.
joint arthroplasty are not necessarily limited to a sedentary 14. Daniels R, van Rossum E, de Witte L, et al: Interventions to
prevent disability in frail community-dwelling elderly: A system-
lifestyle. The methods and technology in the areas of joint
atic review, BMC Health Serv Res 8(1):278, 2008.
arthroplasty will continue to evolve, and so will the possi- 15. Evans WJ: Effects of exercise on body composition and func-
bilities to return to physical activity and athletics. tional capacity of the elderly, J Gerontol A Biol Sci Med Sci 50
Spec No:147–150, 1995.
16. Fiatarone MA, Marks EC, Ryan ND, et al: High-intensity
Conclusion strength training in nonagenarians. Effects on skeletal muscle,
JAMA 263(22):3029–3034, 1990.
The population of masters athletes will continue to increase 17. Fielding RA: The role of progressive resistance training and
as the world’s population ages. Better health care and tech- nutrition in the preservation of lean body mass in the elderly,
nology is allowing the continuation of athletic activity in J Am Coll Nutr 14(6):587–594, 1995.
724 SECTION IV • Special Populations and Epidemiology
18. Hess JA, Woollacott M: Effect of high-intensity strength-training 39. Tanaka H, Seals DR: Invited review: Dynamic exercise perfor-
on functional measures of balance ability in balance-impaired mance in masters athletes: Insight into the effects of primary
older adults, J Manip Physiol Ther 28(8):582–590, 2005. human aging on physiological functional capacity, J Appl Physiol
19. Seynnes O, Fiatarone Singh MA, Hue O, et al: Physiological and 95(5):2152–2162, 2003.
functional responses to low-moderate versus high-intensity pro- 40. Tanaka H, Seals DR: Endurance exercise performance in Masters
gressive resistance training in frail elders, J Gerontol A Biol Sci athletes: Age-associated changes and underlying physiological
Med Sci 59(5):503–509, 2004. mechanisms, J Physiol 586(1):55–63, 2008.
20. Going S, Williams D, Lohman T: Aging and body composition: 41. Coyle EF: Integration of the physiological factors determining
Biological changes and methodological issues, Exerc Sport Sci endurance performance ability, Exerc Sport Sci Rev 23:25–63,
Rev 23:411–458, 1995. 1995.
21. Kavanagh T, Shephard RJ: Can regular sports participation slow 42. Fitzgerald MD, Tanaka H, Tran ZV, Seals DR: Age-related
the aging process? Data on masters athletes, Phys Sports Med declines in maximal aerobic capacity in regularly exercising vs.
18:94–104, 1990. sedentary women: a meta-analysis, J Appl Physiol 83(1):160–165,
22. Grimby G: Physical activity and effects of muscle training in the 1997.
elderly, Ann Clin Res 20(1–2):62–66, 1988. 43. Tanaka H, Desouza CA, Jones PP, et al: Greater rate of decline
23. Grimby G: Muscle performance and structure in the elderly as in maximal aerobic capacity with age in physically active vs.
studied cross-sectionally and longitudinally, J Gerontol A Biol Sci sedentary healthy women, J Appl Physiol 83(6):1947–1953,
Med Sci 50 Spec No:17–22, 1995. 1997.
24. Thompson LV: Skeletal muscle adaptations with age, inactivity, and 44. Pimentel AE, Gentile CL, Tanaka H, et al: Greater rate of decline
therapeutic exercise, J Orthop Sports Phys Ther 32(2):44–57, 2002. in maximal aerobic capacity with age in endurance-trained than
25. Thompson LV: Effects of age and training on skeletal muscle in sedentary men, J Appl Physiol 94(6):2406–2413, 2003.
physiology and performance, Phys Ther 74(1):71–81, 1994. 45. Eskurza I, Donato AJ, Moreau KL, et al: Changes in maximal
26. Chandler JM, Duncan PW, Kochersberger G, Studenski S: Is aerobic capacity with age in endurance-trained women: 7-yr
lower extremity strength gain associated with improvement in follow-up, J Appl Physiol 92(6):2303–2308, 2002.
physical performance and disability in frail, community-dwelling 46. Zachazewski JE: Range of motion and flexibility. In Magee DJ,
elders? Arch Phys Med Rehabil 79(1):24–30, 1998. Zachazewski JE, Quillen WS, editors: Scientific foundations and
27. Weiner DK, Long T, Hughes MA, et al: When older adults face the principles of practice in musculoskeletal rehabilitation, Philadelphia,
chair-rise challenge. A study of chair height availability and height- 2007, Saunders.
modified chair-rise performance in the elderly, J Am Geriatr Soc 47. Altman RD, Lozada CJ: Clinical features of osteoarthritis. In
41(1):6–10, 1993. Hochberg MC, Weinblatt ME, Silman AJ, et al, editors: Practical
28. Brown M: Effects of aging—growth changes and lifespan concerns. theumatology, St Louis, 2004, Mosby.
In Magee DJ, Zachazewski JE, Quillen WS, editors: Scientific foun- 48. Felson DT, Chaisson CE, Hill CL, et al: The association of bone
dations and principles of practice in musculoskeletal rehabilitation, marrow lesions with pain in knee osteoarthritis, Ann Intern Med
Philadelphia, 2007, Saunders. 134(7):541–549, 2001.
29. Brown M, Sinacore DR, Host HH: The relationship of strength 49. Felson DT, Gale DR, Elon Gale M, et al: Osteophytes and
to function in the older adult, J Gerontol A Biol Sci Med Sci 50 progression of knee osteoarthritis, Rheumatology (Oxford) 44(1):
Spec No:55–59, 1995. 100–104, 2005.
30. Thompson LV: Age-related muscle dysfunction, Exp Gerontol 50. Felson DT, Lawrence RC, Dieppe PA, et al: Osteoarthritis: New
44(1–2):106–111, 2009. insights. Part 1: The disease and its risk factors, Ann Intern Med
31. Tuite DJ, Renstrom PA, O’Brien M: The aging tendon, Scand J 133(8):635–646, 2000.
Med Sci Sports 7(2):72–77, 1997. 51. Boissonnault WG, Goodman CC: Bone, joint and soft tissue dis-
32. Strocchi R, De Pasquale V, Guizzardi S, et al: Human Achilles orders. In Goodman CC, Boissonnault WG, editors: Pathology:
tendon: Morphological and morphometric variations as a func- Implications for the physical therapist, Philadelphia, 2000,
tion of age, Foot Ankle 12(2):100–104, 1991. Saunders.
33. Birch HL, Smith TJ, Tasker T, Goodship AE: Age related changes 52. Hoare K, Donahoe KM: Alteration of musculoskeletal function.
to mechanical and matrix properties in human Achilles tendon, In McCance KL, Huether SE, editors: Pathophysiology: The bio-
Transactions of the 47th Annual Meeting of the Orthopaedic logic basis for disease in adults and children, St Louis, 1990,
Research Society, San Francisco, CA, 2001. Mosby.
34. Maffulli N, Barrass V, Ewen SW: Light microscopic histology of 53. Felson DT, Zhang Y, Hannan MT, et al: The incidence and
achilles tendon ruptures, A comparison with unruptured natural history of knee osteoarthritis in the elderly. The
tendons, Am J Sports Med 28(6):857–863, 2000. Framingham Osteoarthritis Study, Arthritis Rheum 38(10):
35. Maffulli N, Ewen SW, Waterston SW, et al: Tenocytes from rup- 1500–1505, 1995.
tured and tendinopathic achilles tendons produce greater quanti- 54. Felson DT, Naimark A, Anderson J, et al: The prevalence of knee
ties of type III collagen than tenocytes from normal achilles osteoarthritis in the elderly. The Framingham Osteoarthritis
tendons. An in vitro model of human tendon healing, Am J Study, Arthritis Rheum 30(8):914–918, 1987.
Sports Med 28(4):499–505, 2000. 55. Cameron H, Brotzman SB: The arthritic lower extremity.
36. Heath GW, Hagberg JM, Ehsani AA, et al: A physiological com- In Brotzman SB, Wilk KE, editors: Clinical orthopedic rehabilita-
parison of young and older endurance athletes, J Appl Physiol tion, Philadelphia, 2003, Mosby.
51(3):634–640, 1981. 56. Neyret P, Donell ST, DeJour D, DeJour H: Partial meniscectomy
37. Hagberg JM, Coyle EF: Physiological determinants of endurance and anterior cruciate ligament rupture in soccer players. A study
performance as studied in competitive racewalkers, Med Sci Sports with a minimum 20-year followup, Am J Sports Med 21(3):
Exerc 15(4):287–289, 1983. 455–460, 1993.
38. Joyner MJ: Physiological limiting factors and distance running: 57. Neyret P, Donell ST, Dejour H: Results of partial meniscectomy
Influence of gender and age on record performances, Exerc Sport related to the state of the anterior cruciate ligament. Review at
Sci Rev 21:103–133, 1993. 20 to 35 years, J Bone Joint Surg Br 75(1):36–40, 1993.
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 725
58. Honkonen SE: Degenerative arthritis after tibial plateau fractures, of the hip or knee—The MOVE consensus, Rheumatology
J Orthop Trauma 9(4):273–277, 1995. (Oxford) 44(1):67–73, 2005.
59. Lundberg M, Thuomas KA, Messner K: Evaluation of knee-joint 77. Van Baar ME, Dekker J, Oostendorp R, et al: The effectiveness
cartilage and menisci ten years after isolated and combined rup- of exercise therapy in patients with osteoarthritis of the hip
tures of the medial collateral ligament. Investigation by weight- or knee: A randomized clinical trial, J Rheumatol 25(12):
bearing radiography, MR imaging and analysis of proteoglycan 2432–2439, 1998.
fragments in the joint fluid, Acta Radiol 38(1):151–157, 1997. 78. Iwamoto J, Takeda T, Sato Y: Effect of muscle strengthening
60. Roos H, Laurén M, Adalberth T, et al: Knee osteoarthritis after exercises on the muscle strength in patients with osteoarthritis of
meniscectomy: Prevalence of radiographic changes after twenty- the knee, Knee 14(3):224–230, 2007.
one years, compared with matched controls, Arthritis Rheum 79. Deyle GD, Henderson NE, Matekel RL, et al: Effectiveness of
41(4):687–693, 1998. manual physical therapy and exercise in osteoarthritis of the knee.
61. Gillquist J, Messner K: Anterior cruciate ligament reconstruction A randomized, controlled trial, Ann Intern Med 132(3):
and the long-term incidence of gonarthrosis, Sports Med 27(3): 173–181, 2000.
143–156, 1999. 80. Currier LL, Froehlich PJ, Carow SD, et al: Development of a
62. Moskowitz RW: Clinical and laboratory findings in osteoarthritis. clinical prediction rule to identify patients with knee pain and
In Koopman WJ, editor: Arthritis and allied conditions: A text- clinical evidence of knee osteoarthritis who demonstrate a favor-
book of rheumatology, Baltimore, 1997, Williams and Wilkins. able short-term response to hip mobilization, Phys Ther
63. Hannan MT, Felson DT, Pincus T: Analysis of the discordance 87(9):1106–1119, 2007.
between radiographic changes and knee pain in osteoarthritis of 81. Cliborne AV, Wainner RS, Rhon DI, et al: Clinical hip tests and a
the knee, J Rheumatol 27(6):1513–1517, 2000. functional squat test in patients with knee osteoarthritis: Reliability,
64. Flores RH, Hochberg MC: Definitions and classifications of os- prevalence of positive test findings, and short-term response to hip
teoarthritis. In Brandt KD, Doherty M, Lohmander LS, editors: mobilization, J Orthop Sports Phys Ther 34(11):676–685, 2004.
Osteoarthritis, Oxford, UK, 2003, Oxford University Press. 82. Deyle GD, Allison SC, Matekel RL, et al: Physical therapy treat-
65. Bedson J, Croft PR: The discordance between clinical and radio- ment effectiveness for osteoarthritis of the knee: A randomized
graphic knee osteoarthritis: A systematic search and summary of comparison of supervised clinical exercise and manual therapy
the literature, BMC Musculoskelet Disord 9:116, 2008. procedures versus a home exercise program, Phys Ther
66. Fisher NM: Osteoarthritis, rheumatoid arthritis, and fibromyalgia. 85(12):1301–1317, 2005.
In Myers JN, Herbert WG, Humphrey R, editors: Clinical exercise 83. Moss P, Sluka K, Wright A: The initial effects of knee joint mobi-
physiology. Musculoskeletal, neuromuscular, neoplastic, immunologic, lization on osteoarthritic hyperalgesia, Man Ther 12(2):109–118,
and hematologic conditions, Philadelphia, 2002, Lippincott 2007.
Williams and Wilkins. 84. Sasaki T, Yasuda K: Clinical evaluation of the treatment of osteo-
67. Szebenyi B, Hollander AP, Dieppe P, et al: Associations between arthritic knees using a newly designed wedged insole, Clin
pain, function, and radiographic features in osteoarthritis of the Orthop Relat Res (221):181–187, 1987.
knee, Arthritis Rheum 54(1):230–235, 2006. 85. Yasuda K, Sasaki T: The mechanics of treatment of the osteoar-
68. Brandt KD: Nonsurgical management of osteoarthritis, with an thritic knee with a wedged insole, Clin Orthop Relat Res
emphasis on nonpharmacologic measures, Arch Fam Med (215):162–172, 1987.
4(12):1057–1064, 1995. 86. Andriacchi TP: Dynamics of knee malalignment, Orthop Clin
69. Felson DT, Lawrence RC, Hochberg MC, et al: Osteoarthritis: North Am 25(3):395–403, 1994.
New insights. Part 2: Treatment approaches, Ann Intern Med 87. Finger S, Paulos LE: Clinical and biomechanical evaluation of the
133(9):726–737, 2000. unloading brace, J Knee Surg 15(3):155–158; discussion 159,
70. Hurley MV, Scott DL: Improvements in quadriceps sensorimo- 2002.
tor function and disability of patients with knee osteoarthritis 88. Lindenfeld TN, Hewett TE, Andriacchi TP: Joint loading with
following a clinically practicable exercise regime, Br J Rheumatol valgus bracing in patients with varus gonarthrosis, Clin Orthop
37(11):1181–1187, 1998. Relat Res (344):290–297, 1997.
71. Fisher NM, Pendergast DR, Gresham GE, Calkins E: Muscle 89. Pollo FE, Otis JC, Backus SI, et al: Reduction of medial com-
rehabilitation: Its effect on muscular and functional performance partment loads with valgus bracing of the osteoarthritic knee,
of patients with knee osteoarthritis, Arch Phys Med Rehabil Am J Sports Med 30(3):414–421, 2002.
72(6):367–374, 1991. 90. Self BP, Greenwald RM, Pflaster DS: A biomechanical analysis of
72. O’Reilly SC, Muir KR, Doherty M: Effectiveness of home exer- a medial unloading brace for osteoarthritis in the knee, Arthritis
cise on pain and disability from osteoarthritis of the knee: A Care Res 13(4):191–197, 2000.
randomised controlled trial, Ann Rheum Dis 58(1):15–19, 91. Ramsey DK, Briem K, Axe MJ, Snyder-Mackler L: A mechanical
1999. theory for the effectiveness of bracing for medial compartment
73. Bennell KL, Hinman RS, Metcalf BR, et al: Efficacy of physio- osteoarthritis of the knee, J Bone Joint Surg Am 89(11):
therapy management of knee joint osteoarthritis: A randomised, 2398–2407, 2007.
double blind, placebo controlled trial, Ann Rheum Dis 64(6): 92. Nakajima K, Kakihana W, Nakagawa T, et al: Addition of an arch
906–912, 2005. support improves the biomechanical effect of a laterally wedged
74. Fransen M, McConnell S, Bell M: Exercise for osteoarthritis of insole, Gait Posture 29(2):208–213, 2009.
the hip or knee, Cochrane Database Syst Rev (3):CD004286, 93. Kuroyanagi Y, Nagura T, Matsumoto H, et al: The lateral
2003. wedged insole with subtalar strapping significantly reduces
75. Devos-Comby L, Cronan T, Roesch SC: Do exercise and self- dynamic knee load in the medial compartment gait analysis on
management interventions benefit patients with osteoarthritis of patients with medial knee osteoarthritis, Osteoarthritis Cartilage
the knee? A metaanalytic review, J Rheumatol 33(4):744–756, 15(8):932–936, 2007.
2006. 94. Kerrigan DC, Lelas JL, Goggins J, et al: Effectiveness of a lateral-
76. Roddy E, Zhang W, Doherty M, et al: Evidence-based recommen- wedge insole on knee varus torque in patients with knee osteoar-
dations for the role of exercise in the management of osteoarthritis thritis, Arch Phys Med Rehabil 83(7):889–893, 2002.
726 SECTION IV • Special Populations and Epidemiology
95. Crenshaw SJ, Pollo FE, Calton EF: Effects of lateral-wedged 113. Quintana JM, Arostequi I, Escobar A, et al: Prevalence of knee
insoles on kinetics at the knee, Clin Orthop Relat Res (375): and hip osteoarthritis and the appropriateness of joint replace-
185–192, 2000. ment in an older population, Arch Intern Med 168(14):
96. Ogata K, Yasunaga M, Nomiyama H: The effect of wedged 1576–1584, 2008.
insoles on the thrust of osteoarthritic knees, Int Orthop 114. Felson DT, Zhang Y: An update on the epidemiology of knee
21(5):308–312, 1997. and hip osteoarthritis with a view to prevention, Arthritis Rheum
97. Butler RJ, Marchesi S, Royer T, Davis IS: The effect of a subject- 41(8):1343–1355, 1998.
specific amount of lateral wedge on knee mechanics in patients 115. Garstang SV, Stitik TP: Osteoarthritis: Epidemiology, risk
with medial knee osteoarthritis, J Orthop Res 25(9):1121–1127, factors, and pathophysiology, Am J Phys Med Rehabil 85
2007. (11 Suppl):S2–11; quiz S12–4, 2006.
98. Toda Y, Tsukimura N: Influence of concomitant heeled footwear 116. Lievense A, Bierma-Zeinstra S, Verhagen A, et al: Influence of
when wearing a lateral wedged insole for medial compartment work on the development of osteoarthritis of the hip: A system-
osteoarthritis of the knee, Osteoarthritis Cartilage 16(2): atic review, J Rheumatol 28(11):2520–2528, 2001.
244–253, 2008. 117. McAlindon TE, Wilson PW, Aliabadi P, et al: Level of physical
99. Brockmeier SF, Shaffer BS: Viscosupplementation therapy for activity and the risk of radiographic and symptomatic knee osteo-
osteoarthritis, Sports Med Arthrosc 14(3):155–162, 2006. arthritis in the elderly: The Framingham study, Am J Med
100. Dixon AS, Jacoby RK, Berry H, Hamilton EB: Clinical trial of 106(2):151–157, 1999.
intra-articular injection of sodium hyaluronate in patients with 118. Coggon D, Croft P, Kellingray S, et al: Occupational physical
osteoarthritis of the knee, Curr Med Res Opin 11(4):205–213, activities and osteoarthritis of the knee, Arthritis Rheum
1988. 43(7):1443–1449, 2000.
101. Puhl W, Bernau A, Greiling H, et al: Intra-articular sodium hyal- 119. Cooper C, Inskip H, Croft P, et al: Individual risk factors for hip
uronate in osteoarthritis of the knee: A multicenter, double-blind osteoarthritis: Obesity, hip injury, and physical activity, Am J
study, Osteoarthritis Cartilage 1(4):233–241, 1993. Epidemiol 147(6):516–522, 1998.
102. Dougados M, Nguyen M, Listrat V, Amor B: High molecular 120. Vossinakis IC, Georgiades G, Kafidas D, Hartofilakidis G: Unilat-
weight sodium hyaluronate (hyalectin) in osteoarthritis of the eral hip osteoarthritis: Can we predict the outcome of the other
knee: A 1 year placebo-controlled trial, Osteoarthritis Cartilage hip? Skeletal Radiol 37(10):911–916, 2008.
1(2):97–103, 1993. 121. Vingård E, Hogstedt C, Alfredsson L, et al: Coxarthrosis
103. Lohmander LS, Dalén N, Englund G, et al: Intra-articular hyal- and physical work load, Scand J Work Environ Health 17(2):
uronan injections in the treatment of osteoarthritis of the knee: 104–109, 1991.
A randomised, double blind, placebo controlled multicentre trial. 122. Vingård E, Alfredsson L, Malchau H: Osteoarthrosis of the hip
Hyaluronan Multicentre Trial Group, Ann Rheum Dis 55(7): in women and its relation to physical load at work and in the
424–431, 1996. home, Ann Rheum Dis 56(5):293–298, 1997.
104. Henderson EB, Smith EC, Pegley F, Blake DR: Intra-articular 123. Vingård E, Alfredsson L, Goldi I, Hogstedt C: Occupation and
injections of 750 kD hyaluronan in the treatment of osteoarthritis: osteoarthrosis of the hip and knee: A register-based cohort study,
A randomised single centre double-blind placebo-controlled trial Int J Epidemiol 20(4):1025–1031, 1991.
of 91 patients demonstrating lack of efficacy, Ann Rheum Dis 124. Maetzel A, Mäkelä M, Hawker G, Bombardier C: Osteoarthritis
53(8):529–534, 1994. of the hip and knee and mechanical occupational exposure—A
105. Dahlberg L, Lohmander LS, Ryd L: Intraarticular injections of systematic overview of the evidence, J Rheumatol 24(8):
hyaluronan in patients with cartilage abnormalities and knee pain. 1599–1607, 1997.
A one-year double-blind, placebo-controlled study, Arthritis 125. Croft P, Coggon D, Cruddas M, Cooper C: Osteoarthritis of the
Rheum 37(4):521–528, 1994. hip: An occupational disease in farmers, BMJ 304(6837):
106. Lo GH, LaValley M, McAlindon T, Felson DT: Intra-articular hy- 1269–1272, 1992.
aluronic acid in treatment of knee osteoarthritis: A meta-analysis, 126. Walker-Bone K, Palmer KT: Musculoskeletal disorders in farmers
JAMA 290(23):3115–3121, 2003. and farm workers, Occup Med (Lond) 52(8):441–450, 2002.
107. Wang CT, Lin J, Chang CJ, et al: Therapeutic effects of hyal- 127. Holmberg S, Stiernström EL, Thelin A, Svärdsudd K: Musculosk-
uronic acid on osteoarthritis of the knee. A meta-analysis eletal symptoms among farmers and non-farmers: A population-
of randomized controlled trials, J Bone Joint Surg Am 86(3): based study, Int J Occup Environ Health 8(4):339–345, 2002.
538–545, 2004. 128. Thelin A: Hip joint arthrosis: An occupational disorder among
108. Bellamy N, Campbell J, Robinson V, et al: Viscosupplementation farmers, Am J Ind Med 18(3):339–343, 1990.
for the treatment of osteoarthritis of the knee, Cochrane Database 129. Thelin A, Holmberg S: Hip osteoarthritis in a rural male
Syst Rev (2):CD005321, 2005. population: A prospective population-based register study, Am
109. Arrich J, Piribauer F, Mad P, et al: Intra-articular hyaluronic acid J Ind Med 50(8):604–607, 2007.
for the treatment of osteoarthritis of the knee: Systematic review 130. Thelin A, Jansson B, Jacobsson B, Ström H: Coxarthrosis and
and meta-analysis, CMAJ 172(8):1039–1043, 2005. farm work: A case-referent study, Am J Ind Med 32(5):497–501,
110. Jackson DW, Evans NA, Thomas BM: Accuracy of needle place- 1997.
ment into the intra-articular space of the knee, J Bone Joint Surg 131. Thelin A, Vingard E, Holmberg S: Osteoarthritis of the hip joint
Am 84(9):1522–1527, 2002. and farm work, Am J Ind Med 45(2):202–209, 2004.
111. Tepper S, Hochberg MC: Factors associated with hip 132. Lloyd-Roberts GC: The role of capsular changes in osteoarthritis
osteoarthritis: Data from the First National Health and of the hip joint, J Bone Joint Surg Br 35(4):627–642, 1953.
Nutrition Examination Survey (NHANES-I), Am J Epidemiol 133. Altman RD, Hochberg M, Murphy WA Jr, et al: Atlas of
37(10):1081–1088, 1993. individual radiographic features in osteoarthritis, Osteoarthritis
112. Altman R, Alarcón G, Appelrouth D, et al: The American Cartilage 3 Suppl A:3–70, 1995.
College of Rheumatology criteria for the classification and 134. Karachalios T, Karantanas AH, Malizos K: Hip osteoarthritis:
reporting of osteoarthritis of the hip, Arthritis Rheum 34(5): What the radiologist wants to know, Eur J Radiol 63(1):36–48,
505–514, 1991. 2007.
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 727
135. Steultjens MP, Dekker J, van Baar ME, et al: Muscle strength, 155. Siebold R, Lichtenberg S, Habermeyer P: Combination of
pain and disability in patients with osteoarthritis, Clin Rehabil microfracture and periostal-flap for the treatment of focal full
15(3):331–341, 2001. thickness articular cartilage lesions of the shoulder: A prospective
136. Rasch A, Byström AH, Dalen N, Berg HE: Reduced muscle study, Knee Surg Sports Traumatol Arthrosc 11(3):183–189,
radiological density, cross-sectional area, and strength of major 2003.
hip and knee muscles in 22 patients with hip osteoarthritis, Acta 156. McCarty LP, Cole BJ: Nonarthroplasty treatment of glenohu-
Orthop 78(4):505–510, 2007. meral cartilage lesions, Arthroscopy 21(9):1131–1142, 2005.
137. Arokoski MH, Arokoski JP, Haara M, et al: Hip muscle strength 157. Ruckstuhl H, de Bruin ED, Stussi E, Vanwanseele B: Post-
and muscle cross sectional area in men with and without hip traumatic glenohumeral cartilage lesions: A systematic review,
osteoarthritis, J Rheumatol 29(10):2185–2195, 2002. BMC Musculoskelet Disord 9:107, 2008.
138. Ganz R, Parvizi J, Beck M, et al: Femoroacetabular impinge- 158. Millett PJ, Gobezie R, Boykin RE: Shoulder osteoarthritis:
ment: A cause for osteoarthritis of the hip, Clin Orthop Relat Res Diagnosis and management, Am Fam Physician 78(5):605–611,
(417):112–120, 2003. 2008.
139. McCarthy JC, Noble PC, Schuck MR, et al: The Otto E Aufranc 159. Iannotti JP, Kwon YW: Management of persistent shoulder pain:
Award: The role of labral lesions to development of early degen- A treatment algorithm, Am J Orthop 34(12 Suppl):16–23, 2005.
erative hip disease, Clin Orthop Relat Res (393):25–37, 2001. 160. WIlliams MD, Edwards RB: Glenohumeral arthritis in the
140. McCarthy JC, Noble PC, Schuck MR, et al: The watershed labral athlete: Evaluation and algorithm for management, Op Tech
lesion: Its relationship to early arthritis of the hip, J Arthroplasty Sports Med 16:2–8, 2008.
16(8 Suppl 1):81–87, 2001. 161. Neer CS: Replacement arthroplasty for glenohumeral osteoar-
141. Hoeksma HL, Dekker J, Ronday HK, et al: Comparison of thritis, J Bone Joint Surg Am 56(1):1–13, 1974.
manual therapy and exercise therapy in osteoarthritis of the hip: 162. Walch G, Ascani C, Boulahia A, et al: Static posterior subluxation
A randomized clinical trial, Arthritis Rheum 51(5):722–729, of the humeral head: An unrecognized entity responsible for
2004. glenohumeral osteoarthritis in the young adult, J Shoulder Elbow
142. Arokoski MH, Haara M, Helminen HJ, Arokoski JP: Physical Surg 11(4):309–314, 2002.
function in men with and without hip osteoarthritis, Arch Phys 163. Buscayret F, Edwards TB, Szabo I, et al: Glenohumeral arthrosis
Med Rehabil 85(4):574–581, 2004. in anterior instability before and after surgical treatment:
143. Birrell F, Croft P, Cooper C, et al: Predicting radiographic hip Incidence and contributing factors, Am J Sports Med 32(5):
osteoarthritis from range of movement, Rheumatology (Oxford) 1165–1172, 2004.
40(5):506–512, 2001. 164. Hovelius L, BG Augustini, H. Fredin, et al: Primary anterior
144. MacDonald CW, Whitman JM, Cleland JA, et al: Clinical dislocation of the shoulder in young patients. A ten-year prospec-
outcomes following manual physical therapy and exercise for tive study, J Bone Joint Surg Am 78(11):1677–1684, 1996.
hip osteoarthritis: A case series, J Orthop Sports Phys Ther 165. Neer CS, Craig EV, Fukuda H: Cuff-tear arthropathy, J Bone
36(8):588–599, 2006. Joint Surg Am 65(9):1232–1244, 1983.
145. Rasch A, Dalen N, Berg HE: Test methods to detect hip and 166. Burbank KM, Stevenson JH, Czarnecki GR, Dorfman J: Chronic
knee muscle weakness and gait disturbance in patients with hip shoulder pain: Part II. Treatment, Am Fam Physician 77(4):
osteoarthritis, Arch Phys Med Rehabil 86(12):2371–2376, 2005. 493–497, 2008.
146. Marti B, Knobloch M, Tschopp A, et al: Is excessive running 167. Nowinski RJ, Schiffern SC, Burkhead WZ: Biological resurfacing
predictive of degenerative hip disease? Controlled study of of the glenoid: Longer term results and newer innovations,
former elite athletes, BMJ 299(6691):91–93, 1989. Semin Arthroplasty 16:274–280, 2005.
147. Vingård E, Alfredsson L, Goldie I, Hogstedt C: Sports and os- 168. Ball CM, Galatz LM, Yamaguchi K: Meniscal allograft interposi-
teoarthrosis of the hip. An epidemiologic study, Am J Sports Med tion arthroplasty for the arthritic shoulder: Description of a new
21(2):195–200, 1993. surgical technique, Tech Shoulder Elbow Surg 2:247–254, 2001.
148. Panush RS, Schmidt C, Caldwell JR, et al: Is running associated 169. Brislin KJ, Savoie FH, Field LD: Surgical treatment fo glenohu-
with degenerative joint disease? JAMA 255(9):1152–1154, meral arthritis in the young patient, Tech Shoulder Elbow Surg
1986. 5:165–169, 2004.
149. Konradsen L, Hansen EM, Sondergaard L: Long distance 170. Maffulli N, Kenward MG, Testa V, et al: Clinical diagnosis of
running and osteoarthrosis, Am J Sports Med 18(4):379–381, Achilles tendinopathy with tendinosis, Clin J Sport Med 13(1):
1990. 11–15, 2003.
150. Lane NE, Oehlert JW, Block DA, Fries LF: The relationship 171. Crossley KM, Thancanamootoo K, Metcalf BR, et al: Clinical
of running to osteoarthritis of the knee and hip and bone features of patellar tendinopathy and their implications for
mineral density of the lumbar spine: A 9 year longitudinal study, rehabilitation, J Orthop Res 25(9):1164–1175, 2007.
J Rheumatol 25(2):334–341, 1998. 172. Fredericson M, Moore W, Guillet M, Beaulieu C: High
151. Kettunen JA, Kujala UM, Kaprio J, Sarna S: Health of master hamstring tendinopathy in runners: Meeting the challenges of
track and field athletes: A 16-year follow-up study, Clin J Sport diagnosis, treatment, and rehabilitation, Phys Sports Med
Med 16(2):142–148, 2006. 33(5).32–43, 2005.
152. Kettunen JA, Kujala UM, Kaprio J, et al: Lower-limb function 173. Lequesne M, Mathieu P, Vuillemin-Bodaghi V, et al: Gluteal
among former elite male athletes, Am J Sports Med 29(1):2–8, tendinopathy in refractory greater trochanter pain syndrome:
2001. Diagnostic value of two clinical tests, Arthritis Rheum 59(2):
153. Matsen FA, Rockwood CA, Wirth MA, et al: Gleno-humeral 241–246, 2008.
arthritis and its management. In Rockwood CA, Matsen FA, 174. Lewis JS: Rotator cuff tendinopathy, Br J Sports Med 43(4):
Wirth MA, Lippitt SB, editors: The shoulder, Philadelphia, 2004, 236–241, 2009.
WB Saunders. 175. Bisset L, Paungmali A, Vicenzino B, Beller E: A systematic
154. Memel D, Francis K: The Disability Discrimination Act: an review and meta-analysis of clinical trials on physical interven-
opportunity more than a threat, Br J Gen Pract 50(461): tions for lateral epicondylalgia, Br J Sports Med 39(7):411–422;
950–951, 2000. discussion 422, 2005.
728 SECTION IV • Special Populations and Epidemiology
176. Maffulli N, Wong J, Almekinders LC: Types and epidemiology of 198. Stanish WD, Rubinovich RM, Curwin S: Eccentric exercise in
tendinopathy, Clin Sports Med 22(4):675–692, 2003. chronic tendinitis, Clin Orthop Relat Res (208):65–68, 1986.
177. Alfredson H, Lorentzon R: Intratendinous glutamate levels and 199. Alfredson H, Pietila T, Jonsson P, et al: Heavy-load eccentric calf
eccentric training in chronic Achilles tendinosis: A prospective muscle training for the treatment of chronic Achilles tendinosis,
study using microdialysis technique, Knee Surg Sports Traumatol Am J Sports Med 26(3):360–366, 1998.
Arthrosc 11(3):196–199, 2003. 200. Alfredson H, Cook J: A treatment algorithm for managing
178. Khan KM, Cook JL, Kannus P, et al: Time to abandon the Achilles tendinopathy: New treatment options, Br J Sports Med
“tendinitis” myth, BMJ 324(7338):626–627, 2002. 41(4):211–216, 2007.
179. Fredberg U: Tendinopathy—Tendinitis or tendinosis? The 201. Ohberg L, Lorentzon R, Alfredson H: Eccentric training in
question is still open, Scand J Med Sci Sports 14(4):270–272, patients with chronic Achilles tendinosis: Normalised tendon
2004. structure and decreased thickness at follow up, Br J Sports Med
180. Maffulli N, Khan KM, Puddu G: Overuse tendon conditions: 38(1):8–11, 2004
Time to change a confusing terminology, Arthroscopy 14(8): 202. Fahlström M, Jonsson P, Lorentzon R, Alfredson H: Chronic
840–843, 1998. Achilles tendon pain treated with eccentric calf-muscle training,
181. Puddu G, Ippolito E, Postacchini F: A classification of Achilles Knee Surg Sports Traumatol Arthrosc 11(5):327–333, 2003.
tendon disease, Am J Sports Med 4(4):145–150, 1976. 203. Maffulli N, Testa V, Capasso G: Similar histopathological picture
182. Schubert TE, Weidler C, Lerch K, et al: Achilles tendinosis is in males with Achilles and patellar tendinopathy, Med Sci Sports
associated with sprouting of substance P positive nerve fibres, Exerc 36(9):1470–1475, 2004.
Ann Rheum Dis 64(7):1083–1086, 2005. 204. Jonsson P, Alfredson H, Sunding K, et al: New regimen for
183. Rees JD, Wilson AM, Wolman RL: Current concepts in the man- eccentric calf-muscle training in patients with chronic insertional
agement of tendon disorders, Rheumatology (Oxford) 45(5): Achilles tendinopathy: Results of a pilot study, Br J Sports Med
508–521, 2006. 42(9):746–749, 2008.
184. Cook JL, Khan K M, Zoltan Z S, et al: Prospective imaging study 205. Silbernagel KG, Thomeé R, Eriksson BI, Karlsson J: Continued
of asymptomatic patellar tendinopathy in elite junior basketball sports activity, using a pain-monitoring model, during rehabilita-
players, J Ultrasound Med 19(7):473–479, 2000. tion in patients with Achilles tendinopathy: A randomized
185. Cook JL, Kiss ZS, Khan KM: Patellar tendinitis: The significance controlled study, Am J Sports Med 35(6):897–906, 2007.
of magnetic resonance imaging findings, Am J Sports Med 206. Purdam CR, Jonsson P, Alfredson H, et al: A pilot study of the
27(6):831, 1999. eccentric decline squat in the management of painful chronic
186. Major NM, Helms CA: MR imaging of the knee: Findings in patellar tendinopathy, Br J Sports Med 38(4):395–397, 2004.
asymptomatic collegiate basketball players, AJR Am J Roentgenol 207. Young MA, Cook JL, Purdam CR, et al: Eccentric decline squat
179(3):641–644, 2002. protocol offers superior results at 12 months compared with
187. Cook JL, Khan KM, Harcourt PR, et al: Patellar tendon ultraso- traditional eccentric protocol for patellar tendinopathy in volley-
nography in asymptomatic active athletes reveals hypoechoic ball players, Br J Sports Med 39(2):102–105, 2005.
regions: A study of 320 tendons. Victorian Institute of Sport 208. Jonsson P, Wahlström P, Öhberg L, Alfredson H: Eccentric train-
Tendon Study Group, Clin J Sport Med 8(2):73–77, 1998. ing in chronic painful impingement syndrome of the shoulder:
188. Cook JL, Khan KM, Kiss ZS, et al: Reproducibility and clinical Results of a pilot study, Knee Surg Sports Traumatol Arthrosc
utility of tendon palpation to detect patellar tendinopathy in 14(1):76–81, 2006.
young basketball players. Victorian Institute of Sport tendon 209. Cook J, Purdam CR: Is tendon pathology a continuum? A
study group, Br J Sports Med 35(1):65–69, 2001. pathology model to explain the clinical presentation of load-
189. Shalaby M, Almekinders LC: Patellar tendinitis: The significance induced tendinopathy, Br J Sports Med 43(6):409–416, 2009.
of magnetic resonance imaging findings, Am J Sports Med 210. Assendelft W, Green S, Buchbinder R, et al: Tennis elbow, Clin
27(3):345–349, 1999. Evid (11):1633–1644, 2004.
190. Almekinders LC, Weinhold PS, Maffulli N: Compression etiol- 211. Assendelft WJ, Hay EM, Adshead R, Bouter LM: Corticosteroid
ogy in tendinopathy, Clin Sports Med 22(4):703–710, 2003. injections for lateral epicondylitis: A systematic overview, Br J
191. Bey MJ, Ramsey ML, Soslowsky LJ: Intratendinous strain fields of Gen Pract 46(405):209–216, 1996.
the supraspinatus tendon: Effect of a surgically created articular- 212. Clark SC, Jones MW, Choudhury RR, Smith E: Bilateral patellar
surface rotator cuff tear, J Shoulder Elbow Surg 11(6):562–569, tendon rupture secondary to repeated local steroid injections,
2002. J Accid Emerg Med 12(4):300–301, 1995.
192. Brosseau L, Casimiro L, Milne S, et al: Deep transverse friction 213. Lambert MI, St Clair Gibson A, Noakes TD: Rupture of the
massage for treating tendinitis, Cochrane Database Syst Rev triceps tendon associated with steroid injections, Am J Sports Med
(4):CD003528, 2002. 23(6):778, 1995.
193. Melham TJ, Sevier TL, Malnofski MJ, et al: Chronic ankle pain 214. Jones JG: Achilles tendon rupture following steroid injection,
and fibrosis successfully treated with a new noninvasive J Bone Joint Surg Am 67(1):170, 1985.
augmented soft tissue mobilization technique (ASTM): A case 215. Kleinman M, Gross AE: Achilles tendon rupture following
report, Med Sci Sports Exerc 30(6):801–804, 1998. steroid injection. Report of three cases, J Bone Joint Surg Am
194. Sevier TL, Wilson JK: Treating lateral epicondylitis, Sports Med 65(9):1345–1347, 1983.
28(5):375–380, 1999. 216. Scarpone M, Rabago DP, Zgierska A, et al: The efficacy of
195. Davidson CJ, Ganion LR, Gehlsen GM, et al: Rat tendon prolotherapy for lateral epicondylosis: A pilot study, Clin J Sport
morphologic and functional changes resulting from soft tissue Med 18(3):248–254, 2008.
mobilization, Med Sci Sports Exerc 29(3):313–319, 1997. 217. Fullerton BD: High-resolution ultrasound and magnetic reso-
196. Gehlsen GM, Ganion LR, Helfst R: Fibroblast responses to nance imaging to document tissue repair after prolotherapy: A
variation in soft tissue mobilization pressure, Med Sci Sports Exerc report of 3 cases, Arch Phys Med Rehabil 89(2):377–385, 2008.
31(4):531–535, 1999. 218. Rabago D, Best TM, Beamsley M, Patterson J: A systematic
197. Nirschl RP: The etiology and treatment of tennis elbow, J Sports review of prolotherapy for chronic musculoskeletal pain, Clin J
Med 2(6):308–323, 1974. Sport Med 15(5):376–380, 2005.
Selected Rehabilitation Needs of the Masters Athlete • CHAPTER 29 729
219. Willberg L, Sunding K, Ohberg L, et al: Sclerosing injections to 238. Schmalzried TP, Callaghan JJ: Wear in total hip and knee replace-
treat midportion Achilles tendinosis: A randomised controlled ments, J Bone Joint Surg Am 81(1):115–136, 1999.
study evaluating two different concentrations of Polidocanol, 239. Kuster MS: Exercise recommendations after total joint
Knee Surg Sports Traumatol Arthrosc 16(9):859–864, 2008. replacement: A review of the current literature and proposal of
220. Alfredson H, Ohberg L, Zeisig E, Lorentzon R: Treatment of scientifically based guidelines, Sports Med 32(7):433–445,
midportion Achilles tendinosis: Similar clinical results with US 2002.
and CD-guided surgery outside the tendon and sclerosing poli- 240. Kuster MS, Stachowiak GW: Factors affecting polyethylene wear
docanol injections, Knee Surg Sports Traumatol Arthrosc in total knee arthroplasty, Orthopedics 25(2 Suppl):S235–S242,
15(12):1504–1509, 2007. 2002.
221. Zeisig E, Ohberg L, Alfredson H: Sclerosing polidocanol injec- 241. Clifford PE, Mallon WJ: Sports after total joint replacement,
tions in chronic painful tennis elbow-promising results in a pilot Clin Sports Med 24(1):175–186, 2005.
study, Knee Surg Sports Traumatol Arthrosc 14(11):1218–1224, 242. McGrory BJ, Stuart MJ, Sim FH: Participation in sports after hip
2006. and knee arthroplasty: Review of literature and survey of surgeon
222. Hoksrud A, Ohberg L, Alfredson H, et al: Ultrasound-guided preferences, Mayo Clin Proc 70(4):342–348, 1995.
sclerosis of neovessels in painful chronic patellar tendinopathy: 243. Healy WL, Iorio R, Lemos MJ: Athletic activity after joint
A randomized controlled trial, Am J Sports Med 34(11): replacement, Am J Sports Med 29(3):377–388, 2001.
1738–1746, 2006. 244. Mallon WJ, Liebelt RA, Mason JB: Total joint replacement and
223. Moon YL, Jo SH, Song CH, et al: Autologous bone marrow golf, Clin Sports Med 15(1):179–190, 1996.
plasma injection after arthroscopic debridement for elbow tendi- 245. Mallon WJ, Callaghan JJ: Total joint replacement in active
nosis, Ann Acad Med Singapore 37(7):559–563, 2008. golfers, J South Orthop Assoc 3(4):295–298, 1994.
224. James SL, Ali K, Pocock C, et al: Ultrasound guided dry needling 246. Mallon WJ, Callaghan JJ: Total knee arthroplasty in active
and autologous blood injection for patellar tendinosis, Br J Sports golfers, J Arthroplasty 8(3):299–306, 1993.
Med 41(8):518–521; discussion 22, 2007. 247. Mallon WJ, Callaghan JJ: Total hip arthroplasty in active golfers,
225. Suresh SP, Ali KE, Jones H, Connell DA: Medial epicondylitis: J Arthroplasty 7 Suppl:339–346, 1992.
is ultrasound guided autologous blood injection an effective 248. Diduch DR, Insall JN, Scott WN, et al: Total knee replacement
treatment? Br J Sports Med 40(11):935–939; discussion 9, 2006. in young, active patients. Long-term follow-up and functional
226. Mishra A, Pavelko T: Treatment of chronic elbow tendinosis outcome, J Bone Joint Surg Am 79(4):575–582, 1997.
with buffered platelet-rich plasma, Am J Sports Med 34(11): 249. Fortin PR, Clarke AE, Joseph L, et al: Outcomes of total hip and
1774–1778, 2006. knee replacement: Preoperative functional status predicts
227. Rabago D, Best TM, Zgierska A, et al: A systematic review of outcomes at six months after surgery, Arthritis Rheum 42(8):
four injection therapies for lateral epicondylosis: Prolotherapy, 1722–1728, 1999.
polidocanol, whole blood and platelet rich plasma, Br J Sports 250. Nicholls MA, Selby JB, Hartford JM: Athletic activity after total
Med 43(7):471–481, 2009. joint replacement, Orthopedics 25(11):1283–1287, 2002.
228. Paoloni JA, Murrell GA, Burch R, et al: Randomised, double 251. Mitchell K, Banks S, Morgan D, Sugaya H: Shoulder motions
blind, placebo controlled, multicentre dose-ranging clinical trial during the golf swing in male amateur golfers, J Orthop Sports
of a new topical glyceryl trinitrate patch for chronic lateral Phys Ther 33(4):196–203, 2003.
epicondylosis, Br J Sports Med 43(4):299–302, 2009. 252. Wilcox RB, Arslanian LE, Millett P: Rehabilitation following
229. Paoloni JA, Murrell GA: Three-year followup study of topical total shoulder arthroplasty, J Orthop Sports Phys Ther 35(12):
glyceryl trinitrate treatment of chronic noninsertional Achilles 821–836, 2005.
tendinopathy, Foot Ankle Int 28(10):1064–1068, 2007. 253. Jensen KL, Rockwood CA: Shoulder arthroplasty in recreational
230. Paoloni JA, Appleyard RC, Nelson J, Murrell GA: Topical golfers, J Shoulder Elbow Surg 7(4):362–367, 1998.
glyceryl trinitrate application in the treatment of chronic supra- 254. Schmidt-Wiethoff R, Rapp W, Mauch F, et al: Shoulder rotation
spinatus tendinopathy: A randomized, double-blinded, placebo- characteristics in professional tennis players, Int J Sports Med
controlled clinical trial, Am J Sports Med 33(6):806–813, 2005. 25(2):154–158, 2004.
231. Paoloni JA, Appleyard RC, Nelson J, Murrell GAC: Topical 255. Meister K: Injuries to the shoulder in the throwing athlete. Part
glyceryl trinitrate treatment of chronic noninsertional achilles one: Biomechanics/pathophysiology/classification of injury, Am
tendinopathy. A randomized, double-blind, placebo-controlled J Sports Med 28(2):265–275, 2000.
trial, J Bone Joint Surg Am 86(5):916–922, 2004. 256. McGuire MR, Kyle RF, Gustilo RB, Premer RF: Comparative
232. Chandler HP, Reineck FT, Wixson RL, McCarthy JC: Total hip analysis of ankle arthroplasty versus ankle arthrodesis, Clin
replacement in patients younger than thirty years old. A five-year Orthop Relat Res (226):174–181, 1988.
follow-up study, J Bone Joint Surg Am 63(9):1426–1434, 1981. 257. Kitaoka HB, Patzer GL, Ilstrup DM, Wallrichs SL: Survivorship
233. Kilgus DJ, Dorey FJ, Finerman GAM, Amstutz HC: Patient analysis of the Mayo total ankle arthroplasty, J Bone Joint Surg
activity, sports participation, and impact loading on the durability Am 76(7):974–979, 1994.
of cemented total hip replacements, Clin Orthop Relat Res 258. Kofoed H, Sorensen TS: Ankle arthroplasty for rheumatoid
(269):25–31, 1991. arthritis and osteoarthritis: Prospective long-term study of
234. Bradbury N, Borton D, Spoo G, Cross MJ: Participation cemented replacements, J Bone Joint Surg Br 80(2):328–332,
in sports after total knee replacement, Am J Sports Med 26(4): 1998.
530–535, 1998. 259. Wood PL, Deakin S: Total ankle replacement. The results in
235. Mont MA, LaPorte DM, Mullick T, et al: Tennis after total hip 200 ankles, J Bone Joint Surg Br 85(3):334–341, 2003.
arthroplasty, Am J Sports Med 27(1):60–64, 1999. 260. Anderson T, Montgomery F, Carlsson A: Uncemented STAR total
236. Ries MD, Philbin EF, Groff GD, et al: Effect of total hip arthro- ankle prostheses. Three to eight-year follow-up of fifty-one con-
plasty on cardiovascular fitness, J Arthroplasty 12(1):84–90, 1997. secutive ankles, J Bone Joint Surg Am 85(7):1321–1329, 2003.
237. Ries MD, Philbin EF, Groff GD, et al: Improvement in cardio- 261. Valderrabano V, Pagenstert G, Horisberger M, et al: Sports and
vascular fitness after total knee arthroplasty, J Bone Joint Surg Am recreation activity of ankle arthritis patients before and after total
78(11):1696–1701, 1996. ankle replacement, Am J Sports Med 34(6):993–999, 2006.
30
CHAPTER
730
Applied Sports Injury Epidemiology • CHAPTER 30 731
Case Series
Study Designs Often the most direct way to obtain information on sports-
The science of epidemiology is devoted to the study of related injuries is to get lists of people who have been
health conditions in human populations. To understand injured. These lists can come from such places as clinics,
these processes, most of which occur outside the laboratory medical sites, and schools. From these lists, it is also possible
setting, a series of study designs and related statistics have to collect additional information on the injury event, its
been developed. Sports injuries are an excellent example of severity, the tasks surrounding the event, use of protective
the type of diseases or conditions that epidemiologists gear if any, and other elements to further describe the
study. To understand and interpret data on sports injuries, injured population. However, without uninjured people for
a basic understanding of study design and related terms is comparison, there is no way to identify risk factors for
necessary. There are two basic types of study designs: injury. Case series are useful for getting an idea of the scope
descriptive and analytical. Descriptive studies (i.e., case-series of the problem. For example, if there are no tibial stress
Table 30-1
Types of Study Designs
Study Design Uses Population
fractures during a year of clinic visits, then it is not feasible are usually relatively cheap to conduct because there is no
to design a study to look at risk factors for tibial stress frac- waiting time for an injury to occur. The downside of this
tures in this population. However, if there were 2 tibial efficiency is that the researchers have to find a way to docu-
stress fractures in 1 year and 24 tibial stress fractures in the ment retrospectively the potential risk factors, such as play-
next year, without denominator data one has no way of ing time. It is also not possible to obtain rates of injury or
knowing whether this is even an important increase. If one to assess severity of injury with this type of study design.
can estimate a denominator and determine that this repre- The particular outcome (in this case, degree of ACL injury)
sents an increase in tibial stress fractures, one still cannot must be clearly identified prior to conducting the study and
look for risk factors because one does not have an uninjured this may prove to be a limitation if the researchers decide
group for comparison. In summary, case series can often they want to study a slightly different outcome (such as any
help the clinician or researcher generate ideas for sports knee ligament injury) while the study is in progress. This
injury studies that need to be done and can help plan for design is only useful for studying risk factors that are not
care, but they are very limited in terms of their ability to affected by injury, such as genomics, or anatomical charac-
track trends or identify risk factors for prevention. teristics. If the injury changes the risk factor, this design
cannot be used.12 If the investigator is relying on self-
reported data, then recall bias is another problem with case-
Cross-Sectional control studies. Recall bias occurs if cases remember their
Studies that are conducted on a random sample of a target risk factor data with greater clarity than controls.
population provide valuable information on the prevalence The most fundamental point concerning case-control
of (or percentage of the target population currently studies is that controls serve as a sample from the population
experiencing) certain diseases, conditions, or risk factors. A in which the cases occurred. The control and the case groups
cross-sectional study on concussions, for example, can be should come from the same core “source population.” They
conducted on a target population of high school athletes.10 should not be two random groups of patients who have no
If information is requested of all high school athletes (both logical relationship to one another. This simple rule is often
injured and uninjured), then there is a denominator to use ignored. The first step in designing a case-control study is to
to calculate the number of concussions that have occurred. identify the source population from which the cases arose.
In time, the rates of concussions can be calculated from This could be all basketball or soccer players in a geograph-
multiple cross-sectional studies to observe trends. This can ical area, for example. Then work out how to draw a sample
be useful information to determine if there are unusual from this population—for example, from team members
increases in concussions, but cross-sectional studies have or lists of league members. These are the controls. If the
limited ability to identify risk factors for concussion injuries investigator cannot identify the core source population of
because all of the information on injuries and behaviors or the cases, perhaps another type of study design should be
equipment use is collected at the same time. Therefore, considered.
there is no way to know which came first—the risk factor
(not wearing protective gear) or the injury (which gener-
ated a need to wear protective gear). Other study designs Clinical Point
are used to assess risk factors. For case control studies, the case group and control group must
come from the same core “source population.”
Case-Control
One example of a study design that can be used to assess
risk factors is the case-control study. In this design, cases Case-Crossover
(for example, injured athletes) are selected, and then com- In certain situations, it is possible for a case to serve as its
parable controls (uninjured athletes) are selected so that the own control, thus eliminating potential biases (such as
two groups can be compared on possible risk factors. For recall) inherent in traditional case-control studies. With this
example, one may be interested in studying female high type of study, it is possible to assess whether the injury was
school athletes who incurred or did not incur an anterior preceded by something that happened immediately prior to
cruciate ligament (ACL) injury during a basketball or soc- the injury. The injured person would be assessed for devia-
cer game.11 For each person with an ACL injury (a case), tions from usual activity in a period at some point prior to
another soccer or basketball player without an ACL injury the injury. Because each person serves as his or her own
would be selected as a “control.” Then potential risk factors control, the problems of finding an appropriate control
could be explored. For example, did hamstrings or quadri- group are not present. For certain acute injuries, this is a
ceps muscle strength vary among cases and controls? There very strong design that maximizes efficiency. It is well-
are many advantages of the case-control design. These studies suited for studying transient factors that have an immediate
Applied Sports Injury Epidemiology • CHAPTER 30 733
or near-immediate effect on injury, for example, fatigue or helmets compared with athletes with the standard head
hormonal factors. gear. In practice, it is often easier to randomize at the level
of the team or school, rather than to randomize individuals.
This is called cluster-randomization, and it does decrease
Prospective Cohort the statistical power of the study, further increasing the
One of the strongest study designs for assessing risk factors need for large numbers of athletes to be studied.
is the prospective cohort study. In this design, a healthy An RCT study designed by Gilchrist and colleagues14 to
group of athletes is followed for a period of time (usually a prevent ACL injury in women collegiate soccer players
season or until an injury occurs). Baseline information can illustrates the power of this study design. In this study,
include potential risk factors and, at follow-up, comparisons National Collegiate Athletic Association (NCAA) division I
can be made to see if the injury risk is similar among ath- women’s soccer teams were randomly assigned to a treat-
letes with different initial exposures. For example, to study ment or control group. The treatment group participated in
the effect of a particular type of helmet on the occurrence a program that included stretching and strengthening
of concussions among college athletes, a prospective cohort activities three times a week during the season while the
study could follow two groups of athletes during the control group did their usual activities. This study was able
season: those who wore the special helmet and those who to document a reduction in ACL injuries occurring during
wore the traditional helmet. Then the rate of new concus- practice and games throughout the 2002 season. In spite of
sions in each helmet group could be compared, thus mak- the strength of these types of studies, which are considered
ing some conclusions about the efficacy of the new helmet the gold standard of study designs, they are often difficult
in preventing or reducing concussion injuries. The key char- to carry out in practice. First of all, the random assignment
acteristic of this type of study is that the risk factor (in this is difficult to achieve. For studies assessing types of equip-
case helmet use) is identified prior to the injury (in this case ment, for example, it is difficult to randomly assign special
concussion).13 Although this type of study is very powerful equipment to an individual because players on the same
in its ability to identify potential risk factors, evaluate the team have different equipment (and it may be difficult to
performance of interventions, and identify the incidence ensure that everyone wears the assigned equipment). As
(new cases) of an injury, it is also very costly because it re- mentioned previously, if randomization is done on a team
quires a large sample size and a period of follow-up time or school level, then a much larger sample size is needed
before an injury occurs. For a relatively rare injury (such as because the unit of measurement becomes the team or
concussion), thousands of athletes need to be followed to school rather than the subject. This leads to a more complex
have a sufficient sample size to attain statistical power. Thus, statistical analysis plan. Finally, if the intervention is a knee
for injuries with a low rate of incidence, a case-control study brace or a training program, it is often difficult or impossi-
might be more feasible. ble to blind subjects and study staff as to which athletes are
in the treatment group and which are in the control group.
Thus, double-blind RCTs are rare in sports medicine.
In summary, there are several types of study designs, each
with specific advantages and disadvantages (Table 30-2).
Clinical Point
The time factor may be an important consideration in con-
The key feature and strength of the prospective cohort study, as ducting a specific study and in understanding one that has
compared with other observational epidemiological designs, is that been conducted (Figure 30-1). For example, case series
the risk factor is identified prior to the injury. studies are collected in the present and use records that are
available for other purposes, which makes data collection
very time efficient. However, without a control group only
limited inferences can be drawn. A cross-sectional study
includes those with and without injury, but because all data
Randomized Control Trial are collected in the present, it is possible to look for associa-
An RCT is a special case of the prospective study that tions within the sample but not to identify risk factors. Case-
randomly assigns healthy subjects to a “treatment” or control and case-crossover studies provide a comparison
“control” group. For example, to assess the benefits of group, but the temporal sequence of the risk factor and the
wearing a special protective helmet among college football outcome (injury) may be harder to identify. The prospective
players, randomly selected athletes would wear these special cohort and the randomized clinical trial study designs are
helmets while other athletes would wear traditional head the most powerful studies from which to draw inferences
gear. If all other factors were the same (e.g., playing time, about cause and effect (risk factors), but these are also the
other equipment), then one would expect the rate of con- most difficult to conduct and can be quite expensive and
cussions to be lower among the athletes with the special take a long time to complete.
734 SECTION IV • Special Populations and Epidemiology
Table 30-2
Advantages and Disadvantages of Various Study Designs
Study Design Advantages Disadvantages
Case Cohort
Control Study
Prevalence, itself, cannot directly tell one anything about Given the huge variations in the definitions of injury used,
how frequently new cases occur in the population. How- it is not surprising that the injury rates reported by these stud-
ever, if one knows the average healing time, then one can ies also vary widely. Note that the variation in injury rates is
deduce something about incidence. due to more than just the variations in injury definitions. It is
To define incidence and prevalence, one needs a clear also due to differences in the methods used to collect the
and unambiguous injury definition and some denominator injury data, and to underlying differences in the real incidence
data on the athletes being monitored. For injury preva- of injury in the different populations under study.
lence, injury risk, and injury odds, this means some simple There is no obvious solution to the problem of injury
way of determining the size of the population at risk (such definitions that vary between studies. Definitions that
as a team roster). For injury rate, this means some mecha- involve access to health care are plagued by the problem
nism for tracking the number of team sessions (e.g., games that different populations have widely differing levels of
and practices) for the athletes being monitored. access to health care. Most NCAA Division I teams, for
Earlier, the importance of having a study design that is example, have ready access to clinical services through the
appropriate for the research question that a study is address- provision of certified athletic trainers (ATCs), whereas
ing was stressed. However, even if the study design is many high schools and recreational club athletes have very
correct, additional problems can occur. Two particularly limited access to on-site services. Definitions that involve
important areas in sports injury epidemiology are the time lost from the sport are even more problematic. A
study’s injury definition, and the collection of denominator sprained ankle that is a debilitating injury for a track athlete
data on exposure to athletic participation. Methodological might only be a mild inconvenience in crew (rowing).
errors in either of these areas can result in serious flaws in a Furthermore, chronic injuries such as low back pain or
study. The next two subsections discuss these important bone stress reactions may cause considerable distress for the
areas in more detail. athlete without resulting in any time lost from the sport.
There are profound differences in physiological and psycho-
logical make-up between athletes—some athletes might be
Injury Definition able to play with an injury that would be debilitating to
Injury definition refers to the criteria used to include an another athlete. There are wide variations in clinician man-
injury in the study. An injury definition should be clear and agement of some injuries. For example, two concussions
unambiguous. A wide range of injury definitions have been that have identical severity and presentation might be
used in the literature. Most injury definitions involve some managed very differently by different clinicians. One might
minimal criteria for time lost from participation in the sport. become a lost-time injury and the other might not.
For example, a researcher might decide to include only
those injuries that caused the athlete to miss at least a week
of participation. Injury definitions also often involve some
Clinical Point
minimal criteria for clinical attention, such as requiring a
physician’s assessment. Some studies use different criteria An explicit and clear injury definition should be reported in every
for different injuries. The North Carolina High School study.
Athletic Injury Study, for example, defined an injury as
“a result of participation in a high school sport that either
limited the student’s full participation in the sport the day
following the injury or required medical attention by a In summary, the best possible recommendation is simply
health care professional (i.e., athletic trainer, physician, that every study should have an explicit and clear injury
nurse, emergency medical technician, emergency room per- definition and that the injury definition should be reported
sonnel, or dentist).”16 In addition, all fractures, concus- in all publications from the study data. If the goals of the
sions, and eye injuries were included because the researchers study are broad-based injury surveillance, it is highly prefer-
considered those injuries to be serious. able to provide a qualified primary data collector, such as an
The fact that there is no standard, universal definition of ATC, at the data site, if one does not already exist. It is also
injury makes it exceedingly difficult to compare different preferable to capture all injuries that require evaluation, not
studies. As an example, Table 30-3 lists a sequence of rugby just those that result in lost time.
injury studies from the 1980s and 1990s.17-26 As can be
seen, the definition of injury used in these studies varied
widely, and included criteria such as (1) prevented play for Denominator Data
any period, (2) required any health care, (3) prevented play In general, regardless of how good the injury data is, it is
for any period or required any health care, (4) prevented meaningless unless some denominator data is also collected.
play 7 days or more, and (5) prevented play 7 days or more At a minimum, the denominator should at least quantify the
and required health care. number of athletes in the population under study. However,
Applied Sports Injury Epidemiology • CHAPTER 30 737
Table 30-3
Studies of Injury in Rugby Showing Effect of Variations in Study Methodology
Definition Data Collection No. of Rate per 100
Study Year Country Population of Injury Method Injuries Player-Years
Nathan et al.17 1983 South Africa High school boys Prevented play Interview players 79 16.99
7 days who missed games
Sugerman18 1983 Australia High school boys Prevented play Teacher and coach 258 114.67
or school report
Roux et al.19 1987 South Africa High school boys Prevented play Teacher and coach 495 10.31
7 days and all report; some
concussion personal visits
Davidson20 1987 Australia High school boys Required medical School physician or 1444 10.56
care nurse in central
location
Clark et al.21 1990 South Africa Adult men Prevented play Self-administered 114 95.00
7 days or form; contact at
medical care club
Dalley et al.22 1992 New Zealand Mixed age and Required medical Club and team 921 8.37
gender care contacts
Hughes and 1994 Australia Adult men Prevented play or Team trainer 133 110.83
Fricker23 required medical
care
Garraway and 1995 Scotland Adult men Prevented play Club contact; 358 29.44
Macleod24 volunteer observers
Lee and 1996 Scotland High school boys Prevented play School contact 210 12.32
Garraway25
Bird et al.26 1998 New Zealand Mixed age and Prevented play or Weekly telephone 569 159.83
gender required medical follow-up of all
care players
detailed denominator data collection can become exceed- that epidemiologists refer to as “person-time.” Thus,
ingly time-consuming. Fortunately, denominator data can although athlete-exposures is typically presented as counts, it
often be approximated (or estimated) from pre-existing is in fact conceptually measured in units of time. Some
sources of information, such as team rosters and practice researchers go the extra step of multiplying the count of
schedules. athlete-exposures by the average number of minutes per
An important point about the denominator is that injury exposure; however, this is an approximation of the true
risk and injury odds only require simple head counts of the athlete-time. Only in a very few settings—for example, in
number of athletes under observation and the definition of professional basketball27—can participation truly be tracked
the length of the monitoring (or follow-up period). Injury at the individual level in terms of minutes and seconds. Thus,
rate, on the other hand, requires a much more detailed athlete-exposures has become the “industry standard,”
accounting of the number of games and practices in which despite the fact that important methodological details of its
the athletes participate. Despite this considerable obstacle, estimation remain underdeveloped (see discussion later in
most researchers prefer injury rate to injury risk because this chapter).
injury rate has the ability to account for differences between
athletes in their denominator, and allows the researcher to
identify risk factors and compare sports in a manner that is
Clinical Point
scientifically more rigorous.
The most common type of denominator used in injury Athlete-exposures is the preferred denominator to help increase
rate studies is “athlete-exposures.” Athlete-exposures is com- comparisons of injury rates across sport studies. Comparisons of
puted by summing up the total number of athletes who risks across sports often use athletes (rather than athlete-exposures)
participated in every game and every practice during the in the denominator. Although use of risks is rare in the literature, they
monitoring or follow-up period. Although it is not immedi- are important and their use should be encouraged.
ately obvious, athlete-exposures is a type of measurement
738 SECTION IV • Special Populations and Epidemiology
To date, most studies have attempted to do the best pos- Table 30-4 presents two example calculations of injury
sible job of collecting denominators with the limited risk, injury odds, and injury rate. The data (originally pre-
resources available. However, collecting denominator data sented by Knowles and colleagues15) are taken from two
is a thankless task and the sports injury epidemiology field real high school teams enrolled in the North Carolina High
is distinguished by a lack of creativity or originality to the School Athletic Injury Study: a football team and a volley-
issue of denominator data collection. Much denominator ball team. On the football team, 22 of the 36 athletes were
data is probably not as accurate as the researchers would injured; therefore, the injury risk for this season was 22 of
have liked. In general, there is a desperate need for method- 36, or 61%. Thus, the average risk of injury on this team in
ological research to streamline the collection of denomina- this season was 61%. Put another way, the probability of
tor data without sacrificing data quality. being injured in this season playing football at this school
was 0.61 or just over 6 out of 10.
It is very important that the period for which the
Injury Risk and Injury Odds athletes are followed is specified, because a 10-season
Injury risk is the number of injured athletes divided by the risk is obviously going to be much larger than a 1-season
total number of athletes. The unit of analysis is the athlete. risk. The way to report injury risk is to always state
Athletes who have multiple injuries are counted only once in the monitoring period, for example, “the risk of injury
the numerator of injury risk. Risk is the same as probability, in a season of football is 61%.” One should never state
and therefore risk must always be a positive number and can “the injury risk was 61%” without also specifying the
never exceed 1. period.
Table 30-4
Comparing the Three Measures of Injury Incidence (Risk, Odds, and Rate)
Football Volleyball
(One Season for One High (One Season for One High Football Team vs.
School Team) School Team) Volleyball Team Comment
Athletes 36 17
Injuries 44 5
Injured 22 (Two injuries per injured athlete) 5 (one injury per injured athlete)
athletes
Athlete- 3,860 (107 exposures per athlete) 741 (44 exposures per athlete)
exposures
The average odds of being injured The average odds of being Footballers have nearly Tracks close to
in a football season is 1.6 to 1 injured in a volleyball season is four times greater the risk ratio if
(approximately 3:2). approximately 0.4 to 1 odds of injury, per risk is 10% or
(approximately 1:2). season, relative to less; otherwise
volleyballers. useless
Injury 44 5 Rate ratio 1.7
11.3 per 1,000 athlete-exposures 6.8 per 1000 athlete-exposures
rate 3860 741
The average rate of injury on the The average rate of injury on the Footballers have Useful for
football team is 11.3 per 1000 volleyball team is 6.8 per 1000 nearly twice the rate scientists
athlete-exposures. athlete-exposures. of injury, per game
or practice, relative
to volleyballers.
Applied Sports Injury Epidemiology • CHAPTER 30 739
To compute a 95% confidence interval (CI) for injury In Table 30-4, note that there are 44 injuries on
risk in this study, take 0.611 and add and subtract 1.96 the football team, and 3860 athlete-exposures during the
0.08125. Then multiply by 100 to get 45% and 77%. Where follow-up period. Therefore, the injury rate per 1000 athlete-
do these numbers come from? The 1.96 is a standard mul- exposures is:
tiplier used to compute 95% CIs and it is taken from the
44
bell-shaped normal curve. The 0.08125 is called the 1000 11.3
3860
standard error of injury risk and is computed as:
The choice of multiplier - 1000 - is arbitrary. Its purpose
0.611 (10.611) is simply to make the result more readable. To compute a
36 95% CI for the injury rate, one simply divides 44 by 3860
in which 36 is the number of athletes on the team (the de- to get 0.0113, and then adds and subtracts 1.96
nominator of injury risk). The scientific interpretation of this 0.001718 to get 0.0079 and 0.0147, and multiply both
interval is that if the study was repeated 100 times, and 100 numbers by 1000. The resulting 95% CI is 7.9 to 14.7.
estimated injury risks were computed, 95% of them would As with injury risk, the interpretation of this interval is that
contain the true (unobservable) injury risk. When communi- if the study was repeated 100 times, and 100 injury rates
cating with nonscientists, it is sufficient to point out that the were computed, 95% of them would contain the true
estimate of 61% is subject to statistical error and state that (unobservable) injury rate. More informally, there is a 95%
there is a 95% probability—on average—that the CI (45% to probability—on average—that this interval contains the
77%) contains the true injury risk. true injury rate.
Note that the numerator and denominator of injury risk Note that there were 12 athletes having a single injury,
are counts of athletes—the count of injured athletes divided four athletes having two injuries, and six athletes having
by the count of total athletes. Historically, some researchers three injuries, and one unfortunate athlete having six
have divided the count of injuries by the total athletes. This injuries. All of these injuries are used in calculation of
calculation is not a risk, odds, or rate. It has no meaning as the injury rate, and this is an important advantage of
a personal measure of injury incidence. However, it is useful injury rate over injury risk: it uses all the injury data,
from the standpoint of allocation of clinical resources. For whereas multiple injuries on the same athlete are not
this reason, the term clinical incidence has been suggested reflected in injury risk. Injury risk uses only the 22 “first
for this measure.15 injuries”—the first injury for each athlete during the
Injury odds is simply injury risk divided by 1 minus risk. follow-up period.
The odds of injury for the football season in Table 30-4 was Note that a single event, such as a collision on the field
0.61 (1 0.61) or 1.57 to 1. The usefulness of injury of play, can give rise to more than one injury. For example,
odds is simply that it can be a useful surrogate for injury risk if two soccer players collide in midair when trying to head
in some situations in which risk cannot be estimated directly the ball, one could be concussed and the other might suffer
(such as case-control studies). Other than that, odds has no a fractured clavicle. Should the one event, or the two inju-
direct use. ries, be used in the numerator of the injury rate? It depends
Note that the term risk is used very loosely in science. on the purposes of the study, but, in general, both should
For example, if a surveillance study found that football be used, because injury rate should be the rate of incident
had twice the injury rate of volleyball, people might say “the injuries, not the rate of events that give rise to injuries.
risk is twice as high in football.” However, the fact that the Technically, these multiple events are not statistically inde-
rate is twice as high in football does not mean that the risk pendent; however, this is a minor issue and typically can be
is twice as football. safely ignored as most injury events do not give rise to mul-
tiple injuries.
Another issue is whether only “new” injuries should be
Injury Rate used in the calculation of injury rate and injury risk, or
Injury rate is the number of injuries divided by the total whether the “reinjuries” to a body part (i.e., the athlete had
number of athlete-exposures. The unit of analysis is the previously sustained an injury) should be included. As with
injuries. Athletes who have multiple injuries are counted the other aspects of injury definition, limiting the range of
multiple times—once for each injury—in the numerator of injuries that are to be included is fraught with peril, and
injury rate. A rate must always be a positive number and it there are no standard clinical criteria for defining a reinjury
has no upper bound, that is, it can exceed 1. to the same body part. Thus, the injury rate (or risk) mea-
Note that one divides injured athletes by total athletes sure should typically include all injuries, both “new” and
to get injury risk, and one divides injuries by athlete- “reinjuries.” However, if there are multiple injuries to the
exposures to get injury rate. One should not divide inju- same body part during the course of the follow-up period,
ries by athletes if one’s goal is to measure the personal the conditional risk methods discussed in the following
incidence of injury. section should be used.
740 SECTION IV • Special Populations and Epidemiology
Table 30-5
Statistical Analyses Overview
Recommended Statistical Analysis
Dependent Variable Independent Variable
(Outcome Measure) (Predictors or Risk Factors) Nonparametric Regression
Continuous data are measurements such as body height or P Values and Confidence Intervals
miles run per week, whereas categorical data are binary, There is widespread use of p values in the biomedical sciences,
nominal, or ordinal measures, such as sex, race, or sprain and p values and hypotheses can provide a useful means for
status (e.g., first degree, second degree, third degree). quantifying study findings, especially in randomized studies.
However, researchers have become overly dependent on
the p value and hypothesis test when interpreting the results
Multivariate Regression of their studies. This is dangerous, because p values can
Multivariate regression is an important tool in sports injury be very misleading in some situations.29-32 Researchers in
epidemiology, because it allows the researcher to account any area of sports injury medicine should not depend solely
for nonrandomized covariates that potentially might on p values when interpreting their data. They should also
confound an analysis. The solutions (“beta coefficients”) consider and report meaningful measures of effect (e.g.,
produced by a regression model have useful interpretations: means, or rate ratios) that provide a context for the p values.
linear regression produces means, binomial regression pro- A statistically significant finding may have little or no clinical
duces risk ratios, logistic regression produces odds ratios, meaning, and there is no way to know this if only the p value
and Poisson regression produces rate ratios. A variant of is reported.
Poisson regression named negative binomial regression is In addition, the authors recommend reporting CIs for all
often used for injury rates. Finally, the popular Cox model major findings in any study. A profound limitation of the
(proportional hazards regression) is used if the outcome p value is that it combines two pieces of information—the
measure is a time-to-event variable (such as number of days precision of the study, and the magnitude of the treatment
to injury). effect—that really should be kept separate. The CI allows
In all cases, these measures can be adjusted for the con- the precision of the study to be quantified as separate piece
founding effect of other factors simply by including the of information, to be considered alongside the magnitude
relevant factors, including covariates, in the model. Caution of effect.
is required, however. Regression models are not a panacea, P values can be particularly misleading when reported as a
and will give misleading results if variables are entered into simple inequality (e.g., p 0.05), rather than as a numerical
the model without thought. It is good advice to develop a value (e.g., p 0.06). It is important that sports injury
written analysis plan and make sure that the regression researchers are able to distinguish a p value of 0.06 from a
models (and all statistics) directly address the aims of the p value of 0.99, because these two results represent very dif-
study in a logical and coherent fashion. In particular, the ferent sets of findings and would probably have different
thoughtless inclusion of interaction terms in a regression implications. The truth is that p 0.06 has much more in
model can often produce highly misleading and confusing common with p 0.04 than it does with p 0.99. Perhaps,
results. with the addition of a few more subjects, or a slightly different
742 SECTION IV • Special Populations and Epidemiology
random sample, the p 0.06 result would become p 0.04, is low, and frequency data can be generated.33 This approach
purely because of slight improvements in study precision can be useful when there is a low occurrence of injury but
(statistical power). However, the blind adherence to rules of the injury type is severe or catastrophic as in head and spinal
hypothesis testing would mislead one to conclude that the cord injuries. However, there are several distinct disadvan-
p 0.06 result and the p 0.99 result convey the same in- tages to the case-series approach.33 First, it is usually impos-
formation, whereas the p 0.04 finding is somehow vastly sible to determine the completeness of reporting (i.e., if all
different from the p 0.06 result - clearly, a ludicrous situa- or only some injuries are reported). This may lead to inac-
tion. Sadly, many investigators downplay, or even disregard, curate conclusions. Second, the setting in which the data is
potentially useful findings simply because the result failed to collected can introduce a bias in the injury profile. These
attain the somewhat arbitrary cut-off criteria (p 0.05) used systems tend to identify acute and more severe sport-related
for statistical significance. injuries, which limits the generalizability of the data. For
example, reporting on snowboarding injuries, the number of
injuries occurring in the general population would be under-
Clinical Point estimated but the severity of injury may be overestimated.
Third, and probably the main disadvantage of the case-series
The reporting of confidence intervals is encouraged as a supplement approach is that these systems do not collect data on nonin-
or even replacement for p values. Confidence intervals allow the jured athletes or participants or exposure. Thus, because the
investigator to consider the precision and the magnitude of effect as population at risk and exposure information is not collected,
two separate items, whereas the p value collapses these items into
risk and causal associations cannot be determined.
a single summary measure.
Cohort Design
In contrast to the case-series design, sports injury surveil-
General Injury Surveillance Systems lance systems collect data on a group of uninjured athletes
Sports injury surveillance or reporting systems exist to serve (a cohort) at the beginning of the study and follow them
a variety of functions. The data collected may be used forward in time. Thus, the main advantage of the cohort
to estimate the total burden of morbidity or mortality, or design is that it offers the ability to examine characteristics
to identify risk factors and high-risk groups in sport between injured and noninjured athletes.33 Accordingly, the
populations.33 This information can also be used as a basis researcher can estimate both injury rates and injury risk
for safety decision making and for the allocation of health (injury rate ratio).33 Thus, cohort systems can determine
care and other resources. Finally, the data may serve as an casual associations from the data. In sports injury, as previ-
outcome measure for research on injury prediction and ously mentioned in the section on denominator data, the
form the basis for assessing the effectiveness of interven- most commonly used measure of participation is the athletic
tions aimed at injury prevention.33 exposure (AE), in which one AE is one athlete participating
During the past three decades, a wide variety of injury in a practice or game. The disadvantages of these systems
surveillance systems have been developed to assess sport- are the time and costs associated with collecting the expo-
related injury. Table 30-6 summarizes selected surveillance sure information.
systems by design type, years of existence, data collected
and source of data.16,34-46 The systems vary in the method Cohort Personal-Estimation versus Cohort
used in the reporting of athletic injuries. Some systems are Team-Estimation
based on the reporting of a specific injury type, whereas There are two types of cohort design systems based on their
others are sport-specific. Some systems are aimed at specific method of how exposure data (denominator) is collected. In
athletic populations, whereas other systems survey the the cohort design with personal-measurement system, the
general population. An important issue in distinguishing total amount of AE is based on the sum of all individual
between these systems is to determine the design used for athlete participations (i.e., an athlete is credited with an AE
collecting the data.33 The design is what places limitations only if he or she actually participates in a practice or game).
on how data may be interpreted and how it may be used. In Thus, athletes are not credited with an AE if they missed or
general, two design types are used: case-series and cohort.33 did not participate in a practice because of injury or nonin-
Each design type has its strengths and limitations. jury reasons. This method is more time consuming but
allows the ability to record varying amounts of participation
(exposure) for each athlete, providing a more precise injury
Case-Series Design rate or risk estimate. In contrast, the systems that use the
The case-series design approach is the least complex. The cohort design with team estimation estimate individual expo-
advantages of this approach are that data on a variety of in- sure rather than measuring it directly. The exposure for a given
jury or diseases can be easily collected in many settings, cost situation is calculated as the number of players multiplied by
Applied Sports Injury Epidemiology • CHAPTER 30 743
Table 30-6
Sports Surveillance Systems
Years
Surveillance System of Existence Data Collected Source of Data
Case-Series Design
National Electronic Surveillance 1972-present All injuries Hospital emergency department injury records
System 34
National Football Head & 1975-present Football head and neck Survey, direct contact with athlete, parent, or
Neck Injury Registry35 injuries school official at colleges and high schools
National Center for 1982-present Any severe injury incurred Coaches, athletic trainers, athletic directors,
Catastrophic Sports Injury during high school– or executive officers of state and national
Research36 college-sponsored sport athletic organizations, a national newspaper
events clipping service, and professional associates
of the researchers
Children’s Hospital Injury, 1989-present All injuries in persons Hospital records
Research and Prevention younger than 20 years of
Program37 age
Cohort Team-Estimation
National Athletic Injury 1974-1983 Sport-related injuries, Injury report form completed by medical
Reporting System38 participation data (AEs) personnel and athletic trainers from
professional teams, colleges, and high schools
Canadian Athletic Injury/ 1979-1986 Sport-related injuries, Injury report form completed by medical
Illness Reporting System39 participation data (AEs) personnel or athletic trainers from profes-
sional teams, colleges, and high schools
(teacher and coach)
NCAA Injury Surveillance 1982-present Sport-related injuries, Injury report form completed by athletic
System40 participation data (AEs) trainers from US colleges
Sports Injury Monitoring ?-present Sport-related injuries and Injury report form completed by medical
System41 participation data (AEs) personnel and athletic trainers from
professional teams and colleges
National High School Athletic 1985-? Sport-related injuries and Injury report form completed by athletic
Injury Registry42 participation data (AEs) trainers from US high schools
Big Ten Conference43 1986-present Sport-related injuries and Injury report form completed by medical
participation data (AEs) personnel and athletic trainers from Big Ten
Conference colleges
University of North Carolina 1996-2000 Sport-related injuries and Injury report form completed by athletic
High School Athletic Injury participation data (AEs) trainers from 100 North Carolina (US) high
Registry16 schools
High School Sports-Related 2005-present Sport-related injuries and Injuries reported by athletic trainers from 100
Injury Surveillance Study44 participation data (AEs) US high schools (nationally representative)
weekly via Internet-based surveillance system
Cohort Personal-Estimation
Athletic Health Care System45 1978-1995 Sport-related injuries and Injury report form completed by athletic
participation data (AEs) trainers or coaches from Washington state
(US) high schools
Canadian Intercollegiate Sport 1993-present Sport-related injuries and Injury and medical report forms and weekly
Injury Registry46 participation data (AEs) exposure sheet completed by athletic trainers
from Canadian Collegiate sports
the number of games or practices. The main advantage of this 1000 AEs. This difference could be important when compar-
approach is the data collection is significantly minimized ing rates with other studies or when making important deci-
(e.g., need to count only the number of team players and sions regarding program planning for health care allocation.
total number of practices and games from the team roster for It is unlikely that one universal system will fit all the needs
the entire season or any specified amount of time). In addi- of injury reporting in all populations and settings. Thus, a
tion, injury risk can be computed for the team. However, general sports injury surveillance system can be useful for
there are some disadvantages with the team-estimation answering questions about the incidence and severity of the
method. First, it assumes that all team members are sports injury problem in various subsets of a population.48
“exposed” on each and every practice and game throughout Such a general sports injury surveillance system requires
the season. Thus, athletes who (1) start the season late, easy-to-use, uniform, and unambiguous definitions of the
(2) do not complete the entire season because of injury or variables. If the purpose of the surveillance system is to iden-
noninjury reasons, or, (3) miss several or many practices or tify causal factors or to assess the effectiveness of preventa-
games because of absences or injury are still credited with tive measures, then the sports injury surveillance system
the same amount of exposures. Similarly, in many sports, should be tailored to the specific research situation.48 Some
although most players participate in each practice, many important components of sports injury systems as recom-
non–first team members may not participate in games. How- mended by Finch49 are presented in Box 30-1.
ever, in this team-estimation system, those who did not play
or participate in the game are still awarded a game exposure.
In summary, injury rates calculated from the cohort team-
estimation system may underestimate the true injury rate or Clinical Point
injury risk as compared with the cohort personal-estimation
method. For example (Table 30-7), in a study of 423 high Sports injury data are important for a number of reasons. It is impor-
school cross-country runners, Rauh and colleagues47 tant that definitions of injury and collection of meaningful exposure
data be determined and agreed on before injury surveillance activities
reported an injury rate of 17 injuries per 1000 AEs using the
are undertaken. In addition, the system should also collect information
cohort personal-estimation method whereby only practices
in a form that is of relevance across a broad range of potential users
and competitions in which runners actually participated of the data: sports participants themselves, sport medicine physicians,
(absences and time loss from injury days not counted in ex- other sports medicine professionals and researchers, coaches,
posure estimation) were counted. If the study had used the trainers, and sports administrators.49
cohort team-estimation method, the injury rate would have
been observed as 13.7 injuries per 1000 AEs. Thus, using the
cohort team-estimation method, there would have been an
excess of 4510 total AEs (practices: 3683, competitions: 827)
because of counting exposures for practices or competitions
in which all runners did not participate. This would Box 30-1 Recommended Components of a Sports
have caused an underestimation of almost four injuries per Injury Surveillance System49
• The sports activity the injured person was engaging in at the time
of the injury (e.g., football, running)
Table 30-7
• The location where the injury was incurred (e.g., football field,
Example of Cohort Personal-Estimation versus Cohort basketball course, running surface)
Team-Estimation in High School Cross-Country Runners • The particular activity initiating the injury (e.g., pitching, tackling)
Design Type Injuries Athletic Exposures Rate • What went wrong? (e.g., collided with another player)
• The level of supervision of the initiating activity (e.g., recreation vs.
Cohort Personal-Estimation competition, organized sporting event)
• The nature of the injury (e.g., sprain, fracture, concussion)
Practices 272 15447 17.6 • The body regions injured (e.g., head, shoulder, knee)
Competitions 44 3161 13.9 • The severity of the injury (e.g., number of participation days lost,
Total 316 18608 17.0 emergency department visit)
• The characteristics of the injured person (e.g., age, gender,
Cohort Team-Estimation race, etc.)
• The places of the presentation and referral for treatment (hospital
Practices 272 19130 14.2 emergency room, physical therapist, athletic trainer)
Competitions 44 3,988 11.0 • Sports participation data (e.g., number of exposures, hours, or
Total 316 23118 13.7 minutes spent in an activity, competition vs. training)
• The use of sports injury countermeasures (e.g., modified rules,
Data from Rauh MJ, Koepsell TD, Rivara FP et al: Epidemiology of
protective equipment, clothing, appropriate training)
musculoskeletal injuries among high school cross-country runners,
Am J Epidemiol 163(2):151-159, 2006.
Applied Sports Injury Epidemiology • CHAPTER 30 745
Table 30-8
A Comparison of Injury Rates in Prospective Studies of Girls’ Selected High School Sports
Number of Injury Rate/ Injury Rate/
Data Number of Number Injured 100 Athlete 1000 Athletic
Study Collection Duration Participants of Injuries Athletes/N Seasons Exposures
Basketball
Cross-Country Running
Field Hockey
Gymnastics
Lacrosse
Soccer
Table 30-8
A Comparison of Injury Rates in Prospective Studies of Girls’ Selected High School Sports—cont’d
Number of Injury Rate/ Injury Rate/
Data Number of Number Injured 100 Athlete 1000 Athletic
Study Collection Duration Participants of Injuries Athletes/N Seasons Exposures
Softball
Swimming
Tennis
Volleyball
AT, Athletic trainer reports; DM, direct monitoring; DNP, data not provided; I, interview; IRF, injury report form; Q , questionnaire.
748 SECTION IV • Special Populations and Epidemiology
Table 30-9
A Comparison of Injury Rates in Prospective Studies of Selected Boys’ High School Sports
Injury Injury
Number Rate/100 Rate/1000
Data Number of Number of of Injured Athlete Athletic
Study Collection Duration Participants Injuries Athletes/N Seasons Exposures
Baseball
Basketball
Cross-Country Running
Football
Gymnastics
Table 30-9
A Comparison of Injury Rates in Prospective Studies of Selected Boys’ High School Sports—cont’d
Injury Injury
Number Rate/100 Rate/1000
Data Number of Number of of Injured Athlete Athletic
Study Collection Duration Participants Injuries Athletes/N Seasons Exposures
Lacrosse
Soccer
Swimming
Tennis
Volleyball
Wrestling
AT, Athletic trainer reports; DM, direct monitoring; DNP, data not provided; I, interview; IRF, injury report form; Q , questionnaire.
750 SECTION IV • Special Populations and Epidemiology
For boys’ high school sports, the highest injury rates per Baseball-B 0.95
Softball-G 0.96
1000 AEs are reported in cross-country running (range: 1.7 Track-B 1.09
to 15.0), football (range: 3.2 to 8.1), and wrestling (range: Track-G 1.18
Basketball-G 1.28
1.49 to 7.6). It should be noted that although injury rates Volleyball-G 1.31
per 1000 AEs were not reported for gymnastics, swimming, Wrestling-B 1.49
Basketball-B 2.32
tennis, and men’s volleyball, the reported injury rates per Soccer-G 2.35
100 athletes in these sports were low. Soccer-B 2.81
Football-B 3.54
Caution should be used when making comparisons of
0 0.5 1 1.5 2 2.5 3 3.5 4
incidence rates across studies because of study differences
and methodological limitations, including varying sample Injury Rates per 1000 AEs: Knowles et al., Am J Epidem 2006 (58)
definition and data collection methods (i.e., designated data Soccer-G 2.36
not all high school sports were included in these studies, Field Hockey-G 3.7
Basketball-G 4.4
especially girls’ and boys’ cross-country running that have Soccer-B 4.6
reported high injury rates per 1000 AEs.47,64 Basketball-B 4.8
Soccer-G 5.3
Wrestling-B 5.6
Football-B 8.1
Clinical Point 0 1 2 3 4 5 6 7 8 9
Injury Rates per 1000 AEs: Powell & Barber-Foss, J Athl Train 1999 (41)
Clinicians and researchers should carefully consider the following
methodological issues when making comparisons of injury incidence Figure 30-4
across studies: A comparison of injury rates in prospective studies of selected high
school sports. Girls (G), Boys (B).
• Different injury definitions
• Type of denominator use
• Varying sample sizes
• Different methods of data collection
• Variable data collection periods
Baseball-M 2.9
Softball-W 3.25
Lacrosse-W 3.97
Volleyball-W 4.31
Collegiate. At the collegiate level, women’s soccer had Field Hockey-W 4.61
the highest incidence rate injury followed by men’s wres- Lacrosse-M 4.59
tling and soccer between 1988 to 2004 (Figure 30-5).40 Basketball-W 4.81
4.9
Men’s baseball and women’s softball had the lowest inci- Basketball-M
Football-M 6.08
dence of injury, which is similar to the high school level. 6.81
Gymnastics-W
Soccer-M 7.2
Gender Differences Wrestling-M 7.58
ing incidence rates per 1000 AEs for both girls and boys in 0 1 2 3 4 5 6 7 8 9
Injury Rate per 1,000 AEs
same sports is provided in Table 30-10. Significantly higher
incidence rates were reported for girls than boys in softball,41 Figure 30-5
A comparison of injury rates in selected National Collegiate Athletic
basketball,57 cross-country running,47,64 and soccer.41 None Association (NCAA) collegiate sports: 16-year longitudinal study of
of the studies reported injury rates that were significantly NCAA collegiate men’s and women’s sports.40 Women (W),
higher for boys as compared with girls in same sports. men (M).
Applied Sports Injury Epidemiology • CHAPTER 30 751
Table 30-10
A Comparison of Injury Rates in Prospective Studies of Similar Girls’ and Boys’ High School Sports
Injury Rate
Girls/Boys
Study Girls Boys Rate Ratio 95% CI
Softball and Baseball
Basketball
Cross-Country Running
Lacrosse
Soccer
CI, Confidence interval; DNP, data not provided (denominator) to determine confidence intervals.
*p 0.05.
Collegiate. At the collegiate level, although incidence rates per 1000 AEs for girls’ and boys’ high school sports
rates of injury were significantly higher among women than are presented in Table 30-11. The incidence rates were
men in soccer (rate ratio [RR] 1.08, 95% CI: 1.05-1.11) consistently higher in competition and games than practice
and softball (RR 1.12, 95% CI: 1.08-1.16), men had a for girls’ basketball,41,44,57,60,61 field hockey,41 soccer,41,44,66
significantly higher incidence injury rate in lacrosse than and softball.41,44 For boys, the rate of injury was consistently
women (RR 1.15, 95% CI: 1.11-1.21) (Figure 30-6).40 greater in competition and games than practices for base-
The incidence of injury was similar for women’s and men’s ball,41,44,68 basketball,41,44,57,61 football,41,44,70 lacrosse,65 and
basketball. wrestling.41,44,73 In several girls’ and boys’ cross-country
running studies,47,64 and in girls’ lacrosse65 and volleyball41
Exposure (Practice versus Competition the incidence of injury was higher in practices than in
or Games) Setting competition/games.
High School. Most studies on participation setting have Collegiate. As shown in Table 30-12, the incidence rates
reported on percent of injury in practice and competitions of injury were higher in games than in practices for all women’s
or games. Studies reporting competition and practice injury and men’s collegiate sports.74-86 The risk of incurring an injury
752 SECTION IV • Special Populations and Epidemiology
9
∗ and men’s collegiate sports with the exception of men’s
8 7.77 baseball. The ankle was the most common lower-extremity
7.2
injury for basketball,76,77 gymnastics,80 lacrosse,81,82 men’s
Injury Rate per 1,000 AEs
7
soccer,84 and volleyball,85 whereas the knee was more com-
6
∗ mon for field hockey,78 football,79 softball,74 and women’s
5
4.9 4.81
4.58 soccer.83 Women’s softball74 and baseball75 had the highest
∗
3.97 percent of upper-extremity injury, with the shoulder most
4
3.25 commonly affected. The percent of head and spine injuries
2.9
3
are highest in wrestling,86 field hockey,78 and women’s
2 lacrosse,81 with the head and face being the most commonly
injured sites. Gymnastics,80 volleyball,85 and wrestling86 have
1
the highest percent of injuries in the trunk region, with the
0
lower back being the most commonly injured body site.
-M
-M
M
-W
-W
W
ll-
ll-
ll-
se
er
ll-
er
se
ba
ba
ba
a
cc
cc
os
os
ftb
et
se
et
So
So
cr
cr
sk
So
sk
Ba
Severity of Injury
La
La
Ba
Ba
Table 30-11
A Comparison of Injury Rates in Competition and Practice Settings in Selected High School Sports (per 1000 AEs)
Girls Boys
Study Competition Practice C/P Ratio Competition Practice C/P Ratio
Baseball
Basketball
Cross-Country Running
Field Hockey
Football
Lacrosse
Soccer
Softball
Volleyball
Wrestling
Table 30-12
A Comparison of Injury Rates in Game and Practice Settings in Selected Collegiate Sports (per 1000 AEs)*
Women Men
Study Game Practice G/P Ratio Game Practice G/P Ratio
Softball
Baseball
Basketball
Agel et al.,76 Dick et al.77 7.68 3.99 1.92 9.9 4.3 2.30
Field Hockey
Football
Gymnastics
Lacrosse
Dick et al.,81 Dick et al.82 7.15 3.30 2.17 12.58 3.24 3.88
Soccer
Dick et al.,83 Agel et al.84 16.4 5.20 3.15 18.75 4.34 4.32
Volleyball
Wrestling
Collegiate. Although there is some small variation by ankle ligament sprains, these injuries accounted for approxi-
sport, gender, and exposure type (i.e., practice or game), the mately one quarter of all injuries in men’s (1.30 per 1000
most frequently reported injuries at the collegiate level are AEs) and women’s basketball (1.15 per 1000 AEs) and
sprains, strains, and contusions.91 Ligamentous injuries to women’s volleyball (1.01 per 1000 AEs). During this same
the ankle were the most common injury occurrence (14.9% period, approximately 5000 ACL injuries (0.15 per 1000
of all injuries, 0.83 per 1000 AEs), regardless of sport or AEs) were reported for average of 313 per year. Football had
exposure type. More than 27,000 ankle ligament sprains the highest number of reported ACL knee injuries (fall 2159
were reported in 16 sports during 16 academic years, yield- [0.18 per 1000 AEs], spring 379 [0.33 per 1000 AEs], 53%
ing an average of approximately 1700 per year. Although of all reported ACLs). Three of the four sports with the high-
spring football (1.34 per 1000 AEs) had the highest rates of est rates of ACL injuries were women’s sports: gymnastics,
Table 30-13
A Percent Comparison of Injuries by Body Location Among Selected Girls’ High School Sports
Cross- Field Track
Basketball Country Hockey Lacrosse Soccer Softball and Field Volleyball
Powell Powell Powell Powell Powell
and and and and Watson and
Borowski Messina Barber- Rauh Rauh Barber- Hinton Barber- Yard Barber- Rechel and Barber- Rechel
Study et al.57 et al.61 Fosss41 et al.64 et al.47 Foss41 et al.65 Foss41 et al.66 Foss41 et al.87 DiMartino67 Foss41 et al.87
Number of 745 1748 776 157 510 370 1771 DNP 910 DNP 11 628 DNP
injuries
Head/Face/ 14.2 7.5 11.0 0.0 0.0 16.6 14.9 9.7 14.6 11.2 19.5 0.0 4.5 3.9
Neck/Spine
Head 14.2a 7.5 11.0a 16.6a 14.1 9.7a 14.6 11.2a 4.5a
Neck/spine 1.6
Upper 12.0 13.1 12.7 0.0 0.0 15.8 15.2 6.4 6.1 39.2 36.1 0.0 20.8 18.8
Extremity
Shoulder 2.5b 2.8 2.4b 3.1b 4.1 1.9b 1.3 16.3b 9.4b
Upper arm 1.6h 4.8j
Elbow
Forearm 9.5c 2.3f 10.3c 12.7c 4.5c 22.9c 11.4c
Wrist 9.5i
f
DNP, data not provided. Includes arm and wrist injuries.
a g
Includes head, neck and spine injuries. Includes hip and thigh injuries.
b h
Includes shoulder and arm injuries. Includes upper arm, elbow, and forearm injuries.
c i
Includes forearm, wrist, and hand injuries. Includes wrist and hand injuries.
d j
Includes hip, thigh, and leg injuries. Includes torso, spine, and neck.
e k
Includes ankle and foot injuries. Includes upper arm, elbow, forearm, wrist, and hand injuries.
755
756 SECTION IV • Special Populations and Epidemiology
Table 30-14
A Percent Comparison of Injuries by Body Location Among Selected Boys’ High School Sports
Number of 431 861 773 543 1933 846 159 2228 10557
injuries
Head/Face/ 16.5 10.8 12.8 13.6 13.3 0.0 0.0 10.0 15.5
Neck/Spine
Head/face 15.8 10.8a 12.8a 13.6 13.3a 9.0 15.5a
Neck/spine 0.7 1.0
Upper 39.9 44.3 12.2 16.8 13.8 0.0 0.0 23.0 26.2
extremity
Shoulder 15.5 19.7b 2.8b 6.1 2.4b 11.0 12.0b
Upper arm 1.2
Elbow 7.2 4.0
Forearm 2.1 24.6c 9.4c 3.4f 11.4c 14.2c
Wrist 3.7
Hand 10.2 8.8 8.0
Trunk 5.8 7.2 7.1 6.1 7.7 3.4 2.4 9.0 8.6
Chest 1.6 0.4 0.0 0.0 0.0
Abdomen 0.5 0.0 0.0 0.0
Back 3.7 5.7 3.4 2.4 9.0
Lower 35.7 37.5 65.4 60.4 64.8 94.2 97.6 55.0 47.7
extremity
Hip/groin 1.8 14.5d 8.2d 10.5g 14.4d 5.5 9.8 7.0 16.7d
Upper leg/ 7.6 8.5 4.3
Thigh
Knee 8.6 10.5 10.6 9.7 11.1 24.3 25.8 20.0 15.1
Lower leg 3.0 3.4 4.4 29.2 31.3 8.0
Ankle 14.2 12.5e 43.2e 31.9 39.3c 18.4 19.0 18.0 15.9e
Foot 0.5 3.9 8.3 7.4 2.0
Other 2.1 0.1 2.4 3.9 0.4 2.4 0.0 2.0 2.0
a
Includes head, neck, and spine injuries.
b
Includes shoulder and arm injuries.
c
Includes forearm, wrist, and hand injuries.
d
Includes hip, thigh, and leg injuries.
e
Includes ankle and foot injuries.
f
Includes arm and wrist injuries.
g
Includes hip and thigh injuries.
h
Includes upper arm, elbow, forearm, and wrist injuries.
i
Includes torso, spine, and neck injuries.
j
Includes lower leg, ankle, and foot injuries.
k
Includes upper arm, elbow, and forearm injuries.
l
Includes upper leg and lower leg injuries.
m
Includes wrist and hand injuries.
n
Includes upper arm, elbow, forearm, wrist, and hand injuries.
Applied Sports Injury Epidemiology • CHAPTER 30 757
Track and
Football Lacrosse Soccer Field Wrestling
18.6 11.5 14.4 18.6 8.7 13.1 0.0 19.0 16.5 16.2
Table 30-15
A Percent Comparison of Injuries by Body Location Among Selected Women’s Collegiate Sports
Field
Study Basketball Hockey Gymnastics Lacrosse Soccer Softball Volleyball
Agel Dick Marshall Dick Dick Marshall Agel
et al.76 et al.78 et al.80 et al.81 et al.83 et al.74 et al.85
soccer, and basketball (0.33, 0.28, 0.23 per 1000 AEs, Time Loss
respectively). Although ACL injuries accounted for only 3% An often used and useful measure of injury severity in the
of all injuries, 88% of these injuries resulted in 10 or more sports injury literature is the duration of restriction from
days of time loss. The rate of ACL injury increased 1.3% on athletic performance. Although the length of time lost be-
average during the 16-year period. cause of sports injury likely provides the most precise indi-
Overall, 9150 concussions, or a rate of 0.94 concussions cation of the consequences of injury to an athlete,55 it is
per 1000 AEs, were reported among the 16 collegiate recognized that subjective factors such as personal motiva-
sports between 1988 and 2004.91 The rate of concussion tion, peer influence, or coaching staff reluctance may deter-
increased significantly by 7% on average during this period. mine if and when athletes return to play.90 In addition, as
The rate of concussion ranged from 0.07 (men’s baseball) shown in Table 30-17, there is presently no consensus on
to 0.91 (women’s ice hockey) per 1000 AEs. Football had what amount of time loss constitutes the degree of severity
the largest number of reported concussions (n 5016) of an injury. In general, time loss has been defined as any
with higher rates in spring (0.54 per 1000 AEs) than in fall injury that restricts the athlete from completing a practice
(0.37 per 1000 AEs) football. Higher rates of concussion or competitive event or prevents the athlete from returning
were reported among women than men for basketball, to a subsequent practice or competitive event with an unre-
hockey, soccer, and softball. stricted participation status.47,92 At the high school level,
although time-loss severity classifications of mild ( 8
days), moderate (8 to 21 days), or major ( 22) have been
Clinical Point advocated to standardize injury severity,41 others have used
different classifications (1 to 4 days, 5 to 14 days, 15 or
Sprains, strains, and contusion are the most commonly reported type more days, respectively47,64 or 1 to 6 days, 7 to 21 days, 22
of injury at high school and collegiate levels.
or more days, respectively44,66). Beachy and colleagues59
also included a fourth category of no time lost. The lack of
Applied Sports Injury Epidemiology • CHAPTER 30 759
Table 30-16
A Percent Comparison of Injuries by Body Location Among Selected Men’s Collegiate Sports
Study Baseball Basketball Football Lacrosse Soccer Wrestling
Dick Dick Dick Dick Agel Agel
et al.75 et al.77 et al.79 et al.82 et al.84 et al.86
consensus in reporting severity of injury has been apparent colleagues87 reported that a significantly greater proportion
at the collegiate level. Although Powell and Dompier93 used of competition injuries (19.2%) resulted in more than
the classification of less than 8 days, 8 to 21 days, and 22 or 3 weeks of time loss than injuries that occurred in practice
more days to describe mild, moderate, and major time-lost (15%) (proportion ratio [PR] 1.28, 95% CI: 1.08-1.52).
injuries, an NCAA compendium of 16 sports used less than Competition injuries were more likely to result in 3 or more
10 days or 10 or more days to denote severity of injury.40 weeks of time loss or the end of the athletes’ season than
Thus, these differences in definitions make the comparabil- practice injuries in baseball (23.9% vs. 6.9%; PR 3.47,
ity within and across competitive levels difficult. 95% CI: 1.48-8.11) and girls’ volleyball (21.3% vs. 7.4%;
PR 2.88; 95% CI: 1.01-8.24). Finally, in two separate
studies of cross-country runners, Rauh and colleagues,47,64
Clinical Point reported that girls had significantly higher rates of injuries
resulting in 15 or more days of time lost (RR 1.5, 95%
Because there is no standard definition of what constitutes the degree
of severity of an injury, in terms of amount of time loss, making CI: 1-2.2; RR 3.2, 95% CI: 1.4-8, respectively) or
comparisons within and across sport studies can be difficult. out-for-season (RR 1.8, 95% CI: 1.2-2.6; RR 3.3, 95%
CI: 1-14.5, respectively) than boys.
Collegiate. As shown in Table 30-18, most injuries
that occurred in practices or games resulted in nine or
High School. Of the few studies that have reported fewer participation days lost for both women’s and men’s
time lost from injury, most indicated that the majority of sports.74-81,83-86 The distribution of injuries resulting in 10
injuries in girls’ and boys’ high school sports are minor in or more days of time loss was slightly higher during games
nature (see Table 30-17).41,44,47,57,64,66,68 One study com- for most sports with the exception of spring football79 and
pared time loss relative to AE or gender. Rechel and men’s lacrosse.82
760 SECTION IV • Special Populations and Epidemiology
Table 30-17
Percent Comparison of Severity Rates in Selected High School Sports
Girls Boys
Study Minor Moderate Major Minor Moderate Major
Baseball
Basketball
Cross-Country Running
Field Hockey
Football
Soccer
Softball
Volleyball
Wrestling
G, Games; P, practices.
*Borowski et al.57 and Collins and Comstock68: Minor 1 week, Moderate 1-3 weeks, Major 3 weeks.
†
Comstock et al.44: Estimated from figure (categories do not add up to 100% because of nonreporting of injuries); Yard et al.66: Minor 1-6,
Moderate 7-21, Major 22
days.
‡
Powell and Barber-Foss41: Minor 8 days, Moderate 8-21 days, Major 22
days.
§
Rauh et al.47,64: Minor 1-4 days, Moderate 5-14 days, Major 15
days.
Applied Sports Injury Epidemiology • CHAPTER 30 761
Lacrosse
Catastrophic Injury
Catastrophic injuries are rare but severely debilitating
Dick et al.,81
21.9 23.9 21.0 21.0 events. The most comprehensive review of catastrophic in-
Dick et al.82 juries comes from the National Center for Catastrophic
Sports Injury Research (NCCSI).36 Data on catastrophic
Soccer injury among high school and collegiate sports have been
monitored by the NCCSI since 1982. According to the
Dick et al.,83 21.8 16.5 18.7 14.6 NCCSI, catastrophic injuries are considered direct (i.e., in-
Agel et al.84
juries that result directly from participation in the skills of
the sport) and indirect (i.e., injuries that were caused by
Volleyball
systemic failure as a result of exertion while participating in
Agel et al.85 23.0 19.0 — — a sport activity or by a complication that was secondary to
a nonfatal injury). Catastrophic injuries are also divided into
Wrestling three classifications: fatal, nonfatal (i.e., permanent, severe
functional disability), and serious (i.e., no permanent func-
Agel et al.86 — — 34.0 28.0 tional disability but severe injury—e.g., cervical vertebral
fracture with no paralysis).
Longitudinal, 16-year study of National Collegiate Athletic Association
High School. According to the NCCSI’s twenty-fifth
Collegiate Men’s and Women’s Sports.
annual report, during the 25-year period from the fall of
1982 through the spring of 2007, a total of 1303 cata-
strophic injuries were associated with high school sports.36
This indicates that approximately one out of every 100,000
(0.89 per 100,000) high school athlete suffers some type of
762 SECTION IV • Special Populations and Epidemiology
catastrophic injury. Of these, 864 were direct (0.59 per had the greatest number of catastrophic injuries for all
100,000) and 439 indirect (0.30 per 100,000) injuries. Of collegiate sports. When assessing the risk by incidence
these, 580 (0.39 per 100,000) were fatal, 370 (0.25 per rates, gymnastics and ice hockey had the highest rates for
1000 participants) were nonfatal and 353 (0.24 per direct injuries for both men’s and women’s sports. How-
100,000) were considered serious. The rate of any cata- ever, for indirect injuries, the highest rates were found for
strophic injury was almost five times greater for boys’ sports rowing and basketball in men’s sports, and gymnastics in
(1.22 per 100,000; n 1173 injuries) than in girls’ sports women’s sports.
(0.25 per 100,000; n 130 injuries). Football had the
greatest number of catastrophic injuries for all high school Step 2: Identification of Risk Factors
sports. However, when assessing the risk by incidence rates A critical step in injury sequence is to establish the causes.
(i.e., number of injuries per total number of athlete at risk), This includes obtaining information on why a particular
for both boys’ and girls’ sports, the rates are highest for athlete may be at risk in a given situation (i.e., risk factors)
gymnastics and ice hockey for direct injuries, and water polo and how the injuries happen (i.e., injury mechanisms).
for indirect injuries. Furthermore, a comprehensive understanding of injury
Collegiate. During the 25-year period from the fall of causation needs to address the multifactorial nature of
1982 through the spring of 2007, a total of 306 cata- sports injuries. Meeuwisse98 developed a model to ac-
strophic injuries were reported in college sports.36 This count for all factors involved. As shown in Figure 30-7,
indicates that almost 4 of every 100,000 (3.81 per 100,000) although an injury may appear to have been caused by
college athletes suffered a catastrophic injury. Of these, a single inciting event, it may result from a complex
204 were direct (2.54 per 100,000) and 102 indirect (1.27 interaction between athlete-related internal (intrinsic)
per 100,000) injuries. Of these, 100 (1.51 per 100,000) and external (extrinsic) environmental risk factors.98-101
were fatal, 65 (0.81 per 1000 participants) were nonfatal, Intrinsic risk factors (e.g., age, gender, body composition,
and 120 (1.49 per 100,000) were considered serious. The previous injury, or psychosocial factors) may influence
rate of any catastrophic injury was similar between men’s the risk of sustaining injuries, predisposing the athlete
sports (74.1 per 100,000; n 182 injuries) and women’ to injury. Once the athlete is predisposed to injury, extrin-
sports (77.9 per 100,000; n 124 injuries). Football also sic factors (e.g., sports equipment, rules, weather, or
Figure 30-7
A comprehensive injury causation model developed by Bahr and Krosshaug99 based on the epidemiologi-
cal model of Meeuwisse98 and the biomechanical model of McIntosh.100 (From Bahr R, Krosshaug T:
Understanding the injury mechanisms—A key component to prevent injuries in sport, Br J Sports Med
39(6):327, 2005.)
Applied Sports Injury Epidemiology • CHAPTER 30 763
field conditions) may make the athlete more susceptible “Reinjury” section in the discussion of “Severity of Injury”
to injury. Although the presence of both intrinsic earlier in this chapter), particularly for some injury types
and extrinsic factors make the athlete more vulnerable such as concussion or ankle sprain in which a history of
to injury, the presence of these factors may not be concussion or ankle injury is a significant predictor of future
sufficient to cause injury. The cumulative number and concussion or ankle sprain in high school football
interaction of these factors “set up” the athlete for players.108,109 These findings suggest an underestimation of
injury in a given situation, and an inciting event (e.g., the severity of the primary injury, inadequate rehabilitation,
playing situation, player behavior, biomechanical descrip- or premature return to sports activity.28,64,96 Subsequent
tion) is the final link in the chain that causes the injury injuries at a different site might be indicative of kinetic
occurrence.98,99 chain dysfunction.95 Previous injuries can lead to fibrosis,
with adhesions and limited joint motion and function.
Long-standing joint injuries resulting in chronic instability,
Clinical Point or even a slight effusion, can result in reflex inhibition of the
muscles and secondary alteration of body biomechanics.
Although an injury may appear to have been caused by a single
inciting event, it typically has resulted from a complex interaction
Restricted motion (hypomobility) will increase stresses on
between athlete-related internal (intrinsic) and external (extrinsic) other areas, and joint instability may result in muscle atro-
environmental risk factors. phy and increased compensatory stresses on other areas.95
Age, Grade Level, and Experience Level. The rela-
tionship between age, grade, or experience levels appears to
be sport-specific. Two football studies indicated that the older
Risk factors can also be divided into modifiable and non- or more experienced players were more likely to incur an in-
modifiable factors.99,101 Modifiable risk factors are those jury.69,70 In a study of 418 wrestlers, Pasque and Hewett73
that can be altered by injury prevention strategies to reduce found that older, experienced athletes sustained more injuries.
injury rates.102-104 Nonmodifiable risk factors cannot be These studies suggested that older or more experienced
altered, but still may affect the relationship between modifi- athletes are at increased risk because of increased playing time,
able risk factors and injury. Although nonmodifiable risk increased aggressiveness, or increased likelihood of attempt-
factors such as age, gender, and previous injury may be ing a high-risk skill. In contrast, Emery and colleagues110
worthy of consideration in studies of sport injury prediction reported a significantly higher injury rate among younger
and prevention, it is important to study factors that are (younger than 14) soccer players than older (younger than 18)
potentially modifiable, such as physical training, flexibility, players. They reported that this finding may be due to physi-
balance and proprioception, or psychological and social ological differences or under-reporting of injuries, particularly
factors.101,104 For the purposes of this chapter, risk factors minor injuries, among older players. The greatest risk was
that have been subjected to statistical tests for association or found among the elite playing divisions in the younger-than-
predictive value in prospective or retrospective studies of 14 and younger-than-16 age groups. They reported that the
high school sports are summarized in Table 30-19. increased risk was likely due to increased intensity of play in
higher divisions. Finally, in several studies of cross-country
Nonmodifiable Intrinsic Factors runners,47,63 age, grade, level, or running experience were not
Gender. In studies of high school athletes, in sports played associated with increased risk of injury.
by both sexes, there is evidence that girls may be at greater
risk of injury, including softball vs. baseball,105 basketball,61,105 Nonmodifiable Extrinsic Factors
cross-country running,47,64,106 lacrosse,65 and soccer.66,97 The Sport Type. As discussed in the section on overall inci-
reasons for girls being at greater risk of injury may be related dence, sport-specific rates for high school sports indicate
to lower skill level, training differences, or some physiological that the highest rates of injury per 1000 AEs are found for
or neuromuscular factor. girls’ high school sports in cross-country running,47,63,64
Previous Injury. Although an important aspect of in- soccer,41,44,58,66 basketball,41,44,60,61 and field hockey.41 For
jury prevention is to minimize the risk of the athlete’s initial boys’ high school sports, the highest injury rates per 1000
(first) injury, an equal goal is to minimize the occurrence of AEs are in football,41,44,58,70 cross-country running,47,63,64
a previous (subsequent) injury to the same (reinjury) and wrestling.41,44,58,73 The high incidence rate of injury in
body location or additional injuries to new body both girls’ and boys’ cross-country running is likely related
locations.28,41,47,58,64,95 Several high school studies have to the repetitive nature of motor pattern activity in combi-
shown prior history of injury to be a risk factor for future nation with the varying sport surfaces for training and com-
injury.28,47,58,64,70,107 The risk of subsequent injury has been peting. The relatively high incidence injury rates for foot-
reported significantly greater than the risk of the initial ball, wrestling, soccer, basketball, and field hockey are likely
(first) occurrence in multiple studies of cross-country because these sports involve direct player contact and a
runners.28,47,64 As mentioned previously, the effect of rein- large amount of pivoting, jumping, and quick-burst and
jury to the same body part or injury type is evident (see the sprinting activities.
764 SECTION IV • Special Populations and Epidemiology
Table 30-19
Risk Factor Studies for Selected High School Sports
Number of Significant Intrinsic Significant Extrinsic
Study Duration Participants Risk Factors Risk Factors
Baseball/Softball
Powell and Barber- 3 seasons 635 (F: 311, Gender (girls) Position (pitching)
Foss (2000)105 M: 324)
Basketball
Plisky et al. 1 season 235 (F: 105, Poor dynamic balance for lower-
(2006)111 M: 130) extremity injury
McGuine et al. 2 seasons 301 (F: 91, Poor balance (higher postural
(2000)109 M: 210) sway) for ankle sprains
Messina et al. 1 season 1863 (F: 890, Gender (girls) for any knee or Setting (increased risk of injury
(1999)61 M: 973) ACL injury during competition) for boys
and girls
Powell and Barber- 3 seasons 801 (F: 395, Gender (girls) for overall knee
Foss (2000)105 M: 406) injury and ACL injury
Cross-Country Running
Rauh et al. 1 season 393 (F: 171, Q-angle 20° associated with
(2007)112 M: 222) any injury for girls, knee and
8 days-lost injuries
Q-angle 15° with any injury
(males)
Q-angle right-left 4° difference
with any injury, shin injury, and
ankle foot injury (males)
Plisky et al. 1 season 105 (F: 46, High BMI and gender (females)
(2007)63 M: 59) with MTSS injury
Rauh et al. 1 season 421 (F: 186, Gender (female) Setting (increased risk of injury
(2006)47 M: 235) Q-angle 20° in practice vs. competition)
Previous summer running injury Girls only
(females)
Any prior running injury (males)
Bennett et al. 1 season 125 (F: 68, Greater navicular drop and gender
(2001)106 M: 57) (females) predicted MTSS
Rauh et al. 15 seasons 3233 (F: 1202, Gender (female) Setting (increased risk of injury
(2000)64 M: 2031) in practice vs. competition)
Football
Table 30-19
Risk Factor Studies for Selected High School Sports—cont’d
Number of Significant Intrinsic Significant Extrinsic
Study Duration Participants Risk Factors Risk Factors
Lacrosse
Hinton et al. 5 seasons 6528 (F: 2658, Gender (boys) Setting (increased risk of injury
(2005)65 M: 3870) for boys in competition than
girls
Setting (increased risk of injury
for girls in practice than boys)
Webster et al. 2 seasons 1386 females Protective eyewear reduced
(1999)121 forehead and periorbital injuries
Soccer
Yard et al. 2 seasons 1524 (F: 744, Gender (girls) increased risk of knee Setting (increased risk of injury
(2008)66 M: 780) ligament sprains during games in competition vs. practice)
Player-to-player contact during Setting (increased risk of
competition knee ligament sprain during
Noncontact mechanisms during practice—girls only)
practices
Emery et al. 1 season 317 (F: 164, Gender (girls) for knee ligament Setting (increased risk of injury
(2005)110 (Canada) M: 153) sprain in competition vs. practice)
Previous injury
Competition (elite)
Age (younger) with minor injury
Wrestling
Pasque and 1 season 418 males Increased wrestling experience Setting (increased risk of injury
Hewett (2000)73 Age (older) in competition vs. practice)
Decreased ligament laxity with
shoulder injury
Combined Sports
Knowles et al. 3 seasons 15,038 (F: Gender (males) Increased playing experience
(2006)58 5801, History of injury
M: 9237)
Hewett et al. 1 season 205 females Increased dynamic valgus
(2005)113 Increased knee abduction movement
ACL, Anterior cruciate ligament; BMI, body mass index; F, female; M, male; MTSS, medial tibial stress syndrome,
NA, not applicable.
766 SECTION IV • Special Populations and Epidemiology
Sport Position. Few studies have compared risk of that a large navicular drop predicted injury among cross-
injury by sport position. In a study of 1092 football players, country runners, especially among girl runners. However,
Turbeville et al.70 reported that lineman were almost two Plisky and colleagues63 found no relationship between cross-
times more likely to incur an injury than nonlineman. In country runners with a greater navicular drop ( 10 mm).
contrast, among 5100 football players, Ramirez and col- Two biomechanical measures of neuromuscular control
leagues69 found that offensive backfield (i.e., quarterback, have predicted ACL risk in a prospective study of female
running back, full back, wide receiver) and defensive back- soccer, basketball, and volleyball players. Hewett and
field (i.e., cornerback, defensive back, linebacker, safety) colleagues113 found that female athletes with increased
players had a 20% higher risk of injury when compared with dynamic valgus and high abduction loads at the knee were
linemen. They reported that the level of physical activity in at increased risk of an ACL injury.
a specified position coupled with player’s physique was an Body Composition. In some sports, such as football,
important marker for risk. Offensive linemen, who are often athletes try to increase their size or weight to become more
larger in size, station their bodies to block or tackle, whereas effective players. However, the evidence suggests that
backfielders move with greater speed. The transmission of increased weight and size may increase the likelihood of
energy forces from larger lineman to backfielders, or half- injury. Gomez and colleagues114 reported that a high body
backs being tackled rather than blocking, may increase the fat and increased body mass index (BMI) were associated
risk of injury to backfielders. Finally, when looking at the with lower-extremity injury among football players. Simi-
same position by gender, Powell and Barber-Foss105 larly, two other football studies reported that being over-
reported that pitchers in boys’ baseball were injured more weight, as indicated by BMI, increased the risk for ankle
often in practices and games than girls’ softball pitchers sprains.107,115
(p 0.001). Hence, future research should address biome- In sports such as cross-country and gymnastics, a large
chanical and training activities that might explain the BMI has been thought to increase the risk of injury.47,102 A
increased risk difference. Further, as few studies have exam- study of 105 cross-country runners by Plisky and colleagues63
ined the risk of injury by position in team sports, or by provides some support. They found that runners with a
event type (e.g., swimming, track and field, tennis), more higher BMI (20.2-21.6) were five times more likely to incur
studies are warranted in this area. a medial tibial stress syndrome (MTSS) injury than runners
with a lower BMI (18.8-20.1). However, a study of 421
cross-country runners found no association between high
BMI ( seventy-fifth percentile) and running injury.47
Clinical Point Psychosocial. Limited evidence exists on the role
In terms of injury prevention, a higher priority should be placed on of psychosocial variables and risk of injury. Using a
studying factors that are potentially modifiable (alterable) rather than modified version of the Life Events Survey for Collegiate
nonmodifiable (unalterable) factors. Athletes, Gunnoe and colleagues116 found that football
players with higher levels of preseason total and negative
lifestyle changes were more likely to incur an injury
during the season.
Potentially-Modifiable Intrinsic Factors
Neuromuscular. Several recent studies suggest that Potentially-Modifiable Extrinsic Factors
dynamic balance may increase the risk of injury. Plisky Exposure and Setting. Evidence from cohort studies
and colleagues111 found that a decreased normalized right during the past two decades suggest that for most girls’ and
composite reach distance and greater anterior right and left boys’ high school sports the risk of injury is higher during
reach distance difference on the Star Excursion Balance Test competition or games than in practice for baseball and soft-
predicted lower-extremity injury in girl and boy basketball ball,41,44,68 basketball,44,57,61 field hockey,41 football,41,44,69,70
players, respectively. These findings are consistent with soccer,41,44,66,97 and wrestling.41,44,73 However, in cross-
those reported by McGuine and colleagues,109 who country running47 and girls’ volleyball,41 the incidence of
reported that basketball players with poor balance were injury has been reported higher in practices than in compe-
more susceptible to ankle injury. titions or games. In lacrosse, the rates vary by gender, with
Anatomical and Biomechanical. Two lower-extrem- the risk of injury being higher in games for boys and during
ity anatomical measures have been found to be associated practices for girls.65 In the latter study, the authors sug-
with running injuries. In a prospective study of 421 cross- gested that the finding was likely because boys are allowed
country runners, Rauh and colleagues112 reported that a more purposeful contact than girls during competitions and
large Q-angle ( 20° for girls and 15° for boys), was as- games, which increases their risk of injury, particularly to
sociated with a twofold increased risk of injury. Runners the neck, shoulder, arm, and trunk.
with a large Q-angle were almost six times more likely to The proportion of injuries is greater in practice than com-
incur a knee injury.112 Bennett and colleagues106 reported petition or games in most high school and collegiate sports.
Applied Sports Injury Epidemiology • CHAPTER 30 767
This finding is likely due to the greater amount of time spent risk of injury was found among athletes who had incurred a
in practice compared with competition.41,87 On a practical previous ankle sprain. Yang and colleagues122 reported that
basis, this relationship indicates the need for a strong pro- high school athletes who used protective equipment were
gram of early recognition and treatment of practice-related less likely to incur a lower-extremity injury. However, the
injuries to potentially minimize game-related injuries.41 protective effect was largely attributed to protective knee
However, the findings from competition levels indicate the pad use. Athletes who used braces and who did not have a
rates of injury are actually greater during competition than history of knee or ankle injury were more likely to incur an
practices in most sports. The higher rates of injury during ankle or knee injury.
competition or games may be due to increased play inten- Coaching Experience and Education. It has been
sity,110 increased legal and illegal contact,117,118 and increased speculated that coaches with more educational training
exposure to high-risk activities (e.g., tackling in football).87 or experience are more likely to implement training
The increased rate of game injuries suggests a need to methods or teach techniques to minimize the number of
incorporate drills of potentially high-risk situations into injuries among their athletes. Only a few studies have
practice under controlled conditions in an effort to decrease examined this relationship at the high school level.
competition- or game-related injuries.87 Schulz and colleagues123 found a lower risk of injury
Environment. Few studies have assessed the effect of among competitive cheerleaders whose coaches had a
environmental conditions on risk of injury among high college degree and more years of coaching experience
school athletes. Regarding playing surface, the findings compared with cheerleaders whose coaches had only a
appear equivocal. Meyers and Barnhill119 compared the in- high school diploma and few years of experience. Con-
jury rates on FieldTurf and natural grass during games versely, in a similar study of athletes in multiple sports,
among high school football players during a 5-year period Schulz and colleagues108 reported no difference in risk of
and found no significant difference. Conversely, during a concussion injury among athletes who coaches had a
2-year period, Garlock and colleagues120 found that the in- master’s degree than athletes whose coaches did not have
jury risk was 1.3 and 1.94 times greater for football and a master’s degree.
girls’ soccer players, respectively, on natural grass than
FieldTurf (p 0.0001). In a study of 5118 football players,
Ramirez and colleagues69 found that playing on an artificial Step 3: Injury Prevention Programs—What Works
turf surface increased the risk of injury 1.6-fold (95% CI: and Does Not Work
1.3-1.9) as compared with natural grass. They also reported A summary table (Table 30-20) provides a snapshot of the
that playing on a wet or muddy surface was also significantly level of evidence for a variety of interventions.124 Some of
associated with risk of injury (RR: 1.2, 95% CI: 1–1.5). the interventions in the “proven” column are sometimes
Finally, in a study of 421 cross-country runners, Rauh and based on only one positive study, or are still contentious (as
colleagues47 reported that running on a concrete surface or in the case of ACL injury prevention programs). Neverthe-
irregular terrain significantly increased the risk of injury 12% less, this table provides a sense that there is a large number
for each mile run. of “proven” interventions. However, there has been little
Two studies have found associations between weather translational research to date on how best to implement
conditions and injury among football players. Ramirez and more widespread use of these interventions.
colleagues69 reported that playing in foggy, rainy, or clear The authors stress that just because an intervention is
night conditions increased the risk of injury when compared proven in one study, it does not mean that research on
with playing on sunny days. Meyers and Barnhill119 that topic should be halted. In fact, it should encourage
reported a significantly higher incidence of injury (62.8%) a whole new phase of research, dealing with how to
during hot days on FieldTurf when compared with natural encourage athletes to adopt the intervention, in addition
grass (50.9%). to studies that replicate the original trial or extend the
Equipment. Protective equipment devices are often intervention to a new population. An example of this
worn by high school athletes in many sports. Current evi- occurred with a series of studies of safety bases in softball
dence from three studies reported equivocal findings on the and baseball.125-127 These studies demonstrated the
risk of injury. Webster and colleagues121 assessed the rate of effectiveness of safety bases in recreational youth, recre-
head and facial injuries in 1386 female lacrosse players and ational adult, and elite softball. It is clear from these
reported that the risk of certain head and facial injuries were studies that use of safety bases should be encouraged at
lower in players that wore protective eyewear, especially all levels of the game. It is curious, however, that the line
during games. Partly, as a result of this evidence, female of research addressing safety bases phased out in the
lacrosse players must now wear eye protection during 1990s. One would expect that these studies would
games.65 Tyler and colleagues107 observed an increased risk have generated follow-up research on how best to get
of injury in football players who used ankle braces or tape safety bases adopted by as many users as possible (i.e.,
compared with players who did not. Further, the increased behavioral change research).
768 SECTION IV • Special Populations and Epidemiology
Table 30-20
Examples of Injury Prevention Intervention in Common Activities
Not Evaluated,
Insufficient or
Activity Proven Promising/Potential Conflicting Evidence
From Gilchrist J, Saluja G, Marshall SW: Interventions to prevent sports and recreation-related injury. In Doll LS, Bonzo SE, Mercy JA, Sleet
DA: Handbook of injury and violence prevention, New York, 2007, Springer.
Applied Sports Injury Epidemiology • CHAPTER 30 769
7. Garrick JG, Requa RK: Sports and fitness activities: The nega- 29. Poole C: Low p-values or narrow confidence intervals: Which are
tive consequence, J Am Acad Orthop Surg 11(6):439–443, more durable? Epidemiology 12(3):291–294, 2001.
2003. 30. Marshall SW: Testing with confidence: The use (and misuse) of
8. Caine CG, Caine DJ, Lindner KJ: The epidemiologic approach to confidence intervals in biomedical research, J Sci Med Sport
sports injuries. In Caine DJ, Caine CG, Lindner KJ, editors: Epide- 7(2):135–137, 2004.
miology of sports injuries, Champaign, 1996, Human Kinetics. 31. Wolfe R, Cumming G: Communicating the uncertainty in
9. Rothman KJ, Sander G, Lash TL: Modern epidemiology, ed 3, research findings: Confidence intervals, J Sci Med Sport 7(2):
Philadelphia, 2008, Lippincott Williams & Wilkins. 138–143, 2004.
10. Gessel, LM, Fields SK, Collins CL, et al: Concussions among 32. Cordova ML: Giving clinicians more to work with: Let’s incor-
United States high school and collegiate athletes, J Athl Train porate confidence intervals into our data, J Athl Train 42(4):445,
42(4):495–503, 2007. 2007.
11. Myer GD, Ford KR, Barber-Foss KD, et al: The relationship of 33. Meeuwisse WH, Love EJ: Athletic injury reporting: Develop-
hamstring and quadriceps strength to anterior cruciate liga- ment of universal systems, Sports Med 24(3):184–204, 1997.
ment injury in female athletes, Clin J Sports Med 19(1):3–8, 34. Duvall DP: The National Electronic Injury Surveillance System:
2009. A description of its role in the U.S. Consumer Product Safety
12. Schootman M, Powell JW, Torner JC: Study designs and poten- Commission, Division of Hazard and Injury Data Systems, U.S.
tial biases in sports injury research: The case-control study, Sports Consumer Product Safety Commission, 1990.
Med 18(1):22–37, 1994. 35. Torg JS, Vegso JJ, O’Neill MJ, Sennett B: The epidemiologic,
13. Collins M, Lovell MR, Iverson GL, et al: Examining concussion pathologic, biomechanical, and cinematographic analysis of
rates and return to play in high school football players wearing football-induced cervical spine trauma, Am J Sports Med
newer helmet technology: A three-year prospective cohort study, 18(1):50–57, 1990.
Neurosurgery 58(2):275–286, 2006. 36. National Center for Catastrophic Sport Injury Research (NCCSI):
14. Gilchrist J, Mandelbaum BR, Melancon H, et al: A randomized 25th Annual Report, NCCSI, 2008. Accessed Jan 25, 2009, at
controlled trial to prevent noncontact anterior cruciate ligament http://www.unc.edu/depts/nccsi/AllSport.htm.
injury in female collegiate soccer players, Am J Sports Med 37. Mackenzie SG, Pless IB: CHIRPP: Canada’s principal injury
36(8):1476–1483, 2008. surveillance program. Canadian Hospitals Injury Reporting and
15. Knowles SB, Marshall SW, Guskiewicz KM: Estimating rates and Prevention Program, Inj Prev 5(3):208–213, 1999.
risks in sports injury research, J Athl Train 41(2):201–215, 38. Levy IM: Formation and sense of the NAIRS athletic injury sur-
2006. veillance system, Am J Sports Med 16 (Suppl 1):S132–S133,
16. Weaver NL, Mueller FO, Kalsbeek WD, Bowling JM: The North 1988.
Carolina high school athletic injury study: Design and methodology, 39. Pelletier R: Canadian Athletic Injury/Illness Reporting System:
Med Sci Sports Exerc 31(1):176–182, 1999. CAIRS 1 recorder’s handbook, Ottawa, 1992, University of Ottawa.
17. Nathan M, Goedeke R, Noakes TD: The incidence and nature of 40. Dick R, Agel J, Marshall SW: National Collegiate Association
rugby injuries experienced at one school during the 1983 rugby Injury Surveillance System Commentaries: Introduction and
season, S Afr Med J 64(4):132–137, 1983. methods, J Athl Train 42(2):173–182, 2007.
18. Sugerman S: Injuries in an Australian schools Rugby Union 41. Powell JW, Barber-Foss KD: Injury patterns in selected high
season, Aust J Sports Med Exerc Sci 15:5–14, 1983. school sports: A review of the 1995-1997 seasons, J Athl Train
19. Roux CE, Goedeke R, Visser GR, et al: The epidemiology of 34(3):277–284, 1999.
schoolboy rugby injuries, S Afr Med J 71(5):307–313, 1987. 42. Powell JW: National High School Injury Registry, Am J Sports
20. Davidson RM: Schoolboy rugby injuries, 1969-1986, Med J Aust Med 16 (Suppl):S134–S166, 1988.
147(3):119–120, 1987. 43. Big Ten Sports Injury Reporting System, Am J Sports Med 16
21. Clark DR, Roux C, Noakes TD: A prospective study of the inci- (Suppl):S166–S200, 1988.
dence and nature of injuries to adult rugby players, S Afr Med J 44. Comstock RD, Knox C, Yard E, Gilchrist J: Sports-related inju-
77(11):559–562, 1990. ries among high school athletes—United States, 2005–06 school
22. Dalley DR, Laing DR, Rowberry JM, Caird MJ: Rugby injuries: year, MMWR 55(38):1037–1040, 2006.
An epidemiological survey, Christchurch 1980, N Z J Sports Med 45. Rice SG: Development of an injury surveillance system: Results
10:5–17, 1982. from a longitudinal study of high school athletes. In Ashare AB,
23. Hughes DC, Fricker PA: A prospective survey of injuries to first- editor: Safety in ice hockey, vol 3, West Conshocken, 2000,
grade rugby union players, Clin J Sports Med 4(4):249–256, American Society for Testing and Materials.
1994. 46. Meeuwisse WH, Love EJ: Development, implementation, and
24. Garraway M, Macleod D: Epidemiology of rugby football validation of the Canadian Intercollegiate Sport Injury Registry,
injuries, Lancet 345(8963):1485–1487, 1995. Clin J Sport Med 8(3):164–177, 1998.
25. Lee AJ, Garraway WM: Epidemiological comparison of injuries 47. Rauh MJ, Koepsell TD, Rivara FP, et al: Epidemiology of mus-
in school and senior rugby, Br J Sports Med 30(3):213–217, culoskeletal injuries among high school cross-country runners,
1996. Am J Epidemiol 163(2):151–159, 2006.
26. Bird YN, Waller AE, Marshall SW, et al: The New Zealand 48. Van Mechelen W: Sports injury surveillance systems. One size fits
Rugby Injury and Performance Project V. Descriptive epidemi- all? Sports Med 24(3):164–168, 1997.
ology of a season of rugby injury, Br J Sports Med 32(4): 49. Finch CF: An overview of some definitional issues for sports
319–325, 1998. injury surveillance, Sports Med 24(3):157–163, 1997.
27. Lombardo S, Sethi PM, Starkey C: Intercondylar notch stenosis 50. Blair SN, Kohl HW, Barlow CE, et al: Changes in physical fitness
is not a risk factor for anterior cruciate ligament tears in profes- and all-cause mortality: A prospective study of healthy and
sional male basketball players: An 11-year prospective study, Am unhealthy men, JAMA 273(14):1093–1098, 1995.
J Sports Med 33(1):29–34, 2005. 51. Jebb S, Moore M: Contribution of a sedentary lifestyle and inactiv-
28. Rauh MJ, Macera CA, Ji M, Wiksten DL: Subsequent injury pat- ity to the etiology of overweight and obesity: Current evidence and
terns in girls’ high school sports, J Athl Train 42(4):486–494, research issues, Med Sci Sports Exerc 31(11 Suppl):S154–S541,
2007. 1999.
Applied Sports Injury Epidemiology • CHAPTER 30 771
52. Paffenbarger RS, Kampert JB, Lee IM, et al: Changes in physical Collegiate Athletic Association Injury Surveillance System,
fitness and other lifestyle patterns influence longevity, Med Sci 1988-1989 through 2003-2004, J Athl Train 42(2):286–294,
Sports Exerc 26(7):857–865, 1994. 2007.
53. Koh J, Dietz J: Osteoarthritis in other joints (hip, elbow, foot, 75. Dick R, Sauers EL, Agel J, et al: Descriptive epidemiology of
ankle, toes, wrist) after sports injuries, Clin Sports Med 24(1): collegiate men’s baseball injuries: National Collegiate Athletic
57–70, 2005. Association Injury Surveillance System, 1988–1989 through
54. Van Mechelen W, Hlobil H, Kemper HCG: How can sports inju- 2003-2004. J Athl Train 42(2):183–193, 2007.
ries be prevented? Nationaal Instituut voor Sport GezondheidsZorg 76. Agel J, Olsen DE, Dick R, et al: Descriptive epidemiology of
publicatie, nr 25E, Papendal, 1987. collegiate women’s basketball injuries: National Collegiate
55. Van Mechelen W, Hlobil H, Kemper HCG: Incidence, severity, Athletic Association Injury Surveillance System, 1988-1989
aetiology and prevention of sports injuries: A review of concepts, through 2003-2004, J Athl Train 42(2):202–210, 2007.
Sports Med 14(2):82–99, 1992. 77. Dick R, Hertel J, Agel J, et al: Descriptive epidemiology of
56. Robertson LS: Injury epidemiology, New York, 1992, Oxford collegiate men’s basketball injuries: National Collegiate Athletic
University Press, Inc. Association Injury Surveillance System, 1988-1989 through
57. Borowski LA, Yard EE, Fields SK, Comstock RD: The epidemi- 2003-2004, J Athl Train 42(2):194–201, 2007.
ology of US high school basketball injuries, 2005–2007, Am J 78. Dick R, Hootman JM, Agel J, et al: Descriptive epidemiology of
Sports Med 36(12):2328–1235, 2008. collegiate women’s field hockey injuries: National Collegiate
58. Knowles SB, Marshall SW, Bowling JM, et al: A prospective study Athletic Association Injury Surveillance System, 1988–1989
of injury incidence among North Carolina high school athletes, through 2003–2004, J Athl Train 42(2):211–220, 2007.
Am J Epidemiol 164(12):1209–1221, 2006. 79. Dick R, Ferrara MS, Agel J, et al: Descriptive epidemiology of
59. Beachy G, Akau CK, Martinson M, Olderr TF: High school collegiate men’s football injuries: National Collegiate Athletic
sports injuries. A longitudinal study at Punahou School: 1988 to Association Injury Surveillance System, 1988–1989 through
1996, Am J Sports Med 25(5):675–681, 1997. 2003–2004, J Athl Train 42(2):221–233. 2007.
60. Gomez E, DeLee JC, Farney WC: Incidence of injury in Texas 80. Marshall SW. Covassin T. Dick R, et al: Descriptive epidemiology
girls’ high school basketball, Am J Sports Med 24(3):686–687, of collegiate women’s gymnastics injuries: National Collegiate
1986. Athletic Association Injury Surveillance System, 1988–1989
61. Messina DF, Farney WC, DeLee JC: The incidence of injury through 2003–2004, J Athl Train 42(2):234–240, 2007.
in Texas high school basketball. A prospective study among 81. Dick R, Lincoln AE, Agel J, et al: Descriptive epidemiology of
male and female athletes, Am J Sports Med 27(3):294–299, collegiate women’s lacrosse injuries: National Collegiate Athletic
1999. Association Injury Surveillance System, 1988–1989 through
62. McLain LG, Reynolds S: Sports injuries in high school, Pediatrics 2003–2004, J Athl Train 42(2):262–269, 2007.
84(3):446–450, 1989. 82. Dick R, Romani WA, Agel J, et al: Descriptive epidemiology of
63. Plisky MS, Rauh MJ, Heiderscheit B, et al: An epidemiological collegiate men’s lacrosse injuries: National Collegiate Athletic
investigation of medial tibial stress syndrome among high school Association Injury Surveillance System, 1988–1989 through
cross country runners, J Orthop Sports Phys Ther 37(2):40–47, 2003–2004, J Athl Train 42(2):255–261, 2007.
2007. 83. Dick R, Putukian M, Agel J, et al: Descriptive epidemiology of
64. Rauh MJ, Margherita AJ, Koepsell TD, et al: High school cross collegiate women’s soccer injuries: National Collegiate Athletic
country running injuries: A longitudinal study, Clin J Sports Med Association Injury Surveillance System, 1988–1989 through
10(2):110–116, 2000. 2003–2004, J Athl Train 42(2):278–285, 2007.
65. Hinton RY, Lincoln AE, Almquist JL, et al: Epidemiology of 84. Agel J, Evans TA, Dick R, et al: Descriptive epidemiology of
lacrosse injuries in high school-aged girls and boys: A 3-year collegiate men’s soccer injuries: National Collegiate Athletic
prospective study, Am J Sports Med 33(9):1305–1314, 2005. Association Injury Surveillance System, 1988–1989 through
66. Yard EE, Schroeder MJ, Fields SK, et al: The epidemiology of 2003–2004, J Athl Train 42(2):262–277, 2007.
United States high school soccer injuries, 2005.2007, Am J 85. Agel J, Palmeri-Smith RM, Dick R, et al: Descriptive epidemiol-
Sports Med 36(10):1930–1937, 2008. ogy of collegiate women’s volleyball injuries: National Collegiate
67. Watson MD, DiMartino PP: Incidence of injuries in high school Athletic Association Injury Surveillance System, 1988–1989
track and field athletes and its relation to performance ability, Am through 2003–2004, J Athl Train 42(2):295–302, 2007.
J Sports Med 15(3):251–254, 1987. 86. Agel J, Ransone J, Dick R, et al: Descriptive epidemiology of
68. Collins CL, Comstock RD: Epidemiological features of high school collegiate men’s wrestling injuries: National Collegiate Athletic
baseball injuries in the United States, 2005–2007. Pediatrics Association Injury Surveillance System, 1988–1989 through
121(6):1181–1187, 2008. 2003–2004, J Athl Train 42(2):303–310, 2007.
69. Ramirez M, Schaffer KD, Shen H, et al: Injuries to high school 87. Rechel JA, Yard EE, Comstock RD: An epidemiologic compari-
football athletes in California, Am J Sports Med 34(7): son of high school sports injuries sustained in practice and
1147–1158, 2006. competition, J Ath Train 43(2):197–204, 2008.
70. Turbeville SD, Cowan LD, Owen WL, et al: Risk factors for 88. Shankar P, Fields SK, Collins CL, et al: Epidemiology of high
injury in high school football players, Am J Sports Med 31(6): school and collegiate football injuries in the United States,
974–980, 2003. 2005–2006, Am J Sports Med 35(8):1295–1303, 2008.
71. DeLee JC, Farney WC: Incidence of injury in Texas high school 89. Yard EE, Collins C, Dick RW, Comstock RD: An epidemiologic
football, Am J Sports Med 20(5):575–580, 1992. comparison of high school and college wrestling injuries, Am J
72. Prager BI, Fitton WL, Cahill BR, Olson GH: High school foot- Sports Med 36(1):57–64, 2008.
ball injuries: A prospective study and pitfalls of data collection, 90. Caine D, Caine C, Maffuli N: Incidence and distribution of
Am J Sports Med 17(5):681–685, 1989. pediatric of sport-related injuries, Clin J Sport Med 16(6):
73. Pasque CB, Hewett TE: A prospective study of high school 500–513, 2006.
wrestling injuries, Am J Sports Med 28(4):509–515, 2000. 91. Hootman JM, Dick R, Agel J: Epidemiology of collegiate injuries
74. Marshall SW, Hamstra-Wright KL, Dick R, et al: Descriptive for 15 sports: Summary and recommendations for injury preven-
epidemiology of collegiate women’s softball injuries: National tion initiatives, J Athl Train 42(2):311–319, 2007.
772 SECTION IV • Special Populations and Epidemiology
92. Rice SG, Schlotfeldt JD, Foley WE: The Athletic Health Care and 112. Rauh MJ, Koepsell TD, Rivara FP, et al: Quadriceps angle and
Training Program. A comprehensive approach to the prevention risk of injury among high school cross country runners, J Orthop
and management of athletic injuries in high schools, West J Sports Sports Phys Ther 37(12):725–733, 2007.
Med 142(3):352–357, 1985. 113. Hewett TE, Myer GD, Ford KR, et al: Biomechanical
93. Powell JW, Dompier TP: Analysis of injury rates and treatment measures of neuromuscular control and valgus loading of the
patterns for time-loss and non-time loss injuries among collegiate knee predict anterior cruciate ligament injury risk in female
student athletes, J Athl Train 39(1):56–70, 2004. athletes: A prospective study, Am J Sports Med 33(4):492–501,
94. Fuller CW, Bahr R, Dick R, Meeuwisse WH: A framework for 2005.
recording recurrences, reinjuries, and exacerbations in injury 114. Gomez JE, Ross SK, Calmbach WL, et al: Body fatness and
surveillance, Clin J Sports Med 17(3):197–200, 2007. increased injury rates in high school football linemen, Clin J
95. Renstrom PA: Mechanism, diagnosis, and treatment of running Sport Med 8(2):115–120, 1998.
injuries, Instr Course Lect 42:225–234, 1993. 115. McHugh MP, Tyler TF, Tetro DT, et al: Risk factors for non-
96. Lysens R, Steverlynck A, van der Awuweele Y, et al: The predi- contact ankle sprains in high school athletes: The role of hip
catability of sports injuries, Sports Med 1(1):6–10, 1984. strength and balance ability, Am J Sports Med 34(3):464–470,
97. Emery CA, Meeuwisse WH: Survey of sport participation and 2006.
sport injury in Calgary and area high schools, Clin J Sports Med 116. Gunnoe AJ, Horodyski M, Tennant LK, Murphey M: The effects
16 (1):20–26, 2006. of life events on incidence of injury in high school football
98. Meeuwisse WH: Assessing causation in sport injury: A multifac- players, J Athl Train 36(2):150–155, 2001.
torial model, Clin J Sport Med 4(3):166–169, 1994. 117. Stuart MJ: Gridiron football injuries, Med Sport Sci 49:62–85,
99. Bahr R, Krosshaug T: Understanding the injury mechanisms—A 2005.
key component to prevent injuries in sport, Br J Sports Med 118. Guskiewicz KM, Weaver NL, Padua DA, Garrett WE Jr: Epide-
39(6):224–229, 2005. miology of concussion in collegiate and high school football
100. McIntosh AS: Risk compensation, motivation, injuries, and bio- players, Am J Sports Med 28(5):643–650, 2000.
mechanics in competitive sport, Br J Sports Med 39(1):2–3, 119. Meyers MC, Barnhill BS: Incidence, causes, and severity of high
2005. school football injuries on FieldTurf versus natural grass: A
101. Bahr R, Holme I: Risk factors for sports injuries—A method- 5-year prospective study, Am J Sports Med 32(7):1626–1638,
ological approach, Br J Sports Med 37(5):384–392, 2003. 2004.
102. Caine D, Maffulli N, Caine C: Epidemiology of injury in child 120. Garlock PG, Rauh MJ, Hummel-Berry K, Bateman MJ: Injury
and adolescent sports: Injury rates, risk factors and prevention, rates on FieldTurf and natural grass for high school football and
Clin Sports Med 27(1):19–50, 2008. soccer, Med Sci Sports Exerc 41(5):S587, 2009.
103. Meeuwisse WH: Predictability of sports injuries: What is the 121. Webster DA, Bayliss GV, Sparado JA: Head and face injuries in
epidemiological evidence? Sports Med 12(1):8–15, 1991. scholastic women’s lacrosse with and without eyewear, Med Sci
104. Emery CA: Injury prevention and future research. In Maffuli N, Sports Exerc 31(7):938–941, 1999.
Caine DJ, editors: Epidemiology of pediatric sports injuries, 122. Yang J, Marshall SW, Bowling JM, et al: Use of discretionary
Medicine and Sport Science, Basil, 2005, Karger. protective equipment and rate of lower extremity injury in high
105. Powell JW, Barber-Foss KD: Sex related injury patterns among school athletes, Am J Epidemiol 161(6):511–519, 2005.
selected high school sports, Am J Sports Med 28(3):385–391, 123. Schulz MR, Marshall SW, Yang J, et al: A prospective cohort
2000. study of injury incidence and risk factors in North Carolina
106. Bennett J, Reinking M, Pluemer B, et al: Factors contributing high school competitive cheerleaders, Am J Sports Med 32(2):
to the development of medial tibial stress syndrome in high 396–405, 2004.
school runners, J Orthop Sports Phys Ther 31(9):504–510, 124. Gilchrist J, Saluja G, Marshall SW: Interventions to prevent
2001. sports and recreation-related injury. In Doll LS, Bonzo SE,
107. Tyler TF, McHugh MP, Mirabella MR, et al: Risk factors for Mercy JA, Sleet DA, editors: Handbook of injury and violence
non-contact ankle sprains in high school football players: The prevention, New York, 2007, Springer.
role of previous ankle sprains and body mass index, Am J Sports 125. Janda DH, Bir C, Kedroske B: A comparison of standard vs.
Med 34(3):471–475, 2006. breakaway bases: An analysis of a preventative intervention for
108. Schulz MR, Marshall SW, Mueller FO, et al. Incidence and risk softball and baseball foot and ankle injuries, Foot Ankle Int
factors for concussion in high school athletes, North Carolina, 22(10):810–816, 2001.
1996–1999, Am J Epidemiol 160(10):937–944, 2004. 126. Janda DH, Wojtys EM, Hankin FM, Benedict ME: Softball
109. McGuine TA, Greene JJ, Best T, Leverson G: Balance as a pre- sliding injuries. A prospective study comparing standard and
dictor of ankle injuries in high school basketball players, Clin J modified bases, JAMA 259(12):1848–1850, 1988.
Sports Med 10(4):239–244, 2000. 127. Sendre, RA, Keating TM, Hornak, JE, Newitt PA: Use of the
110. Emery CA, Meeuwisse WH, Hartmann SE: Evaluation of risk Hollywood Impact Base and standard stationary base to reduce
factors for injury in adolescent soccer: Implementation and vali- sliding and base-running injuries in baseball and softball, Am J
dation of an injury surveillance system, Am J Sports Med Sports Med 22(4):450–453, 1994.
33(12):684–687, 2005. 128. Schneider S, Seither B, Tönges S, Schmitt H: Sports injuries:
111. Plisky PJ, Rauh MJ, Kaminski TW, Underwood FB: Star Excursion Population based representative data on incidence, diagnosis,
Balance Test as a predictor of lower extremity injury in boys and sequela, and high risk groups, Br J Sports 40(4):334–339,
girls high school basketball players, J Orthop Sports Phys Ther 2006.
36(12):911–919, 2006.
Index
A Acclimatization to altitude, 119b, 445 Adhesive capsulitis, in diabetics, 449
Ab Slide, 393 circulatory adaptations in, 119-120 Adhesive tape
Abdomen exercise performance and, 120 for custom padding, 485
anatomy of, 605f neuropsychologic function and, protective wrap under, 465t
three regions of, 606, 606t 120-121 Adhesives
Abdominal injuries, internal, 596, pulmonary ventilation and, 118, 119f for custom padding, 485
596b Acclimatization to cold, 114 for wound closure, 457, 587
acute life-threatening conditions in, Acclimatization to heat, 102-103, ADLs (activities of daily living), in
623b, 628 103b, 103f older adults, 706, 710
bladder, 612 Acetabular labrum, injury to AED (automated external defibrillator),
evaluation of, 604-606, 604b golf swing and, 222, 223b 627
hepatic, 609 osteoarthritis secondary to, 712 Aerobic capacity. See Oxygen uptake,
intestinal tract, 609-610 in runners, 307 maximum (VO2 max).
kidney, 450, 610-612 N-Acetylcysteine, 156-157 Aerobic conditioning tests, 32-33
pediatric, 610, 610b Achilles notch, of running shoe, 322 Aerobic exercise
types of, 610-611, 610f Achilles tendinopathy energy sources for, 67
misleading physical examination in, corticosteroid injection for, 716-717 after total hip arthroplasty, 719
604, 606t in dancers, 666-667, 666f, 667b Aerobic training
pancreatic, 612 eccentric training for, 715-716, 716b fat as fuel and, 84
penetrating, 604-606, 604b in masters athletes, 714 heat acclimatization and, 103
return-to-play criteria for, 608b pathophysiology of, 714-715 AEs. See Athlete-exposures (AEs).
signs and symptoms of, 598t, 604, topical glyceryl trinitrate for, 717 Agility, testing of, 31, 32f, 34t
604b Achilles tendon, aging and, 707 Aging. See also Masters athlete.
splenic, 606-609, 607f Achilles tendonitis, in cyclists, 210t benefits of exercise and, 704, 704b
structures involved in, 605f, 606b, ACL. See Anterior cruciate ligament cold exposure and, 113
606t (ACL). heat intolerance and, 104
ureteral, 612 Acne mechanica, 461, 461f musculoskeletal decline in, 704, 706
Abdominal muscles Acquired immunodeficiency syndrome of population, US and world, 704,
in golf swing, low back pain and, (AIDS), 448 705t
224-225, 225b Acrochordons, 466-467 AIDS (acquired immunodeficiency
tendinopathies of, in soccer players, Acromioclavicular joint syndrome), 448
298 football shoulder pads and, 512 Air management pads, 480-481
Abdominal surgery sprain of, protection for, 496-499 Air pollution, 123-124. See also
return-to-activity guidelines for, Actinic keratoses, 472 Asthma, air pollution and;
603t Activities of daily living (ADLs), in Carbon monoxide; Nitrogen
wound healing after, 604, 604f older adults, 706, 710 dioxide; Ozone; Particulate air
Abdominal wall, anatomy of, 597f Acupuncture, for delayed onset muscle pollution; Sulfur dioxide.
Abdominal wall injury, 596-604, soreness, 434 altitude and, 132
596b. See also Hernia. Acute mountain sickness, 118, 121, cold exposure and, 132
vs. blow to solar plexus, 597, 598t 122-123t heat stress and, 131
contusion as, 596-597, 604, 605-606 pre-existing lung disease and, 121 interactions between pollutants in,
vs. intra-abdominal injury, 598t ADD/ADHD (attention deficit 131
muscle strain as, 597-598, 619-620 disorder/attention deficit national standards for, 123, 124t
Abrasions, 457-458 hyperactivity disorder), 50-51, vocal cord dysfunction and, 128
corneal, 589 51b, 182 Aircast sport stirrup, 516-518, 517f
in disabled athletics, 688t, 690t, Adenosine receptors, caffeine and, Airway injuries
691-692 154-155, 160-161 laryngeal, 581-582, 582b, 583f
prosthetic socket and, 692 Adenosine triphosphate (ATP) nasal, 590, 590f
of head and face, 583 endurance exercise and, 141-142 rib fracture with, 617, 618b
Acceleration, running, testing of, 31, high-intensity exercise and, 158, 160 sternoclavicular dislocation with,
31t, 34t muscle nociceptors and, 424 620b
Page numbers followed by f refer to illustrations; page numbers followed by t refer to tables; page numbers followed by b refer to boxes.
773
774 Index
Airway management, 581-582 Androgens. See Anabolic-androgenic Anterior cruciate ligament (Continued)
Airway obstruction, checking for, steroids. in female soccer players, 299,
623-624 Androstenedione, testing for, 178-179 302, 632, 635, 733
Alcohol Anemia in jumping, 257, 261
caloric content of, 85 vs. dilutional pseudoanemia, 87, 87b, osteoarthritis secondary to, 166,
cold injury and, 114 446-447 632, 709
endurance contests and, 85-86 iron-deficiency, 86-87, 446-447, return to play after, 25-26
after exercise, 93 447b in soccer, 299, 302, 632, 635, 733
hypertension and, 442-443 preparticipation evaluation and, 21 valgus angle of knee and, 302
muscle metabolism and, 86 Angina pectoris lunge exercises and, 401-403, 402t
physiologic effects of, 85-86 carbon monoxide exposure and, 129 squat exercises and, 397-399, 398t
Alcohol abuse cold exposure and, 114 Anterior knee pain syndrome. See also
in athlete with disability, 690 high altitude and, 121 Patellofemoral pain.
in young athlete, 53, 53b Angiotensin-converting enzyme (ACE) Q-angle and, 320
Allergic dermatitis, 464-465 inhibitors, for hypertension, 443 in soccer players, 298
Allergy Ankle taping for, 524, 528, 528b
asthma in, 124, 126 in ballet, 657-662, 658f, 659f, Anterograde amnesia, 539
in athlete with disability, 688t 659t, 660b, 660f, 661f Antibiotics, facial wounds and, 587
Alopecia, 462, 462f in cycling, injury to, 208 Anticholinergic drugs, heat intolerance
Altitude. See High altitude. hypermobile, gluteus medius and, caused by, 106
Amenorrhea 314-315 Antihistamines, heat disorders and, 20
bone density and, 18-19, 87, impingement syndromes of, 664-666 Anti-inflammatory drugs
641-642, 643 anterior, 665-666, 666b breast trauma and, 622
diagnostic testing in, 642-643 posterior, 665, 665f, 666b for delayed onset muscle soreness,
exercise-induced, 18-19 in running 429-430
in female athlete triad, 53, 641-642 kinematics of, 309-310, 309t in iontophoresis, 432
Amino acids, 77 knee pain and, 320b in phonophoresis, 432
ATP generation from, 141-142 muscle activity and, 315-316 for exercise-induced bronchospasm,
branched-chain, 79 in soccer 444
central fatigue and, 144 injury to, 297, 300 Antioxidants
as ergogenic aid, 152-153 jumping and, 296-297 for delayed onset muscle soreness,
plant sources of, 82 sprains of 435
Amnesia, concussion with, 539, 539b bracing and, 508 as ergogenic aids, 156-157, 157b
Amphetamines impingement syndromes second- Aorta, rib fracture with injury to, 617,
heat stroke caused by, 106 ary to, 665-666, 666b 618b
reasons for use of, 175 os trigonum and, 665, 673 Aortic coarctation, preparticipation
testing for, 180-181 overweight and, 766 examination and, 17-18
Amputees as athletes, 694b in soccer players, 300 Aortic rupture, 627-628
as cyclists, 209-211, 209b, 212f taping of. See Taping, of ankle. Aphasia, 699
injuries of, 692-695, 693f total joint arthroplasty of, 722-723 Aphthous ulcer, 460
as runners, energy requirements for, Ankle braces, 508, 509f Apocrine glands, 456
694-695 risk of injury and, 767 Apolipoprotein E, concussion and,
Anabolic Steroid Control Act, 177-178 vs. taping, 516-518, 517f, 518f, 542, 545
Anabolic-androgenic steroids, 55, 519, 521 Apophysitis, in runners, 307
164-165 cost-effectiveness of, 508, 523-524, Appendectomy, return-to-activity
adverse effects of, 165, 165b 524b guidelines for, 603t
hypertension as, 442 Ankylosing spondylitis, 638-639 Arches, height of, in runners, 318,
pectoralis major rupture as, 622 Anorexia nervosa, 22-24t, 54, 54b, 319f, 320-321
common examples of, 177t 641 Arnica, for delayed onset muscle
testing for, 174-175, 176-179, 177t Antacids, 446 soreness, 434-435
young people’s use of, 55-56 Anterior cord syndrome, 573 Arthritis. See Osteoarthritis.
Anaerobic conditioning tests, 32, 33t, Anterior cruciate ligament (ACL) Artificial turf, injury rates and, 767
34t deficiency of Ascorbic acid. See Vitamin C.
Anaerobic metabolism cycling and, 196-198, 198f, 199f Asteatotic eczema, 475, 475f
energy sources for, 67 knee brace and, 504-506, 506f Asthma, 124-126, 445
at high altitude, 120 injury to air pollution and, 126
for high-intensity exercise, 158, 158b case study of, 6-7, 7f nitrogen dioxide in, 131
Analytic studies, 731 in dancers, 668-670, 669f, 670b, ozone in, 131
Analytical epidemiology, 745 670t, 671-672 sulfur dioxide in, 129, 131
Androgen insensitivity syndromes, in female athletes, 25-26, 632-635, cold-induced, 114, 132
185 633t, 634f, 669-670, 766 definition of, 125b
Index 775
Cardiac. See also Heart. Cerebral blood flow Cervical spine injuries (Continued)
Cardiac dysrhythmia, sports participa- concussion and, 537, 545 types of, 551-556
tion with, 22-24t during exercise, 144 brachial plexus, 551, 553f
Cardiac injuries, 626-628. See also Cerebral edema fractures, subluxations, and
Sudden cardiac death. high-altitude, 122, 122-123t, 122b, dislocations, 552-554, 554f,
aortic rupture and, 627-628 445 555f
commotio cordis in, 444, 627, hyponatremia with, 109 sprains and strains, 551-552, 553f
627b Cerebral palsy, athletes with stenosis with neurapraxia, 555-556,
contusion as, 626-627, 626b, 627b aphasia in, 699 556b, 556f, 557f, 576t
tamponade in, 623-624, 627, 627b as cyclists, 209, 211-212, 213f Cervical stenosis, 555-556, 556b,
Cardiac output dysarthria in, 699 556f, 557f
altitude and, 119-120 dysphagia in, 698 return to play and, 576t
carbon monoxide exposure and, injuries of, 692 Chafing, 464
129 knee instability and, 694 Chain of custody, in drug testing,
cold exposure and, 111 seizures in, 699 175-176, 175b
heat stress during exercise and, 101, sports participation by, 22-24t Change. See Behavior change.
102f Cervical collars Cheerleading
hypertension and, 442 rigid, for immobilization, 570-571, cervical spine injuries in, 559
Cardiorespiratory fitness, 707-708. 571f, 572f coaches of, risk of injury and, 767
See also Oxygen uptake, maximum soft, for sprains and strains, 552 Chemosis, 589
(VO2 max). Cervical spine Chest injuries. See Thoracic injuries.
Cardiovascular adaptations, to congenital conditions of, 576t Chest pain, costochondritis with, 617
endurance training, 142, 142b fusion of, return to play and, 578t Chest protection, 500-501, 503f
Cardiovascular disease, 441-444 of soccer player Chest radiography, of trauma patient,
carbon monoxide exposure and, biomechanics and, 294-296, 294b 624-625, 625f, 626
129 injury to, 300-301 Chilblains, 116, 116-117t, 474
cold exposure and, 114 Cervical spine injuries, 549-580 Chin straps, 490-491, 491f
congenital, sports participation equipment standards and, 563b Chiral analysis, for banned stimulants,
with, 22-24t hospital management of, 571-574 180-181
high-altitude exercise with, 121 helmet and, 571, 573-574, 575f Chlorpromazine, heat intolerance with,
Cardiovascular examination, prepartic- introduction to, 549 106
ipation, 17-18, 17b, 18f legal considerations in, 560-562, Chondroitin, 166
Carditis, sports participation with, 560b Chondromalacia patellae
22-24t mechanism of, 554, 554b, 554f, cycling and, 208-209
Carnitine 555f, 559-560, 560b, 561f taping for, 525
for delayed onset muscle soreness, on-site management of, 562-571 CK. See Creatine kinase (CK).
435 algorithms for, 564f, 565f Clavicle
as ergogenic aid, 157-158 for conscious athlete, 566-568 injury to, in weight training, 416
Carpal tunnel syndrome face mask removal in, 566, 567f shoulder pads and, 512
in diabetics, 449 guidelines for, 562b Clean, 385, 406
in wheelchair athletes, 691-692 helmet in, 568-569, 569b, 571 segment mechanics of, 406-410,
Case series, 731-732, 731t, 733, 734f, immobilization in, 568-571, 408f, 409t, 410f
734t 568b, 568f, 569b, 570b, system mechanics of, 410-412,
surveillance system design and, 742, 570f, 572f 411f, 412b, 412t, 413t
743t initial actions in, 564-565, 564b, Clean and jerk. See Clean.
Case-control studies, 731-732, 731t, 565b Clean and snatch, 406
732b, 733, 734f, 734t medical team in, 563, 563b Clearance for participation, 21
Case-crossover studies, 731, 731t, planning for, 560, 562b, 563-564, contact level and, 10b, 21
732-733, 734t 564b intensity level and, 19t, 21
Casein, as protein supplement, 162 players and coaches during, 563b pass/fail criteria and, 21b
Casting materials, 484-485, 484b, 485f training for, 560, 560b, 564, specific medical conditions and,
Casts, legality of, in high school 575-578 22-24t
football, 484b for unconscious athlete, 566, 567f Cleats, 508, 510-511, 510f
Catastrophic injuries, epidemiology of, return to play and, 574-575, 576t, Clinical incidence, 739
761-762 577t, 578t Clothing. See also Protective equipment.
Cauliflower ear, 493, 582-583, 584f sport-specific incidence of, 556-559, cold exposure and, 110, 112-113,
Cecal slap syndrome, 446 557f 474
Central cord syndrome, 573 in soccer, 300-301 heat stress and, 105
CERA (methoxy glycol–epoetin beta), tracking and surveillance of, 550-551, protective, 465t
180 550f, 551f, 552t sun exposure and, 133
Cluster-randomization, 733
778 Index
Golf injuries (Continued) Ground reaction forces (Continued) Headache, concussion with, 540,
spinal biomechanics and, 223-225, shock attenuation and, 316-318, 540b, 545
223b, 225b 316f Heart. See also Cardiac entries.
club length and, 229 speed and, 317 age-related changes in, 708b
stresses leading to, 217-218 in soccer athlete’s, 17-18, 442
upper limb biomechanics and, during cutting, 292-293 vs. hypertrophic cardiomyopathy,
225-228, 225b, 228b during landing, 296-297, 302 442, 442t
elbow in, 225, 226-227, 226b, in tennis Heart murmur, sports participation
226f, 227b, 227f, 228b kinetic chain and, 268, 270 with, 22-24t
shoulder in, 225-226, 226b, 228b reaction time and, 282-283 Heart rate
wrist and hand in, 225, 227-228, surface and, 279, 279f altitude and, 119-120
228b, 228f in vertical jumping, 237-239, 238b, in exercise training, 121
Golf shoes, 221, 230, 231b 239f cold exposure and, 110-111
Golf swing arm swing and, 247, 248-249 heat stress with exercise and,
difficulty of, 217 in high jump, 252 101, 102f
general biomechanics of, 218-221 muscle activity and, 242, 244f acclimatization of, 103, 103f
grip tension in, 227 squat vs. countermovement, 249, dehydration and, 103-104
hand positions in, 226-227, 226f, 250f training precautions and, 105
227f Growth hormone, 180 neurologic lesions and, 695
injury and. See Golf injuries. Gymnastics normal ranges of, by age group, 16t
kinematic sequence of, 220, 220b body composition and injury in, 766 Heat acclimatization, 102-103, 103b,
lead and trail designations for, cervical spine injuries in, 559 103f
218-221 spondylolysis and, 638 Heat cramps, 106, 107-108t
muscle activation in, 220, 220t, Heat disorders, preparticipation
221t H evaluation and, 20, 22-24t
neutral grip in, 226-227, 227f Hair Heat exhaustion, 106, 107-108t
phases of, 218-221, 218b, 219f chemical damage to, 474-475 miliaria profunda and, 109
Golfer’s elbow. See Medial epicondylitis friction-induced loss of, 462, 462f Heat illness, 106-109, 106b, 107-108t
(golfer’s elbow). Hair follicles, 455-456, 456f, 457f Heat intolerance
Granular cell layer, 455 Hallux pressure, in sidestep cutting, drugs associated with, 106
Granuloma, pyogenic, 460 292 populations susceptible to, 105-106,
Graphite Rollbar system, 322-324 Hallux saltans tenosynovitis, 667 105b
Great vessel injuries Hamstrings Heat loss, pathways of, 99, 99f
rib fracture with, 617, 618b activity of, in running, 315 Heat production, metabolic, 99
sternoclavicular dislocation with, cycling biomechanics and, in cold climate, 110
620b 200-201 in endurance exercise, 142
Groin pain flexibility testing of, 31 Heat rash (miliaria rubra), 106,
in athletic pubalgia, 600-602, 600b, knee injury and 107-108t, 109, 466, 466f
601f on landing, 261, 261b Heat stress, exercise-associated.
differential diagnosis of, 599t in women, 633 See also Heat illness; Heat
hernia with, 598-599, 600 strains of intolerance.
hip joint causes of, 602 protection for, 501 acclimatization and, 102-103, 103b,
obturator nerve entrapment with, in runners, 307 103f
603 in soccer players, 298 aging and, 104
protective equipment and, 501 Handball, vertical jumping in, 252, air pollution and, 131
sacroiliac conditions with, 639 253f cardiovascular responses to, 101, 102f
soccer-related, 298, 300, 303, 598 Hands, protection for, 499, 499b, cerebral response to, 101, 144b
in testicular or scrotal injury, 613-614 501f clothing and, 105
Ground reaction forces in wheelchair athletes, 691-692 core temperature and, 100-101,
in disabled athletics, with amputees, Hang clean or snatch, 406 100b, 100f
693 Harman’s equation for average dehydration in, 103-104, 104b,
in golf, 221-222, 230 power, 29 104f, 105
in landing, 257-258, 260-261, 262 Harris-Benedict equation, 94, 94b fatigue and, 101, 152
gender and, 260, 260b, 633-634 Head injury. See also Brain; gender and, 104-105
in running, 309, 316-318, 316b, Concussion; Maxillofacial injuries. glycerol-induced hyperhydration
318f pupillary differences in, 15 and, 148
arch height and, 318, 319f soccer-related, 300-301, 300b metabolic responses to, 101
on curved pathway, 292 electroencephalogram and, reducing, 105, 105b
point of impact and, 317-318, 537-538 Heat syncope, 107-108t
317b, 317f, 318f sports participation with history of, Heat wrap, for delayed onset muscle
pronation and, 312 22-24t soreness, 431
786 Index
Lunate, dislocation of, in weightlifter, Masters athlete (Continued) Metabolic testing, 32-33, 33f, 33t
415 muscle and, 706-707, 706b, Metatarsal fractures
Lunge exercises, 393-397, 395t, 396t, 707b, 707f fifth, 667-668, 668f
401-406, 402t, 403b, 404f, 405f, tendon and, 707, 707b stress fractures, 668, 669f
406b sports medicine practitioner and, Metatarsalgia, in cyclists, 210t
705-706 Metatarsophalangeal joints
M tendinopathy in, 714-717, 716b first, in dancers
Macronutrients, 67-86. See also world records of, in track, 705, 705t osteoarthritis of, 672, 672b
Carbohydrate; Fat; Protein. Maxillary fractures, 591, 591f, 592b sesamoiditis and, 673-674, 674f
calories per gram of, 83t Maxillofacial injuries, 581-595 in jumping, 250-251
dietary reference intakes (DRIs) airway, 581-582, 582b, 583f Methacholine challenge test, 126
acceptable ranges, 77t concluding summary of, 595 Methicillin-resistant S. aureus
additionally limited, 79t dental, 594-595, 594b, 594f, 595b (MRSA), 448-449, 448b
recommended intakes, 78t fractures in. See Facial fractures. Methoxy glycol–epoetin beta (CERA),
recommended distribution of, initial management of, 581, 581b, 180
83t 582t Methylprednisolone, for spinal cord
Macrophages, delayed onset muscle introduction to, 581 injury, 574
soreness and, 428 ocular, 587-590, 588b, 589b, 590b Microcurrent electrical neuromuscular
Maladaptive fatigue syndrome, 48-49, soft tissue, 582-583. See also Abra- stimulation (MENS), 433
48b sions; Contusions; Lacerations. Microfailure zone, 321-322, 321f
Malignancy, sports participation with, Maximum voluntary isometric Micronutrients, 67, 86-91. See also
22-24t contraction (MVIC), 350, 352 Minerals (elements); Vitamins.
Malocclusion, 592, 593f Medial collateral ligament, of knee, Midfacial fractures, 590-591, 591f,
Mandible injury to, 504 592b
dislocation of, 592-593 Medial epicondylitis (golfer’s elbow), Midfoot motion, in running, 312
fracture of, 591t, 592-593, 592b, 226, 227b Midfoot pronation, in running, 320
593f in baseball pitchers, 362, 380 Midfoot strikers, in running, 317-318,
zygomatic fracture and, 591 Medial tibial stress syndrome 317b, 317f, 318f
Manual therapy (shin splints) Migraine, post-traumatic, 540
for osteoarthritis in cyclists, 210t Miliaria, 466
of hip, 712 diagnosis of, 637 Miliaria crystallina, 466
of knee, 710 pathogenesis of, 637 Miliaria profunda, 107-108t, 109, 466
for tendinopathy, 715 in runners, 307 Miliaria rubra, 106, 107-108t, 109,
Manubrium, 616f, 620 body composition and, 766 466, 466f
Marathon runners, physical fitness female, 637, 637b Milk-based protein supplement, 162
profile for, 27 foot abnormalities and, 320 Minerals (elements), 86-91
Marfan syndrome, 17-18, 441, 443, in women, 637, 637b dietary reference intakes (DRIs),
443t Median nerve, entrapment of, in 70t, 74-75t, 80t
Marijuana, testing for, 181 baseball pitchers, 381 supplementation of, 86-87
Massage, for delayed onset muscle Medical history iron-deficiency anemia and, 447
soreness, 433-434 maxillofacial injury and, 581 multivitamin with, 94
Mast cells, delayed onset muscle in nutritional assessment, 58 Mitochondria, endurance training and,
soreness and, 425f, 428-429 in preparticipation evaluation, 142
Masters athlete, 10b, 704-729. 12-15, 13f Mitral valve prolapse, sports participa-
See also Aging; Elderly athlete, Medicine ball throw distance, 29, 34t tion with, 22-24t
preparticipation evaluation of. Melanocytes, 455 Moles, 472-473
competitive events for, 705 Melanoma, 132, 472-473 Molluscum contagiosum, 470
definition of, 705 Menopause, 644-645 sports participation with, 22-24t
introduction to, 704-706 MENS (microcurrent electrical Mononucleosis, infectious, 447, 447b,
joint replacement in. See Total joint neuromuscular stimulation), 433 608-609
arthroplasty. Menstrual cycle Monounsaturated fats, dietary sources
osteoarthritis and, 708-714 anterior cruciate ligament injury of, 85t
hip, 711-713 and, 634 Morton’s foot, in ballet vs. folk
knee, 709-711, 709f, 710b, body temperature and, 104-105 dancing, 660
712 Menstrual history, 18-19 Mountain sickness. See Acute
shoulder, 713-714 Metabolic rate. See also Caloric mountain sickness.
physiology of aging in, 706-708 expenditure. Mouth
body composition and, 706 basal (BMR), 94 aphthous ulcers of, 460
cardiorespiratory fitness and, cold exposure and, 110 mucosa of, 455
707-708, 708b exercise-heat stress and, 101 Mouthguards, 493, 493f, 594-595
flexibility and, 708, 708b food restriction and, 94b ulcer prevention by, 460
Index 791
Movement patterns, physical fitness Muscle mass. See also Muscle(s), National Athletic Training Association
profile and, 24-25 hypertrophy of. Board of Certification
Movement screening, 28, 28b, 34t ergogenic aids and, 162-164, (NATABOC), 2, 2b
MRSA (methicillin-resistant S. aureus), 162b National Football League (NFL)
448-449, 448b resistance training and, 161-162 combine, 26
Multiple sclerosis Muscle pain National Operating Committee on
cold-induced motor control and, 114 causes of, 423, 423b, 424t Standards for Athletic Equipment
heat intolerance in, 106 receptors of, 423-424, 425f (NOCSAE)
hypotension in, 698 Muscle soreness. See Delayed onset baseball helmets and, 488
neurogenic bladder and, 697-698 muscle soreness (DOMS); football helmets and, 478, 479b,
temperature regulation and, 695 Soreness. 486, 486b, 487b
Multi-RM testing, 28-29 Muscle strain, 435-436, 435f. See also lacrosse helmets and, 490
Multivariate regression, 741, 741t Muscle damage. Navicular drop
Multivitamin with minerals, 94 abdominal, 597-598, 619-620 medial tibial stress syndrome and, 637
Muscle(s) cervical, 551-552 running injuries and, 766
aging and, 706-707, 706b, 707b, chest wall, 619-620 Nearsightedness, 15
707f continuum of, 424t Neck. See also Cervical spine.
biarticular, jumping and, 242-243, in disabled athletics, 688t injury to
244-245 vs. muscle soreness, 423, 423b laryngeal trauma in, 582, 582b,
caffeine effect on, 155 rates of, 758b 583f
cold stress and, 110 in soccer players, 300 in soccer players, 300-301
endurance training and, 142, 143b thigh and hip protection and, 501 stresses on, in golf, 221
force-length relationship of, 238b in weightlifters, 415, 415b Neck pain, cycling and, 209, 210t
glycogen in, 67 Muscle strength. See also Strength Neck protection, 494, 494f, 495f
diet and, 67, 77 training. Nedocromil, for exercise-induced
endurance exercise and, 141-142 anabolic steroids and, 165 bronchospasm, 444
endurance performance and, cold exposure and, 111 Neoprene elbow sleeve, 506, 507f
149 creatine supplementation and, 163 Neoprene knee braces, 506, 507f
exercise-heat stress and, 101 gender differences in, 631, 632t Neurogenic bladder, 697-698
replacement of, 93 high altitude and, 120 Neuroleptic drugs, heat intolerance
heat stress and, 101 testing of, 28-29, 34t with, 106
hypertrophy of. See also Muscle mass. Musculoskeletal disorders, sports Neurologic examination
anabolic steroids and, 165 participation with, 22-24t preparticipation, 17
fiber types and, 706 Musculoskeletal examination, in suspected cervical injury
for optimizing speed and power, preparticipation, 15-17 at hospital, 573
159 MVIC (maximum voluntary isometric on-site, 566-568
through strength training, 159, contraction), 350, 352 Neutrophils, delayed onset muscle
162 Myocardial contusion, 626-627, 626b, soreness and, 425f, 427-428, 429
of masters athlete, 706-707, 707f 627b Nevi, dysplastic, 472-473
red blood cell destruction in, 447 Myocardial infarction, cold exposure Niacin, toxic effects of, 86
strength training and, 159, 159b and, 114 Nipples
Muscle actions, in physical fitness Myofascial force transmission, 303 chafing of, 464
profile, 25 Myoglobin, 86-87 trauma to, 623
Muscle activity. See Electromyography muscle damage and, 427-428 Nitrogen dioxide, 124t, 129-130, 131
(EMG). Myokinase, high-intensity exercise Nitrogen oxides, 129-130
Muscle cramps, 423 and, 158-159 Nociceptors, muscle, 423-424, 425f,
fluid replacement and, 147 Myopia, 15 429
Muscle damage. See also Creatine Myositis ossificans, 451-452, 452f NOCSAE. See National Operating
kinase (CK); Muscle strain. Committee on Standards for
coenzyme Q10 and, 435 N Athletic Equipment (NOCSAE).
delayed onset muscle soreness and, N-acetylcysteine, 156-157 Nonsteroidal anti-inflammatory drugs
426f, 427-428, 427f, 429 Nails, 456, 456f (NSAIDs). See also Anti-
beta-hydroxy-beta-methylbutyrate fungal infection of, 467-468 inflammatory drugs.
and, 163-164 hemorrhage under, 459, 462, 462f breast trauma and, 622
Muscle endurance ingrown, 462-463 delayed onset muscle soreness and,
acclimatization to altitude and, Nandrolone (19-nortestosterone), 429-430
120 177-178 19-Nortestosterone (nandrolone),
local, testing of, 29, 34t Nasal trauma, 590, 590b, 590f 177-178
Muscle fibers fractures in, 590, 590b, 590f Nose
aging and, 706-707, 707b, 707f hockey-related, 591t cerebrospinal fluid leakage from, 591
types of, 706 lacerations in, 586 injury to. See Nasal trauma.
792 Index
Patellar tendinitis Peritoneal irritation, 604, 605-606, Plantar pressures. See Foot plantar
cycling and, 208-209, 210t 609, 612 pressures.
running and, 320b Peritoneal lavage, 605, 606t Plantar warts, 469, 470f
Patellar tendinopathy (jumper’s knee), Pes anserine bursitis, in cyclists, 210t Plasma volume, glycerol-induced
257, 261b, 262, 714 Pes cavus, running shoe for, 318, 322 hyperhydration and, 148
eccentric training for, 716 PET (positron emission tomography), Plastazote, 484
pain of, 714-715 concussion and, 537 Plastics. See Thermomoldable plastics.
soccer-related, 299, 301-302 Petechiae, 458-459, 458f Platelet-rich plasma, for tendinopathy,
Patellar tendinosis, in weightlifter, PFP. See Physical fitness profile (PFP). 717
416 Pharmacology, sports, 174-175, 174b Playgrounds, injury prevention in,
Patellar tendon rupture, in weightlifter, Pharyngitis, 445 768t
415 Phonophoresis, 432 Plyometric training
Patellar tendon strain, in weightlifter, Phosphocreatine. See Creatine depth jumps in, 253b
415-416 phosphate (CP). push-ups in, 391
Patellofemoral forces Photo injury. See Sun exposure. for swimmers, 347
in lunge exercises, 404-406, 404f, Physical Activity Guidelines, of US Pneumothorax, 624-625, 624b, 625b,
405f, 406b federal government, 704-705 625f
in squat exercises, 399-401, 400f, Physical examination. See Preparticipa- rib fracture with, 618, 618b,
401b, 401f tion evaluation (PPE), physical 624-625
Patellofemoral joint examination in. spontaneous, 625
injury to Physical fitness profile (PFP), 21-36 tension, 623-624, 625, 625b, 626f
in runners, 309 data quality in, 27, 27b, 33 Polidocanol, for tendinopathy, 416,
in soccer players, 299 developing test battery for, 33, 34t 717
neoprene stabilizers for, 506, 507f important uses of, 25-27, 25b Polyunsaturated fats, dietary sources
Patellofemoral pain. See also Anterior introduction to, 21-24, 24b of, 85t
knee pain syndrome; Knee pain. needs analysis for, 24-25, 25b Popliteus tendinitis, in cyclists, 210t
in cyclists, 210t safety considerations in, 27, 27b Positron emission tomography (PET),
in runners for skill- or strategy-intensive sports, concussion and, 537
foot pronation and, 319-320 27, 27b Postconcussion syndrome, 537
hip abduction weakness and, sports medicine team and, 25, 25b, Posterior cord syndrome, 573
314-315 33-36 Posterior cruciate ligament (PCL)
management of, 320b strength and conditioning lunge exercises and, 401-403, 402t
Q-angle and, 319-320 coordinator in, 21-24 squat exercises and, 397-399, 398t
in soccer players, 298-299 test classifications in, 27-28, 27b Postpubescent athlete, preparticipation
taping for, 524-528, 524f, 525f, tested constructs in, 28-33, 28b evaluation of, 9
526f, 529-530t agility, 31, 32f Postural instability, in concussed
in women, 635-637, 635t for common sports, 34t patients, 537-538, 540
PCL. See Posterior cruciate ligament flexibility and range of motion, Potassium
(PCL). 31-32 dietary, 70t, 74-75t
Peak stresses, of sports, 18, 19t local muscle endurance, 29 hypertension and, 443
Pectoralis major metabolic capacity, 32-33, 33f, 33t muscle nociceptors and, 424
anatomy of, 621, 621f movement screening, 28, 28b Potential energy, definition of,
rupture of, 621-622 muscular strength, 28-29 238-239
Pedal designs, joint loads and, 196, power, 29-30, 30f Power
196f velocity and acceleration, 30-31, definition of, 239
Pedal reaction forces, 191-193, 191f, 31t muscle
192f, 193f Physical therapist, sports, 2-3, 3b, 3f defined, 29
Pelvic drop, in running, 314-315, 315f competency statements for, 3b testing of, 29-30, 30f, 34t
Pelvis injury management and, 6 in vertical jumps, 239-240, 240f,
running injuries to, 307 Physician. See Team physician. 240t
soccer-related dysfunctions of, 297b, Phytochemicals, antioxidant, 156-157 Power activities. See High-intensity
298 Piezogenic papules, 459-460, 459f exercise.
Penile injury, 614 Pink eye, 450 Power clean or snatch, 406
Performance-enhancing substances, Pitching. See Baseball pitching. Power endurance tests, 32, 33f, 34t
174-175, 174b. See also Drug Pitted keratolysis, 467, 467f Power Wheel, 393
testing; Ergogenic aids. Plantar fasciitis Powerlifting, 406
Pericardial effusion, rib fracture with, in runners squat exercise and, 386-387
618 foot abnormalities and, 320-321 PPE. See Preparticipation evaluation
Pericardial tamponade, 623-624, 627, incidence of, 307 (PPE).
627b stride length and, 310 Pre-existing conditions, 10-11
Perineum, injuries to, 614-615 taping for, 523
794 Index
Psychosocial aspects of youth sports QT interval, prolonged, in eating Rearfoot strikers, in running,
(Continued) disorders, 642 317-318, 317b, 317f, 318f
parents and Quadriceps Rearfoot varus
clinician’s role with, 44-45, 45b, 46 contusions of, protection for, 501 knee injury and, in soccer players,
key tools for, 43-44, 43b in female athletes, 633 299
positive attitudes of, 44, 44b patellofemoral pain and, 636 medial tibial stress syndrome and,
unhealthy involvement by, 41, 43, in running, 315 637
44-46, 48 strains of, protection for, 501 pronation associated with, 320
performance enhancement and, Quadriceps angle. See Q-angle. Recommended dietary allowances
43-44, 43b Quadriceps tendon, strains of, in (RDAs), 66
slump and, 48 weightlifters, 415 Recreational drugs, 174-175, 174b
staleness and, 48-49 Quadrilateral space syndrome, in Rectus abdominis muscle
steroid abuse and, 55-56 baseball pitchers, 380 athletic pubalgia and, 602
substance abuse and, 53, 53b Quadriplegia. See also Spinal cord injury. hematoma in, 598, 604
winning and, 43-44 autonomic dysreflexia in, 698 strain of, 597-598
Pubalgia, athletic, 600-602, 600b, 601f cervical spinal stenosis and, 555-556 Rectus femoris, vertical jumping and,
Pubescent athlete, preparticipation heat and cold intolerance in, 695 242-243, 244f, 245f, 251
evaluation of, 9 Quercetin, 156-157 Rectus femoris strain, in soccer
Pudendal nerve, cycling trauma to, 614 players, 298
Pulmonary artery pressure, altitude R Regression models, 741, 741t
and, 119 Radial nerve, entrapment of, in Rehabilitation. See also Return to
Pulmonary compromise, sports baseball pitchers, 381 competition.
participation with, 22-24t Radiant heat exchange, 99 physical fitness profile used in,
Pulmonary disease, 444-445, 445b Radiocapitellar joint, injury to, in 25-26
carbon monoxide exposure and, 129 baseball pitchers, 363, 381 Rehydration, 91, 91b, 93, 93b.
high altitude and, 121 Radiologic examination. See also See also Fluids and exercise.
Pulmonary edema Computed tomography (CT). caffeine and, 92
high-altitude, 121-122, 122-123t, of cervical spine injury, 571, intravenous, 146
122b, 445 573-574, 573b sodium solution for, 87, 93b
hyponatremia with, 109 of knee osteoarthritis, 709-710, 710b Reinjury
Pulmonary examination, of rib fractures, 618, 618b rates of, 761
preparticipation, 18 Randomized controlled trials, 731, risk of, 763
Pulmonary function testing, 125 731t, 733 Repoxygen, 181-182
Pulmonary hypertension, high altitude advantages and disadvantages of, Resistance training, 161-162. See also
and, 121-122 733, 734t Strength training; Weight
Pulmonary injuries, 624-626 Range of motion (ROM). See also training.
contusion as, 624, 624b Flexibility. beta-hydroxy-beta-methylbutyrate
hemothorax in, 618, 618b, 623-624, aging and, 708 and, 163-164
625-626 in cycling, 187-188 carbohydrate-protein supplements
mediastinal emphysema in, 626, 626b kinematics of, 188-189, 188f, and, 162-163, 162b
pneumothorax in, 624-625, 624b, 190, 191b conjugated linoleic acid and, 164
625b, 625f stationary bicycle adjustments and, creatine and, 163
tension, 625, 625b, 626f 206b Respiratory rate, normal ranges of,
subcutaneous emphysema in, 618, in running, 309-310, 309t by age group, 16t
626, 626b testing of Resveratrol, 156-157
Pulmonary ventilation, at high altitude, in physical fitness profile, 31-32, 34t Retinal detachment, 15, 22-24t
118-119, 119f preparticipation, 15 Retrograde amnesia, 539
Pupil diameter, baseline differences in, Rate ratio, 738t, 740, 740b Retroperitoneal abdomen, 606, 606t
15 RDAs (recommended dietary Retroperitoneal hematoma, 604-605,
Purpura. See Bruising. allowances), 66 606
Push-up, 391 Reach height, 235-236, 236b, 237f Retroperitoneal hemorrhage, 611
Pyogenic granuloma, 460 Reactive nitrogen species, antioxidants Return to competition
and, 156-157 psychological aspects of, 4-5
Q Reactive oxygen species, antioxidants as team decision, 6
Q-angle and, 142, 156-157 team physician’s responsibility for,
gender differences in, 261, 631, 635 Rearfoot motion 4-5, 5b
knee injury and, in runners, 766 ankle bracing and, 508 in youth sports, 48, 48b
knee pain and, 319-320 in running, 312-314, 313f, 314t, Revolution helmet, 486-487, 487f,
in runners, 319-320 320-321 512
in women, 635-636 shoe selection and, 511 Rib belts, 616-617, 618-619, 618b
796 Index
Shin splints. See Medial tibial stress Sit-and-reach test, 31, 34t Snapping scapula, in baseball pitchers,
syndrome (shin splints). Sit-ups, 391, 393 380
Shingles, 460 Skate bite, 464, 464f Snatch, 385, 406
Shivering, 110 Skateboarding, injury prevention in, segment mechanics of, 406-410,
endurance training and, 113 768t 407f, 409t, 410f
glycogen and, 113-114 Skaters, female, scoliosis in, 640-641 system mechanics of, 410-412,
hypoglycemia and, 113-114 Skating, inline, injury prevention in, 411f, 412b, 412t, 413t
in hypothermia, 114-115, 115t 768t Snowboarding
spinal cord injury and, 114 Skier’s toe, 462 cervical spine injuries in, 558
subcutaneous fat and, 113 Skiing injury prevention in, 768t
Shock pads, 496 cervical spine injuries in, 558 Snowmobiling, cervical spine injuries
Shoe inserts. See Orthosis, foot. injury prevention in, 768t in, 558
Shoes, 508-512, 510f knee brace in, after ACL reconstruc- Soccer
for cycling, 208 tion, 505 physical fitness profile for, 34t
for dancing en pointe, 656-657, after total hip arthroplasty, 719 protective equipment for
657f, 658f Skin helmets, 512
for golf, 221, 230, 231b aging of, 457, 473 shin guards, 506-508, 508f
for running, 508, 510f cold climate and, 110 shoes, 510f
categories of, 322-324, 323b, 324f heat dissipation in, 142 Soccer biomechanics, 287-306
construction of, 322-324, 323b overview of, 455-457, 456f approach to, 288
high arch and, 318 Skin cancers, sun exposure and, 132, of cutting, 288, 290-293, 291b
knee pain and, 320b 472-473 crossover, 291-292, 291f, 291t,
last types of, 323 Skin conditions 293
rearfoot stabilization by, 311, 314t of communal contact. See Skin injuries and, 290-291, 292-293,
recommendations for, 322-325, infections. 298-300, 299b
325b of environmental exposure, 471-475, pelvic rotations in, 292-293
selection of, 511b 471b, 473b, 475f sidestep, 291-293, 291f, 291t
surfaces and, 510-511, 510f equipment-related, 461-465, of heading, 288, 293-297, 294b,
Shoulder. See also Acromioclavicular 461b 294t, 295f
joint; Glenohumeral joint, heat- and sweat-related, 465-467, injuries and, 300-302, 300b
osteoarthritis of. 466b hypermobile joints and, 671-672
flexibility testing of, 31-32 heat intolerance in, 106 introduction to, 287
in golf, 221, 221b prophylactic measures for, 465t of jumping/landing, 296-297
protection of. See Protective trauma-related, 457-461, 457b injuries and, 300, 300b, 301-302,
equipment, for shoulders. Skin infections, 467-471, 467b 302f
taping for, 528-532, 532f bacterial, 470-471 of kicking, 288-290, 288b, 288t,
total joint arthroplasty of, 721-722, prevention of, 471, 471b 289f
721t, 722t pseudomonal, 470-471 injuries and, 297-298, 297b
Shoulder harnesses, 499 staphylococcal, 448, 448b, pelvic rotations in, 290, 290t, 298
Shoulder injuries 449-451, 470-471, 471b Soccer-related injuries, 297-302
in baseball pitchers, 367, 376-380, fungal, 467-469, 468f, 469b of abdominal wall, 598
377b, 378-379t parasitic, 471 biomechanical basis of. See Soccer
vs. football passers, 376 sports participation with, 22-24t biomechanics.
in golfers, 217, 221, 221b viral, 469-470, 469f, 470f capability-demand reasoning about,
osteoarthritis secondary to, 713 Skin tags, 466-467 287, 288t, 297
in swimmers, 341-343 Sleep deprivation rehabilitation and, 303
in weightlifters, 416 caffeine and, 155 complexities of the sport and, 287
in wheelchair athletes, 691 tyrosine supplementation and, 154 cutting-related, 290-291, 292-293,
Sickle cell disease Sleep disturbances, in concussed 298-300, 299b
high altitude and, 121 athletes, 541, 545 epidemiology of, 287
sports participation with, 22-24t Slipped capital femoral epiphysis, heading-related, 300-302, 300b
Sickle cell trait, 447 in runners, 307 jumping/landing-related, 300,
sports participation with, 22-24t Slump, in young athlete, 48 300b, 301-302, 302f
Side-ache, 603-604 Slump stretching, 640, 640f kicking-related, 297-298, 297b
Silicone elastomer, 484 Smoking. See also Tobacco. overview of, 297
Single-leg standing hyperextension carboxyhemoglobin and, 129 playing surface and, 767
test, 638-639, 638f particulates inhaled in, 130 prevention of, 768t
Single-photon emission computed Snapping hip rehabilitation for, 302-303, 303b
tomography (SPECT), in dancers, 670-671, 670f in women, to anterior cruciate
concussion and, 537 in runners, 307 ligament, 299, 302, 632, 635
798 Index
Sodium, 87-91. See also Hyponatremia; Spine. See also Cervical spine; Lumbar Sports medicine team (Continued)
Salt supplementation. spine. physical fitness profile and, 25, 25b,
in hydration fluid, 91, 93b recommended exercises for, 393, 33-36
muscle cramps and, 147 393b preparticipation physical examination
hypertension and, 442-443 stabilization of. See Weight training, and, 6, 6f
in sweat, 146-147 spine in. responsibility to the athlete, 4b
Sodium bicarbonate, as ergogenic aid, Spine board immobilization, 568-571, Sports pharmacology, 174-175, 174b
160 568b, 568f, 569b, 570b, 570f, Sprains
Softball 572f cervical, 551-552
injuries in, to pitchers, 766 Spirometry, 125 costochondral joint, 617
injury prevention in, 768t Spleen rates of, 758b
safety bases in, 767 enlarged of rib-vertebral attachment, 616
Solar plexus, blow to, 597, 598t in infectious mononucleosis, sternal joint, 620
Sorbothane, 481-482 608-609 thumb, splint for, 499, 499b
Sore throat, 445 sports participation with, 22-24t Squamous cell carcinoma, 472
Soreness. See also Delayed onset injury to, 606-609, 607f Squamous cells, 455
muscle soreness (DOMS). rupture of, mononucleosis and, 447, Squash, eye injuries in, 492
vs. pain, 339-341 608 Squat, barbell, 393, 399-400, 404
swimming and, 341, 342t Splints Squat jump, 234, 235f. See also
Soy protein, 162 legality of Jumping, vertical.
Spearing, 479 at elbow or below, 499 vs. countermovement jump, 249,
Spear-tackler’s spine, 576t in high school football, 484b 250f
SPECT (single-photon emission materials for, 483t, 484-485 depth of squat in, 238b
computed tomography), for ulnar collateral ligament sprain, Squat lift, 386-387, 387f, 388b, 388f,
concussion and, 537 499, 499b 389f
Speed activities. See High-intensity Split clean or snatch, 406 Squat wall exercises, 393-394, 395t,
exercise. Split jerk, 406 396t, 397-406, 398t, 399b, 400f,
Spermatic cord, torsion of, 614 segment mechanics of, 412-414, 401b, 401f
Spider veins, 460 413f Stacking, of anabolic steroids, 165
Spinal cord, cervical neurapraxia of, system mechanics of, 401-406, 414b Staleness
555-556, 556b, 556f, 557f Spondylolisthesis, 638-639 overtraining and, 450
Spinal cord injury. See also Wheelchair preparticipation evaluation and, 17 in young athlete, 48-49
athletes. Spondylolysis, 638-639 Staphylococcus aureus infections, 448,
autonomic dysreflexia in, 688t, 698, in weightlifters, 415, 415b 470
698b Sports, classification of methicillin-resistant, 448-449,
cervical, 554, 571. See also Cervical by dynamic and static demands, 448b, 470-471, 471b
spine injuries. 18, 19t, 21 Statistical methods, 740-742, 741t
cold sensitivity and, 114, 696 by level of contact, 10b, 21 Stellate lacerations, 583, 585f
epidemiology of, 549, 550f Sports anemia, 87, 87b, 446-447 Sternoclavicular joint, dislocation of,
heat intolerance in, 106, 697 Sports beverages, 91, 93, 93b 620, 620b
hypotension in, 698 Sports hernia, 600-602, 600b, 601f Sternum
in ice hockey, 558 Sports medicine anatomy of, 616f
neurogenic bladder and, 697-698 philosophy of, 704 fractures of, 620-621
patterns of, 573 physician training and certification injuries of, 620-621
substance abuse and, 690 in, 3 Steroid abuse. See Anabolic-androgenic
sunburn risk in, 696-697 Sports medicine team, 1-8. See also steroids.
temperature regulation and, 695 Athletic trainer; Physical therapist, Stieda process, 665, 665f
treatment of, 574 sports; Team physician. Stimulants
Spinal injury. See also Back injury; cervical injuries and, 549, 563, 563b hypertension and, 442
Cervical spine injuries; Spinal communication among, 4, 4b, 6 testing for, 180-181
cord injury. composition of, 1-5, 1b, 2f Stingers, 551, 553f
golf-related, 223-225, 223b, 225b confidentiality and, 4 Stitch in the side, 603-604
red flags associated with, 638, core principles of, 5-8, 5b, 6b Stoop lift, 386, 388b, 388f, 389f
638b emergency management plan of, Stork test, 638-639, 638f
sports participation with history of, 549b Straddle injury, 614-615
22-24t goal of, 1 Straight leg raise test, 31
in women, 638-641, 638b as influence on young people, 8 Strain. See Muscle strain.
Spinal instability, preparticipation injury management by, 6 Stratum corneum, 455, 465-466
evaluation and, 17 case studies of, 6-8, 7f, 8f Strength and conditioning coordinator,
Spinal shock, 573, 573b necessity of, 1, 1b 21-24, 25, 25b
Index 799
Strength training. See also Resistance Sudden cardiac death, 441 Swimming, 331-349
training; Weight training. chest protectors and, 501 backstroke in, 337-338
dietary protein and, 161-162 commotio cordis and, 444, 627 conditioning for, 345, 347t
ergogenic aids in, 161-162 coronary artery abnormalities and, humeral hyperextension in, 332,
carbohydrate-protein supplements, 443 333f, 338
162-163 coronary artery disease and, 444 breaststroke in, 338-339, 339f, 341
conjugated linoleic acid, 164 hypertrophic cardiomyopathy and, conditioning for, 345, 347t
creatine, 163 441-442 butterfly stroke in, 335-337
beta-hydroxy-beta-methylbutyrate, in Marfan syndrome, 443 conditioning for, 345, 347t
163-164 risk factors for, 441, 441b humeral hyperextension in, 332,
sodium bicarbonate, 160 Sudden death 333f, 335
lower-body, jump performance and, causes of, in athletes, 18 mechanics of, 335, 337f, 341
252-253, 253b preparticipation examination and, muscle activity in, 335-337, 337f
physiologic adaptations in, 159, 159b 17-18 concluding summary of, 348
Stress fractures Sulfur dioxide, 124t, 129, 131 conditioning for, 345, 347t
amenorrhea and, 642-643 Sulfur oxides, 129 flexibility screen for, 343-345,
in dancers, 668, 669f Summation of speed principle, 220 343b, 344f
little league shoulder as, 380 Sun exposure, 132-133 freestyle stroke in, 334-335
pars interarticularis, lumbar, 638-639 skin conditions caused by, 472-473 conditioning for, 345, 347t
rib, 619, 619f protection from, 473b humeral hyperextension in, 332,
sacral, 639 Sunburn, 132-133, 473 333f, 334-335
sternal, 621 heat intolerance and, 106 mechanical changes in, 341,
tibial, 637 Sunscreen, 133, 465t, 473, 473b, 342-343, 342t
Stress management, blood pressure 696-697 mechanics of, 334-335, 334f
and, 443 “Superman” exercise, 392, 393t muscle activity in, 335, 336f
Stress test, preparticipation, 18, 18f Suprascapular nerve, entrapment of, painful phases of, 332, 332f, 334
Stress urinary incontinence, 645-646 in baseball pitchers, 380 humeral hyperextension in, 332
Stretching Supraspinatus tendinopathy in backstroke, 332, 333f, 338
delayed onset muscle soreness and, eccentric training for, 716 in butterfly, 332, 333f, 335
434 topical glyceryl trinitrate for, 717 in freestyle, 332, 333f, 334-335
general guidelines for, 345 Suprasternal notch, 616f injury in
for golfers, pregame, 230-231 Surface clinical issues and, 341-343
for swimmers, 343-345, 343f, 344f, injury rates and, 767 mechanical changes and, 341,
346f shoes and, 510-511, 510f 342t
Stride length, in running, 310, 310b tennis biomechanics and, 279, 279f pain and, 339-341, 340f, 342t
Stroke Surfer introduction to, 331
cold exposure and, 114 bony spurs in ear canal of, 474 pain associated with
shoulder strapping and, 531 nodules on feet of, 460-461 characteristics of, 331-332, 332f
Subacromial impingement, taping for, Suturing of wounds, 457, 586-587 mechanical changes and, 341, 342t
531 Sweat glands, 456, 456f. See also rehabilitation for, 345-348
Subconjunctival hemorrhage, 589 Miliaria. return to swimming and, 347-348,
Subdural hematoma, 540 Sweating 347t
Substance abuse. See also Drug disorders with impairment in, stretching for, 343-345, 343f, 344f,
testing. 105-106 346f
in athlete with disability, 690 miliaria profunda as, 109 Syncope, heat-associated, 107-108t
in young athlete, 53, 53b spinal cord injury as, 695, 697
Subtalar joint gender differences in, 104-105 T
patellofemoral pain syndrome and, heat acclimatization and, 103, 103f T cells, delayed onset muscle soreness
636 iron loss through, 87 and, 429
in runners, 309 medications interfering with, 695 Talocrural joint, in runners
injuries and, 320-321 rates of, 146 knee pain and, 320b
knee pain and, 320b sodium loss through, 87-91 range of motion of, 309-310
orthoses and, 325-326 sunscreen interfering with, Tamponade, pericardial, 623-624,
pronation and, 313, 313f, 314t, 696-697 627, 627b
319 Swede-O ankle brace, 516-518, 518f, Tanning salons, 473
in soccer, pronation and, 296-297, 519 Taping, 515-535
299 Swimmer’s ear, 450 of ankle, 515-521, 518b
SubTalar Support brace, 516-517 Swimmer’s itch, 471 vs. ankle bracing, 516-518, 517f,
Subungual hemorrhage, 459, 462, Swimmer’s shoulder, 331-332, 518f, 519, 521, 523-524,
462f 341-343 524b
800 Index
Thermomoldable plastics, 480, Total joint arthroplasty, 717-723 Upper respiratory tract infections,
482-484, 483t, 484f, 485 ankle, 722-723 444-445
custom fabrication with, 485b, hip, 717-719, 718t sports participation with, 22-24t
486f implants for, 719 Ureteral injury, 612
of thumb splint, 499, 499b implant longevity in, 717-718, Urethral injury, 614
Thermotherapy, for delayed onset 718b, 723 Urinalysis, preparticipation, 19
muscle soreness, 431 knee, 717, 719-721, 720t Urinary catheter, athlete’s manage-
Thigh, injuries to, in runners, 307 implants for, 720-721 ment of, 697-698
Thigh protection, 501, 503f, 512 patient education following, 719, Urinary incontinence
Thiol oxidation, 156-157 719b adequate fluid intake and, 697
Thomas test, of hip flexor flexibility, return to sport after, 723 stress, 645-646
31-32, 34t shoulder, 721-722, 721t, 722t Urinary tract bleeding, in runners, 447
Thoracic injuries, 596 ski poles following, 719-720, 720b Urinary tract infections, 688t, 697-698
of chest wall, 615-623 Trace minerals, 86-87 Urine
to breast, 622-623 Tracheostomy, 582 blood in. See Hematuria.
effort thrombosis as, 623 Track and field, physical fitness profile protein in, 449-450
muscle strain as, 619-620 for, 34t Urine testing, 175-176. See also Drug
to pectoralis major, 621-622 Trainer. See Athletic trainer. testing.
to ribs. See Rib injuries. Trampoline, cervical spine injuries Urogenital examination,
to sternum, 620-621, 620b with, 559 preparticipation, 18-19
concluding summary of, 628 Transcutaneous electrical nerve Urticaria, 474
intrathoracic, 623-628 stimulation (TENS), 432-433
acute life-threatening conditions Traveler’s diarrhea, 446 V
in, 623, 623b Treadmill, stride length on, 310 Vagina
cardiac. See Cardiac injuries. Trench foot, 116, 116-117t lacerations of, 614-615
esophageal, 628 Tretinoin water injection injuries of, 615
evaluation of, 623-624 for acne mechanica, 461 Varicose veins, 460
pulmonary. See Pulmonary in scar revision, 476 Vasculature, age-related changes in,
injuries. Triceps tendinitis, in baseball pitchers, 708b
structures involved in, 615b, 616f, 381 Vastus medialis oblique
621f Trigger toe, 667 gender differences in, 632f
Throat protectors, 494, 495f Trochanteric bursitis patellar taping and, 527-528,
Thrombophlebitis, in athlete with cycling and, 209, 210t 529-530t
disability, 698 in runners, 307 Vegetarian diets
Thrombosis, subclavian or axillary Trolamine salicylate, 432 categories of, 79-82
vein, 623 True abdomen, 606, 606t food pyramid for, 85f
Thumb, protective splint for, 499, Truss, 599-600 iron sources in, 91t
499b Tryptophan, fatigue and, 144, nutrients to focus on, 82b
Thyroid cartilage, fracture of, 582, 152-153 protein in, 79-82, 82b, 85f
583f T-test of agility, 31, 32f, 34t sample menu for, lacto-vegetarian,
Tibial torsion Turf toe, vs. sesamoiditis, 673-674, 85f
dancer’s turnout and, 663 674f Veins, leg, unattractive conditions of,
gender differences in, 631, 632f, 24-hour recall, of nutrient intake, 59 460
633 Tyrosine, as ergogenic aid, 153-154 Venous thrombosis, subclavian or
Tibial varus, pronation and, 320 axillary, 623
Tibiofemoral forces U Ventral hernia, 603, 603t
in lunge exercises, 401-403, 402t Ulcers Ventricular fibrillation
in squat exercises, 397-399, 398t aphthous, 460 chest protectors and, 501
Tinea, 467-469, 469b decubitus, 688t, 690t as commotio cordis, 444, 627, 627b
Title IX, 730, 769 Ulnar collateral ligament injury Vertical jump biomechanics. See
Tobacco, hypertension and, 442. See in baseball pitchers, 362-363, 381 Jumping, vertical.
also Smoking. splint for, 499, 499b Vertical jump height, 29, 30f, 34t, 239b
Tobogganing, cervical spine injuries Ulnar neuritis, in baseball pitchers, Vertical jump repetitions, 32-33, 34t
in, 558 381 Viscosupplementation, for knee
Toenails. See Nails. Ultrasound therapy, for delayed onset osteoarthritis, 711
Tongue, lacerations of, 586 muscle soreness, 432 Vision. See also Eyes.
antibiotics and, 587 Ultraviolet light, 132-133, 472 in one eye, 21, 22-24t, 492-493
Tooth injuries, 594-595, 594b, 594f, Umbilical hernia, 602, 603t with one eye, 15
595b Unconsciousness. See Loss of zygomatic fractures and, 591
Torso Track, 393 consciousness. Visual examination, preparticipation, 15
802 Index
Wrist Y Z
fractures of, in weightlifters, 415 Young adult athlete, preparticipation Zinc, in vegetarian diets, 82b
golf-related injuries of, 217, 221, evaluation of, 9 Zygomatic fractures, 590-591, 591f,
221b Youth sports. See also Psychosocial 591t, 592b, 592f
protection for, 499 aspects of youth sports.
taping of, 523 numbers dropping out of, 41
numbers participating in, 40
X Yo-yo intermittent test, 33, 33f, 34t
X-factor stretch, 219
Xiphoid process, 616f, 620