Aerobic fitness:

Aerobic ftness may be defined as the ability to deliver oxygen to the muscles and to utilize it to generate energy to support muscle activ-ity during exercise. Aerobic fitness therefore depends upon the pul-monary, cardiovascular, and haematological components of oxygen delivery and the oxidative mechanisms of exercising muscles.Maximal oxygen uptake (VO2 max), the highest rate at whichoxygen can be consumed by the muscles during an exercise test to exhaustion, is widely recognized as the best single measure of aerobic ftness. However, only a minority of children satisfy the classical VO2 plateau criterion for achieving VO2 max in a sin-gle exercise test, and it has become conventional to use the term peak VO2 when discussing young people’s aerobic ftness. 
The dis-tinction between VO2 max and peak VO2 will be clarified in theMethodological issues section and thereafter the term peak VO2 will be adopted when referring to children or adolescents. In the meantime, the conventional term VO2 max will be used unless the  research cited specifically refers to peak VO2.Maximal VO2 limits the capacity to perform aerobic exercisebut it does not define all aspects of aerobic ftness.
The ability to sustain submaximal exercise is aptly represented by blood lactate accumulation, which also provides a sensitive means of evaluating improvements in muscle oxidative capacity with exercise training, often in the absence of changes in VO2 max. However, in every-day life young people’s spontaneous play and participation in sport are more concerned with short duration, intermittent exercise, and rapid changes in exercise intensity. Under these conditions  VO2 max and blood lactate accumulation might be considered variables of investigative convenience rather than factors underpin-ning exercise behaviour, and it is the kinetics of pulmonary VO2(pVO2) which best describe this aspect of aerobic fitness.
To provide an appropriate framework for subsequent discussion of aerobic fitness initially the concepts of VO2 max, blood lactateaccumulation, and pVO2 kinetics will be introduced. Thereafter the focus will be on aerobic fitness in relation to chronological age, body size, biological maturity, and sexual dimorphism. It is recog-nized that aerobic fitness has a genetic component, with the herit-ability of VO2 max estimated to be ~50%,1 but genetics are outsidethe scope of this chapter and the topic is addressed. The following terms are used throughout the chapter: ‘prepu-bertal children’ when prepuberty is confirmed in the research cited; ‘children’ to represent those 12 years and younger but with-out proof of pubertal status; ‘adolescents’ to refer to 13- to 18- year- olds; and ‘youth’ or ‘young people’ to describe both children and adolescents.

Measures of aerobic fitness Maximal oxygen uptake

The seminal work of Hill and Lupton2 in the 1920s gave rise to the concept of VO2 max in humans. They were, of course, constrainedby the available technology and for context their experimental pro-tocol is worth describing in their own words,In determining the rate of oxygen intake during running at various speeds, the subject ran with a constant measured velocity around a grass track carrying a Douglas bag, and breathing through mouthpiece and valves, the tap being turned to allow the expired air to escape into the atmosphere. 
After continuing this for a time known to be suficient for the oxygen intake to attain a steady value, the tap was turned for a measured interval (usually about 1 min) to allow a sample of expired air to be collected in the bag, the running being continued at the same speed. After the interval, the running ceased, and the measurement and analysis of the expired air were carried out in the usual manner. Experiments were made at a variety of speeds and on several subjects (which amply confirm one another).
Their observations revealed a near- linear relationship and even-tual plateau between pVO2 and running speed during discontinu-ous, incremental exercise (but see the section on Methodological issues). Hill and Lupton’s findings evolved into the development of a range of laboratory protocols designed to investigate the pVO2response to incremental exercise, based on the concept of VO2 max being achieved when a levelling- off or plateau in pVO2 emerged. 
By the late 1930s boys were participating in labo-ratory determinations of VO2 max.The first laboratory- based investigations of boys’ VO2 max were carried out by Robinson3 and Morse et al.4 in the US, on either side of the Second World War. They determined 6-  to 18- year- old boys’ VO2 max using a treadmill protocol involving a 15 min walk at 3.5 miles · h–1 up an 8.6% gradient, followed by a 10 min rest, and a run to exhaustion at a speed of 6 or 7 miles · h–1 up an 8.6% gradient. 
Åstrand’s5 doctoral thesis, published in Scandinavia in 1952, was the first study to report the VO2 max of both girls andboys, aged 4–18 years. e three studies reported VO2 max inratio with body mass (mL · kg–1 · min–1) but Åstrand insightfully expressed reservations about whether this approach was appro-priate with children (see the section on Peak oxygen uptake and body size).Åstrand5 criticized the Robinson3 and Morse et al.4 methodol-ogy as ‘certainly practical from the investigator’s point of view but hardly so from that of the subject, especially if he is 6– 10 years o l d ’. 5 He commented that on the basis of the exercise protocol and the post- exercise blood lactate accumulation, ‘the work in sev-eral cases must have been submaximal’,5(p110), a point conceded by Morse et al.,4 who observed that, ‘undoubtedly all of the boys did not push themselves to the same state of exhaustion, and some had not reached the limit of their capacity in 5 min of running at 7 m.p.h.’
In his studies Åstrand used a discontinuous, incremental protocol in which the first session was carried out on a horizontal treadmill running at 7–8 km · h–1. He described subsequent sessions as follows: ‘after a couple of days the experiment was repeated with a higher speed of 1– 2  km · h–1 etc. until the intensity was reached which exhausted the subject in 4–6 min. The determinations for each subject were spread over a period of 3 weeks or more’. The vast major-ity of subsequent investigations of young people’s VO2 max fol-lowed Åstrand’s lead and adopted either a discontinuous or (more recently) a continuous, incremental exercise protocol to voluntary exhaustion.

Oxygen uptake response to incremental exercise

Incremental exercise to VO2 max requires the cardiopulmonary oxygen delivery and muscle oxygen utilization mechanisms to accommodate the rising metabolic demands. Interested readers are invited to peruse for a comprehensive review of pul-monary function during exercise for an insightful analysis of cardiovascular function during exercise, but the main points can be summarized as follows.Pulmonary ventilation (VE) increases in accord with exercise inten-sity, but it is primarily driven by carbon dioxide (CO2) production and the need to minimize metabolic acidosis. 
Pulmonary ventilation is therefore only matched with exercise intensity and pVO2 until the ventilatory threshold (TVENT) is reached. The TVENT is dened as the point during incremental exercise at which VE begins to increase out of proportion to the increase in pVO2. Beyond the TVENT the bicarbonate buffering of hydrogen ions accompanying lactic acid dissociation to lactate causes CO2 and therefore VE to rise faster than  pVO2. As VO2 max is approached, a further reduction in blood pH causes VE to compensate (ventilatory compensation point) by increasing at a disproportionately higher rate than carbon dioxide expired (VCO2).The general pattern of the VE response to progressive exercise is similar in children and adults, but there are clear age and maturity differences in the quantitative and relative responses of VE. 
Data on sex differences in the pulmonary response to exercise are equivocal.Children have a higher ratio of respiratory frequency (fR) to tidal volume than adults and during maximal exercise a fR > 60 breaths · min–1 is not uncommon compared with ~40 breaths · min–1  in adults. Children display a higher VE and therefore a less effcient response to a given metabolic demand than adults, which suggests that there is some maturation of the ventilation control mecha-nisms during childhood and adolescence. However, gas exchange in the alveoli is determined by alveolar, rather than pulmonary, ventilation and young people’s alveolar ventilation is more than adequate to optimize gas exchange. 
Although at VO2 max the ven-tilatory equivalent (VE/VO2) is generally lower in adults than in children, VE at VO2 max seldom exceeds ~70% of maximal vol-untary ventilation. With healthy children and adolescents, VE does not normally limit VO2 max. Oxygen delivery in the blood and subsequent uptake by the mus-cles is conventionally described by the Fick equation, where pVO2  is the product of cardiac output (Q) and arteriovenous oxygen dif-ference  (a- vO2 di), where Q is the product of heart rate (HR) and stroke volume (SV). 
Ethical and methodological issues related to the determination of Q, SV, and a- vO2 di during exercise have clouded the interpretation of cardiovascular data, but the introduc-tion of technologies such as Doppler echocardiography, thoracic bioimpedance, and near- infra red spectroscopy (NIRS) has clari-ed responses to incremental exercise.Heart rate rises in a near- linear manner before tapering prior to reaching HR max. Maximal HR is independent of age during youth and typical mean values at VO2 max on a treadmill and a cycle ergometer are ~200 and ~195 beats · min–1, respectively.
In the upright position untrained young people’s SV rises progres-sively with incremental exercise to values ~30– 40% higher than resting but at ~50% of VO2 max SV plateaus and remains stable to the end of the test. In contrast, trained young people’s SV has been reported to increase progressively to exhaustion. Stroke volume and Q are normally expressed in relation to body surface area, as the stroke or cardiac index respectively. Prepubertal boys’ peak cardiac index has been reported to be ~10% higher than that of prepubertal girls, but in both sexes values appear to remain stable from ~10 years of age into young adulthood.
Investigations of a- vO2 di during youth are sparse but a- vO2 di has been observed to increase with incremental exercise before plateauing at near- maximal exercise in both children and adults, with adults having a greater maximum a- vO2 di than children. Data are equivocal, but at least one study has reported prepubertal boys to have a significantly higher maximum a- vO2 di than pre-pubertal girls. 

Blood lactate accumulation

At rest, lactate is continuously produced in skeletal muscles, but with the onset of exercise there is an increased production and accumulation of lactate in the muscles. Muscle lactate accumula-tion is a dynamic process where active muscle fibres produce lactate and adjacent fibres simultaneously consume it as an energy source. 
Some of the lactate discuses into the blood where it can be sampled and assayed to provide an estimate of the anaerobic contribution to exercise and therefore an indication of submaximal aerobic fit-ness. Lactate is, however, continuously removed from the blood by oxidation in the heart or skeletal muscles or through conversion to glucose in the liver or kidneys. Blood lactate accumulation must therefore be interpreted cautiously as lactate sampled in the blood cannot be assumed to reflect a consistent or direct relationship with muscle lactate production.Hill and Lupton2 described the production of lactate in humans in relation to the ‘limit of muscular exertion’, but much of the subse-quent research concerned the interpretation of blood lactate accu-mulation during submaximal exercise and was initially published in the post- Second World War German literature. 
The hypothesis of an ‘anaerobic threshold’ to describe blood lactate accumulation during progressive exercise was popularized in the 1970s, but more recent research has both challenged and defended the threshold hypothesis. Current thought on lactate thresholds in adults can be found in the work of Wassermann and his colleagues.

Blood lactate accumulation during incremental exercise

During an incremental exercise test to exhaustion blood lactate accumulation typically increases. The onset of the test stimulates minimal change in blood lactate accu-mulation, which often does not significantly rise above resting values. It is not unusual for blood lactate accumulation to initially increase and then fall back to near resting values due to the inter-play between type I and type II muscle fibre recruitment. 
However, as the exercise progresses blood lactate accumulation gradually increases until an infection point is reached where lactate begins to accumulate rapidly. The blood lactate accumulation infection point is defined as the lactate threshold (TLAC), which serves as a useful estimate of submaximal aerobic fitness. The highest exercise intensity which can be sustained without incurring a progressive increase in blood lactate accumulation is termed the maximal lactate steady state (MLSS). It corresponds to the highest point at which the discusion of lactate into the blood and removal from the blood are in equilibrium.
Exercise can be sus-tained for prolonged periods at or below the MLSS, and it therefore has the potential to provide an indicator of aerobic tness, but for methodological reasons secure data from children and adolescents are not currently available. To avoid taking multiple blood samples from young people, non- invasive alternatives to blood lactate reference values have become the preferred option in many paediatric exercise science laborato-ries. Robust methods have been developed to determine and evalu-ate the TVENT18 (or V- slope19) and the critical power (CPo)20 of children. 
The V- slope, which is often the preferred method of esti-mating a threshold, is determined using linear regression to detect the point at which VCO2 begins to rise at a more rapid rate than pVO2, and is independent of the VE response. Critical power is defined as the power asymptote of the theoretical hyperbolic rela-tionship between muscle power output and the time to exhaustion. The TVENT (or V- slope) and CPo are often used to replace TLAC and MLSS respectively, for example, in defining exercise domains and monitoring training programmes.
Peak blood lactate accumulation following an exercise test to exhaustion has been used routinely to estimate whether a young person has given a maximal efort. Some authors have advocated the use of specific values of post- exercise blood lactate accumula-tion (e.g. 6 to 9 mmolL1⋅−) to confirm maximal eforts during tests to determine peak VO2. There  is, however, considerable vari-ability in young people’s blood lactate accumulation. Post- exercise values of blood lactate accumulation at peak VO2 of untrained 11- to 13- year- olds have been observed to range from 4 to 13 mmolL1⋅−, using the same exercise protocol, blood sampling, and assay techniques. Post-exercise blood lactate accumulation is dependent on mode of exercise, protocol employed and timing of the post- exercise blood sample relative to the cessation of the exercise. The recommendation of a spe-cific minimum post- exercise blood lactate accumulation to validate peak VO2 as a maximal efort during youth is therefore untenable.

Pulmonary oxygen uptake kinetics

A high VO2 max and/ or the ability to sustain submaximal exercise are prerequisites of elite performance in some sports, but exer-cise of the intensity and duration required to elicit VO2 max or to sustain performance at the TLAC or MLSS is rarely experienced by most young people. The outcome is that there is no mean-ingful relationship between daily (or habitual) physical activity during youth and either VO2 max or blood lactate indices of aerobic fitness.
The vast majority of young people’s daily phys-ical activity is intermittent and consists of periods of rest inter-spersed with physical activity of short duration. Furthermore, in many sports the ability to engage in rapid changes in exercise intensity is at least as important as VO2 max or TLAC. Under these circumstances, it is the kinetics of pVO2 which best reflect the eective integrated response of the pulmonary, circulatory, and muscular systems.The introduction of breath- by- breath respiratory gas exchange technology in the late 1960s enabled innovative scientists, includ-ing Margaria, Wasserman, and Whipp, to map out the kinetic response of pVO2 following the onset of exercise. 
Critical reviews of the assessment and interpretation of the respiratory gas kinetics of both adults30 and youth are available elsewhere. The following paragraphs summarize current understanding of the phenomenon.Kinetics of the pulmonary oxygen uptake response at exercise onset the pVO2 response to a step change from rest (experimentally usu-ally from unloaded pedalling on a cycle ergometer) to moderate- intensity exercise (i.e. exercise intensity below the TLAC or TVENT) is characterized by three phases.  
Phase I (the cardiodynamic phase), which lasts ~15– 20 s in young people, is associated with an increase in Q which occurs prior to the arrival at the lungs of venous blood from the exercising muscles and is therefore independent of muscle VO2 (mVO2). Phase I is followed by an exponential increase in pVO2 (phase II)  that drives pVO2 to a steady state (phase III) within ~2 min. Phase II  (the primary component) is described by its time constant (τ), which is the time taken to achieve 63% of the change in pVO2. 
The shorter the primary component τ, the smaller the oxygen de-cit and the anaerobic contribution to the energy required for the change in exercise intensity.In contrast to the pVO2 response at the onset of moderate- inten-sity exercise, a step change from rest to heavy- intensity exercise (i.e. exercise intensity above the TLAC or TVENT, but below CPo or the MLSS) elicits a phase III, where the oxygen cost increases over time as a slow component of pVO2 is superimposed and the achieve-ment of a steady state is delayed by ~10 min in children32 and 10– 15 min in adults.
 Although largely ignored in the physiology literature for over 60 years, initial indications of the presence of a pVO2 slow com-ponent lie in the 1913 data of Krogh and Lindhard.33 Ten years later, Hill and Lupton2 observed what was probably a pVO2 slow component in a subject running at constant speed, but reported that, ‘the gradual rise in oxygen consumption is probably to be attributed to a painful blister on the foot causing ineficient movement’. It required the advent of data from more sophis-ticated breath- by- breath technology before Gaesser and Poole34 were able to provide an insightful clarification of the sources of the  pVO2 slow component. The mechanisms still remain speculative, but compelling arguments suggest that ~85% of the pVO2 slow component originates from the exercising muscles, perhaps largely due to a change in muscle fibre recruitment as exercise progresses. 
In prepubertal children32 and adolescents35 neither the primary component τ nor the pVO2 slow component are significantly related to peak VO2. The very heavy- intensity exercise domain encompasses exercise intensities lying between the MLSS (or CPo) and VO2 max. In this domain a pVO2 steady state is not achieved and in adults the pVO2 slow component rises with time and projects to VO2 max. The higher the work rate is above CPo the faster the projection of the pVO2 slow component to VO2 max.
This phenomenon has not to date been reported in children where it has been observed that pVO2 projects progressively towards peak VO2 but stabilizes at ~85– 90% of peak VO2. The severe- intensity exercise domain describes step changes in exercise intensity in which the primary component of pVO2 is pre-dicted to project to or above VO2 max and the maximal rate of pVO2 is achieved within 2–3 min of exercise onset. In the severe- intensity exercise domain a pVO2 slow component is not discern-ible from the primary component, but it is unclear whether this is due to the prominence of the primary component of pVO2 or insuficient time for a pVO2 slow component to be expressed.
It has been suggested that as there is a large slow phase in recovery from exercise in this domain it is likely that a pVO2 slow component also exists during the onset of exercise. An alternative classification scheme of pVO2 kinetics defines all exercise intensities that achieve VO2 max to reside within the severe domain irrespective of whether pVO2 projects to VO2 max through the primary component or via the pVO2 slow component. In this schema there exists a domain termed extreme intensity in which the exercise intensity is so great that fatigue intervenes before VO2 max can be attained.
Peak oxygen uptakeMaximal (and later peak) VO2 has been the criterion measure of young people’s aerobic fitness since the pioneering studies of Robinson, Morse etc al. and Åstrand, yet the assessment and interpretation of VO2 max or (peak VO2) during growth and mat-uration remain shrouded in controversy. This section identifes pertinent methodological issues in the determination of peak VO2, clarifies the distinction between VO2 max and peak VO2, discusses the increase in peak VO2 with chronological age, challenges the conventional interpretation of peak VO2 in relation to body size; demonstrates the independent contribution of biological maturity to peak VO2; and addresses sexual dimorphism in peak VO2.

Methodological issues Maximal or peak oxygen uptake?

Classically, VO2 max was determined in a laboratory using a dis-continuous, incremental exercise test to exhaustion on a treadmill or cycle ergometer. Typically, the participant exercised at a predeter-mined, submaximal intensity for about 3– 5 min to obtain a steady state pVO2 and then rested for ~60 s (in some cases submaximal stages were carried out on diferent days) before completing a more intense exercise stage. This protocol continued until a stage beyond which a pVO2 plateau was reached. The additional energy required to exercise above the point where the pVO2 plateau occurred was assumed to be provided exclusively by anaerobic metabolism, resulting in an intracellular accumulation of lactate, acidosis, and eventual termination of exercise. 
In practice a genuine plateau in pVO2 with increasing exercise intensity seldom occurred and less stringent criteria for establishing the existence of a plateau were developed. In order to increase confidence that a true VO2 max  had been achieved, subsidiary criteria related to HR, respiratory exchange ratio (i.e. VCO2/ pVO2; R), and blood lactate accumula-tion at the termination of the VO2 max test were introduced. The VO2 plateau concept has retained primacy in the literature as the principal criterion for establishing VO2 max, but the validity of the classical model has been a topic of lively debate for several years.
The practice of reporting submaximal pVO2 steady states or describing exercise intensities as % VO2 max in the heavy-  and very heavy- exercise intensity domains has fallen into disrepute with evidence of a pVO2 slow component emerging at exercise intensities above the TLAC in adults,30 adolescents,35 and prepuber-tal children.Åstrand’s5 studies revealed that a pVO2 plateau was found in ‘70 of 140 running experiments with school children’. It was subsequently argued by some authors that the failure of some chil-dren to elicit a pVO2 plateau was related to low motivation or low anaerobic capacity.
But others demonstrated that with both pre-pubertal children42 and adolescents43 those who exhibited a pVO2 plateau at the termination of an incremental exercise test to volun-tary exhaustion were indistinguishable in terms of HR, R, or blood lactate accumulation at test termination from those who did not. This raised the question of whether a pVO2 plateau was required to indicate a maximal index of aerobic fitness during youth. The problem was addressed experimentally by determining the peak VO2 of 20 boys and 20 girls, mean age 9.9 years, on three occasions, 1 week apart. On the first occasion, the children com-pleted a discontinuous, incremental protocol on a treadmill with the belt speed held at 1.94 m · s–1 but with the gradient increasing every 3 min. 
The children exercised until voluntary exhaustion. Using a <2 mL · kg–1 · min–1 increase in pVO2 as the criterion, six boys and seven girls exhibited a pVO2 plateau. No significant dif-ferences in either anthropometrical or peak physiological data were revealed between those who did and did not exhibit pVO2 plateaus. The second and third tests were performed at the same belt speed as test one (i.e. 1.94 m · s–1) but, following a 3 min warm- up running at  1.67  m · s–1, the children ran up gradients which were 2.5% and 5% greater, respectively, than the highest gradient achieved on the first test. 
The children were strongly motivated and the data were accepted if the child ran for at least 2 min up the higher gradient. Eighteen girls and 17 boys completed all tests and although they exhibited significantly higher post- exercise blood lactate accumu-lation, peak VE, and peak R in tests two and three than in the initial test, there were no significant diferences in peak VO2 across the three tests. These data and those from a similar study45 imply that with well- motivated children ‘true’ VO2 max values can be achieved in a single, incremental test to exhaustion despite the majority of participants not demonstrating a pVO2 plateau. 
There is, however, no easy solu-tion to the problem of whether an individual child has delivered a maximal efort in an incremental test to exhaustion. Habituation to the laboratory environment, subjective criteria of intense efort (e.g. facial pushing, sweating, hyperpnoea, unsteady gait), and the paediatric exercise testing experience of the experimenters are vital ingredients in making this decision. Various other physiological indicators of a maximal efort such as HR and R at peak VO2 and peak post- exercise blood lactate accumulation have been proposed as subsidiary criteria, they are all protocol dependent. 
Furthermore, there is no ‘one size ts all’ criterion of a maximal efort. For example, at the termination of an incremental treadmill exercise test HR at peak VO2 has a mean  ±  standard deviation of ~200 ± 7 beats · min– 1, in the age range 8–16 years.8 As ~95% of young people’s HRs at peak VO2 would therefore be expected to fall in the range 186– 214 beats · min–1 it is futile to interpret a spot HR of, for example, 195 or 200 beats · min–1 as is commonly advocated, as reflecting maxi-mal efort. As the term VO2 max conventionally requires a pVO2 plateau to be exhibited, it has become common practise in paediatric exercise science to define the highest pVO2 observed during a progressive exercise test to exhaustion as peak VO2 rather than VO2max.

Respiratory gas analysis

The determination of peak VO2 depends upon the accurate meas-urement of inspired and/ or expired air per unit of time and the fraction of oxygen and carbon dioxide therein. Automated respira-tory gas analysis systems and sophisticated metabolic carts with appropriate calibration facilities are commercially available and commonplace in research laboratories. Paediatric physiologists must, however, be cautious of measuring children’s respiratory responses to exercise using apparatus primarily designed for use with adults.
Most respiratory gas analysis systems measure volume using a breathing valve (normally a lightweight turbine or pneumotacho-graph) connected to the participant via a mouthpiece and nose clip or facemask. With children it is imperative that the mouthpiece and nose clip or facemask is comfortable and appropriately sized to prevent leakage. To prevent the signicant inspiration of previously expired air the combined dead space of the mouthpiece/ facemask and breathing valve should be minimized, although this must be balanced against the resulting increase in resistance tomorrow.
To periodically sample respiratory gases metabolic carts nor-mally use either a mixing chamber, which stores expiratory gases over a given interval, or a breath- by- breath system. Large mixing chambers may cause substantial measurement errors as children have smaller exercise tidal volumes than adults. Breath- by- breath systems with rapid gas analysers allow continuous measurement of volume and respiratory gas content and overcome the potential size limitations of mixing chambers. However, breath- by- breath systems are challenged by the large inter- breath variations of exer-cising children in relation to their pVO2 response amplitude (i.e. high  noise- to- signal  ratio).
In addition, the breath- by- breath gas sampling interval can have a significant impact on the reported pVO2. Short sampling intervals increase the variability in measuring pVO2 and with their smaller peak VO2 this is more marked in children than in adults. However, large sample intervals may ‘over- smooth’ the data and artificially reduce the ‘true’ VO2 response. A  sampling interval of ~15– 30 s is optimum for children and adolescents, but whatever the chosen interval it should be recorded and reported to allow cross- study comparisons.

Ergometry

Young people’s peak VO2 has been determined using a wide range of ergometers, and although it is important to simulate competitive performance when testing and monitoring young athletes, cycles and treadmills remain the ergometers of choice in most paediatric exercise science laboratories.Cycle ergometry provides a portable, relatively cheap, and more quantitable mode of exercise than treadmill running and it tends to induce less anxiety in young children. 
Cycle ergom-eter crank lengths may need to be modified for young children who sometimes experience dificulty with the need to maintain a fixed pedal rate when cycling on mechanically braked ergometers. Electronically braked cycle ergometers which adjust resistance to pedalling frequency alleviate this dificulty to some extent, but the increase in resistance required to maintain exercise intensity fol-lowing a reduction in pedal rate may in itself cause problems with young children.
Limited upper body movement during cycle ergometry facilitates the measurement of ancillary variables such as HR, blood pressure, and blood lactate accumulation. However, a disadvantage of cycle ergometry with young children is that a high proportion of the total power output is developed by the quadriceps muscles and the efort required to push the pedals during the later stages of an incre-mental test may be high in relation to children’s muscle strength. This leads to blood row through the quadriceps being restricted and results in increased anaerobic metabolism and consequent ter-mination of the test through peripheral muscle fatigue. Treadmill running engages a larger muscle mass than cycling. 
The increased venous return and reduced peripheral resistance during running enhances Q, and peak VO2 is more likely to be lim-ited by central than peripheral factors. Peak VO2 is typically about 8–10% higher during treadmill running than cycle ergometry, although some adolescents have been reported to achieve higher peak VO2 on a cycle ergometer. Pearson product- moment correla-tions between peak VO2 rigorously determined on a treadmill and a cycle ergometer are ~0.90.

Exercise protocols

Peak VO2 during youth is a robust variable which, on a specific ergometer, is normally independent of exercise protocol with a coeincient of variation in repeated tests of ~5% on both treadmill and cycle ergometer. Incremental, continuous, or discontinuous protocols on a treadmill have traditionally been the exercise tests of choice in paediatric exercise research laboratories. However, with clear experimental evidence that children and adolescents exhibit a pVO2 slow component during exercise above the TLAC, the avail-ability of commercial breath- by- breath metabolic carts, and the development of electromagnetically braked cycle ergometers, ramp protocols have become popular. 
In many paediatric exer-cise science laboratories ramp cycle tests, where power output is increased linearly with time, have replaced classical, discontinu-ous, ‘steady state’, incremental protocols. Ramp protocols have the advantages of exibility of rate and magnitude of power output, short test duration (~10 min), and the ability to determine other parameters of cardiopulmonary function (e.g. V- slope) during a single test.In a single ramp test to exhaustion a pVO2 plateau is an infre-quent occurrence. However, a study of 10-  and 11- year- old children, across three ramp tests each 1 week apart, reported a typical error in peak VO2 of ~4%, which compares favourably with the reliability of adults’ VO2 max, regardless of protocol.
A short duration ramp test coupled with children’s ability to recover quickly from exhaustive exercise57 allows the use of a follow- up supramaximal test to verify whether a maximal efort was elicited in the initial test. The following protocol has been found to be appropriate for chil-dren: After a 3 min period of cycling at 10 W, participants under-take a ramp incremental test to exhaustion with power output increasing by 10 W · min–1. Cycling cadence is maintained at 75 revs · min–1 throughout the test and exhaustion is defined as a drop in pedal cadence below 60 revs · min–1 for 5 consecutive sec-onds. 
Immediately after exhaustion, power output is reduced to 10 W and the child cycles at this intensity for 10 min followed by 5 min of rest. The participant then performs a supramaximal test consist-ing of 2 min pedalling at 10 W, followed by a step transition to 105% of the peak power achieved during the ramp test. The pedalling cadence is maintained at 75 revs · min–1 with the same criterion as in the initial test to define exhaustion. The power output is then returned to 10 W until the HR has recovered to ~120 beats · min–1. With prepubertal children the time to exhaustion in the supramaxi-mal test is ~90 s. On the rare occasions (<5%) that the peak VO2 is higher than in the ramp test, the supramaximal test can be repeated at 110% of peak power following full recovery.

Peak oxygen uptake and chronological age

The peak VO2 of children and adolescents has been extensively documented with data available from children as young as 3 years of age. The validity of peak VO2 determinations in children younger than 8 years has been questioned since the original studies of Robinson. He noted that, ‘the youngest boys were unwilling to continue work after it ceased to be fun, whereas all of the boys of 8 years and older could be encouraged to carry on for some time after the first signs of fatigue’. As very young children typically have short attention spans, poor motivation, and lack suficient understanding of experimental procedures it is dificult to elicit genuine maximal eforts.
Equipment and protocols designed for adults make exercise testing with young children problematic, and the smaller the child, the greater the potential problem. Reports of peak VO2 in very young children are often dificult to interpret. Small sample sizes are common and several studies have pooled data from boys and girls. Whether the children exhibited maximal values is unclear in some reports, and there is a strong tendency to report only mass- related data (mL · kg–1 · min–1). One study suggested that it is possible with rigorous techniques to estimate the peak VO2 of most young children and reported achieving ‘maximal’ values in ~84% of 706 6-  to 7- year- olds. 
Boys were noted to have peak VO2 values (L · min–1) ~11% higher than girls, confirming the importance of not pooling boys’ and girls’ val-ues and reporting data in relation to sex, even at a young age. There are, however, few secure data from children aged less than 8 years in the literature and the focus herein will therefore be on the age group 8–18 years.A comprehensive review of the extant literature generated graphs representing ~10 000 peak VO2 determinations of untrained eight-  to 16- year- olds. Because of the ergometer dependence of peak VO2  data from treadmill and cycle ergometry were graphed separately and the treadmill- determined peak VO2 values (n = 4937). 
The data must be interpreted cautiously, as means from a range of studies with varying sample sizes are included. No information is available on randomly selected groups of young people, and since participants are generally volunteers selection bias cannot be ruled out. This type of analysis tends to smooth data, a near- linear increase in peak VO2 in relation to age. Linear regression equations indicate that peak VO2 increases by ~80% from 8 to 16 years in girls and by ~150% in boys over the same time period.
Longitudinal studies provide a more granular analysis of peak VO2 in relation to age, but few longitudinal studies have reported data from a broad age range and coupled rigorous determination of peak VO2 with substantial sample sizes. Data from rigorous longi-tudinal studies of treadmill- determined peak VO2, but between studies comparisons should be interpreted with caution.Longitudinal data from boys are consistent. The pooled data show an increase in peak VO2 of ~150%, from 8 to 18 years, with the largest annual increases occurring between 13– 15 years. It has been suggested that the greatest increase in boys’ peak VO2 accompanies the attain-ment of peak height velocity (PHV),66 but others have noted a stable increase in peak VO2 from 3 years before to 1 year after PHV.
Longitudinal data from girls are sparse and when pooled they indi-cate an increase in peak VO2 of ~98%, from 8 to 17 years. One study observed a growth spurt in peak VO2 aligned with PHV, but when data across studies are compared they suggest, on bal-ance, that girls’ peak VO2 rises progressively from 8 to 13 years and then begins to level of from ~14 years. The most comprehensive longitudinal study reported is the Amsterdam Growth and Health Longitudinal Study (AGHLS) which followed 12- to 14- year- old boys and girls for a period of 25 years. Boys demonstrated a linear increase in peak VO2 of ~57%, from age 12– 17 years. Girls’ values increased by ~11% over the same time period, with a marked levelling- off from 14– 17 years (~2% change). The Dutch data contrast with a mixed longitudi-nal study from England, which reported increases in peak  VO2, from 12– 17 years, of ~70% and ~24% for boys and girls respectively. As Dutch values at age 12 years were ~12% and ~22% higher than English values, for boys and girls respectively, the conflicting data may be at least partially explained by the initial high level of aerobic fitness of Dutch youth compared with English youth.

Peak oxygen uptake and body mass

Peak VO2 is strongly correlated with body mass and, in particular, with lean body mass (LBM). Much of the age- related increase in peak VO2 reflects the increase in mus-cle mass during the transition from childhood into young adult-hood. Because of the problems in assessing LBM, researchers have conventionally focused on controlling for body mass diferences by dividing peak VO2 by total body mass and expressing it as the sim-ple ratio mL · kg–1 · min–1 (ratio scaling). When peak VO2 is expressed in this manner a diferent picture emerges from that apparent when absolute values (L · min–1) are used. 
Cross- sectional data indicate that boys’ mass- related peak VO2 decreases slightly or remains unchanged at ~48 mL · kg–1 · min–1, from 8 to 18 years, while in girls a progressive decline, from ~45– 35 mL · kg–1 · min–1, is apparent. Boys consistently demonstrate higher mass- related  peak VO2 than girls throughout childhood and ado-lescence, with the sex diference being reinforced by the greater accumulation of body fat by girls in puberty. The AGHLS data are intriguing in this context as, in conflict with the extant literature, they indicate that from 12– 17 years boys’ peak VO2 decreases from ~59– 52 mL · kg–1 · min–1 and girls’ values fall from ~57– 45 mL · kg–1 · min–1.
Although informative in relation to the performance of, for example, track athletes who carry their body mass, the conven-tional use of ratio values has clouded the physiological understand-ing of peak VO2 during growth. Rather than removing the influence of body mass, ratio scaling ‘over scales’ and favours light individuals and penalizes heavy individuals. Tanner described the fallacy of ratio scaling in 1949 and Åstrand noted its limitations in relation to expressing children’s peak VO2 in 1952, but its use has persisted in the paediatric literature.  The interpretation of exercise performance data in relation to body size has been critically reviewed elsewhere, but the inadequacy of ratio scaling can be explained simply.To create a size- free variable in this context requires a product- moment correlation coeficient between peak VO2, expressed in mL · kg–1 · min–1, and body mass in kg, which is not significantly diferent from zero. 
Significant negative correlations between ratio scaled peak VO2 and body mass have been reported on numer-ous occasions, but data drawn from the first year of a longitudi-nal study64 of 11- to 13- year- olds illustrate the phenomenon. Significant positive correlations between peak VO2 (L · min–1) and body mass (kg). Describes the presence of significant negative correlations between ratio scaled peak VO2 (mL · kg–1 · min–1) and body mass (kg), and confirms the inability of the simple ratio to remove the influence of body mass from peak VO2. However, presents the same data and shows that correlations between allometrically scaled peak VO2 (mL · kg–0.68 · min–1) and body mass (kg) are not significantly diferent from zero. Body mass has therefore been appropriately controlled for using allometric scaling with, in this case, a common mass exponent of 0.68.
Several studies have generated data illustrating how inappropriate ratio scaling has led to misplaced interpretation of physiological vari-ables, whereas studies in which the use of more appropriate means of controlling for body size have provided new insights into peak VO2 during growth. For instance, an early exploration of scaling children’s peak VO2 used a simple linear regression model to investigate changes in peak VO2 with chronological age in two groups of boys aged 10 and 15 years. The mean values for peak VO2 were 1.73 and 3.12 L · min–1 respectively, but when ratio scaled, the two groups had identi-cal mean values of 49 mL · kg–1 · min–1. 
However, the regression lines for the relationship between peak VO2 and body mass described two clearly diferent populations. Intuitively this appears appropriate and is in accord with the observed diferences in 10-  and 15- year- olds’ performance in athletic events primarily dependent on aerobic fitness. A more sophisticated analysis avoiding the limitations of lin-ear regression scaling used both ratio and allometric (log- linear analysis of covariance) scaling to partition size effects from peak VO2 data in groups of males and females spanning the age range 11– 23 years. 
The results of the ratio analyses con-formed to the conventional interpretation with mass- related peak VO2 consistent across the three male groups (11, 14, and 23 years). In the females mass- related peak VO2 did not change from  11– 13 years, but there was a significant decrease in peak VO2 from 13– 22 years. In direct contrast, allometric scaling revealed significant, progressive increases in peak VO2 across male groups demonstrating that, with body size appropriately controlled for, peak VO2 is, in fact, increasing during growth rather than remaining static. In females, peak VO2 increased significantly from 11– 13 years, subsequently remaining constant with no decline into adulthood evident.
The application of allometry to longitudinal data is complex, but its use is increasing and evidence to support the cross- sectional analyses is accumulating. Multilevel modelling techniques repre-sent a sensitive and exible approach to the interpretation of lon-gitudinal exercise data which enable body size, chronological age, and sex effects to be partitioned concurrently within an allomet-ric framework. 
The interested reader is referred to Welsman and Armstrong, where the theoretical principles of allometry and mul-tilevel modelling are explained and applied to paediatric data sets. The independent effect of age on peak VO2 was clearly demon-strated in a longitudinal study which used multilevel regression modelling to interpret peak VO2 in 11– 13- year- old boys and girls. The analysis was founded on 590 peak VO2 determinations over three annual occasions.
Peak oxygen uptake and biological maturation
As young people grow they also mature, and the physiological responses of adolescents must be considered in relation to bio-logical maturity as well as chronological age. Some studies indicate  an adolescent growth spurt in peak VO2 in boys, with the spurt reaching a maximum gain near the time of PHV, but secure data are insuffcient to offer any generalization for girls. With stage of maturity classified using secondary sexual characteristics, more mature young people have been reported to have a higher peak VO2 in L · min–1 than those less mature, but ratio scaled peak VO2  (mL · kg–1 · min–1) has been reported to be unrelated to state of maturity, indicating no additional effect of biological maturity on peak VO2 above that due to growth.
Armstrong etc al. argued that the true relationship between peak VO2 and biological maturity may have been obscured through an inappropriate means of controlling for body mass. They deter-mined the peak VO2 of 176 12- year- olds and classified them according to the stages of pubic hair development described by Tanner. In accord with the extant literature, mass- related peak VO2 (mL · kg–1 · min–1) was not significantly diferent across stages of pubic hair development in either boys or girls. However, when body mass was controlled using allometry (log- linear analysis of covariance with mass as the covariate) peak VO2 was demon-strated to significantly increase with biological maturity in both sexes. 
None of the children were classified as in stage 5 for pubic hair development (PH5), but, with body mass controlled for, boys in PH4 exhibited peak VO2 values 14% higher than similarly aged boys in PH1. The corresponding difference in girls was 12%, thus demonstrating that in both boys and girls there is a significant independent effect of biological maturity on peak VO2 above that attributed to chronological age and body mass. Armstrong and Welsman65 introduced the same criterion of bio-logical maturity into their multilevel regression model of 11– 17- year- olds and confirmed their earlier findings on 11– 13- year- olds by showing incremental effects of stage of maturity on peak VO2 inde-pendent of chronological age and body mass.
The posi-tive effect of biological maturity on aerobic tness was consistent for both boys and girls. When skinfold thicknesses were introduced into the model, the stage of pubic hair development remained a significant covariate in all but stage PH5, but the magnitudes of the effect were reduced, indicating the relationship between stage of biological matu-rity and body composition. With body mass, skinfold thicknesses, and pubic hair development accounted for, peak VO2 was shown to increase throughout the age range studied in both sexes. The girls’ data are noteworthy as earlier longitudinal studies using conventional analyses to control for body mass suggested a decline in females’ peak VO2 from age ~14 years. The authors concluded that LBM was the predominant influence in the increase in peak VO2 through adoles-cence, but that both chronological age and stage of biological maturity were additional explanatory variables, independent of body size and fatness.

Peak oxygen uptake

Boys’ peak VO2 values are consistently higher than those of girls by late childhood and the sex difference becomes more pronounced as young people progress through adolescence.46 e data pre-sented indicate that peak VO2 is ~12% higher in boys than in girls at age 10 years, increasing to ~25% higher at 12, ~30% higher at 14, and ~35% higher at 16 years of age. Longitudinal data support this trend, although with small sample sizes there is some variation in the magnitude of sex differences, particularly within the age range 12– 14 years, which is likely to be due to individual varia-tions in the speed of biological clocks. These sex differences in peak VO2 during adolescence have been attributed to a combination of factors including differences in daily physical activity, body compo-sition, and blood haemoglobin concentration ([Hb]).Boys are generally more physically active than girls, but reviews of current physical activity patterns demonstrate that both sexes rarely experience the intensity, frequency, and duration of physical activity associated with increases in peak VO2.
Data are remarkably consist-ent and demonstrate no meaningful relationship between objectively measured daily physical activity and directly determined peak VO2 (see Armstrong etc al. for a table of relevant studies to date). There is therefore no compelling evidence to suggest that current levels of phys-ical activity are likely to contribute to sexual dimorphism in peak VO2.Muscle mass increases through childhood and adolescence, but although boys generally have more muscle mass than girls, marked sex differences do not become apparent until the adolescent growth spurt. Girls experience a growth spurt in muscle mass but it is less dramatic than that of boys. Between 5 and 16 years of age, boys’ rela-tive muscle mass increases from ~42– 54% of body mass, whereas in girls muscle mass increases from ~40– 45% of body mass between 5 and 13 years of age, and then, in relative terms, it declines due to an increase in fat accumulation during adolescence. 
Girls have slightly more body fat than boys during childhood, but during the growth spurt, girls’ body fat increases to ~25% of body mass while boys decline to ~12– 14% of body fat. These dramatic changes in body composition in adolescence contribute to the progressive increase in sex differences in peak VO2 over this period. Boys’ greater mus-cle mass not only facilitates the use of oxygen during exercise, but also supplements the venous return to the heart, and therefore aug-ments SV through the peripheral muscle pump.In adolescence there is a marked increase in [Hb] and hence oxy-gen- carrying capacity in boys, whereas girls’ values plateau in their mid- teens. 
As [Hb] is significantly correlated with peak VO2 during adolescence it would be expected that differences in [Hb] between boys and girls, which are ~11% at 16 years, would be a contributory factor to the observed sex difference in peak VO2 during the late teens.8 However, when [Hb] was investigated longitudinally as an additional explanatory variable to body mass, stature, skinfold thick-nesses, age, and pubic hair development (as an indicator of stage of maturity), in a multilevel regression model of peak VO2 a non- sig-nificant parameter estimate was obtained with 11– 17- year- olds.
Prior to the onset of puberty there are only small sex differences in muscle mass and [Hb], but even with body size controlled for, prepubertal boys have consistently been demonstrated to have higher peak VO2 than prepubertal girls. For example, in a sample of 164 (53 girls) 11- year- old prepubertal children, boys’ peak VO2 was observed to be ~22% higher than that of girls. With the removal of the influence of body mass using a log- linear adjustment model, boys’ peak VO2 remained significantly higher (~16%) than girls’ values despite there being no sex dierence in either skinfold thick-ness or [Hb]. Why prepubertal boys have significantly higher values of peak VO2 than prepubertal girls is not readily apparent, but the explana-tion might lie in the Fick equation. There is no evidence to indicate sex differences in HR max, but boys have generally been observed to have higher SV max, and therefore higher Q max, than girls, although there are conflicting data.
The trend for boys to have higher SV max during exercise has been attributed to their greater heart mass (or size) in relation to body mass (or size), but conflicting data indicating no sex dierences in relative heart size are available. Exercise SV is, however, not just a function of ven-tricular size and it is difficult to distinguish between the complex and inter- related effects of ventricular preload, myocardial contrac-tility, and ventricular aerload.Vinet et al.compared the cardiovascular responses of prepu-bertal boys and prepubertal girls using Doppler echocardiography during maximal cycle exercise. They reported no significant sex differences in a- vO2 di or HR at peak VO2, but the boys demon-strated significantly higher peak VO2 and SV max. They therefore concluded that the only component of peak VO2 that distinguished girls from boys was their lower SV max. 
The data indicated no sig-nificant sexual dimorphism in diastolic function indices or short-ening or ejection fractions. Vinet and her colleagues84 concluded that it is unlikely that overall cardiac contractility, relaxation, and compliance properties or loading conditions contribute to the sex difference in SV max, which is therefore due to differences in car-diac size rather than function.In a similar study, Rowland etc al. compared prepubertal boys and premenarcheal girls and demonstrated that SV max was the sole cardiac variable responsible for sexual dimorphism in peak VO2 these authors noted that a characteristic that distinguished girls from boys was a lower rise in SV at the onset of exercise in girls. They suggested that cardiac functional factors (skeletal mus-cle pump function, systemic vascular resistance, and adrenergic responses) rather than intrinsic le ventricular size are responsible for the sex differences in SV max during childhood. 
There are few secure data on young children’s a- vO2 di at peak VO2, but a study which used thoracic bioelectrical impedance to determine the Q at peak VO2, of  (13 girls) 10- year- olds provided some interesting insights into prepubertal differences in peak VO2.  The boys had a significantly higher mean peak VO2 than the girls (~19%) but no significant sex differences in stature, body mass, LBM, % body fat, body mass index, body surface area, [Hb], HR at peak VO2, R at peak VO2, SV at peak VO2, or Q at peak VO2 were observed.
 Furthermore, heart size variables determined at rest using magnetic resonance imaging (MRI) revealed no significant sex differences in le ventricular muscle mass, le ventricular muscle volume, posterior wall thickness, septal wall thickness, le ventricular end- diastolic chamber volume, or le ventricular end- systolic chamber volume. The only significant sex difference was in a- vO2 di at peak VO2 where boys’ values were ~17% higher than those of girls. The emergence of non- invasive technology has opened up new avenues of research with, for example, NIRS allowing the non- invasive measurement of microcirculatory changes in deoxy-genated haemoglobin and myoglobin ([HHb]). 
An initial study demonstrated a more rapid rate of change in [HHb] during ramp exercise to peak VO2 in prepubertal girls than in prepubertal boys. These intriguing data indicate that a poorer matching of muscle oxygen delivery to muscle oxygen utilization in prepubertal girls might contribute to their lower peak VO2, but they require con-formatory evidence from different exercise models. Blood lactate accumulationPO Åstrand’s experimental studies of physical working capacity popularized the use of blood lactate accumulation as an objective measure of young people’s effort, and blood sampling for lactate is a common procedure in many paediatric exercise physiology laboratories. The extant literature is, however, confounded by methodological issues which have contributed to the controversy surrounding the interpretation of young people’s blood lactate responses to exercise. This section outlines methodological issues, comments on blood lactate thresholds and reference values of performance during youth, and reviews the data on blood lactate responses to exercise in relation to chronological age, biological maturity, and sexual dimorphism.

Methodological issues

Research with children should not employ blood sampling as a rou-tine procedure and for ethical reasons a strong case should always be made to justify it in relation to the research question. Strict prac-tices must be followed at all times in the sampling and handling of blood with the health and safety of both the child and the investiga-tor paramount. Detailed health and safety issues in haematology are beyond the scope of this blog, and readers are referred to Maughan etc al. for further guidance. Similarly, a detailed review of blood lactate assessment techniques during youth appears else-where, and only key issues are outlined here.
Muscle lactate produced during leg exercise discuses into the femoral veins, and then rapidly appears in the arterial circulation. It has been demonstrated that blood sampled from the arm arter-ies provides a close reflection of the extent of lactate discusion into the systemic circulation. The ethical, technical, and medical haz-ards associated with arterial blood sampling preclude its use with healthy young people, but it has been shown that arterial lactate levels are closely reflected by capillary lactate levels during tread-mill exercise if a good blood row is maintained at the sampling site. Most paediatric laboratories therefore sample lactate from the capillaries in the fingertip or earlobe. To facilitate blood row the site can be warmed and to reduce children’s anxiety an anaesthetic cream or spray can be applied.
Once sampled, ‘whole blood’ can be immediately assayed in an automatic analyser and results reported as blood lactate accu-mulation. Before making cross- study comparisons of blood lac-tate accumulation during or following exercise, researchers must, however, confirm the comparability of the lactate assay used and the automatic analyser. Prior to the ready availability of auto-matic analysers, lactate was routinely assayed in preparations such as lysed blood, protein- free blood, plasma, or serum, and often reported as ‘blood lactate’. The significant variation in reporting children’s blood lactate accumulation from different assays was clearly illustrated in a study which reported lactate values from the same blood sample as 4 mmolL1⋅− when assayed as whole blood, 4.4 mmolL1⋅− when the blood was lysed, and 5.5 mmolL1⋅− from a plasma preparation.89Young people’s blood lactate responses to exercise are inuenced by mode of exercise, exercise protocol, and time of sampling. Blood lactate reference values are heavily dependent on definition and measurement technique. 
As discussed in the Ergometry section, when cycling during part of the pedal revolution there is a poten-tial for restriction in children’s blood row through the quadriceps, which will promote anaerobic metabolism. Children’s blood lactate accumulation in relation to pVO2 is therefore not directly com-parable during cycling and treadmill running. Regardless of erg-ometer, during an incremental exercise test, increments should be small and each exercise stage must be sustained for at least 3 min to allow adequate diusion of lactate from muscle to blood. If sampled too soon the blood lactate accumulation will not reflect the inten-sity of the exercise and will profoundly influence the blood lactate reference value.
Numerous fixed blood lactate values (e.g. 4 mmolL1⋅−) have been recommended as submaximal reference measures of adult perfor-mance. However, several of these reference values were originally determined using serum or plasma samples and all are problematic when applied to children. A study of 11– 13- year- olds, for exam-ple, reported that 34% of boys and 12% of girls did not achieve a whole blood lactate value of 4 mmolL1⋅− at peak VO2. The authors suggested that a criterion reference of 2.5 mmolL1⋅− from a whole blood assay might be more appropriate for children,17 but any fixed blood lactate value is likely to be inappropriate throughout child-hood and adolescence as studies suggest an age- dependent trend in blood lactate responses to exercise. 
The TLAC, which represents the individual’s response to increas-ing exercise- induced metabolic demands, has become recognized as an appropriate blood lactate indicator of young people’s sub-maximal aerobic fitness. The TLAC is defined as the first observable increase in blood lactate accumulation above resting levels. It can be determined from visual inspection of the infection in blood lac-tate accumulation, but a clear inflection point is not always discern-ible and some investigators have used mathematical interpolation or defined the point of infection as a 1 mmolL1⋅− increase over baseline. The MLSS represents the upper point at which the processes of blood lactate accumulation and elimination are in equilibrium and theoretically provides a sensitive measure of submaximal aerobic fitness. However, because of the requirement for multiple blood  samples over several ~20 min stages at the border of heavy and very heavy- intensity exercise, it is difficult to motivate children to participate in this type of test. Furthermore, there is no consensus over the optimum test time or magnitude of acceptable variation in blood lactate accumulation to represent MLSS. Young people’s MLSS data should therefore be interpreted cautiously. Exercise just below CPo has been shown to correspond reasonably well with MLSS in adolescents, and this non- invasive variable may be more appropriate for use during youth.

Pulmonary oxygen uptake kinetics

During a step change in exercise intensity, once the cardiodynamic phase has been deleted, the exponential rise in pVO2 has been dem-onstrated to reflect in adults the kinetics of mVO2 and to therefore provide a non- invasive window into metabolic activity in muscle. The work has not been replicated with children, but a close rela-tionship between children’s intramuscular phosphocreatine (PCr) kinetics during prone quadriceps exercise in a MR scanner and  pVO2 kinetics during upright cycling at both the onset and ofset of exercise has been demonstrated. This relationship has opened up new avenues of research in developmental exercise metabol-ism.
The kinetics of pVO2 and intramusclular PCr (as a surrogate of mVO2) at the onset of exercise are complex, and are compre-hensively analysed, where the theoret-ical principles are explained, the underlying mechanisms explored, and the rigorous methodology required to characterize the kinetic responses critiqued. Discussion here is restricted to identifying methodological issues in the determination of young people’s pVO2 kinetics responses which might influence their interpretation. The focus is on exploring the pVO2 kinetics responses to a step change in exercise intensity in relation to exercise domain, chronological age, and sexual dimorphism. The independent influence (if any) of biological maturity on pVO2 kinetics remains to be rigorously investigated.

Methodological issues

The clarification of the pVO2 kinetics response at the onset of exercise depends upon the ability to rigorously evaluate the speed and the magnitude of the respiratory gas exchange response to a given metabolic demand. This can be achieved by imposing a pre-determined square wave exercise stress and then using non- linear regression and iterative fitting procedures with the response data to at a specified model to return the rate of the exponential rise and the amplitude of the response. Unfortunately, a wide array of mod-els with various degrees of rigour have been employed to evalu-ate pVO2 kinetics, and interested readers are referred to Fawkner and Armstrong, who have critiqued and tabulated chronological models used with children and adolescents.
The confounding effect of different modelling techniques on the interpretation of young people’s response parameters has been shown empirically by apply-ing several different models to the same dataset in both the moder-ate and heavy- intensity exercise domains. The use of different models, several with limited physiological rationales, has made understanding the extant paediatric literature problematic. Even with an appropriate modelling procedure, the rigorous resolution of the pVO2 kinetics of children and adolescents is chal-lenging. Children’s inherently erratic breathing pattern reduces the signal- to- noise ratio of their pulmonary gas exchange kinetics.
Large inter- breath fluctuations reduce the condence with which  pVO2 kinetic responses can be estimated, and confidence intervals are likely to be beyond acceptable limits unless sufficient identical transitions are time aligned and averaged to improve the signal to noise ratio. The number of transitions that are required to achieve suitable confidence is directly proportional to the amount of data being at, the variability of the data, and the magnitude of the signal, and will thus vary from one person to another. With children, as many as ten transitions may be required in the moderate- intensity exercise domain to establish an acceptable confidence interval for the primary component τ.
Fewer transitions are required in heavier- intensity exercise domains because the magnitude of the signal is greater.Young people’s lower peak VO2, and therefore smaller range of metabolic rates achievable, may compromise the integrity of work-ing within specic exercise domains. Children’s TVENT occurs at ~60– 70% of peak VO219 and to ensure that the prescribed exer-cise is clearly within the moderate domain, the upper border of  exercise intensity is normally set at ~80% of TVENT. 
With children, the  pVO2 kinetics responses to exercise intensities above TVENT have rarely been investigated within carefully defined parameters. This is most likely because the assessment of CPo, the upper boundary of heavy- intensity exercise, and the threshold of very heavy- inten-sity exercise is demanding in terms of both subject effort and test-ing time.20 Investigators in adult studies normally use 40– 50% of the difference between TVENT and peak VO2 (e.g. 40% ) as describing exercise within the heavy- intensity domain30. It has been demon-strated that CPo occurs at ~70– 80% of peak VO2 in children, similar to relative values reported for adults, and that exercise at an intensity of 40% this below CPo and falls within the heavy- intensity exercise domain.103 However, the absolute range of pVO2 between TVENT and CPo is small in children and there is considerable individual variation in the relative position of both TVENT and CPo in relation to peak VO2. The 40% concept is therefore less secure on an individual basis with children than with adults.

Conclusion:

The laboratory assessment of young people’s peak (or max) VO2 dates back to 1938 and it is the most researched variable in pae-diatric exercise science. Yet, debate over the determination and terminology of peak and/ or maximal values of VO2 persists. The fallacy of expressing peak VO2 in ratio with body mass has been documented for over 65 years, but ratios are still reported. Decisive action and insistence on contextual reporting of peak VO2 by  academic journal editors is required to disseminate the appropriate interpretation of aerobic fitness during growth and maturation. 
Nevertheless, analysis of data using sophisticated modelling tech-niques has enhanced understanding of sexual dimorphism and the independent effects of chronological age, body size, and biological maturity on peak VO2. The mechanisms underlying sex differ-ences in peak VO2 prior to puberty remain to be elucidated, but the introduction of recent non- invasive technology such as NIRS provides promising avenues for future research.Despite its ubiquity in the literature, the use of fixed post- exercise values of blood lactate accumulation to verify a maximal effort dur-ing an exercise test to elicit peak VO2 is untenable. 
The monitoring of blood lactate accumulation and the determination of blood lac-tate accumulation thresholds (e.g. TLAC) during exercise provides an indicator of the ability to sustain submaximal exercise and a sensitive means of evaluating improvements in muscle oxidative capacity with exercise training. The relationship between blood lac-tate accumulation and chronological age is well- documented, but sex differences in blood lactate accumulation during youth remain to be proven. A persuasive theoretical argument can be presented for an independent effect of maturity on blood lactate accumula-tion, although there is no compelling empirical evidence to sup-port the case and more research with appropriate methodology and power to adequately address the problem is required.
Young people’s physical activity patterns and participation in most organized sports are reliant on intermittent exercise and rapid changes in exercise intensity. Under these conditions peak VO2 and blood lactate accumulation thresholds are variables of investigative convenience rather than factors underpinning exercise behaviour, and it is the kinetics of pVO2 which best describe aerobic fitness. Rigorously determined and appropriately analysed studies of young people’s pVO2 kinetic responses to step changes in exercise inten-sity are sparse.
The extant data describe intriguing chronological age-  and sex- related differences across exercise domains, although independent effects of biological maturity are yet to be revealed. Unique insights into aerobic fitness during youth rest in the tran-sient response to and recovery from a forcing exercise regimen. The challenge is to identify and explain the underlying mechanisms and how they evolve during childhood and adolescence.No single measure describes fully aerobic fitness and this chapter has focused on arguably the three most important variables in rela-tion to chronological age, body mass, biological maturity, and sex. We conclude that although aerobic fitness is the most researched trait in paediatric exercise physiology, much remains to be learned.

Summary:

• Aerobic fitness can be defined as the ability to deliver oxygen to the exercising muscles and to utilize it to generate energy during exercise. No single variable describes fully aerobic fitness.
• Boys’ peak VO2 expressed in L · min–1 increases in a near- linear manner with chronological age. Girls’ data demonstrate a similar but less consistent trend with several cross- sectional and longitu-dinal studies indicating a tendency for peak VO2 to plateau from ~14 years of age.
•  With body mass appropriately controlled for using allometry, boys’ peak VO2 increases from childhood through adolescence and into young adulthood. Girls’ values increase from prepuberty until mid- teens, then level- off as they approach young adulthood.
• Biological maturation exerts a significant and positive effect on the peak VO2 of both sexes independent of that due to chrono-logical aging, body composition, and body mass.
• Prepubertal boys have higher peak VO2 values than prepubertal girls.
• There is a progressive divergence in sex differences in peak VO2 in puberty largely due to sex- related growth in muscle mass.
• Interpretation of blood lactate accumulation during exercise is clouded by methodological issues related to mode of exercise, exercise protocol, timing of blood sample, site of sampling, and assay technique
• The lactate threshold normally occurs at a higher % of peak VO 2  in children than in adults, and there is no compelling evidence to suggest sexual dimorphism.
• Empirical studies have consistently failed to detect an independ-ent effect of biological maturation on blood lactate accumulation during exercise.
• The confident estimation of the primary component time con-stant and appropriate modelling of the amplitude of the slow component is challenging and rigorous studies of pVO2 kinetics during youth are sparse.
• The primary component time constant is negatively related to chronological age in both sexes across the moderate, heavy, and very heavy exercise domains.
• During exercise above the ventilatory threshold, boys’ primary component time constant is shorter than that of girls, whereas the amplitude of the pVO2 slow component is greater in girls. Little is known about pVO2 kinetic responses to severe exercise.
• The relative contribution of oxygen delivery and oxygen utiliza-tion to the speed of the primary component time constant in dif-ferent exercise domains remains to be elucidated.
• In contrast to adults, the primary component time constant is not related to peak VO2 during youth.
• The amplitude of the pVO2 slow component of oxygen uptake is positively related to chronological age during exercise above the ventilatory threshold
• Data on the pVO2 kinetics recovery from exercise in different domains are sparse.
• Whether there is an independent effect of biological maturation on the pVO2 kinetics response at the onset and ofset of exercise is unknown.

Effects of Aerobic Training

• Aerobic capacity: Maximum aerobic capacity increases with aerobic training. The resting Vo2 is stable, as is the Vo2 at a given workload. The changes are specific to the trained muscles.
• Cardiac output: Maximum CO increases, whereas resting CO is stable. Resting SV increases, with a corresponding decrease in the resting HR.
• Heart rate: Resting HR decreases with aerobic training and is lower at any given workload. The maximum HR is unchanged.
• Stroke volume: SV increases at rest and is maintained at a lower HR, resulting in a lower RPP for a given level of exertion.
• Myocardial oxygen capacity: Maximum Mvo2 usually does not change, but at a given workload, Mvo2 decreases with training. This reduces episodes of angina.
• Peripheral vascular resistance (PVR): Aerobic training reduces arterial and arteriolar tone, thereby decreasing cardiac “afterload” and PVR. The reduction in PVR results in a lower RPP and a lower Mvo2 at a given workload and at rest.

Dynamic Aerobic and Endurance Exercise

Aerobic exercise involves regular body part (e.g., arms or legs) movements that increase workload on the cardiovascular system. It is convenient and useful to think of the intensity of aerobic exercises in metabolic equivalents, or METs. One MET represents the amount of energy used at rest, and two METs is twice that much energy expenditure per unit of time, and so on. Aerobic exercise is widely recommended in contemporary guidelines. However, guidelines also indicate that exercise regimens are contraindicated in patients with unstable cardiovascular conditions, including but not limited to uncontrolled severe hypertension (BP ≥ 180/110 mm Hg). Conditions under which stress testing should be performed before initiation of an exercise regimen have been described.
Meta-analyses and reviews are useful for getting an overall sense of the many studies of aerobic exercise and BP. A 2007 meta-analysis of the effects of endurance exercise on BP found that exercise significantly reduced resting and daytime ambulatory BP.38 A more recent review (2010) found again that regular aerobic exercise lowered clinical BP. In both the 2007 meta-analysis and the 2010 review, aerobic exercise appeared to reduce BP more in patients with hypertension compared with those without hypertension. Five small studies in women systematically reviewed in 2011 showed a nonsignificant change in BP in response to aerobic interval training of walking. Walking programs appeared to reduce BP in some 9/27 trials reviewed in 2010. Larger trials with increased intensity or frequency of exercise for longer periods tended to be the ones that showed a significant effect. The authors concluded that further high-quality trials are needed. The most comprehensive and latest meta-analysis of all types of exercise clearly demonstrates the ability of aerobic exercise to lower BP within 8 to 12 weeks. In 105 trials, endurance exercise significantly lowered BP by 3.5/2.5 mm Hg. The effect was much larger in patients with preexisting hypertension (−8.3/6.8 mm Hg).
A recent randomized crossover trial of lower-intensity or high-intensity exercise showed decreases in clinical SBP with both types of exercise. However, there was no decrease in mean day or nighttime ambulatory BP with either form of exercise. Aerobic interval training (AIT) combines episodes of high-intensity with episodes of low-intensity aerobic exercise. At least two randomized studies have suggested an advantage of AIT over continuous aerobic exercise. Some patients, of course, have limited ability to use their legs, and upper extremity aerobic exercise also has been shown to lower BP.
The question of BP lowering with aerobic exercise in type 2 diabetics has been studied. In the Early Activity in Type 2 Diabetes (ACTID) trial, 593 newly diagnosed diabetics were randomized to use of a pedometer in a program that included intense counseling or standard or intense dietary advice.46 There was no difference in SBP or DBP after 6 or 12 months, even though the participants using pedometers increased their steps by 17% on average. Whether the exercise was merely of too low a “dose” to be effective is unclear. There may be some male-female differences in BP response to aerobic exercise, with women exhibiting BP lowering with resistance compared with aerobic exercise and men responding similarly to both types of exercise.47 The 2013 AHA Scientific Statement recommends at least 30 minutes of moderate intensity aerobic exercise per day most days of the week.2 T
he authors assigned dynamic aerobic exercise a Class I, level of evidence A recommendation in those for whom it is not contraindicated. Our review of the evidence since 2013, as well as that from another group, confirm these recommendations.41,48 Whether or not high versus moderate (or interval) intensity training is optimal for BP-lowering as well as other aspects of the dose-response effect (i.e., ideal duration of cumulative exercise per week) and the potential impact of different types of aerobic activity requires further investigation.

Cardiac disease and dysfunction

1. Aerobic exercise and, in some reports, muscular strength exercise can contribute significantly to the reduction in future cardiac disease morbidity and mortality in individuals with and without cardiac disease.
2. Aerobic fitness, related to both aerobic power (max) and aerobic endurance, is a strong independent risk factor of cardiac morbidity and all-cause mortality.
3. Physical activity, related to an individual's weekly energy expenditure above basal metabolic rate, is inversely related cardiac disease related morbidity and mortality.
4. Aerobic fitness is a stronger independent predictor of morbidity and mortality compared with physical activity. However, it is difficult sometimes to delineate between the individual effects of aerobic fitness versus total weekly caloric energy expenditure (physical activity). Furthermore, measuring total weekly energy expenditure in both free-living and structured exercise is much more difficult than measuring aerobic fitness.
5. Exercise professionals need to assess the risk of adverse cardiac events in patients prior to their participation and in order to determine an exercise intensity which optimizes safety, efficacy and personal needs (physically, psychologically and socially).
6. In planning safe and effective exercise, cardiac function related to overall physical function needs to be considered in light of autonomic-electrical rhythm control, coronary artery and myocardial integrity.
7. Neurological Rehabilitation

Maintaining aerobic capacity

Aerobic capacity is a measure of the ability to perform oxidative metabolism. Multiple systems are involved, including the pulmonary, cardiac, vascular, and musculoskeletal systems. Patients with MD have lower aerobic capacity, especially those patients with aggressive forms of MD (Sockolov et al., 1977; Edwards, 1980; Haller and Lewis, 1984; Lewis, 1984; Wright et al., 1996). Poor aerobic capacity results in reduced activity levels. Other organ dysfunction, such as decline in pulmonary status and cardiomyopathy, may further contribute to declining levels of aerobic capacity.
A major component of rehabilitation of children with MD is to prevent or slow functional losses. Aerobic activity is at the heart of improving and maintaining physical functioning. Despite the weakness, fatigue, loss of joint range of motion, and orthopedic changes, maintaining aerobic activity must be part of a comprehensive rehabilitation program. Studies have shown that aerobic capacity can be increased, improving functional abilities (Wright et al., 1996; Taivassalo et al., 1999). Continuous low to moderate resistive and aerobic exercises to promote fitness are suggested (Ansved, 2003). However, few if any studies have evaluated the long-term benefit or risks. Cardiac disease is one of the most common causes of death in patients with DMD. Potentially, cardiomyopathies and conduction abnormalities pose serious risks for patients with MD during aerobic and/or resistance training. The American Academy of Pediatrics (2005) recommended that, after the confirmation of DMD or Becker muscular dystrophy (BMD), a referral for cardiac evaluation with a specialist be made. The cardiac evaluation should include a complete history and physical, ECG, and transthoracic echocardiography (TTE). A complete cardiac evaluation should be completed every other year. In addition, starting at the age of 10 years or after the onset of cardiac signs/symptoms, cardiac evaluations should be completed annually. Specifically, symptoms of dilated cardiomyopathy, heart failure, cardiac arrhythmias, and respiratory abnormalities should be identified and treated.
Similarly, there is potential for overuse or repetitive injury, fractures, and falls in this population. Clinicians should carefully monitor patients with MD before and during exercise programs.

How Do We Measure Performance?

Typically aerobic fitness is measured as the highest oxygen consumption achieved by a subject on a treadmill or cycle ergometer. Figure 46.8 shows that O2 uptake increases with leg power output to the limit of uptake at VO2max. This power output by the legs represents a direct measure of aerobic exercise performance that can be related to the muscle properties governing the demand and supply of ATP. Our focus is on how these muscle properties determine aerobic leg performance; specifically, how muscles generate and use ATP in power production and how the changes in muscle properties with age affect muscle power production.

The Role of Physical Activity and Exercise in Managing Obesity and Achieving Weight Loss

Aerobic Exercise:

Aerobic exercise involves the continuous and rhythmic use of large muscle groups, such as walking, jogging, cycling, and swimming. In practical terms, this means sustaining a self-perceived moderate-to-vigorous exercise intensity for a prolonged period. Current guidance stipulates that people with obesity should engage in aerobic exercise –7 days/week, with each session lasting 45–60 min4, such that the amount of exercise undertaken within in a week totals a minimum of 150 min. This recommendation serves as the minimum amount of exercise needed to maintain health, not weight loss however. Those individuals seeking to lose weight or prevent weight regain over the long term are advised to increase exercise duration to 200–300 min/week.6,8,9 For most individuals, this equates to expending over 2000 kcal/week (or over 400 kcal/session). To put this into perspective, most individuals would need to walk or jog 1 mile to expend 100 calories, which is the same as one slice of bread or four heaped tablespoons of sugar. Based on this guidance, it is clear that a substantial amount of aerobic exercise is needed for people with obesity to lose weight or maintain weight loss in those who have successfully lost weight. However, weight loss resulting from aerobic exercise is highly variable due, at least in part, to individual differences in total energy expenditure for a set amount of given exercise and subsequent compensatory changes in dietary caloric intake.
In studies evaluating weight change in response to aerobic exercise prescription consistent with current guidance, most demonstrate only modest weight loss and some demonstrate no weight loss at all. For example, in the Inflammation and Exercise (INFLAME) study11 (n = 129), 4 months of aerobic exercise training resulted in only minimal weight loss (∼0.4 kg), which was no different to a nonexercise control group. In line with this investigation, the Dose Response to Exercise in Women (DREW) study assessed weight loss in response to performing aerobic exercise consistent with public health recommendations in postmenopausal women (n = 464) over a 6-month duration. Despite achieving adherence rates, the researchers observed no significant changes in weight (∼−2.2 kg). 
Interestingly, in this study the authors found that weight loss remained minimal even when aerobic exercise was performed at 150% of public health recommendations (∼−0.6 kg). The Targeted Risk Reduction Intervention through Defined Exercise (STRRIDE) study13 (n = 84) investigated the interaction between exercise amount and intensity, assessing 6 months of exercise training at  a low amount at a moderate intensity, a low amount at a vigorous intensity, or  a high amount at a vigorous intensity. Irrelevant of the exercise intensity, weight loss was the lowest with the least amount of exercise performed (moderate intensity ∼−0.6 kg vs. vigorous intensity ∼−0.2 kg), and although weight loss was greater when increasing exercise amount, the total weight lost was still minimal (∼−1.5 kg). In a cohort of people with type 2 diabetes, the Diabetes Aerobic and Resistance Exercise (DARE) study14 (n = 251) observed statistically significant weight loss after 22 weeks of aerobic training compared with a nonexercise control group, although the amount of weight lost was once again minimal (0.74 kg).