INTRODUCTION

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METABOLIC RESPONSES to heavy exercise are different in children and adults. In particular, children have lower muscle lactate levels compared with adults in relation to relative workload (10) and reach lower peak lactate levels during all-out exercise (13, 15, 23). Furthermore, during high-intensity exercise, the ratio of P_i to phosphocreatine in muscle increases to a smaller extent in children compared with adults (23). The regulation of these age-related differences is not well understood.

The accumulated O₂ deficit during heavy exercise is lower in children compared with adults (8). Similarly, the kinetics of O₂ uptake (O₂) at the onset of exercise above the gas-exchange threshold have been found to be faster in children compared with adults (1, 16, 18). It has been suggested that children can adapt their oxidative metabolism faster than adults to meet the higher energy requirements and, hence, have a lower need for nonoxidative metabolism at the onset of exercise (1, 3).

A three-phase model best describes the O₂ response at the onset of moderate-intensity exercise (14, 22). Phase I reflects the rapid increase in O₂, as blood pooled in the periphery is returned with the onset of contractions and ends with the arrival of blood from the exercising muscle with a greater level of deoxygenation. Phase II is the further increase in O₂, as venous return continues to increase and more O₂ has been extracted at the exercising muscles. Phase III is the steady state. The faster kinetics of O₂ at the onset of exercise at an intensity above the gas-exchange threshold in children were reported in studies that used a single-exponential equation starting at time 0 (16, 18) or a single-exponential function plus a linear term both starting at time 0 (1). In contrast, no age-related differences in O₂ kinetics were observed at a work rate requiring 75% of the gas-exchange threshold in prepubertal children compared with 15- to 18-yr-old adolescents when a three-phase model was used (9). Therefore, we hypothesized that the differences between children and adults reported for O₂ kinetics might reflect the methodology of data analysis. Thus phase II O₂ kinetics at the onset of exercise could be independent of age when analyzed with a three-phase model. However, at high exercise intensities, age-dependent differences in metabolism might also influence O₂ kinetics.

An analysis of O₂ on-transient responses to low- and high-intensity exercise might offer some insight as to the regulation of metabolism in boys compared with young men. Our interest was targeted especially on very high-intensity exercise, since differences between children and adults should conceptually increase with increasing overall proportions of nonoxidative metabolism.

	METHODS

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Subjects. Nine boys, aged 9-12 yr, and eight young men, aged 19-27 yr, participated in this study, which was approved by the ethics board of McMaster University. The subjects' characteristics are summarized in Table 1. All boys were Tanner pubic hair (PH) development stage 1, except one boy who was Tanner stage PH 2. All men were Tanner PH 5. All subjects were healthy and active but were not competitive athletes.

Design. Subjects came to the laboratory for three visits. The first visit was used to gather descriptive data, including stage of puberty and anthropometric characteristics, and to determine anaerobic performance and peak O₂ (O_{2 peak}). During each of the following two visits, subjects performed four bouts of exercise. Each bout started with unloaded cycling for 2 min. Then exercise intensity was suddenly increased to 50, 100, or 130% O_{2 peak}. Heart rate (HR) and O₂ were monitored continuously to follow subjects' response to the increase in workload.

Visit I. Subjects and their parents, if appropriate, were informed about the study, and informed consent was obtained. Then a medical history was taken, and subjects underwent a physical examination to exclude those with a disease. Sexual maturation was assessed by Tanner staging, according to pubic hair development (21). Height was determined to the nearest 0.1 cm by Harpenden stadiometer, and body weight was assessed to the nearest 10 g with the subjects wearing only light exercise clothing but no shoes. Body adiposity was measured by using bioelectrical impedance technique (model BIA 101A, RJL Systems, Clinton, MI). Subjects performed a continuous incremental all-out cycling task on a calibrated, mechanically braked cycle ergometer (Fleisch Metabo, Geneva, Switzerland) to determine peak: after 2 min of unloaded cycling, work rate was increased to 1 W · kg¹ for 2 min and then to 2 W · kg¹ for another 2 min. Thereafter, work rate was increased by 0.5 W · kg¹ every minute until the subject could not maintain the cycling cadence of 60 rpm despite verbal encouragement. O₂ was measured breath by breath and averaged every 10 s (Vmax229, SensorMedics, Yorba Linda, CA), and HR was recorded continuously by electrocardiogram (ECG) (1500B, Hewlett-Packard, Fort Collins, CO) by using bipolar lead CM5. O_{2 peak} was taken as the highest O₂ over a 30-s period during the test. Peak HR was the average HR at the time of O_{2 peak}. All but two boys reached a respiratory exchange ratio >1.0 at O_{2 peak}; their respective peak HR values were 190 and 206 beats/min. For all subjects, the investigators were convinced that a peak effort was reached at the end of the incremental- exercise test. O₂ and mechanical power were averaged for the final 30 s of the first three exercise intensities. By using individual linear regressions of O₂ over power, the workloads for the subsequent visits were calculated for each subject.

Visits II and III. These visits were scheduled at the same time of the day. Subjects did not eat for at least 2 h before testing and refrained from intense exercise in the preceding 24 h. During each of the visits, subjects performed four cycling tasks on the same calibrated ergometer as in visit I. Each of the tasks consisted of 2 min of unloaded cycling at 80 rpm (20 W). Work rate was then increased to 50% O_{2 peak} for 210 s, to 100% O_{2 peak} for 120 s, or to 130% O_{2 peak} for 75 s. In this paper, the entire exercise bouts including the unloaded cycling are referred to as "50% O_{2 peak} task," "100% O_{2 peak} task," and "130% O_{2 peak} task."

In each session, two 50% O_{2 peak} tasks, one 100% O_{2 peak} task, and one 130% O_{2 peak} task were performed. The 50% O_{2 peak} tasks and the 100% O_{2 peak} task were performed first and in random order, whereas the 130% O_{2 peak} task was always administered last, to avoid confounding effects on the HR and O₂ kinetics during the other tasks. At least 30 min of rest were scheduled between the exercise bouts. Throughout each exercise task, HR was recorded continuously via ECG, and O₂ was determined breath by breath.

Subjects were told to maintain cycling cadence at exactly 80 rpm throughout each task. A visual feedback helped them to keep the right pace. Cycling cadence was monitored and stored second by second by using a computer. The collection of data was ended if cycling cadence fell below 72 rpm for any consecutive 2 s during the exercise.

Obviously, we would have preferred to collect data during longer exercise periods in the 100% O_{2 peak} and 130% O_{2 peak} tasks, but the subjects could not maintain the work rate for a longer period. Actually, four subjects not included in this paper, two men and two boys, were not able to perform for long enough at the high exercise intensities required. All 17 subjects described in this paper completed the four 50% O_{2 peak} and the two 100% O_{2 peak} tasks according to the above criteria. However, only seven boys and two men were able to keep the cycling cadence at 80 rpm for 75 s during both 130% O_{2 peak} tasks. All subjects were, however, able to complete at least 60 s in both 130% O_{2 peak} tasks.

Data analysis. The data were only accepted for analysis if the subject's average cadence was 80 ± 3 rpm during the entire task. For each subject, data of the 130% O_{2 peak} tasks were analyzed only for the duration that was sustained in both trials. In other words, data from a subject who performed, e.g., one 130% O_{2 peak} task for 65 s and the other for 73 s were analyzed only for 65 s.

The breath-by-breath O₂ data of visits II and III were interpolated second by second for each exercise intensity and added together so as to maximize signal-to-noise ratio. The average O₂ during the final 30 s of unloaded cycling was used as baseline for the O₂ response to the steplike exercise increase.

O₂ deficit was calculated as the difference between the estimated O₂ demands and the accumulated O₂ values. Computations were performed for the interval from the end of unloaded pedaling to the end of exercise in the 50 and 100% O_{2 peak} tasks. For the 130% O_{2 peak} task, accumulated O₂ deficit was calculated for the first 60 s of heavy exercise in all subjects to adjust for differences in endurance times.

Phase I of the O₂ response after the increase of exercise intensity was identified visually. Single-exponential functions were fitted to each individual interpolated data set, excluding phase I and allowing for a delayed response (Eq. 1).

(1)

where O₂(t) is the increase in O₂ above baseline at the time t; O₂ is asymptote of O₂(t) above the baseline of unloaded cycling; D is time delay for the exponential; and  is time constant of the exponential. More complex equations, such as a two-exponential function allowing for independent time delays of components A and B (7)

(2)

or those including a linear term with a slope s as a second component [modified from Armon et al. (1)]

(3)

were also tried. All functions were fitted by using an iterative optimization routine (BMDP Statistical Software, Los Angeles, CA). By using the fitted equations, the half-time response was calculated in addition to the O₂ kinetics.

O₂ cost for each exercise intensity was calculated by dividing O₂ derived from the fitted equation by the increase in work rate from unloaded pedaling to cycling at 50, 100, and 130% O_{2 peak}.

HR was determined manually second by second from the ECG strips. The HR responses were then superimposed for each subject and task. Because of the complexity of the HR on-transients, half-response time constants were determined to quantify the time course of the HR response.

Statistics. All values reported are means ± SD unless stated otherwise. Anthropometric and performance data of boys and men were compared by using two-tailed t-test. The fit of Eqs. 1-3 was compared for each data set by using nonparametric statistics on each set of residuals squared excluding phase I from the analysis. The delay times, time constants, and asymptotes derived from Eqs. 1-3, describing the exponential phase II O₂ response to a steplike increase of exercise intensity, were analyzed for effects of age and exercise intensities by using 2 × 3 ANOVA for one repeated measure (age × task). A t-test or paired t-test was employed for post hoc analysis adapting P for the multiple comparisons (Bonferroni). Significance was accepted at P < 0.05.

	RESULTS

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Table 2 summarizes the O₂ deficits accumulated during the 50, 100, and 130% O_{2 peak} tasks in the boys and men. Accumulated O₂ deficit was larger for the 100 and 130% O_{2 peak} tasks in the men compared with the boys, if expressed in absolute terms. O₂ deficit relative to body weight was not different between the age groups at any of the exercise intensities. Similarly, the aerobic contribution to each task was similar in boys and men.

View this table: [in this window] [in a new window]   Table 2.   Accumulated O2 deficit and aerobic contribution after increasing exercise intensity from unloaded pedaling to cycling at 50, 100, and 130% O2 peak in boys and men

Figure 1 shows the O₂ response to an increase in work rate from unloaded pedaling to 100% O_{2 peak} in one man. Phase I was determined visually (here 18 s) and excluded from analysis. Equations 1-3 were fitted to phase II O₂ response, and residuals were calculated. Squared residuals were compared intraindividually to determine best fit. Like the example provided in Fig. 1, somewhat smaller residuals were found with the more complex Eqs. 2 and 3 compared with Eq. 1. The residuals squared were, however, not significantly different between equations for all intraindividual comparisons and tasks. The parameters describing the kinetics of the O₂ response reported in the remainder of this paper are, therefore, derived from fitting Eq. 1, unless stated otherwise.

View larger version (30K): [in this window] [in a new window]   Fig. 1.   Fit of Eqs. 1-3 to O2 uptake (O2) response to transition from unloaded cycling to cycling at 100% of peak O2 (O2 peak) in 1 man at time 0. Phase I = 18 s was excluded from analysis. A: original data and fitted lines for Eqs. 1-3. B: respective residuals squared. Residuals squared were somewhat, but not statistically significantly, smaller with the more complex equations.

Figure 2 shows the time course of O₂ in one boy and one man for the three different exercise tasks. Phase I could be identified visually, and phase II was well described by fitting single-exponential functions (Eq. 1).

View larger version (33K): [in this window] [in a new window]   Fig. 2.   O2 response to transition from unloaded cycling to cycling at 50, 100, and 130% O2 peak in 1 boy (A) and 1 man (B). Dotted lines denote baseline O2 during unloaded cycling and time of increase in exercise intensity; dashed lines mark the fitted curves (Eq. 1).

Table 3 summarizes the duration of phase I in boys and men. Overall, there was no significant difference between the age groups. However, whereas there was no difference in the duration of phase I between the different tasks in the boys, phase I became shorter with increasing exercise intensity in the men. The interaction between age and task was significant. The volume of O₂ taken up during phase I was lower in the boys compared with the men in all tasks. In both age groups, the amount of O₂ consumed was higher in the more intense exercise tasks.

There was no significant difference in the time constants of the exponential increase in O₂ between the boys and the men (Table 3). There was also no interaction with exercise intensity. However, based on the data analysis outlined in METHODS, time constants appeared significantly shorter in the 130% O_{2 peak} task compared with the 50% O_{2 peak} and 100% O_{2 peak} tasks (paired t-test, adjustment of P according to Bonferroni).

The asymptote of the exponential O₂ response above the baseline of unloaded cycling was expectedly higher in the men compared with the boys, when expressed in absolute values. However, when the asymptote O₂ was added to the baseline O₂ and expressed as percentage of O_{2 peak}, no significant differences were observed between the boys and the men (Table 3). When the relative amplitudes of both age groups were combined, the 95% confidence interval for the mean amplitude of the total O₂ response was 48.48-54.54% of O_{2 peak} for the 50% O_{2 peak} task, 85.94-94.02% for the 100% O_{2 peak} task, and 91.52-101.51% for the 130% O_{2 peak} task, respectively. The total amplitudes were not only significantly lower in the 50% O_{2 peak} task compared with the 100% O_{2 peak} task or the 130% O_{2 peak} task, the amplitude was also lower in the 100% O_{2 peak} task compared with the 130% O_{2 peak} task (paired t-test, P < 0.01).

O₂ cost for cycling at 50, 100, and 130% of O_{2 peak} was higher in the boys compared with the men (Table 3). O₂ cost decreased with increasing exercise intensity in both boys and men.

Figure 3 shows the increase in HR at the transition from unloaded cycling to cycling at 50, 100, and 130% of O_{2 peak} in one boy and one man. The HR on-kinetics were more complex than the O₂ kinetics, so that only half response times could be calculated to describe the time course of HR increase at the sudden increase in exercise intensity. Table 4 summarizes the mean half response times of the boys and the men in comparison to the mean half times of the O₂ response (phases I and II). HR half response times were similar in boys and men and significantly shorter than O₂ half response times in both age groups.

View larger version (28K): [in this window] [in a new window]   Fig. 3.   Heart rate (HR) response to transition from unloaded cycling to cycling at 50, 100, and 130% O2 peak in 1 boy (A) and 1 man (B). Dotted lines denote time of increase in exercise intensity. Subjects are different from those shown in Fig. 2 to show HR responses that obviously could not be described by simple mono- or two-exponential equations.

View this table: [in this window] [in a new window]   Table 4.   Half times of the HR and O2 responses to an increase in work rate

	DISCUSSION

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O₂ deficit was higher in the men compared with the boys when expressed in absolute terms but was similar when expressed relative to body weight. Aerobic contribution to the total O₂ requirement of the exercise at 50, 100, and 130% O_{2 peak} was similar in boys and men. This is in line with our finding that the time constant of the phase II response of O₂ to heavy exercise was similar in boys and men.

Accumulated O₂ deficit calculated in the present study was lower in the boys and men than that reported for similar exercise intensities in other studies (8, 12). This might be explained with differences in study design. The present study was not meant to stress the O₂ deficit to its maximum. Our subjects started their exercise from unloaded cycling, so that O₂ was already raised above resting O₂ at the increase of exercise to 50, 100, or 130% of O_{2 peak}. Thus the amplitude of the O₂ response was smaller. Furthermore, exercise was terminated once the subjects had cycled for 2 min at 100% O_{2 peak} (100% O_{2 peak} task) or the analysis was limited to the first 60 s of high-intensity exercise (130% O_{2 peak} task).

One problem with the calculation of O₂ deficit is that O₂ requirement during very high-intensity exercise has to be extrapolated from submaximal exercise data. Saltin (19) and Bangsbo (2) have challenged the validity of this approach. The following computations may show how crucial the precise estimation of O₂ requirements during high-intensity exercise is for the calculations of O₂ deficit: when we recalculated O₂ deficit during the 130% O_{2 peak} task in the present study, assuming the metabolic demand to equal 140% O_{2 peak} instead of 130% O_{2 peak}, computed O₂ deficit increased by 16.0 ± 1.9 and 14.9 ± 1.1% in the boys and men, respectively.

Another problem with the calculation of O₂ deficit is the inclusion of the phase I O₂ reponse. O₂ taken up during this phase reflects venous return and O₂ uptake of the previously pooled blood (4, 6). Since phase I lasts for ~15-20 s, whole body O₂ deficit might, by inclusion of phase I in the calculations, largely overestimate O₂ deficit accumulated by the active muscle, of which O₂ is reflected only in phase II of the O₂ response.

The asymptotes of the exponential O₂ response plus the baseline O₂ during unloaded cycling expressed in relation to O_{2 peak} were comparable in boys and men for all cycling intensities (see Table 3). However, the O₂ cost of the exercise, calculated as the difference between the asymptote O₂ minus the O₂ during unloaded pedaling (O₂) divided by the difference in power output, was significantly lower in the men compared with the boys in all tasks (Table 3). The boys' and the men's O₂ costs of the 50 and 100% O_{2 peak} task are in good agreement with the data reported by Armon et al. (1), who suggested as possible causes for differences in O₂ cost between children and adults either "a more effective cardio-respiratory response to exercise in children than adults," or "a less developed ability of children to support anaerobic (`O₂-sparing') mechanisms of ATP metabolism," or "a greater ability (of children) to oxidize the lactate produced during exercise." Other differences between children and adults might also contribute to the observed differences in O₂ cost of cycling at high exercise intensities. For example, one study has shown that men are more able than boys to use stored elastic energy within the muscle during short, intense exercise (17). It could also be speculated that there are age-related differences in muscle fiber recruitment patterns of boys and men during intense exercise (see below), although direct experimental proof is lacking.

The time constants of the exponential rise in pulmonary O₂ at the transition between unloaded cycling and cycling at 50, 100, or 130% of O_{2 peak} were not different between boys and men. These results extend previous investigations that have been confined to work rates far below 100% O_{2 peak}. Our findings are in line with the study of Cooper and co-workers (9), who studied exercise transients from 20 W to 75% of gas-exchange threshold (40-50% of O_{2 peak}). They found no differences in time constants of the exponential O₂ response during phase II between prepubescent boys and 15- to 18-yr-old male adolescents. The time constants reported in their study (26.5 ± 3.0 and 24.3 ± 2.3 s for boys and adolescents, respectively) are in good agreement with those calculated for the 50% O_{2 peak} task in the present study (Table 3). This same research group (20) also found the time constants of the O₂ response during phase II to be similar in children and adults at the onset of exercise under hypoxic conditions.

In contrast to those studies and our findings, other studies comparing the on-transients of pulmonary O₂ in children and adults have reported significantly faster time constants in the children (1, 16, 18). It is possible that differences in the methods of data analysis might account for the conflicting findings. Two studies (16, 18) used a single-exponential equation to model the entire O₂ response. This approach failed to differentiate between phase I and phase II as well as between the fast component of phase II and its slow component (5, 7). Indeed, when our data were analyzed in the same way, we found time constants for the 50, 100, and 130% O_{2 peak} tasks of 37.3 ± 7.7, 52.2 ± 11.2, and 47.7 ± 12.4 s, respectively, in the boys and 51.3 ± 10.9, 58.1 ± 19.7, and 70.5 ± 26.39 s in the men, respectively. Using this approach, the intergroup differences would have been significant in our study (ANOVA F_age = 5.89, P < 0.05). We believe that sufficient evidence has been accumulated in recent years to negate this approach (5, 7).

In the remaining study showing apparently conflicting results, Armon et al. (1) tried to incorporate the slow component of O₂ kinetics into their model of O₂ transients when analyzing the transients at the onset of 6-min high-intensity exercise. However, they did not exclude phase I from their analysis, and they chose a linear model starting at the origin (time 0) for the slow component. There is evidence that phases I and II have to be distinguished during analysis and that the slow-component O₂ during phase II starts with a considerable delay (5, 7). The finding of Armon et al. (1) of a greater slope of the linear term of the slow component with increasing exercise intensity in the adults, but not in the children, would have biased the calculated time constants of phase II in the adults. Indeed, the children's time constants in the study of Armon et al. (26 ± 8 s at the transition to 80% of gas-exchange threshold, 29 ± 6 s at the transition to 75% of the difference between gas-exchange threshold, and O_{2 peak}) were similar to those in our study (Table 3). In contrast, the time constants for the adults were considerably larger in their study (44 ± 7 s at the transition to 80% of gas-exchange threshold, 41 ± 3 s at the transition to 75% of the difference between gas-exchange threshold and O_{2 peak}) compared with our study. Distinguishing between phases I and II and allowing for a time delay of the slow component Barstow and colleagues (5, 7) found time constants for the fast exponential rise in O₂ during phase II to be 20.2 ± 4.1 and 27.2 ± 3.8 s in the men in their two studies, respectively.

The time constants found by Barstow and colleagues (5, 7) are very similar to the men's time constants in our study, yet we did not use the same model. It could be argued that the 100 and the 130% O_{2 peak} tasks were intense enough in our study to elicit a slow-component O₂ response that was not included in our analysis. However, these work rates were higher than investigated previously. The consequence of this was that the total duration of exercise at this high intensity was quite short. Furthermore, the O₂ requirements for the 100 and 130% O_{2 peak} tasks were so high that no slow component was expected. Indeed, we did not see a slow component. In one man only, did visual inspection of the data cause us to suspect a slow-component O₂ response during the final 20 s of the 100% O_{2 peak} task (Fig. 1). When we analyzed all data sets using the two-exponential model with independent time delays, as suggested by Barstow and colleagues (5, 7), we found no significant improvement of fit compared with a single-exponential model. When looking at the averaged O₂ response from the boys and the men during the 100% O_{2 peak} task, no slow component could be identified visually (Fig. 4).

View larger version (15K): [in this window] [in a new window]   Fig. 4.   Average O2 response to transition from unloaded cycling to cycling at 100% O2 peak in boys and men. Response was calculated as %difference between O2 during unloaded cycling and O2 peak for each subject and was averaged afterward. Exercise began at time 0. There was no difference in O2 response between boys and men, and no slow component of the phase II response could be identified.

We found significantly shorter time constants in the 130% O_{2 peak} task compared with the 50% O_{2 peak} and 100% O_{2 peak} tasks. This pattern occurred in boys and men alike. To our knowledge, no other study has investigated the effects of exercise transients to intensities beyond O_{2 peak} on O₂ kinetics. Barstow et al. (5) have shown that the time constants for the first exponential of the phase II O₂ response were independent of exercise intensity up to O_{2 peak}. This is in agreement with our findings. In this context, the shorter time constants of O₂ kinetics during the 130% O_{2 peak} task compared with the 100% O_{2 peak} task might seem surprising. However, all exponential models assume that the difference between actual and required O₂ determines the velocity of O₂ increase. The requirements for O₂ during the 130% O_{2 peak} task will be higher than during the 100% O_{2 peak} task. If the kinetics of the O₂ response in the 130% O_{2 peak} task, projecting to a O₂ beyond 100% O_{2 peak}, were similar or only slightly slower than the kinetics observed during the lower work intensities, the larger O₂ demands during exercise at 130% O_{2 peak} would result in an O₂ increase per second, which is faster during the 130% O_{2 peak} task compared with the 100% O_{2 peak} task. Because the amplitude of the increase is limited at peak O₂, the method of data analysis used in this study might have resulted in time constants appearing shorter for the 130% O_{2 peak} task than for the 100% O_{2 peak} task.

Children have been shown to possess less ability to rely on nonoxidative energy sources during high-intensity exercise, as evidenced by lower peak muscle and blood lactate levels (10, 13, 15, 23) and lower P_i-to-phosphocreatine ratios at peak exercise (23). Based on previous findings of faster time constants of the O₂ response at the transition from unloaded cycling to more intense exercise in children compared with adults, it was suggested that children may depend less on anaerobic energy sources early in exercise (1). Our data, however, show that, during the first 1-2 min of heavy exercise, the O₂ kinetics of boys and men are similar even at exercise of very high intensity. This finding suggests that the interactions between metabolic and cardiovascular adjustments underlying the fast exponential increase of pulmonary O₂ at the onset of intense exercise are activated at a similar time course and to a similar extent in boys and men. After ~2 min into high-intensity exercise, however, a slow increase of pulmonary O₂ can be expected in addition to the initial increase in O₂ described by the fast exponential rise. This slow component of O₂ uptake kinetics, which has not been investigated in the present study, has been observed to be more pronounced in adults than in children (1). It has been suggested that the main part of the slow component reflects motor unit recruitment pattern during the exercise, possibly the recruitment of fast-twitch fibers (11). Additional O₂ requirements for ventilation will also contribute to the slow-component O₂ (11).

In conclusion, boys and men showed similar fast- component O₂ kinetics during phase II at the onset of moderate- to high-intensity exercise. Both groups exhibited similar O₂ deficits accumulated during exercise of 50, 100, and 130% O_{2 peak} and, consequently, similar aerobic contributions to each tasks. Therefore, our findings are in contrast to common beliefs that children rely less on anaerobic energy turnover early in exercise.