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The following pages contain your course module which contain your courses directions,
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this Course, in the following pages and read all of the directions before beginning your
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After you have completed the reading material, you will need to complete the post-test
examination. You may utilize your course materials to answer the questions. Clearly
write your answers to all of the questions on your answer sheet with a black pen. When
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or you may login to our online testing center from our website and input your test
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Please also keep in mind that you have one-year from the invoice date to complete your
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We hope you enjoy your courses!

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At Home Seminars, LLC

PRESENTS:

Athletic and Sport Issues
in Musculoskeletal
Rehabilitation

Module 7

A Self-Paced study

Athletic and Sport Issues in Musculoskeletal Rehabilitation:
Module 7
a self-paced study distributed by At Home Seminars offered in cooperation with
Elsevier, Inc

Published in cooperation with Elsevier Inc. No portion of the text, Athletic and Sport
Issues in Musculoskeletal Rehabilitation may be used without written consent from
Elsevier Inc. Copyright 2011, Saunders/Elsevier.
HOW TO TAKE THIS COURSE

1. This course is offered in cooperative with Elsevier Inc and utilizes the textbook, Athletic and Sport
Issues in Musculoskeletal Rehabilitation by David J Magee, PT, PhD, Robert C Manske, PT, DPT, SCS,
Med, ATC, CSCS, J ames E Zachazewski, PT, DPT, SCS, ATC and William S Quillen, PT, PHD, SCS,
FACSM. This is module 7 and will utilize chapters 26-29 only.

2. Read the material in the order presented. If you need help with the material, you may contact us by
telephone, mail or by email at: customerservice@athomeseminars.com.

3. Complete the post test examination and course evaluation form. Follow directions and give us
accurate, complete information. Incomplete or illegible information delays or prevents processing of CE
credit. Course materials may be used to assist in answering the post test questions. Completion of the
Course Evaluation Form is not mandatory; however it does help us to evaluate the quality of our courses
and to alert us of any problems that may be present.

4. Complete the examination carefully. The answer sheet will not be returned to you but a letter will
accompany your completion certificates stating your grade for each course. A score of 75% or more is
considered passing. Scores of less than 75% indicate a failure to understand the material and At Home
Seminars will call you by telephone to correct the examination with you. An answer sheet with a passing
grade must be present in our files for CEU credit to be assigned.

5. Office personnel are unable to answer questions regarding test questions or answers. To view the
correct answers for the questions you may miss on your examination, you must complete your test through
our online testing center. If you have problems or questions with a test question, please note it in the
Comments portion of your answer sheet or when taking your test online.

6. Return your post test answer sheet or take your test online. Customers have the ability to take their
test online at no charge from their online account on our website. Simply Log In with your email address
and password and click on My Online Tests for online testing. You may also return your answer sheet by
mailing it to: At Home Seminars, PO Box 94594 Las Vegas, Nevada 89193 or by faxing it to: 1-800-
959-3328. Please do not use UPS, Fed Ex, or Certified Mail to return your tests as it delays processing. If
you fax your answer sheet, please be sure your answers are printed legibly in black ink. If you fax
your answer sheet to us or take your test online, you do not need to return your original answer sheets to us.
The date that your envelope is postmarked , the day your test is received by fax, or the day you complete
your test online will be the date of completion printed on your certificate of completion.

8. Certificates are generally returned within 3-4 days of receipt by our office. Examinations are
processed in our office within 1 business day of receiving them and then certificates are mailed by 1
st
Class
Mail to you. Certificates can be faxed to you before mailing upon request at no charge as long as the
request is made at the time the test is submitted. If you test online, you can print a temporary certificate
from the website once you finish your test. You will still receive the original certificate in the mail if you
test online.

9. Passing tests will be kept at our office for a period of seven years from the date of completion. If
you lose your certificate you can print another copy from your online account or contact us and well be
glad to assist you.

10. You have one-year from the invoice date to complete this course and return the answer sheet to us.
Tests returned after the one-year deadline will be subject to an additional charge of $20 per course for
processing and run the risk of no longer being valid in your state.

Target Audience:

Physical Therapists, Physical Therapist Assistants, Occupational Therapists, Occupational Therapist Assistants,
Athletic Trainers

Instructional Level:

Intermediate

Course Goals: This course is intended to instruct the student through self paced study on the
foundation of treating special populations in athletics including the female athlete, dance medicine, an
athlete with disability, and rehabilitation of the masters athlete.

Student Objectives:

At the end of this course, the student will be able to:
1. Understand the musculoskeletal differences between males and females.
2. Analyze female basketball/soccer players and the rate of ACL injury.
3. Analyze four factors that contribute to ACL injury.
4. Understand the relationship of the female menstrual cycle and ACL tears.
5. Evaluate the Q-angle in the lower extremity.
6. Analyze four muscles as they relate to medial tibial stress syndrome.
7. Understand the correct treatment for MTSS.
8. Understand common locations for spondylolisthesis.
9. Evaluate the relationship of SI dysfunction and lumbar motions.
10. Understand the difference between structural and functional scoliosis.
11. Understand the female athlete triad.
12. Analyze female bone mineral density and age.
13. Understand the exercise parameters for an elite pregnant athlete.
14. Analyze four conditions and exercise during pregnancy.
15. Evaluate four body parts and their likelihood to be injured during dance.
16. Understand the type of dance that will most often cause overuse injuries.
17. Evaluate the anterior talofibular ligament as it relates to different dance positions.
18. Understand the dance position with the greatest potential for injury to the foot.
19. Analyze lower extremity kinematics as it relates to turnout.
20. Understand the relationship of an anteverted/retroverted femoral neck and dancing postures.
21. Evaluate the pain pattern of an os trigonum/steida process in the foot.
22. Evaluate several types of foot fractures common in dance.
23. Understand the biomechanical processes of external hip snapping.
24. Evaluate the differences between a qualitative and quantitative biomechanical analysis.
25. Understand emergency procedures related to autonomic dysreflexia.
26. Analyze the potential for injury for a runner with a below knee amputation.
27. Analyze several medical conditions and their relationship to core body temperature.
28. Understand ideal fluid replacement in athletics.
29. Understand the bodys normal response to aging as it relates to muscle fiber type.
30. Understand the decline of flexibility in the masters athlete.
31. Understand the mechanical processes of knee osteoarthritis.
32. Analyze primary osteoarthritis of the shoulder and its causes.
33. Evaluate four sports and the possibility for an individual with a total hip arthroplasty to
participate in those sports.
34. Analyze four sports and the possibility of an individual to participate in them after total shoulder
arthroplasty.
Directions: After reading the previous material, answer the questions on this post test
and return your answer sheet to At Home Seminars. You may utilize the learning
materials to answer the questions. Upon receipt of your test, it will be graded, and if you
score 75% or higher, we will issue you a certificate of completion.

ATHLETIC AND SPORT ISSUES IN MUSCULOSKELETAL REHABILITATION:
MODULE 7 (COURSE #757)

1. Which of the following is an incorrect statement regarding the musculoskeletal
differences between males and females?
A. Females are more likely to present with an increased Q-angle
B. Females are more likely to present with a wider pelvis
C. Females are more likely to present with increased tibial torsion
D. Females are more likely to present with cubitus varus

2. Female basketball and soccer players are generally ____________ times more likely
to sustain an ACL injury than males.
A. 1
B. 2
C. 3
D. 4

3. Which of the following is an extrinsic factor that may contribute to sex differences
regarding ACL injury?
A. Anterior cruciate ligament size
B. Hip abductor strength
C. Tibial plateau slope
D. Hormonal influences

4. According to research by Hewett and colleagues, during which phase of the menstrual
cycle is a female most likely to tear her ACL?
A. Follicular and ovulatory phases
B. Follicular and luteal phases
C. Ovulatory and luteal phases
D. The menstrual cycle does not contribute to ACL damage

5. A Q-angle of greater than __________ is excessive.
A. 10 degrees
B. 20 degrees
C. 30 degrees
D. 40 degrees

6. Which of the following muscles has not been identified as a possible culprit of medial
tibial stress syndrome?
A. Gastrocnemius
B. Posterior tibialis
C. Soleus
D. Flexor digitorum longus

7. What is the last resort for treatment of MTSS?
A. Ligament release
B. Orthotics for the shoe
C. Osteotomy
D. Fasciotomy

8. What is the most common level of occurrence of spondylolisthesis?
A. L2-L3
B. L3-L4
C. L4-L5
D. L5-S1

9. What grade of spondylolisthesis is a 50-75% anterior slippage of the superior
vertebral body on the inferior vertebral body?
A. Grade I
B. Grade II
C. Grade III
D. Grade IV

10. What two motions would increase pain in a female with right SI dysfunction?
A. Extension and left rotation
B. Extension and right rotation
C. Flexion and right rotation
D. Flexion and left rotation

11. A functional structural scoliosis is reversible.
A. True
B. False

12. Which of the following is not part of the female athlete triad?
A. Disordered eating
B. Amenorrhea
C. Osteoporosis
D. Depression

13. At what age is female bone mineral density the greatest?
A. 30
B. 40
C. 50
D. 60

14. An elite pregnant athlete should exercise at __________ max heart rate.
A. 65-70%
B. 70-75%
C. 75-80%
D. 80-85%

15. Which of the following is an absolute contraindication to exercise during pregnancy?
A. Restrictive lung disease
B. Severe anemia
C. Chronic bronchitis
D. Poorly controlled type I diabetes

16. It is acceptable to provide intervention for a dancer in the traditional sports medicine
model of care.
A. True
B. False

17. What body part is most often injured in dance?
A. Cervical spine
B. Lumbar spine
C. Upper extremity
D. Lower extremity

18. In what type of dance are overuse injuries more common?
A. Ballroom dancing
B. Modern dance
C. J azz
D. Classical ballet

19. When a dancer is in the en-point position, what is the orientation of the anterior
talofibular ligament?
A. Anatomical position
B. Nearly vertical
C. 45 degree angle to the fibula
D. Nearly horizontal

20. What position has the greatest potential for injury to the forefoot and mid foot?
A. Demi- plie
B. Demi-point
C. En-point
D. Releve

21. If the ideal 90 degrees of turnout in one limb can be performed, what amount of this
motion should come from external hip rotation?
A. 40-50 degrees
B. 50-60 degrees
C. 60-70 degrees
D. 70-80 degrees

22. An anteverted femoral neck may mechanically limit a dancers potential for turnout,
whereas a retroverted femoral neck allows for greater turnout.
A. True
B. False

23. Where does the pain from an os trigonum or stieda process typically manifest in the
foot?
A. Anterior/lateral
B. Posterior/lateral
C. Anterior/medial
D. Posterior/medial

24. A spiral fracture of the distal shaft of which metatarsal is termed a dancers fracture?
A. Second metatarsal
B. Third metatarsal
C. Fourth metatarsal
D. Fifth metatarsal

25. What metatarsal is most prone to stress fractures in dance?
A. First
B. Second
C. Third
D. Fourth

26. External hip snapping is created by the iliopsoas tendon running over the anterior
ridge on the femoral head.
A. True
B. False

27. What is the parallel organization to the International Olympic Committee for
disabled individuals?
A. Special Olympics International
B. Special Olympics Incorporated
C. International Paralympic Committee
D. Wheelchair Sports USA

28. A qualitative analysis of biomechanical sporting events to study human movement is
more easily employed than a quantitative analysis.
A. True
B. False

29. Which of the following is incorrect advice for the sports medicine team when dealing
with an athlete that has autonomic dysreflexia?
A. Recline the patient to a supine position
B. Activate EMS
C. Immediately search for the source of the stimulus that caused the dysreflexia
D. Relieve the source of the stimulus immediately

30. Which of the following is not a common site for abrasions and blisters for a runner
with a below knee amputation?
A. Fibula head
B. Distal posterior end of the tibia
C. Distal end of the fibula
D. Medial and lateral femoral condyles

31. Which two diagnoses will often present with problems in regulation of core body
temperature?
A. Spinal cord injury and muscular dystrophy
B. Muscular dystrophy and multiple sclerosis
C. Spinal cord injury and multiple sclerosis
D. Spinal cord injury and cerebral palsy

32. What is the ideal fluid replacement solution for events lasting less than 1 hour?
A. Warm water
B. Cool water
C. Electrolyte solutions with a 4-6% concentration
D. Electrolyte solutions with a 6-8% concentration

33. What is the ideal concentration of glucose and electrolytes solutions in carbohydrate
polymer solutions for rehydration?
A. 1-2%
B. 3-4%
C. 5-7%
D. 6-8%

34. In track and field, masters athletes are considered older than ______ years.
A. 30
B. 35
C. 40
D. 45

35. As one ages type I muscle fibers deteriorate more rapidly than type II fibers.
A. True
B. False

36. Flexibility decreases approximately _______ between 30 and 70 years of age.
A. 5% and 10%
B. 10% and 20%
C. 15% and 25%
D. 20% and 30%

37. The majority of knee osteoarthritis affects which compartment of the knee?
A. Medial compartment
B. Lateral compartment
C. Anterior compartment
D. Posterior compartment

38. Primary osteoarthritis of the shoulder is likely to be caused by which of the following
conditions?
A. Dislocation of the shoulder
B. Subluxation of the shoulder
C. Hill Sachs lesion
D. Rotator cuff disease

39. Which of the following activities are not recommended following total hip
arthroplasty regardless of the athletes level of experience?
A. Doubles tennis
B. J ogging
C. Hiking
D. Bowling

40. Which of the following activities is not recommended following total shoulder
arthroplasty regardless of the level of experience of the athlete?
A. Gymnastics
B. Downhill skiing
C. Bowling
D. Doubles tennis

41. How would you rate this course on a scale of 1 to 7 (1=not informative; 7=very
informative)?

42. How long did it take you to complete this course?
A. Less than 7 hours
B. 7-8 hours
C. 8-9 hours
D. More than 9 hours

43. Would you recommend this course to others?
A. Yes
B. No

RETURN ONLY YOUR POST-TEST ANSWER SHEET TO AT HOME
SEMINARS

Editors
David J. Magee, PT, PhD
Professor and Associate Dean
Department of Physical Therapy, Faculty of Rehabilitation Medicine
University of Alberta, Edmonton, Alberta, Canada
Robert C. Manske, PT, DPT, SCS, MEd, ATC, CSCS
Associate Professor, Department of Physical Therapy
Wichita State University, Wichita, Kansas
James E. Zachazewski, PT, DPT, SCS, ATC
Clinical Director, Department of Physical and Occupational Therapy
Massachusetts General Hospital, Boston, Massachusetts
Adjunct Assistant Clinical Professor, Program in Physical Therapy
MGH Institute of Health Professions, Boston, Massachusetts
William S. Quillen, PT, PhD, SCS, FACSM
Associate Dean, College of Medicine
Professor and Director, School of Physical Therapy and Rehabilitation Sciences
University of South Florida ,Tampa, Florida
Editorial Consultant
Bev Evjen
Swift Current, Saskatchewan, Canada

ATHLETIC AND SPORT
ISSUES IN
MUSCULOSKELETAL
REHABILITATION

3251 Riverport Lane
St. Louis, Missouri 63043
ATHLETIC AND SPORTS ISSUES IN MUSCULOSKELETAL
REHABILITATION ISBN: 9781416022640
Copyright 2011 by Saunders, an imprint of Elsevier Inc.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
mechanical, including photocopying, recording, or any information storage and retrieval system, without
permission in writing from the publisher. Details on how to seek permission, further information about the
Publishers permissions policies and our arrangements with organizations such as the Copyright Clearance
Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions .
This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).
Notices
Knowledge and best practice in this eld are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical treatment
may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating
and using any information, methods, compounds, or experiments described herein. In using such
information or methods they should be mindful of their own safety and the safety of others, including
parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identied, readers are advised to check the
most current information provided (i) on procedures featured or (ii) by the manufacturer of each
product to be administered, to verify the recommended dose or formula, the method and duration
of administration, and contraindications. It is the responsibility of practitioners, relying on their own
experience and knowledge of their patients, to make diagnoses, to determine dosages and the best
treatment for each individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors,
assume any liability for any injury and/or damage to persons or property as a matter of products liability,
negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas
contained in the material herein.
Library of Congress Cataloging-in-Publication Data
Athletic and sport issues in musculoskeletal rehabilitation/editors, David J. Magee . . . [et al.]; editorial
consultant Bev Evjen.
p. ; cm. -- (Musculoskeletal rehabilitation series)
Includes bibliographical references and index.
ISBN 978-1-4160-2264-0 (pbk. : alk. paper) 1. Sports medicine. 2. Sports injuries--Treatment.
3. Sports--Physiological aspects. 4. Human mechanics. I. Magee, David J. II. Series: Musculoskeletal
rehabilitation series.
[DNLM: 1. Athletic Injuries--rehabilitation. 2. Musculoskeletal Diseases--rehabilitation.
3. Biomechanics. 4. Sports Medicine. QT 261 A8705 2011]
RC1210.A82 2011
617.1027--dc22
2010024809
Vice President and Publisher: Linda Duncan
Executive Editor: Kathy Falk
Senior Developmental Editor: Christie Hart
Publishing Services Manager: Catherine Jackson
Project Manager: Sara Alsup
Design Direction: Teresa McBryan
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1
To Teach is to Learn Twice
To those who invested in us that we might in turn pass on their
knowledge and wisdom to future generations of students.
William E. Amonette, MA, CSCS
Fitness and Human Performance Program
School of Human Sciences and Humanities
University of Houston-Clear Lake
Houston, Texas
James R. Andrews, MD
Andrews Sports Medicine and Orthopaedic Center
Birmingham, Alabama
Brant D. Berkstresser, MS, ATC/L
Head Athletic Trainer
Department of Athletics
Harvard University
Boston, Massachusetts
Natlia Franco Netto Bittencourt, BPT
MSc Student in Rehabilitation Sciences
Universidade Federal de Minas Gerais
Belo Horizonte, Minas Gerais, Brazil
Physical Therapist
Ncleo de Integrao das Cincias do Esporte
Minas Tnis Clube
Lori A. Bolgla, PT, PhD, ATC
Assistant Professor
Department of Physical Therapy
Medical College of Georgia
Augusta, Georgia
Rich Bomgardner, MS, LAT, ATC, CSCS
Athletic Training Education Coordinator
Department of Human Performance Studies
Wichita State University
Wichita, Kansas
Brian D. Busconi, MD
Associate Professor
Chief of Sports Medicine and Arthroscopy
Department of Orthopedics and Physical Rehabilitation
University of Massachusetts Medical School
Worcester, Massachusetts
W. Lee Childers, MSPO
PhD Candidate
School of Applied Physiology
Georgia Institute of Technology
Atlanta, Georgia
Contributors
Loren Z.F. Chiu, PhD, CSCS
Assistant Professor
Faculty of Physical Education and Recreation
University of Alberta
Edmonton, Alberta, Canada
Michael W. Collins, PhD
Assistant Professor
Department of Orthopaedic Surgery
Department of Neurological Surgery
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania
Assistant Director
UPMC Sports Medicine Concussion Program
Stephen A. Durant, EdD
Instructor
Department of Psychiatry
Harvard Medical School
Co-Director
MGH Performance And Character Excellence (PACES)
Institute of Sports Psychology
Department of Child Psychiatry
Massachusetts General Hospital
George T. Edelman, MPT, OCS, MTC
Edelman Spine and Orthopaedic Physical Therapy
Dover, Delaware
Adjunct Professor
University of Delaware
Newark, Delaware
Todd S. Ellenbecker, DPT, MS, SCS, OCS, CSCS
Clinic Director, Physiotherapy Associates Scottsdale Sports
Clinic
National Director of Clinical Research, Physiotherapy
Associates
Director of Sports Medicine, ATP World Tour
Scottsdale, Arizona
vi
Rafael F. Escamilla, PhD, PT, CSCS, FACSM
Professor
California State University, Sacramento
Sacramento, California
Professor
Andrews-Paulos Research and Education Institute
Andrews Institute
Gulf Breeze, Florida
Glenn S. Fleisig, PhD
Research Director
American Sports Medicine Institute
Birmingham, Alabama
Adjunct Professor
Department of Biomedical Engineering
The University of Alabama at Birmingham
Birmingham, Alabama
Srgio Teixeira Fonseca, BPT, ScD
Associate Professor
School of Physical Education, Physical Therapy
and Occupational Therapy
Universidade Federal de Minas Gerais (UFMG)
Eileen G. Fowler, PT, PhD
Associate Professor
Peter William Shapiro Chair for the Center for Cerebral
Palsy
UCLA / Orthopaedic Hospital Department
of Orthopaedic Surgery
University of California at Los Angeles
Los Angeles, California
Travis L. Francis, MS, LAT, ATC
Via Christi Sports Medicine
Wichita, Kansas
Gary J. Geissler, PT, DPT, SCS, ATC
Clinical Director of Rehabilitation
Athletic Department
Harvard University
Cambridge, Massachusetts
Assistant Professor
Program in Physical Therapy
MGH Institute of Health Professions
Physical Therapist
Orthopaedic Physical Therapy Services
Wellesley, Massachusetts
Richard D. Ginsburg, PhD
Instructor
Department of Psychiatry
Co-Director
MGH Performance And Character Excellence (PACES)
Institute of Sports Psychology
Department of Child Psychiatry
Gabriela Gomes Pavam Gonalves, BPT, MSc
Physical Therapist
Ncleo de Integrao das Cincias do Esporte
Minas Tnis Clube
Gary A. Green, MD
Clinical Professor
Division of Sports Medicine
Department of Internal Medicine
David Geffen UCLA School of Medicine
Partner
Pacic Palisades Medical Group
Pacic Palisades, California
Steven A. Greer, MD, CAQ
Program Director, Primary Care Sports Medicine
Fellowship
Director, Primary Care Sports Medicine
Assistant Professor, Departments of Family Medicine
and Orthopaedics
Medical College of Georgia
Augusta, Georgia
Robert J. Gregor, PhD, FACSM, FAAKPE
Professor Emeritus
School of Applied Physiology
Georgia Institute of Technology
Atlanta, Georgia
Adjunct Professor
Division of Biokinesiology and Physical Therapy
University of Southern California
Contributors vii
Donald W. Groot, MD, FRCP(C), FACP
Clinical Professor of Medicine
Department of Medicine
Medical Director
Groot DermaSurgery Centre
Michael S. Jellinek, MD
Professor of Psychiatry and of Pediatrics
Chief, Child Psychiatry Service
President
Newton Wellesley Hospital
Newton, Massachusetts
Patricia A. Johnston, BSc, MClSc, MBA
President, InForum
John P. Kelly, DMD, MD, FACS
Associate Clinical Professor
Department of Surgery
Yale University School of Medicine
New Haven, Connecticut
Chief, Section of Oral and Maxillofacial Surgery
Department of Surgery
Hospital of Saint Raphael
New Haven, Connecticut
W. Ben Kibler, MD, FACSM
Medical Director, Lexington Clinic Sports Medicine
Center
Medical Director, Shoulder Center of Kentucky
Lexington Clinic
Lexington, Kentucky
Mark S. Kovacs, PhD, CSCS
Senior Manager, Strength and Conditioning/
Sport Science
United States Tennis Association
Boca Raton, Florida
Richard H. Leu, MD
CAQ Primary Care Sports Medicine
Clinical Associate Professor
Department of Family Medicine
Kansas University School of Medicine
Wichita, Kansas
Faculty Member, Sports Medicine Fellowship, Family
Medicine Residency Program
Department of Family Medicine
Via Christi Regional Medical Center
Wichita, Kansas
David Lindsay, BHMS, BPhty, MSc
Sport Medicine Centre
University of Calgary
Calgary, Alberta, Canada
Janice Loudon, PT, PhD, ATC, SCS
Associate Professor
Department of Physical Therapy and Rehabilitation
Science
University of Kansas Medical Center
Kansas City, Kansas
Caroline A. Macera, PhD, FACSM
Professor of Epidemiology
Graduate School of Public Health
San Diego State University
San Diego, California
David J. Magee, BPT, PhD
Professor and Associate Dean
Faculty of Rehabilitation Medicine
Corrie A. Mancinelli, PT, PhD
Associate Professor
Division of Physical Therapy
Department of Human Performance and Applied Exercise
Science
West Virginia University School of Medicine
Morgantown, West Virginia
Robert C. Manske, PT, DPT, SCS, MEd, ATC,
CSCS
Associate Professor
Wichita, Kansas
viii Contributors
Russell Mark, BS
National Team Performance Support Director
Biomechanics Manager
USA Swimming
Colorado Springs, Colorado
Stephen W. Marshall, PhD
Associate Professor, Department of Epidemiology
Adjunct Associate Professor, Department of Exercise
and Sport Science
School of Public Health
University of North Carolina at Chapel Hill
Chapel Hill, North Carolina
James W. Matheson, PT, DPT
Board Certied in Sports and Orthopaedic Physical
Therapy
Minnesota Sport and Spine Rehabilitation
Burnsville, Minnesota
Consultant
EIP Consulting
Savage, Minnesota
Duane G. Messner, MD
Past President
American Orthopaedic Sports Medicine Society
Gunnison, Colorado
Scott T. Miller, PT, MS, SCS, CSCS
Partner/Director of Clinical Operations
Agility Physical Therapy & Sports Performance, LLC
Portage, Michigan
Michael R. Mirabella, MS, ATC, CSCS
Athletic Trainer
White Plains High School
White Plains, New York
Athletic Trainer/Physician Extender
Westchester Orthopaedic Associates, PC
White Plains, New York
Elizabeth A. Mooradian, MS
Senior Scientist
Gatorade Sports Science Institute
Barrington, Illinois
Dhiren J. Naidu, MD, FRCP(C), Dip Sport Med
Assistant Professor
Division of Physical Medicine and Rehabilitation
Education Director, HealthPointe Medical Centre
Sport Medicine Consultant, Glen Sather Sports Medicine
Clinic
Team Physician, Edmonton Oilers, National Hockey
League
Team Physician, Edmonton Eskimos, Canadian Football
League
Juliana Melo Ocarino, BPT, MSc
PhD Candidate in Rehabilitation Sciences
Assistant Professor
Centro Universitrio de Belo Horizonte (UNI-BH)
Marilyn M. Pink, PhD, PT
CEO, EDUCATA
Calabasas, California
William S. Quillen, PT, PhD, FACSM
Associate Dean, College of Medicine
Professor and Director, School of Physical Therapy
and Rehabilitation Sciences
University of South Florida
Tampa, Florida
Mitchell J. Rauh, BSPT, PhD, MPH, FACSM
Associate Professor
Graduate Program in Orthopaedic and Sports Physical
Therapy
Rocky Mountain University of Health Professions
Provo, Utah
Adjunct Research Faculty
Graduate School of Public Health
School of Exercise and Nutritional Sciences
San Diego State University of Health Professions
San Diego, California
Michael P. Reiman, PT, DPT, OCS, SCS, ATC,
FAAOMPT, CSCS
Assistant Professor
Department of Physical
Wichita, Kansas
Clinician
Via Christi Orthopaedic and Sports Physical Therapy
Wichita, Kansas
Contributors ix
Lars C. Richardson, MD
Clinical Instructor in Orthopaedics
Department of Orthopaedics, Harvard Medical School
Orthopaedic Surgical Consultant
Department of Orthopaedics, Harvard University Health
Services
Clinical Instructor in Orthopaedics
Department of Orthopaedics, Beth Israel Deaconess
Medical Center
Scott A. Riewald, PhD
Senior Sport Technologist
Sport Performance Division
United States Olympic Comittee
Colorado Springs, Colorado
Scott A. Rodeo, MD
Chairman, USA Swimming Sports Medicine Committee
Co-Chief, Sports Medicine and Shoulder Service, Hospital
for Special Surgery
Professor of Orthopaedic Surgery (Academic Track), Weill
Medical College of Cornell University
Attending Orthopaedic Surgeon, Hospital for Special
Surgery
Attending Surgeon (Orthopaedic Surgery),
The New York-Presbyterian Hospital
Assistant Scientist, Department of Research, Hospital for
Special Surgery
Associate Team Physician, New York Giants Football
New York, New York
E. Paul Roetert, PhD, FACSM
Managing Director, Coaching Education and Sport
Science
United States Tennis Association
Boca Raton, Florida
Justin Rohrberg, PT, DPT, ATC
Instructor
Wichita, Kansas
Physical Therapist, Head Athletic Trainer
Player Development Solutions
Wichita, Kansas
Jeffrey A. Russell, MS, ATC
Assistant Professor, Dance Science
Department of Dance
Claire Trevor School of the Arts
University of California, Irvine
Irvine, California
Thales Rezende Souza, BPT, MSc
PhD Student in Rehabilitation Sciences
Barry A. Spiering, PhD, CSCS
Department of Kinesiology
California State University, Fullerton
Fullerton, California
William T. Stauber, PT, PhD, FACSM
Division of Physical Therapy
Department of Human Performance and Applied Exercise
Science
Department of Physiology and Pharmacology
West Virginia University
Morgantown, West Virginia
Alex M. Taylor, PsyD
Neuropsychology Fellow
Department of Sports Medicine
University of Pittsburgh Medical Center
Benjamin M.J. Thompson, MD
Chief Resident, Orthopaedic Surgery
Department of Orthopaedics and Physical Rehabilitation
University of Massachusetts Medical School
Worcester, Massachusetts
Timothy F. Tyler, MS, PT, ATC
Clinical Research Associate
NISMAT at Lenox Hill Hospital
New York, New York
Anthony A. Vandervoort, PhD
Editor-In-Chief
Journal of Aging and Physical Activity
Professor and Associate Dean (Scholarship)
Faculty of Health Sciences
University of Western Ontario
London, Ontario, Canada
x Contributors
Francis Wang, MD
Clinical Instructor
Department of Medicine
Physician
Department of Internal Medicine
Harvard University Health Services
Team Physician
Harvard University
Heidi M. Wells, BS, RD, CSSD, LD
Sports Dietitian/Clinical Dietitian
Via Christi Regional Medical Center
Wichita, Kansas
Kimberly M. White, PhD
Principal Scientist
James E. Zachazewski, PT, DPT, SCS, ATC
Clinical Director
Department of Physical and Occupational Therapy
Adjunct Assistant Clinical Professor
Program in Physical Therapy
MGH Institute of Health Professions
Jeffrey J. Zachwieja, PhD, FACSM
Contributors to Content Used from
Athletic Injuries and Rehabilitation
Susan Cummings, MS, RD
Mary Jane Rewinski, BS, RD
Scott J. Montain, PhD
Beau J. Freund, PhD
Thomas G. McPoil, PhD, PT, ATC
Mark W. Cornwall, PhD, PT
Frank W. Jobe, MD
James C. Puffer, MD
Ethan Saliba, PhD, ATC, PT, SCS
Susan Foreman, MEd, MPT, ATC
Richard T. Abadie Jr., BA, EMC
Donald Hangen, MD
Andrew W. Nichols, MD
Kathleen A. Curtis, PhD, PT
Robert S. Gailey Jr., MSEd, PT
Contributors xi
Musculoskeletal Rehabilitation Series
Musculoskeletal conditions have an enormous impact on
society. Today, musculoskeletal conditions have become the
most common cause of disability and severe long-term pain
in the industrialized world. As we approach the completion
of the Bone and Joint Decade, it is apparent that the knowl-
edge and skill required by the community of health care
providers involved in managing the impairments and func-
tional limitations resulting from acute or chronic musculo-
skeletal injury/illness has grown exponentially as the fre-
quency of visits to practitioners ofces for musculoskeletal
system complaints has continued to rise.
The art and science of musculoskeletal rehabilitation
began as a consequence of the injuries suffered on the bat-
tleelds of Europe during World War I. Since that time,
numerous textbooks have been published regarding muscu-
loskeletal rehabilitation. These texts have encompassed the
areas of basic science, evaluation, and treatment. However,
these books have most often been developed and written in
professional isolation (ie., from a single disciplines per-
spective). As a consequence, topics have either been cov-
ered in great depth but with a very narrow focus, or with
great breadth with very little depth. Our goal in the devel-
opment and production of this series was to develop a series
of textbooks that compliment and build on one another,
providing the reader with the needed depth and breadth of
information for this critical area of health care.
Volume I of the series is the 5
th
edition of David Magees
Orthopedic Physical Assessment. This now classic text pro-
vides the clinician with the most comprehensive text avail-
able on this topic. First published in 1987, it has withstood
the test of time and is the most widely used text in this area.
In 1996, we developed and published the 1000 page text-
book Athletic Injuries and Rehabilitation. Based upon feed-
back from both students and clinicians, we have expanded
and broadened the scope of Athletic Injuries and Rehabili-
tation into three new volumes comprising approximately
2400 pages of information. Volume II , Scientic Founda-
tions and Principles of Practice, provides clinicians with cur-
rently available science regarding musculoskeletal issues and
principles of practice that should guide clinicians regarding
therapeutic intervention. In Volume III, Pathology and
Intervention, we have attempted to provide readers with a
comprehensive text containing information on the most
Preface
common musculoskeletal pathologies seen and the best
evidence behind contemporary interventions directed to-
wards the treatment of impairments and limitations associ-
ated with acute, chronic and congenital musculoskeletal
conditions which occur across the lifespan. Volume IV, Ath-
letic and Sport Issues provides the clinician interested in
sport related injuries with specic in-depth information not
commonly presented elsewhere. Detailed information is
presented regarding non-orthopedic concerns, the biome-
chanics along with clinical impact of physical activities
required for sport and specic patient populations.
International contributors have provided their unique
perspectives on current diagnostic methodologies, clinical
techniques, and rehabilitative concerns. We hope that our
continued use of interdisciplinary author teams has rmly
broken down the professional territorial turf barriers that
have existed in past decades of health care. Health care pro-
fessionals involved in the contemporary care of musculosk-
eletal conditions must continue to share and learn from one
another to advance the provision of the most time- and
cost-efcient care possible in 21
st
century society.
Each volume in our series is liberally illustrated. Key con-
cepts in each chapter are highlighted in text boxes, which
serve to reinforce those concepts for the reader, and numer-
ous tables summarize chapter information for easy reference.
Readers will nd that references are not contained on printed
pages at the end of chapters, but rather contained as part
of a comprehensive electronic resource on CD-ROM or
EVOLVE site (provided with each volume), which allows the
reader to link to MEDLINE abstracts where possible. Because
of the comprehensive nature of this multi-volume series, each
text, although complete in itself, has been edited to build and
integrate with related chapter materials from the other vol-
umes in the series. It is the editors hope that this series will
nd its way into use by faculty as a basis for formal coursework
as well as a friendly companion and frequently consulted refer-
ence by students and those on the front lines of clinical care.
As with our previous collaborations, we look forward to
the feedback that only you, our colleagues, can provide, so
that we may continue the development and improvement of
the Musculoskeletal Rehabilitation Series .
David J. Magee
James E. Zachazewski
William S. Quillen
Robert C. Manske

xiii
Athletic and Sport Issues
Athletic and Sport Issues in Musculoskeletal Rehabilitation is
the 4
th
volume in our series Musculoskeletal Rehabilitation .
For this volume we have added a new editor, Robert
Manske. In this volume we have sought to provide the stu-
dent and practicing clinician with a comprehensive source
of information for this topic area not addressed elsewhere in
this integrated series. Most texts on sports injuries have a
primary focus on musculoskeletal pathology and interven-
tion. Information on these types of problems and condi-
tions are thoroughly addressed in Volumes 1 Orthopaedic
Physical Assessment, Volume 2 Scientic Foundations and
Principles of Practice and Volume 3 Pathology and Inter-
vention . The advantage of Volume 4 Athletic and Sport
Issues in Musculoskeletal Rehabilitation being part of an in-
tegrated series is that the information the reader will nd is
summarized and presented in greater depth than most other
texts. Because of this, we believe the reader will nd this
textbook an exceptional resource for their practice.
Volume 4 is divided into four sections:
Preparation and Prevention in Sports Medicine focuses
on psychological, nutritional, environmental and pharma-
cologic factors associated with sport participation and
health.
Applied Biomechanics of Selected Sport Activities
present in depth reviews of the biomechanics of activities
Preface
and how they may impact injury development and reha-
bilitation including clinically relevant points.
Management of Sports Injury and Illness focuses on
non-musculoskeletal injury and management factors.
Special Populations and Epidemiology presents infor-
mation on sport injury concerns based on gender, age or
physical ability/disability. Also presented in this section is
a comprehensive summary of the epidemiologic injury
data by specic sport.
This volume is again liberally illustrated with multiple
gures, tables and text boxes to allow the reader to quickly
grasp the information being presented. A comprehensive
reference list is provided on an Evolve site with links to
MEDLINE abstracts where available.
We rmly believe that with the addition of this volume
the clinician who practices is the area of sports medicine
will have a set of resources that provide them with compre-
hensive information on the management of this patient
population.
As we continue to develop this series we welcome the
readers feedback to allow us to continue to enhance the
quality and comprehensiveness of the series.
David J. Magee
Robert C. Manske
James E. Zachazewski
William S. Quillen
xv
We would like to gratefully acknowledge the ongoing pro-
fessional assistance of the following individuals who have
steadfastly supported this series from its inception.
Acknowledgments
xvi
Kathy Falk Executive Editor, Health Professions, Elsevier
Christie Hart Senior Developmental Editor, Elsevier
Megan Fennell Associate Developmental Editor, Elsevier
Bev Evjen Editorial Assistant
Ted Huff Artist
SECTION I: PREPARATION AND PREVENTION
IN SPORTS MEDICINE
1
ROLE OF THE SPORTS MEDICINE TEAM - Richard H. Leu,
Robert C. Manske
2
PREPARTICIPATION EVALUATION AND PHYSICAL FITNESS PROFILING
PART A: PREPARTICIPATION EVALUATION - David J. Magee,
William S. Quillen
PART B: PHYSICAL FITNESS PROFILING - William E. Amonette,
Barry A. Spiering
3
PSYCHOSOCIAL ASPECTS OF YOUTH SPORTS - Stephen A. Durant,
Richard D. Ginsburg, Michael S. Jellinek
4
NUTRITION COUNSELING AND ATHLETES - Heidi M. Wells
5
ENVIRONMENTAL CONSIDERATIONS FOR SPORTS - Travis L. Francis,
Rich Bomgardner
6
USE OF ERGOGENIC AIDS IN SPORT - Jeffrey J. Zachwieja,
Elizabeth A. Mooradian, Kimberly M. White
7
SPORTS DRUG TESTING - Gary A. Green
SECTION II: APPLIED BIOMECHANICS
OF SELECTED SPORT ACTIVITIES
8
APPLIED BIOMECHANICS OF CYCLING - Robert J. Gregor,
Eileen G. Fowler, W. Lee Childers
9
APPLIED BIOMECHANICS OF GOLF - David Lindsay,
Anthony A. Vandervoort
10
APPLIED BIOMECHANICS OF JUMPING - Scott A. Riewald
11
APPLIED BIOMECHANICS OF TENNIS - Todd S. Ellenbecker,
E. Paul Roetert, W. Ben Kibler, Mark S. Kovacs
12
APPLIED BIOMECHANICS OF SOCCER - Srgio T. Fonseca,
Thales R. Souza, Juliana M. Ocarino,
Gabriela P. Gonalves, Natlia F. Bittencourt
13
APPLIED BIOMECHANICS OF RUNNING - Scott T. Miller
14
APPLIED BIOMECHANICS OF SWIMMING - Marilyn M. Pink,
George T. Edelman, Russell Mark, Scott A. Rodeo
15
APPLIED BIOMECHANICS OF BASEBALL PITCHING - Glenn S. Fleisig,
Rafael F. Escamilla, James R. Andrews
Contents
16
APPLIED BIOMECHANICS OF COMMON WEIGHT TRAINING EXERCISES -
Michael P. Reiman, Rafael F. Escamilla,
Loren Z.F. Chiu
SECTION III: MANAGEMENT OF SPORTS
INJURY AND ILLNESS
17
DELAYED-ONSET MUSCLE SORENESS - William T. Stauber,
Corrie A. Mancinelli
18
MEDICAL CONDITIONS IN SPORT - Dhiren J. Naidu
19
DERMATOLOGIC CONSIDERATIONS IN ATHLETICS - Donald W. Groot,
Patricia A. Johnston
20
PROTECTIVE EQUIPMENT IN SPORTS - Michael R. Mirabella,
Timothy F. Tyler
21
TAPING FOR ATHLETICS AND REHABILITATION - Robert C. Manske,
Justin Rohrberg
22
SPORTS RELATED CONCUSSION - Alex M. Taylor,
Michael W. Collins
23
TRAUMATIC INJURIES TO THE CERVICAL SPINE - James E. Zachazewski,
Brant D. Berkstresser, Gary J. Geissler,
Francis Wang, Lars C. Richardson
24
MAXILLOFACIAL INJURIES - John P. Kelly
25
ABDOMINAL AND THORACIC INJURIES - Benjamin M.J. Thompson,
Brian D. Busconi
SECTION IV: SPECIAL POPULATIONS
AND EPIDEMIOLOGY
26
THE FEMALE ATHLETE - Janice Loudon, Lori A. Bolgla,
Steven A. Greer
27
MUSCULOSKETAL DANCE MEDICINE AND SCIENCE - Jeffrey A. Russell
28
THE ATHLETE WITH DISABILITY - Duane G. Messner
29
SELECTED REHABILITATION NEEDS OF THE MASTERS ATHLETE -
James W. Matheson, Robert C. Manske
30
APPLIED SPORTS INJURY EPIDEMIOLOGY - Mitchell J. Rauh,
Caroline A. Macera, Stephen W. Marshall
xvii
1
9
40
58
98
141
174
187
217
234
265
287
307
331
350
385
423
441
455
478
515
536
549
581
596
631
651
681
704
730
631
Introduction
The opportunity for women and girls to participate in
sports has increased dramatically. According to statistics
from the National Collegiate Athletics Association (NCAA),
female participation in collegiate sports has increased 456%
between 1971 and 2005.
1
At the high school level, roughly
one in three girls participate in organized sports. Benets
from participating in sports are signicant. It has been dem-
onstrated that athletic women and girls have improved
health, better grades, and increased condence, and are less
likely to use drugs.
Along with these benets comes an increased chance of
injury. In 2000, 10-year NCAA data showed increased risk
of the female knee to injury when compared with the male
knee in comparable sports of soccer and basketball.
2
Several
articles have been written hypothesizing the reason for this
injury trend and some of this research is discussed in this
chapter.
This chapter focuses on issues related to the female
athlete. The physiological and musculoskeletal differences
between males and females are reported rst. This is fol-
lowed by a discussion of common musculoskeletal injuries,
the female athlete triad, and issues related to the older
woman athlete.
Physiological Differences
Between the Sexes
When comparing absolute strength, adolescent males score
considerably higher in strength than adolescent females in
all muscle groups. These differences are dramatic for the
upper body, with males exhibiting 40% to 50% greater
strength than females. In the lower body, the strength
difference is less. Females average 20% to 30% less strength
than males. This strength discrepancy decreases when
relative values based on lean body mass are reported. The
strength difference between sexes is due to males total
muscle mass and the presence of testosterone. There is
no difference between the muscle structure of males and
females.
3
Relative maximal oxygen uptake (VO
2
max) for untrained
women typically averages 15% to 30% below scores for men.
In trained women, the difference becomes less, but women
still present with a 10% to 15% lower VO
2
max. The appar-
ent gender difference in aerobic capacity has been attributed
to lower oxygen carrying capacity, lower blood volume,
fewer red blood cells, lower hemoglobin content, smaller
hearts, lower stroke volume, and smaller muscle ber area in
women. It does not appear that lactate threshold or ef-
ciency varies between men and women.
3
A summary of these
changes can be seen in Table 26-1 .
Musculoskeletal Differences
Between the Sexes
Related to the musculoskeletal system, there are differences
between males and females that may make the female athlete
more susceptible to certain injuries. Figure 26-1 portrays
differences between the sexes. In the lower extremity, fe-
males present with an increased quadriceps angle (Q-angle),
wider pelvis, increased genu valgum, and increased tibial
torsion. Other differences include an increase in joint exi-
bility in the female including genu recurvatum which may
contribute to less knee control. In the upper limb, cubitus
valgus is more common in females.
Musculoskeletal Injuries
Much attention has focused on the causes and management
of musculoskeletal injuries in the female athlete. Four of
the common areas of interest include anterior cruciate liga-
ment (ACL) injury, patellofemoral pain syndrome (PFPS),
medial tibial stress syndrome (MTSS), and spine injuries.
THE FEMALE ATHLETE
Janice Loudon, Lori A. Bolgla, and Steven A. Greer

SECTION IV SPECIAL POPULATIONS AND EPIDEMIOLOGY
26
CHAPTER
632 SECTION IV Special Populations and Epidemiology
The purpose of the following sections is to provide the best
available evidence to guide clinical decision making when
treating the female athlete.
Anterior Cruciate Ligament Injury
ACL injury is one of the most serious knee injuries experi-
enced by physically active individuals. The average esti-
mated annual cost associated with treatment (e.g., diagnos-
tic testing, surgical reconstruction, and rehabilitation) in
the United States has been estimated to exceed $2 billion.
4
Despite progressive treatment, a risk remains for the devel-
opment of knee osteoarthritis.
5 , 6
These ndings have led to
the identication of risk factors and the development of
ACL-injury prevention programs.
7
Nearly 70% of ACL injuries occur from a noncontact
mechanism during sports such as basketball and soccer.
8
A common mechanism of injury involves deceleration or a
sudden change in direction such as a cutting movement.
9
This maneuver may apply excessive torsional force onto the
ACL and result in rupture.
4
Noncontact ACL injuries also
may occur when landing from a jump with the body
positioned in minimal hip and knee exion. DeMorat and
colleagues
10
have shown that excessive quadriceps force
relative to the hamstring muscles can cause excessive tibial
forward translation, especially with the knee positioned in
minimal exion.
Following the passage of Title IX, researchers have re-
ported a higher relative incidence of ACL injury in females
who participate in basketball and soccer.
8 , 11-13
Prodromos
and colleagues
14
recently examined the incidence of ACL
injury across gender and sport. They reported that female
basketball and soccer players were generally three times
more likely to sustain an ACL injury than males.
During the past 25 years, researchers have identied
both intrinsic and extrinsic risk factors that may account for
the ACL injury gender bias ( Table 26-2 ). Intrinsic factors
include anatomical or physiological factors such as intercon-
dylar notch width, ACL size, posterior tibial slope, physio-
logical laxity, and hormonal inuences.
45
Extrinsic inu-
ences include biomechanical or neuromuscular factors such
as in nature. They are modiable to change and are the
basis for many injury prevention programs.
46-48
Intrinsic Risk Factors
ACL injury is thought to occur when the ligament is
stretched excessively over the femoral condyles. This mech-
anism may occur with the abutment of the ACL within the
intercondylar notch when the knee is positioned close to
full extension.
49
Therefore, individuals with a decreased
intercondylar notch size may be more prone to an ACL
injury. Based on this theory, many investigators
15-17
have
Table 26-1
Physiological Differences between Adult Males
and Females
Variable Difference
Upper extremity strength Males are 40% to 50% stronger
Lower extremity strength Males are 20% to 30% stronger
VO
2
max (untrained) Males are 15% to 30% higher
VO
2
max (trained) Males are 10% to 15% higher
VO
2
max

; Maximum oxygen consumption.
Less-musclular
thigh development
A
Less-developed
VMO
Increased
flexibility/
hyperextension
Genu
valgum
Wider
pelvis
Femoral
anteversion
Narrow
femoral notch
Lateral
tibial
torsion
More-musclular
thigh development
VMO
hypertrophy
Less
flexibility
Genu
varum
Narrower
pelvis
Wider
femoral
notch
Medial or
neutral
tibial torsion
B
Figure 26-1
Musculoskeletal differences between the sexes. A, Female lower-extremity posture. B, Male lower-
extremity posture. (From Grifn LY, editor: Rehabilitation of the injured knee, pp 298-299, St Louis,
1995, Mosby.)
The Female Athlete CHAPTER 26 633
examined a possible association between intercondylar
notch size and ACL injury. To date, data have not sup-
ported an absolute relationship between decreased notch
width and female ACL injury. Rather, it appears that both
male and female athletes who have a smaller notch, and thus
a smaller ACL, may be more susceptible to injury.
15 , 17
Recently, Chandrashekar and colleagues
16
and Hashemi
and colleagues
18
examined ACL sex differences using a
cadaveric model (six male, mean age 34 years; six female,
mean age 34 years). Ligaments from female specimens were
smaller with respect to length, cross-sectional area, and
volume, and had less stiffness. They attributed this sex dif-
ference to the amount of collagen brils present, because
male specimens exhibited a higher percentage area lled
with collagen ber (e.g., area of collagen bers/total area of
the micrograph). These ndings suggest that females who
have a smaller intercondylar notch, in combination with a
weaker ligament, may be more susceptible to injury.
A few investigators
19-21
have reported an association be-
tween an increased posterior tibial slope (the angle formed by
the tibial plateau relative to the long axis of the tibia) and
ACL injury. They have theorized that an increased posterior
tibial slope would place the femur in a more posteriorly
directed position and promote anterior tibial translation.
Because of the limited scope of data, additional studies are
needed to better understand this inuence.
Increased ACL laxity has been identied as another risk
factor for the female athlete.
22
Uhorchak and colleagues
23
found that females were 2.7 times more likely to sustain an
ACL injury if they had ligamentous laxity values that were
one or more standard deviations (SDs) above the mean
value. The effect of the menstrual cycle on ligamentous lax-
ity also has received much attention. Refer to the separate
section in this chapter for additional information.
Extrinsic Risk Factors
Extrinsic risk factors include biomechanical and neuro-
muscular characteristics that are amenable to change.
Researchers have identied gender differences in lower-
extremity biomechanics during running,
31
cutting,
32 , 33 , 50

and single-leg landing
34 , 35 , 37 , 51
tasks. Results from these
studies infer that females perform these maneuvers with
greater knee valgus, femoral internal rotation, femoral
adduction, and tibial external rotation. Ireland
52
has
described this pattern as the position-of-no-return
( Figure 26-2 ). High knee valgus loads generated in this
position, especially performed on a minimally exed knee,
are thought to signicantly strain the ACL.
34 , 50 , 53
Neuromuscular factors may further contribute to gender
differences. The hamstrings play an important role in mini-
mizing excessive anterior tibial translation caused by a strong
quadriceps contraction. Females also have demonstrated in-
creased quadriceps activation relative to the hamstrings during
athletic maneuvers.
39
This activation pattern, when performed
in limited knee exion, may contribute to excessive anterior
tibial translation and cause ACL injury.
Researchers have examined the inuence of other muscle
groups to better understand the gender bias. During single-
leg landing
40
and cutting maneuvers,
33
females attenuate
greater energy using the quadriceps and ankle plantar ex-
ors, whereas males disperse more energy using the quadri-
ceps and hip extensors.
40
Fleming and colleagues
54
have
shown how co-contraction of the quadriceps and gastrocne-
mius result in greater ACL strain with the knee exed at 15
and 30. However, others
33
have postulated that gastrocne-
mius activation may reect a means for increasing knee stiff-
ness. Additional works are needed to better understand the
interaction between these muscles.
Differences in lower-extremity strength also may contrib-
ute to the gender bias. Sex differences regarding general knee
strength occur after puberty when males demonstrate greater
increases in strength, power, and coordination compared
with females.
55
Thus, differences in knee strength may con-
tribute to the higher incidence of ACL injury in females. Hip
weakness also may contribute to lower extremity injury.
56

Jacobs and colleagues
41
found a greater association between
hip abductor weakness and knee valgus during a single-leg
landing task in females. Lawrence and colleagues
42
reported
that females with greater hip and knee strength attenuated
ground reaction forces more effectively and generated smaller
external knee adduction and exor moments during a single-
leg landing. These ndings support the importance of strong
hip muscles for maintaining good lower-extremity alignment.
They also support ndings from Decker and colleagues
40
that
strong hip muscles may reduce some of the ground reaction
forces applied to the knee during a drop landing task.
Limitations of prior studies have been the examination of
subjects in controlled laboratory settings that do not repli-
cate aspects of the eld environment, such as fatigue
and decision-making tasks.
57
Kernozek and colleagues
43
reported that females could not reduce anterior knee shear
forces as effectively as males during a single-leg landing fol-
lowing a fatiguing program. Borotikar and colleagues
44
re-
ported increased hip internal rotation, knee abduction, and
knee internal rotation during anticipated and unanticipated
Table 26-2
Summary of Intrinsic and Extrinsic Factors
that May Contribute to Sex Differences Regarding
Anterior Cruciate Ligament Injury
Intrinsic Factors Extrinsic Factors
Intercondylar notch size
15-17
Kinematics
31-38
Anterior cruciate ligament
size
16 , 18
Quadriceps activation
33 , 39 , 40
Hip abductor strength
41 , 42
Fatigue
43 , 44
Tibial plateau slope
19-21
Physiological laxity
22 , 23
Hormonal inuences
24-30

cutting maneuvers following a fatiguing protocol. More-
over, these differences were more pronounced during the
unanticipated task. Together, results from these studies sup-
port the need for additional work that better depicts eld
conditions.
Menstrual Cycle and Anterior Cruciate
Ligament Injury
Some believe that hormonal differences may contribute to
the increased risk of ACL rupture in female athletes. This
line of research is based on the premise that uctuation in
estrogen levels may contribute to ACL injury.
Beginning with the onset of menses, the menstrual cycle
can be divided into the following phases: follicular, ovula-
tory, and luteal. Within this cycle, estrogen levels are lower
during the follicular phase and rise dramatically during the
ovulatory phase and throughout the luteal phase. Research-
ers
24 , 25
believe that increased estrogen levels may contribute
to ACL laxity, thus predisposing the female athlete to
injury. Although investigators
25-28
have examined the rela-
tionship between menstrual cycle and ligamentous laxity,
conicting results exist. Criticisms include small sample size
and the reliance on subjective history for identifying the
phase of menstrual cycle at the time of injury.
45
Hewett and colleagues
58
recently conducted a systematic
review of the literature regarding menstrual cycle and ACL
injury risk. Based on this review, they concluded that a
female is more likely to incur an ACL injury during the
preovulatory phase (follicular and ovulatory phases). This
conclusion contradicts the previous premise regarding
increased estrogen and ACL laxity. Hewett and colleagues
58
suggested that reduced dynamic knee stability (e.g., de-
creased neuromuscular control) might contribute to ACL
injury during earlier phases of the menstrual cycle based
on earlier work by Sarwar and colleagues.
59
However,
more recent works
29 , 30
have not found a relationship be-
tween uctuating estrogen levels and knee neuromuscular
control.
Oral contraceptives (OCs) increase and stabilize either
levels of estrogen and progesterone, or just those of proges-
terone, and prevent the luteinizing hormone surge and
resultant ovulation. Some believe that controlling uctua-
tions in estrogen levels may minimize the risk of ACL
injury. Hewett and Myer
60
reported increased passive and
dynamic knee stability in females who took OCs compared
with those who did not take OCs. Although OC use may
reduce female ACL injury rates,
61-63
further studies are
needed to establish this association.
Prevention Programs
As described previously, extrinsic factors are modiable and
correction of these factors has been the focus on many ACL-
injury prevention programs. Most programs
7 , 46 , 48 , 64
have
included a combination of strengthening, neuromuscular
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.)
training, and instruction in proper landing and cutting tech-
niques. Although ndings from these studies support
the use of prevention programs, it remains elusive as to the
most important element of each. Lephart and colleagues
65

reported favorable changes in neuromuscular and biome-
chanical parameters in healthy high school female athletes
who completed an 8-week intervention of either plyometric
or resistance exercise.
More recent studies
7 , 46
have prospectively followed
female soccer players who have participated in the Prevent
Injury and Enhance Performance (PEP) injury prevention
program ( www.aclprevent.com ). This program is a combi-
nation of strengthening, stretching, plyometrics, agilities,
and instruction in proper technique as part of a warm-up to
play. Gilchrist and colleagues
7
recently reported that female
soccer players who participated in the PEP program were
3.3 times less likely to sustain an ACL injury.
Grindstaff and colleagues
66
conducted a systematic
review and support the use of ACL-injury prevention pro-
grams. Important aspects of a program include dynamic
balance activities, agility skills, plyometrics with an emphasis
on proper knee position (i.e., minimizing a knee valgus
or varus alignment), and core and hip strengthening. Per-
haps the most important aspect of a prevention program is
attention to proper technique. Female athletes should be
encouraged to land softly using a greater degree of hip and
knee exion to minimize external moments applied to the
knee. They also should be instructed to avoid pivoting on a
xed foot and taught to decelerate using a multiple-step
technique.
Although much attention has been focused on the causal
factors and prevention of ACL injury, additional studies are
needed to understand this enigma. Future investigations
should be directed toward examining mechanisms of injury
in an on-eld setting and identifying the critical compo-
nents of prevention programs. Furthermore, Prodromos
and colleagues
14
recently found that injury prevention
programs were more effective at preventing ACL injury in
female soccer players than in those playing basketball. These
ndings infer the need for the development of prevention
programs specic to a particular sport.
Patellofemoral Pain Syndrome
Patellofemoral pain syndrome (PFPS) is one of the most
common pathological conditions of the knee. Unlike re-
search regarding the incidence of ACL injury, limited data
exist regarding the incidence and causes of PFPS in females.
However, clinicians have anecdotally concluded a gender
bias regarding causal factors of PFPS.
Causal Factors
PFPS may result from abnormal patella tracking that causes
excessive compressive stress to the lateral patella facet. Clini-
cians routinely measure the Q-angle to quantify the degree
of lateral patella tracking and consider a Q-angle greater
than 20 as excessive.
67
Although females generally appear
to exhibit higher Q-angles than males, studies have not sup-
ported the relationship between a higher Q-angle and
PFPS.
68
A reason for this nding is that the Q-angle is a
static measure that may not adequately depict patella move-
ment during dynamic activities. Powers
69
has theorized that
increased hip adduction and internal rotation can increase
the Q-angle by moving the patella medial to the anterior
superior iliac spine (referred to as an increase in the
dynamic Q-angle). Based on this premise, a female with
a normal static Q-angle may perform dynamic activities
such as running, jumping, and stair descent with increased
hip adduction and internal rotation. Prior works
31 , 70
have
shown that females perform athletic maneuvers with greater
hip adduction and internal rotation than males; these nd-
ings may support a relatively higher incidence of PFPS in
females. Therefore, assessment of changes in the Q-angle
during dynamic tasks might provide conclusive information
regarding the relationship between PFPS and the Q-angle.
Hip Inuences and Patellofemoral Pain Syndrome
An emerging body of work has focused on the inuence of
the hip on PFPS. To date, many researchers
71-75
have exam-
ined hip strength and consistently found hip abductor,
external rotator, and extensor weakness in females with
PFPS. Because these muscles primarily control hip adduc-
tion and internal rotation during dynamic activities, weak-
ness or faulty timing could cause altered hip kinematics and
possibly contribute to abnormal lateral patella tracking at
the knee. Table 26-3 summarizes reference force values and
test positions that clinicians may use for identifying hip
weakness in females with PFPS.
A few studies have simultaneously examined the interrela-
tionship between hip weakness and altered lower extremity
kinematics in females with PFPS. Bolgla and colleagues
73
were
the rst to examine hip strength and hip and knee kinematics
in this patient population. Although subjects with PFPS dem-
onstrated signicant hip abductor and external rotator weak-
ness, they did not exhibit increased hip adduction, hip internal
Table 26-3
A Summary of Force Values (Expressed as a Percentage
of Body Mass) for Females Diagnosed with Patellofemoral
Pain Syndrome
Hip
Abductors
Hip
External Rotators
Ireland et al.
71
23.3 6.9 10.8 4.0
Robinson and Nee
72
16.0 8.0 16.0 6.0
Cichanowski et al.
74
29.0 8.0 17.0 4.0
Bolgla et al.
73
22.5 5.9 11.1 3.1
Willson and Davis
75
21.1 6.0 9.1 2.6
rotation, or knee valgus during stair descent. Although this
task was representative of one that elicits patellofemoral
joint pain, subjects might have used compensatory patterns
to minimize knee pain when performing this lower demand-
ing task.
76
Others have examined hip and knee kinematics during
more demanding activities such as running, single-leg
squats, and single-leg jumping. Findings from Willson and
colleagues
77
and Willson and Davis
78
showed that females
with PFPS exhibited greater hip adduction, but less hip
internal rotation, compared with controls during running,
single-leg squatting, and repetitive single-leg jumping. They
concluded that decreased hip internal rotation might have
represented a means for reducing lateral patella stress.
Dierks and colleagues
79
reported a strong correlation ( r
0.74) between hip abductor weakness and peak hip ad-
duction following prolonged running. These results implied
that patients with PFPS might not demonstrate altered ki-
nematics until they achieve a certain threshold of weakness.
In summary, females with PFPS commonly demonstrate hip
weakness and use altered lower-extremity mechanics com-
pared with controls. It remains elusive whether hip weak-
ness was the cause of or the result from PFPS. Prospective
studies are needed to understand associations between hip
strength and lower extremity kinematics.
Foot and Ankle Inuences and Patellofemoral
Pain Syndrome
Tiberio
80
has theorized that excessive subtalar pronation
may contribute to PFPS. From a biomechanical standpoint,
increased subtalar joint pronation results in obligatory tibial
internal rotation. Interestingly, tibial internal rotation brings
the patella toward the tibial tubercle and decreases the
Q-angle. However, during gait, the knee must extend dur-
ing the latter phases of stance to propel the limb to the
swing phase. To achieve knee extension, the tibia must be
in an externally rotated position relative to the femur, a
position accomplished via increased femoral internal rota-
tion. As described previously, increased femoral internal
rotation will cause an increase in the dynamic Q-angle and
may contribute to PFPS.
Powers and colleagues
76
examined foot and lower-
extremity rotation in subjects diagnosed with and without
PFPS during gait. They did not nd any between-group
differences regarding the amount or timing of peak foot
pronation or tibial internal rotation. However, subjects with
PFPS exhibited signicantly less hip internal rotation than
controls. These authors concluded that subjects with PFPS
might have reduced the Q-angle using this compensatory
hip strategy.
Recently, researchers
81-83
have prospectively examined
the inuence of increased foot pronation on PFPS causes.
Results from these studies have not supported an associa-
tion between increased pronation and PFPS. Instead, data
from these studies suggested that subjects who exhibited
foot function that impeded shock attenuation (e.g., gait
patterns of greater pressure on the lateral aspect of the foot
and running patterns of greater vertical peak force under
the lateral heel) developed PFPS. It is important to note
that few studies have examined the relationship between
foot function and PFPS; additional studies are needed to
better understand this interrelationship.
Interventions
Unlike ACL-prevention programs specically aimed at
reducing injury in the female athlete, the best treatment
approach for females with PFPS remains elusive. However,
more recent works
84
support the use of hip strengthening
for the treatment of PFPS. Mascal and colleagues
85
reported
positive outcomes for two female subjects who participated
in a 14-week intervention that targeted the hip, pelvis, and
trunk muscles. Tyler and colleagues
86
and Boling and col-
leagues
87
also reported improvements in pain and function
in subjects with PFPS who participated in a program target-
ing the hip musculature. Limitations for these studies
included use of a case report format,
85
inclusion of male and
female subjects,
86 , 87
and use of hip exercise that also affect
the quadriceps. Future works should examine the effects
of isolated hip strengthening on improving impairments
associated with PFPS.
Prior works
88 , 89
have supported the use of quadriceps
strengthening for the treatment of PFPS. Although many
clinicians prefer weightbearing (closed kinetic chain)
exercise, studies have not supported the preferential use
of weightbearing exercise over nonweightbearing (open
kinetic chain) exercise.
84 , 90
Rather, quadriceps exercise
performed in a pain-free manner appears to be the critical
consideration.
Herrington and Al-Sherhi
91
recently conducted a con-
trolled trial of weightbearing and nonweightbearing quad-
riceps exercises for a group of males with PFPS. Regardless
of exercise group, males demonstrated signicant improve-
ments with knee pain, strength, and function. These nd-
ings support the primary use of quadriceps strengthening
for males; however, it is unclear if females with PFPS will
respond similarly. Although females with PFPS may respond
well to quadriceps strengthening,
90
they may receive addi-
tional benet from hip strengthening. Future works should
focus on developing a clinical prediction rule for identifying
a patient cohort that may respond more favorably to a com-
bination of hip and knee strengthening exercise.
Evidence
92 , 93
supports orthosis use for the treatment of
PFPS. Sutlive and colleagues
50
identied aspects of a physi-
cal examination to determine a cohort of subjects with
PFPS that may benet from orthosis prescription in combi-
nation with activity modication. They found that subjects
with PFPS who exhibited a forefoot valgus greater than or
equal to 2, passive great toe extension less than or equal to
78, and a navicular drop less than or equal to 3 mm
responded favorably. These results inferred that subjects
with a more rigid foot type received greater benet from the
orthosis intervention and suggested that shock attenuation
may have reduced PFPS symptoms. These ndings also are
consistent with prospective etiological studies
81 , 82
that re-
ported the development of PFPS in subjects who exhibited
less pronation during gait.
In summary, PFPS is a multifactor problem with no clear
cause or recommended best practice pattern. Prospective
studies are needed to better understand the inuences of the
hip, knee, and foot-ankle complex on the cause of PFPS.
Researchers also should strive to establish both classication
systems and clinical guidelines
94 , 95
to further improve the
management of patients with PFPS. More information on
this topic can be found in Chapter 18 , Patellofemoral
Joint in Pathology and Intervention in Musculoskeletal
Rehabilitation, volume III in this series.
Medial Tibial Stress Syndrome (MTSS)
MTSS is one of the most common causes of exercise-related
leg pain.
96
The term sometimes referred to as shin splints
describes a specic overuse injury producing pain along the
posteromedial aspect of the distal two thirds of the tibia.
The sports in which athletes are most commonly aficted
are cross-country, track, basketball, and volleyball. The
incidence of MTSS in long-distance runners can be as high
as 16.8% and is more prevalent in the female runner.
97 , 98
The pathogeneses of MTSS is controversial. Some
authors characterize the condition as a periostitis (inam-
mation of the periosteum) caused by strain of the medial
tibial fascia. Others describe it as a tearing at the muscle-
bone interface. Muscles that have been identied as possible
culprits include the posterior tibialis,
99 , 100
soleus,
101 , 102
and
exor digitorum longus.
103
However, in a review of litera-
ture, Tweed and colleagues
104
concluded that MTSS is not
an inammatory 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
fracture if not cared for properly.
The diagnosis of MTSS is based on clinical history and
symptoms. Pain and tenderness is usually diffuse and
located along the medial-distal two thirds of the tibia. Com-
monly, athletes will complain of pain at the beginning of a
run. The pain may subside during the middle of the run but
recurs at the end of the run. Provocative tests to rule in
MTSS include pain with passive ankle dorsiexion, resisted
plantar exion, toe raises, or single-leg hops. If the clinician
suspects a tibial stress fracture, then a bone scan should be
sought.
Potential biomechanical risk factors for MTSS include
excessive foot pronation,
98 , 105
increased velocity of prona-
tion, and increased compensated rear- and forefoot varus
alignment.
106
Theoretically, the antipronation muscles fatigu-
ing over time may increase the amount of force attenuated by
the bone and periosteal tissue.
Bennett and colleagues
107
measured tibiobular varum,
weightbearing resting calcaneal position, and gastrocnemius
length in 125 high school cross-country runners prior to
their competitive season. All athletes were monitored for
symptoms of MTSS. After 8 weeks, 15 runners (25 limbs)
presented with MTSS compared with a randomly select
25 limbs. Navicular drop test (NDT) was compared in these
50 limbs. A T-test showed a signicant difference in NDT
between injured and uninjured limbs, with the injured limb
having greater navicular drop (6.8 mm vs. 3.6 mm). Plisky
and colleagues
108
examined bilateral NDT, foot length,
height, body mass index, previous running injury, running
experience, and use of orthoses or tape in a group of high
school cross-country runners. Runners were followed
during the season to determine athletic exposure and occur-
rence of MTSS. Overall injury rate was higher in females.
Only gender and body mass index were signicantly associ-
ated with the occurrence of MTSS. In addition, those
runners with a previous running injury were more than two
times as likely to develop MTSS.
Other contributing factors are repetitive overload, run-
ning on an unyielding surface, and shoe error (wrong type
or wearing too long [i.e., shoe worn out]). It is also specu-
lated that increasing training volume and hills contribute
to MTSS.
Treatment should focus on relative rest in the acute
phase. The athletes biomechanics should be examined and
an off-the-shelf orthotic device prescribed for the athlete
with pes planus to minimize the amount of pronation. In
those athletes who present with a rigid foot, shock absorb-
ing shoes should be worn. Gastrocnemius and soleus length
needs to be assessed and exibility exercises given if the
complex is tight. Strengthening of the hip musculature such
as the gluteus medius is also advocated.
Suggested Parameters for Safe Return-to-Running
Program
Start at 50% of the preinjury state (intensity and duration)
Level surface
Appropriate warmup
Increase 10% per week
Progress duration prior to intensity
The last resort for treatment of MTSS is a fasciotomy.
The decision for surgery is based on the failure of
conservative measures. The literature presents positive
outcomes following fasciotomy.
109
For more information
on repetitive stress injuries see Chapters 21 and 22 on
repetitive stress pathological conditions in Pathology and
Intervention in Musculoskeletal Rehabilitation, volume III
in this series.
Spine Injuries
An epidemiological study by Jackson and Mannarins
110
in-
dicated that 55% of all athletes sustain at least one injury to
the spine during their sports careers with recurrence at 42%.
The highest incidence of spine injuries in females occurs in
sports such as gymnastics, racquet sports, golf, equestrian
skills, and weight lifting.
111
Compared with the general
population, the athlete responds better to conservative
management of musculoskeletal-related spine injuries and
most will recover within 10 days.
112
If symptoms linger and
the athlete cannot participate in her sport, it is likely that
she has sustained substantial damage to either a bony or
collagenous component of the spine. One must keep in
mind that adolescents have a higher incidence of nonmus-
cular causes for low back pain, such as tumor.
113
The clini-
cian needs to be aware of red ags when dealing with spinal
injuries. Any one of the signs is an indication that further
medical workup by a physician is required.
Spondylolisthesis is a bilateral fracture of the pars inter-
articularis with actual slippage forward of the superior ver-
tebra on the inferior vertebra. Nerve root involvement is
possible with the slippage of the vertebra. The most com-
mon level of occurrence is at the L5-S1 level (90%)
followed by L4 then L3.
117
The anterior slippage is graded
on the percent of the vertebral body that has slipped for-
ward. A grade I spondylolisthesis indicates anterior slippage
less than 25% of the vertebral body. A grade II is slippage
between 25% and 50%, grade III is 50% to 75%, and a grade
IV is anything greater than 75% slippage. For grade I treat-
ment, see the following text. For grade II or greater, the
athlete may be prohibited from playing in aggressive, colli-
sion sports such as rugby or repetitive-stress sports such as
gymnastics and dance.
117 , 118
Symptoms include a dull backache with or without but-
tock pain and possible sciatica. The back pain is aggravated
by extension activity and may increase with prolonged
standing. One should not forget that pain in the low back
may be referred from the uterus, indicating the possible
need for a gynecological consult.
The athlete usually presents with hyperlordotic posture
and tight hip exors. The erector spinae and hamstring mus-
cles may present with spasm. The clinician may feel a step-off
at the involved vertebral level. The single-leg standing hyper-
extension test (Stork test) may be positive ( Figure 26-3 ).
Neurological examination may be positive for changes in
Red Flags Associated with Spinal Injury
Indicating the Need for Further Medical Workup
by a Physician
Unrelenting back pain (worse at night)
Progressive neurological decits
Unexplained weight loss
Bladder or bowel paralysis (cauda equina)
Positive Babinski sign
In addition, ankylosing spondylitis, an inammatory
disease, should be considered if the female athlete com-
plains of a gradual onset of pain and stiffness in the thora-
columbar or sacroiliac (SI) area that is not associated
with activity. Further workup including a bone scan and
blood tests (human leukocyte antigen [HLA] B
27
) deserve
consideration.
Spondylolysis and Spondylolisthesis
Spondylolysis is the most common cause of low back pain
in the active adolescent seeking medical attention (70%).
113
Spondylolysis is a stress fracture through the pars interar-
ticularis of the posterior lumbar vertebra. Repeated axial
loading of the pars interarticularis can cause the stress
fracture,
114
but it also can occur developmentally.
115
Hyper-
extension of the normal lordosis alters the biomechanics of
loading force distribution throughout the lumbar spine and
creates abnormal stress upon the pars interarticularis region.
This type of stress is common in sports such as weightlifting
and gymnastics. A 32% incidence of spondylolysis has been
found in female gymnasts, 63% in divers, and 12% to 15% in
dancers.
116
Figure 26-3
Single-leg standing hyperextension (Stork) test.
sensation, reexes, or myotomes. A radiograph using an
oblique view may identify a Scottie Dog sign (fracture
through the pars). Stress fractures may not show-up initially
with radiographs; therefore, a bone scan or magnetic reso-
nance imaging (MRI) scan is recommended.
Spondylolysis and grade I spondylolisthesis are treated
with training modications to correct hyperextension during
techniques.
119
The athlete should be trained to maintain a
neutral spine with static and dynamic activities. Muscle im-
balances, such as tight hip exors, should be restored around
the hip joint. An athlete with a grade II spondylolisthesis
or higher should be cautioned about aggressive sporting
activities that require hyperextension. Radiographs should
be performed annually to check for a progression in the
anterior slippage. External supports may provide stability
and proprioceptive cuing. Joint mobilization of stiff seg-
ments above the fractured level is benecial. Prognosis for a
grade I and II spondylolisthesis is good. Surgical interven-
tion may be required in a low percentage of athletes if neu-
rological signs progress. Low grade slips can be addressed by
direct fusion with return to noncontact sports.
120
Pathological Conditions of the Sacroiliac Joint
The SI joint is inherently a stable joint with little motion.
121
However, injury can occur to this joint from excessive load-
ing or from a fall onto the buttock. The female athlete may
be particularly vulnerable to SI injury secondary to monthly
cycling of hormones or increased ligamentous laxity during
pregnancy. According to Marymont and colleagues,
122
most
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
exion, abduction, and external rotation test (FABER
or Patrick test) and specic 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 specicity. The gold standard is a diagnostic injection
under uoroscopic guidance to conrm a pathological con-
dition of the joint. Blood work (HLA B
27
) will help to
differentiate between sacroiliitis or ankylosing spondylitis.
Exercises to help stabilize the SI joint should include the
hip rotators, especially the posterior bers of the gluteus
medius and the single-joint hip extensors. Exercises such as
wall sits with gluteal squeeze, lateral step-ups with gluteal
squeeze, isometric hip external rotation ( Figure 26-4 ), and
repetitive prone knee curls are helpful. An SI belt helps
with instability and can be worn until muscle strength is
adequate to stabilize the joint. Joint mobilization to hypo-
mobile joints in the lumbar spine also may be indicated.
Biomechanical analysis of running and sport techniques is
appropriate.
Intervertebral Disc Lesion
The intervertebral disc has limited vascularity and therefore
depends on mechanical pumping and movement for health
and repair. Most disc lesions come on gradually and affect
the levels of L4-L5 and L5-S1.
122
A woman who is older
than 25 years old is more prone to disc lesions than the
younger athlete, although the incidence in adolescents
appears to be increasing.
123
The mechanism of injury usu-
ally involves some combination of lumbar hyperexion, axial
compression, and rotation. The disc injury may occur from
a single episode or repetitive trauma. Repeated minor
trauma, such as sustained compression in exion and rota-
tion, gives rise to circumferential ssures usually located
along the inner portion of the annulus.
124
Weakening of the
annular layers reduces the ability of the annulus to contain
the nucleus, which can lead to disc protrusion. Disc injuries
are found in athletes who participate in sports that require
excessive torsion such as golf, racquetball, or tennis. In the
event that the disc material impinges on the nerve root,
neurological signs will be present. Sciatica has a high sensi-
tivity (95%) for disc herniation.
125
Figure 26-4
Gluteal strengthening exercises.
Discogenic pain can range from a minor complaint of
back pain to severe disability. The athlete, in mild cases, may
continue her activity but will notice a gradual increase in
pain and stiffness. In single, acute incidences, the athlete
may be stopped in her tracks by the pain. The lumbar dis-
comfort often worsens at night and the athlete may awaken
with morning stiffness.
97
Physical examination may reveal a lateral shift, positive
straight-leg raise, diminished reexes, or radicular symp-
toms. Symptoms are usually aggravated by trunk exion.
If irritation of the nerve root sleeve is present, the athlete
will present with a positive slump test or straight leg
raise.
126
Other neurological symptoms include tingling,
numbness, paresthesia, muscle (myotome) weakness, and
altered reexes.
Diagnostic testing should include anterior-posterior and
lateral lms with oblique views to visualize the pars interar-
ticularis and ndings should be correlated with physical
signs and symptoms. MRI is the most sensitive test and will
delineate the disc and nerve roots. Abnormal ndings may
not be the source of the athletes pain. Disc degeneration
and protrusion has been demonstrated on MRI in 20% to
25% of asymptomatic individuals.
127
Fortunately, the symptoms of an acute disc injury often
resolve without surgery. In acute stages, the goal is to
minimize pain and muscle spasm. Unloading of the disc is
performed by positioning the athlete in a side lying posi-
tion to increase the size of the intervertebral foramen with
the convex side up. Sustained lumbar traction may offer
relief. Clinically, McKenzies extension protocol seems to
help a high percentage of patients with disc injury.
107
A
corset sometimes helps stabilize the spine as the athlete
recovers from acute symptoms, but its use should be
closely monitored. In extreme cases, epidural injections
are helpful.
For chronic disc injury, a more aggressive approach is
indicated. Heavy mechanical traction has been proposed by
Saunders and Saunders.
126
Joint mobilizations, including
central techniques and rotations,
128
may also be effective.
Clinical prediction rules have become increasingly available
to the clinician to identify the appropriate candidate for
manipulation.
49 , 129
In the presence of adverse neural ten-
sion, slump stretching and ossing is indicated ( Figure
26-5 ). Once symptoms and signs are controlled, the athlete
should be placed on a lumbar stabilization exercise pro-
gram. Manipulation is contraindicated when neurological
decit is present or if the patient presents with ligamentous
laxity. If joint instability is accompanied by neurological
signs, the athlete may need to undergo surgical intervention
(fusion).
Lumbar Spine Strain and Sprain
A lumbar strain or sprain or low back pain refers to injury
in the musculotendinous or ligamentous tissue. Common
mechanisms of injury include high-velocity torsion or twist-
ing movements or repetitive overload. This loading creates
excessive and abnormal tension in collagen bers causing
microtearing.
130
An acute, violent torsion may be associated
with avulsion of the transverse process by strong contrac-
tion of the quadratus lumborum or iliopsoas. Chronic over-
load strains are due to poor posture or faulty mechanics.
Growth spurts may increase the incidence of back strain
because of soft tissue inextensibility.
131
The athlete will complain of local pain with trunk
motion. Motion is usually restricted in exion and rotation.
Pain or weakness will be present with resisted trunk motion.
In chronic situations, trigger points, localized areas of
increased sensitivity, or irritability in soft tissue structure
may cause referred pain.
In the acute stage, rest and local modalities will help with
pain and muscle guarding. A brace or corset worn for 2 to
3 weeks will sometimes help with debilitating pain. Soft
tissue mobilization including trigger point therapy along
with posture correction is started on day 2 or 3 following
injury. Improper body mechanics, poor conditioning, and
poor warmup should all be addressed in chronic situations.
Structural Scoliosis
Scoliosis is dened as a lateral spinal curvature usually
associated with rotation of vertebral body. Idiopathic ado-
lescent scoliosis is relatively common in the general popula-
tion and is unrelated to sporting activity. A structural curve
as seen in idiopathic scoliosis refers to a xed, bony defor-
mity. A functional curve, as seen in a disc lesion, is reversible
and is due to muscle imbalance. A mild idiopathic spinal
deviation is usually well tolerated and the female athlete has
no trouble participating in sports. However, if scoliosis
progresses to a severe deformity (greater than 40 to 50
Figure 26-5
Slump stretching.
Cobb angle), compromise of the cardiopulmonary system is
probable. There appears to be an association between
scoliosis and participation in sports such as gymnastics, ice
skating, and dance. Smith and Micheli
116
found the preva-
lence of scoliosis to be 33% in female skaters compared with
the general population.
In mild cases, the athlete may be asymptomatic. In other
cases, the athlete will complain of back pain that may be
aggravated by prolonged positioning or intense exercise.
Radiographic evidence will reveal a scoliotic curve. Clinical
signs include a lateral curvature of the spine, lateral shift, leg
length discrepancy, and rib hump (structural scoliosis).
The key to managing scoliosis is early diagnosis and
intervention. As well, the clinician must counsel the young
athlete on sport participation. Although sports are not con-
traindicated, the athlete needs to alert the health profes-
sional of spine pain during activity. Rehabilitation focuses
on maintaining trunk mobility, muscle balance, soft tissue
techniques, and breathing exercises. In moderate cases,
bracing may be appropriate. In contact sports, the brace
must be padded to prevent lacerations and contusions.
Surgery is indicated for severe progressive curves.
Costochondral Joint
The costochondral joint may be injured from direct impact
or overuse.
132
Possible joint separation may occur when a
force is applied to the chest, causing the costal cartilage
to separate from the sternum. The athlete complains of
pain and tenderness in one of the costochondral joints.
A snapping sensation may also be present. Symptoms will be
made worse by sudden movements, strain, and coughing. It
appears that this condition is more common in young
adults; is related to exercise; and is more common in sports
such as golf, rowing, and throwing sports.
133
Radiological
examination is normal. Effective treatment includes cortico-
steroid injections into the region and nonsteroidal anti-
inammatory drugs (NSAIDs). Modalities such as phono-
phoresis and electrical stimulation may be used initially for
pain, followed by a progressive exercise program focusing
on the pectoralis and serratus muscles. Joint mobilization
and manipulation may be indicated for associated hypomo-
bile joints in the thoracic spine or costal articulations.
134
Strapping or taping may help with pain or instability.
Taping can be applied over the affected joint in a criss-cross
or L-shaped manner to help stabilize the joint. Differential
diagnosis includes cardiac involvement because Tietze dis-
ease is a condition involving the same area of the anterior
chest, but is associated with swelling. Polyarthritis is charac-
terized by inammation of ve or more joints.
Female Athlete Triad
The female athlete triad was rst described in 1992 as
a combination of disordered eating, amenorrhea, and
osteoporosis in female athletes.
135
Each of these areas rep-
resents a spectrum of three interrelated aspects of womens
health: energy availability, menstrual function, and bone
health. Therefore, alterations in one or more of these areas
may adversely affect the health of the female athlete.
136
Energy Availability
Bonci and colleagues
137
have stated that low energy avail-
ability is the hallmark factor contributing to the other
aspects (amenorrhea and osteoporosis) of the triad. Energy
availability is dened as the energy intake minus the exer-
cise energy expenditure per kilogram of lean body mass.
136
An athlete may lessen energy availability by either decreas-
ing intake (e.g., disordered eating or eating disorder) or
increasing expenditure (e.g., excessive exercise).
Disordered eating refers to an entire spectrum of abnor-
mal behavior such as fasting, restrictive consumption, or the
use of laxatives or diuretics.
137
In contrast, eating disorders,
such as anorexia and bulimia nervosa, represent clinical
syndromes dened by strict diagnostic criteria.
137
However,
both represent a means of reducing the available energy by
reducing intake. Conversely, an athlete can reduce energy
availability by increasing energy expenditure through exces-
sive exercise. Therefore, an athlete need not necessarily
present with disordered eating to be at risk for detrimental
effects caused by low energy availability.
When energy availability decreases, the body attempts
to maintain energy balance by disrupting reproduction,
cellular maintenance, thermoregulation, and growth.
138
Decreased energy availability associated with disordered
eating may further lead to an increased risk of depression
and anxiety and adversely affect the cardiac, gastrointestinal,
endocrine, reproductive, skeletal, renal, and central nervous
systems.
139
Menstrual Dysfunction
Menstrual function may be described as eumenorrhea
(menstrual cycle at a 28-day median interval), oligomenor-
rhea (menstrual cycle at a 35-day or longer median inter-
val), or amenorrhea (absence of a menstrual cycle),
136

with dysfunction resulting from altered hypothalamic reg-
ulation. Specically, decreased secretion of gonadotropin-
releasing hormone by the hypothalamus reduces the
pulsatility of the luteinizing hormone produced by
the pituitary.
140
Loucks and Thuma
141
and Loucks and
colleagues
142
have reported a reduction in luteinizing hor-
mone pulsatility when decreasing energy availability in
females who have a regular menstrual cycle. These ndings
suggest that a loss in energy availability may contribute to
amenorrhea.
Amenorrhea associated with a decrease in estrogen
143
may lead to anovulation (failure to ovulate), infertility, and
decreased bone density. Although infertility is generally
reversible with the restoration of menses, it is important to
note that ovulation may return prior to menses restoration.
Therefore, an athlete may become pregnant should she not
use an adequate form of birth control during this time.
Unfortunately, bone density loss may remain even after the
restoration of menses.
144 , 145
Other adverse effects associated with lack of estrogen
include decreased oxidative metabolism in skeletal muscle,
increased low-density lipoprotein (LDL) cholesterol lev-
els,
146 , 147
and vaginal dryness.
148
Decreased oxidative me-
tabolism translates to decreases in performance. Increased
LDL levels may increase the risk of cardiac disease. Vaginal
dryness can increase the prevalence of candidal infection
and dyspareunia (abnormal pain during sexual intercourse).
In summary, although reduced estrogen is commonly
manifested with menstrual dysfunction, it adversely affects
other systems.
Bone Mineral Density
Reduced bone mineral density (BMD) has important impli-
cations for the female athlete as it may lead to osteoporosis
as well as the incidence of stress fracture. When associated
with amenorrhea, the risk of incurring a stress fracture
increases twofold to fourfold.
149
In females, BMD normally increases until approxi-
mately age 30 and signicantly tapers after menopause.
Reduced BMD occurs when bone resorption exceeds bone
formation. Risk factors associated with reduced BMD
include female sex, low weight, and decreased estrogen.
136

Estrogen is needed to facilitate bone remodeling as it has
an inhibitory effect on osteoclast activity in studies exam-
ining osteoporosis and decreased estrogen in postmeno-
pausal females.
150
Evidence has suggested a similar decrease in estrogen
in response to low energy availability.
122 , 130
Ihle and
Louks
151
have quantied a dose-response relationship
between energy availability and bone turnover in young
exercising females. They found that reduced energy avail-
ability suppressed estradiol and altered selected bone
marker concentrations indicative of increased bone re-
sorption. These ndings suggest that low energy avail-
ability can adversely affect hypothalamic function, as
manifested by reduced estrogen secretion, and lead to
decreased BMD.
Evaluation
Up to 84% of athletes with disordered eating are asymp-
tomatic.
152
This is particularly concerning given that the
incidence of eating disorders in athletes may be as much as
20 to 30 times higher than age-matched peers.
153
Because
of this, practitioners must be aware of the various aspects of
the spectrum and be vigilant for clues to its presence when
working with the female athletes. Interaction with the
female athlete may occur during a preparticipation evalua-
tion, an annual health visit, and or a health visit associated
with one or more areas of the triad. Bonci and colleagues
137
have recommended the use of self-report questionnaires to
facilitate the detection of disordered eating as athletes are
commonly less apt to disclose these behaviors. More impor-
tant, health care providers and coaches should observe and
monitor athletes for behavior changes such as excessive
weight loss, fatigue, excessive exercise, and decreased
performance.
137
The medical history should focus on diet and energy
intake, exercise, weight changes, menstrual history, fracture
history, and the patients satisfaction with current weight.
Mental health practitioners should be consulted if disor-
dered eating is discovered. Because early intervention is
preferred, Diagnostic and Statistical Manual criteria need
not be strictly observed.
154
The physical examination should address signs of eating
disorders, such as lanugo (ne soft hair covering body),
bradycardia, and hypercarotenemia (high levels of carotene
in blood giving the skin a yellow appearance). The practi-
tioner also should assess height and weight. Fingernails
should be examined for brittleness; the backs of the hands
should be examined for signs of callus or abrasion from
induced vomiting.
137
A pelvic examination may reveal vagi-
nal atrophy. An electrocardiogram may show a prolonged
QT interval.
Clinical Signs and Symptoms Associated
with the Female Triad
Lanugo (a soft, ne hair covering all parts of the body)
Bradycardia (decreased heart rate)
Hypercarotenemia (excessive carotene in bloodabnormal yellow
skin)
Low body weight
Fingernail discoloration
Vaginal atrophy
Abnormal electrocardiogram (prolonged QT interval)
Laboratory tests should include a complete blood cell
count with differential blood chemistries and electrolytes,
thyroid stimulating hormone, erythrocyte sedimentation
rate, and urinalysis to identify abnormalities indicative of
malnutrition or its sequelae. Secondary amenorrhea should
be evaluated by a pregnancy test, follicle stimulating hor-
mone, leuteinizing hormone, prolactin, and cortisol levels.
If these are normal, the physician should perform a proges-
terone challenge. In the presence of estrogen, withdrawal
bleeding will occur in 7 to 10 days. Possible diagnoses will
then include progesterone deciency, polycystic ovarian
syndrome, some medications and normogonadotropic hy-
pogonadism. If the challenge fails, test for androgen excess
caused by tumors, adrenal hyperplasia, or certain genetic
disorders such as Turner syndrome should be performed.
If all of the testing is normal, functional hypothalamic
amenorrhea is diagnosed by exclusion. One exception is
that an athlete in recovery may respond to the progesterone
challenge.
BMD testing should be performed on any individual
with a 6-month history of disordered eating or amenorrhea
or after suffering multiple stress fractures.
155
The World
Health Organization (WHO)
156
has established criteria
based on BMD, as measured using techniques such as dual-
energy x-ray absorptiometry, for diagnosing osteoporosis.
The diagnosis is based on a T-score, which represents the
number of SDs above or below the average BMD for
young, healthy, white women.
157
The WHO
156
considers a
person with a T-score more than 2.5 SD below the average
BMD as having osteoporosis. A limitation of this classica-
tion system is that the WHO has based these criteria on
studies using postmenopausal women.
158
The International Society for Clinical Densitometry
(ISCD) recommends comparing young individuals bone
density with that of age- and sex-matched controls to deter-
mine those with low bone density (dened as a Z-score ).
158
The ISCD denes osteoporosis as a Z-score below 2,
meaning that the BMD is less than that expected for a
specied age range. This system may be more advantageous
than that used by the WHO osteoporosis scale as it ac-
counts for differences in age and sex. Refer to the National
Athletic Trainers Association Position Statement: Prevent-
ing, Detecting, and Managing Disordered Eating in
Athletes
137
for comprehensive guidelines for additional
information.
Treatment
Because bone density loss may not be fully recoverable,
prevention is paramount. Prevention programs should
include nutrition and exercise counseling and education.
Once diagnosed, treatment of the triad should be compre-
hensive and include a variety of players. The primary team
should include a physician, dietitian, and coach. When avail-
able, family members; an athletic trainer or sports physical
therapist; an exercise physiologist; and a psychologist, psy-
chiatrist, or clinical social worker also should be consulted.
The initial intervention should focus on increasing energy
availability to greater than 45 kcal/kg per day. Simply
increasing body weight will promote bone density and re-
store normal menstruation for an athlete with low body
weight.
136
Athletes with disordered eating also should enter
into a contract with the treatment team and be allowed to
participate only if they adhere to the treatment plan and
show signs of improved health.
Antidepressants may assist in the treatment of eating
disorders; however, medications have not been effective for
improving bone density in young athletes. Prior research
159
has shown that hormone replacement therapy (HRT) and
OCs are ineffective in individuals with eating disorders.
In those without eating disorders, data are inconclusive.
Although bisphosphonates are a mainstay of treatment in
postmenopausal women, their benet is unproven in pre-
menopausal women. Evidence
160
suggests that use in a
premenopausal female may adversely affect the growth and
development of a fetus should she become pregnant. There-
fore, bisphosphonates are contraindicated in athletes of
childbearing age because of possible detrimental effects on
a fetus. Given the time these drugs stay in human bone and
their slow release, the detrimental effects are not assuaged
by simply stopping when trying to become pregnant.
160
Pregnancy and Exercise
The recommendations for exercising while pregnant have
become clearer in the last decade. Most research has shown
that females will benet from aerobic exercise.
161-163
The
level at which they exercise depends on prepregnancy tness
level and should be guided by their physicians. The Ameri-
can College of Obstetricians and Gynecologists (ACOG)
has led the way in setting guidelines for exercising while
pregnant, rst with a statement in 1985 and subsequent
updates in 1994 and 2002 (available at www.acog.org/
publications/patient_education/bp119.cfm ).
164
Many physiological changes occur during pregnancy that
have an effect on exercise. With regard to the cardiovascular
system, there is a 50% increase in cardiac output, blood
volume increases by 45%, and resting heart rate can increase
up to 15 beats per minute.
165
The respiratory system
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-
drates are the preferred fuel source. Related to the muscu-
loskeletal system, there is an increase in joint laxity, weight
gain ranges from 20 to 40 pounds (9 to 18 kg), and there
is an increase in lumbar lordosis.
163
All these factors will
affect the intensity and mode in which the pregnant woman
can exercise.
The benets of exercising while pregnant can be both
physical and psychological. It has been shown that exercis-
ing women have improved strength and posture and there
is a prevention of excessive maternal weight gain.
167
These
factors undoubtedly help with a reduction in low back
pain.
167
Related directly to birthing, Clapp
168
found that
women who take part in some form of exercise on the aver-
age had a shorter active labor during vaginal births. Plasma
glucose has been shown to be signicantly reduced by
45 minutes of exercise a day at least three times per week,
and it may help to control or prevent gestational diabe-
tes.
169
Some of the psychological benets of exercise include
a reduction of depression
170
and improved self-esteem.
171
The exercise prescription should be designed in conjunc-
tion with the womans physician. Guidelines have been
dened by both the American College of Sports Medicine
(available at www.acsm.org/AM/Template.cfm?Section
current_comments1&Template/CM/ContentDisplay.
cfm&ContentID8638 )
172
and the ACOG (available at
www.acog.org/publications/patient_education/bp119.
cfm ).
164
Both groups recommend aerobic exercise such as
walking or swimming at moderate intensity (3-4 metabolic
equivalent tasks). Running is appropriate only if the indi-
vidual was running prior to her pregnancy. In general, peak
heart rate should not exceed 140 beats per minute. Regard-
ing duration and frequency of exercise, the 2002 position
statement from the ACOG states that in absence of either
medical or obstetric complications, 30 minutes or more of
moderate exercise a day on most, if not all days of the
week is recommended for pregnant women.
173
For more
specic guidelines based on prepregnancy training level see
Table 26-4 .
The effect of high-volume exercise during pregnancy
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.
Beilock and colleagues found that highly trained women
who limited their aerobic and strength training during
pregnancy did not signicantly affect their postpartum
training program.
175
Further recommendations and warning signs are found
in Table 26-5 . There are few absolute and relative contrain-
dications to aerobic exercise in pregnancy and these are
found in Table 26-6 . In conclusion, it appears that healthy
females with uncomplicated pregnancy can continue to
exercise at moderate levels without harm to themselves or
their child.
Older Female Athlete
It has been reported that one of the fastest growing groups
of exercisers is the middle-aged and older woman. Benets
of choosing a physically active lifestyle include a lower inci-
dence of chronic degenerative disease, lower age-specic
mortality rate, and the ability to live independently. The
older athletic woman has unique challenges that may affect
her ability to be active, including hormonal changes
that inuence tissue health and the cardiovascular system.
Benets of Exercising While Pregnant
Physical Benets
Improves posture
Improves strength
Improves endurance
Prevention of excessive weight gain
Reduces low back pain
Shorter active labor
Controls blood glucose levels
Psychological Benets
Improves self-image
Reduces depression
Table 26-4
Exercise Prescription During Pregnancy
Sedentary
Frequency 3 times per week
Intensity Perceived exertion: moderately hard;
HR: 65% to 75% max
Type Low impact (walking, bicycling,
swimming, aerobics)
Time/duration 30 minutes
Recreational Athlete
Frequency 3 to 5 times per week
Intensity Perceived exertion: moderately hard
to hard, HR: 65% to 80% max
Type Low impact (running, tennis,
cross-country skiing)
Time/duration 30 to 60 minutes
Elite Athlete
Frequency Minimum 4 to 6 times per week
Intensity Perceived exertion: hard, HR:
75% to 80% max
Type As with recreational athlete, can
include competitive activities
Time/duration 60 to 90 minutes
Adapted from Joy EA: Exercise and pregnancy. In Ratcliffe SD:
Family practice obstetrics, ed 2, Philadelphia, 2001, Hanley & Befus.
HR, Heart rate.
In addition, with aging, there is a decline in strength that
can lead to injury and stress urinary incontinence (SUI).
Hormonal Changes
For women in their late 40s and early 50s, cessation of men-
struation (menopause) will occur. Problems associated with
menopause include an increase incidence of osteoporosis
and a decline in cardiovascular health caused by diminishing
estrogen levels.
145
In addition, after approximately age 30,
women begin to lose muscle mass and strength. Age-related
decline in lean body mass correlates with several alterations,
including a decrease in endogenous growth hormone, a
decrease in pituitary responsiveness to growth hormone
releasing hormone, and neuromuscular alteration.
Many of these detriments that occur with aging can be
prevented or minimized with a consistent routine of aerobic
exercise and strength training. Researchers have found that
exercise along with proper calcium-rich diet can enhance
bone density and reduce bone loss.
176
The increased me-
chanical stress associated with weightbearing exercise can
increase bone mineralization. In addition, upper-extremity
bone mass can be improved with strengthening exercise.
Table 26-5
Recommendations and Warning Signs Related to Exercise and Pregnancy
164

,

172

Recommendations
Warning Signs to Stop Exercise
and Seek Medical Evaluation
Drink plenty of water before, during, and after exercise
Eat small, frequent meals throughout the day
Avoid exercises that require bouncing, jarring, leaping, risk of abdominal injury
such as contact sports, downhill skiing, scuba diving, horseback riding
Do not exercise on the back as this may reduce blood ow to the heart
Avoid heavy weightlifting and any activities that require straining
Avoid exposures to extremes of air pressure as in high altitude (unless you are
accustomed) or scuba diving
Do not increase intensity of your workout beyond prepregnancy levels
Vaginal bleeding
Dyspnea prior to exertion
Dizziness
Headache
Chest pain
Muscle weakness
Calf pain or swelling
Preterm labor
Decreased fetal movement
Amniotic uid leakage
Table 26-6
Absolute and Relative Contraindications to Exercise during Pregnancy
Absolute Contraindications to Exercise during Pregnancy Relative Contraindications to Exercise during Pregnancy
Hemodynamically signicant heart disease
Restrictive lung disease
Incompetent cervix or cerclage
Multiple gestation at risk for premature labor
Persistent second or third trimester bleeding
Placenta previa after 26 weeks gestation
Premature labor during the current pregnancy
Ruptured membranes
Pre-eclampsia or pregnancy-induced hypertension
Severe anemia
Unevaluated maternal cardiac arrhythmia
Chronic bronchitis
Poorly controlled type I diabetes
Extreme morbid obesity
Extreme underweight (body mass index 12)
History of extremely sedentary lifestyle
Intrauterine growth restriction in current pregnancy
Poorly controlled hypertension
Orthopedic limitation
Poorly controlled seizure disorder
Poorly controlled hyperthyroidism
Heavy smoking
Data from the American College of Obstetricians and Gynecologists.
Regarding the risk of cardiovascular disease, exercise
along with a low-fat diet may reduce this risk. Higher levels
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.
Training-induced improvements in strength and balance
may provide an added benet by preventing the falls that
cause a great number of fractures among the elderly.
177
Help-
ing young women learn how to strength train (i.e., proper
technique, proper loading) during the years when they are
able to increase bone mass may help to prevent osteoporosis
and related fractures.
HRT is a choice for some women following menopause.
HRT will help to decrease vasomotor symptoms, urogenital
atrophy, cardiovascular disease risk, and bone loss. Unfortu-
nately, accompanying these benets are side effects such as
weight gain, headaches, leg cramps, and a potential
increased risk of breast cancer. Natural hormones made
from soy or yams are becoming more popular.
Stress Urinary Incontinence
As more women engage in regular exercise, the issue of
bladder leakage has surfaced.
177-179
Nygaard and col-
leagues
178
reported 47% of women who exercise regularly
have some degree of urinary incontinence. Complaints of
SUI during physical activity have prompted greater atten-
tion to conservative management techniques that support a
womans goal of tness and establishment of healthy pelvic
muscles simultaneously, especially those of the pelvic oor.
Pelvic oor muscles form a hammock of muscular tissue
that provides support for the pelvic organs in addition to
sphincter control. These muscles are sensitive to hormonal
status and are rich in estrogen receptor sites. High-impact
physical activities, estrogen depletion,
180
and pelvic muscle
weakness are among the risk factors associated with SUI.
Conservative treatment for SUI includes a pre-exercise
routine of voiding prior to exercise and avoiding beverages
that include caffeine and alcohol. It may be necessary to
restrict uids, although not to the point of dehydration,
during the exercise session. While exercising, the athlete
may need to wear a minipad or, in some cases, an intravagi-
nal support such as a pessary or bladder neck support pros-
thesis. Strengthening exercises and muscle re-education
should be a component of the womans tness routine.
Physical therapists and other health care providers can ask
women more questions about pelvic oor function, encour-
age women to exercise these muscles, and seek medical care
when they exhibit problems such as SUI. Health care pro-
viders should promote preventative pelvic muscle exercises
rather than restorative.
Conclusion
During the last 25 years, the opportunities for females
in sports have grown tremendously. The high number
of females participating in sports has been associated with
an increase in a number of musculoskeletal injuries and
other high-level activity problems. In some circumstances,
there appears to be a predisposition of the female to
injury. This chapter presented the most common muscu-
loskeletal injuries, including ACL injury, PFPS, MTSS,
and other problems common to the female athlete.
Strategies and programs to prevent injury are also
discussed. Along with musculoskeletal injuries, the exist-
ing knowledge on the female triad is summarized with
information given on the symptoms, diagnosis, and treat-
ment. The chapter concludes with unique issues facing
the older woman athlete.

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651
Introduction and Objectives
Dance medicine and science is a specialized eld concerned
with studying and caring for a fascinating type of individual
who is often overlooked as an athlete, that is, the dancer.
Dancers in all genres of dance will benet from a cadre of
well-trained, compassionate health care clinicians and scien-
tists. This chapter is not an exhaustive compendium of dance
medicine and science. Rather, its primary aim is to present
information about the musculoskeletal aspects of dance
medicine and science so that musculoskeletal clinicians and
scientists can:
1. Recognize the rigorous physical performance that is
required of dancers.
2. Appreciate the psyche of dancers and how it relates to
effective provision of care for dance injuries.
3. Understand some fundamental skills of dancers as
they pertain to common dance injuries.
4. Gain insight into specic injuries that are common in
dance so that, in consultation with the other volumes
of the Musculoskeletal Rehabilitation series, the reader
will be equipped to deliver excellent care to the
multitude of dancers who need it.
Intertwining Science and Art
At rst impression, the melding of something as artistic as
dance with something as analytical as science may seem
unusual. However, dance is an anatomical art, founded at its
core in movement. As such, it actually lends itself well to an
understanding through scientic study in much the same way
sports movement does. Thus, dance medicine and science, as
a eld of expertise, is not unlike sports medicine and science.
Both elds are professional disciplines based on scientic and
clinical principles. Both elds focus on studying the attributes
and abilities of physically active peoplemany of whom are
extraordinarily skilledand applying the knowledge to
improving performance and preventing and managing inju-
ries and conditions suffered by participants in their respective
domains. This chapter introduces musculoskeletal health care
practitioners to concepts that will help them appropriately
manage injuries in dancers and understand some of the idio-
syncrasies that make dance medicine and science a challeng-
ing, yet rewarding, subspecialty in musculoskeletal practice.
Sports medicine and science in Western civilization can
be traced to Herodicus in the fth century BC.
1
In America,
however, Dr. Edward Hitchcock is credited as the rst
sports medicine physician,
2
practicing at Amherst College in
the 1850s. Although the rst known published material
about the benets of therapeutic treatments and exercises
for injuries were books by Avicenna, an Islamic medical
practitioner in the tenth century AD,
1
the rst report locat-
able in the medical literature that clearly shows an emphasis
on dance medicine and science appeared in 1952 in the
British journal Physiotherapy.
3
(It is important to note here
that dance medicine and science is a distinctly different eld
from dance therapy, with the latter referring to psychoemo-
tional interventions using dance as the medium.)
The most prominent professional society devoted exclu-
sively to the medical and scientic aspects of dance is the
International Association for Dance Medicine and Science
(IADMS). Founded in 1990, by the following year its mem-
bership was 48 clinicians, scientists, educators, and dancers.
4

Today the group comprises more than 900 members from a
wide variety of dance-related disciplines. The stated purpose
of IADMS is to enhance the health, well-being, training,
MUSCULOSKELETAL DANCE MEDICINE
AND SCIENCE
Jeffrey A. Russell

27
CHAPTER
and performance of dancers by cultivating educational,
medical, and scientic excellence.
4
Worldwide, several other
professional associations are either totally devoted to dance
medicine and science or embrace this specialty as part of the
broader performing arts medicine eld. In addition, some
national dance associations maintain subgroups focused on
dance medicine and science. Table 27-1 identies many of
these organizations.
The relative newness of dance medicine and science com-
pared with sports medicine and science, combined with the
complex technical intricacies of dance means that there are
many fertile areas for research to advance the eld. Some of
the demands of dance on the musculoskeletal system are
inferred by supposition or anecdote rather than by scientic
inquiry. However, an increasing number of researchers
are accelerating the elds knowledge base. For example, a
casual review of the Medline and the Cumulative Index to
Nursing and Allied Health Literature (CINAHL) databases
reveals that the number of articles therein containing either
the word dance or the word ballet in their titles and that are
devoted to some aspect of dance medicine and science has
increased substantially in the last ve decades; there were no
such articles in 1959. This point, of course, excludes
publications not indexed in those two databases, conference
presentations, and similar dissemination avenues. Clearly,
the disciplines breadth is increasing.
Dance as an Athletic Endeavor
Anyone who spends time in a dance teaching, rehearsal, or
performance venue will have little doubt about the vigor and
athleticism of dancers. Stretanski has called classical ballet a
full contact sport
5
because of its potential for injury. Others
corroborate the view that dancers as artists certainly possess
characteristics associated with traditional athletes.
6-11
Any
dissenting opinion is likely based solely in ones unwillingness
to understand the extent to which aerobic and anaerobic
power; exibility; muscular strength, endurance, and power;
proprioceptive function; coordination; agility; and other
parameters commonly associated with sports participation
are required for success in dance. Although typical dance
trainingwithout ancillary physical conditioning workouts
does not improve maximum oxygen consumption and other
physiological variables to the same degree that sports training
does,
7 , 12-17
dancers bodies must withstand high physical
stresses like those of their sports counterparts.
18
The daily
regimen of training that is common in dance creates a level of
exposure and movement repetition that increases susceptibil-
ity to injury when compared with nondancers.
19
Differences in Working with Dancers
versus Traditional Athletes
It is not required that the health care professional have
dance experience to administer care to dancers, although it
is helpful. Experience in sports medicine is generally useful
for the clinician working with dancers, but there is not an
automatic knowledge transfer. Understanding these points
and motivating oneself to understand dancers in the context
of their sphere of physical activity will prevent many misun-
derstandings and grievances.
Table 27-1
Representative Professional Organizations Wholly
or Partially Devoted to Dance Medicine and Science *
Country Organization
Organizations Primarily Focused on Dance
(or Performing Arts) Medicine and Science
France Mdecine des Arts (Arts Medicine)
Germany Tanz Medizin Deutschland e.V. (TaMeD,
Dance Medicine Germany)
Monaco Association Danse Mdecine Recherche
(Dance Medicine Research Association)
The Netherlands Nederlandse Vereniging voor Dansen
Muziek Geneeskunde (Dutch
Performing Arts Medicine Association)
New Zealand Arts Medicine Aotearoa New Zealand
Spain Asociacin Espaola de Medicina de la
Danza (Spanish Association of Dance
Medicine)
United Kingdom British Association for Performing Arts
Medicine
United States International Association for Dance
Medicine and Science
Performing Arts Medicine Association
National Athletic Trainers Association,
Clinical & Emerging Practices Athletic
Trainers Committee, Performing Arts
Medicine Workgroup
American Physical Therapy Association,
Performing Arts Special Interest Group
National Dance Associations with Specic Focus
on Dancer Health
Australia Ausdance
New Zealand DANZ
United Kingdom DanceUK
United States DanceUSA

* Not an exhaustive list.
Dance is an Athletic Activity
Dance is a rigorous physical performance activity that requires the
same high levels of physical capacities as those required in sports
Dancers clearly are athletes in their own right
Because of its artistic component, dancers cannot and should not
be forced into a traditional sports medicine model of care
Musculoskeletal Dance Medicine and Science CHAPTER 27 653
It may be helpful to the clinician anticipating or wishing
to work with dancers to rst understand a small amount of
background about dance. Dance is a multifaceted perform-
ing art that increasingly dees classication because there is
such breadth in its practice and performance. Many differ-
ent genres of dance are presented on stage and dancers train
rigorously to participate in these. Although ballet and mod-
ern dance (also called contemporary dance ) are two domi-
nant genres, there is a vast assortment of others. Some of
these include tap, jazz (including hip-hop and break dance),
and ballroom. There also is a virtually limitless collection of
world dance forms with rich national or cultural roots, such
as amenco, belly dance, Irish step dance, dances of India
like Bharatanatyam and Kuchipudi, and many types of
Latin American theatrical folk dances. In addition, public
interest has been fueled by a number of television programs
partly or fully devoted to competitive dance.
The accoutrements of dance differ markedly from the
uniforms and equipment of sports. Overall, classical ballet is
structured according to a codied movement vocabulary
named in French. The clothing usually is tights and leotards
for women and tights and close-tting shirts for men. Foot-
wear may be ballet slippers or pointe shoes. Modern dance
is a more freeform genre with wider variability in choreog-
raphy. Modern dancers typically do not wear shoes, and
their attire may range from minimal clothing to casual street
clothes to elaborate, very colorful costumes. Many of these
features of modern dance also are seen in some contempo-
rary ballet performances.
Injuries in ballet
20-29
and modern dance
29-32
have received
the most attention in the orthopaedic and sports medicine
literature. Although research about the demands on the
musculoskeletal system of most of the other genres is scant
at best, enough is known about some of them to indicate
that substantial numbers of injuries do occur.
33-45
This sug-
gests that there are many dancer-patients requiring muscu-
loskeletal practitioners motivated to skillfully and compas-
sionately care for them, a need that was identied as early
as 1978 when Washington
46
encouraged orthopaedic sur-
geons to care for dancers because he foresaw an enlarging
dance populationwith a resulting proliferation of dance
injuriesin the United States.
The Dancers Psyche
A cardinal rule for health care providers without a dance
background who work with dancers is to understand and
respect the dancers psyche. This is related to the rigor of
the physical regimen to which they apply themselves. Danc-
ers are artistsathletically so, as previously describedand
they approach their craft with intensity and fervor. They
also are typically very grateful for well-delivered care. How-
ever, within any group of dancers, several will relate stories
of well-meaning but ill-informed practitioners giving the
poorly conceived advice to stop dancing as a standard
cure for physical ailments. Sadly the prevalence of such
episodes have frustrated many dancers and planted in
them seeds of distrust toward allopathic health care
47
(although a notable contrast to this generality exists in the
Netherlands
48
). Obviously there are injuries (e.g., stress
fracture) when complete rest from dancing is the appropri-
ate standard of care. Nonetheless, nding alternative meth-
ods to keep an injured dancer active and prevent decon-
ditioning is important, as it is with any athlete. In cases in
which some degree of dance can continue, the practitioner
must work with the dancerand his or her teachers and
directors when possibleto develop a moderated activity
plan that reduces the load on the compromised body region
while still allowing the dancer to engage in as much of his
or her usual activity as possible.
Another means of counteracting dancers skepticism
toward health care providers is judicious attention to the
history portion of the commonly used injury evaluation
methodology of history, observation, movement assess-
ment, special testing, and palpation. Listening intently to
symptom descriptions offered by the dancer-patient will
yield valuable information as a foundation to the remainder
of the evaluation, in part because dancers know their bodies
very well. Furthermore, they will sense the practitioners
respect for dance and for the information they are providing
and respond accordingly. Still another way for medical pro-
fessionals to understand dance, and thereby demonstrate
their interest to dancers, is attending dance performances.
Dancers consider this to be a very important characteristic
in their health care providers.
49
Understanding how dancers approach pain is fundamen-
tal to success in caring for them. They possess both a
higher threshold and a higher tolerance for pain than do
nondancers.
50
That is, in comparison with nondancers,
not only is more pain required for dancers to perceive it
(threshold), they also can withstand greater levels of pain
(tolerance). Experiencing pain as a dancer is so customary
that it could be considered normal.
51
However, dancers
may not differentiate well between pain brought on by per-
forming their usual dance activities and pain that results
from injury.
52
The obsessive passion for dance (as opposed
to harmonious passion) that many dancers exhibit has been
associated with willful neglect of injuries.
53
Dancing
Health Care Access for Dancers
Although ballet and modern dance are the most well-known
genres in the United States, many varieties of dance are
performed around the world
In spite of a very high injury rate in dance, many dancers do not
have access to necessary injury care
There is a great need for musculoskeletal health care practitioners
to gain expertise in dance medicine to increase proper care for
dancers
through injuries is typical,
47
especially in dancers with
more experience
48
or in those who believe that engaging in
a treatment regimen will interfere with their ability to par-
ticipate in dance.
49
Regardless of dancers general propen-
sity to tolerate pain, injuries create psychological stress that
can adversely affect their ability to dance.
20 , 54 , 55
Further-
more, the psyche of the dancer that allows him or her
to achieve excellence may be a contributor to injury
incidence,
53
particularly in classical ballet.
22
practitioners has been shown to reduce both time loss from
dancing and medical expenses.
31
Limitations Imposed by Wardrobe and Performance
One of the most noticeable differences between dancers
and traditional athletes is the amount of taping and bracing
that is possible. While these prophylactic and protective
measures are taken for granted as part and parcel of sports,
the appearance requirements for dancers on stage and the
range of motion necessary for their successful performance
restrict some of the clinicians options. The aesthetic faux
pas of a tutu-clad ballerina wearing a knee-stabilizing brace
over her tights is obvious. Another common example is
ankle taping; most dancers likely will reject taping such as
that used for basketball or football players because it is too
restrictive of plantar exion and they do not wear socks plus
sneakers or cleats that would hide the tape. When a dancer
does permit taping, a reduced volume will be used; esh-
colored tape is preferable, or the dancer will apply makeup
cream or powder to blend white tape into the skin. Modern
dancers pose even greater challenges with their bare feet
because foot pads, supports, and orthotics are not easily
afxed, they detach easily, they change how the dancer
senses the interface between the foot and the oor, and they
may be evident to the audience.
The Panoply of Injuries in Dance
Dance participation is associated with a high frequency of
injury.
20 , 21 , 27 , 29 , 31 , 46 , 51 , 59-72
The percentage of participants
affected is high; 95% is not unheard of in a professional
ballet company.
27 , 51
Table 27-2 provides overall injury rates
reported by various authors. Although epidemiological
correction is not made for the variety of possible denitions
of injury that would aid comparisons among studies
73-78

and in spite of the fact that vast numbers of dancers lie
outside the medical professions sphere of data collection
ability, it is clear that dancers sustain substantial numbers of
injuries. The data on dance injuries are less sophisticated
simply because dancers as a subpopulation have not
enjoyed the same level of access to injury evaluation and
recording processes compared with those available in a
typical sports medicine setting; consequently, more system-
atic research is required.
Several reasons for such a high injury incidence are
apparent. Chief among these, especially for amateur danc-
ers, is their lack of the body structure (e.g., tissue strength,
exibility) and biomechanical capability that allows them to
succeed in dance.
79
This is particularly true in ballet, in
which the requirements are very regimented and can be
unforgiving to the musculoskeletal system. Injurious techni-
cal errors may develop from inadequate dance training,
maladaptation to choreography that is beyond the dancers
skill level, or neuromuscular compensation because of
injury. If such errors are not corrected they may be carried
Dance Health Care
Dancers are extremely diligent in their work ethic and they
typically take dance classes and rehearse for many hours daily
Dancers tend to dance through injuries rather than seek health
care advice
Although a sports medicine model is helpful in working with
dancers, these athletic artists must be respected for their unique
talents and abilities that require adaptation of sports medicine
methods
Stop dancing is injury care advice that is universally deplored by
dancers
Environmental Differences
Athletes in typical sports environments are usually accus-
tomed to the cadre of professionals who surround them:
physicians, athletic trainers, physical therapists, and a variety
of other specialists. In fact, it is unlikely in professional and
Olympic sports and extremely unusual at the university
level, and even at most large- to medium-sized high schools,
for there to be no sports medicine provision whatsoever. In
addition, American sports receive unprecedented public
attention and they usually enjoy a nancial state in which
health care for their participants is both possible and pre-
sumptive. Virtually the opposite is true of most dance
programs below the top echelon of professional companies;
furthermore, many dancers are medically uninsured or un-
derinsured.
56 , 57
This problem is particularly exacerbated for
dancers in small professional companies or who dance part-
time.
56
Ambegaonkar and Caswell
58
found that university-
level dance students in the United States are woefully
underserved by the medical profession. A discussion about
the relative merits of funding either sports or dance is not
the place of this chapter, but it seems indisputable that
nancial disparity exists between sports and the arts and one
effect of this is a negative effect on dancers access to health
care. Moreover, because they have not progressed through
systems in which specialized health care providers were
readily available, dancers tend to be more independent
when confronted by injuries. In light of this, it is important
to note that management of injuries by qualied health care
throughout a dancers career, thus compounding their
deleterious effects.
The inherent nature of dance requires countless repeti-
tions of movements in the quest to perfect choreography to
the satisfaction of the artistic director, teacher, and audi-
ence. Dancers usually spend far more hours daily in the
studio than traditional athletes spend on the eld, court, or
track, and the lack of the well-dened season and off-season
periods characteristic of most sports requires dancers to stay
at peak performance continuously.
59
This creates not only
increased exposure time in which injuries can occur, but it
induces fatigue, a known contributor to injury.
80-83
Other
factors associated with the high injury rate include poor
training,
51
suboptimal lower body muscular power,
84
and
low aerobic tness.
85
Injuries to the lower extremity account for the vast pro-
portion of all dance injuries,
20 , 27 , 29 , 46 , 62 , 65 , 68 , 70 , 86
with most
of these occurring in the ankle and foot. One factor report-
edly contributing to this is low thigh torque and power.
87
A number of studies report that trunk or spine injuries com-
pose 20% or more of all injuries in dancers.
21 , 51 , 61-63
Overuse
injuries generally are more common than traumatic injuries
simply because of the repetitive nature of dance rehearsal.
Nilsson
27
found that incidences in overuse versus traumatic
injuries were related to gender. In their study of profes-
sional ballet dancers, men suffered more lower-extremity
traumatic injuries, whereas women suffered more overuse
injuries in this region. Men also experienced more upper-
extremity injuries than women because of the partner-lifting
that is integral to their role in classical ballet. However, this
Table 27-2
Injury Data for Dancers Reported by Various Authors
Authors Type of Dancer Injury Data
Duration of
Data Collection
Arendt and
Kerschbaumer
67
Professional ballet 7.4 injuries per dancer (567 injuries in 77 dancers) 5 years
Bowling
62
Professional ballet and
modern
84% of dancers injured (118 of 140)
12% had 5 or more injuries
Career
Byhring and
B
20
Professional ballet 75% of dancers injured (31 of 41)
3.2 injuries per dancer
5 months
Gamboa et al.
86
Elite preprofessional
ballet
1.3 injuries per dancer (198 injuries in 151 dancers)
5 years
Garrick
279
Female
preprofessional ballet
20 months
Garrick and
Requa
21
Professional ballet 2.97 injuries per dancer (309 injuries in 104 dancers)
23% of dancers accounted for more than 50% of all injuries
3 years
Kerr et al.
61
Female university
dance students
2.4 injuries per dancer
8 months
Laws
63
Student and professional
dancers, all genres
80% of all dancers injured
more injuries in ballet than modern
1 year
Liederbach
et al.
29

Professional ballet and
modern dancers
2.5 injuries per dancer per year (3721 injuries in
298 dancers)
5 years
Luke et al.
102
Preprofessional
dancers
112 self-reported injuries in 39 dancers
71 injuries in 39 dancers reported to and identied by a
physical therapist
95% of dancers reported at least 1 injury during their careers
1 season
Nilsson et al.
27
Professional ballet 95% of dancers injured (93 of 98)
5 years
Rovere et al.
65
Dance students,
all theatrical genres
85% of dancers
1 year
Solomon et al.
28
Professional ballet average of 84% of dancers injured per year
560 total injuries in 5 years in a company with an average
size of 62 dancers per year
5 years
Thomas and
Tarr
280
Professional and
student dancers,
all genres
90% of 204 dancers injured at least once
no dancer older than age 35 had not been injured
in dancers younger than age 35, the number of uninjured
dancers decreased with increasing age
Career
Note: Reported data is not the same for all authors because of differences in how the studies were done.
difference may disappear in modern dancers because the
nature of their partnering work is different and they per-
form more upper-extremity weightbearing maneuvers on
the oor than do ballet dancers.
32
dance and Irish dance and the weightbearing contact
between the head and the ground seen in break dance.
The Pointe Shoe
Dancing en pointe and wearing pointe shoes do not seem to
be conducive to healthy feet. Nonetheless, pointe is a beau-
tiful and integral part of classical ballet that will remain. All
dancers need both support and the ability to sense the oor
to execute their choreography. Therefore, health care prac-
titioners must learn about the technique to best advise
pointe dancers under their care. In the rst two decades of
the nineteenth century when dancing en pointe started gain-
ing popularity,
88
pointe shoes did not exist; rather, dancers
darned the soles of their soft ballet slippers with additional
yarn to provide some further support.
89
The rst use of stiff
blocking in pointe shoes to offer a more stable platform on
which to balance on the toe tips occurred in 1880,
90
an
achievement accomplished by the use of paper, cardboard,
and cloth stiffened by soaking them in glue and letting
them dry. By the middle of the twentieth century pointe
shoes were constructed with even greater stiffness to ac-
commodate increasingly demanding choreography.
89
Most
of todays pointe shoes retain the traditional satin, burlap,
paper, leather, and glue construction ( Figure 27-2 and
Figure 27-3 ), but modern materials like thermoplastics and
microber fabric have been incorporated by some shoe
companies, including Gaynor Minden
91
and Bloch.
92
Every
ballet dancer who dances en pointe engages in an individual-
ized routine to break in a new pair of pointe shoes, some-
thing which often is a daily or every-other-day custom in
professional ballet companies. A careful method of padding
the toes in the shoe also is employed by many dancers. A
prima ballerinathe most prominent female dancer in a
Dancers and Injury
Research suggests that the proportion of dancers who suffer
injuries is 95% or higher
The lower extremity is the most commonly affected body region,
with the ankle being the joint most frequently injured
The high injury rate in dance and the relatively low probability that
dancers have adequate access to specialized health care (compared
with traditional athletes) presents an opportunity for musculoskeletal
health care providers to care for these athletic artists
Clinically Relevant Concepts
in Dance Kinesiology
There are some characteristics of dance movement that may
predispose dancers to certain types of injuries and create an
environment in which injuries are exacerbated or, at best,
heal more slowly than usual. Long hours, repetitive
motions, and unusual movement patterns are examples.
Because most of these are generally ingrained in dance prac-
tice, a properly motivated health care worker will learn as
much as possible about dance and dancers to deliver effec-
tive care and offer sound advice for reducing the likelihood
of injury. A few clinically relevant aspects of dance tech-
nique are described in this section.
Different types of injuries are incurred in different dance
genres. Classical ballet requires hundreds of repetitions of
very prescriptive movements; thus, overuse injuries are
more likely compared with other genres and these usually
occur in the lower extremity in which the majority of
weightbearing movements are performed. In ballet there
also are differences between injury types in men and
women,
27
largely because of differences in technique that
include the male dancer lifting his female partner off the
oor and even over his head. Male ballet dancers suffer
more traumatic injuries and a greater percentage of knee,
upper extremity, and lower back injuries than do their
female counterparts. Male dancers also tend to jump higher
because their thighs and legs typically are stronger than
those of females. On the other hand, modern dance, with
its freer movement patterns, heavy emphasis on oor work,
and greater incorporation of the upper extremities in part-
nering and weightbearing (an example is shown in Figure
27-1 ) yields a greater proportion of traumatic injuries that
are spread across both sets of extremities and the trunk.
29
Different still are the rapid percussive movements that sub-
ject the feet to signicant repetitive forces in amenco
Figure 27-1
An example of partnering in modern dance. Note the requirement
for special capacity in strength, exibility, agility, balance, and other
physical parameters. ( iStockphoto.com/Alexander Yakovlev.)
balletmay use one, two, or even three different pairs of
pointe shoes in a single performance.
The anatomy of a pointe shoe has been well described
elsewhere,
89 , 93 , 94
and it is illustrated in Figure 27-4 . Knowl-
edge about the shoes is important when consulting with a
dancer about foot injuries, or with parents about their
youngsters beginning pointe work. Pointe shoes do not
come in right and left; neither are their sizes related to
womens street shoe sizes, although conversion charts
are available.
89
Dancers and teachers have very particular
preferences from both tting and aesthetic perspectives. In
general the shoes should t closely about the foot and not
unduly compress the sides of the forefoot. Subungual
hematoma, hallux valgus, Mortons neuroma and other
forefoot problems may result from poorly tting shoes.
From an injury-prevention perspective, a properly tting
pointe shoe provides key support to the dancer; the shoe is
especially important for stability of the midfoot as it aug-
ments the ligaments of the Lisfranc joints,
95
which include
the dorsal tarsometatarsal, plantar tarsometatarsal, and
interosseous ligaments.
96 , 97
Additional dependable informa-
tion about pointe shoes is available from sources for both
health care providers
93
and performers and teachers.
89
The Ankle and Foot in Demi-pli , Demi-pointe,
and en Pointe
Of all athletic activities, only classical ballet requires its
participants to repeatedly move from full forced dorsiexion
(in the demi-pli position) to full forced plantar exion (the
Figure 27-2
Typical pointe shoes, including a close-up of three different styles of
the platform on which the dancer stands when en pointe. Ballet danc-
ers select their shoes with specic features they prefer and then pre-
pare the shoes for use by a customized conditioning process accord-
ing to their personal taste.
A
B
Satin
Heavy Muslin
Insole
Burlap
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
of a pointe shoe after the rest of the shoe has been cut away. The
several layers of materials used in constructing pointe shoes are
shown, as well. These are typically impregnated with glue to form
and harden the toe box.

en pointe position). Demi-pointe or half pointe is distin-
guished from full pointe by hyperextended metatarsophalan-
geal joints. (These three positions are shown in Figure 27-5 .)
Demi-pointe essentially places the ankle in full plantar exion,
but to successfully stand in this position, at least 90 of hyper-
extension is required in the rst metatarsophalangeal joint
( Figure 27-6 ). Whereas the typical ankle range of motion for
nondancers is 20 of dorsiexion and 50 of plantar exion,
98-
100
dancers normally exhibit much greater motion.
101-106
This
is especially true in plantar exion for which dancers ideally
need 90 to 100 of weightbearing plantar exion; motion up
to 113 has been reported in female professional ballet
dancers.
101
Table 27-3 summarizes various authors measure-
ments of ankle range of motion in female dancers.
However, all such plantar exion does not occur in the
anklethat is, the talocruraljoint. A substantial amount
of plantar exion in nondancers has been attributed to the
joints of the foot; in other words, goniometry of the ankle
includes movements in the foot joints.
101 , 103 , 106-109
Clinically
measured ankle motion is greater than talocrural motion,
110
but clinical measurement of talocrural motion is difcult.
111
As much as 40% of plantar exion motion occurs in the
joints of the midfoot,
107 , 111
but the relative amounts attrib-
utable to each of these joints varies widely among subjects.
These researchers reported mean talocrural motion as 23
of dorsiexion and 28 of plantar exion.
107
Russell and
Shave developed an x-ray measurement technique to evalu-
ate the motion of the tibia and bones of the foot relative to
A
C
C
B
B
Figure 27-4
Left to right: Bottom, side, and top views of a pointe shoe showing its
anatomy. A, Rear seam; B, waist seams; C, ribbons. White lines with
circle ends heel counter or heel quarter. White dotted line outsole.
Black lines with circle ends shank, a rigid spine along the bottom of
the shoe between the insole and outsole. White arrowheads plat-
form, the surface on which the dancer stands when en pointe. White
dashed line toe box or block. Black line with arrowhead ends
vamp. Black dotted line wing (side of toe box). Black line coursing
around the collar of the shoe indicates the drawstring casing, the pos-
terior part of which is dashed to show the edge of the heel counter
that compresses the Achilles tendon.

Demi-pli
Demi-pointe
En Pointe
Figure 27-5
The lower extremity positions in ballet that require maximum range
of motion: dorsiexion in demi-pli and plantar exion in demi-pointe
and en pointe.

the talus in the en pointe positions of female professional
ballet dancers.
112
They found a mean talocrural motion of
58 and motion of the navicular, second cuneiform, and
rst metatarsal ranging from 5 to 9 each. This translates
to approximately 30% of the total en pointe plantar exion
occurring in the bones of the foot. The percentage likely
varies depending on the foot exibility of a given dancer
and, perhaps, the age a dancer began training, the total
number of years dancing, and the predominant genre.
Additional research about dancers ankle and foot ranges of
motion certainly is warranted.
Figure 27-6
A, Modern dancer standing in demi-pointe showing the 90 of rst meta-
tarsophalangeal joint hyperextension required to attain this position. B,
X-ray showing positions of the bones in demi-pointe. ( B from Kennedy
JG, Hodgkins CW, Columbier J-A et al: Foot and ankle injuries in danc-
ers. In Porter DA, Schon LC, editors: Baxters the foot and ankle in sport,
ed 2, p 478, Philadelphia, 2008, Mosby.)

A B
Table 27-3
Ankle Range of Motion in Female Dancers Reported by Various Authors
Authors Measurement Method
Mean Age
of Participants
Mean SD
Dorsiexion
Mean SD
Plantar Flexion
Bennell et al.
281
Active WB inclinometry 9.6 yr 32.9 6 NR
Bennell et al.
282
Active WB inclinometry 10.7 yr 33.8 6.2 NR
Hamilton et al.
101
Active NWB goniometry 29.3 yr 10 113
Khan et al.
283
Active WB inclinometry 16.9 yr R: 33.7 4.5
L: 34.2 4.3
NR
Lin et al.
284
Active ve camera motion
analysis en pointe
19.2 yr NR R: 52.9 4.3
L: 53.8 6.0
Luke et al.
102
Active NWB goniometry 15.8 yr R: 8.8 3.7
L: 7.0 4.9
R: 76.2 7.0
L: 75.4 8.0
Novella
285
Active NWB
inclinometry
23 yr NR 98 3
Steinberg et al.
104
Passive NWB goniometry 16 yr 12 87
Wiesler et al.
105
Active NWB goniometry 17.5 yr R: 78.0 2.3
L: 77.4 2.2
R: 96.3 2.7
L: 101.0 2.5
NR, Not reported; NWB, nonweightbearing; WB, weightbearing.
The laterally located anterior talobular ligament and
the calcaneobular ligament are the most commonly
injured ankle ligaments
113-115
; thus, it is important to gain
an understanding of how they are situated during the ankle
range of motion required for dance. These ligaments
change position substantially between demi-pli and
en pointe.
116
When the ankle is in anatomical position, the
anterior talobular ligament is approximately horizontal
and the calcaneobular is nearly vertical. Upon moving to
demi-pli, the positions of the ligaments in space change
very little, but their orientations relative to the bula
change. The anterior talobular ligaments angle with the
bula becomes more acute and the calcaneobular
ligament becomes almost parallel to the bula. When
en pointe, the anterior talobular ligament is nearly vertical
while the calcaneobular moves to a somewhat horizontal
position. Figure 27-7 shows the relationships of the
ligaments to the bones of the ankle and foot.
The anterior talobular ligament is weaker than the cal-
caneobular ligament.
108 , 117 , 118
Furthermore, as plantar
exion increases, the anterior talobular ligament under-
goes increasing strain
117 , 119-121
as it is stretched between its
proximal and distal attachments. On supercial analysis,
this would seem to predispose dancers to lateral ankle
sprain, especially of the anterior talobular ligament.
However, in the en pointe position the ankle receives
added stability from compressive locking of the posterior
tibial plafond against the posterior talus and superior
calcaneus
11 , 122-125
and from contraction of the leg, ankle,
and foot musculature.
126
Therefore, although ankle sprains
are common in dancersas in most sportsthe extreme
plantar-exed position en pointe is not necessarily an
inuencing factor for this.
CFL
ATFL
CFL
ATFL
CFL
ATFL
Figure 27-7
Orientations of the anterior talobular ( ATFL ) and calcaneobular ligaments ( CFL ) in different ankle
positions. The ligament positions are based on investigations performed in nondancers
108 , 113 , 114 , 274-278

because these ligaments have not previously been studied in situ in a dancer population. The bula 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.)
Ballet Positions and Movements
The position of demi-pli requires maximum weightbearing
dorsiexion
The en pointe position requires maximum weightbearing plantar
exion
Standing on demi-pointe requires maximum plantar exion
and approximately 90 of rst metatarsophalangeal joint
hyperextension
Relev is the movement of rising to the toes, such as is done to
reach demi-pointe
Classical ballet requires repetitive movement from maximum
forced dorsiexion to maximum forced plantar exion and back
again. This puts tremendous stress on the dancers ankles and
heightens the likelihood of injury
Of the three positions demi-pli , demi-pointe, and
en pointe, the latter produces the greatest potential for
injury to the forefoot and midfoot. It is crucial that dancers
receive proper instruction in pointe work from the initial
time they undertake training in this skill. The lengths of the
toes relative to one another do not seem to have an
effect on the pressure per unit area applied to the hallux
en pointe
94
; that is, the hallux receives the same amount of
pressure regardless of the length of the other toes. How-
ever, toe length is related to foot pain. Ballet dancers with
their rst and second toes of the same length or their rst
toe longer than the second toe reported lower pain scores
and less rst metatarsophalangeal joint inammation.
127

Conversely, in ballet dancers with the second toe longer
than the rst (Mortons foot), more forefoot signs and
symptoms were present. Additionally, unlike in ballet danc-
ers, second-toe length has no bearing on forefoot problems
in folk dancers.
127
Dancing en pointe yields some generalized patterns of
toe placement in the shoes.
128
This is simply related to the
need to t a variety of foot shapes into the toe box. When
en pointe, force is exerted on the medial edge of the great
toe
128 , 129
because of the truncated ellipsoid cone shape of
the toe box (see Figure 27-3 ) that forces the hallux later-
ally and possibly hastens the development of hallux valgus
and bunions. An undesirable winging of the foot en
pointe aggravates this tendency. The force on the medial
aspect of the great toe moves the forefoot into valgus as
shown in Figure 27-8 , A . The opposite of winging the
foot is termed sickling, a position in which the force is
directed laterally, the forefoot moves toward varus, and
the heel inverts. Figure 27-8 , B-D compare proper foot
alignment with sickling and winging. Sickling and winging
can be problematic whether a dancer is en pointe or en
demi-pointe, so strong feet and ankles and proper instruc-
tion will help alleviate these technical faults, both of which
can lead to stress injuries.
Appropriate Age at Which to Start Pointe Work
Few questions are as common among parents and teachers of
girls in ballet than, At what age can she start pointe work?
Although it may seem desirable to answer with a denite age,
this does not serve the dancer well. Ages most often pro-
posed are 11 to 14. One study of ballet dancers with exor
hallucis longus (FHL) tendinopathy found the range of ages
at initial training en pointe to be 4 to 16 years old, with a
mean of 10.
130
Meck and colleagues
131
discovered that age
was the most common parameter used by ballet schools
to determine a students ability to begin pointe; 96% of
the schools studied incorporated age into their pointe readi-
ness evaluation programs and the mean age when pointe was
initiated was 11.2 years. Nonetheless, chronological age must
not be the most heavily weighted variable informing the
Medial
A
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 oor and the
arrowhead identies where this dancers 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.
The Lower Extremity and Turnout
Ballet is the dance genre in which turnout (i.e., the ability
to laterally rotate the entire lower extremity) is exceedingly
important and in which it receives the most attention (often
excessively so, to the point of injury). The ideal ballet turn-
out is 180; that is, in a fully turned-out position a dancer
wishes to set his or her calcanei back-to-back with the lon-
gitudinal axes of the feet along a straight line. This is termed
rst position, one of six fundamental stances in ballet ( Figure
27-9 and Figure 27-10 ). Functional turnout is the amount
of turnout motion attained by a dancer in his or her usual
studio setting. The vast majority of dancers are unable to
achieve the desired 180, although they try various
methods to squeeze a few more degrees from their lower
extremities. First-position turnout values reported in the
literature include 127 for university dancers
135
and 128
for preprofessional dancers.
70
Turnout is not a simple movement of hip external rota-
tion, even though that is its primary component. A ratio
of 60% of turnout motion occurring above the knee and
40% of the motion occurring below the knee has been
proposed as an appropriate guideline.
69 , 101
If the ideal
90 of turnout in one limb can be performed, this is
accumulated from 60 to 70 of hip external rotation and
20 to 30 spread across the natural positioning of the
knee, ankle, and foot.
136
Actual external rotation range of
motion may be less of a limiting factor compared with the
lack of experience and technical ability that prevents danc-
ers from maximizing their turnout when dancing. In fact,
improved neuromuscular coordination and strengthening
the hips external rotators can yield an additional 15 to
30 of turnout.
137
Femoral neck version plays a role in a dancers ability
to attain turnout. An anteverted femoral neck may me-
chanically limit a dancers potential for turnout, whereas a
retroverted femoral neck allows greater turnout ( Figure
27-11 ).
126 , 136 , 138 , 139
It has been postulated that dancers who
begin their training early in life experience a molding
of the femoral neck that accommodates to the turned out
position by the time the skeleton solidies. Some reports
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
In another study, however, students who participated in at
least 6 hours of ballet training per week between the ages
of 11 and 14 showed less femoral neck anteversion
than students who trained less than 6 hours per week.
141
Counterintuitively, these authors did not nd an association
between age of starting ballet training and femoral
neck version, passive hip external rotation, nor functional
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 colleagues
143
calculated an average neck version
angle of 11.4 using data from ve studies containing a total
of 1436 subjects; the range of measurements in these
studies was 20 of retroversion to 50 of anteversion. Then
Baumans group compared this value with version angles in a
contingent of professional ballerinas. The dancers exhibited a
mean femoral version angle similar to the general population:
11.9 of anteversion (range 4 to 24). Practically speak-
ing, the more a dancer tends toward femoral neck antever-
sion, the more potential turnout limitation he or she will
have. Conversely, the more he or she tends toward retrover-
sion, the easier it will be to achieve turnout. Longitudinal
studies that periodically measure femoral version in a cohort
of dancers from age of initiating ballet training (often age 4)
through to adulthood are the only way to conrm the effect
of ballet training on the femoral neck.
Factors for Deciding When to Begin Training
En Pointe
133
Stage of physical development
Quality of trunk, abdominal, and pelvic control (i.e., core stability)
Hip-knee-ankle-foot alignment
Strength and exibility of the feet and ankles
Frequency and duration of the students ballet training
Age
decision to allow a young dancer to commence pointe work.
The consequences of starting too early are far greater than
those of starting too late. The ability to succeed technically is
improved and the risk of injury is reduced if the youngster
waits until the skeleton and musculature are strong
enough.
11 , 132-134
Balance and coordination are additional important
factors.
129
Strength in the ankles and feet are not the only
important components; strong and well-controlled muscu-
lature in the trunk, hips, and thighs are equally important
to dancing en pointe, and are even more critical for dancers
with hypermobile feet and ankles.
132
The attributes outlined in the following textbox offer a
guideline that, although seemingly a rule-of-thumb,
must not be applied without careful evaluation of the indi-
vidual dancer. If the student began serious ballet training at
age 8 or later, participates in ballet class at least twice a
week, and possesses adequate maturity in the areas listed
previously, then pointe work is usually appropriate begin-
ning in the fourth year of ballet training. Dancers taking
instruction only once per week, who are not intending to
engage in preprofessional ballet training, or who lack the
necessary skeletal maturity and muscular strength must be
discouraged from pointe work.
133
For further information,
the reader is referred to a detailed history and physical
examination for young dancers that is offered by Shah.
134
Sixth (Parallel)
Fifth
First
Second
Third
Fourth
Figure 27-10
The six primary foot positions used in ballet. The dancer faces in the
direction of the rst diagram. These feet show ideal turnout of
180. Other than the parallel position, these are achieved mainly
by externally rotating the hips and placing the feet in the specied
positions.
A B
Figure 27-9
A, A dancer standing in rst 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 dancers functional turnout.
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)
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 dancers ability
to achieve his or her desired turnout
Forcing ones turnout can lead to foot pronation, knee valgus
stress, anterior pelvic tilt, and lumbar lordosis
Apart from femoral neck version, other factors contrib-
ute to the amount of turnout a dancer can attain, including
tibial torsion
144 , 145
and soft tissue exibility (especially of
the anterior hip ligaments). Forcing turnout beyond a
dancers natural range of motion results in foot pronation,
knee valgus stress,
126 , 130 , 136 , 146
anterior pelvic tilt, and lum-
bar lordosis.
137 , 147
One very unhealthy technique used by
some dancers to maximize their functional turnout is set-
ting the feet as close to the desired 180 turnout angle as
possible with the knees exed in demi-pli and then raising
the body by straightening the knees and maintaining the
feet in the set position. This puts undue stress on the knees
as they are screwed home into extension. It also is likely
to force the feet into pronation ( Figure 27-12 ).
The difference between a dancers hip external range
of motion and his or her functional turnout angle may be
related to injury. This difference was signicantly larger in
With feet in Parallel After turning out
12
o
Anteversion
(typical)
25
o
Anteversion
Impingement
Impingement
Impingement
15
o
Retroversion
Figure 27-11
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
rotation to the point at which the femoral neck impacts the posterior
lip of the acetabulum (dark shaded circles). Dancers with greater
anteversion will be more limited in their turnout ability, whereas
retroverted femoral necks are favorable to attaining turnout.
dancers who were injured versus dancers who were not in-
jured (25.4 vs. 4.7), suggesting that forcing ones turnout
is related to incidence of injury.
148
In a group of 28 elite
professional ballet dancers
101
and another group of 29
preprofessional dancers,
70
those with less functional turnout
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.
Selected Musculoskeletal Injuries
in Dancers
Injuries in dancers are, in general, pathologically similar to
injuries sustained by traditional athletes even though the
exact mechanisms of injury may differ. That is to say, the
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
North Am 17(4):815, 2006.)
pathological nding of posterior ankle impingement in a
soccer player is not appreciably different from that of the
same injury in a dancer even though the mechanism of on-
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
intended to be an exhaustive monograph describing all
common dance injuries. A few injuries are highlighted here
because of their prevalence in the dance population or
because the circumstances surrounding their occurrence in
dancers are particularly unique and interesting.
Ankle Impingement Syndromes
The requirement that dancers repeatedly plantar ex and
dorsiex the ankle in weightbearing can give rise to impinge-
ment syndromes on both the posterior and anterior aspects
of the ankle. These types of injuries often are related to ana-
tomical variations in the foot (e.g., os trigonum)
149-153
in
addition to the pathomechanics of executing dance skills
such as demi-pli, demi-pointe, and pointe.
150-152 , 154 , 155
Medial
tubercle
Lateral tubercle
Talar dome
Lateral
process
FH
FH FH
Os trigonum
Stiedas process
A B C
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
tubercle are illustrated and the position of the tendon of exor
hallucis longus is indicated by the circle marked FH. A, A typical
talus. B, A talus with an os trigonum. C, A talus with a Stieda process.
under the tibia during relev, or rising on the toes. In this
scenario, the talus slides anteriorly in the ankle mortise and the
superior calcaneus similarly moves forward, impinging against
the posterior edge of the tibial plafond and causing pain.
Regardless of the exact pathogenesis, any space-
occupying structure in the posterior compartment of the
ankle can create symptoms when the calcaneus and talus
approach the posterior distal tibia during plantar exion.
Pain associated with posterior impingement, especially an
os trigonum or Stieda process, most often occurs postero-
laterally, thus differentiating these problems from FHL
tendinopathy, a syndrome that produces pain at the pos-
teromedial ankle.
180 , 184
Dancers with posterior impinge-
ment syndrome complain of posterior ankle pain and
describe a limitation of motion in their demi-pointe or
en pointe positions. During a clinical examination, forced
plantar exion of the ankle reproduces these symptoms. In
cases of failed conservative measures, operative treatment
has been shown successful.
168 , 173 , 182 , 185 , 186
Anterior Ankle Impingement
As in the posterior ankle, impingement syndrome in the
anterior region of the ankle can arise from bone or soft tis-
sue. Symptoms originating in bone can be initiated by
repetitive impact of the anterior edge of the tibial plafond
and the dorsal talus that causes exostoses to form on either
or both bones.
139 , 151 , 155 , 187-194
Although contact between
the tibia and talus does not usually occur, dancers may
experience impingement when they repeatedly force their
ankles into maximum dorsiexion during demi-pli.
151 , 155
Because of this required repetition, exostosis formation
occurs more frequently in dancers than nondancers,
155 , 195
and both pes cavus
79 , 151
and limited subtalar motion
145
can
increase the likelihood that a dancer will develop exostoses.
Another possible result of repeated forced dorsiexion in
demi-pli is a deepened sulcus on the dorsal talar neck.
196
Posterior Ankle Impingement
The cause of posterior impingement most familiar to clini-
cians is os trigonum, an anatomical variation that appears in
5% to 25% of adults.
156-162
Closely related to this is a pro-
truding lateral talar tubercle, or Stieda process.
132 , 163-166
Figure 27-13 illustrates three anatomical variations of the
talus. Some debate exists about whether what appears to be
an os trigonum in certain individuals may in fact be a Stieda
process separated from the body of the talus by a compres-
sion fracture secondary to forced plantar exion.
167-169
Soft
tissue structures, including the FHL tendon,
149 , 170-175
deep
posteromedial deltoid ligament,
176
posterior intermalleolar
ligament,
177 , 178
and posterior tibiotalar ligament,
179
also can
produce posterior impingement symptoms.
Peace and colleagues
153
used magnetic resonance imag-
ing (MRI) scans to study ballet dancers with posterior
impingement symptoms; 30% of the subjects exhibited os
trigonum. This is higher than the prevalence reported in
the general population, perhaps because of the forced plan-
tar exion of ballet during the years when the secondary
ossication center of the lateral talar tubercle is adjoining
the tubercle and the talar body. An os trigonum might be
quiet for years until it becomes symptomatic following a
sprained ankle or other traumatic episode.
149 , 180 , 181
This
may be related to force created by the posterior talobular
ligament during ankle trauma because the ligament attaches
to the lateral talar tubercle.
Additional anatomical variations have been shown to pre-
dispose dancers to pathological conditions of the ankle, espe-
cially posterior impingement syndrome.
149 , 153 , 154 , 167 , 168 , 182 , 183

Greater than 5 mm of downward protrusion of the posterior
lip of the tibial plafond (posterior malleolus) and greater than
5 mm of upward protrusion of the superior calcaneal tuberos-
ity both have been cited as contributory to pathological
conditions resulting in posterior impingement.
153
These are
depicted in Figure 27-14 .
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
Calcaneus
Anterior
Talus
Tibia
CT
PM
Fibula
Figure 27-14
Lateral view of ankle anatomy showing a protruding posterior malleolus
( PM ) and calcaneal tuberosity ( CT ), either of which increases the likeli-
hood of posterior ankle impingement in dancers.
Ankle Impingement
Ankle impingement syndromes result from bony or soft tissue
symptoms that have been irritated by compression during the
extreme range of ankle motion required of dancers
A lateral ankle sprain in a dancer can precipitate posterior
impingement symptoms when an os trigonum is present or an
anterior impingement when hypertrophic scar tissue develops in
the region of the anterior talobular ligament
The relative positions of tibial and talar exostoses usually
preclude them impinging on one another.
188
Tibial spurs
generally occur lateral to the sagittal midline of the ankle
and talar spurs occur medial to the midline. The inner sur-
face of the medial malleolus and the medial surface of the
talus are common locations for exostoses in dancers because
maximum weightbearing dorsiexion generally forces the
foot into pronation against the medial malleolus.
151
A
lateral radiograph taken in full dorsiexion may be helpful
in assessing bony impingement
194 , 197
because this view
improves the ability to see anterior exostoses; however, it is
easy to underestimate their sizes if the spurs overlap.
197 , 198
Moreover, true lateral radiographs may be insufcient to
identify the pathological condition in many cases.
18 , 191 , 199 , 200
Tol and colleagues
191
recommend a special oblique antero-
medial impingement view they designed that improves the
sensitivity of radiographic diagnosis from 40% to 85%.
Soft tissue causes of anterior impingement include
thickened and inamed soft tissue caught between the
tibia and talus
189 , 190 , 192
; the anterior inferior tibiobular
ligament
169 , 190 , 192-194 , 201-204
; and inamed, hypertrophic tis-
sue in the lateral gutter following a typical lateral ankle
sprain.
175 , 198 , 205-210
The lateral gutter is signicant clinically
because its anterior aspect is the site of most anterolateral
soft tissue impingement.
197 , 206 , 211-213
Inasmuch as ankle
sprains are a common occurrence in physical activity
77 , 214-216
and the ankle is the most frequently injured body region in
dance,
63 , 65 , 102
it is wise to consider post-traumatic soft tissue
impingement as a sequela that may hamper a dancers
return to activity following an ankle sprain.
Achilles Tendinopathy
Tendinopathy
217
or tendinosis
218
are the terms currently
employed to describe tendon overuse injury because the
classic signs of inammationdenoted by the sufx in the
word tendinitis are generally not present in this type of
condition.
217 , 219
The distinguishing difference between
these two terms is the presence of intratendinous degenera-
tion in tendinosis
218 , 220
; tendinopathy refers to any abnormal
state of a tendon. The Achilles tendon is prone to injury in
any genre of dance in which repeated dorsiexion and plan-
tar exion are required; however, classical ballet presents a
greater challenge to the tendon than other types of dance.
One suggested cause of tendinopathy is variable force dis-
tribution across a tendons diameter that creates abnormal
frictional forces between the bers
221
and disrupts the
bers microstructure.
222
The Achilles tendon is compressed
in ballet when the foot and ankle are maximally plantar
exed in the en pointe position. The posterior upper edge of
the pointe shoes heel counter, the shoes ribbons tied
around the distal leg and ankle, and the compressed skin
folds over the tendon all create a fulcrum that forces the
tendon into a curved path and creates indentations
that exert pressure on it ( Figure 27-15 ). Also, a drawstring
encircles the shoes opening, a feature that, when tightened,
can further bind against the tendon and its insertion.
Figure 27-15
T1-weighted magnetic resonance images of ballet dancers standing
en pointe. In the larger image, the black arrows indicate the band of
hypointense signal of the Achilles tendon. The white arrow indicates
the indentation made by the posterior lip of the pointe shoe and the
gray arrows indicate the impressions of the shoes ribbon. The inset
image is a different dancer exhibiting an even more pronounced
curve in the tendon substance, as indicated by the open arrows. To
understand the components of the overlaying shoe, compare these
images with the photo of the ankle and foot en pointe in Figure 27-5
and the en pointe x-ray image in Figure 27-7 .
With very few exceptions (e.g., the mens ballet troupe
Les Ballets Trockaderos de Monte Carlo ), pointe dancers are
women. Following exercise-induced collagen degradation,
the rate of collagen synthesis is reduced in women com-
pared with men,
223
a phenomenon possibly related to circu-
lating estradiol levels,
224 , 225
but apparently independent
of menstrual phase.
223 , 226
If a hormonal mediation of rela-
tive collagen strength exists, it may intimate a greater inci-
dence of Achilles tendinopathy in women dancers, especially
in conjunction with the potential for added insult to the
morphological structure of the tendon that is elicited by the
en pointe position as just described. Further insight into
pathological changes in tendon can be found in Tendon
Pathology and Injuries: Pathophysiology, Healing, and
Treatment Considerations, which is Chapter 3 in Scientic
Foundations and Principles of Practice in Musculoskeletal
Rehabilitation, another book in this series.
Flexor Hallucis Longus Tendinopathy
FHL tendinopathy, also known as dancers tendinopathy,
is a very common dance injury, and the FHL tendon is the
involved structure in nearly all medial ankle tendon prob-
lems that occur in dancers.
227
This is not surprising given
the large number of dance movements requiring relev. As
they do with many injuries, dancers often try to dance
through FHL tendinopathyin one study, they tolerated
the symptoms longer than did nondancers prior to seeking
treatment.
130
Hamilton
227
calls this tendon the Achilles
tendon of the foot in dancers who work en pointe. The
tendon courses from the FHL muscle in the deep posterior
muscle compartment behind the tibia, along a groove
between the medial and lateral talar tubercles that lie poste-
rior to the talus, around a bend and through a tunnel that
lies under the sustentaculum tali, then along the underside
of the rst ray to attach on the proximal plantar surface of
Tendinopathies in Dancers
Tendinopathies in dancers are very common because of the heavy
repetition in dance classes, rehearsals, and performances
Achilles tendinopathy and exor hallucis longus tendinopathy are
two of the most common because of dancers emphasis on rising
to their toes (relev) , jumping, and, in classical ballet, dancing
en pointe
the rst distal phalanx. In particular, the bend in the tendon
just before it enters the bro-osseous tunnel under the
sustentaculum tali ( Figure 27-16 ) heightens the chance of
injury from a nonhomogeneous force distribution through
the tendon
221
during rising to and lowering from the toes,
and when jumping. In an advanced stage, the FHL tendon
and its synovial sheath may swell and develop adhesions, or
the tendon may develop areas of degeneration. Any or all of
these can cause a hallux saltans (trigger toe) tenosynovitis
when the tendon does not slide smoothly through its
tunnel.
139 , 180 , 228 , 229
FHL tendinopathy may be precipitated by the presence
of an unstable os trigonum
171
because the trigonal bone is
a nonunited protrusion of the lateral tubercle that creates
the lateral border of the groove for the tendon. Several
authors corroborate a strong, direct relationship between
symptoms in these two structures
149 , 170 , 171 , 173-175 , 230 , 231
because of their proximity to one another.
Sustentaculum tali of calaneus
Medial tubercle of talus
Flexor hallucis
longus tendon
Aream of
common
pathology
Retinaculum
(gray)
Figure 27-16
Medial view of the foot showing the path of the exor 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

Fracture of the Fifth Metatarsal
A spiral fracture of the distal shaft of the fth metatarsal is
termed a dancers fracture
138 , 232-234
because of its association
with an inversion mechanism of a dancer falling from demi-
pointe or en pointe . An unstable landing from a jump can
also induce a dancers fracture.
146
Torsion of the foot exerts
the rotational force that results in this fractures characteris-
tic appearance ( Figure 27-17 ).
A Jones fracture ( Figure 27-18 ) occurs at the junction
of the diaphysis and proximal metaphysis of the fth
metatarsal.
232 , 234 , 235
Named for the author who rst
described it in 1902, Jones
236
reported that this injury
occurred in his own footrecounting that he sustained it
while dancingand in patients seen in his practice. This
particular fracture must be cared for surgically because of
its propensity to proceed to malunion or nonunion, often
because of a poor or disrupted blood supply.
235
Further-
more, those who participate in sports and dance are
unlikely to accept an extended period of immobilization
and the risk of nonunion that can complicate treatment of
a Jones fracture.
Stress Fractures
Stress fractures are a common overuse injury in dance,
especially in the foot.
237
The second metatarsal shaft is the
most frequently affected; because of its length, it bears
more force than the other metatarsals when a dancer stands
in demi-pointe.
232
Cortical hypertrophy of the diaphyses in
such areas is not unusual in response to arduous schedules
of dance rehearsal and performance ( Figure 27-19 ). Perios-
teal elevation indicates the presence of the reparative callus
associated with stress fractures.
238
The second metatarsal
can also exhibit a stress fracture at its base, an injury that is
rare in nondancers because it is induced by the repetitive
longitudinal forces through the foot that are sustained
during dance.
239-242
Other common sites for stress fractures
in dancers are the tibia (often related to later stages of shin
splints), bula, and lumbar spine.
232 , 237 , 243 , 244
The rigors of dance training combined with intervals of
amenorrhea have been suggested as risk factors for stress
fractures in dancers.
237 , 243 , 245
Dancers may ignore the early
symptoms of stress reactions and stress fractures because of
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,
particularly in a weightbearing bone like the tibia.
246
For
more information on stress fractures, see Repetitive Stress
PathologyBone, Chapter 21 , in Pathology and Interven-
tion in Musculoskeletal Rehabilitation, another book in this
series.
Anterior Cruciate Ligament Sprain
Injury to the anterior cruciate ligament (ACL) is much less
common in dancers than in most traditional athletes,
29 , 30 , 247
yet it is debilitating when it occurs. Because of the sophisti-
cated jumping and cutting maneuvers required of dancers,
a dancer with a torn and unrepaired ACL would likely be
unable to continue performing. Meuffels and Verhaar
30
reported the incidence of ACL tear in 253 Dutch profes-
sional ballet and modern dancers to be 1.6 per 100,000
Figure 27-17
Spiral dancers fracture of the fth metatarsal shaft. (From Kadel
NJ : Foot and ankle injuries in dance, Phys Med Rehabil Clin North
Am 17(4):818, 2006.)
Figure 27-18
Jones fracture (arrow) of the proximal fth metatarsal diaphysis.
(From Kennedy JG, Hodgkins CW, Columbier J-A et al: Foot and
ankle injuries in dancers. In Porter DA, Schon LC, editors: Baxters
the foot and ankle in sport, ed 2, p 474, Philadelphia, 2008, Mosby.)
dancing days, or 3.2 per 100,000 dancing days when con-
sidering classical ballet dancers only. In fact, in their 10-year
study, the modern dancers experienced no ACL tears
whereas the classical dancers sustained six. The left knee was
involved in every case and, of these, four occurred in men
and two occurred in women. All were treated operatively,
but three dancers had to retire from dance because of post-
surgical symptoms. These authors calculated the risk of
a dancer suffering an ACL rupture of the left knee in a
10-year classical ballet career to be 7%.
In another study, Liederbach and colleagues
29
prospec-
tively studied 298 professional ballet and modern dancers
for 5 years. In this cohort, 12 ACL sprains occurred, 10 of
which were in women. Contrasting with the data of
Meuffels and Verhaar, in this study, modern dancers experi-
enced a higher risk than did classical ballet dancers: 9 of the
12 injuries were in modern dancers. The ACL injury rate
in ballet was 0.005 injuries per 1000 exposures and for
modern dance, it was 0.012 injuries per 1000 exposures
(an exposure was a single class, rehearsal, or performance in
which a dancer participated). Overall, the injury rate of
ACL injury in all dancers was 0.009 per 1000 exposures.
It is important to note that Meuffels and Verhaar studied
ACL rupture, whereas Liederbach and colleagues recorded
ACL injuries (an injury being a rst-time partial or com-
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
rehearsals en pointe over several weeks, extreme midfoot pain, and
exquisite point tenderness on the second and third metatarsals.
Dotted boxes highlight second, third, and fourth metatarsal shafts
with cortical thickening. Arrowheads indicate areas of periosteal
elevation suggesting stress fractures of second and third metatarsals.
plete rupture of the ligament conrmed by clinical and
radiological examination
29
).
Substantial evidence exists that women athletes who
participate in sports that elicit rotational forces across the
kneesuch as those requiring cutting and jumping
are much more likely than men to sustain an ACL
injury.
215 , 248-250
Jump landings have been proposed as one
mechanism for such injury.
251
Both studies of ACL inju-
ries in dance outlined previously reported virtually identi-
cal injury mechanisms in their samples of dancers: knee
valgus and external rotation forces upon landing from a
jump ( Figure 27-20 ). One set of investigators proposed
this landing style as the single most important risk factor
for ACL tear in dancers.
30
With the large proportion of
dancers being women and the heavy emphasis on jumping
in many dance genres, it is perhaps surprising that more
ACL injuries are not reported. Although it does not
appear that male and female dancers differ in their jump
landing biomechanics,
252
several parameters about dance
and dancers may account for the contrast of these results
with ACL injuries in a sports environment. These include
more forgiving shoe-to-oor or foot-to-oor interfaces,
more controlled (i.e., choreographed) movements, and
generally greater exibility among dancers. Consistent
exposure to balance training and jump training may also
Figure 27-20
Characteristic landing pattern of a dancer that is associated with
anterior cruciate ligament injury. Note the externally rotated hip and
pronated foot with resulting valgus stress to the left knee. (From
Meuffels DE , Verhaar JAN: Anterior cruciate ligament injury in
professional dancers, Acta Orthop 79(4):516, 2008.)
play a role.
29 , 252
One more crucial factor to contemplate
was identied by Liederbach and colleagues study. As
shown in Table 27-4 , most ACL injuries occurred in the
evening, at the end of a season, and during performances,
suggesting that fatigue may play a role in these dance
injuries.
Knee Ligament Injuries in Dancers
Anterior cruciate ligament (ACL) rupture is not a common occurrence
in dancers, but the nature of dance likely precludes participation by
a dancer with a torn ACL
Occurrence of ACL injuries in dancers seems to be associated with
fatigue and related factors because research shows that most of
the injuries occur late in the day, at the end of the season, and
during performances
Table 27-4
Potential Role of Fatigue in Dance ACL Injuries
Number of ACL
Injuries
(Total 12)
Time of Day Morning
Mid-day
Evening
1
3
8
Time of Season Off-season
Early season
End of season
2
1
9
Type of Activity Class
Rehearsal
Performance
1
4
7
ACL, Anterior cruciate ligament.
Note: Bold gures show greatest incidence of injury when dancers
were most fatigued or under the most intense conditions.
Data from Liederbach M , Dilgen FE, Rose DJ: Incidence of anterior
cruciate ligament injuries among elite ballet and modern dancers: A
5-year prospective study, Am J Sports Med 36(9):1779-1788, 2008.
Internal Snapping Hip
Snapping hip, or coxa saltans, is a frequent nding in
dancers; many will report it, although it may be neither
painful nor necessarily restrictive. Of all dancers in a study
by Winston and colleagues,
253
91% reported snapping hip;
in 80% of these cases the snap was bilateral. Although coxa
saltans can encompass a number of pathological entities,
254
one customary way of categorizing the condition is as either
external or internal snapping hip. The nature of hip motion
in dance requires as large a range of motion in this joint as
possiblethis capability is integral to success. The varied
movements along with the concentration on external rota-
tion for turnout in ballet routinely draw soft tissues across
bony prominences. External snapping hip is created by the
posterior iliotibial band or anterior edge of the gluteus
maximus muscle sliding across the greater trochanter.
254
On
the other hand, the internal type may resultamong several
causesfrom the iliopsoas tendon rubbing over the ante-
rior ridge on the femoral head,
140
the iliopectineal ridge,
11
or a portion of the iliacus muscle belly.
253 , 255
Jacobs and
Young
256
found certain kinesiological characteristics in
dancers with a snapping hip compared with dancers without
a snapping hip: narrow width between the pelvic ilia,
increased hip abduction range of motion, decreased hip
external rotation range of motion, and increased external
rotation strength.
The iliopsoas is the most frequently involved anatomical
structure in snapping hip.
253
This complex is a combination
of the iliacus and psoas major muscles with their distal
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
Figure 27-21
Deep anatomy of the anterior hip joint with a portion of the iliopsoas
muscle and tendon resected. The area labeled Exposed head of femur is
the location where the distal muscle belly and tendon of iliopsoas can
snap across the anterior edge of the femoral head during hip move-
ment. A bursa lies between the muscle-tendon and the femur and can
become inamed, as well. (From Neumann DA: Kinesiology of the
musculoskeletal system: Foundations for physical rehabilitation, p 400,
St Louis, 2002, Mosby.)
P
ubis
I
l
i
a
c
u
s

P
s
o
a
s

Ischiofemoral
ligament
Iliofemoral
ligament
Pubofemoral ligament
Obturator
externus
Iliopsoas tendon (cut)
Exposed head of femur
Anterior view
muscle and tendon. In addition to a snapping tendon, ilio-
psoas tendinopathy and iliopsoas bursitis often occur con-
currently because the structures are so close anatomically.
257
Ultrasonography is helpful in establishing a pathoanatomi-
cal diagnosis.
253 , 255
If neither external nor internal snapping
hip is suspected in a dancer presenting with pain and crepi-
tus in the hip region, intra-articular injuries such as labral
tears or loose bodies should be suspected.
258
Joint Hypermobility
In dance parlance, the objective of training is to exhibit a
good line, meaning that the technical form of the body
in its dance positioning should be aesthetically pleasing.
A portion of executing a desirable line depends on the
dancers natural form, including the ranges of motion of the
joints. It is customary for dancers to exhibit better exibility
than nondancers.
259
This is undoubtedly because of the
nature of their training and the aesthetic requirements of
dance, but there may also be some self-selection bias
involved as presumably many individuals with less than
desirable exibility opt out of dance participation. Ballet
dancers tend to be more exible than modern dancers.
260
Nonetheless, this generally increased exibility is often un-
balanced between opposing joint motions (e.g., internal hip
rotation versus external hip rotation), a characteristic that
may predispose ballet dancers to injury in the knee and
hip.
259
One reason for such imbalances is a exibility
emphasis based on the perceived need to accentuate a par-
ticular skill (e.g., turnout) and the concomitant neglect of
the opposite motion.
One widely accepted and easily administered screening
tool for joint hypermobility is the Beighton score.
261-263
This method is shown in Table 27-5 and is composed
of four bilateral assessments plus trunk exion, for a total of
9 possible points. A score of 4 or greater is suggestive of
joint hypermobility
262-264
and may additionally point to
benign joint hypermobility syndrome.
265 , 266
Interestingly,
a longitudinal study of ballet dancers reported that
their Beighton scores increased across a 4-year follow-up
period.
267
This result appeared to stem from improvement
in the trunk exion component that was gained by training;
the authors further suggested that trunk exion ability in
dancers develops over at least 4 years rather than being an
innate quality of the body.
Several studies conrm that hypermobility can be a liabil-
ity for dancers
262 , 263 , 267 , 268
; however, none suggest that the
condition should preclude dance participation. Moreover,
there appears to be no relationship between joint hypermo-
bility and technical excellence.
267
The main challenges for
the hypermobile dancer are an increased likelihood of
injury,
262
increased rehabilitative time following injury,
263 , 268
and proprioceptive difculty attaining proper positioning in
technical training.
263
Hypermobility prevalence was found
to be inversely proportional to rank within a professional
ballet company,
263
suggesting that perhaps the dancers who
are elevated to higher skill levels are not the hypermobile
ones because they are not burdened by the detriments
associated with hypermobility. Decient collagen structure
has been proposed as the root of many of the adverse con-
sequences of joint hypermobility syndrome
265 , 266
; because
this is unalterable, dancers who display hypermobility symp-
toms must be carefully educated about how best to adapt to
the rigors of their training.
Table 27-5
Grading Scale for Determining Joint Hypermobility Based
on Beightons Criteria
261
Score
Passive fth metacarpophalangeal
joint hyperextension 90
Right
Left
0
0
1
1
Passive wrist exion to touch
thumb to volar forearm
Right
Left
0
0
1
1
Elbow hyperextension
(cubitus recurvatum) 10
Right
Left
0
0
1
1
Knee hyperextension
(genu recurvatum) 10
Right
Left
0
0
1
1
Trunk exion to place both
palms at on oor
0 1
Total score ( 4 suggests
hypermobility):
0 1 2 3 4 5 6 7 8 9
A score of 0 Not Present, 1 Present.
Hypermobility and Dancers
Joint hypermobility is more common in dancers than in
nondancers
Hypermobile dancers are more prone to injury and have a greater
challenge achieving proper positioning in their technical training
compared with nonhypermobile dancers
Hypermobility is not a contraindication for participating in dance
A study of female soccer players revealed an intriguing re-
lationship between hypermobile (Beighton score 4) players
and loading of the medial foot during barefoot walking.
264

Two factors about this research are worth noting when con-
sidering hypermobile dancers. First, the study was conducted
with the subjects in bare feet; modern dancers usually wear no
shoes and a ballet slipper provides little more substance than
a bare foot. Second, although the subjects were soccer players
the medial loading hypothesis is important to consider
because of the tendency for dancers forcing turnout to
Dancing and Osteoarthritis
Osteoarthritic changes seen on x-ray examinations are a typical
nding in dancers
The rst metatarsophalangeal joint is the most common site for
osteoarthritis in dancers
Even among older, retired dancers, physical symptoms usually
do not correlate with x-ray examination manifestations of
osteoarthritis
pronate and, thus, load the medial foot (see Figure 27-12 )
and because a common mechanism of ACL injury involves
landing from a jump with substantial medial loading (see
Figure 27-20 ). Whether hypermobile dancers are more prone
to injury because they also exhibit a proclivity to medially load
the lower extremity warrants study.
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
arthritic changes in dancers joints is widely variable. The nd-
ing of degenerative joint disease is not, by itself, necessarily
adverse to dancing.
271-273
Teitz and Kocoyne
271
found that
radiographically conrmed hip capsule calcications and knee,
ankle, and rst metatarsophalangeal joint changes occurred in
young (late 20s to early 40s) retired dancers, yet did not cor-
relate with the dancers symptoms. Neither was the x-ray evi-
dence associated with dancers retirement from dance. Van
Dijk and colleagues
272
studied retired dancers between 50 and
66 years old and found no clinical complaints among them in
spite of a plethora of hip, ankle, subtalar, and rst metatarso-
phalangeal arthroses on x-ray examination. Andersson and
colleagues
269
studied the same joints in a cohort of former
dancers ranging in age from 44 to 80 years and, although the
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
dancers with backgrounds other than just classical ballet. The
long-term effect of other dance genres on joint degeneration
represents a fertile eld for research.
Case Studies
The following two case studies illustrate the importance
of careful diagnostics in dance medicine. In both of these
cases, the dancers involved sought care for recalcitrant
injuries, but sadly that care was not helpful and the danc-
ers became frustrated with their injuries and their caregiv-
ers. However, once a dance medicine specialist established
a correct diagnosis, the dancers were able to proceed
toward recovery. Both of these are fairly recent cases. The
intent is not to show the clinical progression to a success-
ful resumption of activity, but, rather, to focus on how a
health care providers familiarity with the demands of
dance and special attention to a dancer-patients com-
plaints can yield an appropriate diagnosis and treatment
regimen.
Case Study 1: Posterior Ankle Pain
A 19-year-old female ballet and modern dancer presented
to a dance medicine clinician complaining of persistent pos-
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
Ambr and Nilsson
273
20 F 28 7 Ballet NR NR NR NR Yes (minor)
Anderss on et al.
2 69
29 F
15 M
44-80 Ballet Yes Yes 1 case NR Yes
Brode lius
270
13 F
3 M
21-46 Ballet NR NR Yes NR NR
Schneider et. al.
196
39 F
13 M
12-41 Ballet 4 cases 2 cases 6 cases NR Yes
Teitz and Kocoyne
271
9 F
5 M
27-46 Ballet and
modern
Yes 5 cases Yes NR Yes
Van Dijk et al.
272
19 F 50-66 Ballet No NR Yes Yes Yes
F, Female; M, male; MTP, metatarsophalangeal joint; NR, not reported.
X-ray examination ndings are indicated Yes or No for arthroses, or NR for not reported.
this ankle region of more than 2 years duration. The work-
ing clinical impression given to her by a previous clinician
was Achilles tendinopathy. This was the impetus for various
treatments during the 2 years. In addition, she reported a
history of lateral ankle injury, but indicated that her symp-
toms from two prior sprains were resolved except for the
persistent pain that accompanied her current complaint.
Interestingly, she connected the initial ankle sprain to
her current condition. She also disclosed a prior visit to
a primary care physician who had ordered an ankle x-ray
examination and corroborated the diagnosis of Achilles
tendinopathy. Conservative treatments did not ameliorate
the symptoms; only rest from dance was benecial in reduc-
ing her pain. The dancer reported that she continued to
dance, interspersing periodic rest as necessary for pain relief.
Her exasperation with being persistently unable to partici-
pate fully in dance was readily evident.
On examination, the dance medicine clinician found her
Achilles tendon was neither swollen nor markedly tender.
The dancer reported that the greatest pain emanated from
the posterolateral portion of the ankle, indicating that she
felt it was down inside somewhere. She also described pain
during relev and a feeling that something was keeping her
from fully plantar exing to demi-pointe and en pointe .
Edema was present between the posterior aspect of the
lateral malleolus and the lateral border of the Achilles ten-
don. Tenderness was noted in this area, as well. Forced
passive plantar exion provoked pain and the dancer
described crepitus and a rm, uncomfortable endpoint of
the motion. Active maximum plantar exion evaluation
revealed that the involved side was slightly reduced in this
ability compared with the uninvolved side.
The dance medicine clinicians clinical impression was os
trigonum, so the patient was referred back to her primary
care physician for a review of her previous radiographs. The
os trigonum was conrmed based on the lateral x-ray view
on which this accessory bone was originally missed ( Figure
27-22 ). The dancer was scheduled for orthopaedic consul-
tation and surgery for resection of the offending ossicle.
Following this procedure, her healing was uneventful, and
she has returned fully to dance.
This case study demonstrates the importance of two
functions of the clinician: understanding what is required
of the ankle in dance and carefully evaluating an injury in
light of the history reported by the dancer. Of note is the
dancers belief that the origin of the intractable posterior
pain seemed to coincide with a lateral ankle sprain. This is
not an unusual mechanism by which a previously asymp-
tomatic os trigonum can be disrupted. Furthermore,
close attention to pathoanatomy is a must. In this in-
stance, localizing the pain and swelling and coordinating
these with the dancers symptom description was an
effective combination for developing an accurate clinical
impression.
Case Study 2: First Metatarsophalangeal Joint Pain
A 14-year-old female ballet dancer presented to a dance
medicine clinician with the chief complaint of rst metatarso-
phalangeal joint pain in her left foot. She was highly skilled in
ballet, having participated in well-known training programs
in New York City. She also had performed with a professional
dance company. Her symptoms were several months in dura-
tion; the diagnosis provided on initial assessment by another
clinician was rst metatarsophalangeal joint sprain, or turf
toe, and the dancer was treated accordingly. Nonetheless,
conservative treatment for this condition did not allow the
dancer to return to full dance activity.
A visit to an orthopaedic surgeon did not reveal further
insight. This spurred the dancers mother to seek the advice
of the dance medicine clinician. At this point in the case, the
dancers foot had been completely rested for 6 weeks. The
dancer reported that relev was painful and working in the
demi-pointe position elicited more pain under the ball of the
foot than did working en pointe . She felt an increase in pain
as she moved through relev to rise to her toes. Periods of
rest had reduced the pain, but it returned when she re-
sumed any substantial amount of dance. All methods of
padding had not alleviated her symptoms.
On assessment, the dancer denied a traumatic onset.
Her pain was plantar and slightly proximal to the rst
metatarsophalangeal joint rather than periarticular, such as
would be expected in a turf toe injury. The lateral sesa-
moid was particularly tender. Dancing in a pointe shoe
greatly exacerbated the symptoms because of the shoes
Figure 27-22
Lateral x-ray examination of the ankle of a 19-year-old ballet and
modern dancer who complained of pain posterior to the ankle and
limited plantar exion. Arrowhead indicates an os trigonum.
relatively hard and stiff sole. The dancer denied paresthesia
in her toes and swelling was unremarkable in any part of
the forefoot. As a result of the history and examination
and considering the concentration of symptoms at the
lateral sesamoidthe dance medicine clinicians clinical
impression was bipartite lateral sesamoid. Lateral sesa-
moiditis was a differential impression. The dancer was
referred to her orthopaedic surgeon again, and radio-
graphs conrmed a bipartite lateral sesamoid ( Figure
27-23 ). The surgeon advised against surgery (surgery is
contraindicated in the rst metatarsophalangeal joint of
dancers because of the likelihood that the joints crucial
hyperextension range will be compromised), but acknowl-
edged a lack of expertise for working with dancers and
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
the extent of bone and soft tissue involvement. The MRI
examination conrmed the diagnosis, demonstrating bone
marrow edema and soft tissue inammation, so the dancer
was removed from participation to allow the greatest
chance for healing. Following 6 months of rest, the dancer
began to test her injured foot in a very controlled fashion,
but relev remained painful. Because the load on the sesa-
moids during ballet is substantial, she continued pursuing
the conservative course of rest in the hope of being able to
return to dance later. After a complete year of rest, she
undertook a very gradual and methodical resumption of
her dance activity, with hopefulness that her symptoms will
not recur.
Signicant to this case was the need to listen to the
dancers history to establish the probable mechanism. It
was thought that, apart from trauma, a turf-toe type of
injury that was so painful and persistent was unlikely.
Furthermore, the intense focal pressure on the sesamoids
during demi-pointe especially considering how a pointe
shoes sole could amplify thiswas deemed important
and, in fact, this is what elicited the greatest pain. Point
tenderness over the lateral sesamoid added further to the
suspicion of bipartite sesamoid or sesamoiditis. Once
again, careful attention to the injury history and to the
dancers equipment and regimen provided vital assistance
to caring for her. Moreover, it is not a minor point that
this case is saddled with the added emotional challenge of
a very talented dancer requiring an extended period of
discontinuance from dance.
Conclusion
Dancers certainly are athletes and dance injuries are com-
monplace. Unquestionably, working with dancers presents
many challenges to the musculoskeletal health care provider;
but the challenges are also what make the task enjoyable.
Health care providers will nd in dancers an extremely
creative, interesting, and grateful group of patients. A tradi-
tional sports medicine model is helpful in working with
dancers, yet it is not an ideal match because of several unique
characteristics of a dance environment. These include the
dancers intense psyche, limitations imposed by wardrobe
requirements, and unrelenting training regimens.
The majority of dance injuries are of the overuse variety. It
is highly unlikely that a dancer will escape injury during his or
her career; most musculoskeletal conditions are exacerbated
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
CaliforniaIrvine who served as models for some of my
gures: 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
current colleagues, Dr. Lisa Naugle and Dr. Nancy Ruyter,
provided invaluable reviews of portions of this chapter. Finally,
my wife, Ruth, deserves a special accolade for the encourage-
ment she gave me to undertake this writing project.
Figure 27-23
X-ray examination of the forefoot of a 14-year-old ballet dancer with
pain and exquisite point tenderness over the lateral hallux sesamoid.
Arrowhead points to the bipartite sesamoid that was the source of the
dancers symptoms.
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681
Introduction
Twenty to thirty years ago, on any given afternoon, a local
charity organization would host a track meet for the
handicapped at which an indiscriminate number of
events would be offered. Participants would often compete
in their street clothes and everyday wheelchairs, prostheses,
or braces. Many competitors had never practiced or even
attempted some of the events before the day of competi-
tion. However, everyone would have a day of fun and
excitement.
Today, for the accomplished athlete with a disability,
athletics is a world of aerodynamic wheelchairs and high-
tech equipment costing thousands of dollars; scientic per-
formance analysis; and year-round training for regional,
national, and international competitions. The grassroots
infrastructure of disabled athletics is still rmly in place,
with charity groups, public schools, and local disabled
sports organizations (DSOs) hosting improved, structured
weekend competitions for novice- and intermediate-level
competitors. In addition, the potential vertical growth of
competition has ourished within disabled athletics for
gifted and serious competitors.
During the past 30 years, disabled athletics has matured
into a nely structured group of organizations dedicated
to providing athletes of all disabilities with an equitable
playing eld for competition, while allowing individual
athletes the opportunity to rise through the ranks of com-
petition, depending on their athletic ability. Thanks to the
relentless efforts of a persistent few, disabled competitors
are beginning to enjoy the satisfaction of training, com-
peting, and receiving the recognition so richly deserved
yet frequently bestowed only on able-bodied athletes.
Only recently have a few disabled athletes found them-
selves featured in the sports section of newspapers, maga-
zines, and television. Unfortunately, the majority of
the media still regards these talented athletes as human
interest stories. This chapter provides a comprehensive
overview of the complexities and challenges of disabled
athletics, focusing on the enlightenment of rehabilitation
providers as possible advocates in a variety of capacities.
Most importantly, knowledgeable rehabilitation profes-
sionals can identify future disabled athletes and educate
other professionals about the world of disabled athletics
and the benets for those who choose to get involved.
Organizational Structure of Disabled
Athletic Events
The organizational structure of disabled athletic events
appears complex to newcomers to disabled athletics. In
most instances, the basic structure follows the same format
used for able-bodied amateur athletics, with one exception.
Because most DSOs arose to meet the needs of athletes
with similar disabilities, disabled athletics has historically
been governed by disability-specic organizations as
opposed to sport-specic organizations as in able-bodied
sports. For example, each of the eight DSOs offers track
and eld to its athletes; therefore, eight governing bodies
exist for rules, competitions, and medal criteria ( Table
28-1 ).
1
In contrast, in able-bodied sports in the United
States, all track and eld is governed by the national govern-
ing body (NGB), Track and Field USA.
Currently, many philosophic and structural changes are
occurring at all levels of disabled athletics. Some sports are
moving toward becoming entirely sport-specic with regard
to organizational structure, whereas other more complex
THE ATHLETE WITH DISABILITY
Duane G. Messner

Note: This chapter includes content from previous contributions by
Kathleen A. Curtis, PhD, PT, and Robert S. Gailey Jr., MSEd, PT, as it
appeared in the predecessor of this bookZachazewski JE, Magee DJ,
Quillen WS, editors: Athletic injuries and rehabilitation, Philadelphia,
1996, WB Saunders.

28
CHAPTER
sports are weighing the advantages and disadvantages
of such a change. The evolution of disabled sports has
been rapid and appears to be gaining momentum. The
organizational structure presented in this text will change
to some degree in the future, as will some of the organiza-
tions names, but the basic format will probably remain
the same.
The International Olympic Committee (IOC) presides
over all international Olympic-sanctioned sporting events
and governing bodies. The parallel organization for the
disabled is the International Paralympic Committee (IPC).
The IPCs primary responsibility is to sanction disabled
sporting events and act as a coordinating committee among
the host city of the Paralympic Games and the six interna-
tional DSOs (IDSOs), which are the Comite International
des Sports des Soudes, Cerebral Palsy International Sports
and Recreational Association, International Blind Sport
Association, International Stoke-Mandeville Wheelchair
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.
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
Archery
Basketball
Bocce
Bowling
Canoeing
Cross country
Cycling
Diving
Equestrian
Figure skating
Floor hockey
Goal ball
Gymnastics
Handball
Ice hockey
Judo
Nordic skiing
Poly hockey
Powerlifting
Racquetball
Road racing
Roller skating
Shooting
Slalom
Soccer
Softball
Speed skating
Swimming
Table tennis
Team handball
Tennis
Track and eld
Volleyball
Weight lifting
Wrestling
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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.
The Athlete with Disability CHAPTER 28 683
Sports Federation, International Sports Organization for the
Disabled, and International Sport Federation for Persons
with Mental Handicaps. Representation to the IDSOs is
granted to DSOs from all countries that meet the criteria for
membership. The IDSOs process information from partici-
pating countries and communicate directly to the IPC or the
hosting Paralympic Games city. Policy and international
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-
tees (NOCs) and international sports federations. The
United States Olympic Committee (USOC) is the NOC for
the United States and is the coordinating body for amateur
sports, with the primary purpose of preparing Olympic and
Pan American Games teams. The ve membership categories
within the USOC are group A, Olympic/Pan American
sports organizations, which includes the 42 NGBs for
each sport; group B, community-based multisport organiza-
tions, armed forces, and education-based multisport organi-
zations; group C, afliated sport organizations; group D,
state Olympic organizations; and group E, organizations of
sport for the disabled ( Figure 28-2 ).
The Committee on Sports for the Disabled currently
recognizes six DSOs: American Athletic Association for the
Deaf, Dwarf Athletic Association of America, United States
Cerebral Palsy Athletic Association, United States Associa-
tion for Blind Athletes, Wheelchair Sports USA (WSUSA),
and Disabled Sports USA. The United States Les Autres
Sports Association is currently not recognized by the USOC,
but the organization contributes signicantly to the disabled
sports movement. Each of the US DSOs has representation
to its respective international DSO as a voting member.
Classication of Athletes with Disabilities
Classication systems have existed almost as long as sports
for persons with disabilities. The systems are intended to
provide a means to ensure equitable competition, in which
ability and skills, not degree of physical disability, are the
variables among competitors. Accordingly, athletes of similar
levels of disability are grouped together in a class desig-
nated for competition. Individuals in the same class compete
against each other in individual sports, such as track and eld
or swimming. In team sports, athletes in various classes are
allowed to compete as a team only in prescribed combina-
tions, which serve to ensure that the most severely disabled
players will not be excluded from the sport.
Figure 28-1
Organizational Chart for the International Sports Organizations.
AAAD, American Athletic Association for the Deaf; CISS, Comit
International des Sports des Soudes; CP-ISRA, Cerebral Palsy
International Sports and Recreational Association; DAAA, Dwarf
Athletic Association of America; DSUSA, Disabled Sports USA; IBSA,
International Blind Sport Association; IOC, International Olympic
Committee; IPC, International Paralympic Committee; ISMWSF,
International Stoke-Mandeville Wheelchair Sports Federation; ISOD,
International Sports Organization for the Disabled; USABA, United
States Association for Blind Athletes; USCPAA, United States
Cerebral Palsy Athletic Association; USLASA, United States Les
Autres Sports Association; WSUSA, Wheelchair Sports USA.
(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.)

Traditionally, athlete classication was primarily a medi-
cal decision, based on the results of a physical examination
of such criteria as neurological function, degree of visual
decit, or length of residual limbs. There were inherent
problems in both the intent and the implementation of such
systems. These systems classied athletes within a disability
group for all sports in which they competed, regardless of
the relative advantage of having certain functions for a par-
ticular sport. For example, a sport such as wheelchair racing
requires considerably less trunk rotation for performance
than a sport such as wheelchair basketball. In addition, the
divisions between classes were arbitrary and did not reect
parallel increments in performance across all sports. Fur-
thermore, it became apparent that as DSOs such as WSUSA
tried to mix athletes with different disabilities in a classica-
tion system designed for spinal cordinjured athletes, the
system clearly favored certain athletes. Weiss and Curtis
2
studied the distribution of disabilities across nalists in each
class of competition at a national WSUSA multisport cham-
pionship. They found that a disproportionate number of
nalists were athletes with postpolio paralysis and athletes
with amputations compared with the number of athletes
with paraplegia and spina bida in the organization.
Athletes with cerebral palsy were also under-represented in
the nalist groups.
Classication systems in disabled sports provide equitable competition
when ability and skills are the variables for competition.
Classication Systems
For some of these reasons, athletes within a DSO were
prevented from competing against athletes from other DSOs,
as each DSO developed separate meets for its national cham-
pionships. At the world championship events, at which mul-
tiple DSOs represented various countries, amputees compet-
ing in wheelchairs had a different competition from paraplegics
in wheelchairs for each distance of a track meet. In the 1988
Seoul Paralympics, this division by classication and by dis-
ability group resulted in more than 40 different 100-meter
races being run. This was confusing and nonproductive for
meet organizers, athletes, and spectators.
Dissatisfaction with classication systems has been the
norm, rather than the exception, throughout the history of
sports for the disabled. In the mid-1980s, Horst Strohkendl
developed the rst classication system that was based on
observation of an athletes function during actual wheelchair
basketball competition rather than the athletes neurological
level.
3
Other sports have followed, in an effort to consolidate
athletes by classication in their sports rather than by their
disabilities. Sport-specic functional classication systems have
now been developed for track and eld, swimming, table ten-
nis, and shooting.
4
For example, between the 1988 and 1992
Paralympics, a 10-class function classication system for swim-
ming was implemented. This system combines cerebral palsy,
amputee, and wheelchair athletes who would have competed
in 25 classes in the 1992 Paralympic Games. The 10-class
system is intended to reduce the time and organizational
effort required to hold the competition. Despite the benets
of simplifying an athletic event, Richter and colleagues
5
argue
that this system lacks reliability and validity by integrating
disability groups and applying arbitrary criteria that disadvan-
tage certain disability groups. Classication systems are cur-
rently in ux and are expected to evolve further as a result
of the experiences in sport-specic functional classication.
Performance and degree of disability do not always show a
direct relationship. In 2009, the International Paralympic
Committee issued a position statement mandating the devel-
opment of evidence-based classication systems related to
health and functioning as advocated by the International
Classication of Functioning, Disability and Health (ICF),
and the use of selective sport classication.
6
To describe each
classication system currently used goes beyond the scope of
this chapter. Table 28-2 summarizes the various systems used
in some competitive sports.
Rehabilitation professionals and physicians have tradition-
ally been involved as classiers in most DSOs, because tradi-
tional classication involved physical examination and disabil-
ity assessment. These traditional observations still play a
part in some functional classication systems, but more
important now is the observation of athletic performance in
the sport. Thus the role of the classier in the era of functional
classication is to observe performance in sports competition.
Classication is frequently carried out by a team of classiers,
including medical personnel, sports technical experts, ath-
letes, and coaches. Physical therapists are particularly well
suited for this role because of their strengths in the observa-
tion of normal and abnormal movement.
Figure 28-2
Organizational chart for the National Organization Committees. The United States Olympic Committee
coordinates the ve organizations identied and reports to the International Olympic Committee.
Clinical Point
An ability of the classier to observe movement carefully during
functional performance is critical to the classication process.
Technical Assessment
Traditionally, a coach is responsible for the training of an ath-
lete, and the medical team plays a supportive role, responding
to injuries or implementing injury prevention programs.
Table 28-2
Classication Systems for Athletes with Disabilities
Organization Sport Classication System
DAAA, DSUSA, WSUSA, USABA, USABA,
USCPAA, USLASA
Alpine skiing 10 classications, based on type of ski equipment
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
classication 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
classication for breast-stroke, backstroke, and
freestyle
DSUSA, USLASA Table tennis (standing) 5-class system for standing athletes
DSUSA, WSUSA, USLASA Table tennis
(wheelchair)
5 seated classes based on upper extremity and trunk
function
DSUSA Track and eld
(amputees, standing) *
9-class system based on upper- vs. lower-extremity
involvement and level of amputation
DSUSA, WSUSA, USLASA Track and eld (wheel-
chair)
4 classes for track events; 7 seated classes for eld
events; 1 standing class for eld events
DSUSA, USLASA Volleyball (sitting) All players must sit
DSUSA Volleyball (standing) 8-class system; uses combined classication 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 eld and acuity

USCPAA All sports for
USCPAA

8-class system, based on level of function of
extremities and ambulatory status
USLASA All sports for
USLASA

6-class system, based on extremity and trunk
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 specic functional classications for wheelchair or ambulatory athletes.
Disabled athletes present a unique situation in which a grow-
ing number of therapists and other medical professionals have
become involved in the training process. One reason for their
involvement is that the coaching process of a disabled athlete
must include some knowledge in the following areas: sport
performance (the actual biomechanics of the event), pathology,
kinesiology, pathokinesiology, adaptive physiology, prosthetics
or orthotics, and motivational psychology. The criteria for
coaching the disabled athlete go well beyond those required to
coach an able-bodied athlete, in terms of assessing physical and
technical methods for performance enhancement.
Areas to Consider When Performing Movement
Analysis for Disabled Athletes
Physiological laws related to the neuromuscular and musculoskel-
etal systems
Mechanical laws based on Newtons Laws of Motion
Physical environmental and external conditions
Movements before and after the desired skill
Mechanical efciency of adaptive equipment
Identify performance enhancement methods
process can be either complex or general. In many cases, an
educated coach can visually observe the majority of biome-
chanical constraints that may hinder an athletes perfor-
mance. Often an in-depth quantitative analysis only conrms
what the coach has observed. The following is a brief outline
suggesting the major topic areas that should be considered
when performing a movement analysis:
The Physiological Laws That Relate
to the Neuromuscular and Musculoskeletal Systems
The athletes body size and weight, strength, range of
motion, muscular tone, limb length, sensation, balance,
coordination, agility, vision, hearing, endurance, and other
physiological considerations that may be inherent to the
type of disability or to the athletes current physical condi-
tion must be analyzed. For example, athletes with quadri-
plegia or paraplegia are able to maximize their performance
using different wheelchair strokes and trunk position as a
result of the level of disability and the motor function avail-
able. Likewise, many swimmers with various disabilities nd
the backstroke to be faster for them than the crawl stroke
and therefore choose the backstroke when competing in
freestyle events.
The Mechanical Laws Based on Newtons Laws
of Motion
The effects of physical laws such as gravity, friction, inertia,
and momentum should be examined, especially as they relate
to any physical compensation by an athlete. Likewise, me-
chanical advantages and disadvantages with regard to adaptive
devices should be explored to determine the best modication
for a particular athlete participating in a specic sport. Dis-
abled athletics has been the catalyst for numerous technical
advances as a result of modications developed by athletes.
The Physical Environment and External Conditions
The playing surface (e.g., concrete, grass, wood, or syn-
thetic surface) can have a tremendous effect on an athletes
performance. For example, a wheelchair racer may vary tire
pressure with different track surfaces such as asphalt or a
synthetic material. Every athlete must make important deci-
sions based on environmental and external conditions.
Another example would be a blind sprinter having the
option of a sighted guide or a caller who provides auditory
instruction to keep the athlete on line. In a noisy stadium,
a caller may not be possible or too confusing, and a sighted
guide would be mandatory.
The Movements Immediately Preceding
or Following the Desired Skill
As with any movement skill, all the components of that skill
build on each other and have a direct cause and effect. For
example, all throwing performances depend on the windup,
acceleration, release, and deceleration or follow-through
phases. No one phase acts independently of the others.
Two approaches to the analysis of biomechanical events
may be employed to study human movement. The rst is
the quantitative approach, which applies numerical values to
describe all movements. This method is the most explicit,
but it is complex, expensive, time consuming, and, for the
average athlete, unnecessary. In contrast, the qualitative ap-
proach describes movement in non-numerical terms using
observation, qualitative data, and applied physical principles
as the foundation for interpretations made by the observer.
Qualitative analysis is more easily employed than quantita-
tive analysis. Qualitative analysis can be performed simply
by general observation, memory of a performance, or use of
videotape. Obviously, videotaped recordings provide a more
accurate account of the movement being analyzed and can
be reviewed to verify the impressions of the observer.
7
The disability of the athlete adds another factor to the
equation when attempting to enhance athletic performance
and prevent injury. Each athlete presents with some form of
biomechanical restriction: either a physical limitation, such as
increased tone, weakened muscles, loss of range of motion,
or vision loss, or the need for an additional mechanical device
such as a wheelchair or prosthesis. A systematic assessment of
each component of the athletes sport must be made, as with
able-bodied athletes, yet the therapist or coach must now
take into consideration how each component of the skill be-
ing learned can be mastered by either physical or mechanical
compensation. This is the challenge put before all those who
work with disabled athletes, and that is what makes this work
so exciting and gratifying.
Regardless of the approachquantitative, qualitative, or
a combination of the twomovement analysis must be
performed in a systematic manner. The following is provided
to give some insight into the performance enhancement
process and the role that the medical professional can play.
Dene the Movement or Skill to Be Analyzed
Before any analysis of movement can begin, the specic
movement or skill to be analyzed must be dened. The
more specically the movement is dened, the greater the
chance of success. For example, if a track sprinter is being
analyzed, the rst question that would have to be asked is
what part of the sprint requires analysis? The start, mid-
distance, or nish? Once the phase of the sprint has been
determined, a host of sprinter components would have to
be identied and assessed for that phase ( Figure 28-3 ).
Identify the Biomechanical Principles
That Govern the Desired Movement or Skill
Once the component parts of the sprint have been identied,
the mechanical effects throughout the kinetic chain of the
sprinters body must be examined to determine the effect
one body segment has on another. The mechanical effects
can be the result of either internal or external inuence. This
Therefore, if a cerebral palsy athlete has increased tone in the
throwing arm (or anywhere throughout the body), one if
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
performance. Throwing the implement backward over the
shoulder or sideways over the head may help increase the arc
of motion during the acceleration or deceleration phase.
The Mechanical Efciency of Adaptive Equipment
Once all the aspects of movement analysis have been com-
pleted, the evaluation team must ask how an adaptive device
can provide a mechanical advantage to overcome a given limi-
tation. Historically, the majority of innovative adaptive devices
for disabled athletics have arisen through the efforts of dis-
abled athletes themselves. One of the most signicant advances
in recent years has beneted lower-extremity amputees. Pros-
thetic designs have been developed to maximize athletic per-
formance rather than just to facilitate walking. Contemporary
socket designs take muscular efciency into account, prosthetic
knees meet the superior cadence demands placed on them, and
newer foot materials and congurations optimize athletic
performance. The same can be said about wheelchairs, or-
thotic devices, and other adaptive innovations that have been
introduced in recent years. Despite these achievements, there
is still considerable room for improvement in this area.
Identify Performance-Enhancement Methods
Finally, after each of the component skills has been identi-
ed and the athletes current level of performance has been
evaluated, a program designed to improve the performance
must be outlined. For a disabled athlete, training, equip-
ment, and motivation are paramount when designing a
strategy to prepare for competition. Performance enhance-
ment in itself is a major topic of discussion. The following
is a brief overview of some considerations for planning a
training program for a disabled athlete:
Training Methods
Today there are as many different training programs for
athletes as there are successful athletes who would like to
share their secret to success. Many of these training meth-
ods are sound and well worth taking under advisement.
Coaches and medical professionals must consider the nature
of the athletes disability and what, if any, limitations must
be placed on the athlete to prevent injury or unnecessary
medical complications. Although few disabled athletes have
Figure 28-3
A model of the components of sprinting, divided into three phases: start, mid-distance, and nish.
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.)

activity restrictions, there are many athletes who will benet
from preventive measures when participating in sports or
training as outlined in Table 28-3 .
Once any precautions are identied, the disabled athlete
must begin a physical training program comparable to that of
any able-bodied athlete. Similar training principles apply when
Table 28-3
Injuries and Disability-Specic Medical Conditions of Athletes with Disabilities
Problem Prevention Treatment
Chronic overuse syndromes
(shoulder impingement,
tendonitis, bursitis, carpal
tunnel syndrome)
Taping, splinting, protective padding,
proper wheelchair positioning, good
technique
Rest; apply injury-specic principles of
care; selective strengthening, muscle
balancing, exibility; analysis of
technique
Overexertion (muscle strains) Warm-up and stretching; proper
conditioning and equipment
Rest; gradual progression of exercise
program
Falls, physical contact (sprains,
contusions)
Equipment safety; appropriate padding
for sport; appropriate sport-specic
spotting; qualied assistance/guides for
athletes
Apply injury-specic principles of care;
check for signs of fracture in athletes
without movement or sensation
Blisters Encourage callus formation; protective
taping, gloves, padding, cushioning;
adequate clothing
Apply injury-specic principles of care; be
aware of areas that lack sensation; make
prosthetic adjustments
Abrasions/lacerations Check equipment for sharp or abrasive
surfaces; wear protective clothing; use
cushions or towels in all transfers; use
mats on hard surfaces; camber
wheelchair wheels
Apply injury-specic principles of care; be
aware of areas that lack sensation
Decubitus ulcers and burns Adequate cushioning; proper weight
shifting; dry clothing; special precautions
for areas without sensation; skin
inspection; good nutrition and hygiene
Bed rest if necessary to remove all pres-
sure from a weight-bearing surface;
open wound care as necessary; check
equipment
Hyperthermia Minimize exposure to direct sun; provide
shade; wear adequate clothing for
insulation and maintain hydration; spray
externally with water; avoid hot and
humid conditions
Remove from ambient conditions; cool
immediately; seek medical assistance
Hypothermia Minimize exposure; wear adequate
clothing, keeping head covered;
maintain hydration; avoid exposure to
cold and wet conditions
Cover and seek medical assistance
Autonomic dysreexia Encourage regular bowel and bladder
habits in competitive situations
Lift to sitting position; search for source
of stimulus, usually full bladder or bowel;
attempt to relieve condition; this is a
medical emergency
Orthostatic hypotension Wear elastic stockings or corset supports;
avoid heat
Recline in wheelchair or on ground/bed;
encourage deep breathing
Seizures Avoid stress, dehydration, extremes of
temperatures, and fatigue
Protect head and keep airway open by jaw
thrust; avoid putting objects in the
mouth
Unexplained fever (often
urinary tract infections)
Drink uids; practice good hygiene for
self-catheterization
Seek medical treatment
Allergies (bee sting, drug) Notify medical personnel at competition
site of potential problem; be prepared
Seek medical treatment
Eye injuries Protective eyewear, goggles, safety glasses Apply injury-specic principles of care
selecting a strengthening, endurance, agility, speed, or any
other type of program. Often a brief biomechanical analysis
must be performed when creating a training program. If the
athlete cannot use a traditional weight-training apparatus
because of physical limitations, such as an inability to use
the hands to grip, alternative methods, such as securing the
Some athletes with disabilities self-treat serious injuries
rather than seeking medical assistance.
11 , 12
This may result
in reinjury and the progression to chronic disability. Their
training programs may also lack sufcient attention to
exibility and conditioning.
13
The sports rehabilitation
teams ability to intervene and prevent chronic soft tissue
changes, which increase further risk of injury, is of critical
importance.
The active socialization and actual physical activity
involved with sports participation may provide benets for
an individual with a disability. Active individuals with dis-
abilities have been reported to have fewer problems with
body image, a higher degree of physical function, and fewer
medical complications than members of the inactive
disabled population.
8 , 14 , 15
It is also important to look at the skills developed
through athletic participation. Athletics is an acceptable
way to reintegrate with the community. Through athletic
participation, there is a de-emphasis on the disability and
a focus on goal-oriented objectives and resources. Ath-
letic participation encourages the development of net-
working skills and interpersonal relationships that may be
Considerations for Planning a Training Program
for Disabled Athletes
Training method
Equipment enhancement
Clinical Point
It is very important to assess the individual athletes goals and pre-
injury performance level and design realistic programs accordingly
whether he or she is an able bodied or disabled athlete.
In addition, it is important to remember that disabled
individuals may have different experiences with the health
care system than their able-bodied counterparts. Their
access to the health care system has traditionally been
through rehabilitation medicine rather than sports medi-
cine. The goals of the health professionals who treat these
patients may vary from merely returning these individuals
to an everyday level of performance to returning them to an
elite athletic level.
Clinical Point
Injured disabled athletes should be seen as athletes with injuries who
also happen to have permanent disabilities rather than disabled
persons with injuries.
hand to the handle, may have to be employed. If environmen-
tal conditions such as poor weather prohibit a wheelchair
athlete from performing the necessary road work for cardio-
vascular endurance, a roller trainer may be used. In short, the
problem-solving process must continue with training as
it does with competition, placing as few limitations on the
athlete as possible.
Equipment Enhancement
As previously discussed, sport- and disability-specic adap-
tive equipment can enhance an athletes performance in a
number of ways. The selection and development of adaptive
equipment for an individual athlete should be a collective
decision, including the athlete, coach, therapist, orthotist,
prosthetist, or equipment manufacturer.
Motivation
The motivation of a disabled athlete is no different from the
motivation of an able-bodied athlete. As with all athletes,
the intrinsic desires that compel an individual to succeed
may vary, but the positive methods of motivation available
to coaches remain the same. A discussion of the various
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
success. It is important to keep in mind that success is not
always dened by winning.
Psychosocial Considerations
Sports involvement has been reported to have positive
effects on the physical conditioning and self-image of adults
with disabilities.
8
In fact, elite wheelchair athletes have psy-
chological proles that are similar to those of elite able-
bodied athletes.
9
An athlete with a disability is likely to
present similar challenges to medical professionals as an
able-bodied athlete, with a few exceptions.
Depending on the age at the onset of the disability and
the time since its onset, an athlete with a disability may still
be actively engaged in the various stages of the coping pro-
cess, such as denial, anger, or depression. Frustrations en-
countered in athletic competition or following an athletic
injury may compound already existing feelings of loss or
anger. An individuals ability to cope with outside stresses
may vary widely, depending on the nature of the disability
and the persons internal resources and social support
system. However, there is considerable evidence in the lit-
erature to support the premise that sports involvement
among adults with disabilities promotes improved self-
concepts and psychological well-being.
10
useful in work settings as well. An individual who partici-
pates in athletics becomes less dependent on society
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-
pline often carries over to educational and employment
endeavors.
16
Like their able-bodied counterparts, some individuals
with disabilities who participate in sports have substance
abuse problems with alcohol or drugs. Many athletes with
spinal cord injuries were initially injured in an alcohol- or
drug-related incident.
17
Sports medicine professionals who
work with athletes with disabilities need to be aware of the
signs and symptoms of substance abuse and know the
appropriate referrals to make.
Another segment of the population of athletes with dis-
abilities has various cognitive and sensory disorders. Ath-
letes who have sustained brain injuries sometimes exhibit
behavior that is difcult to understand. Any athlete who
becomes combative, abusive, or a danger to himself or her-
self or to other athletes should be removed to an area where
he or she can refocus and calm down, away from any over-
stimulation that might add to the problem. Athletes who
are unable to communicate verbally may use sign language
or communication boards. Although not all athletes
with disabilities are able to understand instructions, health
professionals should not address a companion or coach
instead of the athlete.
Common Injuries and Disability-Specic
Medical Problems of Athletes
with Disabilities
Preventive practices for disabled athletes are becoming a
growing concern among coaches and medical staff alike.
Coaches and athletes must be educated in proper warmup
techniques, including stretching, elevating core body tem-
perature, and sport-specic drills. Moreover, all athletes
should be required to wear or use the recommended safety
gear for every sport. Coaches and event organizers should
also be obligated to provide certied or skilled spotters,
sighted guides, or assistive personnel to ensure every
athletes safety during competition.
The health professional providing care to athletes with
disabilities needs to be aware of common injuries and con-
ditions that are inherent to certain disability groups. Table
28-3 provides information concerning prevention and treat-
ment of common injuries and medical problems of athletes
with disabilities. Table 28-4 presents the type and frequency
of commonly reported injuries sustained by wheelchair
athletes.
Table 28-4
Common Injuries of Wheelchair Athletes
128 Adult Athletes,
All Sports
11
(% of
291 Reported
Injuries)
90 Adult Athletes,
All Sports
18
(% of
346 Reported
Injuries)
69 Pediatric Track
Athletes
29
(% of
Athletes Reporting)
19 Elite Adult
Athletes
12
(% of 50
Reported Injuries)
Soft tissue injuries 33 32 34 52
Blisters 18 25 77 6
Lacerations/abrasions 17 27 38 24
Decubitus/pressure
areas
7 3 14 Not reported
Arthritis/joint
inammation
5 1.5 Not reported Not reported
Fractures 5 2 6 6
Head weakness/
numbness
5 Not reported Not reported Not reported
Bruises/contusions Not reported 8 41 10
Temperature
regulation disorders
3 Not reported 49 Not reported
Head injury/
concussion
2 2 Not reported Not reported
Dental injury 1 1 Not reported Not reported
Dislocation Not reported 1 Not reported Not reported
Eye injury Not reported 1 Not reported Not reported
Wheel burns Included with
lacerations
Not reported 71 Not reported
Other illness Not reported Not reported Not reported 2
Injuries to Athletes Who Compete in Wheelchairs
Athletes with disabilities experience athletic injuries related
to the specic risks and demands of their sport. Track, road
racing, and wheelchair basketball are among the highest-
risk sports for athletes who compete in wheelchairs.
11 , 18
Athletes who train more hours per week and for a longer
period generally report more injuries than those who have
a short-duration and less-intense training history.
11
The most common injuries to athletes competing in
wheelchairs are soft tissue injuries of the shoulder, elbow, and
wrist; abrasions and contusions of the arms and hands; and
blisters of the hands.
11 , 12
In addition, the spinal cordinjured
population may experience some unique problems, including
skin ulceration, temperature regulation disorders, and
delayed recognition of injuries in areas that lack sensation.
Soft Tissue Injuries of Upper Extremities
Both novice and veteran wheelchair athletes experience
chronic soft tissue problems of the upper extremities. Wheel-
chair basketball players often practice and play in excess of
15 to 20 hours per week during the basketball season. Elite
road racers frequently have training schedules that entail total
distances in excess of 100 miles per week. Propelling a wheel-
chair such distances requires specic repetitive upper extrem-
ity motion and therefore stresses the shoulder, elbow, and
wrist joints. Rotator cuff injuries, bicipital tendinitis, shoulder
impingement syndromes, lateral epicondylitis (tennis elbow),
radial extensor muscle tendinitis, and carpal tunnel syndrome
are common problems in wheelchair users.
11 , 19-23
The exces-
sive forces imposed by weightbearing and continuous shoul-
der use are implicated in the development of chronic shoulder
problems. Bayley and colleagues
24
reported shoulder intra-
articular pressures to be 2.5 times greater than arterial pres-
sure during wheelchair transfers. Impingement positioning is
also frequent in this population, which must frequently
engage in overhead activity, even to carry out daily activities.
25

Surgical decompression via acromioplasty has been reported
to be effective in relieving chronic shoulder pain.
26 , 27
In addi-
tion to chronic soft tissue problems, osteonecrosis of the
shoulder has been reported in wheelchair users.
28
Poor exibility may be a predisposing factor to the devel-
opment of chronic shoulder problems. Wheelchair pushing
stresses development of the chest, anterior shoulder, triceps,
and biceps muscles. Specic stretching must be done before
and after activity to emphasize exibility in shoulder exion,
extension, horizontal abduction, and external rotation
and to achieve full length of the triceps and biceps muscles,
because they are two-joint muscles.
Strength training should emphasize achieving balance at
the shoulder, specically strengthening of the posterior
shoulder, including the posterior deltoid, latissimus dorsi,
external rotators, rhomboids, and middle and lower trape-
zius muscles. Many chronic soft tissue injuries can be
prevented and managed by achieving such balance.
Athletes with chronic soft tissue problems of the shoulders
or elbows may benet from preventive use of ice after train-
ing. Preventive taping may also be useful with hand, wrist,
and elbow problems. The well-known principles of rest,
ice, compression, and elevation (RICE) apply to injuries
sustained by athletes who compete in wheelchairs. The use of
anti-inammatory medications is also of value in assisting
athletes with acute or chronic soft tissue problems. Stretching
and strengthening are essential to prevent reinjury.
Abrasions and Contusions
When athletes use equipment such as wheelchairs, they are
also at risk for accidental injury from incidental contact with
the wheelchair parts.
11 , 29
For example, athletes frequently
report friction burns of the inner arms from accidental con-
tact with the large tires during the downstroke in pushing a
racing wheelchair. Beginning athletes who are not using
equipment that is specic for sports may attempt to train in
wheelchairs with wheelchair brakes that are placed danger-
ously close to the wheelchair push rim. Traumatic injuries
of the thumb can easily result from a slip forward during
high-intensity pushing.
Simple preventive measures include protecting the upper
arm from accidental contact with wheelchair tires, wearing
gloves, and wearing a bicycle-type helmet to prevent head
injury in the event of collision. Many athletes nd it useful
to protect the upper arm with the elasticized top of an
athletic sock ( Figure 28-4 ). All wheelchair parts or sharp
surfaces that could accidentally result in a contact injury
should be removed or covered with protective foam.
Blisters
Blisters are a frequent problem for most wheelchair athletes.
Because the hands are used continuously for propulsion,
athletes may experience frequent problems with blisters of
the ngers and thumb from contact with the wheelchair
push rim. Thick calluses may develop on the palm of the
Figure 28-4
Wheelchair racers wear protection on the upper arms and use gloves.

hand; they can crack and result in painful ssures, open to
infection.
Hands should be cleaned frequently and calluses led
with a pumice stone. Open cracks or ssures, blisters, and
other abrasions should be managed with antibiotic creams
and covered with bandages or dressings, as appropriate.
Wheelchair athletes often develop symptoms of carpal tun-
nel syndrome from the repetitive trauma of wheelchair
propulsion, causing compression in the carpal tunnel
area.
11 , 30
Gloves are recommended for training and compe-
tition, but recent evidence questions their efcacy in
preventing carpal tunnel syndrome.
30
Any athlete with
symptoms of hand tingling or numbness should be referred
for evaluation for carpal tunnel syndrome.
Leather batting gloves or handball gloves are most easily
adapted and reinforced for wheelchair pushing, with layers
of tape applied to the areas of highest pressure. Custom-
designed leather mitts with reinforced neoprene use hook-
and-loop fasteners to keep the hand in a closed position,
creating a st, and are widely used in road racing. This
innovative glove design incorporates high-friction materials
and maximizes the force generated during contact with the
push rim. Because of the enhanced power available to the
athlete, stroke dynamics have changed, and wrist and elbow
injuries may decrease in frequency.
Lack of Protective Sensation
Spinal cord injury, multiple sclerosis, and other neurological
disorders interfere with the normal protection that pressure,
temperature, and pain sensation provide. Pressure points,
especially under sitting areas, may lead to skin breakdown,
ulceration, and infection. Insensitive skin must be inspected
frequently.
Any time there is persistent redness of the skin, that area
should have all pressure from sitting, clothes, or equipment
relieved until the redness resolves and normal skin color
returns. Otherwise, these areas may go on to ulcerate and
may progress to serious infections. Athletes with open pres-
sure sores should not participate in competition. Training
should cease, and the athlete should avoid sitting or any
position that may place him or her at risk for additional
pressure damage, until the area is completely healed.
Athletes with chronic pressure sore problems may need
customized seating systems that alleviate areas of pressure.
Wheelchair cushions can be modied to accommodate an
athletes individual needs. If an athlete has chronic prob-
lems caused by positioning in the sports wheelchair, he
or she should be referred to a physical or occupational
therapist for evaluation and recommendations for possible
adaptations.
Fractures account for less than 5% of all injuries sustained
by wheelchair athletes.
11
However, osteoporosis is fre-
quently associated with lower-extremity paralysis. As a
result, athletes may be susceptible to lower-extremity frac-
tures from relatively minor injuries. These fractures may go
unnoticed because of the lack of sensation that would nor-
mally accompany a bony fracture. Therefore, following any
injury, one must be aware of signs and symptoms such as
abnormal body position, bruising, edema, or grinding sen-
sations with movement. The athlete should be evaluated by
x-ray examination to rule out a fracture, as movement
of bony fragments may interfere with healing and cause
further damage to muscles and blood vessels.
By using such simple preventive techniques, athletes
who compete in wheelchairs can have safe and productive
competitive careers.
Injuries of Athletes Who Compete Standing
Athletes with disabilities who compete while standing rep-
resent a variety of physical disabilities and sports interests.
They often compete with disabilities such as upper and
lower extremity amputations, visual decits, and cerebral
palsy. These athletes do not appear to be at greater risk for
the common musculoskeletal problems associated with
sports participation in the general population.
13
Although
musculoskeletal problems may be no more frequent for
athletes with disabilities, disability-related problems are seen
among athletes who wear prostheses for running and ath-
letes who sustain falls and other accidental injuries second-
ary to their disabilities or the use of assistive devices.
Abrasions and Blisters to Bony Prominences
Within Prosthetic Socket
Many lower-extremity amputees run wearing prostheses.
Common problems are skin breakdown, bruising, abrasion,
blistering, skin rashes, and swelling on the residual limb,
within the prosthetic socket, after or during exercise. These
problems can sometimes be prevented by proper adjust-
ment of prosthetic t and alignment and prompt manage-
ment of developing skin lesions.
Common sites for these problems in below-knee ampu-
tees are the bula head, distal anterior end of the tibia,
distal end of the bula, medial and lateral femoral condyles,
over the patella, and over scar tissue and poorly healed skin.
Above-knee amputees may experience similar problems
over the pubic or ischial rami, over the ischial tuberosities,
at the distal lateral femur, over the greater trochanter, or
over sites of scar tissue or poor healing.
Depending on the nature of the injury or trauma sus-
tained, it may be appropriate to use a number of different
management strategies. For bruising and blisters, the athlete
can relieve friction by wearing additional (dry) stump socks
or foam pads, or by applying abrasion protection products
(e.g., Second Skin, Bioclusive, DuoDerm, Tegaderm, Ampu-
Balm) over soft tissue areas that commonly break down as
a result of continual friction. Unfortunately, in most cases
the application of foam or leather padding may cause total-
contact suction sockets to lose suction, and pistoning may
result.
Ideally, the pads are used prophylactically prior to the
event. However, often they are applied after a blister has
formed to permit continued participation. Use of these
protective pads must be monitored regularly, especially dur-
ing long-distance events, because once the inner silicone gel
dries out, the outer covering material can become a source
of irritation.
It may be appropriate to use rest, ice, and compression
and to decrease additional trauma to the limb through sup-
ported ambulation with crutches or a cane.
Compression Injuries
The absorption of ground reaction forces generated during
support-limb impact in able-bodied athletes is accomplished
by the mechanics of the foot-ankle complex, rotation of
long bones, exion of all lower-extremity joints, and insula-
tion of muscle. Amputee runners lack many, if not all, of
these shock-absorbing mechanisms and thus are prone to
many impact or compression injuries. All these injuries
are the result of the ground forces being transmitted to the
socket via the prosthetic pylon. Above- and below-knee
amputees often experience bruising over the bony promi-
nences listed previously. In addition, above-knee amputees
with ischial containment socket designs often complain of
excessive pressure from the medial wall.
Recurrent skin problems, bruising, or recurrent tendini-
tis should lead to suspicion of prosthetic malalignment or a
mistting socket. The prosthetist, coach, and athlete should
be able to work together to evaluate the athletes needs and
adjust or redesign an appropriate prosthesis. Modication
of the patella tendon bar for below-knee amputees or
modication of the height of the anterior or medial socket
wall for above-knee amputees may provide some relief from
compressive forces.
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
ssures 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
help prevent accidents. Wearing reective clothing at night,
running defensively when there are cars or bicycles present,
carrying identication that includes pertinent medical infor-
mation, and dressing appropriately for a workout will help
improve safety margins.
It is strongly recommended that athletes with disabilities
train with other athletes or groups who can provide com-
panionship, support, and an extra measure of safety. Volun-
teers who run with blind athletes especially must be able to
concentrate on obstacles and sudden environmental changes,
as well as individual athletic needs and performance.
Low Back Pain
Some athletes with disabilities also experience chronic low
back pain. Athletes with tightness of the hip exor muscles
often compensate with increased mobility in the lumbar
spine. Amputees often overuse the lumbar spine as a com-
pensatory mechanism. Because of the forces transmitted
through a rigid, unforgiving prosthesis, amputees, especially
above-knee amputees, must compensate for the lack of
lower-extremity joint exion with excessive lumbar spine
lateral exion and extension ( Figure 28-5 ). Greater lateral
lumbar exion is observed during early support, and
increased lumbar extension is observed during late support
Figure 28-5
Above-knee amputee sprinter.
as the maximal hip extension is being achieved. As a result
of daily ambulation and running, an imbalance in back mus-
culature, as well as a functional scoliosis, may be observed
in many amputees.
Muscle balancing, stretching, and traditional prophylac-
tic low back pain measures may be employed to assist an
athlete experiencing low back pain as the result of excessive
lumbar movement or hip exor tightness.
Bursitis
Rarely, amputees complain of bursa pain from socket irrita-
tion. On these occasions, below-knee amputees most fre-
quently experience prepatellar, infrapatellar, or pretibial
bursa pain. Above-knee amputees complain of ischial and
trochanteric bursitis. Bursitis, when it occurs in amputees, is
often the result of poor prosthetic t. Necessary prosthetic
modications should be made.
Knee Injuries
Athletes with cerebral palsy often show genu valgum and
mechanical instability at the knee. In addition, quadriceps
muscles may be spastic and tight. Even though knee insta-
bility and muscle imbalance may be present, it is not
clear that these predispose such athletes to a higher risk of
injury.
Below-knee and Syme amputees may be considered vul-
nerable to many more knee injuries than actually occur
because of the rigid lever constituted by the prosthesis.
Most socket designs bring the medial and lateral wall well
above the knee joint line, reducing the chance of collateral
ligament injury. In most cases, the residual limb pulls away
from the socket rather than being xed within the socket.
Jumping events such as the long jump put amputees at
the greatest risk of knee injury. Occasionally, hyperexten-
sion injuries occur as a result of the bodys forward momen-
tum over a xed prosthesis and residual limb.
Injuries to the Sound Limb
In amputee athletes, the sound limb often sustains injuries
as a result of the stresses endured by compensating for the
prosthetic limb. Frequently, chronic hamstring problems
arise as a result of the altered hip exion of both lower
extremities.
The sound limb foot also must adapt to the additional
weightbearing that is often associated with amputees who
hop on and use the sound limb more than the prosthetic
limb. Some individuals develop plantar fasciitis, stretched
plantar ligaments, or foot imbalances such as pronation
because of the additional abnormal forces.
Treatment of injuries to runners with disabilities should
follow the same principles and guidelines that apply to able-
bodied and sighted runners. RICE, sport orthotics, athletic
taping, and sports rehabilitation are all effective techniques
for treating the musculoskeletal problems of runners with
disabilities.
Injuries to the Upper Extremities in Crutch Users
Some lower-extremity amputees prefer to compete with-
out a prosthesis, using crutches to assist in their mobility.
As with all crutch users, care must be taken to avoid hand
and wrist injuries such as carpal tunnel problems at the
wrist and neurovascular compression at the axilla. Ath-
letes who use crutches should be encouraged to use and
frequently replace rubber padding on hand grips and
under axillae.
Energy Requirements for Amputee Runners
The metabolic cost of ambulation has been well docu-
mented as being 15% to 30% higher for transtibial ampu-
tees while walking at a pace 10% to 40% slower than
nonamputees
31-38
and 40% to 65% higher for transfemoral
amputees who ambulate at a pace 15% to 50% slower than
nonamputees.
38-41
The discrepancy in metabolic cost of
ambulation is directly related to age, cause of amputation,
length of residual limb, and prosthetic design.
38 , 42 , 43
To
date, no studies have been published examining the meta-
bolic cost of amputee running, but it appears that a
considerable physiological demand is placed on amputee
runners for several reasons. In addition to the reasons
previously stated, alteration of the normal kinematics of
the running gait, such as a transfemoral amputees inabil-
ity to ex the prosthetic knee during stance or the lack of
normal foot-ankle motions, increases the physiological
demands.
44-48
There are also kinetic and musculoskeletal
disadvantages, such as the fact that an amputees knee
musculature absorbs only 1.4 times as much energy as it
generates, compared with 3.6 times as much for a nonam-
putee jogger.
44 , 46
Increased demands are placed on the
sound limb as well; for example, the sound limb is respon-
sible for approximately 90% of the total energy generated
during running.
44
The loss of the amputated limb also
decreases the total body surface area available for physio-
logical thermoregulation for cooling the body.
For Amputee Athletes
Metabolic costs are greater
Physiological demands are greater
Greater stress is placed on the sound limb (both biomechanically
and physiologically)
Collectively, all these inuences can increase the physio-
logical demands placed on an amputee runner and result in
greater fatigue, potential hyperthermia, and injuries related
to musculoskeletal imbalances. Hyperthermia is rarely a
problem in running events, because 1500 meters is the
longest distance permitted in international amputee track
competition. However, there are a few amputee marathon
runners and a great number of cyclists who could be at risk
for developing hyperthermia.
Rehabilitation of Sports Injuries
The rehabilitative management of disabled athletes is similar
to that of any other athlete. The rehabilitation must be a
comprehensive program designed to return the disabled
athlete to his or her sport with the greatest degree of func-
tion and in the shortest time possible. Just as an able-bodied
athletes program must be progressive and functional, so
must a disabled athletes rehabilitation program. Therefore,
a general rehabilitation program should include warm-up,
strengthening, exibility, coordination, proprioception,
balance, speed, agility, and muscular and cardiovascular
endurance and conclude with a cool-down period. Some
exercises may have to be adapted to meet the needs of the
individual athlete.
One such adaptation is for cardiorespiratory endurance
training. Athletes with sympathetic nervous system involve-
ment, such as individuals with neurological lesions above
T4, have diminished heart rate and blood pressure re-
sponses to exercise. This diminished sympathetic response
limits the use of heart rate and blood pressure as effective
indicators of exercise intensity. Age-adjusted formulas for
calculating target heart rates cannot be used easily with this
population. Therefore, exercise prescriptions for these ath-
letes may include parameters of speed, duration, frequency,
or mechanical resistance rather than using a target heart rate
to vary intensity.
Education and Injury Prevention
Educating athletes as to the most effective means of preven-
tion is an important task for both coaching and sports
medicine staff. Common-sense coaching and sports medi-
cine techniques; familiarization with the disability by the
athlete, coach, and volunteers; planned workouts; and con-
sideration of safety can help prevent injuries, minimize risks,
and ensure success.
Disability-Specic Medical Problems
In addition to injuries, pre-existing medical conditions, the
requirements of sport participation, and environmental
conditions expose athletes with disabilities to the risk of
specic medical problems.
Temperature Regulation Disorders
Exposure to heat and cold often provides unique challenges
to an athlete with a disability.
49
The athlete may be intoler-
ant to conditions that would not particularly trouble an
able-bodied athlete, because of sensory impairments, sym-
pathetic nervous system dysfunction, and inadequate body
mechanisms for cooling or warming. In addition, specic
medications (tranquilizers, diuretics, sedative-hypnotics, al-
cohol, sympathomimetics, anticholinergics, and thyroid re-
placement drugs) predispose an athlete to problems with
temperature regulation.
Clinical Caution
For disabled athletes with neurological lesions above T4, diminished
sympathetic response limits heart rate and blood pressure use as
effective indications of exercise intensity.
It is also important to note that an athlete with a dis-
ability is often unable to rest an injury completely because
of the demands for continued daily function. For exam-
ple, a wheelchair athlete who sustains a shoulder injury is
unable to rest because demands of everyday mobility
require the use of the shoulder joint. An amputee who
injures the sound limb will have increased difculty with
ambulation if the prosthetic limb becomes the dominant
limb. To regain the ability to perform everyday tasks, the
temptation to increase the use of the injured extremity
prematurely may increase recovery time and the risk of
injury. Alternatives to daily activities, rehabilitation, and
training methods designed to reduce the risk of insult to
the injured limb should be explored by the physical
therapist and athlete.
Clinical Point
Thermal injuries and temperature regulation are common problems
in all athletes with disabilities.
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
have impaired circulation, with a tendency to develop swell-
ing of their feet, because their muscles do not assist in ve-
nous return. There is also a relatively lower blood ow to
the skin and deep tissues. This makes the limb more suscep-
tible to sunburn or frostbite, and even lesser degrees of heat
or cold may cause serious deep tissue damage.
In addition, in spinal cord injury and in multiple sclero-
sis, there are problems with regulation of core body tem-
perature caused by a loss of normal blood ow regulation
via the central nervous system. Athletes with quadriplegia
often report heat and cold intolerance.
11
This is com-
pounded by an inability to sweat below the level of a spinal
cord injury. Many medications used for pain, depression,
allergy, bladder dysfunction, high blood pressure, and other
problems also interfere with normal sweating.
Hypothermia
Tolerance to cold is affected by an athletes level of physical
tness, percentage of body fat, wind, and water immersion.
There are adverse effects on athletic performance if the
bodys core temperature drops. Early symptoms of hypo-
thermia include weakness, fatigue, clumsy movements, slur-
ring speech, and a decreased shivering response. Later
symptoms are collapse and unconsciousness. Hypothermia
is potentially serious, or even fatal, because it may result in
cardiac arrhythmias and dysfunction of other body sys-
tems.
50
The risk of hypothermia is greatly increased by
exercising in extremely cold weather, especially if there is a
high windchill factor or the athlete does not pay attention
to skin and clothes wetness.
An athlete who has had a spinal cord injury (usually
competing in a wheelchair or sit-ski) may not have sensation
below the level of the neurological lesion to feel cold
extremities. In addition, normal mechanisms of piloerection
(goose bumps), shivering, and circulatory shunting for
warming may not take place. This is especially a problem
when it is both cold and wet. Even temperatures at ap-
proximately 50F (10C) may be a problem for an athlete
with a spinal cord injury above the midthoracic level.
49
The following general principles apply to prevent hypo-
thermia in an athlete with a disability. Protective clothing
should be worn whenever possible, and the clothing should
keep the athlete comfortable during the activity. Multiple
layers of clothes should be used to take advantage of air
trapped between the layers. The innermost layer should
carry moisture away from the body, as cooling occurs more
rapidly if the skin surface is wet. Polypropylene and cotton
are recommended materials. In addition, the head should
be covered to prevent heat loss, because as much as 25% of
heat loss can occur from the head especially if it is uncov-
ered. Wearing hats and helmets when training or competing
in cold weather is essential to maintain body temperature.
Athletes should be encouraged to drink adequate uids.
Thirst is an unreliable indicator of the state of hydration,
and athletes may become as quickly dehydrated in cold,
dry climates as in hot climates. Water is lost with hard
breathing and perspiration under cold conditions as well as
hot conditions.
Those athletes who are predisposed to cold intolerance
should take special precautions during training and com-
petition. Athletes with a past history of cold injury
(e.g., frostbite) may suffer further trauma. Older athletes
may have poorer circulation to the extremities and may be
subject to greater intolerance to cold. In addition, an
athlete who has a communication or cognitive disorder
may not be able to communicate symptoms of cold intol-
erance readily. Special attention must be given to making
sure that these athletes are well supervised to recognize
potential problems.
Special attention should be given to awareness of environ-
mental conditions (e.g., windchill factor, wet conditions),
wearing appropriate clothing and head covering, hydration,
and training intensity and duration. After training or compe-
tition, the athlete should go to a warm, dry environment
and remove cold or wet garments and dress in warm, dry
garments so that there is no postexercise lowering of the
body temperature. Supercial frostbite can be treated by
placing the affected area under a warmer body part or by
blowing warm air onto the body part.
50
The most effective
treatment for an athlete with hypothermia is medically super-
vised rewarming by using thermal blankets, intravenous uid
replacement, and warm baths. Hypothermia can be a
life-threatening condition, requiring prompt medical atten-
tion.
51
The principles of treating a hypothermic athlete
with a disability are essentially the same as for treating ath-
letes without disabilities, with added awareness of the possi-
bility of pre-existing sensory and autonomic nervous system
dysfunction.
Hyperthermia
Intolerance to heat is exacerbated by the environmental
temperature and humidity. Mild symptoms of heat illness
are characterized by muscle cramps after exercising in the
heat. More severe heat illness results in heat exhaustion, and
the athlete may complain of headache, nausea, vomiting,
lightheadedness, weakness, cramps, and general malaise.
Most severe is heatstroke, in which the athletes body tem-
perature may rise dangerously high. The athletes perfor-
mance will deteriorate, and he or she may become confused
and disoriented and may faint. He or she may not sweat
normally and may experience personality changes. This ath-
lete is at risk for multiple organ damage, which can be
prevented with quick treatment.
Athletes with disabilities should exercise extreme cau-
tion when high temperatures are accompanied by high
humidity. High humidity prevents cooling of the body by
normal sweating. High ambient temperatures do not allow
for heat dissipation from the body to the environment. In
warm climates, under these conditions, athletes and
coaches should plan training and competitions in the early
morning or evening hours to prevent exposure to peak
heat conditions.
Clothing should be worn to provide shade and hold
moisture for heat loss. Light clothing, in light colors, with
breathable bers are the best attire for exercise in very
hot conditions. Disabled athletes should be encouraged to
wear shirts and clothing designed to act as a sunscreen,
instead of removing them in hot conditions, because of the
added protection. Clothing can provide protection from
the suns rays as well as assist with cooling by holding mois-
ture close to the skin.
Sunscreens should be used whenever athletes will be ex-
posed to the sun. An athlete with a spinal cord injury may
have a particularly increased risk of sunburn in areas without
sensation because of circulatory changes. Although sunscreens
are helpful in protecting against sunburn, water-resistant
sunscreens can also make the athlete more susceptible to heat
intolerance by impeding perspiration. Thus, care should be
taken to cover only those areas exposed to the sun, especially
in athletes who may not perspire normally.
Athletes with disabilities sometimes lack physiological
mechanisms for cooling. Athletes with spinal cord injuries
(especially quadriplegia) and others with neurological dys-
function above the level of the rst thoracic segment (T1)
are particularly susceptible to heat intolerance. These ath-
letes do not sweat below the level of the neurological lesion
and therefore cannot lower their body temperature by this
form of heat exchange.
Close monitoring and preventive measures, such as
spraying the surface of the face, neck, upper trunk, and arms
with water from a spray bottle, should be routine. Although
there is no evidence that spraying with water lowers the
core temperature of normal athletes, the experience of spi-
nal cordinjured athletes seems to support that this is a
useful practice. Even more important, however, is staying
out of the sun and wearing protective clothing.
Special attention should be paid during eld event
competition, which may involve hours of waiting in hot,
sunny conditions. Athletes should be encouraged to rest in
shaded, cooler, well-ventilated areas prior to and following
competition.
Athletes who have medical conditions that predispose
them to heat intolerance should be closely monitored.
Older athletes and young children may also experience
more severe problems. In addition, athletes with heart dis-
ease, diabetes, high blood pressure, and sweat gland dys-
function may have a higher incidence of heat illness. Of
course, any athlete who has an acute problem such as an
infection, nausea, vomiting, fever, diarrhea, fatigue, or pre-
existing dehydration may be particularly intolerant to the
heat. These individuals should refrain from training and
competition until the acute condition improves. Close
monitoring of clothing, uid intake, and body temperature
is essential to the safe participation of high-risk athletes in
extreme environmental conditions.
Any athlete showing signs of heat intolerance should be
removed to a shaded, cool, well-ventilated area and treated
for heat illness. Any athlete displaying headache, lighthead-
edness, or general malaise in the heat should discontinue
exercise and be taken to a shaded, well-ventilated area.
Medical attention is essential to cool the athlete as quickly
as possible. Fluid replacement and cooling at the neck,
groin, and armpits are often adequate to reverse symptoms,
although more extensive treatment may be indicated.
Athletes who have communication or cognitive disorders
may not communicate symptoms of heat intolerance readily.
Special attention must be given to making sure that these
athletes are well supervised to recognize potential prob-
lems. Fluid replacement should be offered frequently
by coaches or staff to all cognitively impaired athletes to
prevent heat illness.
Hydration
Thirst is an unreliable indicator of the state of hydration.
Athletes should be encouraged to drink water continually,
regardless of thirst, and to avoid salt tablets and undiluted
electrolyte solutions. Athletes should drink at least 1 liter
(approximately a quart) of water 1 to 2 hours before com-
petition or training and half a liter (16 oz or 500 cc) of
water 15 to 30 minutes before the event. Fluid replacement
should continue at a rate of at least 400 to 500 cc (13 to
16 oz) every 15 to 30 minutes during training or competi-
tion. Following practice or competition, the athlete should
continue with 1 to 2 liters (0.3 to 0.5 gallons) of uid.
51
Cool (4555F or 7.212.8C) water is the best
form of uid replacement for events lasting less than
1 hour, as they tend to be more rapidly absorbed than
warm water.
51
Glucose and electrolyte solutions and car-
bohydrate polymer solutions may be benecial in events
lasting more than 1 hour, as they delay the onset of
fatigue. Solutions should be of a concentration of less
than 10%; a concentration of 6% to 8% is ideal. If an ath-
lete drinks electrolyte solutions or sweetened drinks, he or
she should be sure that the drink is well diluted or should
drink an equal amount of water. Alcoholic beverages and
caffeine-containing beverages should be avoided because
they cause further dehydration.
Certain athletes with developmental disabilities may not
be able to reliably monitor their own uid intake. Coaches
should be especially cognizant of the uid needs of this
population of cognitively impaired athletes. It may be help-
ful to monitor the athletes weight daily in hot conditions
and increase uid replacement accordingly. Any change in
weight greater than 2% daily may indicate dehydration and
should be treated accordingly.
Some athletes with disabilities restrict water intake
because of bladder incontinence. Coaches need to ensure
that athletes have access to adequate bathroom facilities
rather than risk heatstroke caused by poor uid intake in
hot weather.
Bladder Dysfunction
Athletes with neurological disorders such as spinal cord in-
jury or multiple sclerosis often have a neurogenic bladder.
Because the bladder does not always empty properly or
completely, bladder infections, bladder stones, and bladder
obstruction are common to wheelchair athletes with neuro-
genic bladder.
Those who have indwelling catheters to drain the blad-
der and, to a lesser degree, those who use catheters to drain
the bladder on an intermittent schedule usually have fre-
quent, if not constant, bacteria in their urine. When bacteria
invade the bladder wall, the infection can spread into the
kidneys and blood stream, causing severe illness and death.
Therefore, any infection needs prompt treatment with
Autonomic dysreexia is a medical emergency. The
individual should assume or remain in a sitting position if
possible to minimize blood pressure changes. The bladder
should be emptied and the bowel evacuated; the condi-
tion should then be re-evaluated. Immediate medical
intervention should follow if the hypertension has not
resolved.
Recent studies have revealed that many elite wheelchair
athletes with quadriplegia routinely self-induce autonomic
dysreexia to increase sympathetic outow and improve
performance during competition.
52 , 53
With autonomic dys-
reexia, the athlete experiences uncontrollably high hyper-
tension, which may lead to cerebral hemorrhage and death.
Boosting via clamping a catheter or inducing a painful
stimulus is a dangerous and foolhardy practice and should
be discouraged among all athletes.
Blood Flow
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
be increased by generalized increased blood ow with exer-
cise or prolonged sitting with straps around the legs or
trunk. If blood ow is obstructed, there may be problems
with venous return and development of thrombophlebitis.
Persistent swelling in a leg that does not get better with
elevation may indicate thrombophlebitis, although symp-
toms usually occur without warning. Fragments of the
thrombus may break off, resulting in pulmonary embolus,
often a life-threatening complication.
Edema should resolve with elevation of the extremities.
Redness or heat in the area can signify a serious problem.
Edema of the lower extremities should be treated by re-
moving obstructive straps and reclining and elevating the
limbs above the heart. Individuals with persistent edema
with signs of inammation should be properly evaluated
for infectious processes or thrombophlebitis and treated
appropriately.
Dysphagia
Athletes with cerebral palsy sometimes present with dyspha-
gia or difculty swallowing. An athlete with dysphagia may
drool saliva from the mouth, which can cause a great deal
of uid loss. In addition, an athlete who has difculty swal-
lowing may choke on water or soft drinks.
Because an athlete with dysphagia is at risk for losing
uids by drooling, coaches and supportive personnel should
ensure that the athlete has access to uids that are easy to
swallow and that straws are available. Generally, athletes
with dysphagia are able to swallow frequent small amounts
of thicker liquids, such as juices, more easily than water.
Because dehydration may be a problem, avoiding exposure
to the sun is also important.
antibiotics. Athletes should refrain from competition and
training for at least 8 hours after the initiation of antibiotic
treatment and should be without a fever for at least
24 hours before resuming participation.
To prevent recurrent bladder infection, athletes should
ensure adequate uid intake to ush the bladder regularly.
They must also have access to clean areas to allow good
technique to avoid contamination during the handling and
use of catheters and connecting tubing and bags.
If catheter tubing becomes blocked, the athlete may
develop a bladder obstruction and be unable to urinate.
Bladder obstruction can obstruct blood ow back to the
heart by pressure on the inferior vena cava, or cause abnor-
mally high blood pressure by stimulation of reex activity.
If bladder obstruction precipitates autonomic dysreexia,
blood pressure can rise dangerously high and even cause a
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-
bate these problems.
Hypotension
Wheelchair athletes with multiple sclerosis and spinal cord
injury may experience hypotension with rapid position
changes, caused by the inability of the sympathetic nervous
system to accommodate for a rapidly shifting blood volume.
Infections from pressure sores may also cause pressure drop.
Pain, antispasticity, antiseizure, and bladder and bowel
medications may all affect blood pressure regulation. This
may cause problems in endurance activities and even lead to
lightheadedness or fainting.
If an athlete in a wheelchair experiences lightheadedness
caused by hypotension, the individual should be helped into
a recumbent position or the wheelchair should be tipped
back. These maneuvers will help increase venous return.
Gentle pressure on the abdomen with deep breathing may
also be helpful. If problems with lightheadedness continue,
the athlete should be referred to a physician for evaluation
of the problem.
Hypertension
Autonomic dysreexia is a serious problem of spinal
cordinjured athletes whose lesions are above the midtho-
racic level. This reexive process, causing massive sympa-
thetic outow, often begins from an obstruction of bowel
or bladder.
Clinical Caution
Any spinal cordinjured athlete with sudden hypertension or pounding
headache should be suspected of having autonomic dysreexia.
Dysarthria
Dysarthria, or difculty controlling the oral and vocal mus-
culature to speak, may be seen in the cerebral palsy and
brain-injured populations. Although many athletes have
both dysphagia and dysarthria, the two conditions are not
always present together. An athlete with dysarthria may not
be able to express his or her needs quickly or in a way that
is easy to understand. Health professionals should be care-
ful not to assume, however, that expressive problems also
mean that the athlete does not understand. They should
take the time to communicate simply and directly. It
may help to speak clearly and slowly, using simple, direct
instructions.
Aphasia
Brain-injured athletes and a small percentage of cerebral
palsy athletes may present with aphasia. This is a problem
either in receiving and processing the verbal information
presented (usually uent aphasia) or in formulating a verbal
message to be expressed (usually nonuent aphasia).
It may be helpful to use writing or gestures to commu-
nicate if there is a language problem. Those with signicant
communication problems may need to communicate
through a coach. Always use direct communication with the
athlete rst, before communicating through another per-
son. Athletes with pre-existing medical problems should
carry written instructions or wear Medic-Alert bracelets at
all times in the event that a coach or team member is not
present and an emergency arises.
Behavioral Problems
With the overstimulation of athletic competition, some
brain-injured athletes may become agitated, excited, or
occasionally hostile or abusive. Specic intervention tech-
niques to remove the athlete from the situation and redirect
his or her attention may help reduce distress. It may be
helpful to isolate the athlete from the stimulus in a medical
tent or other quiet area. Attempting to reason, argue, or
debate may only make the situation worse and provoke a
more agitated response. It is usually helpful to redirect the
athletes attention.
Seizure Disorders
Some cerebral palsy athletes have a history of seizure disor-
ders. Seizures do not often occur during sports competition
because the state of metabolic acidosis that frequently
accompanies hypoxia stabilizes neuronal membranes. The
most likely time for a seizure to occur is during travel and
other times of stress, dehydration, and extremes of tem-
perature. Seizure activity should be suspected following a
syncopal episode in which there is no other explanation.
Routine safety measures apply during seizure activity to
protect the head and airway. Following the seizure or in the
postictal period, it is important to do a neurological exami-
nation to look for decits, signs of head injury, contusions,
or neck pain. The athlete may be confused and should be
encouraged to rest. Hospitalization is required only if the
seizure activity is new or different from that experienced
previously. A coach or other responsible party should, how-
ever, check the athletes responsiveness every 2 hours for
the rst 24 hours.
A medication history and schedule should be reviewed,
as athletes often forget to take seizure medications such as
phenytoin (Dilantin), carbamazepine (Tegretol), or pheno-
barbital in the excitement of travel and competition.
Fatigue and dehydration may also precipitate the onset of
seizure activity and may need to be addressed.
Considerations for Travel
with Disabled Athletes
There are numerous areas in which sports medicine applies
to athletes and teams that are traveling for competition.
A medical staff member with a group of athletes with dis-
abilities has many signicant roles in the pretrip planning, as
well as providing services during the competition.
Pretrip Health Screening and Emergency
Contact Information
Athletes should complete forms that include current name
and address, physicians name and address, emergency con-
tacts, insurance coverage, past medical history, a list of cur-
rent medications, and current medical problems. Some
organizations and teams require that athletes have a physical
examination within 3 to 6 months of departure. It is also
important to have a mechanism to ensure that other medi-
cal problems have not developed in the interim between
sending in the medical information and the departure date.
Infections, pressure sores, traumatic injuries, seizures, or
hospitalizations that have occurred in this interim period
require attention by the medical staff to determine the cur-
rent stability of the athletes condition and his or her tness
for travel and competition.
Education on Doping for International Competitions
Athletes with disabilities are subject to the same antidoping
regulations as able-bodied athletes, regardless of their medi-
cal problems. Athletes need to be educated about banned
over-the-counter and prescription medications. In the United
States, if an athlete is taking a medication that is banned,
the athlete needs to call the USOC Drug Hotline (1-800-
233-0393) in Colorado Springs, Colorado to discuss alterna-
tives. The athlete then needs to consult with the athletes
physician to determine which nonbanned medications could
be substituted. Athletes with disabilities must be especially
careful, because even traces of prescription medications such
as sympathomimetics, antihypertensives, diuretics, cortico-
steroids, or pain medications routinely prescribed in the
management of their chronic medical conditions may
result in a positive drug test. It is critical that alternative non-
banned medications be prescribed well in advance of the
competition, as some banned medications can be detected in
the urine as long as several months after the last dose was
taken. It is also important to remember that all over-the-
counter medications and prescription medications that the
medical team brings should meet the USOC or SMSCC
guidelines as well.
Pretrip Information and Planning
Athletes who are traveling must bring sufcient medications
and supplies, such as catheters and gloves, for their care for
the duration of the trip. This needs to be emphasized in
writing to all athletes, as medications, services, and supplies
are often difcult to nd in other countries. State Depart-
ment and Centers for Disease Control advisories for pretrip
immunizations should be followed. Athletes and staff must
receive this information several months prior to departure,
in many cases, to achieve desired immunity.
Jet Lag Education
Athletes traveling through several time zones often expe-
rience problems with eating and sleep cycles because of
the abrupt time change. These changes can affect perfor-
mance dramatically. To minimize changes, athletes are
encouraged to change watches to the destination time
zone immediately on departure. They are encouraged to
sleep and wake at a time appropriate for the destination.
Meals should also be adjusted accordingly. Athletes are
encouraged to stay well hydrated and to use natural light,
rather than stimulants such as caffeine, to assist in staying
awake during the day in the new time zone. Sleep cycles
should remain at 6 to 8 hours, and athletes should avoid
the temptation to take long naps during midday. Alcohol
should be avoided during the trip because of its depres-
sant and diuretic effects.
Attention to Hydration and Nutrition
Outside North America
Athletes may not tolerate all food and water in other coun-
tries, and water and food may not meet standards of sanita-
tion. Unlabeled water sources, in particular, may not be safe
for consumption. It is important to provide a clean water
source for the athletes hydration needs, which may mean
that the team must immediately purchase cases of bottled
water to be kept in the housing area and brought to
the competition site. Athletes should be aware of when it is
essential to drink bottled water and to be cautious about
food choices. Food from street vendors in any country
should be avoided. Ice made from contaminated water is
often overlooked and may cause serious gastrointestinal
problems when added to bottled water.
Athlete nutrition may suffer from changes in diet. With
decreased protein intake, immune system function may be
compromised.
54
It is a good idea to advise athletes to bring
a supply of high-protein food sources from home for emer-
gencies and for supplementation of the local diet. Choices
such as nuts, trail mix, peanut butter, cans of tuna sh, and
small packages of cereal may provide protein to supplement
the diet at the competition site.
Equipment for Travel
Medical staff who are traveling with groups of athletes with
disabilities should bring a well-stocked trainers bag, includ-
ing rst-aid supplies and emergency equipment ( Box 28-1 ).
It is helpful to have electrical stimulation and ultrasound
units that are battery operated, can be recharged, or run on
local current. Because voltages (and wall plugs) often vary,
staff should be prepared with a variety of adapters and con-
verters. It is often easier to use a battery-operated unit and
bring a supply of batteries.
Foreign Facilities
It is important to remember that the facilities for treating
athletes or acquiring ice in other countries may be quite
different from those at home. A treatment room may not
be available, and a medical staff person must sometimes
improvise by providing treatment on the team bus, in the
athletes room, or on a bench at a sport venue. Ice is fre-
quently not as available as it is in North America.
The medical staff must be aware of the mechanism for
managing a serious injury or problem. Emergency services
and contacts should be established, and the local hospital
identied. Local organizers should provide emergency sys-
tems access at competition sites and a mechanism for doing
so at the housing site as well. In cases of severe injury or
illness, the US or Canadian consulate may be able to assist
with information on local resources to provide appropriate
care to injured or ill athletes.
Injury Management Principles
Serious Injuries
Serious injuries or illnesses may require hospitalization. It is
important to remember that medical personnel are not usu-
ally licensed to practice in other countries. Plans for trans-
port of injured or ill athletes should be established early.
An athlete who is seriously ill in a foreign country is often
hospitalized in an environment where he or she may not
speak the same language and the standards for treatment
any circumstances. Injuries that may become worse with
continued physical activity should be identied. Athletes
and coaching staff should be educated about the serious
sequelae of continued activity. Medical staff members should
enforce precautions and activity restrictions as needed and
look to the team administrative leaders for support of those
recommendations.
Organization of Disabled Athletic Events
The logistics of hosting and organizing an event for dis-
abled athletes is an enormous task. The process of organiz-
ing an event is not a topic specic to this chapter, but clini-
cians are frequently asked to assume many roles when they
become involved with event organizing committees. Most
commonly, they are asked to provide medical coverage or,
if certied as a classier, to classify athletes or assume the
role of a technical consultant. Boxes 28-2, 28-3, and 28-4
list the specic needs of organizing, medical, and classica-
tion committees, respectively.
Conclusion
The past 30 years have shown signicant advancements in
sport for disabled athletes. The scope of this progress can be
attributed to many organizations.
Newer methods of teaching adaptive sports have spread
through activities ranging from alpine skiing to shooting,
cycling, horseback riding, and shing. In the United States,
the inclusion of persons with disabilities in this variety of
activities can be attributed to organizations such as Profes-
sional Ski Instructors of America, US Tennis, US Sailing,
Box 28-1 Suggested Items for First-Aid Kit
for Travel with Disabled Athletic Teams
Scissors: 7-inch tape scissors, small suture scissors
Tape cutter
Fingernail cutter
Penlight
Tongue forceps
Tweezers
1-inch adhesive tape (2-3)
1
1
2-inch adhesive tape (6-8)

1
2-inch adhesive tape (2)
2-inch elastic tape (2-3)
1-inch dermal tape (1-2)
Elastic wraps 2-inch, 4-inch, 6-inch (2 each)
Contact lens solution
Eye wash
Taping base (Tuf Skin spray)
Tape underwrap (4-6)
Gauze pads (4 4, 3 3, large) (46 each)
Telfa pads (nonadherent, various sizes) (23 each)
Finger splints
Petroleum jelly
Antiseptic soap
Aspirin, acetaminophen, ibuprofen
Antacid (liquid or tablets)
Bandages (various sizes)
Steri-strips (buttery bandages are second choice)
Cotton-tipped applicators
Padding: cotton; sponge (miscellaneous)
1
4 and
1
2 inch; only felt
(miscellaneous)
1
4 and
1
2 inch
Fungicide ointment
Alcohol and/or Betadine swabs
Antibacterial cream
Plastic bags for ice or instant cold packs
Moleskin
Second Skin Blister Pak
Peroxide, 6 oz
Ampu Balm
Sterile catheters
Sterile and nonsterile rubber gloves
Mirror (small)
Thermometer (oral)
Sunscreen lotion (seasonal/location)
Small spray bottle
Triangular bandage or sling
Pocket cardiopulmonary resuscitation mask or shield
Portable, battery-operated ultrasound and electrical stimulation units
may differ markedly. It is usually benecial to evacuate a
seriously injured athlete as soon as it is medically advisable.
Minor Injuries
Even minor injuries and illnesses that occur at the competi-
tion site may affect athlete participation in competition. It
is inadvisable for an athlete with a fever to compete under
Box 28-2 Typical Committees for a Competition
for Athletes with Disabilities
Sponsorship
Medical
Classication
Technical, event, and ofciating
Manpower
Accommodations
Meals and refreshments
Transportation
Registration and packets
Command post (on-site information center)
Awards
Computer operations
Correspondence
Entertainment
Equipment
Outtters
Athlete assistance
Public relations and marketing
US Water Skiing, US Kayaking and Canoeing, USA
Volleyball, USA Track and Field, and Professional Associa-
tion of Diving Instructors among others. These organiza-
tions have educated their coaching staffs in the adaptations
necessary for successful participation and competition in
their respective sports. Concurrent with the expanded
knowledge and adaptation of coaching techniques for per-
sons with disabilities has been the development and rene-
ment of adaptive sports equipment using the latest technol-
ogy in materials and engineering. Complementing advances
in technology were the adoption of rules changes by
governing organizations that opened up competition and
reconciled the changes in competition fostered by techno-
logical innovation.
Who would have conceived 30 years ago that a paraple-
gic might race down a ski slope at 60 miles per hour
(97 km/hr) or that an above-knee amputee could complete
a 360 aerial on a snowboard? Could the authors and
readers of this original chapter published circa 1995 have
envisioned an individual pushing a lightweight sport wheel-
chair through a grueling 26-mile marathon in less than
1 hour and 30 minutes, faster than their able-bodied
counterparts?
With all of these developments in coaching techniques,
rules modications, and equipment technologies, extraordi-
nary performances by those with a disability have become
ubiquitous within our society.
Sports medicine team members involved with disabled
athletics have the ability to serve in many roles. The tradi-
tional role of providing emergency and rehabilitative
medical care is only a fraction of the contribution that may
be offered. Classifying, coaching, consulting with coaches,
ofciating, organizing, and administering are some of the
many functions that medical personnel have the profes-
sional training and expertise to perform to enhance the
overall performance of disabled athletes. Another integral
responsibility that must be assumed by medical profession-
als is the education and recruitment of athletes through
hospitals, rehabilitation centers, and other medical facilities
where potential disabled athletes can be educated as to
the availability of various sports organizations and quality
training programs.

Box 28-3 Typical Responsibilities of Medical
Committee Members
Medical history forms (athletes, coaches, staff, and volunteers)
Command post directives and hot lines
Medical information yers (athletes, coaches, staff, and volunteers)
Local hospital notication and coordination
Community medical staff alert (emergency medical staff, doctors,
nurses, etc.)
Event medical coverage
Practice eld medical coverage
Medical tent for events
Adaptive equipment repair tent (wheelchair, prosthesis, etc.)
Injury report forms
Disability emergent care information sheets for staff (a memory jog-
ger for medical staff who dont often work with disabled athletes)
First-aid kit checklist
Appropriate personal coverage
Box 28-4 Typical Responsibilities of Classication
Committee Members
Notication of certied classiers
Current classication manuals
Current classication cards
Appropriate medical information on athletes for classiers
Necessary evaluation equipment as outlined by classiers
Appropriate space for classiers to classify athletes
Processing table and staff to direct athletes
Instruction sheet describing the classication process for coaches
and athletes
Arrangements for protest submission and hearings
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704
Introduction
Sports medicine is often described as the treatment and care
of competitive athletes. Yet any clinician currently practic-
ing sports medicine will tell you that this is only a part of
the denition. If asked, he or she will state that sports
medicine is a philosophy. This philosophy is dened by the
patients will to get back to the specic desired physical
activity. The attitude of the clinician factors into this deni-
tion as well. The role of the sports medicine clinician is to
engage, educate, and facilitate the patients ability to reach
his or her goal. Whether the patient is a star high school
basketball player competing for a full college scholarship or
a 75-year-old grandmother who wants to cross-country
ski with her grandchildren, both are highly motivated indi-
viduals who want to return to their sports. Both need the
expertise of a sports medicine clinician.
The worlds population is aging. The median age of the
global population is increasing because of a decline in fertil-
ity and a 20-year increase in the average lifespan during the
second half of the twentieth century.
1
These factors, com-
bined with elevated fertility in many countries during the
two decades after World War II (i.e., the Baby Boom
generation), will result in increased numbers of persons
aged 65 years or older between 2010 and 2030.
2
World-
wide, the average lifespan is expected to extend another
10 years by 2050.
1
In the United States, the proportion of the population
aged 65 years or older is projected to increase from 12.4% in
2000 to 19.6% by 2030.
3
By the numbers, the population
aged older than 65 years is expected to increase from
approximately 35 million in 2000 to an estimated 71 million
in 2030. The number of persons aged 80 years or older is
expected to increase from 9.3 million in 2000 to 19.5 million
in 2030. Internationally, the worldwide population aged
65 years and older is projected to increase by approximately
550 million to 973 million,
3
increasing from 6.9% to 12%
worldwide ( Table 29-1 ).
2
As a result of the population aging and increased life-
span, more and more people are retiring in their mid to late
60s with plans to engage in physical activity such as golf,
tennis, hiking, swimming, weightlifting, and other forms of
both aerobic and anaerobic exercises. Recently, the US fed-
eral government has issued its rst-ever Physical Activity
Guidelines for Americans.
4
They describe the types and
amounts of physical activity that offer substantial health
benets to Americans of all ages. The driving force behind
these guidelines is the overwhelming body of research and
opinion that moderate exercise and daily physical activity is
a valuable intervention in preventing and controlling dis-
ease and chronic illness.
4-9
There is also a large consensus in
medical opinion that moderate exercise in the senior popu-
lation may markedly reduce the age-related declines in
musculoskeletal function.
SELECTED REHABILITATION NEEDS
OF THE MASTERS ATHLETE
James W. Matheson and Robert C. Manske

Clinical Point
Moderate exercise in the senior population may reduce age-related
decline in musculoskeletal function.
The new Physical Activity Guidelines recommend what
is considered the minimum activity requirements for gen-
eral tness. It is unknown if the growing older population
29
CHAPTER
Selected Rehabilitation Needs of the Masters Athlete CHAPTER 29 705
will follow the new guidelines. Currently, the activity level
of many older Americans falls short of the guideline recom-
mendations. However, there exists a subgroup of the aging
population that exceeds these new activity requirements.
These active individuals represent the upper end of
the functional spectrum among older adults. These are the
masters athletes.
Masters athletes are competitors who exceed a minimum
age specic to each sport and who participate in competitive
events designed for master athletes.
10
Some of these events
include the Senior Sports Classics, the World Veterans
Games, and the events sponsored by the National Senior
Games Association (NSGA) in the United States. The com-
petitive events for the 2009 National Senior Games in-
cluded 18 different sports: archery, badminton, basketball,
bowling, cycling, golf, horseshoe, race walk, racquetball,
road race, shufeboard, softball, swimming, table tennis,
tennis, track and eld, triathlon, and volleyball. The NSGA
holds local and state games for seniors across the nation to
encourage seniors to become active and get involved. These
local and state games are estimated to have 350,000 senior
athlete participants annually.
11
To participate in the Senior
Games, an athlete must be at least 50 years old.
11
The
minimum age of a masters athlete varies according to the
extent to which youth is required for success. For example,
in swimming, the minimum masters athlete age is 25 and in
rowing it is 27.
10
In track and eld, masters athletes are
considered those older than 35 years; in race walking they
must exceed 40. Selected outdoor track world records for
male and female master athletes in the 100 m are shown in
Table 29-2 .
Masters athletes who have pursued lifelong sports activi-
ties do not want to alter activity levels or recreational plans
following a recent diagnosis of osteoarthritis (OA) or a sur-
gical procedure. These veteran athletes do not want or
need clinicians to tell them that they can no longer be as
active as they have been in the past. They want clinicians
who treat them no differently than athletes several decades
younger. This is the challenge to the sports medicine prac-
titioner. Returning masters athletes to their activities is chal-
lenging and involves a specic understanding of the physi-
ological changes that occur within the aging musculoskeletal
system. This chapter begins by discussing the physiological
effects that are altered in the aging athlete. The selected
topics of OA and overuse tendinopathy will be discussed.
Common treatment interventions and the research evi-
dence supporting these interventions is emphasized. Last
but certainly not least, considerations for those returning
to athletics following total joint replacement is addressed.
Table 29-1
United States and World Estimated Population
Location and Age Dates
2000 2030
% Age 65 12.4 19.6
US # Age 65 (millions) 35 71
US #Age 80 (millions) 9.3 19.5
Int % Age 65 6.9 12.0
Int # Age 65 (millions) 550 973
Data from Kinsella K , Velkoff V: An aging world, US Census Bureau,
Editor, Washington, DC, 2001, US Government Printing Ofce;
and US Census Bureau: International database. Table 094. Midyear
population, by age and sex. Available from: http://www.census.gov/
population/www/projections/natdet-D1A.html .
%, Percentage; #, number; Int, international; US, United States.
Table 29-2
World Masters Outdoor Track and Field World Records at 100 Meters
Age Group Marks Athlete Name Country Age Meet Date
Men 45 10.72 Willie Gault USA 45 6/24/2006
Women 45 11.34 Merlene Ottey SLO 47 8/12/2008
Men 55 11.44 William Collins USA 57 4/25/2008
Women 55 13.30 Philippa Raschker USA 55 8/10/2002
Men 65 12.37 Stephen Robbins USA 65 8/2/2008
Women 65 14.10 Nadine OConnor USA 65 6/30/2007
Men 75 13.54 Bruno Kimmel GER 75 7/10/2009
Women 75 15.91 Paula Schneiderhan GER 75 9/6/1997
Men 85 16.16 Suda Giichi JPN 85 8/23/1998
Women 85 19.83 Nora Wedemo SWE 86 8/21/1999
Men 95 21.44 Friederich E. Mahlo GER 95 9/7/2007
Women 90 23.18 Nora Wedemo SWE 90 8/9/2003
Men 100 30.86 Philip Rabinowitz RSA 100 7/10/2004
Data from http://www.usatf.org/statistics/records/masters_outdoorTF_world.asp , accessed on 04/04/2010.
GER, Germany; JPN, Japan; RSA, Russia; SLO, Slovenia; SWE, Sweden; USA, United States.
In April, 2010, a team physician consensus statement was
published in Medicine and Science in Sports and Exercise
entitled Selected Issues for the Masters Athlete and the
Team Physician: A Consensus Statement that provides a
guide to the care and treatment of these athletes for selected
conditions.
12
Physiological Effects of Aging
on the Masters Athlete
Progressive loss of muscle strength and endurance resulting
in a loss of athletic performance and function has tradition-
ally been accepted as a consequence of aging. However,
several studies have shown that a signicant portion of these
losses in function may be musculoskeletal adaptations to
physical inactivity.
13-19
These studies have shown that high-
intensity training in the frail elderly can lead to a signicant
increase in their ability to resume activities of daily living
(ADLs). Masters athletes continue to challenge this concept
of age-related decline and may serve as a model from whom
a better understanding may be gained of the inevitable
senescent changes that occur.
Changes in Body Composition
in the Masters Athlete
Body composition comprises body fat and fat free mass,
which includes skin, bone, internal organs, and muscle
mass.
20
In our relatively sedentary society, it is typical to
gain approximately 1 pound (0.5 kg) a year between the
ages of 25 and 65 years. This increase in girth is attributable
to fat mass and generally occurs in the peritoneum, which
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
women who are rigorously active throughout the course of
a lifetime (e.g., masters athletes), there is a change in body
composition reecting the expected increase in fat mass and
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
similar to that of young, active women and lower than that
of sedentary 50- to 60-year-old women. Cross-sectional
data indicate that the percentage of body fat for masters
athletes is relatively constant at approximately 28% between
the ages of 35 and 75.
21
In masters athletes, the percentage
of body fat varies by sport. Those participating in long-
distance track events have a lower percentage body fat
(23.5%) than those participating in short-distance track
events (28.8%).
21
For the same age span, masters athletes
have a lower rate of decline (7.5%) in lean muscle mass than
the general population (25%-30%).
21-23
Thus, maintenance
of a high level of physical activity throughout the lifespan
allows masters athletes to have a slower increase in body fat
and preserve lean mass to a greater extent than the general
population.
Changes in Muscle Structure
and Function in the Masters Athlete
The primary function of skeletal muscle is for movement
and generation of force. This function occurs at both the
macroscopic and microscopic level. Muscle bers are classi-
ed as type I, type IIa, and type IIb bers. Type I bers, also
known as slow-twitch bers, are more resistant to fatigue
than types IIa or IIb, also known as fast-twitch bers.
In comparison with slow-twitch bers, fast-twitch bers
fatigue faster and are mainly anaerobic. It is generally
accepted that slow-twitch bers are mainly used for endur-
ance, whereas fast-twitch bers are used for speed and
power. In regard to hypertrophy (muscle growth), fast-
twitch bers grow faster and larger than slow-twitch bers.
Sarcopenia is of profound importance for the mainte-
nance of posture, locomotion, and the ability to perform
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
is slightly slower early in the decline and accelerates late in
life. Healthy men and women in their seventh and eighth
decades of life demonstrate average reductions of 20% to
40% in maximal isometric strength.
24 , 25
From a functional
perspective, the age-associated reduction of quadriceps
muscle strength is such that the average 80-year-old is at or
near the minimum level of strength required to rise from a
chair.
26 , 27
Clinical Point
Sarcopenia is the progressive decline of muscle mass, force generation,
and quality associated with aging.
This age-associated decline in muscular force genera-
tion also negatively affects the performance capacity of the
masters athlete. The loss in muscle mass and subsequent
loss of muscle force is the consequence of an actual decline
in the number of muscle bers present and the atrophy of
many of the remaining bers, particularly among the fast-
twitch or type II bers. This preferential decline in type II
ber area also affects the ability to recruit muscles quickly,
which makes athletic activities requiring explosive power
(e.g., sprinting, jumping) more difcult. Despite these
senescent changes in muscle tissue, masters athletes con-
tinue to perform at a level much higher than their seden-
tary counterparts.
In a study of elite weightlifters, aged 18 to 82 years,
researchers examined changes in muscle structure. Results
are shown in Figure 29-1 .
28
It is apparent that after age 50,
there is a consistent loss of muscle ber size. Of note is the
oldest lifter, who had ber areas that were comparable to
those of ve physical therapy students who were biopsied as
controls. These data suggest that a large portion of ber
atrophy that occurs with aging may be due to inactivity.
However, the data also illustrate that despite rigorous train-
ing, the masters athlete cannot maintain ber hypertrophy
with advancing age.
28
During the past 20 years, scientists have investigated the
underlying mechanisms for the reduction in strength with
age.
24 , 25 , 28-30
At present, it appears that there is no single cel-
lular or molecular mechanism that can explain the total re-
duction in strength. It is conceivable that age-related weak-
ness may be caused partly by a decreased central drive, and
thus a decline in ability to voluntarily activate a muscle. The
threshold of excitability of the corticospinal tract increases
progressively with age and is signicantly higher in the older
adult. Although this increased threshold of activation inu-
ences performance, masters athletes continue to push their
musculoskeletal systems to the limit and to provide evidence
of the true physiological limitations of muscle force and
structure in the active older adult (see Table 29-2 ).
Changes in Tendon Structure in the Masters Athlete
With aging, there are mechanical and structural changes in
tendon tissue, including increased collagen cross-linking,
decreased content of glycosaminoglycans and water, and
increased stiffness.
31
Strocchi and colleagues
32
reported that
changes in the Achilles tendon included a decrease in the
collagen bril diameter, an increase in bril density, a de-
crease in the number of tenocytes, and a loss of the waviness
(crimp) noted in a young tendon not under tensile load.
Birch and colleagues
33
reported that the ultimate stress
values (mega Pascal) of Achilles tendon decreased with age.
However, other researchers have reported that although
tendons from healthy older adults show these changes,
there is no evidence of degenerative changes in tendons as
seen in tendinosis.
34 , 35
It is possible, however, that the me-
chanical and structural changes in tendons with age may
predispose the tendon to tendinopathy or tendon rupture.
Clinical Point
Aging combined with inactivity leads to loss of muscle mass and
muscle force. It is the result of a decrease in number of muscle bers
and atrophy of remaining bers especially fast-twitch (type II) muscle
bers.
Figure 29-1
Muscle ber area in master lifters. Muscle biopsies from the vastus later-
alis muscle of 22 master athletes aged 18 to 82 years and 5 physical
therapy students who exercise recreationally. Only type IIa ber areas
are presented as this ber type represented approximately 75% of the
total in the lifters. (From Brown M: Effects of aging-growth changes
and lifespan concerns (40). In Magee DJ, Zachazewski JE, Quillen WS,
editors: Scientic foundations and Principles of Practice in Musculoskel-
etal Rehabilitation, p 307, St. Louis, 2007, Saunders.)
Age-Related Changes in Tendon
Increased collagen crosslinking
Decreased glucosaminoglycans
Decreased water
Increased stiffness
Decreased ber diameter
Increased bril density
Decreased tenocytes
Loss of crimp
Cardiorespiratory Fitness in the Masters Athlete
As with skeletal muscle and body composition, senescent
changes occur in the cardiopulmonary system. Decreases
in maximal oxygen consumption, exercise economy, and
the exercise intensity at which a high fraction of the maxi-
mal oxygen consumption can be sustained (lactate thresh-
old) are considered factors that result in a decline in per-
formance of the masters athlete.
36-40
A detailed discussion
of these factors is beyond the scope of this chapter;
however, because maximal oxygen consumption appears
to be the most inuential factor in cardiorespiratory tness
in the masters athlete, it is briey discussed. Maximum
oxygen uptake (VO
2
max) is the gold-standard measure
of cardiorespiratory tness. VO
2
max represents the
upper limit of aerobic power or performance. Maximal
oxygen consumption is generally considered to be a pri-
mary determinant of endurance exercise performance
among young, endurance-trained athletes.
38 , 41
VO
2
max
declines approximately 10% per decade after age 25 to
30 years in healthy, sedentary men and women.
39 , 42-44

Unlike the other physiological variables previously discussed,
endurance exercisetrained men and women demonstrate
greater absolute (1 mL/kg per 1 min) rates of decline
in VO
2
max with age than healthy sedentary adults.
40 , 42 , 44 , 45

It is suspected that this is a result of these athletes having
greater baseline levels of VO
2
max as young adults and a
proportionally greater loss of exercise with aging com-
pared with sedentary adults.
44 , 45
Based on current scien-
tic research, a progressive reduction in VO
2
max appears
to be the primary physiological mechanism associated with
declines in endurance performance in the masters athlete.
of athletic activity. A result of these age-related tissue
changes is a decrease in the passive viscoelastic properties or
exibility of the connective tissue elements.
Connective tissue tends to increase with age in propor-
tion to muscle mass, to become less hydrated, and to
change its relative composition of collagen and elastin, all of
which contribute to its increased density and rigidity. Aging
results in a decrease in the amount of insoluble collagen and
total collagen. Both of these have been correlated with
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
involved joint complex, a condition that contributes to joint
stiffness resulting in range of motion (ROM) loss. Clini-
cally, exibility is dened as the ROM around a joint.
Research suggests that exibility decreases with age
(approximately 20% to 30% between 30 to 70 years of
age).
46
This may make it harder for the masters athlete to
adequately move easily into ranges required for his or her
desired sports activity.
Age-Related Structural Changes
in the Cardiovascular System
From Irwin S: Cardiopulmonary physical therapy: A guide to practice, ed 4,
St Louis, 2004, Mosby.
Heart
Myocardium
Increased wall thickness
Accumulation of lipofuscin
Increased elastin, fat, and collagen
Endocardium
Thickened areas composed of elastic, collagen, and muscle
bers
Fragmentation and disorganization of elastic, collagen, and
muscle bers
Conduction system
Atrophy and brosis of left bundle branches
Decreased number of sinoatrial node pacemaker cells
Valves
Thickening and calcication
Vasculature
Increased size (primarily of proximal vessels)
Increased wall thickness (primarily of distal vessels)
Increased connective tissue and lipids in subendothelial layer
Atrophy of elastic bers in medial layer
Disorganization and degeneration of elastin and collagen
Clinical Point
Maximum oxygen uptake decreases approximately 10% per decade
after 25 to 30 years of age in sedentary adults.
Flexibility
As was true with muscle tissue, the connective tissue ele-
ments that make up tendon, capsule, muscle, fascia, and
aponeurosis also undergo senescent changes. The quantity
of change of the collagen, elastin, and other elements inu-
ence the response of these tissues to the physical stresses
Clinical Point
Flexibility decreases approximately 20% to 30% between 30 and
70 years of age.
In summary, the sports medicine professional needs
to have a basic understanding of the senescent changes
that occur in the injured masters athlete. The challenge to
the clinician is to determine how these changes may inu-
ence clinical decision making. A general understanding of
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.
Osteoarthritis and the Masters Athlete
OA affects more than 20 million individuals in the United
States. This gure is expected to double during the next
two decades. Based on radiographic criteria, OA occurs in
30% of affected individuals aged 45 to 65 years and in more
than 80% by their eighth decade of life, although many
individuals are asymptomatic.
47
The likelihood of develop-
ing OA increases with age and the disease is equally com-
mon among men and women aged 45 to 55 years. After age
55 years, the disease becomes more common in women.
OA is a disease process that causes progressive hyaline
articular cartilage loss and may cause underlying bone to
develop outgrowths (osteophytes) and bony sclerosis.
48-50
OA is categorized as either primary or secondary. Primary
OA has an unknown cause and is thought to lead to joint
destruction caused by an articular cartilage defect, whereas
secondary OA is thought to occur as a result of previous
trauma, hemarthrosis, infection, osteonecrosis, or some
other condition.
51
The pathological process of OA generally
results in the following characteristics: (1) erosion of hyaline
articular cartilage covering long bones; (2) sclerosis, or
thickening, of bone under articular cartilage in an attempt
at a reparative process, (3) formation of bone spurs or
osteophytes ( Figure 29-2 ).
28 , 52
Knee Osteoarthritis
OA of the knee is known to cause more symptoms and dis-
ability than OA affecting any other joint in the body.
53 , 54

Approximately 80% of those with knee OA will develop a
varus deformity caused by medial joint compartment narrow-
ing, with the remaining patients demonstrating a valgus knee
angulation (~5% to 10%) or no angulation (~5% to 10%).
55

Many masters athletes have secondary knee OA because of
ligamentous, cartilage or bone injuries received when par-
ticipating in sports at a younger age. Several studies have
shown a substantial increased risk of knee OA in individuals
with a history of anterior cruciate ligament rupture, meniscal
tears, and fractures.
56-61
Given the increased participation in
varsity sports by todays boys and girls, it is commonplace for
several athletes each year to have a signicant ligament injury
requiring surgery. Although many of these athletes are able
to return to their sports, few clinicians take into consider-
ation the future risk of OA in these athletes.
Imaging of Knee Osteoarthritis
The primary means of evaluation of OA is plain-lm radiog-
raphy. However, a strong correlation between radiographic
severity and loss of function has not been shown. According
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
picture is that many of these individuals may show evidence
of OA on a radiograph, but have absolutely minimal or no
symptoms. Often there is a poor correlation between pain
and actual structural damage.
63
Some of this disparity may
be due to the fact that radiographs do not image synovitis
or bone marrow edema.
64
Bedson and Croft
65
reported
several other reasons for this disparity between radiograph
evidence and function, including (1) insufcient radio-
graphic views to estimate the association between degenera-
tion and pain, (2) the wide variation in denitions of
pain that may result in discrepancy between the score and
the amount of evidence of OA, and (3) the nature of the
study population. Therefore, the prevalence of OA, when
Muscle
Synovial
membrane
Swollen,
thickened,
inflamed
synovial
membrane
Synovial
fluid
Joint capsule
(ligaments)
Bone
Deformity
Osteophyte
Bursa
Tendon
Cartilage
Thinned
cartilage
Cartilage
thinning
Bone ends
rub together
Bone
erosion
Bone
loss
NORMAL JOINT
OSTEOARTHRITIS RHEUMATOID ARTHRITIS
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: Scientic Foundations and
Principles of Practice in Musculoskeletal Rehabilitation, p 307, St. Louis, 2007, Saunders.)
assessed by radiographs, may be much higher than those
actually experiencing pain and disability.
66
Knee-specic OA
has been shown to be present more often when both patel-
lofemoral and tibiofemoral joints are affected, creating
more pain.
67
One of the major diagnostic criteria for arthritis is the
symptom of joint pain. Articular cartilage itself is not
innervated, so where is the pain coming from? The general
consensus is that the pain is a result of inammation of the
synovium, medullary hypertension, microfractures of the
underlying subchondral bone, stretching of periosteal nerve
endings caused by sclerosis, osteophyte formation, or exces-
sive stretching of ligaments and spasm of muscles surround-
ing the affected joint.
68
Symptoms of OA include pain and
stiffness in and around the joint, osteophyte formation,
cartilage degeneration, joint malalignment, weightbearing
difculty, muscle spasm, weakness, and ROM loss.
exercises are a crucial part of any program for those with
OA. Although joints should never be passively forced
through a range, gentle ROM, joint mobilizations, and
stretching exercises should be performed with each exercise
session.
79-81
Both loss of knee exion and extension can be affected
in knee OA, although knee exion is usually limited to a
greater degree. The restoration of full extension is critical
for the establishment of a normal gait pattern and an
adequate of exion is needed for sport-specic activities.
Although the masters athlete with knee OA may only com-
plain about knee pain and loss of motion, the clinician
needs to consider loss of mobility of the entire trunk and
lower extremity. Examining mobility of the lumbar spine,
hip, ankle, and foot is an important part of the physical
examination of a masters athlete with knee pain. Limitations
in the lumbopelvic or lower-extremity kinetic chain may
need to be addressed.
80 , 81
Mobilization techniques specic to the knee include
dorsal and anterior glides of the tibia on the femur; medial
and lateral rotation of the tibia on the femur; and superior,
inferior, and lateral patellofemoral glides. For masters ath-
letes with restricted motion at the knee or hip, combining a
home exercise program with skilled manual therapy appears
to work best. Deyle and colleagues
79 , 82
determined that
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
spine, hip, ankle or foot if it was believed that this
would improve knee function.
79 , 82
A more recent study has
shown that the pain-pressure threshold was signicantly
increased following anterior and posterior glide tibiofemo-
ral joint mobilizations as compared with manual contact
or no contact.
83
For more information on this topic, see
Chapter 27 , Physical Rehabilitation After Total Knee
Arthroplasty, in Pathology and Interventions in Musculo -
s keletal Rehabilitation, Volume 3 of this series.
Unloading Braces and Insoles
for Knee Osteoarthritis
The majority of knee OA affects the medial compartment of
the knee, which bears greater than 60% of the load during
weightbearing.
84-86
As the medial joint compartment
becomes more arthritic, a loss of medial joint space is
observed on radiographs and eventually visually, with the
patient exhibiting a varus or bowlegged knee deformity. To
offset or unload the medial compartment, especially dur-
ing physical activity, two biomechanical interventions have
been suggested.
A specialized counterforce knee brace may be custom
t to the patient. Typically, the athlete is measured and then
the brace is made with an intrinsic valgus correction of 2
to 3. Often, via a small hex wrench or key, the athlete can
Radiographic Evidence of Osteoarthritis
68
Decreased joint space (cartilage degeneration)
Sclerosis of subchondral bone
Osteophyte formation at joint margins
Subchondral cyst formation
Genu varum or valgum joint deformity
Rehabilitation Exercises for Knee Osteoarthritis
Rehabilitation for those with lower-extremity OA should
include all facets of training including exibility, mobility,
muscle strengthening, endurance training, and cardiovascu-
lar training. Consideration of each of these training aspects
is critical when designing a rehabilitation plan of care for the
aging athlete.
The goals of any specic rehabilitation program should
depend on the individual athletes specic needs. For the
aging athlete, this includes ROM, strengthening, and en-
durance training. Lower-extremity strength training allows
the muscular system to work to attenuate impact loads,
provide needed joint stability, and support independent
function.
69
The American College of Sports Medicine has
determined several specic muscle groups that should be
emphasized with a strengthening program for older adults
to maintain independence in ADLs. These muscle groups
include the hip extensors, knee extensors, ankle plantar
exors, and ankle dorsiexors.
9
Exercises for these muscle
groups should be done at functional speeds and using func-
tional patterns specic to the athletes needs.
70-72
There appears to be signicant consensus with respect to
the efcacy of exercise in the case of knee OA.
73-78
Because
ROM of affected joints may be limited due to pain, muscle
spasm, or soft tissue contractures, motion and exibility
increase the valgus force by several additional degrees. This
allows some individual customization of the brace during
different physical activities. Biomechanical analysis has
shown that wearing a valgus unloading brace can alter pain,
joint position sense, strength, and function in the older
athlete.
87-90
The hypothesis surrounding the brace effective-
ness has been the fact that if a brace can place the knee with
medial joint space narrowing in neutral or a slight valgus
alignment, normal biomechanical loading may be restored.
In addition, recent evidence appears to illustrate that
pain relief may also be a result from diminished muscle co-
contractions rather than from so-called medial compart-
ment unloading.
91
Using a knee unloading brace is not
always feasible in the older athlete with knee OA. Custom
unloading braces are very expensive and often are not fully
covered by insurance. Other comorbidities, body size, and
body shape may also prohibit the success of an unloading
brace. In addition, prolonged brace wear can cause skin
breakdown and leg pain. Empirically, it appears the unload-
ing brace works best for the athlete who can wear the brace
for his or her desired athletic activity, but does not necessar-
ily need it for ADLs.
As an adjunct or as an alternative, the clinician may con-
sider the use of a laterally wedged insole for the masters
athlete with medial compartment knee OA. For this to be
effective, the athlete cannot have signicant ankle instabil-
ity. Too much ankle laxity will result in any changes made at
the rearfoot not being transmitted up the kinetic chain. Are
lateral insoles effective? Using insoles to statically alter the
knee in a more upright position by placing the calcaneus
in a position of valgus, Sasaki
84 , 85
and Yasuda reduced the
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
individuals with medial compartment OA.
92-97
This insole
research has yielded some interesting ndings. At present, it
appears that a laterally wedged, full-length orthotic is more
effective than a heel wedge alone,
92-94
that the wedged
insole should not be used with heeled footwear,
98
and that
having the patient self-select wedge size based on numeric
pain ratings before and after wedge use is best.
97
An addi-
tional benet of using a wedged insole is that it is signi-
cantly less expensive than a custom unloading brace. Fur-
ther research is needed to identify which individuals would
benet from an unloading brace and a wedged insole.
Viscosupplementation Therapy
in Knee Osteoarthritis
Many palliative treatments in the form of viscosupplementa-
tion have become available to help reduce symptoms associ-
ated with articular cartilage degradation. These come in the
form of intra-articular injections with hyaluronic acid.
Hyaluronic acid is a normal component of synovial uid,
which bathes the articular surfaces of the normal knee.
In an arthritic knee, this molecule is depleted by a factor of
2 or 3 because of dehydration and dilution.
99
Recom-
mended injection schedules depend on preparations used.
For Hylan G-F 20, an injection weekly for 3 weeks is rec-
ommended, whereas for sodium hyaluronan, the recom-
mended dosage is an injection weekly for 3 to 5 weeks.
99
Most of the clinical studies on the use of injectable hyal-
uronic acid are inconsistent. Early studies demonstrated
relief of symptoms and benet from this form of treat-
ment,
100-103
although others did not.
104 , 105
Problems abound
with these early studies including heterogenicity of patient
populations, different formulations of injected preparations,
and different treatment regimens.
99
Despite these problems in research methodology, several
meta-analyses indicate that viscosupplementation has a
therapeutic effect on pain, function, and patient global
assessment.
106-108
A limitation of these multiple studies is
that, to date, the effect of a placebo response on study par-
ticipants has not been fully analyzed and that adverse effects
of the injections have been reported.
109
One of the problems with use of injectable viscosupple-
mentation is the accurate placement of intra-articular needle.
Jackson and colleagues,
110
using uoroscopic conrmation
of needle position, found that accurate placement was very
difcult. When using an anterolateral approach, only 71% of
injections were performed in the correct position. Injection
site pain and discomfort is another common complication
seen with injectable hyaluronate. Although hyaluronate
injections are used frequently when treating symptoms of
OA, the potentially high placebo effect with the use of hyal-
uronate injections warrants further study before the true
efcacy of this intervention can be determined.
Hip Osteoarthritis
The most common predisposing factor for hip OA is
age.
111-113
Hip arthritis is common and occurs in up to 4%
to 6% of the population.
114
Risk factors for hip OA include
systemic issues such as ethnicity, age, gender, hormonal
status, genetics, bone density, and nutrition. Local biome-
chanical risk factors include joint injury, obesity, occupa-
tion, sports participation, physical activity, altered joint
biomechanics, and muscle weakness.
115
Hip OA is more
common in laborers than those with sedentary jobs. This
probably is accounted for by stress caused by heavy lifting
and carrying in those occupations.
114 , 116-118
Previous hip
injury is also associated with hip OA.
110 , 118
Cooper and
colleagues
119
reported that the odds ratio for hip OA when
having a previous hip injury as 4.3 (95%, condence interval
2.2-8.4). In addition, patients with OA of one hip are at
increased risk of developing OA in the opposite hip.
120
A
masters athletes previous occupation may determine his or
her risk of hip OA. Numerous studies in Europe and the
United States have found a higher prevalence of hip OA in
men whose occupation involves repetitive lifting of heavy
loads.
121-124
Suspected occupational risk factors for hip OA
have been suggested, including regular heavy lifting, oper-
ating machinery, and walking on uneven ground.
124-131
One of the problems in diagnosing hip OA is that symp-
toms can be vague and not localized solely to the hip
region. As other areas aficted with OA, the severity of OA
in the hip may not exactly correlate with the degree of dam-
age seen radiographically. Pain and symptoms associated
with hip OA tend to be of much greater degree than radio-
graphic evidence seems to justify, whereas symptoms may
also be moderate in the presence of severe radiographic
changes.
In hip OA, the entire joint structure and function is af-
fected with joint capsular changes (shortening and lengthen-
ing) along with subsequent articular cartilage degeneration.
132

Later in the disease process, osteophytes or bone spurs may
develop from excessive tensile force on the hip joint capsule
or from abnormal pressure on the articular cartilage.
132 , 133

Other changes also develop, including sclerosis of the sub-
chondral bone from increased focal pressure, and in some
cases, cyst formation.
134
Muscle weakness often develops
around the hip joint with OA,
135
specically the abductor
muscles in the hip.
136
The hip abductor weakness progres-
sively weakens in the later stages of hip OA, which may create
a Trendelenburg gait pattern.
137
Recently, several studies have found an association be-
tween acetabular labral tears and the early onset of hip
OA.
138-140
This is important to understand as the aging
athlete may have had previous injuries or lower-level symp-
toms of hip discomfort that may have gone on for years
without formal treatment.
Rehabilitation of Hip Osteoarthritis
Rehabilitation for hip OA includes therapeutic exercise and
manual therapy. Manual therapy techniques may be bene-
cial for those with restricted hip capsular mobility. Hoeksma
and colleagues
141
performed a clinical trial assessing the
effectiveness of manual therapy compared with exercise
therapy in those with hip OA. Successful outcomes were
found in 81% of those receiving manual therapy compared
with only 50% in the exercise group. Positive effects related
to improvements of pain, hip function, and ROM lasted up
to 29 weeks.
Evidence shows that those with hip OA have limitation in
strength of the hip musculature and limitations in ROM as
compared with those with no hip problems.
137 , 142
One of
the earliest signs of hip OA is restriction of hip ROM.
Altman and colleagues have described hip exion of 115 or
less and medial rotation less than 15 to be prevalent in pa-
tients with hip OA.
112
Birrell and colleagues have noted that
an increased number of restricted planes of ROM increases
the specicity of ruling in hip OA as the actual diagnosis.
143

Therefore, the mainstay of conservative treatment must in-
clude increasing limited motion and strength. Limitations in
rotation can be restored by use of joint mobilization and
passive stretching of the hip musculature. If these limitations
are simply from disuse and are from muscle-tendon unit
shortening, passive stretching should sufce. This is likely
not the case in the masters athlete. If, however, these limita-
tions are from hip capsular attenuation, joint mobilizations
may be more benecial. Joint mobilization techniques may
be required in all planes, but most commonly will involve
increasing hip exion and hip medial rotation in those with
hip OA.
Although evidence for the use of manual therapy for hip
OA is limited, there are several studies that do support its
use. Hoeksma and colleagues demonstrated the superiority
of manual therapy plus exercise over exercise in isolation for
hip OA.
141
Furthermore, a case series from MacDonald and
coauthors described outcomes of individual patients treated
with manual physical therapy and exercise for hip OA.
144
This case series reported reductions in pain and an increase
in hip ROM in subjects with hip OA.
Proximal stability of the hip is required for almost all
weightbearing activities. Studies indicate that patients with
hip OA have decreased strength compared with nonarthritic
control subjects.
137 , 145
Initial exercises can begin in the
hook lying position because of the effects of gravity
and pain that could occur with full weightbearing. Once
exercises are tolerated in hook lying, advancement to pro-
gressive resistive exercises via machine weights or isotonic
exercises may commence.
Does Running Increase the Risk of Hip
or Knee Osteoarthritis in the Masters Athlete?
Many have questioned if running can increase the risk of hip
and knee OA. Multiple studies have attempted to answer
this question. Some studies have reported that running,
especially in excess, does increase the risk of OA.
146 , 147
Other investigations have shown no inuence of distance
running on OA.
148-150
In several studies, moderate distance
running has been reported to perhaps have a protective
effect in preventing the development of hip OA.
151 , 152
At
present, the preponderance of data seems to indicate that
long-distance running in moderation does not appear to
increase the risk of hip or knee OA in healthy individuals
and that running may even have a protective effect on the
risk of OA. Previous trauma to the hip or knee, whether
the result of injury or overuse, excessive running above
the individuals physical threshold, and intrinsic anatomical
instability in the joints may accelerate the onset of OA. The
clinician should weigh the risks of running against the
cardiovascular and musculoskeletal benets of running.
Surgical Treatment for Hip Osteoarthritis
Surgical treatment for hip OA includes but is not limited to
arthroscopic or open procedures. Arthroscopic surgery is
less invasive and is indicated for pathological conditions of
the hip such as symptomatic tears of the labrum, ligamen-
tum teres injuries, snapping hip syndrome, and removal
of loose bodies. Open procedures commonly performed
include a variety of total hip arthroplasty (THA) treatments.
With advances in surgical techniques and high-performance
prosthetic components, many aging athletes are able to
return to an acceptable level of sports both recreational and
competitive following THA. For more information on this
topic see Chapter 26 , Physical Rehabilitation After Total
Hip Arthroplasty, in Pathology and Intervention in Muscu-
loskeletal Rehabilitation, Volume 3 in this series.
Glenohumeral Osteoarthritis
In addition to weightbearing joints, OA affects the shoulder
in an estimated 20% of the elder population.
153
This rate is
well below that of other locations in the body, but its effects
appear to be just as debilitating and are a common cause of
depression, anxiety, activity limitations, and job perfor-
mance decrements.
154
Treating glenohumeral arthritis in
the masters athlete requires providing adequate pain relief
and restoration of ROM and function. Full-thickness artic-
ular cartilage defects in the shoulder have limited capacity
to heal.
155
Multiple causes of articular cartilage abnormali-
ties in the glenohumeral joint occur and include avascular
necrosis, chondrolysis, idiopathic focal defects, OA, osteo-
chondritis dissecans, postsurgical cartilage abnormalities
(iatrogenic injuries and post-traumatic defects).
155-157
Nu-
merous risk factors abound for shoulder OA and include
age, genetics, sex, weight, joint infection, history of shoul-
der dislocation, previous injury, overhead sports, or heavy
labor.
158
Similar to the knee, OA of the shoulder can occur
as either a primary or secondary process. Although primary
OA of the shoulder occurs as a gradual onset of pain, ath-
letes may remember an inciting event or injury that created
symptoms. Secondary OA occurs as the result of some
trauma or damage to the glenohumeral joint. Degeneration
of the glenohumeral joint is a difcult condition for the
masters athlete. This is especially true of athletes who
participate in overhead sports such as baseball, tennis,
swimming, or volleyball. However, competitors in cycling,
football, basketball, and soccer may also nd themselves
with severe post-traumatic, postreconstruction, or primary
cartilage loss in their shoulders. Unfortunately, this may
lead to impeded performance in these elder athletes.
Shoulder OA presents as a gradual onset of pain, crepitus
with decreased motion in those older than 50 years of age
who may have a history of previous shoulder surgery.
159
Classic signs and symptoms include pain, weakness, and
limited shoulder lateral rotation secondary to anterior soft
tissue contracture.
160
Rotator cuff integrity may be difcult
to determine in the presence of pain, and this can make
an exact diagnosis difcult. Diagnostic imaging reveals
joint space narrowing, humeral osteophytes, and posterior
subluxation of the humeral head.
161 , 162
Secondary OA from trauma in the shoulder is often due
to history of dislocation or subluxation. During a sublux-
ation or dislocation, excessive forces may be imparted to the
cartilage of the humeral head and glenoid fossa. Depending
on the mechanism of injury, the result may be either a clas-
sical Hill-Sachs lesion or, if dislocated posteriorly, a reverse
Hill-Sachs lesion. These injuries can cause articular cartilage
to disrupt from bone or cause an osteochondral compres-
sion defect. Recent evidence concludes that arthritic changes
after a dislocation are due to the age of the patient, the time
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
to 76% of patients with cartilage lesions of the shoulder
have associated rotator cuff degeneration or tears, whereas
only 19% of subjects without cartilage problems experience
rotator cuff degeneration or tears.
157
This is probably
caused by progressive wear and the fact that the rotator cuff
tendons have areas of reduced blood supply, making them
more vulnerable to degeneration with increased age.
165
As
with treatment of knee and hip OA, there are several medi-
cal treatment options, including rehabilitation, supplemen-
tation, medicine, and surgery. At present, there is no way in
which the natural progression of OA can be altered.
Rehabilitation Interventions for Shoulder
Osteoarthritis
Rehabilitation depends on whether the OA is treated con-
servatively or following surgical procedures. Conservative
treatment of shoulder OA begins with activity modication
and pain control, followed by progressive ROM and
strengthening exercises. Pain reduction can be attempted
through the use of numerous modalities. Limited evidence
exists regarding the best modality for glenohumeral OA.
Moist heat and electrical stimulation may help alleviate
symptoms, but is generally not long lasting. Use of these
modalities may allow soft tissue relaxation, allowing more
ease with obtaining or regaining valuable shoulder ROM.
Although ROM of the shoulder is important, clinicians must
remember that the patients arthritic glenohumeral joint
surfaces may not be congruent. Aggressive attempts at in-
creasing ROM may exacerbate an already irritated condition.
Therefore, working within a pain-free motion may be more
benecial.
166
Because shoulder joint stiffness is a poor prog-
nostic indicator for surgical outcomes, its avoidance should
be adequately addressed in conservative rehabilitation.
160
Strengthening within the nonpainful range of shoulder
motion is benecial as some physiological overow may
occur. Particular emphasis on the rotator cuff muscles and
scapular stabilizers is important because these muscles pro-
vide a strong foundation on which upper-extremity move-
ment can occur. Because some of these patients may have
chronic rotator cuff arthropathy, strength gains may be
minimal or slow at best. Conservative treatments should be
exhausted before attempts at surgery are considered. For
more information on this topic, see Chapter 25 , Shoulder
Arthroplasty, in Pathology and Intervention in Musculoskel-
etal Rehabilitation, Volume 3 in this series.
Surgical Treatments for Glenohumeral Osteoarthritis
Surgical intervention of glenohumeral OA includes ar-
throscopic debridement, capsular release, glenoidplasty,
corrective osteotomies, and interposition arthroplasty. In
younger, active patients aged 55 to 60 with moderate pain
and associated motion restrictions, arthroscopic debride-
ment with a capsular release may provide signicant
improvement. The debridement component of surgery will
clean out the joint, removing loose bodies, cartilage aps,
or fraying. The capsular release can restore joint mobility
and unload the articular joint surfaces of the humeral head.
Older patients with more severe joint destruction may re-
quire a shoulder arthroplasty because of pain and loss of
function that was not corrected by conservative means. If
both the glenoid and the humeral head have seen destruc-
tion, a total joint arthroplasty is performed, and when only
the humeral head has been damaged, a hemiarthroplasty is
the treatment of choice.
Osteochondral allograft and autograft procedures have
been used predominantly in the knee and hip for years.
Recent surgical advances have allowed use of osteochondral
allografting and autografting, which may prove to be a bene-
cial form of surgical treatment for glenohumeral OA.
167-169
Although OA is known to be a painful joint condition
that limits an athletes function, conservative treatment
methods and selected surgical alternatives can be used judi-
ciously in an effort to help active older adults to maintain
a healthy lifestyle. Although at times expectations for
activities and specic sports participation may need to be
adjusted, most can still participate in active sports recre-
ationally and at times even competitively.
Tendinopathy in the Masters Athlete
Primary disorders of tendons are common and constitute a
high proportion of referrals of the sports medicine clinician.
Certain tendons are particularly vulnerable to degenerative
pathological conditions; these include the Achilles,
170

patella,
171
proximal or high hamstring,
172
gluteus medius,
173

rotator cuff,
174
and common wrist exor and extensor
tendons.
175
It is important to note that both high hamstring
and gluteus medius tendinopathy are often misdiagnosed as
piriformis syndrome or trochanteric bursitis respectively.
172 , 173

The sports medicinetrained clinician should be aware of
this as misdiagnosis can prevent the masters athlete from
receiving the appropriate treatment in a timely manner.
Tendon pain is a common condition in the masters ath-
lete and can cause lasting disability. Signicant advances have
been made in understanding the pathophysiological charac-
teristics of these conditions. Histopathological evidence,
together with advances in imaging techniques, has made
clinicians more appreciative of the degenerative nature of
these conditions. Traditionally, treatments have placed a
heavy emphasis on anti-inammatory strategies, which are
often inappropriate. Recently, however, signicant advances
in the practical management of tendon disorders have been
made. In particular, the advent of eccentric loading train-
ing programs has revolutionized the treatment of Achilles
and patellar tendinopathy in some athletes.
Tendonitis versus Tendinosis and Tendinopathy
It is common practice among health care professionals to
use the term tendinitis indiscriminately to describe all
pathological conditions of the tendon. However, the sufx
-itis is a Greek element used to denote inammation.
Multiple histopathological studies have indicated that the
pathological process in most painful tendons is degenerative
rather than inammatory.
176-179
Accordingly, use of the
term tendinitis appears to be inappropriate in most cases
when describing the pathological condition underlying ten-
don pain. Several experts have suggested that the term
tendinitis be abandoned in favor of the term tendinosis,
which describes a degenerative tendon condition.
178-180
This distinction regarding pathological conditions of the
tendon was rst described by Puddu and colleagues
181
with
regard to classifying Achilles tendon pain. Fredberg
179
chal-
lenged the concept of tendon pain as primarily a degenera-
tive condition, suggesting that a lack of inammatory cells
may not mean the lack of an inammatory process. To
denitively distinguish between -itis and -osis, the diseased
tissue must be biopsied and subjected to histopathological
testing. Given that such histological studies are not com-
mon clinical practice, it is most appropriate for the sports
medicine clinician to describe tendon pain as tendinopathy.
Tendon Pain
A signicant challenge in providing intervention to patients
with tendinopathy or fasciopathy is in understanding the
potential sources of pain. In the traditional histopathologi-
cal model, tendon pain was considered an inammatory
problem, hence the term tendinitis. However, as previously
discussed, there is a lack of inammatory cells in chronically
painful tendons; this observation applies not only to the
Achilles tendon, but to other problematic tendons includ-
ing the patellar, rotator cuff, and wrist extensor tendons.
180
There is some evidence that there may be a neurochemical
aspect of tendinopathy pain. Alfredson and Lorentzon
177
found higher concentrations of glutamate in painful ten-
dons, including Achilles tendon, extensor carpi radialis
brevis tendon, and patellar tendon, and reported the pres-
ence of glutamate receptor sites in nerve endings associated
with painful tendons. Using immunohistochemical analyses
of painful Achilles tendons, Schubert and colleagues
182
found sprouting of substance Ppositive nerve bers, which
may explain the transmission of the tendon pain.
Historically, the mechanical model of tendon pain has
implicated that pain is a consequence of repetitive loading
of the tendon, resulting in collagen disruption.
183
In the
past decade, several imaging studies have seriously ques-
tioned this model. First, studies on patellar tendons
184-187
and Achilles tendons
170
have shown that the tendon can be
partially disrupted without pain, or painful without disrup-
tion.
188 , 189
Other research on pathological conditions of the
tendon at the shoulder and ankle has found the location of
a pathological tendon condition is not in the region sub-
jected to the highest tensile forces, but rather in a region of
relative stress shielding where tensile forces are lower.
190 , 191
These ndings are inconsistent with a model that describes
excessive tensile forces as a primary stimulus for pathologi-
cal conditions of the tendon. To explore new avenues of
examination and intervention for tendinopathy, clinicians
must recognize that research ndings are contrary to a
traditional view of pathological conditions of the tendon as
inammatory conditions caused by repetitive tensile stress
on the tendon. If we continue to allow such a traditional
view to persist, attempts to relieve tensile stress or reduce
inammation will continue to result in frustration for
clinicians and patients alike.
Treatment of Tendinopathy in the Masters Athlete
Management of tendinopathy should address both intrinsic
and extrinsic factors identied in the physical examination.
Correction of training errors, cross-training, and active rest
are common recommendations made in the early stages of
rehabilitation. A multitude of treatment interventions exist
for treating tendinopathy, although more research is neces-
sary to determine their efcacy and effectiveness.
Manual Therapy for Tendinopathy
There are several manual therapies popular in the treatment
of tendon disorders, the two most common being friction
massage and augmented soft tissue mobilization (ASTM).
Made popular by Cyriax, deep transverse friction massage
(DTFM) is a part of many clinical tendinopathy programs.
A Cochrane review in 2002
192
examined the available evi-
dence for DTFM. There were only two randomized con-
trolled trials of sufcient quality to be included: one on the
treatment of lateral epicondylalgia and the other on the
iliotibial band syndrome. Neither of these two trials demon-
strated a lasting benet versus the control group for either
pain or functional status.
192
Therefore, at present, no con-
clusions can be drawn concerning the use or nonuse of
DTFM for the treatment of tendinopathy. A second popular
technique is that of ASTM.
193 , 194
This is an intervention
that involves the use of ergonomically designed instruments
that theoretically assist clinicians in treatment of areas
exhibiting excessive soft tissue brosis.
195 , 196
Following each
ASTM treatment, the patient completes a stretching and
strengthening program. Both DTFM and ASTM are
thought to stimulate blood supply in the vicinity of the
tendinopathy and this is thought to promote healing of the
affected tendon. However, studies in this area are lacking
and currently no high-quality evidence exists for or against
the use of these two manual therapy interventions for treat-
ment of tendinopathy.
Eccentric Training for Tendinopathy
One of the most exciting outcomes of tendinopathy
research has been the positive ndings of eccentric exercise
as a treatment for chronic tendinopathy. Eccentric loading
exercises involve active lengthening of the muscle tendon
unit. Eccentric training as a treatment for chronic tendi-
nopathy is not a new concept.
197 , 198
The original Achilles
tendinopathy eccentric exercise protocol published by
Stanish and colleagues
198
in 1986 has been expanded and
improved. In the protocol by Alfredson and colleagues,
199

the patient groups were required to perform three sets of 15
repetitions of eccentric heel lowering at a slow speed with
the knee straight and bent, twice per day for 12 weeks. The
control group was required to perform concentric
exercises (active shortening of the muscle tendon unit). As
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
of the exercise became painful but not disabling. The sub-
jects were instructed to increase the resistance used once the
exercise became pain-free. High levels of patient satisfaction
were seen in the eccentric loading groups (82%) and all
12 participants returned to their sports activities. In subse-
quent long-term follow-up (mean 3.8 years) Alfredson and
co-workers have conrmed both the initial good results and
a statistically signicant reduction of tendon thickening
and resolved neovasculation.
200 , 201
One problem with the
Alfredson protocol was that it was less successful for patients
with insertional Achilles tendinopathy.
202
Initially, it was
thought that this was because of differences in pathological
conditions; however, this appears to be untrue.
203
Jonsson
and colleagues have reported that modifying the Alfredson
protocol by performing the eccentric Achilles exercises on
the oor instead of off a step improves success in those with
insertional Achilles tendinopathy.
204
These researchers
hypothesize that the avoidance of excessive passive dorsiex-
ion in weightbearing prevents soft tissue impingement be-
tween tendon, bursa, and bone at the calcaneal tendon. In
addition, investigators have determined that the need to
avoid sports activity during eccentric training for Achilles
tendinopathy is not necessary. Silbernagel and colleagues
investigated whether any difference in outcomes could be
found between those subjects who rested and those who
continued their sports activity.
205
The exercise training
group was allowed, with the use of a pain-monitoring
model, to continue Achilles tendonloading activity, such as
running and jumping, whereas the active rest group had to
stop such activities during the rst 6 weeks. No negative
effects could be demonstrated from continuing Achilles
tendonloading activity, with the use of a pain-monitoring
model, during treatment.
205
This is important as it allows
the clinician, with some condence, to permit loading activ-
ity during rehabilitation. This may allow better adherence to
the rehabilitation program by the athlete if he or she does
not feel that the health professional is taking away the
desired activity. The eccentric training program described by
Silbernagel and colleagues is shown in Box 29-1 .
205
The success of eccentric training for Achilles tendinopa-
thy has fostered efforts to determine whether eccentric
training will work for other tendinopathies. Two small stud-
ies on the use of eccentric exercises on a decline board for
treatment of patella tendinopathy have shown positive
results.
206 , 207
A pilot study has also been performed showing
some positive results using eccentric exercises in patients
with supraspinatus tendinopathy.
208
Despite these promis-
ing results, questions remain.
209
Why eccentric training
appears to work is uncertain. The eccentric programs also
seem to be of more benet for active individuals.
200
These
programs require highly motivated people (e.g., the masters
athlete) who are also willing to perform multiple repeti-
tions, twice daily, 7 days a week for 12 weeks, and this will
not suit all patients. Although results appear promising,
future research is still needed to support the use of eccentric
exercise in the management of tendinopathy.
Injection Therapy for Tendinopathy
A systematic review of corticosteroid injection for lateral
epicondylalgia found a total of 12 trials suitable for analysis.
The review authors concluded that corticosteroid injection
was effective in the short term (2 to 6 weeks) but that in the
long term, there was no difference in outcome when com-
pared with those not receiving injections.
210 , 211
There are
several case reports of tendon rupture following corticoste-
roid injection,
212-215
particularly involving the Achilles ten-
don.
214 , 215
Because of the concerns surrounding tendon
integrity following steroid injection, the mounting evidence
shows that the use of intratendinous injections is contrain-
dicated. In contrast, evidence surrounding peritendinous
Phase 1: Weeks 1 to 2
Patient Status: Pain and difculty with all activities, difculty
performing 10 one-legged toe raises
Goal: Start to exercise, gain understanding of the
injury and of the pain-monitoring model
Treatment Program: Perform exercises daily
Pain monitoring model information and advice on exercise activity
Circulation exercises (moving foot up and down)
Two-legged toe raises standing on the oor (three sets 10-15
repetitions per set)
One-legged toe raises standing on the oor (3 10)
Sitting toe raises (3 10)
Eccentric toe raises standing on the oor (3 10)
Phase 2: Weeks 2 to 5
Patient Status: Pain with exercise, morning stiffness, pain
when performing toe raises
Goal: Start strengthening
Treatment Program: Perform exercises daily
Two-legged toe raises standing on edge of stair (3 15)
One-legged toe raises standing on edge of stair (3 15)
Eccentric toe raises standing on edge of stair (3 15)
Quick-rebounding toe raises (3 20)
Phase 3: Weeks 3 to 12 (longer if needed)
Patient Status: Handled the phase 2 exercise program, no pain
distally in tendon insertion, possibly decreased
or increased morning stiffness
Goal: Heavier strength training, increase or start
running or jumping activity
Treatment Program: Perform exercises daily and with heavier load
two to three times per week
One-legged toe raises standing on edge of stair with added
weight (3 15)
Eccentric toe raises standing on edge of stair with added weight
(3 15)
Plyometric training
Phase 4: Week 12 to 6 Months (longer if needed)
Patient Status: Minimal symptoms, morning stiffness not
every day, can participate in sports without
difculty
Goal: Maintenance exercise, no symptoms
Treatment Program: Perform exercises two to three times per week
weight (3 15)
(3 15)
weight (3 15)
(3 15)

Box 29-1 Silbernagels Achilles Tendinopathy Protocol
From Silbernagel KG , Thome R, Eriksson BI, Karlsson J: Continued sports activity, using a pain-monitoring model, during rehabilitation in patients with Achilles
tendinopathy: A randomized controlled study, Am J Sports Med 35(6):897-906, 2007.
steroid injections is lacking, and at present no recommenda-
tions for or against their use can be made.
In contrast to corticosteroid injections, four other injec-
tion therapies are currently being used in the treatment
of tendinopathy. These are prolotherapy,
216-218
sclerosing
polidocanol,
219-222
autologous whole-blood and platelet-rich
plasma (PRP) injections.
223-227
Prolotherapy (proliferative in-
jection therapy) involves injecting an inactive irritant solution
into the tendon for the purpose of strengthening weakened
connective tissue and alleviating musculoskeletal pain. Al-
though several injection agents have been used, hyperosmolar
dextrose and morrhuate sodium are the most common.
216-218

Polidocanol is a vascular sclerosant. In treating tendinopathy,
it is used to sclerose areas of high intratendinous blood ow.
These areas of high blood ow, or neovascularity, are thought
to be associated with the underlying mechanism of lateral
epicondylalgia and other overuse tendinopathies.
219-222

Autologous whole blood and the blood product PRP have
been used as injectants for tendinopathy with the aim of pro-
moting (via cellular mediators) healing in areas of tendon
degeneration. PRP is prepared from autologous whole blood,
which is centrifuged to concentrate platelets in plasma. It
is thought that the platelet-derived growth factors in the
PRP may improve soft tissue healing within the damaged
tendon.
223-227
Unlike steroid injections, these injections theo-
retically try to address the new model of tendinopathy as
being a pathological entity without inammation. Despite
initial positive results in pilot studies, these new injection
therapies need further analysis. Rigorous controlled studies of
sufcient sample size with validated patient reported outcome
and radiological measures are needed to determine long-term
effectiveness and safety, and whether these techniques can play
a denitive role in the management of tendinopathy.
227
Topical Glyceryl Trinitrate for Tendinopathy
One group of researchers has recently completed several
randomized controlled trials examining the effect of topical
glyceryl trinitrate in the treatment of Achilles, wrist exten-
sor, and supraspinatus tendinopathies.
228-231
These research-
ers have shown long-term benets of topical glyceryl
trinitrate use 3 years after the cessation of therapy.
229
The
reasons for these positive ndings are uncertain, although
current speculation is that the topical gel may cause local
vasodilatation that may lead to an increased local blood sup-
ply. To be validated clinically, these positive results need to
be repeated by other research groups. It is also important to
realize that in each of these studies, the use of the topical
gel or patch was not done in isolation but rather in addition
to eccentric strengthening and stretching.
The practicing sports medicine clinician needs to be aware
of the current research investigating manual therapy, eccen-
tric exercise, and injection therapy for the treatment of
tendinopathy. Likely a staged, multimodality program is best.
However, the most effective tendinopathy treatment algo-
rithm to return the masters athlete to sport remains elusive.
Sports Activity in the Masters Athlete
Following Total Joint Arthroplasty
For many masters athletes, joint pain and dysfunction can
pose an insurmountable obstacle in their pursuit to con-
tinue sports activities. In severe pathological conditions of
the joint, total joint arthroplasty offers a viable option to
reduce pain and improve function. Although basic func-
tional tasks are often attainable after surgery, restrictions on
sporting activity after the procedures remain unclear.
Historically, the medical community has viewed postar-
throplasty physical activity with caution. Several studies
have implicated heavy or moderate activity to be a cause of
surgical revision in joint arthroplasty. Chandler and col-
leagues
232
reported that 62% of subjects who participated in
moderate or heavy activities after a THA displayed increased
incidence of prosthetic loosening. Others have found that
patients who participated in high-impact activities had the
highest rates of revision surgery.
233
Despite evidence of potential complications, patients
with total joint arthroplasty are more commonly pursuing
sports activity following surgery. Bradbury and colleagues
234

noted 65% of total knee arthroplasty (TKA) patients re-
turned to sports activities after surgery, although many
chose lower-impact and less physically demanding activi-
ties. Examples in popular sports culture reveal successful
rehabilitation of high-prole sports gures overcoming
total joint arthroplasty and returning to competition at
the professional level. Professional golfer Jack Nicklaus
received a THA in 1999 and returned to the Senior Pro
Tour within 4 months. He continued to compete until
2005. Bo Jackson was at the height of his professional
baseball and football career when he had a THA in the
early 1990s. Jackson returned to play for 2 years of profes-
sional baseball before eventually retiring. These athletes
have challenged the physical limits after joint arthroplasty
and brought notoriety to sports activity following total
joint arthroplasty.
Although exceptions do exist, candidates for total joint
arthroplasty are generally middle-aged to elderly.
235
Patients
in this age group are more susceptible to serious health con-
ditions such as cardiovascular disease, diabetes, and osteopo-
rosis. Physical activity is an important factor in reducing the
risk of such diseases. For many adults, participation in vari-
ous sports and athletic activities offer a vehicle to a healthy
lifestyle. Ries and colleagues
236 , 237
reported improved car-
diovascular function in patients who had undergone knee or
hip arthroplasty compared with their presurgical status.
Total Hip Arthroplasty
Age and activity level are important aspects to consider
when discussing THA. Younger, active individuals
may place high demands on the implants and may place
themselves at risk for implant failure and subsequent revi-
sion. It appears that activity level is the most variable
patient-related factor and may explain why some implants
last longer.
238
Joint load must be considered when dis-
cussing postarthroplasty activity levels with patients. If
patients resume activities that place high loads on the
joint, wear and tear may increase exponentially.
239 , 240
Be-
cause cardiovascular tness is an important preventative
measure, it is important to determine at what level
masters athletes can return to activities that promote this.
Speed walking appears to be a good alternative to run-
ning, while still providing for cardiovascular tness. Com-
pressive loads at the hip joint are 4 to 4.5 times the
athletes body weight when power walking.
239
Jogging or
running will increase hip joint compressive forces to
greater than 5 times the athletes body weight. Unfortu-
nately, there are many activities without documented
evidence on joint forces and loads. Kuster
239
suggests the
following guidelines: during daily activities, loads of 3 to
4 times the athletes body weight may apply; while in
sporting activities, loads of 5 to 10 times the athletes
body weight may occur. Other considerations include
weight training, which will increase loads, and endurance
activities in which load depends on speed.
Patients who have been active and athletically skilled
prior to THA will have the greatest chance for returning to
a high level of skilled activity postoperatively. Individuals
with increased athletic ability typically display less joint
forces than those who are less skilled. Attempting to learn a
new athletic skill is unlikely to be successful and may put the
patient at risk for injury after surgery.
What specic recommendations exist for returning to
exercise and sports activities following total joint arthro-
plasty? Most literature reviews are based on personal opinion
rather than prospective studies. In general, low-impact
activities are tolerated well by patients given that forces and
wear will be lower relative to high-impact exercise and sport.
As impact and torsional loading increase during high-impact
sports and exercise, relative risk associated with activity
increases as well.
239 , 241
Surgeons and residents at the Mayo
Clinic
242
surveyed themselves and reviewed the literature
regarding return to athletics following THA. They deter-
mined that orthopedic surgeons should suggest the follow-
ing low-impact sports to their patients who are interested in
returning to sports: sailing, swimming, scuba diving, cycling,
golf, and bowling. They advise against high-impact activities
such as running, water skiing, football, baseball, basketball,
hockey, handball, karate, soccer, and racquetball. In 1999,
Healy and colleagues
243
conducted a survey of 54 members
of The Hip Society to determine their recommendations for
athletics and sport participation following hip arthroplasty
surgery. The survey was completed by Society members and
they were asked to rate 42 different sports as either recom-
mended or allowed, allowed with experience, no opinion,
and not recommended. See Table 29-3 for a list of these
activities and recommendations.
243
Clinical Points
Activity level, and type and amount of joint loading are better parame-
ters than age when determining implant longevity following total joint
arthroplasty.
Table 29-3
Activities Following Total Hip Arthroplasty1999 Hip Society Survey
Recommended/Allowed Allowed with Experience Not Recommended No Conclusions Made
Ballroom dancing
Bicycling (stationary)
Croquet
Doubles tennis
Golf
Horseshoes
Shooting
Shufeboard
Swimming
Walking
Bowling
Bicycling (road)
Canoeing
Cross-country skiing
Hiking
Horseback riding
Low-impact aerobics
Baseball/softball
Basketball
Football
Gymnastics
Handball
High-impact aerobics
Hockey
Jogging
Lacrosse
Racquetball
Rock climbing
Singles tennis
Soccer
Squash
Volleyball
Fencing
Ice skating
Jazz dancing
Square dancing

Modied from Healy WL , Iorio R, Lemos MJ: Athletic activity after joint replacement, Am J Sports Med 29(3):382, 2001.
Golf has been widely studied and the majority of sur-
geons permit or do not discourage patients to return to golf
after THA, but it is recommended that patients use a cart
while playing. Mallon and colleagues
244-247
determined that
surgeons allow patients to return to golf 19.5 weeks after
surgery. Golfers surveyed stated that their driving distance
decreased 3.3 yards and their handicap increased by
1.1 strokes after THA. These golfers played an average of
3.7 times per week and were followed for 3 or more years.
At an average follow-up time of 61 months, hybrid and
uncemented total hip arthroplasties were associated with
less loosening as determined by radiograph when compared
with cemented total hip arthroplasties. No differences in
pain during or after golf were noted.
244-247
Mont and colleagues
235
evaluated tennis following THA.
For 58 tennis players who had 75 THA surgeries, only 14%
of the patients stated that their physician approved of their
return to tennis. Of these patients, 21% specically had the
surgery to return to tennis and they did so after approxi-
mately 7 months. These individuals played three times per
week and maintained their presurgical national tennis rank-
ing. Revision was necessary for 4% of these patients at a
mean of 8 years after their initial hip arthroplasty.
Healy and colleagues
243
suggest that patient education is
crucial when addressing treatment options and expectations
regarding return to activity and sport. Emphasizing the im-
portance of previous activity and athletic skill, preoperative
rehabilitation, proper choice of components and procedure,
adherence to precautions, and surgeon skill and experience
on THA outcomes are essential. Setting realistic expectations
for return to sport and emphasizing the risks and benets of
specic activities is also important. For the active patient,
Healy and his colleagues
243
recommend a cementless acetab-
ular component, a hemispheric titanium porous-coated im-
plant inserted with an under-ream press-t technique and
supplemental screw xation, with a minimum polyethylene
thickness of 6 mm. Femoral components for active patients
may be cemented or cementless. For cemented techniques
they recommend cobalt-chrome implants with the proper
femoral offset for restoration of abductor biomechanics.
Second-generation cementing techniques with vacuum mix-
ing are also used. For cementless techniques, a cobalt-chrome
tapered wedge stem with porous coating is inserted with the
appropriate offset. A 28-mm ball is used to balance wear and
stability factors.
243
Regarding physical activity, patients should be moti-
vated to maintain appropriate cardiovascular tness levels.
Cardiovascular exercise is benecial for the THA patient
for many other reasons including general health, preven-
tion of cardiac problems, and for improvement of bone
quality and implant xation. Low-impact aerobic exercise
suggestions that allow for increased heart rate are the most
appropriate. Aerobics are completed 3 to 4 days per week
for 30- to 40-minute sessions. Whether the patient wants
to return to recreational or competitive sports is ultimately
up to him or her, although prudent guidance from the
surgeon and rehabilitation clinician physical therapist is
essential. For these individuals, skiing, tennis, and hiking
can be suggested, along with consideration of their previ-
ous athletic participation. Recommendations that help
reduce joint forces are essential to reducing hip joint load-
ing. These include using ski poles when hiking; skiing on
at, groomed runs; and cross-country skiing techniques.
Many of these masters athletes will push the durability and
longevity of arthroplasty implants by engaging in high-
demand sports and activities that repetitively cycle the im-
plant with and without excessive loads. Health care
professionals must learn from these situations as well as
engage in further research to assist in determining what
activities are appropriate and possible for the aging athlete
following THA.
Total Knee Arthroplasty
As with masters athletes with a THA, considerations to the
prosthetic wear and joint-loading forces during sports activ-
ity following TKA is important. Normal and fast walking
speeds have joint loads estimated at 2.8 and 4.3 times body
weight, respectively. Power walking results in tibiofemoral
compressive joint forces of 4 to 4.5 times the athletes
bodyweight.
240
An estimated load during slow jogging is
7.5 to 8 times the athletes body weight for male patients
and 8.5 to 9 times the athletes body weight for women.
Knee joint moments increase with increasing speed, result-
ing in knee joint loads of 10 or more times the athletes
body weight with jogging.
240
Cycling has demonstrated
increasing compressive forces with increasing workload.
Saddle height can also inuence joint load; the higher the
saddle, the lower the compressive force. Cycling demon-
strates a tibiofemoral joint load of 1.2 times the athletes
bodyweight.
240
Hiking is another activity patients may want
to participate in after TKA. Downhill walking places large
loads on the knee joint. Fast downhill walking has demon-
strated loads up to 8 times the athletes body weight. The
use of ski poles is recommended to reduce these joint load-
ing forces by as much as 20%. Unfortunately, there are
many activities without documented evidence on joint
forces and loads. Kuster and Stachowiak
240
report that dur-
ing daily activities, loads of 3 to 4 times the athletes body
weight may apply, whereas in sporting activities, loads of
5 to 10 times the athletes body weight may occur. Other
Patient Education Following Total Joint Arthroplasty
is Essential and Should Include:
Treatment options
Treatment expectations regarding return to activity and sport
Pre- and postoperative rehabilitation
Adherence to precautions
Risks and benets of specic activities
Maintenance of cardiovascular tness
considerations include weight training, which will increase
loads, and endurance activities, in which load depends on
speed.
More than half of these surgeons also suggested that
patients use a golf cart after knee arthroplasty. The golfers
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
of these golfers did use golf carts and 84% did not have pain
when playing golf, but did complain of mild ache after play-
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.
Diduch and colleagues
248
evaluated outcomes of TKA in
young, active patients. The mean age of patients was
51 years and 24% regularly participated in strenuous activi-
ties such as tennis, skiing, bicycling, farm, or construction
work. All but two of the 88 patients experienced increased
activity levels postoperatively. The average survivorship of
the prosthesis for this group was 94% at 18-year follow-up.
Despite the active lifestyles of these patients, loosening was
not a problem. Healy and colleagues
243
recommend an an-
teromedial arthrotomy with a cemented and minimally
constrained PCL-sacricing or PCL-substituting condylar
knee implant for active patients requiring a TKA. They use
intramedullary femoral instrumentation and extramedullary
tibial instrumentation to achieve the correct tibiofemoral
alignment of 5 to 7.0. The femoral component should be
made of cobalt-chrome with a rounded condylar geometry
and conforming patellofemoral joint. The tibial implant is
modular and made of titanium with a high-molecular-
weight polyethylene insert at least six to eight mm thick.
It is recommended that patients avoid recreational and
Clinical Point
Use of ski poles or walking sticks can reduce lower limb joint loading
forces by up to 20%.
Recommendations for Return to Sport
after Total Knee Arthroplasty
Bradbury and colleagues
234
evaluated participation in sports
after TKA. They demonstrated that 65% of their patients
who participated in regular exercise before TKA returned to
sports after the procedure. The majority of these patients
returned to low-impact sports (91%), although some (20%)
returned to higher-impact activities such as tennis. Of
42 patients who underwent simultaneous bilateral TKA,
20 participated in sports prior to surgery. Of those 20 pa-
tients, 15 (75%) returned to sports following completion
of their rehabilitation program. Healy and colleagues
243
surveyed members of The Knee Society regarding recom-
mendations for athletics and sports participation following
TKA. Table 29-4 illustrates the results of this survey.
Mallon and Callaghan
246
investigated members of The
Knee Society and active golfers who had a TKA. Of the
surveyed surgeons, 92% did not discourage patients from
playing golf after knee arthroplasty, nor did they note in-
creased complications in those patients returning to golf.
Table 29-4
Activities Following Total Knee Arthroplasty1999 Knee Society Survey
Bowling
Bicycling (stationary)
Croquet
Dancing (ballroom, square, jazz)
Golf
Horseback riding
Horseshoes
Low-impact aerobics
Shooting
Shufeboard
Swimming
Walking
Bicycling (road)
Canoeing
Cross-country skiing
Doubles tennis
Hiking
Ice skating
Rowing
Speed walking
Weight lifting (machines)
Baseball/softball
Basketball
Football
Gymnastics
Handball
Hockey
Jogging
Lacrosse
Racquetball
Rock climbing
Singles tennis
Soccer
Squash
Volleyball
Downhill skiing
Fencing
Inline skating
Weight lifting (free weights)
athletic activity until their quadriceps and hamstrings are
sufciently rehabilitated in physical therapy.
243
Masters ath-
letes are counseled to maintain cardiovascular tness with
activities such as swimming and cycling. If a masters athlete
wishes to participate in more aggressive activities, the
patient should be assisted in making reasonable choices.
Total Shoulder Arthroplasty
Although hip and knee total joint arthroplasty remain com-
mon procedures in orthopedics, total shoulder arthroplasty
(TSA) is less prevalent. The total number of hip and knee
joint arthroplasties performed annually is nearly 20 times
that of TSA.
249
Trends in pain relief and patient satisfaction
tend to mirror those found in joint arthroplasty of the
hip and knee. Subjectively, 92% of patients describe their
shoulder as much better or better following TSA.
250
Recommendation for Return to Sport
after Total Shoulder Arthroplasty
To assess the appropriateness of athletic activity, one must
consider the sport being pursued following TSA. A survey of
the American Society of Shoulder and Elbow Surgeons re-
ported by Healy and colleagues
243
revealed recommenda-
tions of appropriate sports activity following TSA. These
results are illustrated in Table 29-5 . None of the recom-
mended sports were classied as contact sports and were
relatively low-impact with respect to the upper extremity.
Most activities also involved primarily a uniplanar movement
of the shoulder. Bowling, horseshoes, and cross-country
skiing are all sports that require primarily sagittal plane
movement of the shoulder. In addition, the stress to the
dynamic stabilizers during the deceleration phase of these
activities is partially negated by gravitational forces.
Mitchell and colleagues
251
examined the mechanics of
the shoulder during the golf swing for amateur senior golf-
ers and established normative data characterizing shoulder
motion. Key components of the golf swing required 119
horizontal adduction, 94 of vertical elevation during the
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
103 elevation with 108 horizontal adduction during the
follow-through. The expectation of a patient wishing to
return to golf would require that he or she be able to
achieve these ranges of motion against gravity and hold
these positions against resistance. Table 29-6 compares the
normal ROM after TSA to the normal ROM needed for a
golf swing in an older amateur golfer. These expectations
may be less attainable in patients having a TSA because of
rotator cuff deciency and more realistic in patients with
isolated OA.
252
Jensen and Rockwood
253
studied 24 golfers following
TSA. Of the 24 golfers, 23 were able to return to golf. The
average return to golf took 4.5 months. No radiographic
evidence of component loosening was noted compared
with nongolfers at follow-up evaluations ranging between 2
to 10 years postoperatively. Handicap scores of these patients
were reported to improve on average by ve strokes. Mem-
bers of the American Society of Shoulder and Elbow Surgeons
were surveyed regarding the risks involved with playing golf
after a TSA. Of those surveyed, 91% recommended patients
return to golf and believed there was no increased risk of
postoperative complications by playing golf.
243
In regard to tennis, the survey demonstrated an interest-
ing contradiction. Doubles tennis was recommended, but
no conclusion was made about singles tennis.
243
Ground
strokes would appear to be appropriate if adequate strength
Table 29-5
Activities Following Total Shoulder Arthroplasty1999 American Shoulder and Elbow Society Survey
Bicycling (road or stationary)
Bowling
Canoeing
Croquet
Cross country skiing
Dancing (ballroom, square, jazz)
Doubles tennis
Horseshoes
Jogging
Low-impact aerobics
Shufeboard
Speed walking
Swimming
Downhill skiing
Golf
Ice skating
Shooting
Football
Gymnastics
Hockey
Rock climbing
Baseball/softball
Fencing
Handball
Horseback riding
Lacrosse
Racquetball
Roller or inline skating
Rowing
Soccer
Singles tennis
Volleyball
Weight training
and dynamic control was demonstrated in the affected
shoulder below shoulder height. Traditional serving me-
chanics may have to be altered secondary to predictable
elevation and rotational motion loss following TSA. This
may require even more involvement of the muscles of the
legs and torso to generate power needed to perform an ef-
fective tennis stroke. As a result, a complete evaluation of
the patients trunk and lower extremities with regard to
strength, mobility, and proprioception is critical in making
an appropriate recommendation for the return to sport.
Overhead sports pose interesting challenges. It is well
known that athletes involved in throwing and racquet
sports tend to have differences in rotational ROM, speci-
cally with signicant increases in lateral rotation of the
dominant side.
254 , 255
Optimal lateral rotation as reported in
the literature following TSA averages only 60.
252
This is far
below averages seen in overhead athletes. In addition, limi-
tations in rotator cuff strength may further hinder the
ability to attain sport-specic positions and stabilize the
shoulder in such positions. Follow-through and decelera-
tion phases of overhead throwing require signicant force
from the rotator cuff. Inadequate eccentric strength of
these muscles increases the risk of injury and the inherent
stability of the shoulder.
255
Because of the factors listed previously, it seems unlikely
that many patients having TSA of their throwing arm would
be physically able to perform such tasks. The sports medi-
cine team should consider that loss of functional lateral
rotation ROM may manifest itself in other biomechanical
compensations. Trunk rotation may become excessive to
counteract the lack of shoulder rotation. In this instance,
strength and mobility of the lumbar and thoracic spine may
become an important factor in making an appropriate rec-
ommendation on postoperative throwing. Other muscles of
the legs and arms may compensate for shoulder weakness.
The patient may also alter throwing mechanics with a push-
ing motion similar to throwing a shot put. This requires less
rotation of the shoulder and uses more of the triceps and
pectoralis major musculature to propel the ball. For those
masters athletes wishing to pursue throwing sports, it is
recommended that they have pain free anti-gravity control
of the arm in elevated and laterally rotated position and that
they demonstrate dynamic control of not only the shoulder,
but of the trunk and lower body as well.
Total Ankle Arthroplasty
In the past, athletic activity following total ankle arthro-
plasty (TAA) has been strongly discouraged.
256
In 1994,
Kitaoka and colleagues
257
reported an overall prosthetic
survivorship of 65% at 10 years postoperatively, but only a
42% prosthetic survivorship in a subgroup of patients
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 xation.
258
Pivot-
ing and cutting maneuvers risk dislocation and malleoli
fractures caused by the lack of ligamentous integrity and
dynamic strength that is often compromised with ankle
surgery. Normal postoperative ROM of combined dorsi-
exion and plantar exion is often signicantly less than
what is considered normal. The limited ROM would
likely hinder and dramatically change the mechanics of the
entire lower limb, including the foot, ankle, knee, and hips.
Ankle stability, functional ROM, strength, and balance
require careful assessment before returning to any sport
activity. Low-impact activities with primarily movement in
the sagittal plane logically put the patient at lower risk for
complications.
The emergence of newer surgical techniques is promis-
ing. Wood and Deakin
259
reported a revision rate at 5 years
to be approximately 7% in a sample of 200 ankles. Anderson
and colleagues
260
retrospectively followed patients with
TAA using the Scandinavian total ankle replacement pros-
thesis between the years 1993 and 1999, and reported 30%
of the patients required a revision for their TAA, but noted
the patients who underwent surgery later had much greater
success. Valderrabano and colleagues
261
examined 147 pa-
tients (28 to 86 years of age) 2 to 4 years following TAA.
Patient satisfaction, ROM, American Orthopaedic Foot and
Ankle Society hindfoot score, radiological assessment, rate,
level, and type of sports activity were recorded and com-
pared with the patients preoperative results. At follow-up,
excellent and good outcomes were reported in 83% of cases
and 69% of patients were pain free. The mean ROM preop-
eratively was 21 and after TAA, it was 35. Before surgery,
36% of the patients were active in sports; after surgery, this
Table 29-6
Comparison of Shoulder Range of Motion During the Golf
Swing with Range of Motion Following Total Shoulder
Arthroplasty
Shoulder ROM
Horizontal
Adduction Elevation
Lateral
Rotation
Dominant shoulder
ROM during the
golf swing
108 103 48
Non-dominant
shoulder ROM
during the golf swing
119 94 59
Shoulder ROM
following total
shoulder arthroplasty
Not
available
90 47
Data from Mitchell K , Banks S, Morgan D, Sugaya H: Shoulder
motions during the golf swing in male amateur golfers, J Orthop
Sports Phys Ther 33(4):196-203, 2003; and Wilcox RB, Arslanian LE,
Millett P: Rehabilitation following total shoulder arthroplasty,
J Orthop Sports Phys Ther 35(12):821-836, 2005.
ROM, Range of motion.
percentage rose signicantly to 56%. Overall, sports-active
patients with a TAA showed better functional results than
did inactive ones.
261
Timing of Return to Sport
After Total Joint Arthroplasty
Determining when a total joint arthroplasty patient is
ready to return to sport is essential. Whether it is directly
determined by the treating clinician or physician or self-
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
across the joints involved. Ensuring that the older athlete
has good balance in bilateral and unilateral stance is very
important for those returning to sports. If balance and pos-
tural stability are compromised, risk of injury during sport
may increase. Sport-specic rehabilitation exercises should
be added to the plan of care when the athlete has passed
specic examination- and performance-based criteria. Even-
tually, it is necessary to put the masters athlete through
more rigorous testing to ensure he or she is ready to return
to sport.
As the world of sports medicine has evolved, so has the
context in which athletes are dened. Athletes span the
entire life cycle, and the traditional age-related boundaries
by which athletes are conned have expanded. Athletic
careers and recreation in sports may not be terminated by a
joint arthroplasty procedure. Although there appears to be
some inherent risk to performing sports following arthro-
plasty, low-impact and noncontact sports are usually appro-
priate and generally are encouraged by physicians. Newer
surgical techniques and prosthetic materials have shown
greater durability and have decreased postoperative compli-
cations. Overall survivorship of arthroplasty procedures
demonstrates satisfactory results between 15 to 20 years in
the literature. In many procedures, press t or uncemented
xation is recommended for younger, active patients. Press
t or uncemented xation provides less initial xation, but
allows bone ingrowth for a strong, long-term xation and
preserves greater bone integrity in cases in which a future
revision is needed.
As medical science advances to provide individuals with
greater longevity, expectations of function and recreation
will continue to grow as well. Patients who undergo total
joint arthroplasty are not necessarily limited to a sedentary
lifestyle. The methods and technology in the areas of joint
arthroplasty will continue to evolve, and so will the possi-
bilities to return to physical activity and athletics.
Conclusion
The population of masters athletes will continue to increase
as the worlds population ages. Better health care and tech-
nology is allowing the continuation of athletic activity in
individuals well into their golden years. Because of the
physiological changes associated with aging, the masters
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,
and scrutiny of the physiological demands and musculosk-
eletal stresses of their desired sport. Ultimately, clinicians
and masters athletes must nd a balance between a return
to participation, safety, and a lifelong enjoyment of their
sport.

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773
Index
773
A
Ab Slide, 393
Abdomen
anatomy of, 605f
three regions of, 606, 606t
Abdominal injuries, internal, 596,
596b
acute life-threatening conditions in,
623b, 628
bladder, 612
evaluation of, 604-606, 604b
hepatic, 609
intestinal tract, 609-610
kidney, 450, 610-612
pediatric, 610, 610b
types of, 610-611, 610f
misleading physical examination in,
604, 606t
pancreatic, 612
penetrating, 604-606, 604b
return-to-play criteria for, 608b
signs and symptoms of, 598t, 604,
604b
splenic, 606-609, 607f
structures involved in, 605f, 606b,
606t
ureteral, 612
Abdominal muscles
in golf swing, low back pain and,
224-225, 225b
tendinopathies of, in soccer players,
298
Abdominal surgery
return-to-activity guidelines for,
603t
wound healing after, 604, 604f
Abdominal wall, anatomy of, 597f
Abdominal wall injury, 596-604,
596b. See also Hernia.
vs. blow to solar plexus, 597, 598t
contusion as, 596-597, 604, 605-606
vs. intra-abdominal injury, 598t
muscle strain as, 597-598, 619-620
Abrasions, 457-458
corneal, 589
in disabled athletics, 688t, 690t,
691-692
prosthetic socket and, 692
of head and face, 583
Acceleration, running, testing of, 31,
31t, 34t
Acclimatization to altitude, 119b, 445
circulatory adaptations in, 119-120
exercise performance and, 120
neuropsychologic function and,
120-121
pulmonary ventilation and, 118, 119f
Acclimatization to cold, 114
Acclimatization to heat, 102-103,
103b, 103f
Acetabular labrum, injury to
golf swing and, 222, 223b
osteoarthritis secondary to, 712
in runners, 307
N -Acetylcysteine, 156-157
Achilles notch, of running shoe, 322
Achilles tendinopathy
corticosteroid injection for, 716-717
in dancers, 666-667, 666f, 667b
eccentric training for, 715-716, 716b
in masters athletes, 714
pathophysiology of, 714-715
topical glyceryl trinitrate for, 717
Achilles tendon, aging and, 707
Achilles tendonitis, in cyclists, 210t
ACL. See Anterior cruciate ligament
(ACL).
Acne mechanica, 461, 461f
Acquired immunodeciency syndrome
(AIDS), 448
Acrochordons, 466-467
Acromioclavicular joint
football shoulder pads and, 512
sprain of, protection for, 496-499
Actinic keratoses, 472
Activities of daily living (ADLs), in
older adults, 706, 710
Acupuncture, for delayed onset muscle
soreness, 434
Acute mountain sickness, 118, 121,
122-123t
pre-existing lung disease and, 121
ADD/ADHD (attention decit
disorder/attention decit
hyperactivity disorder), 50-51,
51b, 182
Adenosine receptors, caffeine and,
154-155, 160-161
Adenosine triphosphate (ATP)
endurance exercise and, 141-142
high-intensity exercise and, 158, 160
muscle nociceptors and, 424
Adhesive capsulitis, in diabetics, 449
Adhesive tape
for custom padding, 485
protective wrap under, 465t
Adhesives
for custom padding, 485
for wound closure, 457, 587
ADLs (activities of daily living), in
older adults, 706, 710
AED (automated external debrillator),
627
Aerobic capacity. See Oxygen uptake,
maximum (VO
2
max).
Aerobic conditioning tests, 32-33
Aerobic exercise
energy sources for, 67
after total hip arthroplasty, 719
Aerobic training
fat as fuel and, 84
heat acclimatization and, 103
AEs. See Athlete-exposures (AEs).
Agility, testing of, 31, 32f, 34t
Aging. See also Masters athlete.
benets of exercise and, 704, 704b
cold exposure and, 113
heat intolerance and, 104
musculoskeletal decline in, 704, 706
of population, US and world, 704,
705t
AIDS (acquired immunodeciency
syndrome), 448
Air management pads, 480-481
Air pollution, 123-124. See also
Asthma, air pollution and;
Carbon monoxide; Nitrogen
dioxide; Ozone; Particulate air
pollution; Sulfur dioxide.
altitude and, 132
heat stress and, 131
interactions between pollutants in,
131
national standards for, 123, 124t
vocal cord dysfunction and, 128
Aircast sport stirrup, 516-518, 517f
Airway injuries
laryngeal, 581-582, 582b, 583f
nasal, 590, 590f
rib fracture with, 617, 618b
sternoclavicular dislocation with,
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.
774 Index
Airway management, 581-582
Airway obstruction, checking for,
623-624
Alcohol
caloric content of, 85
cold injury and, 114
endurance contests and, 85-86
after exercise, 93
hypertension and, 442-443
muscle metabolism and, 86
physiologic effects of, 85-86
Alcohol abuse
in athlete with disability, 690
in young athlete, 53, 53b
Allergic dermatitis, 464-465
Allergy
asthma in, 124, 126
in athlete with disability, 688t
Alopecia, 462, 462f
Altitude. See High altitude.
Amenorrhea
bone density and, 18-19, 87,
641-642, 643
diagnostic testing in, 642-643
exercise-induced, 18-19
in female athlete triad, 53, 641-642
Amino acids, 77
ATP generation from, 141-142
branched-chain, 79
central fatigue and, 144
as ergogenic aid, 152-153
plant sources of, 82
Amnesia, concussion with, 539, 539b
Amphetamines
heat stroke caused by, 106
reasons for use of, 175
testing for, 180-181
Amputees as athletes, 694b
as cyclists, 209-211, 209b, 212f
injuries of, 692-695, 693f
as runners, energy requirements for,
694-695
Anabolic Steroid Control Act, 177-178
Anabolic-androgenic steroids, 55,
164-165
adverse effects of, 165, 165b
hypertension as, 442
pectoralis major rupture as, 622
common examples of, 177t
testing for, 174-175, 176-179, 177t
young peoples use of, 55-56
Anaerobic conditioning tests, 32, 33t,
34t
Anaerobic metabolism
energy sources for, 67
at high altitude, 120
for high-intensity exercise, 158, 158b
Analytic studies, 731
Analytical epidemiology, 745
Androgen insensitivity syndromes,
185
Androgens. See Anabolic-androgenic
steroids.
Androstenedione, testing for, 178-179
Anemia
vs. dilutional pseudoanemia, 87, 87b,
446-447
iron-deciency, 86-87, 446-447,
447b
preparticipation evaluation and, 21
Angina pectoris
carbon monoxide exposure and, 129
high altitude and, 121
Angiotensin-converting enzyme (ACE)
inhibitors, for hypertension, 443
Ankle
in ballet, 657-662, 658f, 659f,
659t, 660b, 660f, 661f
in cycling, injury to, 208
hypermobile, gluteus medius and,
314-315
impingement syndromes of, 664-666
anterior, 665-666, 666b
posterior, 665, 665f, 666b
in running
kinematics of, 309-310, 309t
knee pain and, 320b
muscle activity and, 315-316
in soccer
injury to, 297, 300
jumping and, 296-297
sprains of
bracing and, 508
impingement syndromes second-
ary to, 665-666, 666b
os trigonum and, 665, 673
overweight and, 766
in soccer players, 300
taping of. See Taping, of ankle.
total joint arthroplasty of, 722-723
Ankle braces, 508, 509f
risk of injury and, 767
vs. taping, 516-518, 517f, 518f,
519, 521
cost-effectiveness of, 508, 523-524,
524b
Ankylosing spondylitis, 638-639
Anorexia nervosa, 22-24t, 54, 54b,
641
Antacids, 446
Anterior cord syndrome, 573
Anterior cruciate ligament (ACL)
deciency of
cycling and, 196-198, 198f, 199f
knee brace and, 504-506, 506f
injury to
case study of, 6-7, 7f
in dancers, 668-670, 669f, 670b,
670t, 671-672
in female athletes, 25-26, 632-635,
633t, 634f, 669-670, 766
in female soccer players, 299,
302, 632, 635, 733
in jumping, 257, 261
osteoarthritis secondary to, 166,
632, 709
return to play after, 25-26
in soccer, 299, 302, 632, 635, 733
valgus angle of knee and, 302
lunge exercises and, 401-403, 402t
squat exercises and, 397-399, 398t
Anterior knee pain syndrome. See also
Patellofemoral pain.
Q-angle and, 320
taping for, 524, 528, 528b
Anterograde amnesia, 539
Antibiotics, facial wounds and, 587
Anticholinergic drugs, heat intolerance
caused by, 106
Antihistamines, heat disorders and, 20
Anti-inammatory drugs
breast trauma and, 622
for delayed onset muscle soreness,
429-430
in iontophoresis, 432
in phonophoresis, 432
for exercise-induced bronchospasm,
444
Antioxidants
435
as ergogenic aids, 156-157, 157b
Aorta, rib fracture with injury to, 617,
618b
Aortic coarctation, preparticipation
examination and, 17-18
Aortic rupture, 627-628
Aphasia, 699
Aphthous ulcer, 460
Apocrine glands, 456
Apolipoprotein E, concussion and,
542, 545
Apophysitis, in runners, 307
Appendectomy, return-to-activity
guidelines for, 603t
Arches, height of, in runners, 318,
319f, 320-321
Arnica, for delayed onset muscle
soreness, 434-435
Arthritis. See Osteoarthritis.
Articial turf, injury rates and, 767
Ascorbic acid. See Vitamin C.
Asteatotic eczema, 475, 475f
Asthma, 124-126, 445
air pollution and, 126
nitrogen dioxide in, 131
ozone in, 131
sulfur dioxide in, 129, 131
cold-induced, 114, 132
denition of, 125b
Anterior cruciate ligament (Continued)
Index 775
diagnosis of, 125-126
exercise-induced, 444
vs. vocal cord dysfunction,
128-129, 128t
medications for, 125, 126t
prevalence of, 126, 127t
sports participation with, 22-24t
triggers of, 124-125, 125b, 445b
treatment and, 125b
types of, 124, 125t
vs. vocal cord dysfunction, 128-129,
128b, 128t
Atherosclerotic coronary artery disease,
444, 444b
Athlete-exposures (AEs), 737, 737b,
739, 742-744
Athletes foot, 467-468, 468f
Athletes heart syndrome, 17-18, 442
vs. hypertrophic cardiomyopathy,
442, 442t
Athletic pubalgia, 600-602, 600b, 601f
Athletic supporter, penile injury and,
614
Athletic trainer, 2
injury assessment on eld by, 5
injury management by, 6
with physical therapy credential, 2
practice domains of, 2, 2b
present during contact sports, 4
Atlantoaxial dislocations, 553
Atlantoaxial instability, sports
participation with, 22-24t
Atlas, fracture of, 553
Atopic dermatitis, 465
ATP. See Adenosine triphosphate (ATP).
Atrophic scars, 458
Attention decit disorder/attention
decit hyperactivity disorder
(ADD/ADHD), 50-51, 51b, 182
Augmented soft tissue mobilization,
for tendinopathy, 715
Automated external debrillator
(AED), 627
Autonomic dysreexia, 688t, 698, 698b
Autonomic nervous system, endurance
exercise and, 143, 143b
Avulsion fractures, in runners, 307
Avulsive wounds, 583
B
Babinski reex, 573
Back injury. See also Spinal injury.
golf-related, 217, 221, 221b
pushing or pulling and, 388-391,
391b
soccer-related, 298
Back pain, soccer-related, 298. See also
Low back pain.
BALCO scandal, 176-177, 178-179,
183-184
Ball, stability
lower extremity exercises and,
392-393, 399b
spine stabilization and, 392
Ball, Swiss, squat exercises and, 394
Ballet. See Dance.
Barbell squat, 393, 399-400, 404
Basal cell carcinoma, 472
Basal cell layer, of epidermis, 455-456
Basal metabolic rate (BMR), 94
Baseball
bat speed and ground forces in, 222
eye injuries in, 492
injury prevention in, 768t
physical tness prole for, 34t
protective equipment in, 479
catchers chest protector, 501, 503f
catchers shin guards, 506-508,
508f
catchers throat protector, 482
face masks, 490, 491f
gloves, 499
rib stress fractures in, 619
safety bases in, 767
shoes for, 510f
Baseball pitching, 350-384
angular velocity in, 351, 364-365,
367, 368t
ball velocity in, 355t, 365, 367, 368t
body segments in, 350-352
competition levels and, 364-366,
368-372, 370t, 371t
concluding summary of, 382
elbow injuries in, 363, 365, 367,
370-372, 378-379t, 380-381,
381b
vs. football passers, 376
electromyography and, 350, 357t,
363f, 364, 366
experimental set-up for, 350, 351f
vs. football passing, 372-376, 375t,
376t
gender and, 372, 373t, 374t
introduction to, 350
kinematic parameters in, 350, 351f,
352f, 355t
kinetic chain in, 350, 381
kinetic parameters in, 350, 353f,
356t
phases of, 350, 350b, 352b, 354f,
358f
arm acceleration, 354f, 355t, 356t,
357t, 358f, 359f, 361f, 362f,
363-365, 363f, 378-379t
arm cocking, 354f, 355t, 356t,
357t, 358-363, 358f, 359f,
361f, 362f, 363f, 378-379t
arm deceleration, 354f, 356t,
357t, 358f, 359f, 361f, 362f,
363f, 365-366, 378-379t
denitions of, 352b
follow-through, 354f, 357t, 358f,
359f, 361f, 362f, 366
key events of, 354f
stride, 354-358, 354f, 357t, 358f,
359f
time lengths for, 358f
windup, 353, 354f, 357t, 358f,
378-379t
pitch types in, 366-368, 367t, 368t,
369t
rehabilitation and, 381-382, 382b
shoulder injuries in, 367, 376-380,
377b, 378-379t
torques in, 351-352, 361-363,
362f, 363f, 365-366
competition levels and, 368-372
gender and, 372, 374t
pitch types and, 367-368
Basketball
anterior cruciate ligament injury in,
in women, 632
balance and injuries in, 766
eye injuries in, 492
shoes for, 508, 510
thigh pads for, 501, 503f
vertical jumping in, 252, 253f
wheelchair, 691
Behavior change
nutritional, 66-67
action strategies for, 67, 83b
for weight loss, 94
stages of, 66-67, 82t
Beighton score, 671-672, 671t
Beta agonist, exercise-induced
bronchospasm and, 444
Beta blockers, for hypertension, 443
Bicipital tendinitis
in baseball pitchers, 381
in cyclists, 210t
Bicycling. See Cycling.
Bird dog exercise, 392-393, 393t
Birth control, amenorrhea and,
641-642
Bisphosphonates, in premenopausal
women, 643
Black athlete, hypertensive, 443
Black heel, 458-459
Black palm, 458-459
Bladder injury, 612
as contusion, 450, 612
prevention of, 612b
Bleeding. See also Hematoma; Hema-
turia; Hemoptysis; Hemothorax.
anemia and, 447
in head, face, and neck injuries,
581, 583
from ear, 591
Asthma (Continued) Baseball pitching (Continued)
776 Index
from nose, 590
subconjunctival, 589
lower gastrointestinal, 446-447
virus transmission and, 448
Bleeding disorder, sports participation
with, 22-24t
Blisters, 463
in disabled athletics, 688t, 690t,
691-692
prosthetic socket and, 692-693
Blood glucose. See also Glucose.
alcohol consumption and, 85-86
carbohydrate solutions and, 91
glycogen and, 67
meal scheduling and, 83b
Blood injections, for tendinopathy,
717
Blood pressure. See also Hypertension.
measurement of, preparticipation,
15, 16t
normal ranges of, by age group, 16t
Blood testing, 176, 176b. See also
Drug testing.
Blow to solar plexus, 597, 598t
BMR (basal metabolic rate), 94
Body composition
aging and, 706
improvement of
with ergogenic aids. See
Ergogenic aids.
with nutrition and exercise,
161-162
in masters athlete, 706
measurement of, 161
Body fat
aging and, 706
decreasing, 161-162, 164
football injuries and, 766
measurement of, 161
ranges of, for selected sports,
95, 95t
subcutaneous, 455-456, 456f
Body mass index (BMI), injury risk
and, 766
Bodyblade, 391
Bone, ergogenic aids for, 165-166
Bone mineral density (BMD)
female athlete triad and, 642-643
lifespan and, 165
Bone scan, of stress fracture
pars interarticularis, 638-639
rib, 619, 619f
Bounce depth jumps, 253b, 254f, 260
Bowel obstruction, incarcerated hernia
with, 599-600
Bowel rupture, traumatic, 609
Bowes and Church Food Values of
Portions Commonly Used, 66
Boxers
ear protection for, 493
electroencephalograms of, 537-538
event-related potentials of, 538
hematuria in, 610
neurologic and cognitive decits in,
542
Brachial plexus injuries, 551, 553f
Bradykinin, muscle nociceptors and,
424, 425f, 428-429
Brain. See also Cerebral blood ow;
Cerebral edema; Concussion;
Head injury.
exercise-heat stress and, 101, 144b
mild traumatic injury to, 536
soccer-related injury to, 300-301,
512
Brain Pad, 493
Brain-injured athlete. See also Cerebral
palsy.
aphasia in, 699
behavioral problems in, 699
dysarthria in, 699
Branched-chain amino acids, 79
central fatigue and, 144
Brassieres, 501, 622-623
Breasts, injury to, 622-623
Bridging exercises, 391-392, 392t, 393
Broad jump. See Jumping, horizontal.
Bronchospasm. See also Asthma.
in asthma, 445, 445b
exercise-induced, 444
Brown-Squard syndrome, 573
Bruising, 458-459, 458b, 458f. See
also Contusions.
in lower extremities, 447
Bulbocavernosus reex, 573
Bulimia nervosa, 54, 55b, 641
Burners, 551, 553f
Burnout, in young athlete, 41, 48-49,
48b
Burns, heat intolerance and, 106
Bursitis
in amputees, 694
in cyclists, 209, 210t
iliopsoas, in dancers, 670-671
in runners, 307
scapular, in baseball pitchers, 380
C
Caffeine, 92. See also Coffee.
as diuretic, 156
as ergogenic aid, 92
for endurance exercise, 154-156,
155b
for high-intensity exercise, 160-161
threshold reporting level of, 181,
181t
heat disorders and, 20
side effects of, 156
Calcaneal varus
pronation associated with, 320
running shoe and, 322
Calcium, 87
dietary sources of, 91t
muscle damage and, 427, 427f
recommended intake of, 165-166
supplementation with
decreased body fat and, 164
sources of, 91t
in vegetarian diets, 82b
Calcium channel blockers, for
hypertension, 443
Calluses, 463
Caloric expenditure. See also Metabolic
rate.
terrain for walking and, 110, 111f
for various physical activities, 58,
60-64t
Caloric requirements
estimation of, 94, 94b
for men and women age 30, 76t
Canada
certied athletic therapist in, 2
sports physical therapist in, 2
Canker sore, 460
Carbohydrate
calories per gram of, 83t
as energy source, 67
as ergogenic aid
combined with protein, 150-152,
161-163, 162b
149b
to increase muscle mass, 162-163,
162b
recommended intake of, 67-77,
77b, 77t, 78t
after exercise, 93
before exercise, 92, 93b
during exercise, 93, 93b
for life stage groups, 80t
as percent of calories, 83t
summary of, 95
in selected foods and beverages, 92t
Carbohydrate loading, 77
modied, 77, 84f
vegetarian diet and, 82
Carbohydrate solution, 91, 93, 93b,
697
caffeine added to, 154-155
Carbon monoxide, 129-130
at high altitude, 132
in hot climate, 131
national standards for, 124t
particulates with, 131
Bleeding (Continued) Caffeine (Continued)
Index 777
Cardiac. See also Heart.
Cardiac dysrhythmia, sports participa-
tion with, 22-24t
Cardiac injuries, 626-628. See also
Sudden cardiac death.
aortic rupture and, 627-628
commotio cordis in, 444, 627,
627b
contusion as, 626-627, 626b, 627b
tamponade in, 623-624, 627, 627b
Cardiac output
altitude and, 119-120
carbon monoxide exposure and,
129
heat stress during exercise and, 101,
102f
hypertension and, 442
Cardiorespiratory tness, 707-708.
See also Oxygen uptake, maximum
(VO
2
max).
Cardiovascular adaptations, to
endurance training, 142, 142b
Cardiovascular disease, 441-444
carbon monoxide exposure and,
129
congenital, sports participation
with, 22-24t
high-altitude exercise with, 121
Cardiovascular examination, prepartic-
ipation, 17-18, 17b, 18f
Carditis, sports participation with,
22-24t
Carnitine
435
Carpal tunnel syndrome
in diabetics, 449
in wheelchair athletes, 691-692
Case series, 731-732, 731t, 733, 734f,
734t
surveillance system design and, 742,
743t
Case-control studies, 731-732, 731t,
732b, 733, 734f, 734t
Case-crossover studies, 731, 731t,
732-733, 734t
Casein, as protein supplement, 162
Casting materials, 484-485, 484b, 485f
Casts, legality of, in high school
football, 484b
Catastrophic injuries, epidemiology of,
761-762
Cauliower ear, 493, 582-583, 584f
Cecal slap syndrome, 446
Central cord syndrome, 573
CERA (methoxy glycolepoetin beta),
180
Cerebral blood ow
concussion and, 537, 545
during exercise, 144
Cerebral edema
high-altitude, 122, 122-123t, 122b,
445
hyponatremia with, 109
Cerebral palsy, athletes with
aphasia in, 699
as cyclists, 209, 211-212, 213f
dysarthria in, 699
dysphagia in, 698
injuries of, 692
knee instability and, 694
seizures in, 699
sports participation by, 22-24t
Cervical collars
rigid, for immobilization, 570-571,
571f, 572f
soft, for sprains and strains, 552
Cervical spine
congenital conditions of, 576t
fusion of, return to play and, 578t
of soccer player
biomechanics and, 294-296, 294b
injury to, 300-301
Cervical spine injuries, 549-580
equipment standards and, 563b
hospital management of, 571-574
helmet and, 571, 573-574, 575f
legal considerations in, 560-562,
560b
mechanism of, 554, 554b, 554f,
555f, 559-560, 560b, 561f
on-site management of, 562-571
algorithms for, 564f, 565f
for conscious athlete, 566-568
face mask removal in, 566, 567f
guidelines for, 562b
helmet in, 568-569, 569b, 571
immobilization in, 568-571,
568b, 568f, 569b, 570b,
570f, 572f
initial actions in, 564-565, 564b,
565b
medical team in, 563, 563b
planning for, 560, 562b, 563-564,
564b
players and coaches during, 563b
training for, 560, 560b, 564,
575-578
for unconscious athlete, 566, 567f
return to play and, 574-575, 576t,
577t, 578t
sport-specic incidence of, 556-559,
557f
in soccer, 300-301
tracking and surveillance of, 550-551,
550f, 551f, 552t
types of, 551-556
brachial plexus, 551, 553f
fractures, subluxations, and
dislocations, 552-554, 554f,
555f
sprains and strains, 551-552, 553f
stenosis with neurapraxia, 555-556,
556b, 556f, 557f, 576t
Cervical stenosis, 555-556, 556b,
556f, 557f
return to play and, 576t
Chang, 464
Chain of custody, in drug testing,
175-176, 175b
Change. See Behavior change.
Cheerleading
cervical spine injuries in, 559
coaches of, risk of injury and, 767
Chemosis, 589
Chest injuries. See Thoracic injuries.
Chest pain, costochondritis with, 617
Chest protection, 500-501, 503f
Chest radiography, of trauma patient,
624-625, 625f, 626
Chilblains, 116, 116-117t, 474
Chin straps, 490-491, 491f
Chiral analysis, for banned stimulants,
180-181
Chlorpromazine, heat intolerance with,
106
Chondroitin, 166
Chondromalacia patellae
cycling and, 208-209
taping for, 525
CK. See Creatine kinase (CK).
Clavicle
injury to, in weight training, 416
shoulder pads and, 512
Clean, 385, 406
segment mechanics of, 406-410,
408f, 409t, 410f
system mechanics of, 410-412,
411f, 412b, 412t, 413t
Clean and jerk. See Clean.
Clean and snatch, 406
Clearance for participation, 21
contact level and, 10b, 21
intensity level and, 19t, 21
pass/fail criteria and, 21b
specic medical conditions and,
22-24t
Cleats, 508, 510-511, 510f
Clinical incidence, 739
Clothing. See also Protective equipment.
cold exposure and, 110, 112-113,
474
protective, 465t
sun exposure and, 133
Cluster-randomization, 733
Cervical spine injuries (Continued)
778 Index
Coaching staff
team physicians communication
with, 4, 6
Coenzyme Q10, delayed onset muscle
soreness and, 435
Coffee. See also Caffeine.
drug testing and, 92
iron absorption and, 87
Cognitive decits, soccer-related,
300-301
Cohort design, of surveillance systems,
742, 743t, 744t
Cohort studies, 731, 731t, 733, 733b,
734f, 734t
Cold disorders, 114-116, 114b, 115t,
116-117t
Cold exposure. See also Hypothermia;
Shivering.
acclimatization to, 114
aging and, 113
altitude and, 131
arterial spasms in, 698
body morphology and, 113
chronic conditions affected by, 114
clothing and, 110, 112-113, 474
drug-associated sensitivity to, 114
exercise during
aerobic tness and, 113
cardiovascular response to, 110
clothing and, 112-113
metabolic response to, 110, 111f
physical performance in, 111
water immersion and, 112
gender and, 113
skin injury in, 473-474, 473b
protection from, 465t, 474
thermoregulation in, 109-110, 110b
tyrosine supplementation and, 154
vasoconstriction in, 110
at altitude, 131
vasodilatation in, 110
acclimatization and, 114
aging and, 113
weather conditions and, 111-112,
112b
Cold pack, for delayed onset muscle
soreness, 431. See also Ice.
Cold sores, 469
Cold urticaria, 474
Collagen
exercise-induced breakdown of,
429, 667, 714-715
joint hypermobility and, 671
of skin, 456
of tendons
aging and, 707-708
disruption of, 667, 714-715
Collagen hydrolysate, for joint pain, 166
Collodion, 586-587
Commotio cordis, 444, 627, 627b
Compression, for delayed onset
muscle soreness, 433
Computed tomography (CT)
of intra-abdominal trauma,
605-606, 606t
with hematuria, 611-612
hepatic, 609
intestinal tract, 609
pancreatic, 612
splenic, 607-608, 607f
ureteral, 612
of pulmonary contusion, 624
of sternoclavicular dislocation, 620
Concussion, 536-548
assessment of, 538-541
difculty of, 538
multiple informants in, 538
neurocognitive, 541-542, 541b,
543, 543b
at sideline, 538-539, 539b
biomechanics of, 537
complex vs. simple, 52, 537
cumulative effects of, 542
denition of, 536
electrical brain activity and, 537-538
in football
face guards and, 488
helmets and, 486-487
in ice hockey, face shields and,
487-488
imaging studies and, 537
incidence of, 536
mouthguards and, 493
neuropsychological outcomes of,
541-542, 541b
pathophysiology of, 537
preparticipation evaluation and, 17,
22-24t
recovery from, 542-543
factors affecting, 544-545, 544b
return to play following, 52,
542-545, 543b
current criteria for, 543-544, 543b
second impact syndrome following,
51, 51b, 537, 543
signs of, 52b, 538-539, 539b
soccer-related, 300-301, 512
symptoms of, 52b, 538b, 540-541,
540b
under-reporting of, 536, 538, 538b
in young athlete, 51-53, 51b, 544,
544b
Conditional risk, 740
Condence intervals, 739, 741-742,
742b
Condentiality, 4
Confusion, concussion with, 539
Congenital heart disease, sports
Conjugated linoleic acid, 164
Conjunctivitis, 450
Contact lenses, 15, 492
Contact sports
classication of, 10b, 21
preparticipation evaluation for, 9
liver or spleen enlargement and,
19
neurologic, 17
retinal detachment and, 15
solitary paired organ and, 21
spinal instability and, 17
protective equipment in, 479
team physicians presence at, 4
Contrast baths, for delayed onset
Contusions. See also Bruising.
abdominal wall, 596-597, 604,
605-606
bladder, 450, 612
breast, 501, 622-623
cardiac, 626-627, 626b, 627b
in disabled athletics, 690t, 691
external ear, 493, 582-583, 584f
head and face, 582
hepatic, 609
pancreatic, 612
pulmonary, 624, 624b
quadriceps, protection for, 501
rates of, 758b
renal, 610-612, 610f
rib, 615, 615b
sternal, 620
testicular or scrotal, 613-614
Convective heat loss, 99
Convulsive disorder
preparticipation evaluation and,
17, 22-24t
Core temperature. See also Temperature,
body.
carboxyhemoglobin and, 129
central nervous system dysfunction
and, 695
cold exposure and
gender and, 113
in hypothermia, 114-115,
115t
oxygen uptake and, 111
in water immersion, 112
exercise-heat stress and, 100, 100b,
100f
acclimatization to, 102-103,
103b, 103f
dehydration in, 103-104, 104b,
104f
fatigue and, 101
in heatstroke, 106-108
Index 779
measurement of, rectal, 106-108,
108b
menstrual cycle and, 104-105
regulation of, 99
Corneal abrasion, 589
Corns, 463
Coronary artery abnormalities,
congenital, 443
Coronary artery disease, 444, 444b
Corticosteroids
dexamethasone, for muscle soreness,
432
for exercise-induced bronchospasm,
444
for spinal cord injury, 574
for tendinopathy, 716-717
Costal cartilages, 615, 616f
Costochondral junctions
acute injuries of, 617, 641
anatomy of, 615, 616f
chronic injuries of, 617
Costochondritis, 617
Countermovement depth jumps,
253b, 254f
Countermovement jumps, 234, 235f,
249, 250f. See also Jumping,
vertical.
Court shoes, 508, 510f
Coxa saltans. See Snapping hip.
CP. See Creatine phosphate (CP).
CRAFFT screening tool for substance
abuse, 53, 53b
Craniotomy, history of, participation
with, 22-24t
Creatine, as ergogenic aid, 160,
163
Creatine kinase (CK), 427-428, 427f,
429
cryotherapy and, 430-431
diclofenac and, 430
ibuprofen and, 429-430
Creatine phosphate (CP), 158-159,
160, 163
Cromolyn, for exercise-induced
bronchospasm, 444
Cross-sectional studies, 731-732,
731t, 733, 734f, 734t
Crosstrainer shoes, 508
Crunches, 391, 393
Crutch users, upper extremity injuries
in, 694
Cryotherapy
430-431
for warts, 470
CT. See Computed tomography (CT).
Cullen sign, 598
Cup, protective, 501, 613
Curls, abdominal, 391, 393
Cutting
gender differences in, 633-634
in soccer. See Soccer biomechanics,
of cutting; Soccer-related
injuries, cutting-related.
Cycling, 187-216
adjustments to bicycle in, 209b, 213
for chronic conditions, 190
for injury prevention, 206, 210t
for power production, 209b
for rehabilitation, 187, 206b
with amputations, 209-211, 209b,
212f
with cerebral palsy, 209, 211-212,
213f
common injuries in, 206-209, 210t
penile, 614
domains of, 187, 188b
introduction to, 187-188
kinematics of, 188-191, 191b
angle convention for, 188, 188f
ankling and, 189
cadence and, 189
fatigue and, 189
frontal plane motion in, 189-190,
190f
knee pain and, 190
seat height and, 188-189, 189f,
190, 190f
seat tube angle and, 189
three-dimensional, 189-190
kinetics of, 191-201, 201b
effective force in, 193, 193f
joint reaction forces in, 196-198,
196f, 197f, 198f, 199f
muscle moments in, 198-199, 200f
pressure at pedal in, 193-195, 195f
rider-bicycle reaction forces in,
191-193, 191f, 192f, 193f,
194f
torsion at pedal in, 195-196,
195f, 196f
work and power in, 200-201, 201f
muscle mechanics in, 202-206, 206b
activity patterns, 202-205, 203f
muscletendon unit length and
velocity, 205-206, 207f, 208f
recumbent, 193, 205
with cerebral palsy, 212
seat height in
hip injuries and, 209
for injury prevention, 206, 208,
210t
kinematics and, 188-189, 189f,
190, 190f
knee reaction forces and, 197,
197f
muscle length and, 205-206
muscle lengthening velocities and,
205-206
muscle moments and, 199, 200f
pedal reaction force and, 192-193,
192f
stationary vs. outdoor, 187
after total knee arthroplasty,
719-720
unique biomechanical features of,
187
Cystic brosis
heat intolerance in, 105-106
D
Dance, 651-680
as athletic endeavor, 652, 652b
clinically relevant aspects of, 656-664
ankle/foot in ballet and, 657-662,
658f, 659f, 659t, 660b,
660f, 661f
beginning en pointe and, 661-662,
662b
genre and, 656, 656f
pointe shoe and, 656-657, 657f,
658f
turnout and, 662-664, 663b,
663f, 664f, 671-672
genres of, 653
types of injury and, 656
health care and
attitudes of dancers toward,
653-654, 654b
concluding summary on, 674
limited access to, 653b, 654
injuries in, 664-672
Achilles tendinopathy, 666-667,
666f, 667b
ankle impingement, 664-666,
665f, 666b
anterior cruciate ligament sprain,
668-670, 669f, 670b, 670t,
671-672
case studies of, 672-674, 673f,
674f
epidemiology of, 654-656, 655t,
656b
fth metatarsal fracture, 667-668,
668f
exor hallucis longus tendinopathy,
667, 667b, 667f
joint hypermobility and, 671-672,
671b, 671t
osteoarthritis and, 672, 672b, 672t
snapping hip, 670-671, 670f
spondylolysis, 638
stress fractures, 668, 669f
jumping in, 669-670, 669f, 671-672
repetitions of, 258-259, 260b
Core temperature (Continued) Cycling (Continued)
780 Index
medical and scientic specialty for
case studies in, 672-674, 673f,
674f
knowledge base of, 652
professional organizations for,
651-652, 652t
sports medicine compared to,
651-652
pain and, 653-654
psyche of dancer in, 653-654
taping and bracing in, limits of, 654
Dancers fracture, 667-668, 668f
Dancers tendinopathy, 667
Darbepoietin, 179-180
Dead bug exercise, 392
Deadlift, barbell, 393-394, 396t
Decubitus ulcers, 688t, 690t
Dehydration. See also Fluids and
exercise.
body weight and, 697
caffeine-induced, 92
endurance exercise and, 146
exercise-heat stress and, 103-104,
104b, 104f, 105
heat disorders and, 20
physiologic effects of, 91
sickling crisis and, 447
Dehydroepiandrosterone (DHEA),
178-179
Delayed onset muscle soreness
(DOMS), 423-440
concluding summary of, 435-436,
435f
connective tissue and, 429
denition of, 423
factors leading to, 426, 426b
histopathologic changes in, 426f,
427-428, 427f
inammation in, 424, 426f,
427-428, 428f
location of, 424-425
mast cells and, 425f, 428-429
models for study of, 425-426, 426f
vs. muscle pain, 423, 423b
performance decit secondary to,
426-427
prevention and attenuation of, 429
immediate exercise and, 434
stretching and, 434
warmup and, 434
repeated bout effect with, 429
time course of, 425, 425b
treatment of, 429-435, 430f
alternative, 434-435
nutritional, 435
pharmacologic, 429-430
physical, 430-434
Dendritic cells, 455
Denominator data, 736-738, 737b
Dental examination, preparticipation,
20
Dental injuries, 594-595, 594b, 594f,
595b
Depression
symptoms of, 49b
Depth jumps, 234, 253b, 254f, 260,
260t
Depth perception, impaired, 15
Dermatitis, 464-465, 464f
prophylactic measures for, 465t
Dermatologic examination,
preparticipation, 20
Dermatophytes, 467-469, 468f, 469b
Dermis, 455-456, 456f
Descriptive epidemiology, 745
Descriptive studies, 731
Designer steroids, 176-177
Deterministic models of performance,
235, 235b
for horizontal jumps, 253, 254f
for vertical jumps, 235-236, 236f,
237f
Dexamethasone, iontophoresis with,
432
DHEA (dehydroepiandrosterone),
178-179
Diabetes mellitus, 449, 449b
Diarrhea
in acute gastroenteritis, 446
bloody, 446
runners, 446
travelers, 446
Diclofenac, delayed onset muscle
soreness and, 430
Dietary interview, 66
Dietary reference intakes (DRIs), 66
energy requirements, 76t
macronutrients
acceptable ranges, 77t
additionally limited, 79t
recommended intakes, 78t
minerals (elements)
upper intake levels, 74-75t
vitamins
recommended intakes, 68-69t,
88-90t
upper intake levels, 72t
Dip and drive and split, 412-413,
414
Dirt tattoos, 458-459, 459f, 583
Disabled athletics, 681-703
classication systems in, 683-684,
683b, 684b
committees for, 701, 702b
concluding summary of, 701-702
injuries in, 688t
prevention of, 688t, 690, 695
psychosocial aspects of, 689, 689b
rehabilitation for, 695, 695b
of standing athletes, 692-695
treatment of, 688t
of wheelchair athletes, 690, 690t,
691-692
medical problems in, 688t, 695-699
aphasia and, 699
behavioral problems and, 699
bladder dysfunction and, 697-698
blood ow and, 698
dysarthria and, 699
dysphagia and, 698
hydration and, 696-697
hypertension and, 698, 698b
hypotension and, 688t, 698
seizures and, 688t, 699
temperature regulation and, 688t,
695-697, 695b
organization of events in, 701,
701b, 702b
organizational structure of, 681-683,
682t, 683f, 684f, 685t
psychosocial considerations in,
689-690, 689b
technical assessment for
movement analysis in, 685b,
686-687
performance enhancement in,
687-689, 689b
travel considerations in, 699-701
rst-aid supplies for, 700, 701b
Discs. See Intervertebral discs.
Disordered eating, 641-642, 643.
See also Eating disorders.
Diuretics, for hypertension, 443
Diving, spondylolysis and, 638
DOMS. See Delayed onset muscle
soreness (DOMS).
Dopamine, fatigue in endurance
exercise and, 144, 153
DRIs. See Dietary reference intakes
(DRIs).
Drop jump, 234
Drug abuse
Drug education and counseling, 183
Drug testing, 174-186
as accepted part of sports, 174-175,
184b, 185
antihypertensive agents and, 443
Dance (Continued)
Index 781
appeals of positive result, 184
athletes with disabilities and,
699-700
of blood, 176, 176b
for caffeine, 92
collection and chain of custody in,
175-176, 175b
designing programs for, 183, 183b
education and counseling with, 183
ethical considerations in, 183-184,
184b
gender testing and, 185
gene doping and, 181-182
interpretation of levels in, 181, 181t
legal challenges to, 184
limitations of, 174
list of 2010 prohibited substances
and, 176, 177b
methodology in, 176-181
for anabolic-androgenic steroids,
176-179, 177t
for erythropoiesis-stimulating
agents, 179-180
for human growth hormone, 180
for stimulants, 180-181
pharmacologic basis of, 174-175,
174b
at preparticipation evaluation, 21
therapeutic use exemption and,
174-175, 182-183, 182b
for corticosteroids, 444
unregulated dietary supplements
and, 184
of urine, 175-176
Drugs. See also Ergogenic aids.
cold injury associated with, 114
heat intolerance associated with, 106
therapeutic, 174-175, 174b
Duodenum, trauma to, 609
Dynamic constant external resistance
testing, 25, 28
Dysarthria, 699
Dysphagia, 698
Dysplastic nevi, 472-473
Dysrhythmia, cardiac, sports
Dystrophin, muscle damage and, 427
E
Ear
bleeding from, 591
cerebrospinal uid leakage from,
591
external
contusion of, 493, 582-583,
584f
laceration of, 586
otitis externa of, 450
Ear protectors, 493, 493f
Eating disorders, 53-55. See also
Anorexia nervosa; Bulimia nervosa.
female athlete triad and, 641-642,
643
medical complications of, 54b
preparticipation examination and,
19-20
secrecy and denial in, 53, 54b
signs of, 642
Eccentric contractions
jumping and
countermovement, 249
energy absorption in, 257
in high jump, 252
muscle soreness caused by, 423. See
also Delayed onset muscle
soreness (DOMS).
negative work during, 238-239
in pitching rehabilitation, 382
in soccer kicking, 289-290
Eccentric exercise, for tendinopathy,
715-716, 716b
Ecchymosis, 458-459
Eccrine glands, 456
Ectodermal dysplasia, heat intolerance
and, 105-106
Eczema, 464-465, 464f
asteatotic, 475, 475f
Edema
cerebral. See Cerebral edema.
peripheral
high-altitude, 122, 122-123t
pulmonary. See Pulmonary edema.
Efciency of energy burned, 58
Effort thrombosis, 623
EGCG (epigallocatechin gallate),
156-157
Elastic strain energy, in muscles,
vertical jump and, 240, 249
Elbow
protection for, 499
taping of, 523
Elbow injuries. See also Lateral epicon-
dylalgia; Lateral epicondylitis
(tennis elbow); Medial epicondy-
litis (golfers elbow).
in baseball pitchers, 363, 365, 367,
370-372, 378-379t, 380-381,
381b
in golfers, 217
in weightlifters, 415
Elderly athlete, preparticipation evalua-
tion of, 9. See also Masters athlete.
Electrocardiography (ECG), in hyper-
trophic cardiomyopathy, 441-442
Electroencephalogram (EEG),
concussion and, 537-538
Electrolytes
before, during, and after exercise,
93b, 697
heat cramps and, 106
with heat stress, 104, 109
Electromyography (EMG)
in baseball pitching, 350, 357t,
363f, 364, 366
in cycling, lower extremity, 202-206,
207f, 208f
with amputation, 211
with cerebral palsy, 212
in golf swings, 223-226
in obturator nerve entrapment, 603
in running, 315-316
pelvic drop and, 314-315
in soccer, of cervical muscles, 294
in swimming, of freestyle stroke,
335, 336f
with taping
of ankle, 519
of arch, 521-523
patellofemoral, 527-528, 529-530t
of shoulder, 531-532
in tennis
during ground strokes, 272-273
during serve, 267, 270, 271f, 272f
in vertical jumping, 242-243, 244f,
245f, 246
ballet-specic, 252f
in weight training
lower extremities and, 394, 395t,
396-397, 396t
spine and, 385-386, 387f, 388b,
391-392
Electronic health records, 6
Electrophysical agents, for delayed
onset muscle soreness, 432-433
Elements. See Minerals (elements).
EMG. See Electromyography (EMG).
Endurance activities. See also Muscle
endurance.
denition of, 141
energy generation for, 141-142
Endurance exercise
anabolic steroids and, 165
carbohydrate consumption during,
93
ergogenic aids for. See Ergogenic
aids, for endurance exercise.
fatigue during. See Fatigue, in
endurance exercise.
gastrointestinal complaints and, 92
maximum oxygen uptake and,
707-708
perception of effort in, 143
caffeine and, 155, 155b
Endurance training, physiologic adap-
tations in, 142-143, 142b, 143b
Drug testing (Continued)
782 Index
Energy
efciency in burning of, 58
work and, 239
Energy availability
denition of, 641
female athlete triad and, 641-642
Environmental factors, 98. See also Air
pollution; Cold exposure; Heat
stress, exercise-associated; High
altitude; Lightning; Ultraviolet
light.
interactions between, 131-132
skin conditions caused by, 471-475,
471b, 473b
Ephedra, 442
Ephedrine, 180-181, 181t
Epidemiology of sports injury, 730-772
denition of, 731b
incidence and prevalence in, 735-740,
735b, 735f
denominator data and, 736-738,
737b
general determinants of, 730b
injury denition and, 736, 736b,
737t
injury odds and, 735-736, 738t,
739
injury rate and, 735-736, 738t,
739
injury risk and, 735-736, 738-739,
738t
multiple injuries and, 739-740,
740b
injury prevention and, 745-767,
745b, 745f
descriptive basis of. See Injury rate
data.
interventions in, 767, 768t
risk factors and, 762-767, 762f,
763b, 764-765t, 766b
introduction to, 730-731, 730b
recommendations for research on,
769
risk factors in
identication of, 762-767, 762f,
763b, 764-765t, 766b, 769
measuring effects of, 740, 740b
statistical methods in, 740-742,
741t
study designs in, 731-733, 731t
comparison of, 733, 734f, 734t
surveillance systems in, 742-744,
743t, 744b, 744t
recommended components of,
744, 744b
Epidermis, 455-456, 456f
Epididymitis, 614
Epigallocatechin gallate (EGCG),
156-157
Epigastric hernia, 602-603, 603t
Epilepsy. See Convulsive disorder.
Epistaxis, 590
EPO. See Erythropoietin (EPO).
Epstein-Barr virus infection, 447, 447b
Erector spinae
in dead bug exercise, 392
in rowing, 391
in squat exercise, 386-387, 388b
Ergogenic aids, 141-173
for body composition, 161-165
anabolic steroids. See Anabolic-
androgenic steroids.
carbohydrate-protein supplements,
150-152, 161-163, 162b
conjugated linoleic acid, 164
creatine, 163
to decrease fat mass, 164
HMB (beta-hydroxy-beta-
methylbutyrate), 163-164
to increase muscle mass, 162-164,
162b
lacking scientic support, 164,
164b
measurement techniques and, 161
nutrition and exercise in, 161-162
for bones and joints, 165-166
caffeine as, 92
155b
reporting threshold for, 181,
181t
for endurance exercise, 141-158
activities considered for, 141
antioxidants as, 156-157, 157b
branched-chain amino acids as,
152-153
caffeine as, 154-156, 155b
carbohydrate as, 148-150, 149b
carnitine as, 157-158
lacking scientic support, 145b
physiologic basis of, 141-145,
142b, 143b, 145b
pros and cons of, 145, 145b
protein as, 150-152
tyrosine as, 153-154
water and electrolytes as, 146-147,
146b, 147b
genetic manipulation and, 181-182
activities considered for, 158
caffeine as, 160-161
creatine as, 160
lacking scientic support, 159,
159b
physiologic basis of, 158-159,
158b, 159b
protein as, 161
sodium bicarbonate as, 160
sports pharmacology and, 174-175,
174b
web resources on, 166
Erythropoietin (EPO)
altitude and, 119
genetic manipulation involving,
181-182
Esophageal injuries, 628
Estrogen
anterior cruciate ligament injury and,
634
decreased
in female athlete triad, 641-642
urinary incontinence and, 645-646
hypertension associated with, 442
Evaporative heat loss, 99
ambient humidity and, 99b
in endurance exercise, 142
Event-related potentials, concussion
and, 538
Evoked potentials, concussion and,
538
Exercise stress test, preparticipation,
18, 18f
Exercise-heat stress. See Heat stress,
exercise-associated.
Exertional heatstroke, 106-109
Exostosis
at ankle, 665-666
in ear canal, 474
Eyebrow, lacerations involving, 584,
586, 586f
Eyeglasses
protection afforded by, 492
safety lenses for, 15, 492
Eyelid, lacerations involving, 584, 586,
586f
Eyes. See also Vision.
anatomy of, 587-588, 588f
conditions affecting sports
participation, 21, 22-24t
foreign body in, 589
infection of, 450
injuries to, 587-590
anterior segment, 589, 589b
in disabled athletics, 688t
examination of, 588-589
infected, 450
initial management of, 588, 588b
posterior segment, 589-590,
589b, 590b
one-eyed athletes, 15, 21, 22-24t,
492-493
protective equipment for, 15,
491-493, 492b, 492f, 590
Ergogenic aids (Continued)
Index 783
F
Face guards, 488-490, 490f, 490t, 491f
for ice hockey, 487-488, 490
Face mask, removal of, 566, 567f, 571
Facial fractures, 590-593
mandibular, 591t, 592-593, 592b,
593f
nasal, 590, 590b, 590f, 591t
zygomatic, 590-591, 591f, 591t,
592b, 592f
Facial injuries. See Maxillofacial injuries.
Facial nerve
injury to, 585, 586f
repair of, 585
Falls
prevention in elderly, 645
Family of athlete, team physician
and, 6
Family physician, sports medicine
training of, 3
Fasciotomy, for medial tibial stress
syndrome, 637
Fat. See also Body fat; Fatty acids.
dietary sources of, 85, 85t
as energy source, 82, 84
recommended intake of, 67, 77t,
78t, 82-85
as percent of calories, 83t, 84-85
summary of, 95
Fat mass (FM). See Body fat.
Fat-free mass (FFM)
aging and, 706
increasing, 161-162, 163-164
measurement of, 161
Fatigue
in concussed athletes, 540-541
in cyclists, 189
in dancers, 655
anterior cruciate ligament injuries
and, 669-670, 670t
in endurance exercise, 144-145,
145b
antioxidants and, 156-157, 157b
branched-chain amino acids and,
152-153
carbohydrate solutions and,
149-150
central vs. peripheral, 144-145
tyrosine and, 153-154
in exercise-heat stress, 101, 102-103
muscle
in high-intensity exercise, 159-160
in swimmers, 341, 345
in overtraining syndrome, 450
in swimmers, 341, 342t, 343, 345
Fatty acidbinding protein, muscle
damage and, 427-428
Fatty acids
omega-3
bone mass and, 166
joint health and, 166
oxidation of
carnitine and, 157-158
endurance training and, 142
Felt, 482, 482f
Female athlete, 631-650. See also
Gender.
anterior cruciate ligament injury in,
25-26, 632-635, 633t, 634f,
669-670, 766
in soccer players, 299, 302, 632,
635, 733
costochondral joint injury in, 641
differences from male athlete, 631,
632f, 632t
increase in numbers of, 730
landing injuries in, 632, 635,
669-670
medial tibial stress syndrome in,
637, 637b
older, 644-646
patellofemoral pain syndrome in,
635-637, 635t
pregnancy in, 643-644, 644b, 644t,
645t
spinal injuries in, 638-641, 638b
as weightlifter, 406, 407-409, 409t,
411-412
Female athlete triad, 53, 641-643,
642b
Femoral hernia, 598, 599t, 600f, 602
return to activity and, 603t
Femur, stress injuries to, in runners, 307
Fever. See also Hyperthermia, in
disabled athletes.
in disabled athletics, 701
urinary tract infection with, 688t,
697-698
Fever blisters, 469
FFM. See Fat-free mass (FFM).
Fiber, recommended intake of, 78t
Fibrous dysplasia ossicans progressiva,
451
Field hockey, shin guards for, 506-508,
508f
Field tests, in physical tness prole,
27
Finger, taping of, 523
Fingernails. See Nails.
First-aid supplies, in travel for disabled
athletics, 700, 701b
Flack jacket, 502f
Flail chest, 623-624
Flexibility. See also Range of motion
(ROM).
aging and, 708, 708b
of dancers, 671
testing of, 31-32, 34t
Flexion teardrop injury, cervical, 554,
555f
Flexor hallucis longus tendinopathy,
667, 667b, 667f
Flexor relaxation
in rowing, 391
in squat exercise, 386-387
Flexor tenosynovitis, in diabetics,
449
Floating ribs, 615, 618
Fluids and exercise, 91-92, 93.
See also Dehydration;
Hyperhydration; Hypohydration;
Rehydration; Water.
absorption time of, 146
for athletes with disabilities, 697
cognitive impairment and, 697
dysphagia and, 698
sources during travel, 700
caffeine and, 92
for diabetics, 449
endurance exercise and, 93, 146-147,
146b, 147b
carbohydrates with, 91, 149-150
guidelines for, 93, 93b
heat stress and, 104-105, 104f
hyponatremia caused by, 147
Fluids for acute gastroenteritis, 446
Flurbiprofen, delayed onset muscle
soreness and, 430
Foam, protective, 480, 481f
Folate deciency, 447
Folliculitis, 448, 461-462, 470
Folliculitis keloidalis, 461-462
Food frequency questionnaire, 59
Food intake and exercise, 92-93, 93b
Food pyramid, 59, 66f
vegetarian, 85f
Food record, 59
Food value tables, 66
Foot
in ballet, 657-662, 658f, 659f,
659t, 660b, 660f, 661f
injury to
in cycling, 208, 210t
in dance, 667-668, 668f, 669f
in running, 307-308
in soccer, 297, 300
knee pain and, in runners, 320b
red blood cell destruction in, 447
taping of, 521-523, 522f
Foot motion. See Midfoot motion;
Rearfoot motion.
Foot plantar pressures
in running, 318, 319f
784 Index
in soccer
in crossover cutting, 293
in sidestep cutting, 292
Foot pronation
in dancers, 663, 664f, 666, 669f,
671-672
deformities causing, 320
medial tibial stress syndrome and,
637
patellofemoral pain and, 636
in running
early vs. late, 313, 314b, 314t
functional limb varus and, 311,
311b
impact forces and, 317-318
injuries caused by, 320-321
rearfoot motion and, 312-314,
312b, 313f, 314b, 314t
resupination and, 313
shoe types and, 322-324, 325b
structural abnormalities leading to,
319, 319b
in support phase, 309
in soccer, during landing, 296-297
Foot strike, 308-309, 308f
classication of, 317-318, 317b,
317f, 318f
tibialis anterior muscle and, 315-316
Football
collegiate rule changes in, 504
injuries in
body composition and, 766
cervical spine, 556-558, 557f.
See also Cervical spine
injuries.
epidemiology of. See Injury rate
data.
life stress and, 766
playing surface and, 767
by position, 766
weather and, 767
neuropsychological baseline in,
541-542
passing in, vs. baseball pitching,
372-376, 375t, 376t
physical tness prole for, 26, 34t
anaerobic capacity in, 33, 33t
protective equipment in
ankle braces, 767
chin straps, 490-491, 491f
face guards, 488, 490f, 490t
gloves, 499, 501f
helmets. See Helmet(s), football.
hexpad apparel, 512
knee pads, 502, 504f
mouthguards, 493
neck protector, 494, 494f
rib guards, 500, 502f
shoes, 508-511, 510f
shoulder pads, 494-496, 495f,
496b, 496f, 497f, 498f,
500f, 512
for thighs and hips, 501, 503f
Forefoot pressure, in soccer, 292-293
Forefoot strikers, in running, 317-318,
317b
Forefoot varus
medial tibial stress syndrome and, 637
running shoe and, 322, 324, 325b
Formaldehyde, eczema caused by,
464-465, 464f, 465t
Free radicals. See Reactive oxygen
species.
Freezing injury, 115-116, 116-117t
Friction massage, for tendinopathy, 715
Frostbite, 115-116, 116-117t, 474, 696
Fructose, protein supplement with, 163
Functional limb varus, 310-311,
311b, 311f, 312f
Functional magnetic resonance
imaging, concussion and, 537
Furunculosis, 448
G
Gas chromatographycombustion
IRMS, 179
Gas chromatographymass spectrometry
anabolic steroids and, 176-177
erythropoietin and, 179
stimulants and, 180
Gastritis, ischemic, 610
Gastroenteritis, acute, 446
Gastroesophageal reux, 446
Gastrointestinal complaints, 92-93,
445-446, 446b
anemia associated with, 447
Gastrointestinal examination,
preparticipation, 19-20
Gel, shock-absorbing, 481-482, 482f
Gender. See also Female athlete.
baseball pitching and, 372, 373t,
374t
collagen synthesis and, 667
heat tolerance and, 104-105
injury rates and, 750-751, 751t, 752f
injury risk and, 763, 764-765t
landing and, 260-262, 260b,
261f, 633
maximum oxygen uptake and,
631, 632t
muscle strength and, 631, 632t
musculoskeletal differences and,
631, 632f
physiologic differences and,
631, 632t
Gender verication testing, 185
Gene doping, 181-182
Genitalia
female, injuries to, 614-615
male
anatomy of, 613f
injuries to, 613-614, 613b
protection for, 501, 613
Genu valgum
cerebral palsy and, 694
in dancers, 663
gender differences in, 631, 632f, 633
Glenohumeral joint, osteoarthritis of,
713-714
dislocation predisposing to, 713
rehabilitation for, 713
surgery for, 714
Glenoid labrum, tears of, in baseball
pitchers, 360-361
Gloves, protective, 499, 501f
for wheelchair athletes, 691-692
Glucosamine, 166
Glucose. See also Blood glucose.
ATP production and, 141-142
for brain metabolism, 144
in endurance exercise, 141-142, 145
in hydration uid, 91, 149, 697
Glutathione, 156-157
Glycerol, 147-148
Glyceryl trinitrate, for tendinopathy,
717
Glycogen
cold exposure and, 113-114
as energy source, 67
in muscle. See Muscle(s), glycogen
in.
replacement of, after exercise, 93
Glycolysis, high-intensity exercise and,
158-159
Golf, 217-233
biomechanics of. See Golf swing.
driving range mats for, 229-230, 230f
health and tness benets of, 217
after total joint arthroplasty
hip, 719
knee, 720
shoulder, 721, 722t
warmup for, 230-231, 231b
Golf clubs
adjusting length of, 229
spinal biomechanics and, 229, 231b
Golf injuries
epidemiology of, 217
equipment and, 228-230, 228b,
230f, 231b
in follow-through phase, 221, 221b
in impact phase, 220-221, 221b
lower limb biomechanics and,
221-223, 222b, 223b
management strategies for,
217-218, 231, 231f
prevention of, 217-218
Foot plantar pressures (Continued) Football (Continued)
Index 785
spinal biomechanics and, 223-225,
223b, 225b
club length and, 229
stresses leading to, 217-218
upper limb biomechanics and,
225-228, 225b, 228b
elbow in, 225, 226-227, 226b,
226f, 227b, 227f, 228b
shoulder in, 225-226, 226b, 228b
wrist and hand in, 225, 227-228,
228b, 228f
Golf shoes, 221, 230, 231b
Golf swing
difculty of, 217
general biomechanics of, 218-221
grip tension in, 227
hand positions in, 226-227, 226f,
227f
injury and. See Golf injuries.
kinematic sequence of, 220, 220b
lead and trail designations for,
218-221
muscle activation in, 220, 220t,
221t
neutral grip in, 226-227, 227f
phases of, 218-221, 218b, 219f
Golfers elbow. See Medial epicondylitis
(golfers elbow).
Granular cell layer, 455
Granuloma, pyogenic, 460
Graphite Rollbar system, 322-324
Great vessel injuries
rib fracture with, 617, 618b
sternoclavicular dislocation with,
620b
Groin pain
in athletic pubalgia, 600-602, 600b,
601f
differential diagnosis of, 599t
hernia with, 598-599, 600
hip joint causes of, 602
obturator nerve entrapment with,
603
protective equipment and, 501
sacroiliac conditions with, 639
soccer-related, 298, 300, 303, 598
in testicular or scrotal injury, 613-614
Ground reaction forces
in disabled athletics, with amputees,
693
in golf, 221-222, 230
in landing, 257-258, 260-261, 262
gender and, 260, 260b, 633-634
in running, 309, 316-318, 316b,
318f
arch height and, 318, 319f
on curved pathway, 292
point of impact and, 317-318,
317b, 317f, 318f
pronation and, 312
shock attenuation and, 316-318,
316f
speed and, 317
in soccer
during cutting, 292-293
during landing, 296-297, 302
in tennis
kinetic chain and, 268, 270
reaction time and, 282-283
surface and, 279, 279f
in vertical jumping, 237-239, 238b,
239f
arm swing and, 247, 248-249
in high jump, 252
muscle activity and, 242, 244f
squat vs. countermovement, 249,
250f
Growth hormone, 180
Gymnastics
body composition and injury in, 766
spondylolysis and, 638
H
Hair
chemical damage to, 474-475
friction-induced loss of, 462, 462f
Hair follicles, 455-456, 456f, 457f
Hallux pressure, in sidestep cutting,
292
Hallux saltans tenosynovitis, 667
Hamstrings
activity of, in running, 315
cycling biomechanics and,
200-201
exibility testing of, 31
knee injury and
on landing, 261, 261b
in women, 633
strains of
protection for, 501
in runners, 307
Handball, vertical jumping in, 252,
253f
Hands, protection for, 499, 499b,
501f
in wheelchair athletes, 691-692
Hang clean or snatch, 406
Harmans equation for average
power, 29
Harris-Benedict equation, 94, 94b
Head injury. See also Brain;
Concussion; Maxillofacial injuries.
pupillary differences in, 15
soccer-related, 300-301, 300b
electroencephalogram and,
537-538
sports participation with history of,
22-24t
Headache, concussion with, 540,
540b, 545
Heart. See also Cardiac entries.
age-related changes in, 708b
athletes, 17-18, 442
vs. hypertrophic cardiomyopathy,
442, 442t
Heart murmur, sports participation
with, 22-24t
Heart rate
in exercise training, 121
cold exposure and, 110-111
heat stress with exercise and,
101, 102f
acclimatization of, 103, 103f
dehydration and, 103-104
training precautions and, 105
neurologic lesions and, 695
normal ranges of, by age group, 16t
Heat acclimatization, 102-103, 103b,
103f
Heat cramps, 106, 107-108t
Heat disorders, preparticipation
evaluation and, 20, 22-24t
Heat exhaustion, 106, 107-108t
miliaria profunda and, 109
Heat illness, 106-109, 106b, 107-108t
Heat intolerance
drugs associated with, 106
populations susceptible to, 105-106,
105b
Heat loss, pathways of, 99, 99f
Heat production, metabolic, 99
in cold climate, 110
in endurance exercise, 142
Heat rash (miliaria rubra), 106,
107-108t, 109, 466, 466f
Heat stress, exercise-associated.
See also Heat illness; Heat
intolerance.
acclimatization and, 102-103, 103b,
103f
aging and, 104
cardiovascular responses to, 101, 102f
cerebral response to, 101, 144b
clothing and, 105
core temperature and, 100-101,
100b, 100f
dehydration in, 103-104, 104b,
104f, 105
fatigue and, 101, 152
gender and, 104-105
glycerol-induced hyperhydration
and, 148
metabolic responses to, 101
reducing, 105, 105b
Heat syncope, 107-108t
Heat wrap, for delayed onset muscle
soreness, 431
Golf injuries (Continued) Ground reaction forces (Continued)
786 Index
Heatstroke, 106-109, 106b, 107-108t
classic, 106
Heel, piezogenic papules on, 459-460,
459f
Helmet(s)
baseball, 488, 488f
cervical spine injury and
hospital management of, 571,
573-574, 575f
on-site management of, 568-569,
569b, 571
eye protection by, 492b, 492f
football, 486-487
chin straps of, 487
daily inspection of, 486b
tting of, 487, 487b, 489f
jaw pads of, 487
linings of, 488f
recent technology for, 486-487,
487f, 512
reconditioning and recertication
of, 478, 479b
standards for, 478
warning label on, 479b, 486
weekly inspection of, 487b
ice hockey, 487-488
lacrosse, 488f
linings of, 488f
soccer, 512
sports requiring, 486b
standards for, 563b
Hematocele, 613-614
Hematoma, 459
auricular, 493, 582-583, 584f
breast, 622
costochondral injury with, 617
hepatic, 609
intestinal, 609
myositis ossicans secondary to,
451-452, 452f
of nasal septum, 590
penile, 614
perineal, 614
in rectus abdominis muscle, 598, 604
renal, 610-611, 610f
retroperitoneal, 604-605, 606
rib fracture with, 618
splenic, 606-607, 607f
subdural, 540
vulvar, 614-615
Hematuria, 447, 450
differential diagnosis of, 611b
runners, 612
traumatic, 450
in bladder injury, 612
in renal injury, 610-612
Hemoglobin, 86-87
carbon monoxide and, 129
preparticipation measurement of, 21
Hemoptysis, pulmonary contusion
and, 624
Hemothorax, 623-624, 625-626
rib fracture with, 618, 618b,
625-626
Hepatitis B, 448
Hepatitis C, 448
Hernia, 598-603
diagnosis of, 599
epigastric, 602-603, 603t
femoral, 598, 599t, 600f, 602, 603t
groin pain and, 598-599, 600
in athletic pubalgia, 600-602,
600b, 601f
incarceration of, 599-600, 600f
inguinal. See Inguinal hernia.
management of, 599-600
return-to-activity guidelines for,
603t
in runners, 307
strangulation of, 599-600
types of, 599b, 599t
umbilical, 602, 603t
ventral, 603, 603t
Herpes simplex virus infection, 469,
469f
Herpes zoster, 460
Hexpad protective apparel, 512
High altitude, 116-122. See also
Acclimatization to altitude.
chronic diseases and, 121
exercise performance at, 120
exercise training at, 121
neuropsychological behavior at,
120-121
physiologic effects of, 118, 118b,
118t. See also Hypoxia.
circulatory, 119-120, 120f
pulmonary ventilation and,
118-119, 119f
population visiting and living at,
116
sickling crisis at, 447
tyrosine supplementation and,
154
High jump, biomechanics of, 252,
253f
High-altitude cerebral edema, 122,
122-123t, 122b, 445
High-altitude illness, 118, 121-122,
122-123t, 122b, 445, 445b
pre-existing lung disease and, 121
High-altitude peripheral edema, 122,
122-123t
High-altitude pulmonary edema,
121-122, 122-123t, 122b,
445
High-intensity exercise
energy generation for, 158, 158b
ergogenic aids for. See Ergogenic
aids, for high-intensity
exercise.
muscle fatigue in, 159
optimizing performance in,
158-159
physiologic adaptations to, 159
High-threshold mechanosensitive
(HTM) muscle receptors,
423-424, 425f, 429
compression therapy and, 433
summary of, 435-436
Hip
EMG activity in, in runners, 315
exibility testing of, 31-32
injuries to
in cycling, 209, 210t
in dance, 670-671, 670f
in golf, 222, 222b, 223b
osteoarthritis secondary to,
711-712
in running, 307
in soccer, 293, 297-298, 297b
kinematics of, in running, 309-310,
309t
knee pain in runners and, 320b
osteoarthritis of, 711-713
rehabilitation of, 712
running and, 712
surgery for, 712-713
patellofemoral pain syndrome and,
635-636, 635t
in soccer, jumping and, 296-297
total joint arthroplasty of, 717-719,
718t
implants for, 719
Hip pointers, 596-597
Hip power, development of, 253b
Hip protection, 501, 503f, 512
History. See Medical history.
Hives, 474
HMB (beta-hydroxy-beta-
methylbutyrate), 163-164
Homeopathy, for delayed onset muscle
soreness, 434-435
Hormone replacement therapy, 643,
645
Hot tubs, infections transmitted by,
471, 471b
HTM receptors. See High-threshold
mechanosensitive (HTM) muscle
receptors.
Human immunodeciency virus
(HIV) infection, 22-24t, 448
Humerus, spiral fractures of, in
baseball pitchers, 380
Hunting reex, 110
Hyaluronic acid, for knee osteoarthritis,
711
Index 787
Hydration. See Dehydration; Fluids
and exercise; Hyperhydration;
Hypohydration; Rehydration.
Hydrocele, 614
Hydrochlorothiazide, for hypertension,
443
beta-Hydroxy-beta-methylbutyrate
(HMB), 163-164
alpha-Hydroxycitric acid, 164
Hyperbaric oxygen therapy, for
delayed onset muscle soreness,
434
Hyperglycemia
in diabetics, 449
symptoms of, 449, 449b
Hyperhydration, 147-148
Hyperkeratosis, 463
Hypertension, 442-443
in autonomic dysreexia, 698, 698b
exercise recommendations and, 443
hyperadrenergic (hyperdynamic),
442
at preparticipation examination,
15, 17-18
risk factors for, 442, 442b
Hyperthermia, in disabled athletes,
688t, 696-697. See also Fever.
Hypertrophic cardiomyopathy, 18,
441-442
vs. athletes heart syndrome, 442,
442t
Hyperventilation, altitude and,
118-119
Hyphema, 589
Hypoglycemia
cold intolerance in, 113-114
in diabetics, 449
symptoms of, 449, 449b
treatment of, 449b
Hypohydration, 146-147
prevented by hyperhydration,
148
Hyponatremia, 107-108t, 109
uid excess causing, 147
ketogenic diet and, 94
Hypotension, in wheelchair athletes,
688t, 698
Hypothermia, 114-116, 115t,
116-117t
denition of, 114b
in disabled athletes, 688t, 696
in older adults, 113
symptoms of, 696
treatment of, 696
Hypoxia, at high altitude, 118-119,
118b, 120
cardiovascular disease and, 121
cold stress and, 131
exercise performance and, 120
neuropsychologic function and, 120
I
Ibuprofen, delayed onset muscle
soreness and, 429-430
Ice. See also Cold pack, for delayed
onset muscle soreness.
on abdominal wall injuries,
596-597, 598
availability in foreign facilities, 700
on bruises, 458
on cervical sprains and strains, 552
on contusions, 582
abdominal wall, 596-597
for shoulder problems
in swimmers, 345-346
in wheelchair athletes, 691
swimmers conditioning program
and, 340-341
Ice hockey
neuropsychological baseline in, 541
chest guards, 501
face guards, 487-488, 490
gloves, 499
helmets, 487-488
shin guards, 506-508
for thighs and hips, 501
Ice massage, for delayed onset muscle
soreness, 431
Iliac crest
avulsion of, 598
contusion at, 596-597
Iliopectineal bursitis, in runners, 307
Iliopsoas bursitis, in dancers, 670-671
Iliopsoas exibility, in runners, knee
pain and, 320b
Iliopsoas tendinopathy, in dancers,
670-671
Iliopsoas tendonitis, in cyclists, 209,
210t
Iliotibial band friction syndrome,
in runners, 320, 320b
Iliotibial band syndrome
in cyclists, 210t
in runners, 307, 314-315
Immersion foot, 116, 116-117t
Immunizations, preparticipation, 11
Impact Pad, 496-499
Impetigo, 448, 470
Impulse-momentum theorem, 237
Incidence, denition of, 735-740,
735b, 735f
Infections, 447-449. See also Skin
infections; Upper respiratory
tract infections; Urinary tract
infections.
Infectious mononucleosis, 447, 447b,
608-609
Inammation, muscle nociceptors and,
424, 425f
Inuenza, 444-445
Ingrown toenails, 462-463
Inguinal hernia, 600, 600f. See also
Hernia.
diagnosis of, 599
groin pain with, 598-599, 599t, 600
incidence of, 598, 599t
return-to-activity guidelines for, 603t
Injury, denition of, in research
studies, 736, 736b, 737t
Injury odds, 735-736, 738t, 739
Injury rate, denition of, 735-736,
738t, 739
Injury rate data, 745-762
analysis of
by body location, 752, 755t,
756-757t, 758t, 759t
by exposure setting, 751-752,
753t, 754t, 766-767
by gender, 750-751, 751t, 752f,
763
by severity of injury, 752, 752b,
758b, 759b, 760t, 761t
by sport, 745-750, 746t, 748t,
750f, 763
for boys high school sports, 748t,
750f, 751t
by body location, 756-757t
in competition vs. practice, 753t
severity and, 760t
for collegiate sports, 750f, 752f
with 10 or more days lost, 761t
by body location, 758t, 759t
in game vs. practice, 754t, 761t
for girls high school sports, 746t,
750f, 751t
by body location, 755t
in competition vs. practice, 753t
severity and, 760t
literature sources of, 745
Injury risk, 735-736, 738-739, 738t
Injury sites, physical tness prole and,
25
Insole. See Orthosis, foot.
Insulin
carbohydrate-protein supplements
and, 162
carnitine uptake and, 157-158
Insurance, preparticipation evaluation
and, 10-11
Intercostal nerve blocks, 618
Intertrigo, 466
Intervertebral discs
herniation of
cervical, 577t
forces leading to, 224
sciatica with, 639
788 Index
lesions of, 639-640
with functional curve, 640-641
manipulation for injury of, 640
prolapse of, loads required for, 223
Intestinal tract injury, 609-610
Intracranial hemorrhage, 540, 540b
Intrathoracic abdomen, 606, 606t
Ion 4D helmet, 512
Iontophoresis, for delayed onset
IRMS (isotope ratio mass
spectrometry), 178-179
Iron, 86-87
absorption of, 87, 447
recommended intake of, 447
supplementation of, 87
Iron-deciency anemia, 86-87,
446-447, 447b
Ischemic bowel disease, 610
Ischial bursitis, in runners, 307
Isokinetic muscle strength testing, 29
Isometric muscle strength testing, 29
Isotope ratio mass spectrometry
(IRMS), 178-179
Isotretinoin, for acne mechanica, 461
J
Jerk, 385, 406. See also Clean; Split
jerk.
Jersey bruise, 458
Jet lag, 700
Jock itch, 467-469
Joggers toe, 462, 462f
Joint replacement. See Total joint
arthroplasty.
Joints
ergogenic aids for, 166
hypermobility of, in dancers,
671-672, 671b, 671t
preparticipation testing of, 15, 17
Jones fracture, 668, 668f
Jump and land, movement screening
of, 28, 34t
Jumpers knee. See Patellar tendinopathy
(jumpers knee).
Jumping, 234-264
by amputees, 694
bilateral decit in, 251, 251b
concluding overview of, 262
in dance, 669-670, 669f
repetitions of, 258-259, 260b
depth jumps, 234, 253b, 254f, 260,
260t
horizontal, 234, 253-257
arms in, 257, 258f, 259f, 259t
ight biomechanics of, 254f,
255f, 256-257
kinematics and kinetics of, 257,
258f, 259f, 259t
takeoff biomechanics of, 253-256,
254f, 255b, 255f, 256b, 256f
landing from. See Landing.
repetitions in selected sports,
258-259, 260b
in soccer, 296-297
terminology of, 234, 235f
vertical, 234, 235f
arms in, 247-249, 247t, 248f,
249b
countermovement and, 249, 250f
electromyography and, 242-243,
244f, 245f, 246, 252f
full body mechanics of, 236-240,
236b, 238b, 238f, 239b,
239f, 240b, 240f, 240t
in high jump, 252
joint mechanics of, 240-242,
240b, 241f, 242t, 243b, 243t
movement patterns in, 243-245,
245b, 245f
performance factors in, 235-236,
235b, 236b, 236f, 237f
propulsive phase in, 236
single-leg, 235-236, 241f,
249-251, 250t, 251b
sport specicity of, 251-252,
251b, 252f, 253f
submaximal, 245-247, 246f, 247b,
247t
as testing tool. See Vertical
jump height; Vertical jump
repetitions.
as training tool, 252-253, 253b
K
Kallassy ankle brace, 519
Kehr sign, 606-607
Keloid scars, 458, 476
folliculitis with, 461-462
Keratinocytes, 455
Keratolysis, pitted, 467, 467f
Keratoma, 463
Ketoconazole challenge test, 178-179
Ketogenic diets, 94
Ketoprofen, delayed onset muscle
soreness and, 430
Kidney(s)
solitary
participation with, 611, 611b
preparticipation evaluation and,
18, 21, 22-24t
trauma to, 450, 610-612
pediatric, 610-611, 610b
types of, 610-611, 610f
Kinesio tape, 532, 532f
Kinetic chain
in baseball pitching, 350, 381
in soccer, 287-288, 303
in tennis, 265, 268-272, 268b,
270b, 271b
Kinetic energy, denition of, 238-239
Kinetics, and physical tness prole, 25
Knee. See also Anterior cruciate
ligament (ACL); Genu valgum;
Posterior cruciate ligament (PCL).
in cycling
injuries and, 189-190, 206,
208-209, 210t
muscle moments and, 199, 200f
reaction forces and, 196-198,
196f, 197f, 198f, 199f
osteoarthritis of, 709-711, 709f
braces and insoles for, 710-711
in golfers, 223
imaging of, 709-710, 710b
rehabilitation exercises for, 710
running and, 712
viscosupplementation for, 711
protection of, 502-506. See also
Knee braces; Knee pads.
in running
bent, 317-318
kinematics and, 309-310, 309t
muscle activity and, 315
valgus movement of, 314-315
valgus stress at, 311, 311b
in soccer
in crossover cutting, 293
in jumping, 296-297
in sidestep cutting, 292-293
total joint arthroplasty of, 717,
719-721, 720t
implants for, 720-721
Knee braces, 502-504, 504f, 505f, 506f
anterior cruciate ligament and,
504-506, 506f
disadvantages of, 505-506
functional, 502, 504-505, 505f,
506, 506b
medial collateral ligament and, 506
neoprene, 506, 507f
for osteoarthritis, 710-711
prophylactic, 502-504, 504b, 504f,
506
rehabilitative, 502, 506
Knee injuries. See also Anterior
cruciate ligament (ACL); Patellar
entries; Patellofemoral entries.
in cycling, 189-190, 206, 208-209,
210t
in football, collegiate rule changes
and, 504
Intervertebral discs (Continued) Jumping (Continued)
Index 789
in golf, 221-222, 221b, 223, 223b
in jumping sports, 257, 257b,
260-262, 261b
to medial collateral ligament, 504
in runners
epidemiology of, 307-308
exed position and, 309
Q-angle and, 766
in soccer
cutting and, 299
jumping/landing and, 301-302,
302f
kicking and, 297-298, 297b
in weightlifters, 415-416
Knee pads, 502, 504f
Knee pain. See also Anterior knee pain
syndrome; Patellofemoral pain.
in cycling
kinematics and, 190
kinetics and, 195-196
survey of, 208-209
in running
foot pronation and, 319
management of, 320b
L
Labia, injury to, 614-615
Laboratory tests
in physical tness prole, 27
in preparticipation examination,
20-21
Lacerations, 457-458
in disabled athletics, 688t, 690t
of face, scalp, and neck, 583-587
adhesives for, 587
alignment of, 584, 586f
anesthesia for repair of, 584-585
antibiotics for, 587
cleansing and debridement of,
583-584
hemostasis for, 583
special structures and, 585-586,
585b, 586f, 587f
suturing of, 586-587
types of, 583, 583b, 585f
hepatic, 609
pancreatic, 612
renal, 610-612, 610f
vaginal, 614-615
Lacrosse
eye injuries in women players, 492
chest guards, 501, 503f
chin straps, 490
eye protection for women, 767
face masks, 490, 491f
gloves, 499, 501f
helmets, 490
padded shirt, 512
rib guards, 500
throat protector for goalie, 482
Lactate
high-intensity exercise and, 158-159,
160
Landing, 257-262. See also Jumping.
forces exerted in, 257, 257b
gender differences in, 260-262,
260b, 261f, 633
injuries and, 238, 240b, 257, 257b,
260-262, 261b
in dancers, 669-670, 669f,
671-672
in women, 632, 635, 669-670
kinetics of, 257-260, 259b, 259f,
260t
movement screening of, 28, 34t
Langerhans cells, 455, 472
Laryngeal injury, 581-582, 582b, 583f
Laryngoscopy, in vocal cord
dysfunction, 128
Laser treatment
of acrochordons, 467
of aphthous ulcers, 460
of leg veins, 460
of pyogenic granuloma, 460
for scar revision, 462, 475-476
of sun damage, 473
for tattoo removal, 459
of warts, 470
Lateral epicondylalgia, 715, 717
Lateral epicondylitis (tennis elbow)
golf-related, 226, 227b, 227f
taping for, 523
Learning disability, concussion in
athlete with, 545
LeFort fractures, 591, 591f
Left ventricular hypertrophy,
Leg length inequality, and low back
pain, in cyclists, 209
Leg raise test, 31
Legg-Perthes disease, in runners, 307
Lennox Hill derotation brace,
504-505, 506f
Lichen simplex chronicus, 463-464
Lidocaine, with dexamethasone, in
iontophoresis, 432
Lifting. See Weight training.
Lightning, 132
Linoleic acid
conjugated, 164
recommended intake of, 77t, 78t
-Linolenic acid, 77t, 78t
Lips
lacerations of, 586-587, 587f
protective ointments for, 465t
Little league elbow, 365
Little league shoulder, 380
Liver, enlarged, sports participation
with, 22-24t
Load-deformation curve, 321-322,
321f
Local muscle endurance, 29, 34t
Long jump. See Jumping, horizontal.
Loss height, 235-236, 236b, 237f
Loss of consciousness
cervical injury and, 565f, 566
concussion and, 536, 538-539, 543
Low back. See also Lumbar spine.
in soccer, sidestep cutting and, 292
in swimming, 345
Low back injury. See also Back injury;
Spinal injury.
golf-related, 217
pushing or pulling and, 388-391,
391b
Low back muscles, exibility testing
of, 31
Low back pain, 640. See also Lumbar
spine.
in athletes with disabilities, 693-694
core strengthening exercises and,
393
in cyclists, 204, 206b, 209, 210t
in golfers, 223-225, 225b
club and, 229
heat wrap for, 431
muscle activation deciency and, 385
in pregnancy, 643
spondylolisthesis with, 638
spondylolysis with, 638
Lower crossed syndrome, in runners,
knee pain and, 320b
Lower-body power
development of, vertical jumps for,
252-253, 253b
testing of, broad jumps for, 257
Lumbar spine. See also Low back; Low
back pain.
Bodyblade and, 391
injuries to
cumulative load theory of,
223-224
golf-related, 223-225, 223b, 225b
strain or sprain as, 640
muscles providing stability to,
385-386, 386b
push-ups and, 391
rowing and, 391
squatting and, 386-387, 388b,
388f, 389f, 390f
trunk extension exercises and,
391-392, 392t, 393t
trunk exion exercises and, 391
Knee injuries (Continued) Lacrosse (Continued)
790 Index
Lunate, dislocation of, in weightlifter,
415
Lunge exercises, 393-397, 395t, 396t,
401-406, 402t, 403b, 404f, 405f,
406b
M
Macronutrients, 67-86. See also
Carbohydrate; Fat; Protein.
dietary reference intakes (DRIs)
acceptable ranges, 77t
additionally limited, 79t
recommended distribution of,
83t
Macrophages, delayed onset muscle
soreness and, 428
Maladaptive fatigue syndrome, 48-49,
48b
Malignancy, sports participation with,
22-24t
Malocclusion, 592, 593f
Mandible
dislocation of, 592-593
fracture of, 591t, 592-593, 592b,
593f
zygomatic fracture and, 591
Manual therapy
for osteoarthritis
of hip, 712
of knee, 710
for tendinopathy, 715
Manubrium, 616f, 620
Marathon runners, physical tness
prole for, 27
Marfan syndrome, 17-18, 441, 443,
443t
Marijuana, testing for, 181
Massage, for delayed onset muscle
soreness, 433-434
Mast cells, delayed onset muscle
soreness and, 425f, 428-429
Masters athlete, 10b, 704-729.
See also Aging; Elderly athlete,
preparticipation evaluation of.
competitive events for, 705
denition of, 705
joint replacement in. See Total joint
arthroplasty.
osteoarthritis and, 708-714
hip, 711-713
knee, 709-711, 709f, 710b,
712
shoulder, 713-714
physiology of aging in, 706-708
cardiorespiratory tness and,
707-708, 708b
exibility and, 708, 708b
muscle and, 706-707, 706b,
707b, 707f
tendon and, 707, 707b
sports medicine practitioner and,
705-706
tendinopathy in, 714-717, 716b
world records of, in track, 705, 705t
Maxillary fractures, 591, 591f, 592b
Maxillofacial injuries, 581-595
airway, 581-582, 582b, 583f
dental, 594-595, 594b, 594f, 595b
fractures in. See Facial fractures.
initial management of, 581, 581b,
582t
ocular, 587-590, 588b, 589b, 590b
soft tissue, 582-583. See also Abra-
sions; Contusions; Lacerations.
Maximum voluntary isometric
contraction (MVIC), 350, 352
Medial collateral ligament, of knee,
injury to, 504
Medial epicondylitis (golfers elbow),
226, 227b
in baseball pitchers, 362, 380
Medial tibial stress syndrome
(shin splints)
in cyclists, 210t
diagnosis of, 637
pathogenesis of, 637
in runners, 307
female, 637, 637b
foot abnormalities and, 320
in women, 637, 637b
Median nerve, entrapment of, in
Medical history
maxillofacial injury and, 581
in nutritional assessment, 58
in preparticipation evaluation,
12-15, 13f
Medicine ball throw distance, 29, 34t
Melanocytes, 455
Melanoma, 132, 472-473
Menopause, 644-645
MENS (microcurrent electrical
neuromuscular stimulation), 433
Menstrual cycle
anterior cruciate ligament injury
and, 634
body temperature and, 104-105
Menstrual history, 18-19
Metabolic rate. See also Caloric
expenditure.
basal (BMR), 94
exercise-heat stress and, 101
food restriction and, 94b
Metabolic testing, 32-33, 33f, 33t
Metatarsal fractures
fth, 667-668, 668f
stress fractures, 668, 669f
Metatarsalgia, in cyclists, 210t
Metatarsophalangeal joints
rst, in dancers
osteoarthritis of, 672, 672b
sesamoiditis and, 673-674, 674f
in jumping, 250-251
Methacholine challenge test, 126
Methicillin-resistant S. aureus
(MRSA), 448-449, 448b
Methoxy glycolepoetin beta (CERA),
180
Methylprednisolone, for spinal cord
injury, 574
Microcurrent electrical neuromuscular
stimulation (MENS), 433
Microfailure zone, 321-322, 321f
Micronutrients, 67, 86-91. See also
Minerals (elements); Vitamins.
Midfacial fractures, 590-591, 591f,
592b
Midfoot motion, in running, 312
Midfoot pronation, in running, 320
Midfoot strikers, in running, 317-318,
317b, 317f, 318f
Migraine, post-traumatic, 540
Miliaria, 466
Miliaria crystallina, 466
Miliaria profunda, 107-108t, 109, 466
Miliaria rubra, 106, 107-108t, 109,
466, 466f
Milk-based protein supplement, 162
Minerals (elements), 86-91
dietary reference intakes (DRIs),
70t, 74-75t, 80t
supplementation of, 86-87
iron-deciency anemia and, 447
multivitamin with, 94
Mitochondria, endurance training and,
142
Mitral valve prolapse, sports participa-
tion with, 22-24t
Moles, 472-473
Molluscum contagiosum, 470
Mononucleosis, infectious, 447, 447b,
608-609
Monounsaturated fats, dietary sources
of, 85t
Mortons foot, in ballet vs. folk
dancing, 660
Mountain sickness. See Acute
mountain sickness.
Mouth
aphthous ulcers of, 460
mucosa of, 455
Mouthguards, 493, 493f, 594-595
ulcer prevention by, 460
Masters athlete (Continued)
Index 791
Movement patterns, physical tness
prole and, 24-25
Movement screening, 28, 28b, 34t
MRSA (methicillin-resistant S. aureus ),
448-449, 448b
Multiple sclerosis
cold-induced motor control and, 114
heat intolerance in, 106
hypotension in, 698
neurogenic bladder and, 697-698
temperature regulation and, 695
Multi-RM testing, 28-29
Multivariate regression, 741, 741t
Multivitamin with minerals, 94
Muscle(s)
aging and, 706-707, 706b, 707b,
707f
biarticular, jumping and, 242-243,
244-245
caffeine effect on, 155
cold stress and, 110
endurance training and, 142, 143b
force-length relationship of, 238b
glycogen in, 67
diet and, 67, 77
endurance performance and,
149
exercise-heat stress and, 101
replacement of, 93
hypertrophy of. See also Muscle mass.
ber types and, 706
for optimizing speed and power,
159
through strength training, 159,
162
of masters athlete, 706-707, 707f
red blood cell destruction in, 447
strength training and, 159, 159b
Muscle actions, in physical tness
prole, 25
Muscle activity. See Electromyography
(EMG).
Muscle cramps, 423
uid replacement and, 147
Muscle damage. See also Creatine
kinase (CK); Muscle strain.
coenzyme Q10 and, 435
delayed onset muscle soreness and,
426f, 427-428, 427f, 429
beta-hydroxy-beta-methylbutyrate
and, 163-164
Muscle endurance
acclimatization to altitude and,
120
local, testing of, 29, 34t
Muscle bers
aging and, 706-707, 707b, 707f
types of, 706
Muscle mass. See also Muscle(s),
hypertrophy of.
ergogenic aids and, 162-164,
162b
resistance training and, 161-162
Muscle pain
causes of, 423, 423b, 424t
receptors of, 423-424, 425f
Muscle soreness. See Delayed onset
muscle soreness (DOMS);
Soreness.
Muscle strain, 435-436, 435f. See also
Muscle damage.
abdominal, 597-598, 619-620
cervical, 551-552
chest wall, 619-620
continuum of, 424t
vs. muscle soreness, 423, 423b
rates of, 758b
thigh and hip protection and, 501
in weightlifters, 415, 415b
Muscle strength. See also Strength
training.
creatine supplementation and, 163
gender differences in, 631, 632t
testing of, 28-29, 34t
Musculoskeletal disorders, sports
Musculoskeletal examination,
MVIC (maximum voluntary isometric
contraction), 350, 352
Myocardial contusion, 626-627, 626b,
627b
Myocardial infarction, cold exposure
and, 114
Myofascial force transmission, 303
Myoglobin, 86-87
muscle damage and, 427-428
Myokinase, high-intensity exercise
and, 158-159
Myopia, 15
Myositis ossicans, 451-452, 452f
N
N -acetylcysteine, 156-157
Nails, 456, 456f
fungal infection of, 467-468
hemorrhage under, 459, 462, 462f
ingrown, 462-463
Nandrolone (19-nortestosterone),
177-178
Nasal trauma, 590, 590b, 590f
fractures in, 590, 590b, 590f
hockey-related, 591t
lacerations in, 586
National Athletic Training Association
Board of Certication
(NATABOC), 2, 2b
National Football League (NFL)
combine, 26
National Operating Committee on
Standards for Athletic Equipment
(NOCSAE)
baseball helmets and, 488
football helmets and, 478, 479b,
486, 486b, 487b
lacrosse helmets and, 490
Navicular drop
medial tibial stress syndrome and, 637
running injuries and, 766
Nearsightedness, 15
Neck. See also Cervical spine.
injury to
laryngeal trauma in, 582, 582b,
583f
in soccer players, 300-301
stresses on, in golf, 221
Neck pain, cycling and, 209, 210t
Neck protection, 494, 494f, 495f
Nedocromil, for exercise-induced
bronchospasm, 444
Neoprene elbow sleeve, 506, 507f
Neoprene knee braces, 506, 507f
Neurogenic bladder, 697-698
Neuroleptic drugs, heat intolerance
with, 106
Neurologic examination
in suspected cervical injury
at hospital, 573
on-site, 566-568
Neutrophils, delayed onset muscle
soreness and, 425f, 427-428, 429
Nevi, dysplastic, 472-473
Niacin, toxic effects of, 86
Nipples
chang of, 464
trauma to, 623
Nitrogen dioxide, 124t, 129-130, 131
Nitrogen oxides, 129-130
Nociceptors, muscle, 423-424, 425f,
429
NOCSAE. See National Operating
Committee on Standards for
Athletic Equipment (NOCSAE).
Nonsteroidal anti-inammatory drugs
(NSAIDs). See also Anti-
inammatory drugs.
breast trauma and, 622
429-430
19-Nortestosterone (nandrolone),
177-178
Nose
cerebrospinal uid leakage from, 591
injury to. See Nasal trauma.
792 Index
Nosebleed, 590
Nutrient groups, 67, 67b
Nutrient recommendations, 67-92. See
also Carbohydrate; Fat; Minerals
(elements); Protein; Vitamins.
alcohol and, 85-86
assessment for. See Nutritional
assessment.
for bone health, 165-166
uids and, 91-92, 91b
standard tables of. See Dietary
reference intakes (DRIs).
summary of, 95
Nutrition, preparticipation examination
and, 19-20
Nutritional assessment, 58-67
behavior change based on, 66-67
action strategies for, 67, 83b
stages of, 66-67, 82t
for weight loss, 94
determining nutrient intake in,
58-59, 59b
dietary interview in, 66
energy needs and, 58, 60-64t
evaluating nutrient intake in, 59-66
health screen for, 58
recommendations based on. See
Nutrient recommendations.
summary of, 95
for weight loss, 94
Nutritional ergogenic aids. See
Ergogenic aids.
O
Obesity
Obturator nerve entrapment, 603
Odds ratio, 738t, 740, 740b
Odontoid process, fracture of, 553
Oil glands, cutaneous, 455-456,
456f, 457
Older adults. See Aging; Elderly
athlete, preparticipation
evaluation of; Masters athlete.
Olecranon, injury to, in baseball
pitchers, 381
Omega-3 fatty acids
bone mass and, 166
joint health and, 166
110 conditioning test, 33, 33t, 34t
One-repetition maximum (1-RM)
tests, 25, 28-29, 34t
Onychomycosis, 467-468
Oral contraceptives
anterior cruciate ligament injury
and, 634
hypertension associated with, 442
Orbital fractures, 591, 591f, 591t,
592b, 592f
Organ transplant recipient, sports
participation by, 22-24t
Orthogel, 481-482
Orthoglass, 485, 485f
Orthopedic surgeon
certication in sports medicine, 3
as team physician, 3
Orthoplast, 483t, 484, 484f, 486f
Orthosis, foot, 511-512, 512f
cycling kinematics and, 190
for knee osteoarthritis, 711
patellofemoral pain and, 636-637
for runner, 325-327
accommodative, 326-327
biomechanical, 326, 327f
with high arch, 318
impact forces and, 316
knee pain and, 320b
late pronation and, 314t
637
philosophy of, 325, 325b
recommendation for, 325b
resupination and, 313
rigid versus semiexible, 326t
Os trigonum, 664-665, 665f, 666b
case study with, 672-673, 673f
exor hallucis longus tendinopathy
and, 667
Osteitis pubis, in soccer players, 298
Osteoarthritis
in dancers, 672, 672b, 672t
of glenohumeral joint, 713-714
glucosamine and chondroitin for,
166
in golfers
stress on knee and, 223
warmup and, 230
of hip. See Hip, osteoarthritis of.
of knee. See Knee, osteoarthritis of.
in masters athletes, 708-714
hip, 711-713
knee, 709-711, 709f, 710b, 712
shoulder, 713-714
symptoms of, 710
Osteochondral graft procedures, 714
Osteopathy, doctor of, 3
Osteoporosis
diagnosis of, 643
excess protein intake and, 79
exercise-induced amenorrhea and,
18-19
factors contributing to, 87
in female athlete triad, 53, 641-642
lower-extremity paralysis and, 692
postmenopausal, 644-645
Otitis externa, 450
Ovary, absence of one, 22-24t
Overtraining, 450-451, 450b
Overuse injuries
in young athletes, 40
Oxygen partial pressure, altitude and,
118, 118t, 119f
Oxygen saturation
at high altitude, 118-119, 118t, 119f
neuropsychologic function and, 120
Oxygen uptake, maximum (VO
2
max)
aging and, 707-708, 708b
altitude and, 119-121, 120f
in hot climate, 131
gender differences in, 631, 632t
in masters athlete, 707-708
measurement of
in eld tests, 27-28
in laboratory, 27
in physical tness prole, 32, 34t
ozone inhalation and, 130-131
Ozone, 130-131
in hot climate, 131
interactions with other pollutants,
131
national standards for, 123, 124t
P
P values, 741-742
Paget-Schroetter syndrome, 623
Pain
in dancers, 653-654
muscle
causes of, 423, 423b, 424t
receptors of, 423-424, 425f
vs. soreness, 339-341
in swimmers
characteristics of, 331-332, 332f
mechanical changes and, 341, 342t
tendon, 714-715
Pain scale for athletes, 340-341, 340f
Pancreatic injury, 612
Pancreatitis, 612
Parents of young athletes
clinicians role with, 44-45, 45b, 46
key tools for, 43-44, 43b
positive attitudes of, 44, 44b
unhealthy involvement by, 41, 43,
44-46, 48
Parkinson disease, heat intolerance in,
105-106
Parotid duct, injury to, 585, 586f
Pars interarticularis, fractures of,
638-639
Participation. See Clearance for
participation.
Particulate air pollution, 124t,
130-131
Patella, subluxation of, neoprene
braces and, 506
Index 793
Patellar tendinitis
cycling and, 208-209, 210t
running and, 320b
Patellar tendinopathy (jumpers knee),
257, 261b, 262, 714
eccentric training for, 716
pain of, 714-715
soccer-related, 299, 301-302
Patellar tendinosis, in weightlifter,
416
Patellar tendon rupture, in weightlifter,
415
Patellar tendon strain, in weightlifter,
415-416
Patellofemoral forces
in lunge exercises, 404-406, 404f,
405f, 406b
in squat exercises, 399-401, 400f,
401b, 401f
Patellofemoral joint
injury to
in runners, 309
neoprene stabilizers for, 506, 507f
Patellofemoral pain. See also Anterior
knee pain syndrome; Knee pain.
in cyclists, 210t
in runners
foot pronation and, 319-320
hip abduction weakness and,
314-315
management of, 320b
Q-angle and, 319-320
in soccer players, 298-299
taping for, 524-528, 524f, 525f,
526f, 529-530t
in women, 635-637, 635t
PCL. See Posterior cruciate ligament
(PCL).
Peak stresses, of sports, 18, 19t
Pectoralis major
rupture of, 621-622
Pedal designs, joint loads and, 196,
196f
Pedal reaction forces, 191-193, 191f,
192f, 193f
Pelvic drop, in running, 314-315, 315f
Pelvis
running injuries to, 307
soccer-related dysfunctions of, 297b,
298
Penile injury, 614
Performance-enhancing substances,
174-175, 174b. See also Drug
testing; Ergogenic aids.
Pericardial effusion, rib fracture with,
618
Pericardial tamponade, 623-624, 627,
627b
Perineum, injuries to, 614-615
Peritoneal irritation, 604, 605-606,
609, 612
Peritoneal lavage, 605, 606t
Pes anserine bursitis, in cyclists, 210t
Pes cavus, running shoe for, 318, 322
PET (positron emission tomography),
concussion and, 537
Petechiae, 458-459, 458f
PFP. See Physical tness prole (PFP).
Pharmacology, sports, 174-175, 174b
Pharyngitis, 445
Phonophoresis, 432
Phosphocreatine. See Creatine
phosphate (CP).
Photo injury. See Sun exposure.
Physical Activity Guidelines, of US
federal government, 704-705
Physical examination. See Preparticipa-
tion evaluation (PPE), physical
examination in.
Physical tness prole (PFP), 21-36
data quality in, 27, 27b, 33
developing test battery for, 33, 34t
important uses of, 25-27, 25b
introduction to, 21-24, 24b
needs analysis for, 24-25, 25b
safety considerations in, 27, 27b
for skill- or strategy-intensive sports,
27, 27b
sports medicine team and, 25, 25b,
33-36
strength and conditioning
coordinator in, 21-24
test classications in, 27-28, 27b
tested constructs in, 28-33, 28b
agility, 31, 32f
for common sports, 34t
exibility and range of motion,
31-32
local muscle endurance, 29
metabolic capacity, 32-33, 33f, 33t
movement screening, 28, 28b
muscular strength, 28-29
power, 29-30, 30f
velocity and acceleration, 30-31,
31t
Physical therapist, sports, 2-3, 3b, 3f
competency statements for, 3b
injury management and, 6
Physician. See Team physician.
Phytochemicals, antioxidant, 156-157
Piezogenic papules, 459-460, 459f
Pink eye, 450
Pitching. See Baseball pitching.
Pitted keratolysis, 467, 467f
Plantar fasciitis
in runners
foot abnormalities and, 320-321
incidence of, 307
stride length and, 310
taping for, 523
Plantar pressures. See Foot plantar
pressures.
Plantar warts, 469, 470f
Plasma volume, glycerol-induced
hyperhydration and, 148
Plastazote, 484
Plastics. See Thermomoldable plastics.
Platelet-rich plasma, for tendinopathy,
717
Playgrounds, injury prevention in,
768t
Plyometric training
depth jumps in, 253b
push-ups in, 391
for swimmers, 347
Pneumothorax, 624-625, 624b, 625b,
625f
rib fracture with, 618, 618b,
624-625
spontaneous, 625
tension, 623-624, 625, 625b, 626f
Polidocanol, for tendinopathy, 416,
717
Polyunsaturated fats, dietary sources
of, 85t
Popliteus tendinitis, in cyclists, 210t
Positron emission tomography (PET),
concussion and, 537
Postconcussion syndrome, 537
Posterior cord syndrome, 573
Posterior cruciate ligament (PCL)
lunge exercises and, 401-403, 402t
squat exercises and, 397-399, 398t
Postpubescent athlete, preparticipation
evaluation of, 9
Postural instability, in concussed
patients, 537-538, 540
Potassium
dietary, 70t, 74-75t
Potential energy, definition of,
238-239
Power
denition of, 239
muscle
dened, 29
testing of, 29-30, 30f, 34t
in vertical jumps, 239-240, 240f,
240t
Power activities. See High-intensity
exercise.
Power clean or snatch, 406
Power endurance tests, 32, 33f, 34t
Power Wheel, 393
Powerlifting, 406
squat exercise and, 386-387
PPE. See Preparticipation evaluation
(PPE).
Pre-existing conditions, 10-11
794 Index
Pregnancy
exercise and, 643-644
benets of, 643, 644b
contraindications to, 644, 645t
in highly trained women, 644
prescription for, 643-644, 644t
recommendations for, 643-644,
645t
warning signs in, 645t
physiologic changes in, 643
Preparticipation evaluation (PPE),
9-21
extent of, 9
frequency of, 9
group method of, 9, 11-12, 12f
laboratory tests in, 20-21
medical history in, 12-15, 13f
multistation, 9
objectives of, 10-11, 10b
physical examination in, 13f, 15-20
cardiovascular, 17-18, 17b, 18f
dental, 20
dermatologic, 20
gastrointestinal, 19-20
general medical, 20, 20b
general questions in, 15b
musculoskeletal, 15-17
neurologic, 17
prior heat disorders and, 20
pulmonary, 18
sports medicine team and, 6, 6f
urogenital, 18-19
visual, 15
vital signs in, 15, 16t
physicians recommendation based
on, 21
contact level and, 10b, 21
intensity level and, 19t, 21
pass/fail criteria and, 21b
specic medical conditions and,
22-24t
sample form used in, 13f
for specic activities, 9
for specic populations, 9, 10b
structure of, 11, 11b, 12f
timing of, 9
Prepubescent athlete, preparticipation
evaluation of, 9
Prescriptive zone, of ambient
temperature, 100, 100f
Press, in weightlifting, 406, 415
Pressure-mediated pain receptors,
423-424, 425f, 429, 435-436
Prevalence, denition of, 735-740,
735b, 735f
Prevention. See Epidemiology of
sports injury, injury prevention
and; Protective equipment.
Prickly heat. See Miliaria rubra.
Primary care physician
certication in sports medicine, 3
nutritional assessment and, 58
as team physician, 3
Pro-agility test, 31, 32f, 34t
Proling. See Physical tness prole
(PFP).
Progesterone challenge test, 642-643
Prolactin, fatigue and, 144
Prolotherapy, for tendinopathy, 717
Pronation. See Foot pronation.
Pronator teres syndrome, in baseball
pitchers, 381
Prospective cohort studies, 731, 731t,
733, 733b
advantages and disadvantages of,
733, 734f, 734t
Prostaglandins, muscle damage and,
428, 428f, 430
Prostheses. See Amputees as athletes.
Protective equipment, 478-514. See
also Clothing.
for ankles. See Ankle braces.
for chest, 500-501, 503f
custom-made, 479-480
fabrication of, 485, 485b, 486f
for dancers, 654
degree of contact and, 479
with wheelchairs, 691-692, 691f
while standing, 692-693
for elbows, 499
for face, 488-493
chin straps, 490-491, 491f
ear protectors, 493, 493f
eye protectors, 15, 491-493,
492b, 492f, 590, 767
face guards, 488-490, 490f, 490t,
491f
mouthguards, 460, 493, 493f,
594-595
for feet. See Orthosis, foot; Shoes.
for hands, 499, 499b, 501f
of wheelchair athletes, 691-692
for head. See Helmet(s).
for hips, 501, 503f, 512
history of, 478
for knees. See Knee braces; Knee
pads.
legal liability and, 479
materials for, 480-485
air management pads as, 480-481
for casting, 484-485, 484b, 485f
felt as, 482, 482f
foam as, 480, 481f
gel as, 481-482, 482f
thermomoldable. See Thermo-
moldable plastics.
for neck, 494, 494f, 495f
new innovations in, 512
for ribs, 500, 502f
for shins, 506-508, 508f
for shoulders
with acromioclavicular sprain,
496-499
football pads, 494-496, 495f,
496b, 496f, 497f, 498f,
500f, 512
ice hockey pads, 494, 499f
with instability, 499
lacrosse pads, 494, 499f
standards for, 478-479
stock versus custom, 479-480
testing of, factors in, 479b
for thighs, 501, 503f, 512
for wrists, 499
Protein
dietary sources of, 79, 84t
for traveling athlete, 700
energy generation using, 141-142
as ergogenic aid
high-intensity exercise and,
161-163, 162b
excessive, osteoporosis and, 79
recommended intake of, 67, 77-82,
77t, 78t
as percent of calories, 83t
summary of, 95
vegetarian diets and, 79-82, 82b,
85f
water intake needed with, 79
Proteinuria, 449-450
Pseudobursitis, 464, 464f
Pseudomonas, 470-471
Psoriasis, heat intolerance in, 106
Psychosocial aspects of youth sports,
40-57
attention decit disorder and, 50-51,
51b
burnout and, 41, 48-49, 48b
concussion and, 51-53
depression and, 49, 49b
developmental model of Balyi and
Hamilton, 41-42, 42t
dropout majority and, 41
eating disorders and, 53-55
healthy focus for, 40b, 41-43, 41b,
42b, 43b
injury and, 40, 46-48, 46t
with attention decit disorder,
50-51, 51b
return to sport after, 48, 48b
Protective equipment (Continued)
Index 795
parents and
clinicians role with, 44-45, 45b, 46
key tools for, 43-44, 43b
positive attitudes of, 44, 44b
unhealthy involvement by, 41, 43,
44-46, 48
performance enhancement and,
43-44, 43b
slump and, 48
staleness and, 48-49
steroid abuse and, 55-56
substance abuse and, 53, 53b
winning and, 43-44
Pubalgia, athletic, 600-602, 600b, 601f
Pubescent athlete, preparticipation
evaluation of, 9
Pudendal nerve, cycling trauma to, 614
Pulmonary artery pressure, altitude
and, 119
Pulmonary compromise, sports
Pulmonary disease, 444-445, 445b
carbon monoxide exposure and, 129
Pulmonary edema
high-altitude, 121-122, 122-123t,
122b, 445
hyponatremia with, 109
Pulmonary examination,
Pulmonary function testing, 125
Pulmonary hypertension, high altitude
and, 121-122
Pulmonary injuries, 624-626
contusion as, 624, 624b
hemothorax in, 618, 618b, 623-624,
625-626
mediastinal emphysema in, 626, 626b
pneumothorax in, 624-625, 624b,
625b, 625f
tension, 625, 625b, 626f
subcutaneous emphysema in, 618,
626, 626b
Pulmonary ventilation, at high altitude,
118-119, 119f
Pupil diameter, baseline differences in,
15
Purpura. See Bruising.
Push-up, 391
Pyogenic granuloma, 460
Q
Q-angle
gender differences in, 261, 631, 635
knee injury and, in runners, 766
knee pain and, 319-320
in runners, 319-320
in women, 635-636
QT interval, prolonged, in eating
disorders, 642
Quadriceps
contusions of, protection for, 501
in female athletes, 633
patellofemoral pain and, 636
in running, 315
strains of, protection for, 501
Quadriceps angle. See Q-angle.
Quadriceps tendon, strains of, in
weightlifters, 415
Quadrilateral space syndrome, in
Quadriplegia. See also Spinal cord injury.
autonomic dysreexia in, 698
cervical spinal stenosis and, 555-556
heat and cold intolerance in, 695
Quercetin, 156-157
R
Radial nerve, entrapment of, in
Radiant heat exchange, 99
Radiocapitellar joint, injury to, in
baseball pitchers, 363, 381
Radiologic examination. See also
Computed tomography (CT).
of cervical spine injury, 571,
573-574, 573b
of knee osteoarthritis, 709-710, 710b
of rib fractures, 618, 618b
Randomized controlled trials, 731,
731t, 733
advantages and disadvantages of,
733, 734t
Range of motion (ROM). See also
Flexibility.
aging and, 708
in cycling, 187-188
kinematics of, 188-189, 188f,
190, 191b
stationary bicycle adjustments and,
206b
in running, 309-310, 309t
testing of
in physical tness prole, 31-32, 34t
Rate ratio, 738t, 740, 740b
RDAs (recommended dietary
allowances), 66
Reach height, 235-236, 236b, 237f
Reactive nitrogen species, antioxidants
and, 156-157
Reactive oxygen species, antioxidants
and, 142, 156-157
Rearfoot motion
ankle bracing and, 508
in running, 312-314, 313f, 314t,
320-321
shoe selection and, 511
Rearfoot strikers, in running,
317-318, 317b, 317f, 318f
Rearfoot varus
knee injury and, in soccer players,
299
637
Recommended dietary allowances
(RDAs), 66
Recreational drugs, 174-175, 174b
Rectus abdominis muscle
athletic pubalgia and, 602
hematoma in, 598, 604
strain of, 597-598
Rectus femoris, vertical jumping and,
242-243, 244f, 245f, 251
Rectus femoris strain, in soccer
players, 298
Regression models, 741, 741t
Rehabilitation. See also Return to
competition.
physical tness prole used in,
25-26
Rehydration, 91, 91b, 93, 93b.
See also Fluids and exercise.
caffeine and, 92
intravenous, 146
sodium solution for, 87, 93b
Reinjury
rates of, 761
risk of, 763
Repoxygen, 181-182
Resistance training, 161-162. See also
Strength training; Weight
training.
beta-hydroxy-beta-methylbutyrate
and, 163-164
carbohydrate-protein supplements
and, 162-163, 162b
conjugated linoleic acid and, 164
creatine and, 163
Respiratory rate, normal ranges of,
by age group, 16t
Resveratrol, 156-157
Retinal detachment, 15, 22-24t
Retrograde amnesia, 539
Retroperitoneal abdomen, 606, 606t
Retroperitoneal hematoma, 604-605,
606
Retroperitoneal hemorrhage, 611
Return to competition
psychological aspects of, 4-5
as team decision, 6
team physicians responsibility for,
4-5, 5b
in youth sports, 48, 48b
Revolution helmet, 486-487, 487f,
512
Rib belts, 616-617, 618-619, 618b
Psychosocial aspects of youth sports
(Continued)
796 Index
Rib injuries, 615-619
acute costochondral, 617
chronic costochondral, 617
contusion as, 615, 615b
costochondritis as, 617
fracture as, 617-619
in child, 618b, 624
coexisting injuries with, 617-618,
618b
hemothorax secondary to, 618,
618b, 625-626
management of, 618, 618b
pneumothorax secondary to, 618,
618b, 624-625
radiographs of, 618, 618b
respiratory complications of, 618,
618b
return to play with, 618-619
with sternal fracture, 621
stress fracture as, 619, 619f
subcutaneous emphysema second-
ary to, 618, 626, 626b
symptoms of, 618
at vertebral attachments, 616-617,
616f
Rib protection, 500, 502f
Rib strapping, 616-617, 618b
Ribcage
muscle strains at attachments to,
619-620
Ringworm, 467-469
Risk ratio, 738t, 740, 740b
RM. See Multi-RM testing; One-
repetition maximum (1-RM) tests.
Road rash, 459
ROM. See Range of motion (ROM).
Rotator cuff muscles
injuries to
in baseball pitchers, 360-361,
379-380
in golfers, 225-226
in swimmers
in backstroke, 338
cadaver study of, 332
double squeeze of, 332
fatigue and, 341-342
impingement and, 342-343
Rowers rump, 463-464
Rowing
rib stress fractures in, 619
spinal biomechanics of, 391
Rugby
mouthguards in, 493
studies of injuries in, 736, 737t
Runners breast, 622-623
Runners diarrhea, 446
Runners hematuria, 612
Runners nipples, 623
Runners rump, 459
Running, 307-330
by amputees, 692-695, 693f
base of gait in, 310, 311b
blood loss associated with, 447
as hematuria, 610
downhill, soreness caused by,
424-426, 429-430
gender differences in, 633
injuries caused by. See also Medial
tibial stress syndrome (shin
splints).
anatomic variables and, 766
breast trauma as, 622-623
concluding summary on, 327
footwear in management of,
322-325, 323b, 324f,
325b
knee pain in, 320b
load-deformation curve and,
321-322, 321f
orthosis management for,
325-327, 325b, 326t, 327f
surface and, 767
kinematics of, 308-315
foot placement in, 310-311
joint movements in, 309-310,
309t
pelvic drop in, 314-315, 315f
rearfoot motion in, 312-314,
313f, 314t
running cycle in, 308-310, 308b,
308f, 309t, 313
stride length in, 310, 310b
kinetics of, 316-318
bent knees and, 317-318
on curved pathway, 292
with direction change, 292
ground forces in. See Ground
reaction forces, in running.
plantar pressures in, 318, 319f
point of impact and, 317-318,
317b, 317f, 318f
shock attenuation in, 316-318,
316f
speed and, 317
knee pain in
foot pronation and, 319
management of, 320b
long-distance
diarrhea in, 446
myober in, 427
movement screening of, 28, 34t
muscle activity during, 315-316
osteoarthritis risk and, 712
pathomechanics of, 319-321
foot pronation in, 320-321
lower extremity malalignment in,
318b, 319-320
velocity testing in, 30-31, 31t, 34t
S
Sacroiliac joints
pathologic conditions of, 639
soccer-related injury to, 298, 303
stabilization exercises for, 639, 639f
Safety equipment. See Protective
equipment.
Salpingitis, water skiing and, 615
Salt supplementation, 87-91. See also
Sodium.
in heat exhaustion, 106
to prevent heat cramps, 106
Sarcomeres, damage to, 424t, 426f,
427
Sarcopenia, 706, 706b
Saturated fats
Sayerss equation for peak power, 29
Scabies, sports participation with, 22-24t
Scaphoid fracture, case study of, 7-8,
8f
Scapula
snapping, in baseball pitchers, 380
taping of, 531
Scars, 458, 458b
revision of, 475-477, 476b
Schistosomiasis, 471
Sciatica, 639
Sclerosing polidocanol, for
tendinopathy, 416, 717
Sclerotherapy, for leg veins, 460
Scoliosis, 640-641
Scrotum, 613f
injury to, 613-614
Sebaceous glands, cutaneous, 456-457
Second impact syndrome, 51, 51b,
537, 543
Sedentary activities, caloric expenditure
for, 60-64t
Seizures. See Convulsive disorder.
Semi-squat lift, 386, 388b, 388f
Senior athlete. See Masters athlete.
Seroma, 459
Serotonin
fatigue in endurance exercise and,
144, 152-153
muscle nociceptors and, 424, 425f,
428-429
Sesamoiditis, lateral hallux, in dancer,
673-674, 674f
Shin guards, 506-508, 508f
Running (Continued)
Index 797
Shin splints. See Medial tibial stress
syndrome (shin splints).
Shingles, 460
Shivering, 110
glycogen and, 113-114
hypoglycemia and, 113-114
in hypothermia, 114-115, 115t
spinal cord injury and, 114
subcutaneous fat and, 113
Shock pads, 496
Shoe inserts. See Orthosis, foot.
Shoes, 508-512, 510f
for cycling, 208
for dancing en pointe, 656-657,
657f, 658f
for golf, 221, 230, 231b
for running, 508, 510f
categories of, 322-324, 323b, 324f
construction of, 322-324, 323b
high arch and, 318
knee pain and, 320b
last types of, 323
rearfoot stabilization by, 311, 314t
recommendations for, 322-325,
325b
selection of, 511b
surfaces and, 510-511, 510f
Shoulder. See also Acromioclavicular
joint; Glenohumeral joint,
osteoarthritis of.
exibility testing of, 31-32
in golf, 221, 221b
protection of. See Protective
equipment, for shoulders.
taping for, 528-532, 532f
total joint arthroplasty of, 721-722,
721t, 722t
Shoulder harnesses, 499
Shoulder injuries
in baseball pitchers, 367, 376-380,
377b, 378-379t
in golfers, 217, 221, 221b
in swimmers, 341-343
in wheelchair athletes, 691
Sickle cell disease
Sickle cell trait, 447
Side-ache, 603-604
Silicone elastomer, 484
Single-leg standing hyperextension
test, 638-639, 638f
Single-photon emission computed
tomography (SPECT),
concussion and, 537
Sit-and-reach test, 31, 34t
Sit-ups, 391, 393
Skate bite, 464, 464f
Skateboarding, injury prevention in,
768t
Skaters, female, scoliosis in, 640-641
Skating, inline, injury prevention in,
768t
Skiers toe, 462
Skiing
knee brace in, after ACL reconstruc-
tion, 505
Skin
aging of, 457, 473
cold climate and, 110
heat dissipation in, 142
overview of, 455-457, 456f
Skin cancers, sun exposure and, 132,
472-473
Skin conditions
of communal contact. See Skin
infections.
of environmental exposure, 471-475,
471b, 473b, 475f
equipment-related, 461-465,
461b
heat- and sweat-related, 465-467,
466b
prophylactic measures for, 465t
trauma-related, 457-461, 457b
Skin infections, 467-471, 467b
bacterial, 470-471
prevention of, 471, 471b
pseudomonal, 470-471
staphylococcal, 448, 448b,
449-451, 470-471, 471b
fungal, 467-469, 468f, 469b
parasitic, 471
viral, 469-470, 469f, 470f
Skin tags, 466-467
Sleep deprivation
caffeine and, 155
tyrosine supplementation and, 154
Sleep disturbances, in concussed
athletes, 541, 545
Slipped capital femoral epiphysis,
in runners, 307
Slump, in young athlete, 48
Slump stretching, 640, 640f
Smoking. See also Tobacco.
particulates inhaled in, 130
Snapping hip
in dancers, 670-671, 670f
in runners, 307
Snapping scapula, in baseball pitchers,
380
Snatch, 385, 406
407f, 409t, 410f
411f, 412b, 412t, 413t
Snowboarding
Snowmobiling, cervical spine injuries
in, 558
Soccer
protective equipment for
helmets, 512
shin guards, 506-508, 508f
shoes, 510f
Soccer biomechanics, 287-306
approach to, 288
of cutting, 288, 290-293, 291b
crossover, 291-292, 291f, 291t,
293
injuries and, 290-291, 292-293,
298-300, 299b
pelvic rotations in, 292-293
sidestep, 291-293, 291f, 291t
of heading, 288, 293-297, 294b,
294t, 295f
injuries and, 300-302, 300b
hypermobile joints and, 671-672
of jumping/landing, 296-297
injuries and, 300, 300b, 301-302,
302f
of kicking, 288-290, 288b, 288t,
289f
injuries and, 297-298, 297b
pelvic rotations in, 290, 290t, 298
Soccer-related injuries, 297-302
of abdominal wall, 598
biomechanical basis of. See Soccer
biomechanics.
capability-demand reasoning about,
287, 288t, 297
rehabilitation and, 303
complexities of the sport and, 287
cutting-related, 290-291, 292-293,
298-300, 299b
heading-related, 300-302, 300b
jumping/landing-related, 300,
300b, 301-302, 302f
kicking-related, 297-298, 297b
overview of, 297
playing surface and, 767
prevention of, 768t
rehabilitation for, 302-303, 303b
in women, to anterior cruciate
ligament, 299, 302, 632, 635
798 Index
Sodium, 87-91. See also Hyponatremia;
Salt supplementation.
in hydration uid, 91, 93b
muscle cramps and, 147
hypertension and, 442-443
in sweat, 146-147
Sodium bicarbonate, as ergogenic aid,
160
Softball
injuries in, to pitchers, 766
safety bases in, 767
Solar plexus, blow to, 597, 598t
Sorbothane, 481-482
Sore throat, 445
Soreness. See also Delayed onset
muscle soreness (DOMS).
vs. pain, 339-341
swimming and, 341, 342t
Soy protein, 162
Spearing, 479
Spear-tacklers spine, 576t
SPECT (single-photon emission
computed tomography),
concussion and, 537
Speed activities. See High-intensity
exercise.
Spermatic cord, torsion of, 614
Spider veins, 460
Spinal cord, cervical neurapraxia of,
555-556, 556b, 556f, 557f
Spinal cord injury. See also Wheelchair
athletes.
autonomic dysreexia in, 688t, 698,
698b
cervical, 554, 571. See also Cervical
spine injuries.
cold sensitivity and, 114, 696
epidemiology of, 549, 550f
heat intolerance in, 106, 697
hypotension in, 698
in ice hockey, 558
neurogenic bladder and, 697-698
patterns of, 573
substance abuse and, 690
sunburn risk in, 696-697
temperature regulation and, 695
treatment of, 574
Spinal injury. See also Back injury;
Cervical spine injuries; Spinal
cord injury.
golf-related, 223-225, 223b, 225b
red ags associated with, 638,
638b
sports participation with history of,
22-24t
in women, 638-641, 638b
Spinal instability, preparticipation
evaluation and, 17
Spinal shock, 573, 573b
Spine. See also Cervical spine; Lumbar
spine.
recommended exercises for, 393,
393b
stabilization of. See Weight training,
spine in.
Spine board immobilization, 568-571,
568b, 568f, 569b, 570b, 570f,
572f
Spirometry, 125
Spleen
enlarged
in infectious mononucleosis,
608-609
injury to, 606-609, 607f
rupture of, mononucleosis and, 447,
608
Splints
legality of
at elbow or below, 499
in high school football, 484b
materials for, 483t, 484-485
for ulnar collateral ligament sprain,
499, 499b
Split clean or snatch, 406
Split jerk, 406
413f
system mechanics of, 401-406, 414b
Spondylolisthesis, 638-639
Spondylolysis, 638-639
Sports, classication of
by dynamic and static demands,
18, 19t, 21
by level of contact, 10b, 21
Sports anemia, 87, 87b, 446-447
Sports beverages, 91, 93, 93b
Sports hernia, 600-602, 600b, 601f
Sports medicine
philosophy of, 704
physician training and certication
in, 3
Sports medicine team, 1-8. See also
Athletic trainer; Physical therapist,
sports; Team physician.
cervical injuries and, 549, 563, 563b
communication among, 4, 4b, 6
composition of, 1-5, 1b, 2f
condentiality and, 4
core principles of, 5-8, 5b, 6b
emergency management plan of,
549b
goal of, 1
as inuence on young people, 8
injury management by, 6
case studies of, 6-8, 7f, 8f
necessity of, 1, 1b
physical tness prole and, 25, 25b,
33-36
preparticipation physical examination
and, 6, 6f
responsibility to the athlete, 4b
Sports pharmacology, 174-175, 174b
Sprains
cervical, 551-552
costochondral joint, 617
rates of, 758b
of rib-vertebral attachment, 616
sternal joint, 620
thumb, splint for, 499, 499b
Squamous cell carcinoma, 472
Squamous cells, 455
Squash, eye injuries in, 492
Squat, barbell, 393, 399-400, 404
Squat jump, 234, 235f. See also
Jumping, vertical.
vs. countermovement jump, 249,
250f
depth of squat in, 238b
Squat lift, 386-387, 387f, 388b, 388f,
389f
Squat wall exercises, 393-394, 395t,
396t, 397-406, 398t, 399b, 400f,
401b, 401f
Stacking, of anabolic steroids, 165
Staleness
overtraining and, 450
in young athlete, 48-49
Staphylococcus aureus infections, 448,
470
methicillin-resistant, 448-449,
448b, 470-471, 471b
Statistical methods, 740-742, 741t
Stellate lacerations, 583, 585f
Sternoclavicular joint, dislocation of,
620, 620b
Sternum
anatomy of, 616f
fractures of, 620-621
injuries of, 620-621
Steroid abuse. See Anabolic-androgenic
steroids.
Stieda process, 665, 665f
Stimulants
Stingers, 551, 553f
Stitch in the side, 603-604
Stoop lift, 386, 388b, 388f, 389f
Stork test, 638-639, 638f
Straddle injury, 614-615
Straight leg raise test, 31
Strain. See Muscle strain.
Stratum corneum, 455, 465-466
Strength and conditioning coordinator,
21-24, 25, 25b
Sports medicine team (Continued)
Index 799
Strength training. See also Resistance
training; Weight training.
dietary protein and, 161-162
ergogenic aids in, 161-162
carbohydrate-protein supplements,
162-163
conjugated linoleic acid, 164
creatine, 163
beta-hydroxy-beta-methylbutyrate,
163-164
sodium bicarbonate, 160
lower-body, jump performance and,
252-253, 253b
physiologic adaptations in, 159, 159b
Stress fractures
amenorrhea and, 642-643
in dancers, 668, 669f
little league shoulder as, 380
pars interarticularis, lumbar, 638-639
rib, 619, 619f
sacral, 639
sternal, 621
tibial, 637
Stress management, blood pressure
and, 443
Stress test, preparticipation, 18, 18f
Stress urinary incontinence, 645-646
Stretching
434
general guidelines for, 345
for golfers, pregame, 230-231
for swimmers, 343-345, 343f, 344f,
346f
Stride length, in running, 310, 310b
Stroke
shoulder strapping and, 531
Subacromial impingement, taping for,
531
Subconjunctival hemorrhage, 589
Subdural hematoma, 540
Substance abuse. See also Drug
testing.
Subtalar joint
patellofemoral pain syndrome and,
636
in runners, 309
injuries and, 320-321
knee pain and, 320b
orthoses and, 325-326
pronation and, 313, 313f, 314t,
319
in soccer, pronation and, 296-297,
299
SubTalar Support brace, 516-517
Subungual hemorrhage, 459, 462,
462f
Sudden cardiac death, 441
chest protectors and, 501
commotio cordis and, 444, 627
coronary artery abnormalities and,
443
coronary artery disease and, 444
hypertrophic cardiomyopathy and,
441-442
in Marfan syndrome, 443
risk factors for, 441, 441b
Sudden death
causes of, in athletes, 18
preparticipation examination and,
17-18
Sulfur dioxide, 124t, 129, 131
Sulfur oxides, 129
Summation of speed principle, 220
Sun exposure, 132-133
skin conditions caused by, 472-473
protection from, 473b
Sunburn, 132-133, 473
Sunscreen, 133, 465t, 473, 473b,
696-697
Superman exercise, 392, 393t
Suprascapular nerve, entrapment of,
Supraspinatus tendinopathy
Suprasternal notch, 616f
Surface
injury rates and, 767
shoes and, 510-511, 510f
tennis biomechanics and, 279, 279f
Surfer
bony spurs in ear canal of, 474
nodules on feet of, 460-461
Suturing of wounds, 457, 586-587
Sweat glands, 456, 456f. See also
Miliaria.
Sweating
disorders with impairment in,
105-106
miliaria profunda as, 109
spinal cord injury as, 695, 697
gender differences in, 104-105
heat acclimatization and, 103, 103f
iron loss through, 87
medications interfering with, 695
rates of, 146
sodium loss through, 87-91
sunscreen interfering with,
696-697
Swede-O ankle brace, 516-518, 518f,
519
Swimmers ear, 450
Swimmers itch, 471
Swimmers shoulder, 331-332,
341-343
Swimming, 331-349
backstroke in, 337-338
conditioning for, 345, 347t
humeral hyperextension in, 332,
333f, 338
breaststroke in, 338-339, 339f, 341
buttery stroke in, 335-337
333f, 335
mechanics of, 335, 337f, 341
muscle activity in, 335-337, 337f
exibility screen for, 343-345,
343b, 344f
freestyle stroke in, 334-335
333f, 334-335
mechanical changes in, 341,
342-343, 342t
mechanics of, 334-335, 334f
muscle activity in, 335, 336f
painful phases of, 332, 332f, 334
humeral hyperextension in, 332
in backstroke, 332, 333f, 338
in buttery, 332, 333f, 335
in freestyle, 332, 333f, 334-335
injury in
clinical issues and, 341-343
mechanical changes and, 341,
342t
pain and, 339-341, 340f, 342t
pain associated with
characteristics of, 331-332, 332f
mechanical changes and, 341, 342t
rehabilitation for, 345-348
return to swimming and, 347-348,
347t
stretching for, 343-345, 343f, 344f,
346f
Syncope, heat-associated, 107-108t
T
T cells, delayed onset muscle soreness
and, 429
Talocrural joint, in runners
knee pain and, 320b
range of motion of, 309-310
Tamponade, pericardial, 623-624,
627, 627b
Tanning salons, 473
Taping, 515-535
of ankle, 515-521, 518b
vs. ankle bracing, 516-518, 517f,
518f, 519, 521, 523-524,
524b
800 Index
comparisons of materials for,
518-519
cost-effectiveness of, 523-524,
524b
dynamic testing of, 519-520,
520b, 520f
with enhanced subtalar support,
518
with Kinesio tape, 532
meta-analyses and reviews of,
515-516, 516t
peroneal muscle reaction times
and, 519
placebo effect of, 520
postural control and, 521
proprioception and, 521, 521t
rationale for, 515
synopsis of studies of, 522t
concluding critique of, 532-533
of costochondral joint, 641
of elbow, 523
of nger, 523
of foot, 521-523, 522f
Kinesio tape in, 532, 532f
patellofemoral, 524-528, 524f,
525f, 526f, 528b, 529-530t
over shoe, 508-511
of shoulder, 528-532, 532f
with Kinesio tape, 532
uses of, 515b
for wheelchair athletes, 691
of wrist, 523
Tea, iron absorption and, 87
Team. See Sports medicine team.
Team physician, 3-5, 5f
communication by, 4
consultation of specialists by, 5
management of injury by, 6
masters athlete and, 705-706
preparticipation evaluation by, 9,
11-12
responsibilities of, 4-5, 4b
responsibility to athlete, 4
specialties represented by, 3, 3b
trainers handling of injury and, 5
training and certication of, 3
Temperature, body. See also Core
temperature; Fever; Hyperthermia;
Hypothermia.
range of, 98, 98b
normal, by age group, 16t
regulation of, 98-99, 99b, 99f
in athlete with disability, 695-697,
695b
in cold climates, 109-110, 110b
gender differences in,
104-105
Tendinitis
popliteus, in cyclists, 210t
vs. tendinopathy, 714
vs. tendinosis, 714
triceps, in baseball pitchers, 381
Tendinopathy, 666
in dancers, 666-667, 666f, 667b,
667f
iliopsoas, 670-671
in masters athletes, 714-717
treatment of, 715-717, 716b
pain in, 714-715
soccer-related, 298
supraspinatus
vs. tendinitis, 714
tendons with vulnerability to, 714
Tendinosis, 666, 714
in weightlifters, 415b
Tendons, age-related changes in,
707-708, 707b
Tennis, 265-276
anatomic adaptations in, 276-278
in muscular strength, 277-278
in range of motion, 276-277,
277b
biomechanics of, 278-284
applicable data on, 283-284
gravity step in, 279-280, 280b,
281f, 284
jab step in, 279-280, 280b, 280f,
284
lateral, 278, 279-280, 280b,
280f, 281f, 284
pivot step in, 279-280, 280b,
280f, 284
reaction time and, 282-283, 284f
recovery in, 280, 280b, 281f,
282f, 284
split step in, 280-282, 283f
surfaces and, 279, 279f
typical demands and, 278, 278b
velocities and, 282-283, 284f
ground strokes in, 272-273, 272b,
274f, 275f
joint kinematics of, 276
phases of, 265, 272-273, 272b,
274f, 275f
topspin in, 276
two-handed backhand in, 275f,
276
half-volley in, 265
kinetic chain in
activation of, 269-272, 271b
catch-up in, 270
decits in, 270, 270b
force production and, 268-269,
268b
nodes of, 269-270, 269f, 270b,
276
player evaluation based on, 276
serve and, 268, 268b, 269-272,
269f, 270b
muscular activity patterns in, 265-
267, 267b, 271f. See also Elec-
tromyography (EMG), in tennis.
rectus abdominis muscle strains and,
598
serve in
with abbreviated backswing, 266f,
268, 271-272
joint kinematics in, 273, 276
phases of, 265, 265b, 266f, 267
push-through/pull-through, 270-
271, 271b, 271f, 272f, 273f
shoes for, 508
shoulder in
demands on, 267
joint kinematics of, 273-276
kinetic chain and, 268-269,
270-271
muscular strength of, 277
open stance and, 273
range of motion of, 276-277,
277b
after total knee arthroplasty, 720
after total shoulder arthroplasty,
721-722
volley in, 265, 275f
Tennis elbow. See Lateral epicondylitis
(tennis elbow).
Tennis toe, 462
TENS (transcutaneous electrical nerve
stimulation), 432-433
Tensegrity, 303
Tension pneumothorax, 623-624, 625,
625b, 626f
Testicles, 613f
absent or undescended, 21, 22-24t,
614
injury to, 613-614
neoplasms of, 614
preparticipation examination of, 19
torsion of, 613-614
Testosterone, testing for use of,
178-179
Testosterone/epitestosterone (T/E)
ratio, 178-179, 181t
Tetanus immunization, 581, 582t
Tetrahydrocannabinol (THC), 181,
181t
Therapeutic use exemption, 174-175,
182-183, 182b
for corticosteroids, 444
Taping (Continued) Tennis (Continued)
Index 801
Thermomoldable plastics, 480,
482-484, 483t, 484f, 485
custom fabrication with, 485b,
486f
of thumb splint, 499, 499b
Thermotherapy, for delayed onset
Thigh, injuries to, in runners, 307
Thigh protection, 501, 503f, 512
Thiol oxidation, 156-157
Thomas test, of hip exor exibility,
31-32, 34t
Thoracic injuries, 596
of chest wall, 615-623
to breast, 622-623
effort thrombosis as, 623
muscle strain as, 619-620
to pectoralis major, 621-622
to ribs. See Rib injuries.
to sternum, 620-621, 620b
intrathoracic, 623-628
acute life-threatening conditions
in, 623, 623b
cardiac. See Cardiac injuries.
esophageal, 628
evaluation of, 623-624
pulmonary. See Pulmonary
injuries.
structures involved in, 615b, 616f,
621f
Throat protectors, 494, 495f
Thrombophlebitis, in athlete with
disability, 698
Thrombosis, subclavian or axillary
vein, 623
Thumb, protective splint for, 499,
499b
Thyroid cartilage, fracture of, 582,
583f
Tibial torsion
dancers turnout and, 663
gender differences in, 631, 632f,
633
Tibial varus, pronation and, 320
Tibiofemoral forces
in lunge exercises, 401-403, 402t
in squat exercises, 397-399, 398t
Tinea, 467-469, 469b
Title IX, 730, 769
Tobacco, hypertension and, 442. See
also Smoking.
Tobogganing, cervical spine injuries
in, 558
Toenails. See Nails.
Tongue, lacerations of, 586
antibiotics and, 587
Tooth injuries, 594-595, 594b, 594f,
595b
Torso Track, 393
Total joint arthroplasty, 717-723
ankle, 722-723
hip, 717-719, 718t
implants for, 719
implant longevity in, 717-718,
718b, 723
knee, 717, 719-721, 720t
implants for, 720-721
patient education following, 719,
719b
return to sport after, 723
shoulder, 721-722, 721t, 722t
ski poles following, 719-720, 720b
Trace minerals, 86-87
Tracheostomy, 582
Track and eld, physical tness prole
for, 34t
Trainer. See Athletic trainer.
Trampoline, cervical spine injuries
with, 559
Transcutaneous electrical nerve
stimulation (TENS), 432-433
Travelers diarrhea, 446
Treadmill, stride length on, 310
Trench foot, 116, 116-117t
Tretinoin
for acne mechanica, 461
in scar revision, 476
Triceps tendinitis, in baseball pitchers,
381
Trigger toe, 667
Trochanteric bursitis
cycling and, 209, 210t
in runners, 307
Trolamine salicylate, 432
True abdomen, 606, 606t
Truss, 599-600
Tryptophan, fatigue and, 144,
152-153
T-test of agility, 31, 32f, 34t
Turf toe, vs. sesamoiditis, 673-674,
674f
24-hour recall, of nutrient intake, 59
Tyrosine, as ergogenic aid, 153-154
U
Ulcers
aphthous, 460
decubitus, 688t, 690t
Ulnar collateral ligament injury
in baseball pitchers, 362-363, 381
splint for, 499, 499b
Ulnar neuritis, in baseball pitchers,
381
Ultrasound therapy, for delayed onset
Ultraviolet light, 132-133, 472
Umbilical hernia, 602, 603t
Unconsciousness. See Loss of
consciousness.
Upper respiratory tract infections,
444-445
Ureteral injury, 612
Urethral injury, 614
Urinalysis, preparticipation, 19
Urinary catheter, athletes manage-
ment of, 697-698
Urinary incontinence
adequate uid intake and, 697
stress, 645-646
Urinary tract bleeding, in runners, 447
Urinary tract infections, 688t, 697-698
Urine
blood in. See Hematuria.
protein in, 449-450
Urine testing, 175-176. See also Drug
testing.
Urogenital examination,
Urticaria, 474
V
Vagina
lacerations of, 614-615
water injection injuries of, 615
Varicose veins, 460
Vasculature, age-related changes in,
708b
Vastus medialis oblique
gender differences in, 632f
patellar taping and, 527-528,
529-530t
Vegetarian diets
categories of, 79-82
food pyramid for, 85f
iron sources in, 91t
nutrients to focus on, 82b
protein in, 79-82, 82b, 85f
sample menu for, lacto-vegetarian,
85f
Veins, leg, unattractive conditions of,
460
Venous thrombosis, subclavian or
axillary, 623
Ventral hernia, 603, 603t
Ventricular brillation
chest protectors and, 501
as commotio cordis, 444, 627, 627b
Vertical jump biomechanics. See
Jumping, vertical.
Vertical jump height, 29, 30f, 34t, 239b
Vertical jump repetitions, 32-33, 34t
Viscosupplementation, for knee
osteoarthritis, 711
Vision. See also Eyes.
in one eye, 21, 22-24t, 492-493
with one eye, 15
zygomatic fractures and, 591
Visual examination, preparticipation, 15
802 Index
Vital signs
normal ranges, by age group, 16t
in preparticipation evaluation, 15,
16t
Vitamin B
6
, toxic effects of, 86
Vitamin B
1

2

anemia and, 447
Vitamin C, 86
435
iron absorption and, 87
Vitamin D
in older adults, 164
Vitamin E, for delayed onset muscle
soreness, 435
Vitamins, 86, 95
antioxidant, 156-157
dietary reference intakes (DRIs),
68-69t, 72t, 80t, 88-90t
food sources of, 88-90t
supplementation of, 86, 88-90t
recommended multivitamin, 94
VO
2
max. See Oxygen uptake,
maximum (VO
2
max).
Vocal cord dysfunction, 128-129, 128b
vs. asthma, 128-129, 128b, 128t
causes of, 128, 128b
Volleyball
jumping in, 243-244, 251-252,
253f
landing forces in, 257-258
patellar tendinopathy caused by,
262
repetitions per match and,
258-259, 260b
ankle braces, 508
knee pads, 502, 504f
Vulva, injury to, 614-615
W
WADA. See World Anti-Doping
Agency (WADA).
Walking
base of gait in, 310
downhill
loads on knee in, 719-720
soreness caused by, 424, 425-426
ground reaction force in, 316
lumbar spine loading in, 385
vs. running
hip joint forces and, 717-718
knee joint forces and, 719-720
shoes for, 508
after total hip arthroplasty, 717-718
after total knee arthroplasty, 719-
720
Warfarin, 623
Warmup
434
for golf, 230-231, 231b
Warts, 463, 469-470, 470f
Water. See also Fluids and exercise.
bottled, during travel, 700
as ergogenic aid, 146-147, 146b
protein intake and, 79
recommended intake of, 78t
total body, hyperhydration and, 148
Water immersion, cold stress and,
112-113
Water skiing, vaginal injuries in, 615
Water sports, cervical spine injuries in,
558-559
Weight, body
blood pressure and, 443
uid needs and, 147, 147b
normal ranges, by age group, 16t
Weight management, 94
Weight training, 385-422. See also
Resistance training; Strength
training.
competitive. See Weightlifting,
competitive.
lower extremities in, 393-406, 394b
lunge exercises and, 393-397,
395t, 396t, 401-406, 402t,
403b, 404f, 405f, 406b
muscle activity in, 394-397, 395t,
396t, 399b, 403b
squat exercises and, 393-406,
395t, 396t, 398t, 399b,
400f, 401b, 401f
patellofemoral forces in
in lunge exercises, 404-406, 404f,
405f, 406b
in squat exercises, 399-401, 400f,
401b, 401f
spine in, 385-393
clinical points regarding, 393b
commercial devices for, 393
muscles providing stability for,
385-386, 386b
pushing/pulling exercises and,
388-391, 391b
recommendations for, 393
squat exercise and, 386-388,
387f, 388b, 388f, 389f, 390f
trunk extension exercises and,
391-392, 392t, 393t
trunk exion exercises and, 391
unstable surface exercises and, 392
tibiofemoral forces in
in lunge exercises, 401-403, 402t
in squat exercises, 397-399, 398t
vs. weightlifting, 406
Weight-bearing exercise, bone mass
and, 166
Weightlifting, competitive, 385,
406-416
age and muscle ber area in, 707,
707f
historical evolution of, 406
injuries in, 415-416, 415b
pectoralis major rupture,
621-622
407f, 408f, 409t, 410f
of split jerk, 412-414, 413f
411f, 412b
of split jerk, 401-406, 414b
women in, 406, 407-409, 409t,
411-412
Wetness, cold stress and, 112
Wheelchair athletes, 690, 690t,
691-692, 691f. See also Spinal
cord injury.
hypothermia in, 696
Whey, as protein supplement, 162-163
Wind knocked out, 597, 598t
Wind-chill index, 111-112, 112t
Wingate cycle test, 32, 34t
Winter sports. See also Skiing;
Snowboarding.
Women. See Female athlete.
Work
denition of, 238-239
in horizontal jumps, 255-256, 257,
259f, 259t
in vertical jumps
arm swings and, 247, 248-249,
248f, 249b
jump height and, 238-239, 240
jump intensity and, 246-247,
247b, 247t
single-leg, 250-251, 251b
World Anti-Doping Agency (WADA)
blood collection guidelines of, 176
gene doping and, 181-182
laboratory certication by, 176
list of 2010 prohibited substances,
176, 177b
stimulants on, 180
nandrolone and, 178
testosterone/epitestosterone (T/E)
ratio and, 178-179
therapeutic use exemption and,
182-183, 182b
Wound care, 457-458. See also
Abrasions; Contusions;
Lacerations.
Wrestling, ear protection for, 493,
493f
Index 803
Wrist
fractures of, in weightlifters, 415
golf-related injuries of, 217, 221,
221b
protection for, 499
taping of, 523
X
X-factor stretch, 219
Xiphoid process, 616f, 620
Y
Young adult athlete, preparticipation
evaluation of, 9
Youth sports. See also Psychosocial
aspects of youth sports.
numbers dropping out of, 41
numbers participating in, 40
Yo-yo intermittent test, 33, 33f, 34t
Z
Zinc, in vegetarian diets, 82b
Zygomatic fractures, 590-591, 591f,
591t, 592b, 592f

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