Children’s play and sport activities are often intermittent and performed at fairly high intensities (2). Furthermore, the increasing involvement of children in intense, competitive sports, adds both practical and physiological relevance to the understanding of their responses to and recovery from intense exercise. Although the recovery from intense exercise is known to be faster in children than in adults (22), very little experimental data exist concerning the physiological processes that differentiate the two age groups.
It has been widely demonstrated in adults that lactate (La) accumulation is closely associated with muscle fatigue and endurance, as well as with the rate of recovery of dynamic exercise performance (27,28,38,47). The relationship between [La] and subsequent performance is complex and has not so far been fully elucidated. Nevertheless, the relevance of elevated recovery [La] to compromised subsequent performance—likely due to the inverse relationship of La to pH (11,43), as well as to its own direct influence (18,25)—has been shown in many studies (19,28,38,47). Thus, accelerated [La] reduction after intense exercise could be advantageous in adults, and presumably also in children.
[La]peak after maximal and supramaximal exercise in children is characteristically lower than in adults, as is their anaerobic power output (see (46) for a review). Additionally, [La]peak observed after exercise appears sooner in children compared with adults (15,21). In a recent study (15), we found a similar La half-life (T50La) in children and adults during passive recovery from supramaximal exercise, regardless of the large differences in body mass–specific power output and [La]peak attained after the exercise task. Thus, explanations for children’s faster recovery of performance capacity include their shorter time to [La]peak from the end of exercise and, in particular, the fact that they have less to recover from. That is, they need to recover from a lower power output (26) and lower consequent [La]peak. Additional explanations for children’s faster recovery may involve physiological differences such as a shorter circulation time (12) and muscle-to-capillary diffusion distance (7), both of which may contribute to a faster decrease in both muscle and blood [La]. Enzymatic or other biochemical differences may also be part of the explanation. At present, however, such differences can neither be supported nor refuted.
In adults, [La] decrease after intensive exercise is accelerated by active recovery compared with the passive mode (5,9,14,17,31,36). This is due to the fact that, when work intensity is well below the lactate threshold (LT), La removal greatly exceeds La production. Additionally, the elevated muscle blood flow during dynamic exercise expedites La removal (8). During active recovery, [La] decrease was found to be largely dependent on the involved muscle mass and metabolic rate (below the anaerobic threshold) (3,30). Although in normal individuals, maximal removal rates may be reached at recovery intensities above 60% O2peak (23), the suggested recovery intensity for adults is 30–45% O2peak (13,14) because [La] production is much lower than its removal at the latter intensity.
In children, it has not been established whether active recovery is preferential to the passive mode in decreasing postexertion [La] as is the case with adults, and if so, what is its optimal intensity. There are several known differences between children and adults that suggest that children’s optimal recovery intensity would be higher than that recommended for adults: a) the activity of muscle phosphofructokinase is known to be lower in children compared with adults (16); b) even at similar body mass–corrected power outputs, children display a lower blood [La] (15); c) children’s LT occurs at a higher percentage of O2peak than that of adults (33,34,46). These differences suggest that La production at a given relative exercise intensity is lower in children than in adults. On the other hand, there is no evidence to suggest that La removal is different between children and adults. Therefore, at a given active recovery intensity, the reduction in [La] may be greater in children than in adults. It stands to reason, therefore, that children should benefit from active recovery, and that their optimal recovery intensity would be higher than in adults. The purpose of the present study was to investigate children’s [La] dynamics at various intensities of active recovery compared with the passive mode.
Fifteen 9- to 11-yr-old boys (N = 8) and girls (N = 7) volunteered to participate in the study. All subjects were healthy and active, but none was a competitive athlete. All subjects were prepubertal according to the stages of pubic hair and gonadal development as characterized by Tanner (37). Their physical characteristics, HRpeak, and O2peak are described in Table 1.
The nature and purpose of the study was explained to all subjects and their parents. The children gave their verbal consent to participate, and their parents gave their written consent. The study was approved by the ethics committee of our institution.
Subjects attended the laboratory for five sessions, 3–7 d apart. The first visit included the following: a) a physical examination and determination of pubertal stage; b) anthropometry (height, weight, and skin-fold thicknesses); c) a staged cycling test of 5-min stages for the determination of the individual O2-versus-mechanical-power and [La]-versus-O2 relationships; and d) O2peak determination (see measurements for details). Additionally, subjects were familiarized with the procedures of the subsequent visits.
During the next 4 visits, subjects performed 3 supramaximal cycling bouts, followed by one of 4 randomly assigned recovery intensities: passive, and 40, 50 and 60% of the previously determined O2peak (RP, R40, R50, and R60, respectively). [La] was determined at rest and intermittently during the 25-min recovery. HR and O2 were determined during recovery (see protocol and measurements).
Resting [La] was determined in arterialized prewarmed fingertip capillary whole blood. Subsequently, subjects performed a 5-min warm-up on the cycle-ergometer, pedaling at an average of 75 RPM (70–80 RPM), at a power output equivalent to 40% of their previously determined O2peak. After the warm-up, subjects rested for 3 min and [La] was determined 2 min before the beginning of the supramaximal exercise bouts. Subjects performed three 40-s cycling bouts at a work rate corresponding to 150% O2peak, with two 50-s rest intervals, followed by 2 min of passive recovery and 23 min of one of the 4 randomly assigned recovery regimens. [La] was determined at 1:45, 4, 6, 10, 15, 20, and 25 min after exercise. O2 was measured during the last 5 min of recovery. HR was monitored throughout exercise and recovery and was recorded at rest, immediately after exercise and 2, 4, 6, 10, 15, 20, and 25 min after exercise.
Skin-fold thicknesses were determined in triplicate using Skyndex calipers at the standard biceps, triceps, subscapular, and suprailiac sites. The mean of the 3 measurements at each site was recorded.
The O2-versus-mechanical-power relationship was determined individually for each subject. Three to five 5-min submaximal work stages were performed on a Jaeger (Germany) ER900 electrically braked cycle-ergometer (iso-power, with 5-W increments) at ∼70 RPM. That ergometer was used for all subsequent testing as well. Loads commenced at 20 to 60 W, were incremented by 10 or 15 W, and reached maxima of 50 to 100 W. O2 and HR were monitored continuously. Average O2 for the last 3 min, HR within the last 20 s, and rating of perceived exertion (RPE; 15-point Borg Scale) (6) within the last 15 s were recorded for each stage. [La] was determined in finger-tip blood samples from a prewarmed hand 1 min after each stage. Rest intervals between stages were 90-s long.
Cycling O2peak was determined using a progressive protocol. The initial load was 20–30 W, incremented by 15 W in each successive min. Subjects were verbally encouraged by the investigator and the test was terminated upon self-determined exhaustion. The highest mean O2 value obtained for 2 successive 20-s intervals was considered O2peak. O2peak was defined by the achievement of any one of the following 3 criteria: a) a O2 increase of <2.5 mlO2·kg−1·min−1 despite a continued increase in work rate, b) HRpeak > 90% of the age-predicted maximal HR (because true maximal HR is normally attained in running rather than in cycling) or c) RER > 1.15.
The power necessary to promote a O2 equal to 40, 50, and 60% O2peak for each subject was calculated from the individual O2-versus-mechanical-power regression equation and O2peak value (described above). Because the ergometer’s power output could be adjusted by 5 W increments, recovery power outputs were assigned to the nearest possible value. Table 2 shows the mean actual intensities subsequently used for the active recoveries.
[La] for each stage was determined from blood samples taken 60 s after the cessation of each work stage. The [La] values corresponding to 40, 50, and 60% O2peak were interpolated from a manual best-fit curve drawn for each subject. The corresponding HR and RPE values were calculated from the individual regression equations (Table 2). The [La] data were used to ascertain that no subject had exceeded the 3-mM [La] level and that no curve had reached the steep-rising phase characteristic of exertions above the lactate threshold. Given these verifications, actual lactate threshold determination was not necessary because it has been well established that the lactate threshold of prepubertal children occurs at a much higher percentage of O2peak than the 60% used in the highest recovery intensity in the present study (45,46).
O2 was determined using a computerized open-circuit system that included an Applied Electrochemistry S-3A analyzer, a Beckman LB-2 CO2 analyzer, and a Hewlett Packard 47304A Fleisch-type flow transducer. For the purpose of analysis of the submaximal-exercise O2 and recovery O2, consecutive 20-s O2 readings were averaged over the last 3 min of a given measurement interval. HR was monitored using a Polar Sport-Tester (Polar Electro, Finland) at 5-s intervals. The highest HR value during or after the exercise bouts was considered HRpeak.
[La] was determined enzymatically in 25-μL fingertip capillary whole-blood samples, taken from a prewarmed hand, and using the Sport 1500 L-Lactate Analyzer (Yellow Springs Instruments, Yellow Springs, OH) with a lysing agent (42). T50La was defined as the time elapsed from the point of [La]peak (105 s after cessation of exercise) until [La] decreased to 50% of its rise from resting [La] to [La]peak. T50La was determined arithmetically and individually from each subject’s [La] versus time plot.
A one-way ANOVA was performed to assess differences among sessions in baseline resting or preexercise values. Variables measured repeatedly during the session were analyzed using a repeated measures ANOVA (RM-ANOVA) with time and intensity of recovery serving as within-subject factors. The RM-ANOVA was performed between all four recoveries, as well as between the three active recoveries separately. Post hoc analyses were performed using the Bonferroni procedure (24). No differences were found between boys and girls. Therefore, all analyses were performed on the pooled group as a whole. Statistical significance was set at α < 0.05. Data are reported as mean ± SD.
The physical characteristics and O2peak values of the boys and girls are demonstrated in Table 1. The two groups were of similar mean age, height, and body mass. However, they differed in their sum of skinfolds and in their O2peak.
Mean [La], HR, and RPE values, measured during the preliminary staged cycling tests for each of the recovery work-loads are described in Table 2. All three parameters indicate light-to-moderate work-loads throughout the selected intensity range.
No differences were observed among experimental sessions in resting [La] or [La] measured 105 s after the exercise bouts. To facilitate normalized comparison of the [La] decrease in the four recovery intensities, [La] was expressed as a percentage of the [La] increase from rest to 105 s postexercise (Fig. 1a vs 1b). It should be stressed that [La] at 105 s postexercise was the highest [La] value attained in all recovery intensities. The active recoveries, therefore, initiated at 2-min postexercise, were commenced only after the attainment of this [La]peak value.
[La] decreased with time during all recoveries and significantly more so in the active compared with the passive recoveries (Fig. 1). A separate analysis of the active recoveries revealed that [La] was significantly lower in the R40 compared with the R60 recovery. Additionally, a time-intensity interaction was found between R40 and R50. This interaction reflects the fact that during the first 10 min of recovery, [La], when expressed as a percentage of the net increase, was lower in R50 compared with the R40; whereas in the last 10 min of recovery, an opposite situation was observed, namely, lower [La] in the R40 compared with the R50 recovery. The results of the statistical analysis were similar for both the absolute [La] values and the [La] expressed as a percentage of the increase in [La].
At the end of the 25-min recoveries, [La] was significantly lower in all active recoveries compared with the passive one. Within the active recoveries, [La] was significantly lower after 25 min of R40 compared with R60 (Fig. 1). The comparisons among the active recoveries were considered most essential of the comparisons in this study. Therefore, statistical power was determined for pairwise comparisons among active recoveries (40). An effect size of 0.74 was found when comparing R40 with R60. The calculated power was 0.85. On the other hand, the effect size of the R40 versus R50 comparison was 0.38 with a limited power of 0.42.
The calculated T50La was significantly longer in the passive compared with the active recoveries (22.4 ± 5.0, 10.3 ± 1.9, 10.5 ± 2.2, and 11.4 ± 2.1 min in RP, R40, R50, and R60, respectively). No statistically significant differences were found among the active recoveries.
HR, immediately postexercise and 105 s postexercise, was similar in all sessions (Fig. 2). It decreased progressively in the RP; whereas in the active recoveries, it decreased initially, then adapted to recovery intensity and leveled off within 5–10 min. HR during RP was significantly lower than during all active recoveries. Additionally, among the latter, HR decreased with decreasing intensity of recovery. At the end of the 25-min recovery, HR was significantly different between treatments.
Expectedly, O2 was significantly different among all recovery intensities (0.22 ± 0.05, 0.66 ± 0.12, 0.78 ± 0.12, and 0.89 ± 0.12 L·min−1 during RP, R40, R50, and R60, respectively). The measured O2 during the active recoveries was 46.5 ± 7.5, 54.9 ± 7.7, and 62.6 ± 5.5% O2peak in R40, R50, and R60, respectively.
Both HR and [La] are common indices of both exertion and recovery. Their behaviors, however, are not parallel (e.g., Figs. 1 vs 2). We therefore used the %HRpeak × %[La]peak product (HR·La) as a composite index of recovery (Fig. 3) (see discussion for further clarification). HR·La significantly decreased with time in all recovery modes. A significant time-intensity interaction was found when comparing all four modes, reflecting the fact that HR·La was lower in the first few minutes of passive recovery but higher than in all active recoveries in the last 15 min. HR·La during R60 was on average higher than HR·La during R40 or R50. A significant time-intensity interaction was found between R40 and R50, reflecting the fact that at 6 min of recovery, HR·La was similar for R50 and R40, whereas at all other times HR·La at R40 was lower.
The main finding of this study is that [La] decrease after intense exercise in children is faster during active compared with passive recovery. This was demonstrated by the changes in [La], as well as by the calculated La half-life. Although a statistically significant difference was observed between the decrease in [La] during R40 compared with R50, the physiological significance of this small actual difference is questionable. Therefore, in view of the lower HR, lower O2, and lower RPE involved in R40 compared with the R50 recovery intensity, the former should be considered preferable for the overall recovery intensity after supramaximal exercise in children. Our findings, although limited by sample size, do not indicate any differences between boys and girls.
We chose intermittent exercise to obtain [La]peak earlier than would have been possible after a single exercise bout of sufficient intensity. Indeed, [La]peak occurred within 105 s into recovery in all of its modes. Based on the passive recovery, where [La] began to decrease after 105 s with no intervention, it can be assumed that the active recoveries that began 2-min postexercise did not prevent the attainment of higher [La] values. The postexercise [La] values observed in this study are similar to those described by others (15,20,32,41) after the Wingate Anaerobic test in 10- to 12-yr-old boys and girls. On the other hand, others have reported lower values, from 8.0 to as low as 5.4 mM, after the Wingate Anaerobic test in subjects of similar age (4,21). The high postexercise [La] values observed in the present study may be, in part, attributable to the fact that the children performed three supramaximal bouts of exercise, rather than a single bout of exercise (29). [La] differences may also be due to methodological differences in blood collection and [La] determination.
From the fourth min of recovery onwards [La] was lower during R40 and R50 compared with R60 or RP. Although protocols are not quite comparable, this is not much different from the results of previous studies in adults, where the recommended recovery intensity was 30–45% O2peak (14,36).
Based on observations that children’s LT occurs at a higher percentage of O2peak than that of adults (33,34,46), we hypothesized that their optimal recovery intensity would be similarly higher (i.e., ∼50% O2peak). For that reason, a recovery intensity of 30% O2peak was not included in the studied range. Consequently, although that hypothesis was not borne out by our findings, it remains an open question whether or not children’s optimal recovery intensity may reside below 40% O2peak. Judging from the small difference observed between the 50 and 40% intensities, in the present study, it seems reasonable that a 30% recovery intensity would not significantly affect [La] reduction much further.
Our subjects’ [La] values during the preliminary steady-state baseline testing (Table 2) agree well with the above-mentioned findings that children’s LT occurs at a higher percentage of O2peak. For example, Williams and Armstrong (46) found 2.5 mM [La] to occur at 85% O2peak in prepubertal children. In adults on the other hand, higher [La] values are typically found at considerably lower exercise intensities. For example, interpolation of data from Hermansen and Saltin (23) and from McLellan and Skinner (31) reveal [La] values of 2.7 and 4.6 mM or 1.7 and 3.1 mM, at 50 and 60% O2peak, respectively. Thus, it remains unclear why children’s optimal exercise intensity for the reduction of [La] is not indeed higher than what was demonstrated in the present study.
Although active recovery expedites the [La] decrease after intense exercise (5,14,17,31,36), it imposes a degree of exertion, consumes energy, and reduces the rate of muscle glycogen resynthesis (10). Therefore, one should strive to actively recover at the lowest intensity that still promotes efficient La removal. In this study, we therefore put forth the %HRpeak × %[La]peak product as an alternative combined index for the determination of optimal recovery intensity. To normalize the comparison of the four recovery modes using this index, we used its highest value in each mode as 100% and compared subsequent values to it (Fig. 3). In this manner of representing recovery, the differences among the three active modes appear to increase (Figs. 3 vs 1b), suggesting that R60 is still less advantageous, whereas R40 is a more efficient mode of recovery. According to this index, passive recovery has an advantage over the active modes in the first several minutes postexercise. However, it should be noted that in the above index, HR and [La] could be weighted differently or related to each other in a more complex manner. In fact, one of the shortcomings of the above index, in its present form, is its questionable ability to properly reflect metabolic recovery during the first few minutes after exercise, before [La] reaches its peak and begins its own recovery. Further consideration of this index, including actual performance-recovery studies is warranted.
A discussion of recovery is incomplete without reference to the time axis. Passive recovery eventually leads to resting [La] and to full restoration of performance capacity, both of which may not be fully attainable under active recovery. The question, therefore, is not which recovery protocol leads to the lowest [La] but rather what are the dynamics of the different modes of recovery.
Stamford et al. (36) showed, in adults, that during the first 10 min of active recovery after supramaximal exercise, when [La] was still high, work intensity of 70% O2peak reduced [La] more than did exercise at 40%. From 15 min on, when [La] was already considerably lower, 40% O2peak was more efficient in [La] reduction. Although the authors assumed that the 70% level was above their subjects’ anaerobic threshold, it should be pointed out that their steady-state [La] at this exercise intensity was only 3.5 mM, suggesting that it was below their true maximal La steady-state (MLSS). This suggestion is upheld by the data of Dodd et al. (14), whose trained subjects reached [La] of 4.8 mM at only 65% O2peak. Because children are expected to reach MLSS well above 75% O2max (46), a phenomenon such as that reported by Stamford et al. (36) was more likely to be evident in our prepubertal subjects. This, however, was not the case because R60 was at no point more efficient than R40 or R50 in reducing [La] (Fig. 1b).
Previous studies in adults have demonstrated that an active recovery can enhance subsequent performance capacity compared with a passive recovery of similar duration (1,35,39,44). Where measured, [La] at the end of the active recovery was lower than that at the end of the passive recovery (1,39,44). An enhanced exercise performance capacity after an active compared with passive recovery has not yet been demonstrated in children.
In summary, the results of the present study demonstrate that in children, similar to previous findings in adults, active recovery results in faster blood [La] reduction compared with passive recovery. Among the recovery intensities examined in this study, 40 and 50% O2peak resulted in the lowest [La] values after a 25-min recovery. In view of the lower exertion and likely lower muscle glycogen use in the 40% compared with the 50% O2peak recovery intensity, the former should be considered more advantageous for accelerating [La] reduction after supramaximal exercise in prepubertal children. Further research is required to elucidate the possibility that a lower intensity is still more advantageous than the studied intensities.
We would like to thank all the subjects and their parents for volunteering their time, effort, and enthusiasm to this study. Special thanks to Yossy Shorer of Kibbutz Gaash for his help in subject recruitment.
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