During the transition from rest to exercise at an intensity below the lactate threshold (i.e., moderate-intensity exercise), pulmonary oxygen uptake (V˙O2) proceeds, after a short delay representing the muscle to lung blood transit time, along a time course that can be confidently modeled by a single exponential decay term (44). This "phase 2" or "fundamental" response of V˙O2 kinetics is thought to closely represent the kinetics of muscle oxygen consumption, at least in healthy subjects (2,4,38). Perhaps the most potent stimulus to bring about a speeding of V˙O2 kinetics, and thus a faster attainment of a steady state of V˙O2, is exercise training. Several cross-sectional (10,12,27,28,30,37) and longitudinal (1,7,8,21,24,36,46) studies in adults have demonstrated training-induced reductions in the time constant of the fundamental phase of V˙O2 kinetics during both moderate- and heavy-intensity exercise. However, in contrast to this large body of evidence surrounding the impact of training on V˙O2 kinetics in adults, there is a relative dearth of data regarding the effects of training in children and adolescents.
Because children and adolescents are characterized by higher oxidative enzyme activity (23) and faster oxygen uptake kinetics (19) compared with adults, the effects of training on oxygen uptake kinetics may be limited in this population. Alternatively, younger subjects respond to endurance training in a similar manner to adults, with improvements in aerobic capacity reflected by enhancements in blood volume and oxidative enzyme activity (16,17). Given the link between training status and oxygen uptake kinetics in adults, it therefore seems reasonable to also expect faster oxygen uptake kinetics in trained children and adolescents compared with untrained controls. Conversely, in the only previous systematic study of this issue, Obert et al. (35) showed no difference in the fundamental phase of V˙O2 kinetics in either moderate- or heavy-intensity exercise between trained and untrained children. However, there was a dichotomy between the training regimen undertaken and the experimental exercise mode because this study used cycle ergometry as the mode of exercise, yet the experimental group were trained swimmers. Across several different sports, it has been shown that V˙O2 kinetics in trained subjects were markedly slower when the muscle group under investigation was not specific to the training (10). Hence, it is perhaps unsurprising that Obert et al. (35) could show no difference in V˙O2 kinetics during cycle ergometry in trained swimmers versus untrained controls. It is therefore feasible that if the muscle group under investigation is that which is predominately exercised during training, faster V˙O2 kinetics will be demonstrable in trained subjects, versus untrained controls, in children and adolescents.
Exercise training has the potential to augment both oxygen delivery and oxygen utilization mechanisms; hence, it is possible that improvements in oxygen delivery and utilization mechanisms interact to result in the faster V˙O2 kinetics that are demonstrable in trained versus untrained subjects (42). The deoxyhemoglobin signal from near-infrared spectroscopy (NIRS) indicates the balance between oxygen supply and demand in the interrogated tissue; hence, measurement of muscle deoxygenation kinetics in the exercising muscle can be used to examine the relative mismatch in oxygen delivery and oxygen utilization at the onset of exercise. Slower (relative to a relevant control) muscle deoxygenation kinetics would indicate a tipping of the oxygen delivery/utilization mismatch in favor of oxygen delivery, whereas faster muscle deoxygenation kinetics would indicate a tipping of this mismatch in favor of oxygen utilization. Hence, NIRS can be used to help determine mechanisms responsible for alterations in oxygen uptake dynamics (15).
Given the limitations of previous studies (13), the purpose of the present study was to examine pulmonary oxygen uptake kinetics in trained and untrained male adolescents. On the basis of data from adult populations, we hypothesized that the trained subjects would possess faster V˙O2 but unchanged muscle deoxygenation kinetics in response to exercise reflecting adaptations of both oxygen supply and oxygen utilization mechanisms in response to chronic exercise training.
Sixteen trained (15 ± 0.8 yr) and nine untrained (15 ± 0.6 yr) male adolescents volunteered to take part in the study. All subjects were in good health and taking no medications that would influence cardiovascular or muscular function. These subjects were participants in a previously published study examining myocardial functional responses to exercise (39). By self-assessment, the two groups were matched for maturity status (Tanner stage range 2-4, for trained and untrained subjects, see Table 1 for subjects' physical characteristics). Informed written parental consent and subjects' assent were obtained before participation. The study was approved by an institutional research ethics committee.
Fourteen of the trained subjects were soccer players from an English Premier League club youth academy. These subjects reported an average of 7.4 ± 2.2 yr of training, currently practicing 9.9 ± 1.4 months·yr−1, 6.1 ± 1.9 h·wk−1, and have been playing in competitive matches for 6.9 ± 1.8 yr. A further two subjects reporting 7 h of weekly cycle and martial arts training, respectively. The untrained group consisted of nine subjects who reported little regular physical activity and limited recreational sports participation.
Subjects visited the laboratory on two occasions, separated by 3-7 d. At each visit, subjects were asked to have refrained from strenuous exercise in the preceding 48 h and to be 3 h postprandial. At the first visit, subjects performed an incremental exercise test to volitional exhaustion on a cycle ergometer at 60 rpm (Lode Excalibur Sport, Groningen, the Netherlands). The test consisted of 3-min increments of 35 W commencing from an initial workload of 35 W. Maximal oxygen uptake (V˙O2max) was defined as the mean of the two highest 30-s average values during the final stage of exercise. In addition, the lactate threshold was estimated via the v-slope method and confirmatory inspection of the ventilatory equivalent and end-tidal pressure plots for oxygen uptake and carbon dioxide production (5). This process was conducted by two of the named authors with the data confirmed by an independent and appropriately experienced third party. At the second visit to the laboratory, subjects completed two 6-min square wave exercise transitions from a 3-min baseline of 10 W to 80% of the workload, which elicited the lactate threshold. Each exercise transition was separated by a minimum 1 h of passive rest during which time subjects' body composition was assessed via air-displacement plethysmography (BodPod; Life Measurement, Inc, Concord, CA).
Throughout all exercise bouts, HR was measured every 5-s via short-range telemetry (Polar S610, Kempele, Finland). Expired air was measured breath-by-breath via standard open circuit techniques with minute ventilation assessed via pneumotachometer (Zan 600, Oberthulba, Germany). During the square wave exercise bouts, continuous noninvasive measurements of muscle deoxygenation status were also made via NIRS (OxiplexTS; ISS, Champaign, IL). The OxiplexTS uses light at wavelengths of 690 and 830 nm and is a frequency-domain multidistance system, thus enabling direct measurement of the scattering, and therefore absorption coefficient, of NIR light, hence producing absolute values (μM) of oxyhemoglobin (HbO2), deoxyhemoglobin (Hb), and total hemoglobin (THb) concentration. Light source-detector separation distances of 1.50-3.04 cm for each wavelength were used with cell water concentration assumed constant at 70%. For the present study, data were sampled at 2 Hz. The flexible probe was placed longitudinally along the belly of the left vastus lateralis midway between the greater trochanter and the lateral condyle of the tibia and marked with washable pen such that the probe could be placed in the same position for the second exercise bout. The probe was held firmly in place by elastic Velcro strapping, and movement of the optical fibers during cycling was limited by taping them to an adjacent table. After each trial, indentations of the probe on the subject's skin were inspected to confirm that the probe had not moved, which was the case for every exercise transition. The NIRS probe was calibrated before each testing session using a calibration block of known absorption and scattering coefficients. Calibration was then cross-checked using a second block of known but distinctly different absorption and scattering coefficients. Each of these procedures was according to the manufacturer's recommendations.
V˙O2 kinetic analysis
Abnormal breaths due to coughs and swallows were first removed from the V˙O2 data to prevent skewing of the underlying response. The criterion for removal of these breaths was those that were different to the mean of the adjacent four data points by more than three times the SD of those four points. Each data set was then interpolated second-by-second between 0 and 360 s; the two data sets were then ensemble averaged to produce a single response for each subject. The first 20 s of the ensemble data set (cardiodynamic phase 44) were then removed (31). The remaining data set (i.e., up until the end of exercise) was fitted to a monoexponential curve (Origin; MicroCal, Northampton, MA) with a delay relative to the onset of exercise of the form:
where V˙O2(b) is the mean V˙O2 measured during the final minute of baseline (10 W) exercise,
is the asymptotic amplitude of the fundamental (phase 2) response,
is a time delay relative to the onset of exercise, and
is the time constant for the fundamental component of the response. Steady-state oxygen uptake (V˙O2(ss)) is therefore the sum of
and the mean response time
was defined as
NIRS kinetic analysis
The Hb response to exercise was modeled in a similar fashion to V˙O2 kinetics; firstly, the two data sets for each subject were ensemble averaged to produce a single data set for each subject with data points at 0.5-s intervals (i.e., 2 Hz). Secondly, the point at which Hb starts to increase after a short delay of ∼5-10 s (15) was identified. This time point was identified by fitting two linear regression curves to the first 20 s of the ensemble data set and, using custom-written software and the Solver function in Excel (Microsoft Corp., Redmond, WA), determining the time point at which the sum of error squared was minimized. This technique assumes linear characteristics of the data in the first few seconds after the onset of the increase in Hb, which, given the short time frame, seems reasonable. From this point up until the time at which the V˙O2 data achieved 98% of its final value
i.e., effective steady state), the data were fitted to a monoexponential curve (Origin; MicroCal) with a delay relative to the onset of exercise of the form:
where Hb(b) is the mean Hb measured during the final minute of baseline (10 W) exercise, A Hb is the asymptotic amplitude of the response, TDHb is a time delay relative to the onset of exercise, and τHb is the time constant for the response. The absolute value of Hb at
(Hb(Φ3))is therefore the sum of Hb(b) + A Hb, and the mean response time (MRTHb) was defined as τHb + TDHb. Although it is not certain whether the processes underlying the Hb response are exponential in nature, visual inspection of the data and reference to previous literature (15,22,33) suggest that a monoexponential decay model of the form above provides a reasonable estimate of the time course of muscle deoxygenation during this "primary" phase of the Hb response. The average value during the final 30 s of exercise (Hb(360-330) s) was also calculated, as was the difference between Hb(360-330) s and Hb(Φ3) (A 2Hb). Baseline THb and HbO2 concentration were calculated as the average values during the final minute of 10-W cycling.
Estimated capillary blood flow kinetics
Capillary blood flow (Q˙cap) kinetics were estimated by rearrangement of the Fick equation with the substitution of pulmonary oxygen uptake kinetics (V˙O2p, fundamental phase) for muscle oxygen consumption kinetics (V˙O2m) and Hb kinetics for the kinetics of oxygen extraction, (a − v)O2 (20):
This method assumes that muscle oxygen uptake rises exponentially from time zero with the same time course as the fundamental phase of pulmonary oxygen uptake kinetics. To this end, the fundamental phase of pulmonary oxygen uptake kinetics was extrapolated backward to the baseline value, which was given as time zero. The resulting data set were modeled up to 360 s via a monoexponential term with delay of the form,
where Q˙cap(b) is equal to V˙O2/Hb during the last minute of unloaded pedaling and
are the amplitude, time delay, and time constant of the "fundamental" response, respectively. The mean response time was calculated as
are expressed in arbitrary units, and
are expressed in seconds. To determine the optimum fitting window for the "fundamental" phase of Q˙ cap kinetics, all data sets from 0-360 s to 60-360 s were sequentially modeled, and the best fit for each fitting window was determined by nonlinear least squares fitting (see above). The fitting window chosen to represent each transition was that which produced minima in the χ2 value concomitant with a plateau in the time constant of the response.
HR kinetics were modeled via a similar monoexponential function as for V˙O2 kinetics but with the response constrained to start at the onset of exercise (t = 0), i.e., no delay term (11). Baseline HR (HR(b)) was calculated as the average during the last minute of 10-W pedaling, with steady-state HR (HR(ss)) being the sum of the amplitude (A HR) and baseline HR, and τ HR is defined as the time constant of the response.
Confidence intervals of V˙O2 kinetics were analyzed by a paired t-test (SPSS 16.0; SPSS, Inc., Chicago, IL). All other comparisons between groups were made using an independent two-tailed t-test with homogeneity of variance checked via Levene's test. Data are presented as mean ± SD, and statistical significance was accepted at the P ≤ 0.05 level.
Representative plots of an untrained and trained subject are presented in Figure 1 with exponential curve fit and residuals shown. The 95% confidence interval for
laid within acceptable boundaries (trained: 4.0 ± 1.1 s vs untrained: 5.4 ± 1.9 s).
The time constant and mean response time of V˙O2 kinetics was ∼25% (P = 0.05) and ∼13% (P = 0.03) faster in trained subjects compared with untrained, respectively (Table 2). Because of the higher workload in the trained subjects compared with that in the untrained subjects (trained: 114 ± 22 W vs untrained: 90 ± 23 W, P = 0.02), the amplitude of the V˙O2 kinetics and steady-state V˙O2 were higher in trained versus untrained subjects (P < 0.01; Table 2), with no difference in the exercise economy (gain)
of the response (P = 0.1), although this latter result would have been reversed if the variances of the two groups for this parameter had not been unequal (P = 0.05).
Representative plots of Hb kinetics for an untrained and trained subject are presented in Figure 2 with exponential curve fit and residuals shown. The 95% confidence interval for τ Hb was 1.39 ± 0.58 s (trained) and 1.58 ± 0.48 s (untrained). Time constant, time delay, or mean response time of Hb kinetics did not differ between groups.
were all higher in trained versus untrained subjects (P = 0.03, P = 0.001, and P = 0.001, respectively; Table 3). This difference remained when the data were normalized for the increment in oxygen uptake, apart from A Hb in which case this difference was abolished (P = 0.1; Table 3). Representative plots of Hb kinetics are shown in Figure 2.
Baseline THb (81 ± 24 vs 49 ± 19 μM, P < 0.01) and HbO2 (58 ± 18 vs 37 ± 13 μM, P < 0.01) concentrations were significantly higher in the trained subjects compared with untrained.
Q˙ cap kinetics.
Representative plots of Q˙ cap kinetics for an untrained and trained subject are presented in Figure 3 with exponential curve fit and residuals shown. The 95% confidence interval for
was 3.9 ± 1.8 s (trained) and 3.7 ± 1.2 s (untrained). The time delay of Q˙ cap kinetics was not different between groups (trained: 20.3 ± 6.4 s vs untrained: 20.7 ± 4.6 s). However, the time constant (trained: 19 ± 10 s vs untrained: 30 ± 13 s, P = 0.04) and mean response time (trained: 40 ± 11 s vs untrained: 51 ± 10 s, P = 0.03) were significantly faster in the trained subjects.
Representative plots of HR kinetics for an untrained and trained subject are presented in Figure 4 with exponential curve fit and residuals shown. The 95% confidence interval for τ HR was 3.8 ± 1.1 s (trained) and 5.9 ± 1.9 s (untrained). The baseline (trained: 90 ± 12 bpm vs untrained: 93 ± 12 bpm, P = 0.47), amplitude (trained: 43 ± 8 bpm vs untrained: 38 ± 6 bpm, P = 0.17), and steady state (trained: 133 ± 12 bpm vs untrained: 132 ± 12 bpm, P = 0.84) of the HR response to exercise were not different between groups. However, the time constant of HR kinetics was significantly faster in the trained subjects (trained: 37 ± 10 s vs untrained: 49 ± 14 s, P = 0.03).
The main finding of the present study was that pulmonary oxygen uptake kinetics were ∼25% faster in a group of trained male adolescents compared with their untrained counterparts during the transition to moderate-intensity exercise. In addition to faster V˙O2 kinetics, HR kinetics and estimated capillary blood flow kinetics were also faster in the trained subjects. In contrast, muscle deoxygenation (Hb), kinetics, as measured by NIRS, was unchanged between groups. Taken together, the present data suggest that the faster V˙O2 kinetics were due to enhancements in both central (oxygen delivery) and peripheral (oxygen utilization) mechanisms.
The V˙O2 kinetics data are in line with a large body of cross-sectional and longitudinal data in adults (1,7,8,10,12,21,24,27,28,30,36,37,46) but are in contrast to the only previous study to examine the effects of training status on oxygen uptake kinetics in children and adolescents (35). Although there was a difference in the physical maturity of the subjects between the two studies (subjects were prepubescent in the study by Obert et al. (35)), a major limitation of this previous study was the use of cycle ergometry with a group of trained swimmers. During the transition to moderate-intensity exercise in healthy subjects, V˙O2 kinetics are thought to be primarily limited by factors affecting oxygen utilization (i.e., in the peripheral musculature) rather than oxygen delivery (18,26,32,33,45). Hence, it might be expected that the specific muscle group being trained and thence studied is important in establishing a difference between the trained and untrained state. Indeed, in a previous study (10), V˙O2 kinetics in trained swimmers and kayakers were markedly slower during leg compared with arm exercise, with the opposite being shown in trained runners. Hence, the dichotomy between the muscles used during the training and experimental modes of exercise is likely to have accounted for the lack of any effect of training status on V˙O2 kinetics in the study by Obert et al. (35). In contrast, the present study used cycle ergometry with the trained group consisting of athletes whose training predominantly focuses on the leg musculature; hence, there was a match between the muscle used during the training and the experimental exercise.
The cross-sectional nature of the present study does not allow us to rule out the possibility that inherent physiological characteristics predisposed the trained subjects to have faster V˙O2 kinetics compared with the untrained subjects. Nevertheless, given the rapidity of physical changes that can occur in adolescents, cross-sectional designs such as the present study remain an appropriate experimental design to explore the effect of training status on physiological parameters such as V˙O2 kinetics. In the present study, we were careful to select two samples that, as much as possible, differed only in their training status. In this regard, a strength of the present study was the inclusion of 14 subjects from a professional soccer club (English Premiership) where it is possible to confirm the reported volume of training (see Methods) completed in the months and years before the study. The untrained group, although healthy, reported very little and unstructured physical activity in their daily lives. Therefore, we are confident that the significantly faster V˙O2 kinetics demonstrated by the trained group represent adaptations to long-term exercise training rather than differences in inherent physiological characteristics.
The training undertaken by the trained group in the present study involves the mobilization of a large muscle mass and for 15 of the subjects, supporting the mass of the body on the muscle groups under investigation. Hence, central and peripheral adaptations to training will both have the potential to determine the faster V˙O2 kinetic response to exercise versus the untrained group. Certainly, noninvasive imaging techniques have demonstrated that trained adolescents have augmented stroke volume and thus cardiac output in response to maximal incremental exercise relative to their untrained peers (40), demonstrating a central cardiac adaptation to exercise training. However, ethical considerations preclude the analysis of peripheral adaptations to training in adolescents that would ordinarily require invasive techniques such as muscle biopsies. During the transition to exercise, the fundamental phase of V˙O2 kinetics are not thought to be limited by oxygen delivery (18,26,32,33,45); therefore, one could surmise that these peripheral adaptations to training are more important in determining the faster V˙O2 kinetics relative to the untrained subjects. On the other hand, all of these previous studies were conducted with healthy adult populations and it is presently not clear whether the same would follow in children or adolescents. Indeed, although only an indirect measure of muscle oxygen delivery, HR kinetics, and therefore presumably cardiac output kinetics (as has been shown previously in children and adolescents ) and estimated capillary blood flow kinetics were faster in the trained subjects in the present study. Hence, in the present study, the faster V˙O2 kinetics in trained subjects compared with that in untrained may have been due to the enhanced oxygen delivery to the exercising muscle. Furthermore, this may indicate that, in adolescents, V˙O2 kinetics are normally limited by oxygen delivery.
The Hb signal from NIRS represents the balance between oxygen supply and utilization in the interrogated tissue and therefore represents an excellent means to help establish the mechanisms behind the faster V˙O2 kinetics in the trained subjects. Slower Hb kinetics after training would reflect adaptations in oxygen delivery at the onset of exercise that were in excess of enhancements in oxygen utilization. In adolescents, training induces enhancements in ventricular preload and stroke volume (40), estimates capillary blood flow kinetics (present study), and may reduce heterogeneity of oxygen delivery to the active muscle (15). Furthermore, aerobically trained children and adolescents are also characterized by a higher proportion of Type I muscle fibers in the trained musculature (14,34), and it has been shown that muscle composed predominantly of Type I fibers possesses a higher oxygen delivery-to-oxygen consumption ratio during contractions as compared with muscle composed predominantly of Type II fibers (6). Hence, it might therefore be expected that Hb kinetics would be slower and have a reduced ΔHb/ΔV˙O2 in the trained subjects compared with their untrained counterparts. However, the previous finding of no difference in the relative amplitude of the slow component of oxygen uptake kinetics during cycle exercise in trained and untrained children (35) suggests that muscle fiber type and recruitment patterns are unaffected by training in the presently studied population when the same relative exercise intensity is used (3). Faster Hb kinetics after training (in concert with faster V˙O2 kinetics) would be indicative of enhancements in the rate of increase of oxygen utilization at the onset of exercise in the face of relatively little improvement in oxygen delivery. Because enhancements in mitochondrial density and oxidative enzyme activity accompany endurance training in adults, children, and adolescents (16,25,36,41), it might alternatively be expected that Hb kinetics would be faster in the trained group.
The finding that Hb kinetics and ΔHb/ΔV˙O2 were unchanged between the trained and untrained subjects in the present study suggests that enhancements in oxygen utilization, oxygen supply, and Type I muscle fiber recruitment due to training status were equally important in determining the faster V˙O2 kinetic response to exercise. Essentially, the unchanged dynamics of Hb between the trained and untrained subjects during the transition to exercise reflects an unchanged balance in the oxygen delivery-to-oxygen consumption ratio because of parallel enhancements in oxygen delivery (as indicated by faster HR and Q˙ cap kinetics) and oxygen utilization in the trained subjects. The tendency for statistical significance (P = 0.1) in ΔHb/ΔV˙O2 is likely to be due only to group differences in subcutaneous thigh thickness (as indicated by the significantly different percentage body fat) blunting the change in Hb with exercise in the untrained group (43) (see below). Furthermore, any correction for this effect would serve to bring the mean values for the two groups closer together, i.e., increase the mean value of the untrained group. Hence, taken together, the NIRS data strongly suggest that the faster V˙O2 kinetics in the trained, relative to the untrained group were due to the adaptations in oxygen supply and oxygen utilization mechanisms.
The NIRS data from the present study potentially highlight an important methodological consideration when comparing diverse groups as baseline THb, HbO2, and Hb concentrations were significantly higher in the trained compared with the untrained subjects. Fat acts as a low-scattering constant absorber of near-infrared light; therefore, increased subcutaneous fat has the potential to blunt the interrogative depth of near-infrared light into the exercising muscle (9,43) and reduce the detectable change in hemoglobin oxygenation in response to exercise (43). It is therefore possible that the significantly higher percentage whole-body fat in the untrained subjects could also have manifested itself as increased thigh subcutaneous fat at the site of NIRS interrogation. Hence, some of the difference in the steady-state NIRS measures between the two groups may be attributable to differences in subcutaneous fat (the Hb kinetic response should be relatively unaffected, although impacts upon the amplitude of the response will affect the confidence of parameter estimation of Hb kinetics) including those normalized for oxygen uptake (i.e., ΔHb/ΔV˙O2). However, as discussed above, if the change in Hb with exercise is blunted in the untrained subjects, then this will lead to an artificial lowering of ΔHb/ΔV˙O2 and correction for this effect will serve to bring the ΔHb/ΔV˙O2 data for the trained and untrained subjects closer together, demonstrating no effect of training status on this parameter. Unfortunately, in the present study, we did not collect skinfold/subcutaneous fat data and were therefore unable to determine the extent to which enhanced whole-body fat in the untrained subjects manifested as a relative increase in the subcutaneous fat of the thigh. Future studies should therefore consider the depth of subcutaneous fat at the site of interrogation before selecting source-detector distances of the NIRS apparatus, ensuring that subcutaneous fat thickness is well below 50% of the source-detector distance (9).
The present discussion makes the implicit assumption that the region of muscle interrogated by the NIRS probe represents the entire exercising muscle group. However, a recent study showed spatial heterogeneity of muscle deoxygenation during exercise of the vastus lateralis (29). Therefore, although we ensured that the NIRS probe was positioned at the same location for each subject (midway between the greater trochanter and the lateral condyle of the tibia), we cannot rule out the possibility that differences in whole-muscle Hb kinetics between groups were not detected because of intersubject disparities in the site-specific Hb response to exercise.
In conclusion, the present study has demonstrated for the first time faster V˙O2 kinetics in trained adolescents compared with untrained controls, adding to a large volume of similar data in adult populations (1,7,8,10,12,21,24,27,28,30,36,37,46). Although inherent capabilities of the trained subjects cannot be ruled out, we propose that the data represent adaptations to chronic training. Furthermore, muscle deoxygenation data, via NIRS, suggest that faster V˙O2 kinetics were due to the enhancements in both central (oxygen delivery) and peripheral (oxygen utilization) mechanisms.
This work was not funded by the National Institutes of Health, Wellcome Trust, Howard Hughes Medical Institute, or others.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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Keywords:©2010The American College of Sports Medicine
NEAR-INFRARED SPECTROSCOPY; OXIDATIVE METABOLISM; HR KINETICS; EXERCISE