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

ABSTRACT Aim To analyse aerobic fi tness 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

fi tness/performance, and exercise training and peak

oxygen uptake (peak VO 2 ) are reported.

Results Peak VO 2

increases with age and maturation.

Boys’ peak VO 2 is higher than girls’. Despite data show-

ing a decrease in performance test estimates of aerobic

fi tness there is no compelling evidence to suggest that

young people have low levels of peak VO 2 or that it is

declining over time. The primary time constant of the

VO 2 kinetics response to moderate and heavy intensity

exercise slows with age and the VO 2 kinetics response

to heavy intensity exercise is faster in boys. There is

a negative correlation between lactate threshold as a

percentage of peak VO 2 and age but differences related

to maturation or sex remain to be proven. Young athletes

have higher peak VO 2 , 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 VO 2 through exercise training

but a meaningful relationship between aerobic fi tness

and HPA has not been demonstrated.

Conclusions During youth the responses of the com- ponents of aerobic fi tness vary in relation to age, matu-

ration and sex. Exercise training will enhance aerobic

fi tness but a relationship between young people’s cur-

rent HPA and aerobic fi tness remains to be proven.

INTRODUCTION The aims of this review are to analyse aerobic fi tness during growth and maturation and to examine the relationships between aerobic fi tness 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 fi tness/performance and exercise training and peak VO2 are reported.

AEROBIC FITNESS Aerobic fi tness 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 fi tness.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 fi tness. 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 fi tness.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 fi tness 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 fi gure 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 refl ect 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

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 4School 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; [email protected]

Acepted 26 June 2011

Aerobic fi tness and its relationship to sport, exercise training and habitual physical activity during youth Neil Armstrong,1 Grant R Tomkinson,2 Ulf Ekelund3,4

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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 infl uence 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.

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

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 infl uence in the increase in peak VO2 through adolescence.5

Blood haemoglobin concentration is correlated with peak VO2 in both sexes.

19 There are no signifi cant 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 fi gure 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 (TLAC) and heavy (ie, above the TLAC 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 refl ects, 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 fi bre distribution, motor unit recruitment and the matching of oxy- gen delivery to active muscle fi bres.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

Figure 1 Peak oxygen uptake in relation to chronological age. From Armstrong and Welsman6 with permission.

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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 infl uence 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 TLAC. 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 TLAC (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 blood30 lactate responses are related to maturation, whether maturation independently infl uences blood lactate accumulation remains to be proven.

TIME TRENDS IN AEROBIC FITNESS There are no widely recognised recommendations for opti- mum levels of young people’s aerobic fi tness 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 fi tness’ of children and adolescents has declined over time.31 32 There are many factors that make it diffi cult to draw confi dent conclusions regarding historical changes in aerobic fi tness during youth. First, there is a paucity of scientifi c evidence available; second, most of the available scientifi c 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 fi tness’ 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 fi tness (operationalised as mass-related peak VO2) or aerobic perfor- mance (operationalised as maximal fi eld-based endurance run- ning) of healthy (free from known disease or injury) young people aged 9–17 years. Aerobic fi tness data were available for >4002 9–17 year olds from fi ve 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 fi tness (mean change ±95% CI: –0.26 ±0.48% or –0.06 ±0.06SDs) (fi gure 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) (fi gure 3). Changes in aerobic performance, but not aerobic fi t- ness, were consistent for different sex, age and geographical groups (fi gure 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 fi t children.33–37

So why has there been little change in aerobic fi tness but large declines in aerobic performance? Unfortunately, our understanding of the reported changes in aerobic fi tness is confounded by data from different ergometers (eg, cycle,

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.

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Figure 3 Worldwide patterns of change in aerobic fi tness (dashed lines) and aerobic performance (solid lines) of 9–17 year olds over the periods 1962–1994 and 1964–2008, respectively. Data are presented separately for all children, boys, girls, 9–12 year olds, and 13–17 year olds. Data are standardised to 1990 = 100%, with higher values (>100%) indicating better fi tness or performance.

Fitness

Performance

All

Boys

Girls

9–12 years

13–17 years

Percent (1990 = 100%) 110

100

110

100

110

100

110

100

110

100

year of testing 1985 1960 2010

treadmill), and data on relatively small, volunteer samples of young people who might have been athletically inclined. Furthermore, the reported changes in mass-related peak VO2 may refl ect changes in the denominator (body mass in kg) rather than the numerator (peak VO2 in ml/min). Conversely, confi dence in the decline in aerobic performance is high, because of large representative samples, broad geographical coverage and consistent fi ndings. These changes are probably infl uenced by a network of social, behavioural, physical, bio- mechanical, and psychosocial factors as well as physiological variables.38 Causes of a decline over time in maximal aerobic performance are therefore not only a function of changes in peak VO2 but also changes in mechanical effi ciency and frac- 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, 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 also play a role. Nevertheless, changes in maximal aerobic performance – the ability to run faster, play harder and play 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 kinetic response to changes in exercise intensity or blood lac- tate accumulation during submaximal exercise.

AEROBIC FITNESS AND SPORT Peak oxygen uptake 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 swimmers51– 54 and canoeists.50 Young male athletes 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 girls and boys respectively have been regularly observed. As almost all studies report cross-sectional data it is unknown 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- 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 diffi culties of determining young people’s stroke volume during exercise mean that data should be treated with caution.55 However, the literature is consistent in reporting higher stroke volumes56 – 58 and stroke indices47 57 in trained children and adolescents compared with their untrained peers. A single prospective study has supported these fi ndings by observing signifi cant increases in both boys’ (+15%) and girls’ (+11%) stroke volumes following a 13 week endurance training programme, with no changes noted in con- trol groups.59

There are marked inconsistencies in studies exploring the underlying mechanisms of enhanced stroke volumes with

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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 Most60 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- nifi cant training-induced changes in cardiac dimensions62 63 and others reporting signifi cant 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 TLAC. No signifi cant change in the VO2 slow component was observed during exercise above the TLAC. The responses to exercise above TLAC 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 signifi cantly shorter VO2 primary component τ than the control group, thus supporting the specifi city of train- ing on VO2 kinetics. There were no signifi cant 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 signifi cantly 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 infl uenced 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 signifi cantly faster VO2 primary com- ponent τ than the control group. The authors postulated that

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 TLAC 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 specifi cally 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 fi tness on which there are suffi cient 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 identifi ed 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 signifi cant 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-signifi cant 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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10 .5

3 80

% m

ax H

R 30

m in

12 C

on tin

uo us

c yc

lin g

EB 1

.6 0

EG 1

.3 6

C B

1 .6

2 C

G 1

.5 2

1. 66

1. 54

1. 65

1. 52

3. 8

13 .2

1. 9

0. 0

46 .6

39 .3

50 .7

44 .7

47 .2

42 .4

50 .3

43 .0

1. 3

N S

7. 9

N S

− 0.

1 −

3. 8

W ill

ia m

s et

a l9

7† E 1

n =

1 3

B , 1

0. 1

y n

= 1

4 B

, 3

E 1 8

0 –

85 %

m ax

H R

E 2 m

ax sp

ri nt

E 1 2

0 m

in E 2

6 –

8 m

in 8

E 1 c

on tin

uo us

c yc

lin g

E 1 1

.8 0

E 2 1

.8 4

C 1.

1. 93

1. 91

1. 97

7. 2

3. 8

2. 6

54 .7

54 .8

56 .4

57 .5

56 .2

56 .7

5. 1

N S

2. 6

N S

0. 5

E 2 n

= 1

2 B

, 1 0.

1 y

10 .1

y E 2

in te

rv al

r un

ni ng

M an

di go

et a

l9 8†

n =

1 8

B , 1

0. 7

y n

= 1

7 G

, 1 0.

5 y

n =

2 8

B ,

10 .5

y n

= 2

2 G

, 10

.5 y

3 75

– 8

0% m

ax H

co nt

in uo

us 90

% m

H R

in te

rv al

15 –

2 0

m in

nt in

uo us

60 –

9 0

m in

in te

rv al

13 C

on tin

uo us

a nd

te rv

al r

un ni

ng ae

ro bi

c ac

ti vi

tie s

EB 1

.7 0

EG 1

.3 0

C B

1 .6

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G 1

.4 0

1. 84

1. 57

1. 70

1. 50

8. 2

20 .7

6. 2

7. 4

47 .2

38 .6

46 .1

39 .6

49 .2

41 .9

45 .5

39 .5

4. 2*

8. 5*

− 1.

3 0.

2 B

aq ue

t et

a l9

9† n

= 1

3 B

n =

2 0

G 9.

5 y

n =

1 0

B n

= 1

0 G

9. 9

2 80

– 9

5 %

m ax

H R

30 m

in 7

In te

rv al

r un

ni ng

E 1.

54 C

1. 62

1. 68

1. 62

9. 1

0. 0

43 .9

46 .2

47 .5

45 .3

8. 2*

− 1.

O be

et a

l5 9

n =

9 B

, 1 0.

5 y

n =

1 0

G , 1

0. 4

y n

= 9

B ,

10 .7

y n

= 7

G ,

10 .7

3 80

% m

ax H

co nt

in ou

s 90

% m

H R

in te

rv al

60 m

in 13

C on

tin uo

us a

in te

rv al

r un

ni ng

EB –

EG –

C B

– C

G –

– – – –

44 .1

40 .9

51 .5

42 .4

50 .9

44 .2

50 .3

42 .6

15 .4

* 8.

1* −

2. 3

0. 5

M cM

an us

a l10

0 E 1

n =

1 0

B , 1

0. 4y

E 2 n

= 1

0 B

, 1 0.

4 y

n =

1 5

B 10

.5 y

3 E 1

8 5%

m ax

H R

E2 m

ax s

pr in

ts 20

m in

8 w

ee ks

E 1 c

on tin

uo us

c yc

lin g

E 2 in

te rv

al c

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g E 1

1 .6

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6 C

1. 59

1. 72

1. 96

1. 57

4. 2

11 .4

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45 .5

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45 .4

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11 .4

* −

0. 2

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S tu

P ar

ti ci

pa nt

s Tr

ai ni

ng p

ro to

co l

P ea

k V

O 2

(l /m

in )

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k V

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(m l/

kg /m

in )

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ri m

en ta

l (E

) C

on tr

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Fr eq

ue nc

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Ty pe

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e %

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e %

G am

el in

et a

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n =

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3 10

0 –

12 0%

o f M

A V

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% m

ax H

R) 30

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7 In

te rv

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8* −

2. 4

O be

et a

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n =

2 5

14 B

G , 9

-1 1

n =

2 5

13 B

12 G

, 9 -1

1 y

3 10

0– 13

0% o

f M A

V 25

– 30

m in

8 In

te rv

al r

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tt e

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na b7

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ou ps

n =

9 B

in e

ac h,

12 .5

n =

9 B

, 12

.5 y

3 E 1

H R

a t 1

70 –

1 80

at s/

m in

E 2 H

R a

t 1 50

– 1

be at

s/ m

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12 m

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1. 90

1. 80

1. 90

15 .0

5. 6

5. 9

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46 .7

47 .4

46 .6

45 .7

51 .8

48 .0

48 .2

44 .2

10 .8

* 1.

3 N

S 3.

4 N

S −

3. 3

S te

w ar

t an

d G

ut in

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n =

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B ,

10 –

1 2

y n

= 1

1 B

, 10

– 1

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4 90

% o

f m ax

H R

14 –

2 1

m in

8 In

te rv

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1 0

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G ,

15 .6

y 5

70 %

o f m

ax H

co nt

in uo

us 90

% o

f m ax

H R

te rv

S ta

rt ed

a t

9. 7

km /w

ee k

up t

o 32

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m /w

ee k

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on a

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nt in

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2. 8

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s/ m

in 20

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8 G

, 13

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3 75

– 85

% m

ax H

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m in

20 Tr

ea dm

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t s ig

ni fi c

an tly

d if

fe re

nt fr

om p

re tr

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(p ≥

0 .0

5) .

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re nt

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tr ai

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≤ 0.

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ur it

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ed fr

om t

ab le

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ng a

nd B

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A T,

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on tr

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xe rc

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, g ir

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R , h

ea rt

r at

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A V,

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C on

tin ue

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with a 2–5% increase in VO2 max and concluded that, ‘no clear relation can be proved between PA and VO2 max in free living males and females’ (p. 163).87 Other studies have failed to observe a meaningful relationship between children’s HPA and blood lactate indices of aerobic fi tness.88 89 HPA has not been investigated in relation to VO2 kinetics.

CONCLUSIONS Peak VO2 during childhood and adolescence is well- documented but other aspects of aerobic fi tness during youth are less well-understood. There is no compelling evidence

to suggest that low levels of peak VO2 are common and data indicate that youth peak VO2 has remained stable over sev- eral decades. However, young people’s maximal aerobic per- formance involving the transport of body mass is important for health and well-being and successful sport participation 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 submaximal exercise than their untrained peers. Suffi cient dose-response data are available to design exercise training programmes to improve the peak VO2 of both trained and 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 non-existent. Young people rarely experience HPA of suffi cient intensity and duration to enhance peak VO2 and there appears to be no meaningful relationship between peak VO2 and HPA. More research focusing on the mechanisms driving exercise- induced changes in aspects of aerobic fi tness during growth and maturation is needed.

Competing interests None.

Provenance and peer review Not commissioned; externally peer reviewed.

Table 2 Exercise prescription for improvement of peak oxygen uptake

Mode Mixture of continuous and interval training using large muscle groups

Frequency Minimum 3–4 sessions per week Duration 40–60 min Intensity 85–90% of maximum heart rate Programme length Minimum length of 12 weeks

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 Czechoslovakia

1 day heart rate monitoring; questionnaire interview

Cycle ergometer No signifi cant relationships

Saris83 Approx 400 girls, 400 boys; aged 6–10 years The Netherlands

1 day heart rate monitoring; questionnaire

Treadmill No signifi cant relationship between peak VO2 in any of the age groups when TDEE was used as an index for daily physical activity

Andersen et al84 21 girls, 27 boys; aged 13–18 years The Netherlands

1 day accelerometry; questionnaire

Cycle ergometer No signifi cant relationships

Sunnegardh and Bratteby85

49 girls, 52 boys; aged 8–13 years Sweden

1 day accelerometry; questionnaire

Cycle ergometer No signifi cant relationships between accelerometry data and peak VO2. Signifi cant 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; aged 11–16 years England

3 day heart rate monitoring Cycle ergometer or treadmill

No signifi cant relationships. Non-signifi cant correlation coeffi cients ranged from r=0.01 to –0.26

Armstrong et al110 43 girls, 86 boys; aged 10–11 years England

3 day heart rate monitoring Treadmill No signifi cant relationships. Non-signifi cant correlation coeffi cients ranged from r=–0.15 to 0.09

Armstrong et al111 63 girls, 60 boys; aged 12.2 years England

3 day heart rate monitoring Treadmill No signifi cant relationships. Non-signifi cant cor- relation coeffi cients ranged from r=0.13 to 0.16 in boys and from r=–0.02 to 0.04 in girls

Ekelund et al112 40 girls, 42 boys; aged 14–15 years Sweden

3 day heart rate monitoring Treadmill No signifi cant relationships between MVPA and peak VO2. AEE signifi cantly correlated with peak VO2 in both girls and boys but after controlling for body fat and maturity level the relationship in boys was non-signifi cant

Eiberg et al113 309 boys, 283 girls; aged 6–7 years Denmark

3 day accelerometry Treadmill Sustained periods of PA explained 9% of the variance in peak VO2 When children with the 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; aged 8-11 years Sweden

3–4 day accelerometry Cycle ergometer MPA was not signifi cantly correlated with peak VO2. VPA and MDPA were signifi cantly but 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

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