Review
Aerobic fitness and its relationship to sport, exercise
1Children’s Health and Exercise
Research Centre, University of
Exeter, Exeter, UK
2Health and Use of Time
Group, Sanson Institute for
Health Research, University
of South Australia, Adelaide,
Australia
3MRC Epidemiology Unit,
Institute of Metabolic Science,
University of Cambridge,
Cambridge, UK
4 School of Health and Medical
Sciences, Orebro University,
Orebro, Sweden
Correspondence to
Professor Neil Armstrong,
Children’s Health and Exercise
Research Centre, University
of Exeter, Northcote House,
The Queen’s Drive, Exeter EX4
4QJ, UK;
n.armstrong@exeter.ac.uk
Acepted 26 June 2011
Br J Sports Med 2011;45:849–858. doi:10.1136/bjsports-2011-090200
training and habitual physical activity during youth
Neil Armstrong,1 Grant R Tomkinson,2 Ulf Ekelund3,4
ABSTRACT
Aim To analyse aerobic fitness and its relationship with
sport participation, exercise training and habitual physi-
cal activity (HPA) during youth.
Methods Studies were located through computer
searches of Medline, SPORT Discus and personal data-
bases. Systematic reviews of time trends in aerobic
fitness/performance, and exercise training and peak
oxygen uptake (peak VO2) are reported.
Results Peak VO2 increases with age and maturation.
Boys’ peak VO2 is higher than girls’. Despite data show-
ing a decrease in performance test estimates of aerobic
fitness there is no compelling evidence to suggest that
young people have low levels of peak VO2 or that it is
declining over time. The primary time constant of the
VO2 kinetics response to moderate and heavy intensity
exercise slows with age and the VO2 kinetics response
to heavy intensity exercise is faster in boys. There is
a negative correlation between lactate threshold as a
percentage of peak VO2 and age but differences related
to maturation or sex remain to be proven. Young athletes
have higher peak VO2, a faster primary time constant
and accumulate less blood lactate at the same relative
exercise intensity than their untrained peers. Young peo-
ple can increase their peak VO2 through exercise training
but a meaningful relationship between aerobic fitness
and HPA has not been demonstrated.
Conclusions During youth the responses of the com-
ponents of aerobic fitness vary in relation to age, matu-
ration and sex. Exercise training will enhance aerobic
fitness but a relationship between young people’s cur-
rent HPA and aerobic fitness remains to be proven.
INTRODUCTION
The aims of this review are to analyse aerobic
fitness during growth and maturation and to
examine the relationships between aerobic fitness
and participation in sport, exercise training and
habitual physical activity (HPA) during youth.
Studies for review were located through computer
searches of Medline, SPORT Discus and personal
databases. Systematic reviews of time trends in
aerobic fitness/performance and exercise training
and peak VO2 are reported.
AEROBIC FITNESS
Aerobic fitness may be defi ned as the ability to
deliver oxygen to the muscles and to utilise it to
generate energy to support muscle activity during
exercise. Peak oxygen uptake (peak VO2), the high-
est rate at which oxygen can be consumed during
exercise, is recognised as the best single measure
of young people’s aerobic fitness.1 2 Peak VO2 limits
the rate at which oxygen can be provided during
exercise and a high peak VO2 is a prerequisite of
elite performance in many sports but it does not
describe all aspects of aerobic fitness. In several
sports and in everyday life intermittent exercise
and the ability to engage in rapid changes in exer-
cise intensity are at least as important as peak
VO2. Under these conditions, it is the transient
kinetics of VO2 which best describe the relevant
component of aerobic fitness. 3 Furthermore, dur-
ing sustained exercise lactate accumulates within
the muscle and diffuses into the blood to provide
an estimate of the relative aerobic and anaerobic
contribution to the exercise. Blood lactate accu-
mulation therefore provides a useful indicator of
aerobic fitness with reference to the ability to sus-
tain submaximal exercise.4
PEAK OXYGEN UPTAKE
Peak VO2 during youth has been extensively doc-
umented. 5 6 Figure 1 represents ~5000 peak VO2
(l/min) values of 8–16-year-olds. These data must
be interpreted cautiously as they represent mean
values from studies with volunteer samples of
varying sizes. Nevertheless, the figure clearly
shows an almost linear increase in boys’ peak VO2
in relation to chronological age. Girls’ data demon-
strate a similar but less consistent trend with some
cross-sectional studies suggesting a tendency to
plateau at about 14 years of age. Regression equa-
tions generated from these data indicate that peak
VO2 increases from 8 to 16 years by 150% and
80% in boys and girls respectively.6
The few longitudinal studies available reflect
the cross-sectional data with some studies indicat-
ing large age-related increases in boys’ peak VO2
between 13 and 15 years. Girls’ data are less con-
sistent but in accord with cross-sectional fi ndings
they indicate a progressive rise from 8 to 13 years
with a gradual levelling-off in peak VO2 from age
14 years. Longitudinal data indicate that boys’
peak VO2 almost doubles from 11 to 17 years with
girls’ values increasing by ~ 50% over the same
age range. 5
Peak VO2 is strongly correlated with body mass
and this is conventionally controlled for by sim-
ply dividing peak VO2 (ml/min) by body mass
(kg) and expressing it as the simple ratio ml/kg/
min. When peak VO2 is expressed in this man-
ner a different picture emerges with boys’ peak
VO2 remaining remarkably consistent from 6 to
18 years at ~ 48 ml/kg/min with girls’ values
showing a decline from ~ 45 to 35 ml/kg/ min. 5 6
The reporting of peak VO2 in ratio with body mass
is of interest in the context of sports where body
mass is moved or health where the movement of
849
 Review
Figure 1 Peak oxygen uptake in relation to chronological age. From
Armstrong and Welsman6 with permission.
body mass is required for normal locomotion but it has clouded
the physiological understanding of peak VO2 during growth
and maturation.7 8
Numerous studies have showed that ratio scaling can lead to
inappropriate interpretation of physiological variables.9 Using
multi-level modelling, longitudinal studies of both trained10
and untrained11 youth have demonstrated that, in addition to
chronological age, both growth and maturation positively and
independently influence peak VO2. With body mass appropri-
ately controlled for, boys’ peak VO2 increases through child-
hood and adolescence into young adulthood. Girls’ peak VO2
increases at least into puberty and possibly into young adult-
hood.8 In addition, maturation is associated with increases in
peak VO2 above those explained by body size, body composi-
tion, and chronological age.12 13 These changes, although in
confl ict with the conventional interpretation of peak VO2, are
wholly consistent with both the underlying physiological pro-
cesses and improvements in sport performance in relation to
growth and maturation.14 15
Girls’ peak VO2 (l/min) values are about 10% lower than
those of boys during childhood and the sex difference reaches
~ 35% by age 16 years. 5 6 There are no consistent data to sup-
port sex differences in maximal heart rate but the balance of
evidence suggests that maximal stroke index is higher in boys
than in girls although there are confl icting data on whether
this is due to cardiac size or function.16 17 Data on maximal
arterial-venous oxygen difference are sparse and equivocal
with no persuasive evidence to support sex-related differ-
ences during childhood. 5 Sex differences in peak VO2 during
adolescence have been attributed to differences in HPA. Boys
are generally more active than girls but HPA patterns show
that both sexes rarely experience the intensity and duration of
activity associated with increases in peak VO2.18
Physiological explanations for sex differences in peak VO2
during adolescence include boys’ greater muscle mass and
blood haemoglobin concentration. Muscle mass increases
through childhood and adolescence in both sexes but although
boys generally have greater muscle mass than girls in child-
hood marked sex differences do not become apparent until
the adolescent growth spurt. From 5 to 16 years of age, boys’
relative muscle mass increases from about 42–54% of body
mass. Girls experience a less dramatic adolescent growth spurt
than boys and from age 5–13 years muscle mass increases
850
from about 40–45% of body mass. In relative terms it then
declines due to girls’ increase in body fat during adolescence.
Boys’ greater muscle mass not only facilitates the utilisation
of oxygen by the muscles but also supplements the venous
return to the heart and therefore augments stroke volume
through the peripheral muscle pump. Muscle mass appears to
be the dominant influence in the increase in peak VO2 through
adolescence. 5
Blood haemoglobin concentration is correlated with peak
VO2 in both sexes.19 There are no significant sex differences in
haemoglobin concentration in childhood but during puberty
the effect of testosterone on red blood cell production stimu-
lates noticeable increases in boys’ haemoglobin concentration
which reach values ~10% higher than those of girls by late
puberty. It is reasonable to expect that boys’ superior oxygen-
carrying capacity may augment sex differences in peak VO2.
However, the transport and dissociation of oxygen from
haemoglobin during exercise is complex and sex differences
in maximal arterial-venous oxygen difference during youth
remain to be proven. 5
OXYGEN UPTAKE KINETICS
The VO2 kinetic response to step changes in exercise intensity
is described in figure 2 and can be defi ned in relation to a num-
ber of exercise domains. Rigorously determined and analysed
data with young people, however, are only available in the
moderate (ie, below the lactate threshold (T LAC ) and heavy (ie,
above the T LAC but below the maximal lactate steady state
(MLSS) or critical power) intensity exercise domains. 3
At the onset of a step transition from rest to moderate inten-
sity exercise there is an almost immediate increase in VO2
measured at the mouth. This cardio-dynamic phase (Phase I)
lasts about 15 s in children and is associated with an increase in
cardiac output, which occurs before the arrival at the lungs of
venous blood from the exercising muscles. Phase I is indepen-
dent of muscle VO2. The cardio-dynamic phase is followed by
an exponential increase in VO2 (Phase II, the primary compo-
nent) that drives VO2 to a steady-state value (Phase III) within
about 2 min with an oxygen cost of about 10 ml/min/Watt
above that found at rest (or more usually during exercise tests,
unloaded pedalling). The principal variable of interest is the
time constant (τ) of the VO2 primary component which reflects,
within about 10%, the kinetics of VO2 at the muscles. 20 21 The
shorter the τ the smaller the anaerobic contribution to the step
change in exercise intensity. During a step change to heavy
intensity exercise the Phase II oxygen cost is similar to that
observed with moderate intensity exercise. However, the
oxygen cost increases over time as a slow component is super-
imposed and the achievement of a steady-state is delayed by
10–15 min. The mechanisms underlying the slow component
remain speculative but appear to be a function of muscle fibre
distribution, motor unit recruitment and the matching of oxy-
gen delivery to active muscle fibres. 22 23
Boys have a faster τ than girls during the transition from rest
to heavy exercise24 but VO2 kinetic responses to a step change
to moderate intensity exercise are independent of sex. 25 The τ
of the Phase II exponential rise in VO2 during youth has been
showed to be age-dependent during step changes to both
moderate25 and heavy26 27 intensity exercise. A longitudinal
study of the VO2 kinetics of heavy intensity exercise reported
a slowing of the VO2 primary component τ and a reduction
in the Phase II oxygen cost in both boys and girls, who were
prepubertal at the onset of the study.26 A slow component was
Br J Sports Med 2011;45:849–858. doi:10.1136/bjsports-2011-090200

Figure 2 The three phases of the response to a step change in exercise in four different exercise intensity domains. From Fawkner and
Armstrong3 with permission.
demonstrated on both occasions contributing about 10% of
the fi nal VO2 on the fi rst occasion and 15% of the fi nal VO2 on
the second occasion. These fi ndings have been replicated with
13–16-year-old boys27 and are consistent with the presence of
an age-dependent influence on muscles’ potential for oxygen
utilisation. Any independent effects of maturation remain to
be explored.
During youth peak VO2 is not related to the VO2 primary
component τ during the transition to either moderate25 or
heavy27 intensity exercise. This is not surprising as peak VO2 is
largely dependent on oxygen delivery to the muscles whereas
young people’s VO2 kinetics in these exercise domains appear
to be primarily related to oxygen utilisation by the muscles. 3
BLOOD LACTATE ACCUMULATION
Blood lactate accumulation is a function of several dynamic
processes including muscle production, muscle consumption,
rate of diffusion from muscle into blood and rate of removal
from blood. Blood lactate therefore cannot be assumed to
have a direct relationship with rate of muscle production and
values must be interpreted cautiously. At the onset of incre-
mental exercise there are minimal changes in blood lactate
with rate of diffusion from the muscle matched by rate of
removal from the blood. As exercise intensity increases a
point is reached where lactate rises rapidly with a steep rise to
exhaustion. The fi rst observable increase in lactate above rest-
ing level during incremental exercise is referred to as the T LAC .
The highest exercise intensity that can be sustained without
incurring a progressive accumulation of blood lactate is called
the MLSS.4
There are no sex differences in blood lactate accumulation
with exercise during youth. Children accumulate less blood
lactate than adults during both submaximal and maximal
exercise and there is a negative correlation between T LAC (as
a percentage of peak VO2) and age. MLSS has generally been
found to be negatively correlated with age but this fi nding has
been challenged by a recent study. 28 Despite some indications
that both muscle29 and blood 30 lactate responses are related
to maturation, whether maturation independently influences
blood lactate accumulation remains to be proven.
Br J Sports Med 2011;45:849–858. doi:10.1136/bjsports-2011-090200
Review
TIME TRENDS IN AEROBIC FITNESS
There are no widely recognised recommendations for opti-
mum levels of young people’s aerobic fitness and no compelling
evidence to suggest that the current generation of youth have
low levels of peak VO2. 5 Informed debate is, however, divided
on whether the ‘aerobic fitness’ of children and adolescents
has declined over time. 31 32 There are many factors that make
it difficult to draw confident conclusions regarding historical
changes in aerobic fitness during youth. First, there is a paucity
of scientific evidence available; second, most of the available
scientific evidence has only made informal historical compari-
sons, with very occasional rigorous statistical treatment; and
third, researchers have not always been clear on their defi ni-
tion of ‘aerobic fitness’ and how it is operationalised.
Using a systematic review and meta-analytical strategy
one of us (GRT) reviewed 50 studies that examined historical
changes (spanning a minimum of 5 years) in aerobic fitness
(operationalised as mass-related peak VO2) or aerobic perfor-
mance (operationalised as maximal field-based endurance run-
ning) of healthy (free from known disease or injury) young
people aged 9–17 years. Aerobic fitness data were available for
>4002 9–17 year olds from five countries between 1962 and
1994; aerobic performance data were available for >25 245 203
9–17 year olds from 28 countries between 1964 and 2008.
Overall, there has been a very small change in young peo-
ple’s aerobic fitness (mean change ±95% CI: –0.26 ±0.48%
or –0.06 ±0.06SDs) (figure 3). Whereas there has been a large
decline in young people’s aerobic performance since 1975
(mean change ±95% CI: –13.34 ±0.45% or –0.99 ±0.03SDs)
(figure 3). Changes in aerobic performance, but not aerobic fit-
ness, were consistent for different sex, age and geographical
groups (figure 3). As these results describe historical changes
in mean values, it is not clear whether the changes have been
uniform or skewed over time, although data suggest that the
changes have been typically greater in the poorer performing
or least fit children. 33–37
So why has there been little change in aerobic fitness but
large declines in aerobic performance? Unfortunately, our
understanding of the reported changes in aerobic fitness is
confounded by data from different ergometers (eg, cycle,
851
 Review

treadmill), and data on relatively small, volunteer samples

Percent (1990 = 100%) of young people who might have been athletically inclined.
110 All Furthermore, the reported changes in mass-related peak VO2
may reflect changes in the denominator (body mass in kg)
rather than the numerator (peak VO2 in ml/min). Conversely,
confidence in the decline in aerobic performance is high,
because of large representative samples, broad geographical
100 Fitness coverage and consistent fi ndings. These changes are probably
influenced by a network of social, behavioural, physical, bio-
mechanical, and psychosocial factors as well as physiological
Performance
variables. 38 Causes of a decline over time in maximal aerobic
90 performance are therefore not only a function of changes in
peak VO2 but also changes in mechanical efficiency and frac-
110 Boys tional utilisation of oxygen with affective issues (eg, lack of
motivation) and cognitive issues (eg, inability to judge pace)
also important. 39–41 Unfortunately, no historical change
data are available for these factors. Performance is, however,
100 affected by increased fat mass and there is convincing evi-
dence of a worldwide increase in young people’s body fatness
in recent decades.42 43 Increases in fatness explain ~30–70%
of the decline in aerobic performance34 41 but other factors
including reduced experience with maximal sustained efforts
90 also play a role. Nevertheless, changes in maximal aerobic
110 performance – the ability to run faster, play harder and play
Girls
longer – are important for youth health and well-being and
successful sport participation, irrespective of the underlying
mechanisms.
There are no data on time trends in young people’s VO2
100 kinetic response to changes in exercise intensity or blood lac-
tate accumulation during submaximal exercise.

90 AEROBIC FITNESS AND SPORT

Peak oxygen uptake
110 9–12 years Cross-sectional studies have reported that trained young ath-
letes of both sexes have higher peak VO2 than their untrained
peers44–46 and focused studies have reported higher peak VO2
than untrained youth in trained cyclists,47–49 cross-country
skiers, 50 swimmers 51–54 and canoeists. 50 Young male athletes
100
tend to have higher peak VO2 than young female athletes and
although this is probably due to the sex differences described
earlier variations in training volume cannot be ruled out. Peak
VO2 values of >50 ml/kg/min and >60 ml/kg/min for trained
90 girls and boys respectively have been regularly observed. As
almost all studies report cross-sectional data it is unknown
110 13–17 years whether differences in the peak VO2 of trained and untrained
youth are due to initial selection for sport, subsequent training
programmes or both.
There is no compelling evidence to suggest that either maxi-
100 mal heart rate or maximal arterial-venous oxygen difference
change with training during youth and the higher peak VO2
of young athletes appears to be a function of enhanced stroke
volume.46 47 The practical difficulties of determining young
people’s stroke volume during exercise mean that data should
90 be treated with caution. 55 However, the literature is consistent
1960 1985 2010 in reporting higher stroke volumes 56–58 and stroke indices47 57
year of testing in trained children and adolescents compared with their
untrained peers. A single prospective study has supported
these fi ndings by observing significant increases in both boys’
Figure 3 Worldwide patterns of change in aerobic fitness (dashed
(+15%) and girls’ (+11%) stroke volumes following a 13 week
lines) and aerobic performance (solid lines) of 9–17 year olds over the
periods 1962–1994 and 1964–2008, respectively. Data are presented endurance training programme, with no changes noted in con-
separately for all children, boys, girls, 9–12 year olds, and 13–17 trol groups. 59
year olds. Data are standardised to 1990 = 100%, with higher values There are marked inconsistencies in studies exploring the
(>100%) indicating better fitness or performance. underlying mechanisms of enhanced stroke volumes with

852 Br J Sports Med 2011;45:849–858. doi:10.1136/bjsports-2011-090200


training and they are confounded by uncontrolled variables
such as age, maturity, training volume and years of training.
It appears reasonable to suggest that training may enhance
stroke volume through a more effective peripheral muscle
pump and/or plasma volume expansion increasing venous
return but empirical support of this hypothesis is not avail-
able. Data on training-induced changes in cardiac dimensions
are equivocal with some studies reporting larger left ventricu-
lar dimensions at rest47 59 and at maximal exercise47 in trained
youth and others observing no differences in left ventricular
size and mass.44 60 Most 60 61 but not all46 studies have reported
no differences between trained and untrained youth in ven-
tricular wall thickness. Prospective data on young people are
sparse and inconsistent with some studies observing no sig-
nificant training-induced changes in cardiac dimensions 62 63
and others reporting significant increases with training. 59 61
Estimates of shortening fraction and ejection fraction at rest
have been observed to be similar in trained and untrained chil-
dren47 61 but trained children have been reported to increase
their shortening fraction more than untrained children during
maximal exercise.64
Oxygen uptake kinetics
In adults, training results in a shorter VO2 primary component
τ and a smaller VO2 slow component but no prospective data on
young people are available. Two studies from the same research
group compared the VO2 kinetics of trained prepubertal swim-
mers to untrained children.65 66 Both studies determined VO2
kinetics during cycle ergometry and reported no differences in
the VO2 primary component τ during the transition to exercise
either above or below the T LAC . No significant change in the
VO2 slow component was observed during exercise above the
T LAC . The responses to exercise above T LAC were confi rmed in
a similar study that compared the cycle ergometer-determined
VO2 kinetic responses to a step change to heavy exercise of
a group of 11-year-old girl swimmers with an untrained con-
trol group.67 However, when the girls’ VO2 kinetics was deter-
mined during arm (rather than leg) ergometry the swimmers
exhibited a significantly shorter VO2 primary component τ
than the control group, thus supporting the specificity of train-
ing on VO2 kinetics. There were no significant differences in
arm cranking peak VO2 between the two groups suggesting
that training-induced changes in VO2 kinetics are not related
to changes in peak VO2. As heart rate kinetics was also not
related to VO2 kinetics, it was suggested that the mechanism
underpinning the faster VO2 kinetics in the swimmers was
enhanced oxygen utilisation by the muscles.
A similar study by the same research group but with 14-year-
old pubertal girls reported significantly faster VO2 kinetics in
trained girls during both upper and lower body ergometry.
The authors attributed the contrasting results in prepubertal
and pubertal girls to both a greater stage of maturation and a
longer training history in the pubertal girls. Furthermore, they
suggested that, in contrast to their conclusion with prepuber-
tal girls, the faster VO2 kinetics in the trained pubertal girls
was influenced by both central and peripheral factors.68
The only other published study on the topic to date exam-
ined the cycle ergometer-determined VO2 kinetic responses
of 15-year-old boys from a Premier League football academy
to the transition from rest to moderate intensity exercise and
compared them to an age-matched control group. The foot-
ballers demonstrated a significantly faster VO2 primary com-
ponent τ than the control group. The authors postulated that
Br J Sports Med 2011;45:849–858. doi:10.1136/bjsports-2011-090200
Review
the faster VO2 kinetics of the footballers were due to increases
in both oxygen delivery and oxygen utilisation.69
Blood lactate accumulation
The assessment and interpretation of blood lactate accumula-
tion is challenging and the role, in children and adolescents, of
a potential reduction in lactate diffusion from the muscles to
the blood and/or an enhanced lactate clearance from the blood
remains to be investigated. Nevertheless, data consistently
demonstrate that young athletes accumulate less blood lactate
than untrained youth at the same relative exercise intensity.4
It has been reported that T LAC in trained youngsters occurs at a
higher percentage of peak VO2 than in untrained youth.70 71 The
running speed corresponding to a blood lactate accumulation
of 4 mM has been observed to increase following training.72 73
Intervention studies have reported high intensity74 75 but not
low intensity58 76 training to result in a decrease in blood lac-
tate accumulation during subsequent submaximal exercise.
No study has specifically examined the potential mechanisms
underlying training-induced reductions in young people’s blood
lactate accumulation during subsequent submaximal exercise
but data from studies of adults suggest that an increase in oxi-
dative capacity is the primary mechanism.77
AEROBIC FITNESS AND EXERCISE TRAINING
The only component of young people’s aerobic fitness on
which there are sufficient data to estimate a dose-response
relationship with exercise training is peak VO2. In a system-
atic review of the literature one of us (NA) located 69 published
training studies and identified 21 investigations which had rig-
orously examined the effect of structured exercise training on
young people’s peak VO2 (table 1). It was concluded that there
is a small but significant inverse relationship between baseline
(pretraining) peak VO2 and training–induced changes but no
relationship between baseline HPA and peak VO2 responses
to training. An appropriate 12 week training programme will
induce, on average, an 8–9% increase in peak VO2 which is
independent of sex, age and maturation. Greater increases in
peak VO2 are likely with longer periods of training but further
research is required to evaluate the strength of the genetic con-
tribution to responses to training.78
The recommendations of the International Olympic
Committee consensus statement on ‘Training the elite young
athlete’79 are based on the interpretation of these data (table 2).
AEROBIC FITNESS AND HPA
Studies stretching back over 35 years have analysed the peak
VO2 of children and adolescents in relation to their HPA and
consistently shown no meaningful relationship between
the two variables.80 81 All located studies which objectively
estimated HPA and directly measured peak VO2 are tabu-
lated in chronological order in table 3. It could be argued that
pre-1990 studies82–85 did not monitor HPA long enough for it
to be representative of normal physical activity (PA) behav-
iour but as data are sparse all studies have been included for
completeness.
A longitudinal study of over 200 children used multilevel
modelling to examine HPA, from the ages of 11–13 years. Peak
VO2 was investigated as an additional explanatory variable of
HPA but once age, gender and maturity had been controlled
a non-significant parameter estimate was obtained.86 The
Amsterdam Growth and Health Study reported that a 30%
increase in HPA score over a 15-year period was associated
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Review
Table 1 Peak oxygen uptake and exercise training
Participants Training protocol Peak VO2 (l/min) Peak VO2 (ml/kg/min)

Experimental Control Frequency Length

Study (E) (C) (per week) Intensity Duration (weeks) Type Pre Post Change % Pre Post Change %

Lussier and n = 16 n = 10 4 92% maxHR 45 min 12 Continuous running and games E 1.76 1.96 11.4 55.6 59.4 6.8*
Buskirk90 11 B, 5 G, 10.3 y 9B
C 1.83 1.96 7.1 53.1 53.9 1.5
1 G,
10.5 y
Gilliam and n = 11 n = 12 4 HR at 165 beats/min 25 min 12 Enhanced PE programme E 1.29 1.34 3.9 43.4 42.9 −1.2NS
Freedson91 B & G, 8.5 y B & G,
8.5 y C 1.34 1.4 4.5 40.5 40.9 1.0
Becker and n = 11 B, 9.6 y n = 11 B, 3 50% of the way 40 min 8 Continuous cycling E– – – 39.0 47.0 20.5 NS
Vaccaro92 10.0 y between AT and
peak VO2
C– – – 41.7 44.0 5.5
Savage E1 n = 12 B, 8.0 y n = 10 B, 3 E1 85% 2.4 – 4.8 km 10 Interval running E1 – – – 55.9 58.5 4.7*
et al93† E 2 n = 8 B, 8.5 y 9.0 y max HR E2 - – – 52.2 54.6 4.6 NS
E 2 68% C– – – 57.0 55.7 −2.3
max HR
Mc Manus E1 n = 12 G, 9.3 y n = 7 G, 3 E1 80–85% E1 20 min 8 E1 continuous cycling E1 1.30 1.43 10.0 45.4 48.7 7.3*
et al94* E 2 n = 11 G, 9.8 y 9.6 y max HR E 2 8 – 16 min E 2 interval running E 2 1.54 1.67 8.4 48.3 50.3 4.1*
E 2 max C 1.49 1.46 −2.0 44.9 43.8 −2.4
sprints
Welsman E1 n = 18 G, 10.1 y n = 16 G, 3 E1 80% 20 min 8 E1 continuous cycling E1 1.76 1.79 1.7 51.8 52.2 0.7 NS
et al95† E 2 n = 17 G, 10.2 y 10.2 y max HR 20 – 25 min E 2 aerobics and E 2 1.58 1.61 1.9 47.0 47.8 1.7 NS
E 2 75–80% circuit training C 1.72 1.72 0.0 46.2 45.9 −0.6
max HR
Tolfrey n = 12 B, 10.6 y n = 10 B, 3 80% max HR 30 min 12 Continuous cycling EB 1.60 1.66 3.8 46.6 47.2 1.3 NS
et al96† n = 14 G, 10.6 y 10.3 y EG 1.36 1.54 13.2 39.3 42.4 7.9 NS
Br J Sports Med 2011;45:849–858. doi:10.1136/bjsports-2011-090200

n = 9 G, CB 1.62 1.65 1.9 50.7 50.3 −0.1

10.5 y CG 1.52 1.52 0.0 44.7 43.0 −3.8
Williams E1 n = 13 B, 10.1 y n = 14 B, 3 E1 80 – 85% E1 20 min 8 E1 continuous cycling E1 1.80 1.93 7.2 54.7 57.5 5.1 NS
et al97† max HR E 2 6 – 8 min E 2 1.84 1.91 3.8 54.8 56.2 2.6 NS
E 2 n = 12 B, 10.1 y 10.1 y E 2 max E 2 interval running C 1.92 1.97 2.6 56.4 56.7 0.5
sprints
Mandigout n = 18 B, 10.7 y n = 28 B, 3 75 – 80% max HR 15 – 20 min 13 Continuous and EB 1.70 1.84 8.2 47.2 49.2 4.2*
et al98† n = 17 G, 10.5 y 10.5 y continuous continuous interval running EG 1.30 1.57 20.7 38.6 41.9 8.5*
n = 22 G, 90% max 60 – 90 min aerobic CB 1.60 1.70 6.2 46.1 45.5 −1.3
10.5 y HR interval interval activities CG 1.40 1.50 7.4 39.6 39.5 0.2
Baquet n = 13 B n = 10 B 2 80 – 95 % 30 min 7 Interval running E 1.54 1.68 9.1 43.9 47.5 8.2*
et al99† n = 20 G n = 10 G max HR C 1.62 1.62 0.0 46.2 45.3 −1.9
9.5 y 9.9 y
Obert n = 9 B, 10.5 y n = 9 B, 3 80% max HR 60 min 13 Continuous and EB – – – 44.1 50.9 15.4*
et al59 n = 10 G, 10.4 y 10.7 y continous interval running EG – – – 40.9 44.2 8.1*
n = 7 G, 90% max CB – – – 51.5 50.3 −2.3
10.7 y HR interval CG – – – 42.4 42.6 0.5
McManus E1 n = 10 B, 10.4y n = 15 B 3 E1 85% max HR 20 min 8 weeks E1 continuous cycling E1 1.65 1.72 4.2 47.0 50.7 7.8*
et al100 E 2 n = 10 B, 10.4 y 10.5 y E2 max sprints E 2 interval cycling E 2 1.76 1.96 11.4* 45.5 50.7 11.4*
C 1.59 1.57 −0.1 44.7 45.4 −0.2
Br J Sports Med 2011;45:849–858. doi:10.1136/bjsports-2011-090200

Table 1 Continued

Participants Training protocol Peak VO2 (l/min) Peak VO2 (ml/kg/min)

Experimental Control Frequency Length

Study (E) (C) (per week) Intensity Duration (weeks) Type Pre Post Change % Pre Post Change %
Gamelin n = 22 n = 16 3 100 – 120% of MAV 30 min 7 Interval running E– – – 51.6 54.1 4.8*
et al101† 12 B 7B (ie, 80–90% max HR) C– – – 49.9 48.7 −2.4
10 G, 9.8 y 9 G,
9.3 y
Obert n = 25 n = 25 3 100–130% of MAV 25–30 min 8 Interval running E– – – 51.6 55.0 6.6*
et al102 14 B 13 B C– – – 50.3 50.5 −0.4
11 G, 9-11 y 12 G, 9-11 y
Massicotte 3 groups n = 9 B, 3 E1 HR at 170 – 180 12 min 6 Continuous cycling E1 2.00 2.30 15.0 46.7 51.8 10.8*
and n=9B 12.5 y beats/min E 2 1.80 1.90 5.6 47.4 48.0 1.3 NS
Macnab74 in each, E 2 HR at 150 – 160 E 3 1.70 1.80 5.9 46.6 48.2 3.4 NS
12.5 y beats/min C 2.00 1.90 −5.0 45.7 44.2 −3.3
E 3 HR at 130 – 140
beats/min
Stewart n = 13 B, n = 11 B, 4 90% of max HR 14 – 21 min 8 Interval running E– – – 49.8 49.5 -0.6 NS
and Gutin103 10 – 12 y 10 – 12 y C– – – 48.4 49.2 1.7
Burkett n = 10 G, n = 9 G, 5 70% of max HR Started at 20 Continuous and E– – – 45.1 49.4 9.3*
et al104 15.6 y 15.6 y continuous 9.7 km/week interval running C– – – 43.2 43.2 0.0
90% of max HR up to
interval 32.2 km/week
Mahon and n = 8 B, 12.4 y n = 8 B, 4 70 – 80% max HR 20 – 30 min 8 Continuous and E 1.87 2.04 9.1 45.9 49.4 7.6*
Vaccaro105 12.3 y continuous continuous interval running C 1.77 1.84 4.0 45.4 45.9 1.1
90 – 100% peak 100 – 800 m
VO2, 135% HR (from 1.5 to 2.5
At VT interval km) interval
Rowland n = 13 B, n = 13 B, 3 HR at 153 – 184 20 – 30 min 12 Aerobic circuit training E 2.02 2.24 10.9 44.7 47.6 6.5*
and n = 24 G, n = 24 G, beats/min distance running/walking C 1.96 2.02 0.1 44.3 44.7 0.9
Boyajian106† 10.9 – 12.8 y 10.9 – 12.8 y games, basketball
Rowland n = 9 B, n = 9 B, 3 85–90% max HR 30 min 13 Aerobic dance, step EB 2.15 2.29 6.5 45.4 48.2 6.1 NS
et al107† n = 20 G, n = 20 G, aerobics’ EG 1.81 1.97 8.8 43.9 46.1 5.0 NS
11.8 y 11.8 y distance running, CB 2.08 2.15 3.4 45.3 45.4 0.2
circuit activities CG 1.46 1.81 24.0 43.7 43.9 0.4
Stoedefalke n = 20 G, n = 18 G, 3 75–85% max HR 20 min 20 Treadmill running, cycle and E 2.25 2.32 3.1 NS – – –
et al108† 13.6 y 13.7 y rowing ergometry, stair C 2.39 2.45 2.5 – – –
stepping, aerobic dance

NS indicates not significantly different from pretraining value (p ≥ 0.05).

*Indicates significantly different from pretraining value (p≤ 0.05).
†Maturity assessed.
The table is formed from tables in Armstrong and Barker.78
AT, anaerobic threshold; B, boys; C, control group; E, exercise group; G, girls; HR, heart rate; MAV, maximal aerobic velocity; VT, ventilation threshold.

Review
855
 Review

with a 2–5% increase in VO2 max and concluded that, ‘no to suggest that low levels of peak VO2 are common and data
clear relation can be proved between PA and VO2 max in free indicate that youth peak VO2 has remained stable over sev-
living males and females’ (p. 163).87 Other studies have failed eral decades. However, young people’s maximal aerobic per-
to observe a meaningful relationship between children’s HPA formance involving the transport of body mass is important
and blood lactate indices of aerobic fitness.88 89 HPA has not for health and well-being and successful sport participation
been investigated in relation to VO2 kinetics. and this has markedly declined over the last 35 years. Young
athletes have higher peak VO2, faster τ during step changes
in exercise intensity and accumulate less blood lactate during
CONCLUSIONS submaximal exercise than their untrained peers. Sufficient
Peak VO2 during childhood and adolescence is well- dose-response data are available to design exercise training
documented but other aspects of aerobic fitness during youth programmes to improve the peak VO2 of both trained and
are less well-understood. There is no compelling evidence untrained children and adolescents. However, data on the
effects of different exercise training programmes on blood lac-
tate accumulation are sparse and in the case of VO2 kinetics
Table 2 Exercise prescription for improvement of peak oxygen non-existent. Young people rarely experience HPA of sufficient
uptake intensity and duration to enhance peak VO2 and there appears
Mode Mixture of continuous and interval to be no meaningful relationship between peak VO2 and HPA.
training using large muscle groups More research focusing on the mechanisms driving exercise-
Frequency Minimum 3–4 sessions per week induced changes in aspects of aerobic fitness during growth
Duration 40–60 min and maturation is needed.
Intensity 85–90% of maximum heart rate Competing interests None.
Programme length Minimum length of 12 weeks
Provenance and peer review Not commissioned; externally peer reviewed.

Table 3 Habitual physical activity and peak oxygen uptake in youth

Citation Participants Physical activity measures Mode of exercise Outcomes

Seliger et al82 11 boys; aged 12 years 1 day heart rate monitoring; Cycle ergometer No significant relationships
Czechoslovakia questionnaire interview
Saris83 Approx 400 girls, 400 boys; 1 day heart rate monitoring; Treadmill No significant relationship between peak VO2 in
aged 6–10 years questionnaire any of the age groups when TDEE was used as
The Netherlands an index for daily physical activity
Andersen et al84 21 girls, 27 boys; 1 day accelerometry; Cycle ergometer No significant relationships
aged 13–18 years questionnaire
The Netherlands
Sunnegardh and 49 girls, 52 boys; 1 day accelerometry; Cycle ergometer No significant relationships between
Bratteby 85 aged 8–13 years questionnaire accelerometry data and peak VO2. Significant
Sweden relationship between questionnaire data and
peak VO2 in 8-year-old boys and 13-year-old boys
and girls
Armstrong et al109 111 girls, 85 boys; 3 day heart rate monitoring Cycle ergometer No significant relationships. Non-significant
aged 11–16 years or treadmill correlation coefficients ranged from r=0.01
England to –0.26
Armstrong et al110 43 girls, 86 boys; 3 day heart rate monitoring Treadmill No significant relationships. Non-significant
aged 10–11 years correlation coefficients ranged from r=–0.15
England to 0.09
Armstrong et al111 63 girls, 60 boys; 3 day heart rate monitoring Treadmill No significant relationships. Non-significant cor-
aged 12.2 years relation coefficients ranged from r=0.13 to 0.16
England in boys and from r=–0.02 to 0.04 in girls
Ekelund et al112 40 girls, 42 boys; 3 day heart rate monitoring Treadmill No significant relationships between MVPA and
aged 14–15 years peak VO2. AEE significantly correlated with peak
Sweden VO2 in both girls and boys but after controlling
for body fat and maturity level the relationship in
boys was non-significant
Eiberg et al113 309 boys, 283 girls; 3 day accelerometry Treadmill Sustained periods of PA explained 9% of the
aged 6–7 years variance in peak VO2 When children with the
Denmark same peak VO2 were compared, boys were more
active than girls, and in children with the same
level of PA, boys were fi tter
Dencker et al114 101 girls, 127 boys; 3–4 day accelerometry Cycle ergometer MPA was not significantly correlated with peak
aged 8-11 years VO2. VPA and MDPA were significantly but
Sweden weakly (r=0.23 to 0.32) related to peak VO2. In
a multiple forward regression analysis VPA and
MDPA explained 10% of the variability in peak
VO2 (VPA 9%, and MDPA 1%).

AEE, activity-related energy expenditure; MDPA, mean daily physical activity; MPA, moderate physical activity; MVPA, moderate to vigorous physical activity; PA,
physical activity; TDEE, total daily energy expenditure; VPA, vigorous physical activity.
Table adapted from Armstrong and Fawkner.115

856 Br J Sports Med 2011;45:849–858. doi:10.1136/bjsports-2011-090200


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