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J Appl Physiol 98: 1371-1378, 2005. First published December 3, 2004; doi:10.1152/japplphysiol.01028.2004
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Prior heavy-intensity exercise speeds O2 kinetics during moderate-intensity exercise in young adults

Brendon J. Gurd,1,2 Barry W. Scheuermann,4 Donald H. Paterson,1,2 and John M. Kowalchuk1,2,3

1Canadian Centre for Activity and Aging, 2School of Kinesiology, and 3Department of Physiology and Pharmacology, The University of Western Ontario London, Ontario, Canada; and 4Department of Kinesiology, The University of Toledo, Toledo, Ohio

Submitted 16 September 2004 ; accepted in final form 29 November 2004


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics ({tau}O2) was examined in young adults exhibiting relatively fast (FK; {tau}O2 < 30 s; n = 6) and slow (SK; {tau}O2 > 30 s; n = 6) O2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak O2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. O2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). {tau}O2 was lower (P < 0.05) in Mod2 than in Mod1 in both FK (20 ± 5 s vs. 26 ± 5 s, respectively) and SK (30 ± 8 s vs. 45 ± 11 s, respectively); linear regression analysis showed a greater "speeding" of O2 kinetics in subjects exhibiting a greater Mod1 {tau}O2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced (P < 0.05) in Mod2, whereas the HHb mean response time was reduced (P < 0.05) in FK (Mod2, 22 ± 3 s; Mod1, 32 ± 11 s) but not different in SK (Mod2, 36 ± 13 s; Mod1, 34 ± 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of O2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.

near-infrared spectroscopy; muscle deoxygenation; heart rate; muscle oxygen utilization; warm-up exercise

DURING THE TRANSITION TO moderate-intensity exercise, pulmonary O2 uptake (O2) (and muscle O2 consumption) increase exponentially toward a new steady state. The mechanism(s) responsible for limiting the rate of O2 adaptation is unknown; however, blood flow or O2 delivery and activation of enzymes and provision of substrate for mitochondrial oxidative phosphorylation have been implicated (17, 25). Previous studies have shown that in older, but not younger, adults the adaptation of pulmonary O2 during the transition to moderate-intensity exercise became faster when preceded by a priming bout of heavy-intensity exercise (12, 32). This speeding of O2 kinetics was attributed to an attenuation of a muscle perfusion or O2 delivery limitation in the older adults. That O2 kinetics were not affected by the prior bout of heavy-intensity exercise in young adults agrees with previous findings (5, 16, 31) and is consistent with the suggestion that blood flow and O2 delivery do not limit O2 kinetics in younger adults. However, a consistent observation among these studies is that the time constant of the fundamental, phase 2 component of pulmonary O2 (i.e., {tau}O2) is significantly faster in younger (~20–30 s) (5, 12, 16, 31, 32) compared with older adults (~40–60 s) (4, 6, 7, 12, 32). Thus it is unclear from these studies whether the apparent lack of speeding of O2 kinetics (i.e., reduction in {tau}O2) during moderate-intensity exercise in young compared with older adults is a consequence of age-dependent differences between groups or of physiological differences (unrelated to age per se) that contribute to slower adaptation of O2 in older compared with younger adults.

Therefore, the purpose of this study was to examine the effect of a priming bout of heavy-intensity exercise on the adaptation of pulmonary O2 during moderate-intensity exercise in healthy young adults exhibiting a range of {tau}O2 values typically associated with young (i.e., {tau}O2 < 30 s) and older adults (i.e., {tau}O2 > 30 s). We hypothesized that, after a bout of heavy-intensity exercise, 1) the {tau}O2 during moderate-intensity exercise would be reduced in those individuals having the slower O2 kinetics during exercise without warm up and 2) the faster O2 kinetics would be a result of improved local muscle perfusion and O2 delivery before and throughout the exercise transition following warm-up exercise.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects.   Twelve young male adults volunteered and gave written, informed consent to participate in the study. All subjects were healthy, and no subjects were taking medications known to affect the cardiorespiratory system. This study was approved by The University of Western Ontario Ethics Committee for Research on Human Subjects.

Exercise protocol.   Subjects reported to the laboratory on five separate occasions at approximately the same time of day for each subject. An incremental ramp exercise test (25 W/min) to the subject's limit of tolerance was performed on an electromagnetically braked cycle ergometer (model H-300-R, Lode) on the first day of testing to determine the estimated lactate threshold ({theta}L) and peak O2 uptake (O2 peak). The {theta}L was defined as the O2 at which CO2 production began to increase out of proportion relative to O2, combined with a systematic rise in the ventilatory equivalent for O2 and end-tidal PO2 with no concomitant rise in the ventilatory equivalent for CO2 production or end-tidal PCO2. O2 peak was calculated as the average O2 over the final 20 s of the ramp exercise test. From the results of this ramp test, a moderate-intensity work rate (WR) was selected to elicit a O2 equivalent to ~80% of the O2 at {theta}L, and a heavy-intensity WR was selected to elicit a O2 corresponding to ~50% of the difference between the O2 at {theta}L and O2 peak.

In each of the subsequent four visits to the laboratory, subjects performed two step transitions in WR of moderate intensity (Mod1 and Mod2) separated by a step increase in WR of heavy intensity, as described by Scheuermann et al. (32). Exercise was performed continuously; the duration of each step transition was 6 min, and each transition was preceded by a baseline of 20 W of cycling lasting 6 min. Changes in WR were initiated as a step function without a warning to the subject. This protocol was performed four times, resulting in four repetitions for each subject and condition. After testing and analyses of the data were completed, the subjects were divided into two groups based on the {tau}O2 of their initial transition to moderate-intensity exercise: Mod1 {tau}O2 ≤ 30 s ["fast" kinetics group (FK); n = 6] and Mod1 {tau}O2 ≥ 30 s ["slow" kinetics group (SK); n = 6] (Table 1). This was done in an attempt to examine a group of young subjects with O2 kinetics similar to those seen in older adults.


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  		Table 1 Physical characteristics, response to ramp exercise, and {tau}O2 with confidence intervals in FK and SK groups

 
Materials.   Gas-exchange measurements were similar to those described previously (12). Briefly, inspired and expired flow rates were measured with a low dead space (90 ml) bidirectional turbine (Alpha Technologies VMM 110), which was calibrated before each test with a syringe of known volume (3 liters). Inspired and expired gases were sampled continuously at the mouth and analyzed for concentrations of O2, CO2, and N2 by mass spectrometry (Morgan Medical) after calibration with precision-analyzed gas mixtures. Changes in gas concentration were aligned with gas volumes by measuring the time delay for a square-wave bolus of gas passing the turbine to the resulting changes in fractional gas concentrations as measured by the mass spectrometer. Data collected every 20 ms were transferred to a computer, which aligned concentrations with the volume data to build a profile of each breath. Breath-by-breath alveolar gas exchange was calculated by the algorithms of Beaver et al. (2).

Beat-by-beat heart rate (HR) was monitored continuously by electrocardiogram by use of a three-lead placement. We collected the data using Power Lab on a separate collection computer.

Near-infrared spectroscopy (NIRS; Hamamatsu NIRO 300, Hamamatsu Photonics, Tokyo, Japan) was used to continuously measure changes in concentration of local muscle oxy- (O2Hb), deoxy- (HHb), and total hemoglobin-myoglobin (Hbtot) of the vastus lateralis. Optodes were placed on the belly of the muscle midway between the lateral epicondyle and the greater trochanter of the femur. To ensure that the positions of the optodes, relative to each other, were fixed, the optodes were housed in an optically dense plastic holder. The optode assembly was secured on the skin surface with tape, covered with an optically dense black vinyl sheet to minimize the intrusion of extraneous light and loss of near-infrared-transmitted light from the field of interrogation, and wrapped with an elastic bandage to minimize movement of the optodes while still permitting freedom of movement for cycling. This preparation essentially prevented any optode movement relative to the skin surface.

For a detailed description of the theory of NIRS, see Elwell (14). Briefly, the near-infrared light produced by the laser diodes was carried by a fiber-optic bundle to the tissue of interest, and the transmitted light was returned by a second fiber-optic bundle from the tissue to a photon detector (photomultiplier tube) in the spectrometer. Four different wavelength laser diodes (775, 810, 850, and 910 nm) provided the light source. The diodes were pulsed in rapid succession, and the light was detected by the photomultiplier tube. The intensities of incident and transmitted light were recorded continuously at 1 Hz and, along with the relevant specific extinction coefficients and optical path length [assuming a differential path length factor = 3.83 (12)], used for online estimation and display of the relative concentration changes from the "zero" set during the resting baseline of O2Hb, HHb, and Hbtot. The raw attenuation signals (in optical density units) were transferred to the computer and stored for further analyses.

The HHb signal can be regarded as being essentially blood volume insensitive during exercise (9, 15); thus it is assumed to be a reliable estimator of changes in intramuscular oxygenation status and represents the balance between local muscle O2 delivery and O2 utilization within the NIRS field of interrogation (10, 15).

Data analysis: curve fitting.   The breath-by-breath O2 and beat-by-beat HR data obtained during each step increase in WR were filtered and linearly interpolated at 1-s intervals. Each transition was time aligned and ensemble averaged to yield a single profile and then time averaged into 10-s bins to give a single response for each subject. The on-transient response to constant-load, moderate-intensity exercise was modeled as a monoexponential of the form

(1)
where Y(t) represents the variable at any time (t); Y(BSL) is the baseline value of Y before the step increase in WR; Amp is the amplitude (i.e., steady-state increase in Y above baseline); {tau} is the time constant (i.e., the time taken to reach 63% of the steady-state response); and TD is the time delay. O2 data were fit from the phase 1-phase 2 transition to the end of exercise, as previously described (30). Initially, the fitting region included data from only the phase 2 response; as the fitting field sequentially was extended back toward exercise onset (toward t = 0), the {tau}O2 and its 95% confidence limits would, at some point, increase as "nonexponential" data from the phase 1 response were included in the fitting field; the time corresponding to the phase 1-to-phase 2 transition was taken as the time point that preceded the sudden increase in {tau}O2 and its 95% confidence limit (30). HR data were modeled exponentially from the onset to the end of exercise. Because WR changed without warning to the subject, it was expected that HR should not increase until after the WR change, thus the time delay for the HR response was limited to a time of ≥0 s.

The time delay before an increase in HHb after exercise onset (HHb-TD) was determined by second-by-second data and corresponded to the first point greater than one standard deviation above the mean of the pretransition baseline value. The estimation of the HHb-TD was performed for each individual trial and reported as the average of the four trials for each subject. The NIRS-derived O2Hb, HHb, and Hbtot data were then time aligned, ensemble averaged, and time averaged into 5-s time bins to yield a single response for each subject. HHb data between the HHb-TD and 90-s exercise were modeled with an exponential function of the form given in Eq. 1 to determine the time course of muscle deoxygenation. Although we are uncertain whether the underlying processes determining muscle deoxygenation are exponential in nature, visual inspection of the NIRS-derived HHb signal and analysis of least squares residuals suggests that fitting with a monoexponential function provides a reasonable estimate of the time course of muscle deoxygenation (i.e., an "effective" HHb time constant) during the time period corresponding to the phase 2 O2 response. The mean response time (MRT = HHb-TD + {tau}HHb, where {tau}HHb is the HHb time constant) was also calculated to provide a description of the overall time course for muscle deoxygenation. The O2Hb and Hbtot signals did not approximate an exponential response, and thus the analysis of these data was limited to determining the steady-state baseline and end-exercise values.

To verify that exercise was performed in the moderate-intensity domain, in addition to the steady-state O2 being below {theta}L and the response being well fit by a monoexponential function, the actual end-exercise O2 (calculated over the final 30 s of exercise) was compared with the "expected" steady-state O2, as estimated using the following equation

(2)
where O2(SS) is the expected steady-state O2, O2(BSL) is the measured baseline O2 at 20 W cycling, {Delta}O2(ramp)/{Delta}WR(ramp) is the gain of the sub-{theta}L O2-WR relationship calculated after allowing for an appropriate time delay (~60 s) between the onset of the ramp forcing function and a discernible increase in O2, and {Delta}WR(CL) is the increase in WR above the 20-W baseline [i.e., WR(constant load) –20 W]. In addition, the slope of the O2 response between 4 and 6 min of Mod1 was calculated to confirm that the slow component of O2 that is seen during heavy-intensity exercise performed above {theta}L did not exist.

Statistical analysis.   Physical characteristics and peak exercise responses between the FK and SK groups were compared by unpaired t-tests. The parameter estimates for O2, HR, HHb, O2HB, and Hbtot during moderate exercise were analyzed by a two-way repeated measures ANOVA. Linear regression was used to determine the relationship between the {tau}O2 for Mod1 vs. Mod2, {tau}O2 Mod1 vs. {Delta}{tau}O2 (Mod2 – Mod1), and O2 peak (ml·kg–1·min–1) vs. {Delta}{tau}O2. Statistical significance was accepted at P < 0.05. All data are presented as means (± SD).


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects were placed into two groups according to their {tau}O2 determined in response to the O2 transition to moderate-intensity exercise without prior heavy-intensity exercise [i.e., Mod1, faster kinetics (FK), {tau}O2 of <30 s; slower kinetics (SK), {tau}O2 of >30 s]. The groups were the same (P > 0.05) with respect to age, height, and body mass, whereas O2 peak was greater (P < 0.05) in FK than in SK (Table 1).

The moderate-intensity WR used in the present study elicited a O2 that was 88% (SD 6) and 87% (SD 5) of {theta}L and 50% (SD 4) and 50% (SD 6) of O2 peak for FK and SK, respectively. To confirm that these work rates were in the moderate-intensity domain, the expected steady-state O2 and the slope of the O2-time response were calculated. The predicted steady-state O2 results [FK: 2.0 (SD 0.2) l/min; SK: 1.8 (SD 0.1) l/min] were not different from the measured end-exercise steady-state O2 results for Mod1 [FK: 1.8 (SD 0.3) l/min; SK: 1.6 (SD 0.1) l/min] and the slope of the O2-WR relationship (calculated between 4 and 6 min of constant-load exercise) was not different from zero [FK: –2.52 (SD 10.31) ml·min–1·min–1; SK: 0.48 (SD 12.65) ml·min–1·min–1].

O2 kinetics.   The O2 response profiles for transitions to Mod1 and Mod2 for a representative subject is presented in Fig. 1. The {tau}O2 for each individual and a summary of the parameter estimates for the O2 on-transition to Mod1 and Mod2 for FK and SK are presented in Tables 1 and 2, respectively. The baseline O2 was higher (P < 0.05) in Mod2 than in Mod1 with no differences between groups. The O2 amplitude was similar between all conditions, whereas the end-exercise O2 was higher (P < 0.05) in Mod2 than in Mod1 in SK but not in FK (Table 2). During Mod1, {tau}O2 was greater (P < 0.05) in SK [45 (SD 11) s] than in FK [26 (SD 5) s] (Table 2). After heavy-intensity exercise, the {tau}O2 for Mod2 was reduced (P < 0.05) in both SK [30 (SD 8) s] and FK [20 (SD 5) s]; although the reduction in {tau}O2 was greater (P < 0.05) in SK [{Delta}{tau}O2, 15 (SD 8) s] than in FK [{Delta}{tau}O2, 6 (SD 3) s], significant differences in {tau}O2 between groups persisted. Of note, the reduction of {tau}O2 in Mod2 after the heavy-intensity exercise was evident in all six subjects in SK and four of six subjects in FK (Table 1), with the difference in {tau}O2 between exercise transitions being greater than the 95% confidence interval of the parameter estimate (i.e., {tau}C95), as determined by the fitting software.



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  		Fig. 1. Ten-second average of breath-by-breath response of pulmonary O2 uptake (O2) for a representative subject, with line of best fit and residuals to exercise before [({circ}, gray line of best fit and residuals; O2 time constant ({tau}O2) = 30 s)] and after ({bullet}, black line of best fit and residuals; {tau}O2 = 19 s) a bout of heavy-intensity exercise shown.

 

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  		Table 2 Summary of parameter estimates for O2 on-transients to cycle ergometer exercise in the FK and SK groups in Mod1 and in Mod2

 
The {tau}O2 results for Mod1 and Mod2 were significantly correlated to each other (r = 0.85), with the slope of the relationship (m = 0.54) being different from the line of identity (Fig. 2A). The difference in {tau}O2 between Mod1 and Mod2 [i.e., {Delta}{tau}O2 (Mod1 – Mod2)] was positively related to the {tau}O2 (P < 0.05) for the exercise transition without prior warm- up (i.e., Mod1) (Fig. 2B). The {tau}O2 for Mod1 (Fig. 3A) and the difference in {tau}O2 between Mod1 and Mod2 (Fig. 3B) were both negatively correlated (r = 0.61; P < 0.05 and r = 0.73; P < 0.05, respectively) to the O2 peak.



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  		Fig. 2. Relationship between {tau}Mod1 and {tau}Mod2 (A) and between {tau}Mod1 and the change ({Delta}) in {tau}O2 between Mod1 and Mod2 (B) for all subjects (both fast kinetics and slow kinetics). {tau}, Time constant. {Delta}{tau}O2 was directly related to the {tau}O2 value of Mod1. Mod1 and Mod2, moderate-intensity exercise before and after heavy-intensity exercise, respectively.

 


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  		Fig. 3. Relationship between peak O2 and {tau}Mod1 (A) and peak O2 and {Delta}{tau}O2 between Mod1 and Mod2 for all subjects (both fast kinetics and slow kinetics). There was a negative relationship between peak O2 and both {tau}Mod1 and {Delta}{tau}O2.

 
HR kinetics.   A summary of the estimates of the HR on transients is shown in Table 3, and data for a representative subject are shown in Fig. 4. The baseline HR before Mod1 was not different between groups and was elevated (P < 0.05) in both groups before Mod2, with the increase being greater (P < 0.05) in SK than in FK. The HR amplitude was not different between groups in Mod1; however, during Mod2, HR amplitude was lower (P < 0.05) in SK than in FK. End-exercise HR was greater (P < 0.05) in Mod2 than in Mod1 in SK only. The HR time constant was not different between groups during Mod1 or Mod2, although the variability in the HR time constant between subjects was high.


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  		Table 3 Summary of parameter estimates for HR on-transients to cycle ergometer exercise in the FKand SK groups in Mod1 and in Mod2

 


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  		Fig. 4. Ten-second average for beat-by-beat heart rate (HR; A and B), total hemoglobin (Hbtot; C and D), oxyhemoglobin (O2Hb; E and F), and deoxyhemoglobin (HHb; G and H) data for a representative subject in Mod1 (A, C, E, and G) and in Mod2 (B, D, F, and H). HHb data includes line of best fit and residuals. Brackets indicate concentration.

 
NIRS.   Response profiles for Hbtot, O2Hb, and HHb for a representative subject are shown in Fig. 4. Hbtot and O2Hb were elevated (P < 0.05) before and throughout Mod2 compared with Mod1 in both FK and SK (Table 4, Fig. 4).


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  		Table 4 Summary of parameter estimates for NIRS response to cycle ergometer exercise in the FK and SK groups in Mod1 and in Mod2

 
A summary of the estimates for the HHb on transient is shown in Table 4. Baseline and amplitude levels for HHb were similar both between groups and in Mod1 and Mod2. The HHb-TD was shorter (P < 0.05) in Mod2 than in Mod1 with no difference between groups. The HHb time constant was similar between groups in Mod1, whereas, during Mod2, the HHb time constant was greater (P < 0.05) in SK than in FK; for SK only, the HHb time constant tended (P = 0.065) to be greater in Mod2 than in Mod1. During Mod1, the HHb MRT (HHb-TD + {tau}HHb) was similar between groups, whereas, in Mod2, HHb MRT was reduced (P < 0.05) in FK compared with Mod1 and was lower in FK than in SK (Table 4).


   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
The major new findings of this study were as follows: 1) in young adults having relatively slow pulmonary O2 kinetics ({tau}O2 > 30 s) and, unexpectedly, in those having faster kinetics ({tau}O2 < 30 s), a prior bout of heavy-intensity exercise resulted in a faster fundamental phase 2 O2 response (i.e., lower {tau}O2) during Mod2; 2) the magnitude of the decrease in {tau}O2 was related to the "slowness" of the O2 adaptation to moderate-intensity exercise without prior heavy-intensity exercise, with a greater reduction in {tau}O2 seen in those individuals with slower O2 kinetics; 3) the HR and NIRS-derived Hbtot and O2Hb signals were elevated during baseline before the onset of Mod2 compared with Mod1, suggesting cardiac output and muscle perfusion were elevated before the onset of Mod2; 4) the time delay before an increase in the NIRS-derived HHb signal was reduced in both SK and FK in Mod2 compared with Mod1, indicating that the mismatch between local muscle O2 utilization and O2 delivery occurred earlier in the transition to Mod2. This suggests that, despite an apparent improved blood flow and O2 delivery (elevated HR, O2Hb, and Hbtot) in Mod2, muscle O2 consumption was in excess of local O2 delivery (possibly due to faster mitochondrial enzyme activation); and 5) in the SK group, the adaptation of HHb was slower in Mod2 than in Mod1 (i.e., greater HHb time constant), suggesting that during this phase of the transition the adaptation of O2 delivery was greater and/or faster than the adaptation of muscle O2 consumption.

O2 kinetics and prior heavy-intensity exercise.   In two previous studies (12, 32), our group demonstrated that, in older adults exhibiting relatively slow O2 kinetics (~45 s), a prior bout of heavy-intensity exercise resulted in faster O2 kinetics during the transition to moderate-intensity exercise compared with a transition without prior warm up. In the present study, we observed for the first time in young healthy adults performing moderate-intensity exercise a reduction of the {tau}O2 when the moderate-intensity exercise was preceded by prior heavy-intensity exercise. Although the speeding of O2 kinetics was seen in young subjects, demonstrating both slower ({tau}O2 > 30 s) and faster ({tau}O2 < 30 s) O2 kinetics, the reduction in {tau}O2 was greater in those individuals exhibiting the slower O2 kinetics in exercise without prior warm up. The finding of faster O2 kinetics after heavy-intensity warm-up exercise in FK does not support our initial hypothesis or the findings from previous studies showing no effect of prior heavy-intensity exercise on {tau}O2 (5, 16, 32). This may reflect the degree to which O2 kinetics are limited at exercise onset and thus the extent to which O2 kinetics might be expected to speed as a consequence of overcoming these limitations. For example, in the present study, slower O2 kinetics was demonstrated in SK vs. FK when moderate-intensity exercise was initiated without prior warm-up exercise ({tau}O2 of ~45 s for SK; {tau}O2 of ~26 s in FK) and greater speeding of O2 kinetics after heavy-intensity, warm-up exercise (Fig. 2). Also, the O2 kinetics for both of these groups were apparently slower than those results reported in previous studies (very fast kinetics, {tau}O2 of ~16–20 s), where no speeding was observed after heavy-intensity exercise (5, 16, 32). Combined, these observations may reflect a continuum of decreasing limitation(s) to O2 kinetics from SK to very fast kinetics, with the potential to speed O2 kinetics after heavy-intensity exercise being attenuated in those individuals having the fewer limitations.

In the present study, there is evidence that muscle blood flow and perfusion and O2 delivery were elevated before and throughout Mod2 compared with Mod1. Absolute HR changes during exercise likely reflect changes in cardiac output as stroke volume changes minimally with exercise above baseline (20 W) levels (11, 34). The HR time constant was not different between SK and FK and was not affected by prior heavy-intensity exercise, reflecting, also, similar cardiac output and muscle blood flow kinetics between groups. However, a higher absolute HR before and throughout Mod2 suggests that, although blood flow adaptation to the higher steady-state was the same, absolute cardiac output and muscle blood flow likely were higher throughout the exercise transient in Mod2. This is supported by the higher NIRS-derived Hbtot and O2Hb at baseline and throughout Mod2, reflecting an increased volume of total and oxygenated hemoglobin and myoglobin, respectively, within the field of NIRS interrogation. Also, the elevated muscle blood flow combined with an acidosis-induced rightward shift of the O2Hb dissociation curve and improved O2 off-loading from hemoglobin after heavy-intensity exercise will contribute to an increase in both convective and diffusive O2 delivery. Thus improved blood flow redistribution and local muscle perfusion, as well as O2 delivery consequent to prior heavy-intensity exercise, may contribute to the faster O2 kinetics seen in both groups during Mod2.

It often is argued that, in young adults, O2 delivery does not limit muscle O2 utilization during the onset of moderate-intensity exercise. This is based on the relative constancy of O2 kinetics and the apparent inability to "speed" O2 kinetics following variable interventions intended to improve or increase bulk O2 delivery in human and animal models (18, 19, 24, 27). In young adults, prior heavy-intensity warm-up exercise has been shown to speed the overall adaptation of O2 following the onset of a subsequent heavy-intensity but not moderate-intensity exercise (5, 16), but this effect has been attributed mainly to a reduction in the O2 slow component rather than a reduction in the phase 2 {tau}O2 (5), although a shorter {tau}O2 has been observed in some instances (31). However, in older adults having a greater {tau}O2 compared with young adults, moderate-intensity O2 kinetics became faster after a bout of heavy-intensity exercise (12, 32). In these studies, the reduction of {tau}O2 following heavy-intensity exercise was attributed to improved O2 delivery, as suggested by the elevated HR (12, 32), Hbtot, and O2Hb (12). The higher HR, Hbtot, and O2Hb before and throughout Mod2 compared with Mod1 in the present study are also consistent with improved local muscle perfusion and O2 delivery contributing to the faster O2 kinetics in Mod2.

Although the elevated HR, Hbtot, and O2Hb provide evidence of improved muscle perfusion, the NIRS-derived HHb signal represents a balance between local O2 delivery and muscle O2 utilization (13, 21). In both FK and SK, the HHb-TD (i.e., the time required after exercise onset for the HHb signal to increase above the pretransition baseline) was shorter in Mod2, reflecting a faster and/or greater activation of muscle O2 utilization relative to the increase in local muscle blood flow at exercise onset. This is consistent with the faster O2 kinetics, and thus higher absolute O2, that was seen in both groups during the transition to Mod2.

In FK, the faster O2 kinetics in Mod2 was accompanied by a shorter MRT HHb (as a consequence of a shorter HHb-TD and a somewhat lower HHb time constant), reflecting faster overall muscle deoxygenation kinetics. Thus, despite an apparent elevated blood flow and O2 delivery before and throughout Mod2 (as inferred by the greater HR, Hbtot, and O2Hb), the increase in muscle O2 utilization was in excess of O2 delivery early in exercise, resulting in a greater O2 extraction and increase in HHb during the exercise transient in Mod2. We interpret this to suggest that, although elevated blood flow and O2 delivery may have in part contributed to faster O2 kinetics in FK, a shorter time to overcome metabolic inertia, due to faster enzyme activation and improved substrate provision, also contributed to the faster O2 kinetics in Mod2.

In SK, unlike FK, the faster O2 kinetics in Mod2 was accompanied by an unchanged HHb MRT but greater HHb time constant, reflecting slower O2 muscle deoxygenation (and muscle O2 extraction) kinetics during the exercise transient. Thus, in SK, the greater muscle blood flow and O2 delivery observed in Mod2 were in excess of the ability of the muscle to fully utilize the increased O2 delivery, suggesting that the faster O2 kinetics in SK was due primarily to the removal of an O2 delivery limitation. Together, these observations in SK and FK suggest that both O2 delivery and metabolic inertia can play a role in determining O2 kinetics and that the variability in O2 kinetic response to exercise, even in healthy young adults, may depend on the relative contribution of each as a limiting factor.

In addition, it is possible that, as a consequence of prior heavy-intensity exercise, metabolic inertia was overcome earlier in the exercise transition, which could also result in faster O2 kinetics. Recently, in isolated animal muscle, a faster reduction in both intracellular (22) and extracellular (3) PO2 was demonstrated following prior heavy-intensity contractions in the absence of a change in O2 delivery, thereby implicating a metabolic inertia as limiting muscle O2 consumption. Also, prior activation of the mitochondrial enzyme pyruvate dehydrogenase (PDH) by dichloroacetate was associated with reduced breakdown of glycogen and phosphocreatine and a reduced lactate accumulation in humans (33) and a more rapid decrease in intracellular PO2 in isolated amphibian muscle fibers (23), responses consistent with a reduced O2 deficit and faster activation of mitochondrial O2 utilization. However, in humans, no effect of dichloroacetate administration was observed when pulmonary O2 was measured directly or when muscle phosphocreatine kinetics (a proxy for muscle O2 consumption) was measured (1, 20, 26, 29). Information regarding the effects of prior exercise on metabolic activation of a subsequent exercise bout is limited. However, PDH activity remained significantly elevated after 4 min of recovery from a single 30-s bout of supramaximal exercise; after 6 s of exercise, PDH activation and acetyl CoA accumulation were greater during the third compared with the first 30-s supramaximal bout of exercise (28). Parolin et al. (28) argued that a higher intramuscular H+ concentration consequent to the supramaximal exercise would be expected to maintain a high level of PDH activation, thereby contributing to a greater reliance on oxidative, rather than substrate-level, phosphorylation. Whether PDH activation remains elevated after the 6-min recovery from heavy-intensity (but not maximal) exercise used in the present study is unknown; the activation state of other enzymes and the level of substrates involved in the control of mitochondrial O2 utilization are also unknown. However, the findings of Parolin et al. do demonstrate that metabolism remains elevated in recovery and faster enzyme activation along with improved provision of oxidative substrate could be a consequence of the prior bout of heavy-intensity exercise. The shortened HHb-TD at the onset of Mod2 in both SK and FK in the present study reflects a greater increase in muscle O2 consumption relative to the increase in muscle blood flow despite improved perfusion before and throughout Mod2, possibly due to a faster metabolic activation.

Although there is no direct evidence to support that metabolic activation was enhanced after prior heavy-intensity exercise in our study, we cannot rule out the possibility that the decreased {tau}O2 observed in this study was the consequence of faster metabolic adjustments overcoming metabolic inertia.

Aerobic fitness and O2 kinetics.   The {tau}O2 in Mod1 and the reduction in {tau}O2 after the heavy-intensity exercise in young adults of the present study were negatively correlated (P < 0.05) to O2 peak (Fig. 3), as demonstrated previously (8, 32). These findings support the contention in our previous study (32) that cardiorespiratory fitness rather than chronological age modulate O2 kinetics. Thus it appears that those factors that limit maximal O2 utilization may also contribute, in part, to limiting the time course of muscle O2 utilization during the transition to submaximal exercise.

In summary, this study demonstrated that, in young healthy adults, pulmonary O2 kinetics during the transition to moderate-intensity exercise became faster when preceded by a bout of heavy-intensity exercise. The extent of the reduction in {tau}O2 was related to the adaptation of O2 to exercise performed without prior exercise (i.e., Mod1), becoming progressively less in those individuals exhibiting a lower {tau}O2 for Mod1. Because of the noninvasive nature of this study, we are unable to comment with certainty on the mechanisms of the observed speeding; however, prior heavy-intensity exercise resulted in a higher HR, Hbtot, and O2Hb before and throughout Mod2 in both SK and FK groups, which is consistent with an improved muscle perfusion and O2 delivery during Mod2. Although O2 kinetics were faster in Mod2 in both SK and FK, slower deoxygenation kinetics in SK suggested that the improved blood flow and O2 delivery were in excess of the muscle's ability to utilize the extra O2 delivered. In FK, faster deoxygenation kinetics suggested that factors in addition to the improved muscle blood flow and O2 delivery (i.e., related to metabolic inertia) may be involved as O2 utilization was in excess of the extra O2 delivered. Together, these observations suggest that, in young healthy adults, the limitation to the O2 kinetic response may be variable and may consist of a combination of metabolic inertia or O2 delivery rather than one or the other.


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This study was supported by Natural Science and Engineering Research Council of Canada research and equipment grants. Additional support was provided by a University of Western Ontario Academic Development Fund Grant and infrastructure support from the Canadian foundation for Innovation and Ontario Innovation Trust.


   ACKNOWLEDGMENTS
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The technical support of Brad Hansen is greatly appreciated.


   FOOTNOTES
 

Address for reprint requests and other correspondence: J. M. Kowalchuk, School of Kinesiology, 3M Centre, Canadian Centre for Activity and Aging, The Univ. of Western Ontario, London, Ontario, Canada N6A-3K7 (E-mail: jkowalch{at}uwo.ca)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


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