AMERICAN JOURNAL OF HUMAN BIOLOGY 23:517526 (2011)

Original Research Article

The Effects of Time and Intensity of Exercise on Novel and Established Markers
of CVD in Adolescent Youth
DUNCAN S. BUCHAN,1* STEWART OLLIS,1 JOHN D. YOUNG,2 NON E. THOMAS,3 STEPHEN-MARK COOPER,4 TOM K. TONG,5
JINLEI NIE,6 ROBERT M. MALINA,7 AND JULIEN S BAKER8
1
Health and Exercise Sciences, School of Science, University of the West of Scotland, Hamilton, ML3 0JB, Scotland, United Kingdom
2
Life and Environment, School of Science, University of the West of Scotland, Hamilton, ML3 0JB, Scotland, United Kingdom
3
Centre for Children and Young Peoples Health and Well-Being, School of Human and Health Sciences, Swansea University, Swansea,
SA2 8PP, Wales, United Kingdom
4
Cardiff School of Sport, UWIC, Cyncoed Campus, Cyncoed Road, Cardiff, CF23 6XD, Wales, United Kingdom
5
Dr. Stephen Hui Research Centre for Physical Recreation and Wellness, Hong Kong Baptist University, Hong Kong, NAB210, China
6
School of Physical Education and Sports, Macao Polytechnic Institute, Rua de Luis Gonzaga Gomes, Macao, China
7
Department of Kinesiology and Health Education, The University of Texas at Austin, 1 University Station-D3700, Austin, Texas
8
Health and Exercise Sciences, School of Science and Technology, University of the West of Scotland, Hamilton, ML3 0JB, Scotland,
United Kingdom

Objectives: This article examines the effects of brief, intense exercise in comparison with traditional endurance
exercise on both novel and traditional markers of cardiovascular disease (CVD) in youth.
Methods: Forty seven boys and ten girls (16.4 6 0.7 years of age) were divided into a moderate (MOD), high intensity
(HIT), or a control group. The MOD group (12 boys, 4 girls) and HIT group (15 boys, 2 girls) performed three weekly
exercise sessions over 7 weeks. Each session consisted of either four to six repeats of maximal sprint running within a
20 m area with 2030 s recovery (HIT) or 20 min continuous running within a 20 m area at 70% maximal oxygen
uptake (VO2max).
Results: Total exercise time commitment over the intervention was 420 min (MOD) and 63 min (HIT). Training volume was 85% lower for the HIT group. Total estimated energy expenditure was 907.2 kcal (HIT) and 4410 kcal
(MOD). Signicant improvements (P  0.05) were found in systolic blood pressure, aerobic tness, and body mass index
(BMI) postintervention (HIT). In the MOD group, signicant (P  0.05) improvements were noted in aerobic tness,
percentage body fat (%BF), BMI, brinogen (Fg), plasminogen activator inhibitor-1, and insulin concentrations.
Conclusions: These ndings demonstrate that brief, intense exercise is a time efcient means for improving CVD
risk factors in adolescents. Am. J. Hum. Biol. 23:517526, 2011.
' 2011 Wiley-Liss, Inc.

Cardiovascular disease (CVD) is the leading cause

of mortality throughout the world with a reported 17.1
million deaths attributed to the disease in 2004 (World
Health Organization, 2005). Though cardiovascular
events tend to typically occur during mid adulthood, it is
now accepted that CVD risk factors have their origins in
childhood and tend to track into adulthood (Andersen
et al., 2004; Raitakari et al., 2003). Despite the extremely
low risk of early mortality in youth, early and continued
exposure to an unhealthy CVD prole may accentuate the
risk of early mortality. Thus, identication of individuals
presenting with an abnormal CVD risk prole or a prole
just below accepted levels of risk is central to the development and implementation of appropriate health strategies
in youth.
Numerous risk factors have been linked to the development of CVD. These include poor dietary habits,
physical inactivity, low aerobic tness, obesity and overweight, hypertension, and abnormal lipid proles (Ruiz
et al., 2009). Though the etiology of CVD is complex,
many of the risk factors are interrelated. For example,
the increase in prevalence of overweight and obesity in
youth throughout the world is attributed in part to a
decrease in habitual physical activity (Kipping et al.,
2008). Indeed obesity is linked to almost all CVD risk
factors (McMurray and Andersen, 2009), so the prevention of excessive weight gain is vital. The two main
contributors to excessive weight in youth are poor diet
and physical inactivity.
C 2011
V

Wiley-Liss, Inc.

Though regular participation in physical activity protects against future CVD risk (Strong et al., 2005), recent
estimates suggest that current activity levels in youth are
insufcient to meet recommendations (McLure et al.,
2009). As childhood and adolescence are critical periods
for developing favorable activity habits that may continue
into adulthood, lifestyle interventions that target this
modiable contributor to future CVD risk are important.
Despite the strong association between unfavorable cardiometabolic proles, which relates to diseases of the heart
and metabolic disorders, in youth and low physical activity and poor aerobic tness levels (Pan and Pratt, 2008),
much of this evidence is informed through cross-sectional,
epidemiological, and prospective studies. Current ndings
on the effectiveness of programs to increase activity levels
in youth are equivocal (Durant et al., 2009; van Sluijs
et al., 2008). There are relatively few intervention studies
available and many have focused on nonrepresentative
samples of obese and overweight youth who may be more

*Correspondence to: D. S. Buchan, Health and Exercise Sciences, School

of Science, University of the West of Scotland, Hamilton, ML3 0JB, Scotland, United Kingdom. E-mail: duncan.buchan@uws.ac.uk
Received 6 December 2010; Revision received 20 January 2011; Accepted
6 February 2011
DOI 10.1002/ajhb.21166
Published online 4 April 2011 in Wiley Online Library (wileyonlinelibrary.
com).

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D.S. BUCHAN ET AL.

susceptible to change in comparison with the general population (Steele et al., 2008). As such, recommendations
informed from such samples may have major limitations.
Poor cardiorespiratory tness and physical activity
levels are common factors in both metabolic and CVDs.
There is, however, a lack of clinical evidence pertaining to
the quantity of physical activity necessary to prevent or
reduce CVD risk (Steele et al., 2008). Brief, interval training is effective as a means of improving the health status
of obese and overweight adolescents with unfavorable
cardiometabolic proles (Tjonna et al., 2009). As some
have questioned the aptness of current youth PA recommendations (Andersen et al., 2006; Ness et al., 2007),
there is a need to consider the potential of nontraditional
exercise interventions as a means of improving the health
and well being of youth. Previous studies have demonstrated similar metabolic adaptations in adults over 6
weeks when comparing low volume sprint interval and
traditional endurance training (Burgomaster et al., 2008).
Therefore, the purpose of this study is to compare the
effects of two exercise protocols of differing intensities and
durations on traditional and novel markers of CVD risk in
youth.
SUBJECTS AND METHODS
A cohort of adolescent school children (47 boys, 10 girls,
16.4 6 0.7 years) volunteered for the study. The experimental protocol was approval by the University of the
West of Scotland Ethics committee and conformed to the
Declaration of Helsinki. Following initial discussions with
the school principal and relevant teaching staff, written
consent from the principal was obtained. Members of the
research team then visited the intended participants and
discussed their involvement in the project. Information
sheets, participant, and parental/guardian consent forms
were then distributed and returned completed. Only participants who returned the consent forms were eligible for
the study. Test and activity protocols were fully explained
to the participants including possible risks and discomfort
they may experience. All pupils were assured of anonymity and informed that they were free to withdraw from the
project at any time.
Participants were recruited from two PE classes in year
5 and year 6. Year 5 pupils acted as the control group
whereas year 6 pupils were randomly assigned to a high
intensity training (HIT) or a moderate (MOD) intensity
training group by a third party using computer-generated
sequences of random numbers. Participants were
instructed not to change their dietary or lifestyle habits
other than prescribed.
Physical and physiological measures
Stature without shoes was measured to the nearest
1 mm (Seca Stadiometer, Seca, Birmingham, UK). Weight
in normal PE clothing was measured to the nearest 0.1 kg
using electronic weighing scales (Seca 880, Digital Scales,
Seca, Birmingham, UK), which was calibrated against
balanced weighing scales. Body mass index (BMI) was
calculated (weight/(height)2, kg/m2) and used to classify
participants as obese, overweight, underweight, or a
healthy weight using recommended international ageand gender-specic BMI cut-off values (Cole et al., 2000,
2007).
American Journal of Human Biology

Skinfolds were measured at two sites, triceps and calf,

using Harpenden skinfold callipers (John Bull, British
Indicators, Bedfordshire, UK) in accordance with standard procedures (Lohman, 1992). A third skinfold measurement was taken if the rst two measurements differed
by more than 1.0 mm. Percentage body fat (%BF) was estimated with sex-specic skinfold equations for adolescents
(Slaughter et al., 1988). Waist-to-hip ratio (WHR) was calculated to provide an index of relative fat distribution
(Ledoux et al., 1997). Hip circumference was measured at
the widest point between the buttocks and the iliac crest.
Waist circumference was measured at the midpoint
between the lower ribs and the iliac crest in accordance
with standard procedures (Ledoux et al., 1997). Sexual
maturation status was determined using a self report
questionnaire based on the criteria of Tanner (Tanner,
1962) for stage of pubic hair development. Systolic blood
pressure (SBP) and diastolic blood pressure (DBP) were
measured with an automated monitor (Omron M10-IT
Blood Pressure Monitor HEM-7080IT-E, Omron Healthcare UK, Milton Keynes, UK) after each participant had
sat quietly for a period of 10 min as previously documented (Andersen et al., 2003). This device is a valid and
reliable measure of blood pressure and meets the validation criteria of both the British Hypertension Society and
the European Society of Hypertension (de Greeff et al.,
2009). The cuff was placed tightly on the upper left arm
and three measurements were taken. The average of the
second and third measures was used for analysis. Cardiorespiratory tness was measured using the 20-m multistage tness test (20MSFT) as previously documented
(Buchan et al., 2010; Leger et al., 1988).
All measurements were performed before and after
the intervention for the HIT, MOD, and control groups.
Performance in the 20 MSFT was also measured at the
end of week 4 in the intervention groups.
Observational analysis
Observational data was gathered by video recording one
weekly exercise session in the two intervention groups.
Direct behavioral observation provides contextually rich
data and is cited as the criterion measure of PA behaviors
in pediatric populations (Sirard and Pate, 2001). The oneday records permitted quantication of distances covered
during a weekly session in the intervention groups.
Physical activity and dietary questionnaire
All participants completed a validated physical activity
questionnaire for adolescents (PAQ-A) (Kowalski et al.,
1997). The protocol required participants to recall their
PA behaviors from the previous 7 days. This validated
questionnaire has been used in previous research (Janz
et al., 2008). From previous experience, it was anticipated
that completion of the questionnaire would require no longer than 30 min and thus could be completed during
scheduled class time. Daily food intake was monitored
with a validated, self-reported food diary (Food Standards
Agency, 2002) and a food frequency questionnaire. The
collated data was analyzed using nutritional analysis
software by Health Options (Nutri Check, Health Options,
Cirencester, Gloucester, UK). Participants were
instructed to continue their normal eating and drinking
habits throughout the intervention.

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EXERCISE AND CVD RISK IN YOUTH

Fig. 1.

Course outline showing distance and direction taken by participants, during the 30 s HIT protocol. A 5 10 m, B 5 20 m, C 5 10 m.

Intervention protocol
Participants in the HIT group (15 boys, 2 girls) completed a 30 s maximal effort sprint within a 20-m distance
separated by cones (Fig. 1). The start point was located at
the mid-point of the markers. Participants were instructed to sprint from the midpoint to the rst marker, turn,
and then sprint 20 m in the opposite direction to the second marker. Participants then turned and ran again
through the midpoint covering a total distance of 40 m.
Although this protocol has been used and validated as a
measure of anaerobic performance (Baker and Davies,
2002), in this study, participants were instructed to sprint
maximally for a period of 30 s. Following 30 s rest, participants were instructed to repeat this procedure a further
three times, which equated to 2 min of maximal effort
sprinting interspersed with 2 min recovery. Participants
were requested to perform the protocol three times
weekly. Training progression was implemented by
increasing the number of repetitions from four during
weeks 1 and 2, to ve during weeks 3 and 4, and to six
during weeks 5 and 6. During week 7, participants performed six repetitions but interspersed by only 20 s recovery. Participants were given a familiarization trial of four
low intensity runs under test procedures before the start
of the intervention.
Participants in the MOD group (13 boys and 4 girls)
were instructed to exercise at an intensity of 70% VO2max
as observed elsewhere (Tabata et al., 1996) by running
steadily for a period of 20 min. As the 20 MSFT has been
validated as a predictor of VO2max in young people, the
speed of exercise was determined by each participants
performance in the 20 MSFT. Participants were
instructed to keep pace with a CD that emitted a continuous audio signal for a period of 20 min. It was anticipated
that there would be a wide range of aerobic capabilities
among participants; hence, participants were divided into
two subgroups based on performances in the 20MSFT.

Participants then were evenly matched in relation to

initial aerobic capacity. During week 4 all participants
were instructed to perform the 20MST to determine a
training effect. On analyzing performances during week
4, participants were instructed to exercise at an intensity
that elicited 70% of their newly predicted VO2max while
running steadily for 20 min in weeks 57.
This training intervention met, in part, previous PA
guidelines calling for adolescents to engage in three or
more sessions per week of activities that last 20 min or
more at a MOD-vigorous intensity (Sallis and Patrick,
1997). The MOD training intervention thus afforded the
opportunity to determine whether the PA guidelines will
have an effect on components of cardiovascular and
metabolic health of adolescents.
Metabolic measurements
Blood samples were collected between 9:00 am and
11:00 am after an overnight fast before and after the exercise intervention. Postintervention blood sampling was
undertaken within 9092 H of the nal exercise session.
Before sampling participants were instructed to sit quietly
for a period of at least 30 min to control for plasma volume
shifts (Pronk, 1993). A team of qualied phlebotomists,
experienced in pediatric sampling techniques, collected all
blood samples. The samples were allowed to clot and immediately centrifuged at 4,000 rpm for 10 min. The blood
samples were analyzed for total cholesterol (TC), insulin,
high-density lipoprotein (HDL-C), low-density lipoprotein
(LDL-C), high-sensitivity C-reactive protein (CRP), glucose, brinogen (Fg), interleukin-6 (IL-6), adiponectin,
triglyceride (TG), and plasminogen activator inhibitor-1
(PAI-1). All blood analyses were performed using standard
procedures. TC and TG were measured by enzymatic
methods (Randox, Antrim, UK) and a Camspec M107
spectrophotometer (Camspec, Leeds, UK). Concentration
of HDL-C was determined after precipitation of very low
American Journal of Human Biology

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D.S. BUCHAN ET AL.

TABLE 1. Baseline characteristics (mean 6 SD where appropriate) of

TABLE 2. Heart rate response and distance covered (mean 6 SD)

physical and physiological variables

Variables
Age (years)
Gender, boys/girls
Weight status
Obese (%)
Overweight (%)
Normal of healthy weight (%)
Underweight (%)

Control
n 5 24

Moderate
n 5 16

High Intensity
n 5 17

16.3 6 0.5
20/4

16.2 6 0.1
13/4

16.7 6 0.1
15/2

0
21
75
4

0
25
62
13

0
6
88
6

Where n = denoted number, actual sample number is presented in brackets. No

signicant difference found between groups at baseline.

density and low-density lipoproteins by the addition of

phosphotungstic acid in the presence of magnesium ions.
The Friedewald formula (Friedewald et al., 1972) was
used to calculate LDL-C concentration. Glucose was measured with the glucose oxidase method (Randox, Antrim,
UK) and analyzed using a Camspec M107 spectrophotometer (Camspec, Leeds, UK). Plasma insulin was analyzed
with commercially available immunoassay kits (ALPCO,
Salem, NH) and a Camspec M107 spectrophotometer
(Camspec, Leeds, UK). Fg concentration was analyzed
using commercially available immunoassay kits (ALPCO,
Salem, NH) and a MRX microplate reader (Dynatech Laboratories, MA). Concentrations of IL-6, CRP, adiponectin,
and PAI-1 were measured with specic ELISA kits (R&D
Systems, Abingdon, UK) and a MRX microplate reader
(Dynatech Laboratories, MA).
Estimated energy expenditure
Total estimated group energy expenditure for both
interventions was estimated using the following equation
(metabolic equivalent of task (METs) 3 3.5 3 body weight
in kg)/200 5 kcal min21 (American College of Sports Medicine, 2008). Body weight was taken as the average mass of
each group at baseline, whereas METs was taken from
young adult estimates published previously (Bouchard,
1990). As such, the absolute METs of each exercise session
were estimated to be 9.0 for the MOD and 13.0 for the HIT
intervention.
Statistical analysis
Means and standard deviations were calculated for
each observation point. The level of signicance was set at
P  0.05 throughout. The AndersonDarling test was
applied to conrm normality, whereas homogeneity of variance was assessed using Levenes test. For normally distributed data, a two-way analysis of variance (ANOVA)
with repeated measures was used to compare values
within each group (HIT, MOD, Control) at the two data
collection points, whereas a one-way ANOVA was used to
test differences between groups at the two data collection
points. Where residuals were not normally distributed,
the nonparametric KruskalWallis test (H-values) was
used. Bonferroni adjustments for multiple comparisons
were used. For signicant H-values, a Bonferroniadjusted Mann-Whitney U test was applied. In addition,
post hoc, effect size statistics (ES) for all the statistically
signicant t-ratios were also established. These calculations were based on Cohens classication of a small
(0.2  d < 0.5), MOD (0.5 < d < 0.8) and large (d  0.8)
American Journal of Human Biology

during each week in the two intervention groups

Moderate Group n 5 16

Heart Rate Response (bpm)

Week 1
177.1 6 17.7 (10)a
Week 2
177.1 6 13.3 (10)a
Week 3
178.5 6 17.3 (9)a
Week 4
178.9 6 13.0 (10)a
Week 5
173.9 6 14.5 (8)a
Week 6
174.1 6 15.0 (13)a
Week 7
175.6 6 18.2 (12)a
Distance Covered (m)
Week 1
3486.3 6 375.1 (16)a
Week 2
3513.8 6 353.3 (16)a
Week 3
3525.0 6 352.6 (14)a
Week 4
3563.8 6 320.7 (15)a
Week 5
3621.9 6 359.0 (16)a
Week 6
3663.1 6 336.0 (15)a
Week 7
3690.6 6 327.7 (15)a

High Intensity Group n 5 17

177.9 6 14.9 (11)a
178.2 6 13.4 (10)a
174.8 6 15.5 (11)a
178.2 6 16.5 (12)a
177.7 6 18.0 (12)a
175.1 6 18.9 (11)a
174.3 6 19.4 (10)a
495.6 6 45.1 (16)a
496.7 6 44.2 (17)a
617.2 6 55.6 (16)a
622.8 6 60.1 (16)a
761.1 6 32.7 (17)a
763.9 6 39.6 (16)a
748.3 6 41.6 (17)a

Where n = denoted number, actual sample number is presented in brackets.

ES (Cohen, 1988). Knowledge of the ES enabled us to

estimate the power (%) of each signicant analysis.
RESULTS
Baseline characteristics for participants in the three
groups are summarized in Table 1. The three groups did
not differ in any of the variables at baseline (Tables 3
and 4). Overall, 25% of the sample was overweight and 2%
was underweight, the remainders were normal or a
healthy weight. Of the 21 exercise sessions, mean attendance for all participants involved in both interventions
was 17.71 6 4.2. Mean PA levels estimated with the PAQA did not differ between groups, 2.0 6 0.8 (Control), 2.2 6
0.5 (MOD), and 2.2 6 0.4 (HIT). Absences were due to
illness, work placement attendance, or poor weather disrupting transport. No injuries were reported during the
intervention. This is encouraging as HIT in youth is often
dismissed as being unsafe or unfeasible for many to
undertake. No change was noted in dietary intake pre and
post intervention (data not shown). Weekly heart rate
response and distance covered during one session per
week are shown in Table 2. Although individualized target
training heart rate zones were not prescribed, mean heart
rate responses over the 7-week intervention was comparable with intensity recommendations aimed at improving
cardiorespiratory tness (American College of Sports
Medicine, 2008). Total estimated energy expenditure for
the HIT intervention was 907.2 kcal in comparison with
4410 kcal for the MOD intervention.
Postintervention results
Descriptive statistics for physiological and blood variables before and after the intervention are summarized in
Tables 3 and 4, respectively. There was no change in body
mass postintervention within or between groups. Stature
increased over time in each group, control (P 5 0.000),
MOD (P 5 0.000), and HIT (P 5 0.001) but no changes
was observed in stature among groups postintervention.
The BMI decreased in all groups postintervention: control
group (P 5 0.010, ES 5 0.58, power 5 77.2%), MOD group
(P 5 0.009, ES 5 0.75, power 5 79.6%), and the HIT group
(P 5 0.013, ES 5 0.68, power 5 74.9%) but the BMI did
not differ among groups. This reected the maintenance

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EXERCISE AND CVD RISK IN YOUTH

TABLE 3. Physical and physiological variables (mean 6 SD) before (pre) and after (post) the interventions
Control n 5 24

Variables
Physical
Stature (cm)
Body Mass (kg)
BMI (kg/m2)
WHR
Body Fat (%)
SBP (mm Hg)
DBP (mm Hg)
Aerobic Fitness (shuttles)

Moderate n 5 16

PRE

POST

171.1 6 8.7
66.11 6 7.6
22.70 6 2.6
0.82 6 0.0
16.62 6 6.8
113 6 10
68 6 8
81.33 6 25.3

172.5 6 8.8
66.27 6 8.0
22.31 6 2.5c
0.84 6 0.0c
16.62 6 7.2
109 6 11
64 6 7b
80.13 6 24.7
b

High Intensity n 5 17

PRE

POST

172.7 6 9.3
66.60 6 9.9
22.4 6 3.3
0.78 6 0.0 (15)a
19.73 6 8.6 (15)a
112 6 11
66 6 7
73.56 6 21.8

173.8 6 9.3
66.61 6 9.8
22.10 6 3.3b
0.78 6 0.0 (15)a
17.64 6 6.5 (15)ac
108 6 12
66 6 4
93.25 6 23.2b
b

PRE

POST

170.1 6 7.8
63.38 6 9.2
21.61 6 2.2
0.86 6 0.3
18.65 6 7.7
112 6 10
67 6 7
82.00 6 25.8

172.6 6 7.5b
63.69 6 9.3
21.31 6 2.1c
0.84 6 0.1
19.20 6 5.8
106 6 11c
65 6 6
88.78 6 26.4b

Where n = denoted number, actual sample number is presented in brackets.

Different from baseline, P<0.01.
Different from baseline, P<0.05.

a
b
c

TABLE 4. Blood variables (mean 6 SD) before (pre) and after (post) the interventions
Control n 5 24
Blood Variables
Adiponectin (ng/mL)
CRP (mg/L)
Fibrinogen (mg/dL)
IL-6 (pg/ml)
LDL-C (mmol/L)
HDL-C (mmol/L)
Total Cholesterol (mmol/L)
PAI-1 (ng/mL)
Glucose (mmol/L)
Insulin (lIU/mL)
Triglycerides (mmol/L)

PRE

Moderate n 5 16

POST

7751 6 3126 (23)

1.54 6 0.67 (23)a
149.7 6 74.7 (14)a
4.60 6 3.89 (21)a
1.73 6 0.58 (16)a
1.55 6 0.62 (18)a
3.62 6 1.07 (22)a
25.1 6 14.6 (16)a
4.74 6 1.03 (19)a
6.30 6 4.67 (16)a
0.83 6 0.29 (22)a
a

PRE

4766 6 3406 (23)

2.33 6 0.17 (23)ab
114.0 6 72.3 (14)
4.83 6 10.91 (21)a
1.73 6 1.21 (16)a
2.20 6 1.46 (18)a
3.55 6 1.45 (22)a
14.0 6 21.3 (16)ab
4.67 6 0.91 (19)a
4.68 6 4.61 (16)a
1.06 6 0.49 (22)a
ab

High Intensity n 5 17

POST

7028 6 3603 (16)

1.48 6 0.67 (16)a
170.5 6 65.8 (12)a
4.96 6 6.78 (15)a
2.20 6 0.92 (13)a
1.59 6 0.62 (13)a
4.06 6 0.91 (14)a
23.4 6 11.3 (14)a
4.70 6 1.40 (14)a
6.04 6 5.30 (13)a
0.81 6 0.42 (14)a
a

PRE

6111 6 2645 (16)

1.98 6 1.38 (16)a
106.2 6 79.3 (12)ab
4.71 6 8.22 (15)a
1.96 6 1.05 (13)a
1.69 6 0.38 (13)a
3.92 6 0.74 (14)a
11.7 6 9.8 (14)ab
4.80 6 0.97 (14)a
2.02 6 3.13 (13)ab
1.16 6 0.42 (14)ab
a

POST

8633 6 699 (14)

1.38 6 0.63 (14)a
119.5 6 105.7 (9)a
3.78 6 5.89 (13)a
1.91 6 0.84 (10)a
1.52 6 0.51 (14)a
3.84 6 1.37 (14)a
19.8 6 9.0 (11)a
4.68 6 1.27 (13)a
5.15 6 3.31 (11)a
0.77 6 0.26 (13)a
a

4220 6 3416 (14)ac

1.85 6 1.36 (14)a
98.6 6 60.9 (9)a
2.41 6 5.55 (13)a
1.45 6 0.58 (10)a
1.83 6 1.41 (14)a
3.96 6 1.81 (14)a
9.7 6 13.1 (11)a
4.26 6 1.02 (13)a
10.93 6 17.57 (11)a
1.27 6 0.42 (13)ac

ANOVA summaries are provided for selected variables.

No signicant difference was found between groups at baseline or postintervention.
a
Where n = denoted number, actual sample number is presented in brackets.
b
Different from baseline, P<0.05.
c
Different from baseline, P<0.01.

of body mass with continued growth in stature in all

groups over time.
WHR signicantly increased in the control group (P 5
0.015) but not in the MOD or HIT groups postintervention. The control and HIT groups did not differ in the
WHR postintervention, whereas the MOD group differed
signicantly from the HIT (P 5 0.004) and control
(P 5 0.000) groups postintervention.
%BF decreased signicantly in the MOD group postintervention (P 5 0.00, ES 5 0.72, power 5 73.3%), though
there was no change postintervention in both the control
and HIT groups. No differences were observed between
groups.
DBP declined signicantly over time (P 5 0.001) in the
control group (68 6 8 vs. 64 6 7 mm Hg), whereas SBP
did not change. SBP and DBP did not change in the MOD
group. On the other hand, SBP declined signicantly (112
6 10 vs. 106 6 11 mm Hg, P 5 0.017, ES 5 0.65, power 5
70.9%) after the intervention in the HIT group, whereas
DBP did not change. The three groups did not differ in
SBP and DBP at postintervention.
Cardiorespiratory tness of the control group did not
change over time. However, there was a signicant
improvement in cardiorespiratory tness within both the
MOD (73.56 6 21.8 vs. 93.25 6 23.16 shuttles, P 5 0.000,
ES 5 2.29, power 5 100%) and HIT (82.00 6 25.8 vs.
88.78 6 26.41 shuttles; P 5 0.000, ES 5 0.95, power 5
96.8%) groups postintervention.

IL-6, HDL-C, LDL-C, TC, and glucose concentrations

did not change at postintervention in any group (Table 4).
PAI-1, Fg, CRP, or insulin concentrations also did not
change postintervention in the HIT group, while adiponectin and CRP concentrations did not change postintervention in the MOD group. Fg or insulin concentrations
also did not change at postintervention in the control
group.
The control (7751 6 3126 vs. 4766 6 3406 ng/mL,
P 5 0.013, ES 5 0.57, power 5 73.6%) and HIT
(8633 6 699 vs. 4220 6 3416 ng/mL, P 5 0.000, ES 5 1.40,
power 5 99.8%) groups showed a signicant decrease in
adiponectin postintervention, while a signicant postintervention increase was observed in CRP (1.54 6 0.67 vs.
2.33 6 0.17 mg/L, P 5 0.016, ES 5 0.54, power 5 69.8%)
in the control group.
The MOD group experienced a signicant reduction in
Fg concentration (170.5 6 65.8 vs. 106.2 6 79.3 mg/dL,
P 5 0.013, ES 5 0.86, power 5 77%) postintervention,
while signicant reductions were noted in PAI-1 concentrations in both the control (25.1 6 14.6 vs. 14.0 6 21.3
ng/mL, P 5 0.027, ES 5 0.61, power 5 63%) and MOD
(23.4 6 11.3 vs. 11.7 6 9.8 ng/mL, P 5 0.022, ES 5 0.70,
power 5 67.3%) groups. Although there was a reduction
in PAI-1 concentration in the HIT group, it was not signicant (1.98 6 0.90 vs. 0.97 6 1.31 ng/mL, P 5 0.09). A signicant reduction in insulin (6.04 6 5.30 vs. 2.02 6 3.13
lIU/mL, P 5 0.014, ES 5 0.80, power 5 75.7%) and an
American Journal of Human Biology

522

D.S. BUCHAN ET AL.

increase in TG concentration (0.81 6 0.42 vs. 1.16 6 0.42

mmol/L, P 5 0.006, ES 5 0.88, power 5 86.1%) was noted
in the MOD group postintervention. Finally, a signicant
increase in TG concentration (0.77 6 0.26 vs. 1.27 6 0.42
mmol/L, P 5 0.000, ES 5 1.40, power 5 99.6%) was also
noted in the HIT group postintervention.
DISCUSSION
A high number of youth exhibit at least 1 or more CVD
risk factor, which they are likely to retain into adulthood
(Raitakari et al., 2003; Thomas and Williams, 2008).
Although the prevalence of poor metabolic proles may be
lower in youth than in adults, elevated risk factors for
CVD are evident. The prevalence of traditional risk factors in youth varies between 0 and 60% depending on the
criteria and population used (Ekelund et al., 2004). Considering that physical inactivity has been suggested as a
contributor to the prevalence of poor metabolic proles in
youth (Huang et al., 2007), it is crucial to implement
health enhancing strategies early in life. However, information on the effect of activity programs of different
intensities on CVD risk factors in youth is limited. The
purpose of this study was to evaluate the effects of exercise protocols of two different intensities on both novel
and traditional CVD risk factors in a small representative
sample of adolescents.
Overall, results of the study indicated that the two exercise programmes had distinct cardioprotective effects on
adolescent youth. Participants in the MOD intervention
improved several risk factors, including %BF, aerobic tness, insulin sensitivity, Fg, and PAI-1concentrations,
whereas participants in the HIT intervention improved in
SBP and aerobic tness. It is not surprising, perhaps, that
traditional endurance exercise appears to have had the
greatest effect on CVD risk over the 7-week intervention.
However, it is important to note that the HIT group experienced improvements despite a substantially lower exercise time commitment. The exercise time commitment
over 7 weeks was 420 min for the MOD group compared
with only 63 min in the HIT group. Thus, signicant
improvements in CVD risk factors in the HIT group
occurred in only 15% of the exercise time. Recent
literature suggests that aerobic tness may be the most
important marker of current health status and a strong
predictor of early mortality in adulthood (Myers
et al., 2002; Ortega et al., 2008). In this study, signicant
improvements in aerobic tness were observed after only
7 weeks with either MOD of HIT exercises.
MOD and HIT group participants improved 26.8 and
8.3%, respectively, in aerobic tness. It could be suggested
that the MOD intervention placed a greater demand on
the heart given the nature of the continuous protocol more
so than the HIT protocol. As such, the increase in aerobic
tness in the MOD group could be the result of improvements in maximal cardiac output via an enhanced stroke
volume (Blomqvist and Saltin, 1983). Although both central and peripheral factors can affect VO2max, cardiac
output is often identied as one of the main contributors
of oxygen transport and VO2max (Bassett and Howley,
2000). It was not feasible to measure cardiac output given
the time restrictions of the curriculum and the number
of participants. Nevertheless, a recent study in adults
suggested that different exercise intensities may have
specic training effects on both central and peripheral
American Journal of Human Biology

mechanisms affecting VO2max (MacPherson et al.,

2011). Continuous endurance exercise in this study
resulted in an increase in maximal cardiac output (central
adaptation) while no effect was observed in a-vO2
difference (peripheral adaptations). Participants in the
sprint interval running protocol, however, demonstrated
signicant improvements in a-vO2 difference while no signicant improvements were noted in maximal cardiac
output. Similar ndings have also been seen elsewhere
(Daussin et al., 2008; Wisloff et al., 2007), which suggest
that exercise programs of differing intensities may
result in site-specic physiological adaptations. Although
the HIT intervention was sufcient to improve aerobic
capacity, it seems that the 30 s exercise protocol and/or
the duration of the intervention period (7 weeks) was too
brief to induce a similar magnitude of adaptation observed
with the MOD intervention. Recent investigations have
shown that sprint interval training is an effective means
of improving a number of CVD risk factors. Observed
changes were similar (Burgomaster et al., 2008; MacPherson et al., 2011) or to some extent greater (Nybo et al.,
2010; Tjonna et al., 2009; Wisloff et al., 2007) that noted
with a traditional, continuous exercise protocol. Differences in training intensities and volumes, mode of exercise,
and participants limit direct comparisons among studies.
However, it appears that the duration of the intervention
period was important to induce central physiological
adaptations. The rationale of intense interval training is
to challenge the hearts pumping ability so that work may
be completed at higher intensities over shorter periods
(Tjonna et al., 2009).
Based on HR responses (Table 2), it is evident that both
interventions challenged the hearts pumping ability
throughout the intervention period. However, the HIT
protocol was apparently of insufcient duration to
adequately stress the hearts pumping ability to produce
the magnitude of improvements in aerobic tness observed in the MOD group. Improvements in aerobic capacity
were, nevertheless, seen in the HIT group even though
their exercise time commitment was only 15% of that of
the MOD group. Considering that aerobic tness appears
to be the most important predictor of morbidity and mortality for CVD and for all causes (Blair and Brodney, 1999;
Blair and Morris, 2009; Ortega et al., 2008; Tjonna et al.,
2009), it is encouraging that both the MOD and HIT interventions signicantly improved aerobic tness in this
study.
Adiponectin serves as an insulin sensitizing adipokine,
which is produced by adipose tissue; low levels are associated with CVD disease, type 2 diabetes and cancer in
adults with low levels in youth potentially tracking into
adulthood (Ekelund et al., 2004). Adiponectin levels
decreased postintervention in the HIT and control groups
(Table 4). The ndings appear puzzling given that higher
levels of PA in youth are often associated with lower metabolic risk and adiponectin levels (Emken et al., 2010; Froberg and Andersen, 2005). On the other hand, others have
demonstrated a reduction in adiponectin levels with
increasing levels of PA (Metcalf et al., 2009; Platat et al.,
2006). Possible explanations for the variable results may
be that adiponectin levels are reduced by improvements in
insulin action or adiponectin levels are downregulated
when PA levels are sufcient to maintain insulin sensitivity (Metcalf et al., 2009; Yatagai et al., 2003). The rst
mechanism may not be applicable given the healthy glu-

EXERCISE AND CVD RISK IN YOUTH

cose levels (Zimmet et al., 2007) in the three groups at preintervention and postintervention. This would preclude
the presence of insulin resistance among the participants.
The second explanation may be plausible though others
have speculated that increasing PA levels could result in
an upregulation of adiponectin receptors, which can
reduce the need for high levels of circulating adiponectin
given their possible inverse relationship (Emken et al.,
2010). Nevertheless, and as the authors contend, it is not
known whether these mechanisms are applicable to youth
because previous studies investigating the relationship
between PA levels and adiponectin receptors have
involved adults (Emken et al., 2010).
It has also been suggested that a reduction in %BF is
necessary for exercise effects on adiponectin levels to
become apparent in obese youth (Kim et al., 2007). Other
studies that have reported a signicant increase in adiponectin levels with increased PA have also involved obese
participants (Balagopal et al., 2005b). Results of the
present study with a sample of nonobese youth were
thus not consistent with suggestions on obese youth. The
MOD intervention resulted in a signicant reduction in
%BF without signicant changes in adiponectin levels
(Table 4), which was consistent with other studies showing a decrease in adiponectin levels after increased PA
in nonobese subjects (Balagopal et al., 2005b; Metcalf
et al., 2009). It is apparent that the effects of exercise on
adiponectin levels are unclear, and further research is
warranted to establish the relationship between PA and
adiponectin. Nevertheless, the ndings of this study are
in contrast with the suggestion that increasing PA levels
has a positive effect on adiponectin levels. It may be
that adiponectin secretion is blunted, when activity
levels are sufcient to maintain healthy plasma glucose
concentrations in nonobese adolescents.
CRP did not change in the HIT and MOD groups, while
it increased signicantly in the control group after 7 weeks
(Table 4). Although specic reference values are not available for adolescents, values < 1.0 mg/L are considered low
risk, 1.03.0 mg/L medium risk, and >3.0 mg/L high risk
in adults (Pearson et al., 2003). All participants were in
this medium risk category at both preintervention and
postintervention (Table 4). Information on the effects of
exercise interventions of differing intensities on CRP concentrations in nonobese adolescents is not available; the
available data are limited to obese participants (Balagopal
et al., 2005b; Kim et al., 2007).
It has been suggested that increases in cardiorespiratory tness may be associated with a decrease in CRP
concentrations (Plaisance and Grandjean, 2006). This was
not apparent in this study of nonobese adolescents.
Studies of overweight and obese youth have also reported
no changes in CRP concentrations in the presence of
signicant improvements in cardiorespiratory tness
(Barbeau et al., 2002; Kelly et al., 2007; Nassis et al.,
2005). Interestingly, these studies involved either overweight or obese youth participants who experienced no
signicant change in body weight.
A possible explanation for observations of nonobese adolescents may be that concomitant weight loss is required
before a decrease in CRP concentrations becomes apparent (Kelly et al., 2007). Although adiposity decreased
signicantly in the MOD group, participants in the three
groups did not change signicantly in body mass postintervention (Table 3). The signicant increase in CRP

523

concentration postintervention in the control group may

be explained by the increased IL-6 concentration postintervention. IL-6 is known to stimulate CRP production
(McCarty, 1999), whereas regular physical activity is
known to decrease the secretion of IL-6 from adipose tissue (Thomas and Williams, 2008). It is evident that IL-6
concentration postintervention increased in the control
group despite decreasing in both the HIT and MOD
groups. It is possible that the small cohort used in this
study failed to detect a signicant relationship.
Fg concentration decreased postintervention in the
MOD group, whereas concentrations did not change in
the control and HIT groups. This may be a potentially
interesting nding given that elevated plasma Fg concentrations has been linked to an increased risk of
CVD in adults (Ford, 2003). Fg is synthesized in the
liver, is a major coagulation protein in plasma, and is a
determinant of blood viscosity and blood ow (Thomas
and Williams, 2008). At present no specic cut off
points have been recommended for youth populations.
Normal Fg values in adults though range from 150 to
350 mg/dL (El-Sayed, 1996), although these values can
be affected by various lifestyle and biological variables.
Previous studies have found signicant reductions
in Fg concentrations after a 3 month MOD PA and
diet intervention (Balagopal et al., 2005a) and after a
6 month exercise protocol1 H, three times per week
(Meyer et al., 2006). Both studies involved obese adolescents who also experienced signicant reductions in
adiposity postintervention. As in this study, it appears
that a decrease in adiposity may be required to trigger
a reduction in Fg concentration.
Elevated PAI-1 concentrations play a role in the development of atherosclerosis by limiting endogenous brinolysis (Lira et al., 2010). As PAI-1 plays an important role
in hemostasis and is released by endothelial cells, it is
often used as a marker for endothelial dysfunction, which
in turn is known to be a key cause in the development of
atherosclerosis (Ribeiro et al., 2007). Elevated PAI-1 concentrations are also viewed as a powerful predictor of both
myocardial infarction and stroke incidence in adulthood
(Gallistl et al., 2000). Thus, reversing abnormal proles of
PAI-1 during youth may be potentially benecial for adult
health. One recent study of healthy adolescent males did
demonstrate a signicant reduction in PAI-1 concentrations immediately after exhaustive exercise, but it normalized after 24 H (Ribeiro et al., 2007). Participants
in the MOD group however experienced a signicant
decrease in PAI-1 even though blood samples were
taken within 9092 H after the last intervention exercise
session.
Individuals who exercise regularly have an improved
brinolytic prole (Szymanski et al., 1994). Improved PAI1 proles have been noted after an exercise intervention
in adults; the improved proles were attributed to reductions in insulin (Schuit et al., 1997) and/or adiposity
(Mavri et al., 2001; Svendsen et al., 1996). In this study of
adolescents, reductions in insulin and adiposity were
evident only in the MOD group and may help explain the
reductions in PAI-1. It has been suggested that responses
to exercise may be inuenced by age-dependent endothelial dysfunction and as such may show a propensity to
change if high concentrations of PAI-1 is present. Of
potential relevance, PAI-1concentrations in the present
sample were lower than those in a study of healthy adolesAmerican Journal of Human Biology

524

D.S. BUCHAN ET AL.

cents (Ribeiro et al., 2007), 21.9 6 13.3 ng/mL versus 28.2

6 12.1 ng/mL. Apparently, the MOD protocol provided a
substantial dose of exercise, albeit over a relatively short
period of time, which resulted in positive improvements in
endothelial function as evidenced by the signicant
decrease in PAI-1 concentration.
Participants in the MOD group also experienced a signicant improvement in fasting insulin concentrations
postintervention. Fasting insulin concentration is commonly used as an indicator of insulin resistance given the
costly and invasive nature of the gold standard, the hyperinsulinemic-euglycemic clamp technique. As insulin
resistance precedes the development of type 2 diabetes,
interventions that have the potential of improving fasting
insulin levels and perhaps preventing type 2 diabetes in
youth are needed. The ndings for the MOD group are
consistent with investigations that noted a decrease in
fasting insulin concentrations after an aerobic intervention in overweight/obese youth with (Ferguson et al.,
1999) or without (Nassis et al., 2005) a reduction in %BF.
Although one of the studies (Ferguson et al., 1999) noted a
10% reduction in fasting insulin concentrations in overweight/obese youth, the MOD group experienced a mean
reduction of 70%.
Lipid abnormalities and in particular elevated plasma
TG concentrations are strongly linked to CVD in adulthood. As such, exercise interventions that reduce elevated
plasma TG concentrations in youth might be important for
reducing the risk of CVD in later years. Exercise interventions have a benecial effect on plasma TG as documented
in two recent reviews (Kelly et al., 2007; Strong et al.,
2005). Surprisingly, the MOD group experienced a signicant increase in plasma TG concentrations postintervention. However, this response is typical during normal
growth and maturation during adolescence and may
explain this response (Dai et al., 2009). Another possible
explanation for this nding may relate to initial levels of
plasma TG concentrations of participants at preintervention. Several studies that observed a positive effect of
aerobic exercise on plasma TG concentrations included
overweight or obese participants (Ferguson et al., 1999;
Kelly et al., 2007). A cut off point of > 1.7 mmol/L may
serve as a means of detecting abnormal plasma TG concentrations in youth (Zimmet et al., 2007). Plasma TG concentrations of both groups ranged within 0.77 6 0.26 to 1.27
6 0.42 mmol/L at preintervention and postintervention,
respectively. Thus, the inuence of exercise on plasma TG
may only be apparent in those who present with abnormal
preintervention proles (Kelley and Kelley, 2007).
It is evident from Table 4 that denite trends exist
within the data. It appears that there was a decrease in
PAI-1 and LDL-C and an increase in HDL-C concentrations within both intervention groups. Increased physical
activity levels tend to have a positive effect on lowering
PAI-1 levels in healthy adolescents (Ribeiro et al., 2007).
However, the exact mechanisms whereby increased physical activity levels enhance brinolysis in unclear. It has
been hypothesized that reductions in PAI-1 activity, mediated by positive changes in lipid prole through increased
physical activity levels, may be responsible for enhanced
brinolysis (Speiser et al., 1988). This seems plausible
given the responses noted in LDL-C and HDL-C in both
intervention groups. However, this response in addition to
the increase in TG in all groups and the decrease in TC
concentration in the control and MOD groups may also
American Journal of Human Biology

represent normal lipid response patterns during growth

and maturation (Dai et al., 2009).
Furthermore, there also appears to be a reduction
in IL-6 response in both exercise groups. IL-6 is a
proinammatory cytokine and is a strong independent
predictor of increased mortality (Thomas and Williams,
2008). Limited studies have investigated the effects of
PA interventions on IL-6 in youth. Of the studies that
have, some have involved overweight (Kelly et al., 2007)
and/or obese (Balagopal et al., 2005a; Nassis et al., 2005;
Rosenbaum et al., 2007) youth participants. However,
only two of these studies noted a signicant reduction in
IL-6 postintervention either in the presence (Rosenbaum
et al., 2007) or absence (Balagopal et al., 2005a) of weight
loss after exercise. It could be that the resting levels of
IL-6 noted in this cohort were not of a sufcient raised
level to induce signicant changes through exercise as
found in other studies. Nevertheless, it is plausible that a
type II error was committed given the relatively small
sample size used. It may be that future studies that
involve a larger cohort are needed to reveal signicant
changes in these risk factors.
In conclusion, although limited to relatively small samples, the ndings demonstrate signicant improvements
in cardiorespiratory tness, blood pressure, body composition, insulin resistance, Fg, TG, and PAI-1levels in
healthy adolescent youth after a 7 week intervention of
different exercise intensities. Different exercise intensities and durations may have different cardioprotective
effects on youth. Nevertheless, the mechanisms whereby
physical activity improves metabolic health are incompletely understood. To our knowledge, this is the rst
study to demonstrate the effects of a novel interval training program on both traditional and novel CVD risk
factors in adolescents. Although positive adaptations were
noted in the metabolic proles of the participants in a traditional exercise intervention, further research is needed
to evaluate the use of intermittent activity protocols.
Larger scale and extended interventions must be undertaken so that the long-term impact and effects of intermittent training programs on unfavorable metabolic proles
may be investigated further.
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