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1Department of Exercise and Sport Science, Manchester Metropolitan University, Alsager ST7 2HL, United Kingdom; 2Department of Movement and Sports Sciences, Ghent University, 9000 Ghent, Belgium; and 3Department of Kinesiology, Kansas State University, Manhattan, Kansas 66506
Submitted 10 December 2003 ; accepted in final form 12 May 2004
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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O2) kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to O2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to 
105% of the predetermined O2 peak, separated by 3 x 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means ± SD: MAX1: 1.3 ± 0.4 mM vs. MAX2: 7.7 ± 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in O2 was not significantly different between the two conditions (MAX1: 33.8 ± 5.5 s vs. MAX2: 33.2 ± 7.7 s). Rather, the asymptotic "gain" of the primary O2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 ± 0.9 ml·min–1·W–1 vs. MAX2: 9.0 ± 0.7 ml·min–1·W–1; P < 0.05), such that O2 was projecting to a higher "steady-state" amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component O2 response but does increase the amplitude to which O2 may rise following the onset of perimaximal-intensity cycle exercise. priming exercise; warm-up; respiratory gas exchange
O2) rises following the abrupt transition to a higher metabolic rate, such as at the onset of muscular exercise (e.g., Refs. 16, 23, 47, 50). Specifically, it is presently unclear, at least for work rates that elicit a metabolic acidosis [that is, during "heavy" or "severe" exercise performed above the so-called lactate threshold but below the peak O2 (O2 peak)], whether the obligatory O2 deficit that is incurred is related mainly to "peripheral" factors, such as the rate at which one or more of the key metabolic enzymes is activated, or to "central" factors, such as the delivery and distribution of O2 to working muscle.
Gerbino et al. (15) hypothesized that the increased muscle perfusion resulting from the performance of prior exercise (provided that it was of sufficient intensity to cause an accumulation of vasoactive metabolites in the vascular beds of the exercised muscles) should result in a speeding of O2 kinetics following the onset of subsequent heavy exercise if O2 availability represented an important limitation to the increase in O2. In keeping with their hypothesis, these authors demonstrated that the performance of prior heavy exercise resulted in a significant speeding of the "overall" O2 kinetics (measured as the "effective time constant" of the response from 20 s to 6 min) during a bout of heavy exercise performed 6 min later (15). Similar results can also be found in the work of Pendergast et al. (37), who showed, in four subjects, that the half-time of the O2 response from the onset to the end of 5 min of cycle exercise at 90% O2 peak was significantly reduced when it was preceded by 5 min of exhaustive exercise performed by either the arms or the legs. More recently, a number of other studies have been conducted to further investigate the effect of prior exercise on O2 kinetics during subsequent heavy or severe exercise (e.g., Refs. 2, 4, 6–9, 14, 22, 29, 30, 34, 35, 38, 41, 45, 46; for review see Ref. 25). In humans performing upright cycle exercise, the majority of these studies indicate that the performance of prior high-intensity exercise does not alter the time constant of the primary component (
p) of O2 (i.e., phase II) but does result in a reduction of the amplitude of the so-called O2 "slow component" (4, 6–9, 14, 29, 30, 35, 45). In those studies in which the recovery period between the exercise bouts was extended to allow an effective restoration of baseline O2, there is evidence that prior high-intensity exercise results in an increased amplitude of the primary-component O2 response (4, 6–8, 14). A reduced slow-component amplitude alongside a similar or elevated primary-component amplitude will result in a reduction in the effective time constant [or mean response time (MRT)], as originally observed by Gerbino et al. and subsequently confirmed by others (e.g., Ref. 9, 29, 35). However, an unchanged p following the performance of prior high-intensity exercise, despite the existence of both direct (2, 22, 32) and indirect (6, 14) evidence of enhanced muscle blood flow and oxygenation, leads to the conclusion that O2 availability does not limit the primary increase in O2 in the transition to heavy or severe exercise, at least in young healthy subjects performing upright cycle exercise (4, 6–9, 14, 29, 30, 45; see Ref. 25 for review).
In contrast to the studies mentioned above, Tordi et al. (46) have recently reported that prior multiple-sprint exercise caused a significant reduction in p in the transition to a cycle work rate requiring 85% O2 peak and concluded that "the more rapid adaptation of oxidative metabolism was a function of improved O2 delivery." The authors hypothesized that the prior repeated sprint exercise bouts caused a greater accumulation of vasoactive metabolites, and, therefore, a greater muscle perfusion, compared with previous studies that utilized a single 30-s sprint (8) or a 6-min bout of heavy-intensity exercise (e.g., Refs. 6, 9, 29, 35, 45) as the "primer." The conclusions of Tordi et al., that O2 availability represents a limitation to p following the onset of severe-intensity exercise, have important implications for our understanding of the factor(s) that determines the O2 dynamics following the onset of exercise. However, Tordi et al. did not measure either blood lactate concentration ([lactate]) or muscle vasodilatation and thus were unable to verify their claim that their use of prior multiple-sprint exercise speeded the primary O2 kinetics by causing an additional enhancement of muscle O2 availability over and above that caused by a single bout of heavy-intensity exercise. Furthermore, because the six subjects who took part in the study only performed one transition to the severe work rate, the possibility that a type I error occurred cannot be ruled out. It is, therefore, necessary to reexamine the effect of prior multiple-sprint exercise on O2 kinetics during subsequent high-intensity constant work rate exercise by using more robust methods.
The purpose of the present study was to investigate the effect of multiple-sprint exercise (46) on O2 kinetics during subsequent perimaximal-intensity exercise (i.e., at 105% of the work rate associated with O2 peak during a preliminary ramp exercise test). We chose to study the effect of prior multiple-sprint exercise on O2 kinetics following the onset of perimaximal exercise because we reasoned that increasing muscle perfusion would be most likely to cause a speeding of O2 kinetics at such a high-exercise intensity (18, 21). We measured blood [lactate] to assess the extent of the metabolic acidosis and used near-infrared spectroscopy (NIRS) to provide information on changes in muscle blood volume and oxygenation resulting from the prior multiple-sprint exercise. Our subjects performed two transitions of the protocol to improve the precision of our estimate of p (33). Following the work of Tordi et al. (46), we hypothesized that prior multiple-sprint exercise would result in a reduction in p (i.e., speed the phase II O2 kinetics) after the onset of subsequent perimaximal-intensity exercise.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Experimental overview.
Subjects attended the laboratory on a total of 4 days, separated by at least 48 h. On test days, the subjects were required to report to the laboratory rested and fully hydrated, at least 2 h following the consumption of a light meal. Exercise testing took place at approximately the same time of day for each individual subject. On the first day, the subjects completed an incremental (ramp) cycle exercise test to exhaustion for the determination of the gas exchange threshold (GET) and O2 peak (see below). On the second day of testing, the subjects completed a total of four square-wave bouts of moderate-intensity exercise (at a work rate equivalent to 90% GET), each of 6-min duration and separated by 10-min recovery. We included moderate-intensity exercise bouts in our experimental design because, in contrast to the potentially complex O2 dynamics during perimaximal exercise (21, 43, 49), during moderate-intensity exercise, following phase I, O2 increases monoexponentially until a steady state is attained. This allowed us to establish "control" values for p and for the gain [i.e., delta (
) O2/delta work rate (WR)] of the primary-component O2 response in a domain where the response profile is uncomplicated either by the emergence of a O2 slow component (for work rates requiring a O2 > GET but < O2 peak) or by the inability to attain the required O2 for the work rate (for work rates requiring a O2 > O2 peak). If the primary-component O2 kinetics are under linear first-order control, irrespective of exercise intensity, then the p and the asymptotic gain should be similar for moderate and perimaximal exercise (49, 50). On both the 3rd and 4th days of testing, the subjects completed a "square-wave" bout of exhaustive perimaximal-intensity cycle exercise (at a work rate equivalent to 105% O2 peak), followed after 60-min rest by a multiple-sprint exercise protocol (3 x 30 s all-out cycling separated by 5-min recovery), followed 15 min later by a second square-wave bout of exhaustive perimaximal-intensity exercise (Fig. 1). All exercise tests were conducted by using an electrically braked cycle ergometer (Jaeger Ergoline E800), and pulmonary gas exchange was measured breath by breath throughout exercise, as described below.
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O2 peak was determined as the highest 30-s average value recorded before the participant's volitional termination of the test. The GET was determined from a cluster of measures including 1) the first disproportionate increase in CO2 production (CO2) from visual inspection of individual plots of CO2 vs. O2 and 2) an increase in minute ventilation/O2 with no increase in minute ventilation/CO2. The work rates that would require 90% of the GET (moderate exercise) and 105% O2 peak (perimaximal exercise) were calculated. The MRT of the O2 response to ramp exercise (assumed to approximate 2/3 of the ramp rate, i.e., 20 W) was taken into account in the calculation of these work rates. Square-wave tests. Each exercise bout began with 3 min of baseline pedaling (at 20 W, the lowest work rate available on the ergometer), before an abrupt transition to the target work rate, which was maintained for 6 min (for moderate exercise) or until exhaustion (for perimaximal exercise). For the perimaximal exercise bouts, the time to exhaustion (defined as the point at which pedal rate dropped by >5 rpm below the selected pedal rate for >5 s, despite strong verbal encouragement from the experimenters) was recorded to the nearest second. The subjects completed a total of four bouts of moderate exercise (separated by 10-min resting recovery) on a single day. On 2 other days, they performed two bouts of perimaximal exercise separated by a multiple-sprint exercise protocol (Fig. 1). Therefore, the subjects performed a total of four bouts of moderate exercise, two bouts of perimaximal exercise with no prior exercise (i.e., the control condition), and two bouts of perimaximal exercise following the performance of multiple-sprint exercise (i.e., the experimental condition).
Measurements. Pulmonary gas exchange was measured breath by breath throughout all exercise tests. The participants wore a nose clip and breathed through a low-dead space, low-resistance mouthpiece and volume sensor assembly. Pulmonary gas exchange was measured with a mass spectrometer and volume turbine system (Morgan EX670, Morgan Medical, Gillingham, Kent, UK). The system was calibrated before each test by using gases of known concentration and a precision 3-liter calibration syringe. Heart rate (HR) was recorded every 5 s by using short-range telemetry (Polar PE 4000, Kempele, Finland). A fingertip blood sample was collected into a capillary tube immediately before and after one of the exercise bouts in each condition and subsequently analyzed for blood [lactate] (YSI 1500 Sport lactate analyzer, Yellow Springs Instruments, Yellow Springs, OH).
During one of the test days on which perimaximal exercise was performed, the oxygenation status of the right vastus lateralis muscle was monitored by use of a commercially available NIRS system (model Heo-200, OMRON). The system consisted of a probe attached to a data logger that received NIRS signals at 2 Hz. The probe consisted of two light-emitting diodes and two photodetectors, which detected photons at wavelengths of 840 nm [oxyhemoglobin (HbO2)] and 760 nm [deoxyhemoglobin (HHb)]. The penetration depth with this device is 2.5–3.0 cm (manufacturer's instructions). Following shaving and cleaning of the lower one-third of the vastus lateralis muscle, the probe was secured to the skin at 10–12 cm above the knee joint with a Velcro strap and adhesive tape. Pen marks were made above and below the Velcro strap to check for any movement of the device during exercise. The probe gain was set with the subject at rest in a seated position, and NIRS data were collected continuously during both bouts of perimaximal exercise. The data were subsequently downloaded onto a personal computer, and the resulting text files were stored on disk for later analysis. The NIRS data represented a relative gain based on the optical density measured in the first datum collected and could not, therefore, be used to estimate absolute tissue O2 saturation. Similar to the recent study of Grassi et al. (19), we summed the HbO2 and HHb signals to provide an estimate of total Hb (and, therefore, blood volume) in the field of interrogation, and we calculated the difference between the HbO2 and HHb signals to provide an index of muscle oxygenation. It should be noted here that the NIRS signals might also partly reflect oxygenated and deoxygenated myoglobin as well as Hb (see Ref. 19 for discussion).
Analysis of O2 kinetics.
The breath-by-breath O2 data from each test were initially examined to exclude errant breaths caused by coughing, swallowing, sighing, etc., and those values lying >4 SDs from the local mean were deleted. The breath-by-breath data were subsequently linearly interpolated to give 1-s values. For each participant and each exercise condition, the identical repetitions of each work rate were then time aligned to the start of exercise and ensemble averaged to reduce the breath-to-breath noise and enhance the underlying physiological response characteristics. The baseline O2 was defined as the average O2 measured during baseline cycling (20 W) between 150 and 30 s before the start of exercise. The first 20 s after the onset of exercise (i.e., the phase I response) were not included in the fit. Subsequently, a single-exponential model was used to analyze the O2 responses to moderate exercise, and a biexponential model was used for perimaximal exercise, as described in the following equations:
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O2baseline is baseline O2; Ap and As are the primary and slow component amplitude, respectively; Tdp and Tds are the primary and slow component time delay, respectively; and s is the time constant of the slow component. The parameters of the model were determined by using a nonlinear least squares algorithm. In the equations above, O2(t) represents the absolute O2 at a given time t, and O2baseline represents the average O2 through the baseline cycling period. For moderate-intensity exercise, the O2 response was best fit with a single-exponential curve that described the Ap, the Tdp, and the p increase in O2 above baseline. For perimaximal exercise, the O2 response was initially fit with two exponential curves. However, the second term invariably "dropped out" (i.e., there was no slow component), such that the data were adequately described with a monoexponential model. Because the time to exhaustion was not identical in the first and second bouts of perimaximal exercise, we fitted the data 1) to the end of exercise in both bouts; 2) to the same point in time (given by the time to exhaustion in the shortest bout); and 3) to the same point in time (90 s following the onset of exercise).
The primary component "gain" (i.e., Ap/WR) was calculated for both the moderate and perimaximal work rates. For the moderate work rate, this was simply the steady-state increase in O2 above baseline divided by the WR. For the perimaximal exercise bouts, the work rate was, by design, too intense for the required steady-state O2 to be attained. The primary gain was, therefore, calculated from the projected asymptotic O2. In addition, the "actual" gain attained at the end of exercise was calculated.
Analysis of HR and HHb kinetics.
To provide further information on the effect of the prior multiple-sprint exercise on blood flow dynamics and muscle oxygenation, we also modeled the HR and HHb responses to perimaximal exercise. We chose to model HHb because this variable is relatively insensitive to alterations in blood volume. For both analyses, a monoexponential model with delay similar to that described in Eq. 1 above was used, with the exception that the fitting window commenced at the onset of exercise (i.e., at time 0). In addition, we performed a statistical comparison of the values of HR, HHb, and total Hb between the first and second perimaximal exercise bouts for every 10 s of exercise.
Statistical analysis.
The O2 kinetic responses to moderate exercise and the two bouts of perimaximal exercise were compared with a repeated-measures analysis of variance with post hoc Sidak-adjusted paired t-tests, as appropriate. Comparisons between the two bouts of perimaximal exercise (e.g., for HR, HHb, total Hb, and blood [lactate] responses, and the time to exhaustion) were made with paired t-tests. Significance was accepted at P < 0.05. Values are reported as means ± SD.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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O2 peak was 49.1 ± 3.8 ml·kg–1·min–1, with the GET occurring at 48 ± 6% O2 peak. The moderate work rate was 119 ± 23 W, and the perimaximal work rate was 332 ± 33 W. For the perimaximal exercise bouts, the mean time to exhaustion in the control condition (MAX1) was significantly longer than that following prior multiple-sprint exercise (MAX2) (MAX1: 151 ± 20 s vs. MAX2: 123 ± 8 s; P < 0.01).
The blood [lactate], HR, and NIRS results collectively suggest that the prior multiple-sprint exercise probably increased vasodilatation and, therefore, also the potential for enhanced muscle blood flow before the onset of, and during, the subsequent bout of perimaximal exercise (Table 1 and Figs. 2 and 3). Blood [lactate] was significantly higher following multiple-sprint exercise compared with the control condition, both immediately before the onset of exercise (MAX1: 1.3 ± 0.4 mM vs. MAX2: 7.7 ± 0.9 mM; P < 0.01) and at the end of exercise (MAX1: 6.1 ± 0.6 mM vs. MAX2: 8.6 ± 0.9 mM; P < 0.01). However, the accumulation of blood lactate was significantly greater in the control condition compared with the prior sprint exercise condition (MAX1: 4.8 ± 1.6 mM vs. MAX2: 0.9 ± 0.6 mM; P < 0.01). HR was significantly higher in the prior sprint exercise condition compared with the control condition immediately before the onset of exercise and throughout exercise except for at exhaustion (Table 1 and Fig. 2). There was no significant difference in the time constant describing the adaptation of HR following the onset of exercise between the two conditions (MAX1: 28.9 ± 15.0 s vs. MAX2: 30.7 ± 23.4 s). NIRS data indicated that HbO2 (Fig. 3A), tissue oxygenation (Fig. 3C), and total Hb (Fig. 3D) were greater, and HHb (Fig. 3B) was lower in the field of interrogation before and during (at least up to 60–80 s) perimaximal exercise when it was preceded by the multiple-sprint exercise condition compared with the control condition. Modeling of the HHb signal demonstrated no significant difference in the derived time delay parameter preceding the rise in HHb following the onset of exercise (MAX1: 8.0 ± 1.7 s vs. MAX2: 7.5 ± 1.2 s). [Note: A time delay preceding the exponential increase in HHb has been reported previously (12, 19) and attributed to a close matching between increased metabolic demand and increased muscle O2 delivery.] The HHb kinetics were significantly slower in the second compared with the first exercise bout (MAX1: 6.9 ± 0.4 s vs. MAX2: 8.7 ± 1.0 s; P < 0.01). Furthermore, HHb was significantly lower during perimaximal exercise when it was preceded by multiple-sprint exercise at 30 s (P < 0.01), 40 s (P < 0.01), and 50 s (P < 0.05) of exercise. Total Hb was significantly greater during perimaximal exercise when it was preceded by multiple-sprint exercise at 10, 20, 30, and 70 s of exercise (all P < 0.05) and also tended to be greater at 0, 40, 50, 60, and 110 s of exercise (all P < 0.10).
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O2 kinetics are presented in Table 2, and the O2 response to perimaximal exercise, with and without preceding multiple-sprint exercise, is shown in a representative subject in Fig. 4. There was no significant difference in p between moderate and perimaximal exercise (moderate: 27.6 ± 7.5 vs. MAX1: 33.8 ± 5.5; P = 0.10). Baseline O2 was significantly higher before the onset of perimaximal exercise when it was preceded by multiple-sprint exercise compared with the control bout. Importantly, with regard to our experimental hypothesis, there was no significant difference in p between the control and experimental bouts of perimaximal exercise when the entire response was modeled (MAX1: 33.8 ± 5.5 s vs. MAX2: 33.2 ± 7.7 s), when the data were modeled to the same point in time (i.e., when the longest bout was truncated to the time to exhaustion in the shortest bout) (MAX1: 30.4 ± 5.2 s vs. MAX2: 33.2 ± 7.7 s), or when the data were modeled to 90 s only in both bouts (MAX1: 30.4 ± 4.2 s vs. MAX2: 34.7 ± 9.9 s).
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O2 response to perimaximal exercise was significantly greater when it was preceded by multiple-sprint exercise compared with the control condition (see Table 2 and Fig. 4), such that the percentage of O2 peak attained at exhaustion was significantly higher in the experimental bout (MAX1: 88 ± 6% O2 peak vs. MAX2: 94 ± 10% O2 peak; P < 0.01), despite exercise duration being significantly shorter in this condition. The asymptotic gain of the primary component was significantly lower for the control bout of perimaximal exercise compared with moderate exercise (moderate: 9.7 ± 0.8 ml·min–1·W–1 vs. MAX1: 8.1 ± 0.9 ml·min–1·W–1; P < 0.05). However, the asymptotic gain of the primary component for perimaximal exercise was significantly increased by the performance of prior multiple-sprint exercise (MAX1: 8.1 ± 0.9 ml·min–1·W–1 vs. MAX2: 9.0 ± 0.7 ml·min–1·W–1; P < 0.05) (Table 2). Similar results were obtained for the asymptotic gain when the data were modeled to the same point in time (i.e., when the longest bout was truncated to the time to exhaustion in the shortest bout) (MAX1: 8.1 ± 0.6 ml·min–1·W–1 vs. MAX2: 8.9 ± 0.8 ml·min–1·W–1; P < 0.01), or when the data were modeled to 90 s only in both bouts (MAX1: 7.9 ± 0.7 ml·min–1·W–1 vs. MAX2: 9.0 ± 0.9 ml·min–1·W–1; P < 0.05). Figure 5 shows the mean increase in O2 over the first 2 min of moderate exercise and the two bouts of perimaximal exercise when expressed as a gain (i.e., the increase in O2 is normalized to the increase in work rate above baseline).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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O2 kinetics during subsequent high-intensity exercise if the latter were O2-delivery limited in the control (i.e., no prior exercise) condition. In our study design, we used multiple-sprint "priming" exercise to potentially increase the effect of prior exercise on muscle vasodilatation (46), and we elected to study perimaximal constant work rate exercise to maximize the potential for the prior exercise to correct an O2 delivery limitation, if one existed (18). However, despite indirect evidence that muscle blood flow was enhanced, p during perimaximal exercise was not significantly affected by the performance of prior multiple-sprint exercise; rather, O2 projected toward a higher asymptotic amplitude (and, therefore, a higher gain) with the same p. We interpret these data to indicate that O2 availability does not limit p even after the onset of "extreme" upright cycle exercise (i.e., a work rate requiring a "steady-state" O2 
O2 peak). However, it appears that the performance of prior high-intensity exercise enables the attainment of a higher O2 during subsequent perimaximal exercise.
Primary component time constant.
There is both direct (2, 22, 32) and indirect (6, 14) evidence that prior high-intensity exercise results in significantly enhanced muscle blood flow before and during subsequent high-intensity exercise. Bangsbo et al. (2) and Krustrup et al. (32) both reported that leg blood flow was significantly higher throughout supramaximal (120% O2 peak) single-leg knee-extension exercise when it was preceded by a similar bout of high-intensity exercise. Hughson et al. (22) have also recently demonstrated that leg blood flow, estimated by using Doppler ultrasonography, was significantly greater throughout the second of two bouts of two-legged knee-extension and flexion exercise performed at 85–90% O2 peak. Previous estimates of cardiac output (46) and muscle oxygenation status with NIRS (6, 14) also suggest that muscle blood flow and perfusion during exercise are enhanced when it is preceded by a bout or bouts of high-intensity priming exercise. In the present study, the performance of the multiple-sprint exercise resulted in HR being significantly higher both before and throughout perimaximal exercise (except for at the point of fatigue) compared with the control condition (Fig. 2). Furthermore, the prior multiple-sprint protocol elevated whole blood [lactate] to 7.7 mM, the highest value so far reported for "prior exercise" experiments of this type. This degree of metabolic acidosis is likely to have increased muscle vasodilatation and increased the potential for the enhancement of muscle blood flow (20), as well as facilitated muscle O2 availability by right-shifting the HbO2 dissociation curve. In keeping with this interpretation, the NIRS data indicate that the prior multiple-sprint exercise resulted in hyperemia and increased muscle oxygenation before and up to at least 70 s of subsequent perimaximal exercise (Fig. 3). Although possible increases in skin blood flow might partially confound our conclusion that muscle blood flow was enhanced by priming exercise, collectively our blood [lactate], HR, and NIRS data, in combination with the results of previous studies (2, 22, 32), strongly suggest that the prior multiple-sprint exercise enhanced muscle O2 delivery across the on-transient of the subsequent perimaximal exercise bout. However, crucially, despite the likelihood of enhanced muscle blood flow following multiple-sprint exercise, there was no significant effect on p (Table 2 and Fig. 4). Although absolute O2 was higher throughout the experimental exercise bout compared with the control exercise bout, this should not be interpreted to mean that the O2 response was faster. Rather, as can be seen in Figs. 4 and 5, prior sprint exercise resulted in a higher baseline O2 and both a greater asymptotic (Table 2) and end-exercise (Figs. 4 and 5) primary-component gain compared with the bout that was not preceded by multiple-sprint exercise, with no difference in the time constant describing the increase in O2 following the onset of exercise.
Our results are consistent with a number of other studies that reported that prior high-intensity exercise had no effect on p but rather reduced the amplitude of the O2 slow component (4, 6–9, 14, 22, 29, 30, 45) and increased the amplitude of the O2 primary component (4, 6–8, 14) during subsequent heavy- or severe-intensity exercise (at 70–90% O2 peak) (see Ref. 25 for review). That an improved O2 delivery to muscle, facilitated by the performance of prior high-intensity exercise, did not speed the primary-component O2 kinetics in these studies suggests that, in the control condition, O2 availability is adequate and/or that the fundamental increase in muscle O2 is principally regulated and/or limited by intramuscular factors during heavy and severe exercise. The results of the present study extend these earlier findings by demonstrating, contrary to our hypothesis, that the performance of prior multiple-sprint exercise did not alter p, even during subsequent perimaximal exercise. Although it is widely accepted that the O2 peak is limited by maximal cardiac output (and, therefore, muscle O2 delivery) during large-muscle group exercise (e.g., Ref. 42), it does not necessarily follow that p at the onset of perimaximal exercise is similarly limited. It is possible that the O2 on-kinetics might be principally regulated and/or limited by "metabolic" factors but that O2 availability ultimately limits the amplitude of the O2 response that can be attained (i.e., O2 peak unless muscular fatigue ensues before this is achieved). Indeed, in the present study, the performance of prior multiple-sprint exercise enabled the attainment of a higher O2 at the end of exercise with no change in p. Putative mechanisms for this increase in the absolute O2 attained are addressed later (see Primary component gain).
Our data contrast with the recent study of Tordi et al. (46), in which it was reported that prior multiple-sprint exercise resulted in significantly faster primary-component O2 kinetics (p reduced from 29 to 22 s) during subsequent severe-intensity cycle exercise (at 85% O2 peak), an effect that the authors concluded was "a function of improved O2 delivery." The cause of this difference between these two studies is unclear. However, the six subjects in the study of Tordi et al. only performed a single transition to the high-intensity work rate. Given the innate intraindividual variability in the breath-by-breath pulmonary O2 kinetic response to exercise (33, 36), the possibility that a type I error occurred cannot be excluded. Another difference between our study and that of Tordi et al. was the aerobic fitness of the subjects (O2 peak 50 ml·kg–1·min–1 in our study and 66 ml·kg–1·min–1 in theirs). There is some evidence that subjects of higher fitness might be more sensitive to O2 delivery limitations than subjects of lower fitness. For example, breathing hyperoxic gas leads to an increase in O2 peak in trained subjects (27) but not in sedentary subjects (10). It remains to be established whether training status is an important factor in the potential for interventions designed to improve muscle O2 availability (such as prior exercise and hyperoxic inspirates) to cause a speeding of O2 kinetics during high-intensity exercise. Finally, the exercise intensity studied was different between our study (work rate equivalent to 105% O2 peak) and the study of Tordi et al. (work rate equivalent to 85% O2 peak). We extended the reasoning of Tordi et al. and deliberately selected a perimaximal work rate to increase the potential for priming exercise to speed O2 kinetics (18, 21). Surprisingly, this is the first study to investigate the influence of priming exercise on pulmonary O2 kinetics in the transition to a work rate that has an energy equivalent exceeding O2 peak. However, as discussed previously by others (21, 43, 49), modeling the pulmonary O2 response to perimaximal exercise is complicated both by the difficulty in precisely identifying the O2 requirement for the work rate and by the confounding influence of the approach to, and the possible attainment of, O2 peak itself. In the present study, we circumvented these issues by also modeling the first 90 s of the O2 response in each condition. This approach makes no assumption with regard to the "required" O2 or energy equivalent for the work rate (21), prevents any possible contamination of the fit resulting from the approach to O2 peak, and has the added advantage of controlling for the difference in the time to exhaustion between the two conditions. However, this approach did not alter our principal results or conclusions.
Prior heavy exercise has been shown to reduce p during subsequent heavy exercise in different modes of exercise (34, 38, 41) and in subjects with different characteristics (44). For example, Rossiter et al. (41) reported that p was significantly reduced (from 47 to 41 s) in the second of two bouts of heavy leg-extension exercise performed in the prone position. Furthermore, it has been established that prior exercise can speed both blood flow and O2 kinetics during forearm exercise when it is performed in the supine position with the arm extended above the level of the heart (34, 38). Finally, it has been demonstrated that prior heavy exercise can reduce p during subsequent moderate cycle exercise in the elderly (44). However, it should be cautioned that there is likely to be a reduction in perfusion pressure and/or a compromise to muscle blood flow in the control condition in all of these situations, as evidenced by the relatively long p values reported for the control conditions (28, 41, 44). In contrast, during upright cycle exercise in young healthy participants, the available data indicate that, although reductions in muscle O2 availability have the potential to cause a longer p (13; but see also Ref. 51), enhancing muscle O2 availability does not result in a shorter p (present study; Refs. 6, 35), such that O2 availability cannot be considered limiting in this situation.
A number of studies have directly measured blood flow and O2 across an exercising limb during perimaximal exercise (1, 18, 32). Grassi and colleagues demonstrated that pump-perfusing canine muscle at the steady-state blood flow requirement across the transition from rest to contractions, requiring 100% O2 peak (18) [but not 60% O2 peak (17)], resulted in a significant speeding of the O2 on-kinetics. However, this speeding might be partly attributed to a dramatic effect in a single dog (see Fig. 3 in Ref. 18), and the majority of the inertia in p remained unexplained. In humans, Bangsbo et al. (1) reported that O2 delivery to muscle was closely matched with, or in excess of, requirements throughout the transition to single-leg knee-extensor exercise at 120% O2 peak (see Fig. 5 in Ref. 1). Similar conclusions were reached in other experiments from the same group (2, 32). These data might be interpreted to suggest that intramuscular factors (i.e., inertia in the activation of one or more oxidative enzymes and/or limitations to substrate flux; Refs. 16, 50) represent the principal limitation to the acceleration of mitochondrial respiration, even during supramaximal-intensity exercise. However, it should be cautioned that the single-leg knee-extensor exercise model used in these studies (1, 2, 32) would not stress the cardiovascular system to the same extent as the two-legged cycle exercise used in the present study.
Interestingly, there was no significant difference in p between moderate and perimaximal-intensity exercise, although there was a tendency for this to lengthen (from 27.6 to 33.8 s on average, P = 0.10). The literature is divided on the question of whether or not p becomes longer at higher work rates, with some studies demonstrating a significant lengthening (e.g., Refs. 13, 24, 31) and others demonstrating no effect (e.g., Refs. 36, 43). Longer p values at higher work rates have been interpreted to indicate the existence of an O2 delivery limitation (23). However, it should also be considered that higher work rates will require the recruitment of a larger volume of muscle to meet the force requirements of exercise and that the "additional" muscle fibers recruited at the higher work rates will be higher order fibers with generally more fast myosin and lower oxidative capacity. We and others have suggested that the slower O2 on-kinetics in these higher order fibers (11) might impact on the "net" O2 kinetics measured at the lung and result in a trend for p to be longer at higher work rates, irrespective of any changes in muscle O2 availability (5, 24, 31, 40).
Primary-component gain.
There was a significant reduction in the asymptotic gain of the primary component from moderate exercise (9.7 ml·min–1·W–1) to perimaximal exercise (8.1 ml·min–1·W–1). At extreme work rates (O2 requirement > O2 peak), it is by definition impossible for the "steady-state" O2 for the work rate to be attained (the system being constrained by the attainment of O2 peak, or by muscular fatigue even before O2 peak is attained). However, it seems reasonable to expect that O2 would initially project toward an amplitude commensurate with the ATP turnover rate required for the work rate (to eliminate the initial "error signal" as given by, for example, the intramuscular phosphocreatine concentration/t) for extreme as well as for "submaximal" work rates (49). However, despite the fact that the imposed work rate required 105% O2 peak, O2 only projected initially to an amplitude equivalent to 85% O2 peak. It is important to stress that this result was not altered when we modeled only the first 90 s of data, indicating that the result was not caused by contamination of the model fit by a plateauing of O2 as fatigue was approached. A similar significant fall in the primary gain at severe and/or extreme work rates has been reported in a number of recent studies (24, 39, 40, 43). The cause of the fall in the primary gain at severe and extreme work rates is unclear, but it has been suggested that this might be related to the recruitment of type II muscle fibers, which have a lower oxidative capacity and a higher glycolytic capacity than type I fibers. Type II fibers might have an inherently low O2 gain in vivo and/or be obligated to meet a proportion of the energy requirement of exercise (presumed to be equivalent to 10 ml·min–1·W–1) through O2-independent mechanisms (24, 39, 40, 43). Consistent with this suggestion, it has been shown that subjects with a high percentage of type II fibers in the working muscles have a lower primary-component gain compared with subjects with a low percentage of type II fibers (3, 39).
The prior multiple-sprint exercise protocol resulted in a significant increase in the gain of the primary component during perimaximal exercise (from 8.1 to 9.0 ml·min–1·W–1), to a value that was not significantly different from that for moderate exercise (Fig. 5). Why the performance of prior sprint exercise would cause the primary O2 component to project to a value that is closer to what would, at least theoretically, be expected for the work rate (i.e., to "correct" the apparent "underestimation" of the required O2) is unclear. The difference in O2 between the perimaximal bouts performed with and without prior sprint exercise at baseline (130 ml/min) was not as great as the difference measured at exhaustion (200 ml/min), suggesting that the difference does not simply represent the superimposition of the O2 cost of ongoing recovery processes. Indeed, Burnley et al. (7) reported that prior heavy exercise resulted in a higher primary-component amplitude during subsequent heavy exercise, even when the recovery time following the first bout was extended to allow complete restoration of baseline O2. One possible explanation for the higher primary-component gain observed is that the performance of prior sprint exercise (which might be expected to preferentially fatigue the type II fiber population) results in altered fiber recruitment or rate coding during subsequent exercise. Burnley et al. (6) have reported that the integrated electromyogram was significantly increased in concert with an increased primary-component amplitude during heavy exercise when it was preceded by a bout of heavy exercise; the mean power frequency (believed to reflect changes in the recruitment of type II fibers), however, was unchanged. The authors interpreted these results to indicate that the performance of prior exercise increased the overall muscle fiber recruitment and/or activation without appreciably affecting the proportion of type I or type II fibers that was recruited. An increase in integrated EMG during heavy or severe exercise, when it was preceded by high-intensity exercise, has been noted in several other studies, although the natural variability in the measurement of EMG has often precluded the attainment of statistical significance (22, 45, 46). Another explanation for the increased oxidative metabolism following priming exercise is that ATP resynthesis from substrate-level phosphorylation is attenuated either because there is insufficient time following the completion of the priming exercise for muscle phosphocreatine concentration to be restored or because the resultant low pH (or a change in the concentration of some other metabolite) inhibits anaerobic glycolysis (see Ref. 48 for review).
One other consideration is that O2 availability is somehow "sensed" in the muscle or its vascular bed and that this is used to set the amplitude to which O2 initially or eventually projects. In this respect, it is interesting to note that the primary-component gain during heavy exercise is reduced when perfusion pressure is lower, for example during supine compared with upright exercise (28), and increased when hyperoxic compared with normoxic gas is breathed (35). These data suggest that the amplitude (although apparently not the time constant) of the primary O2 response might be sensitive to O2 availability during high-intensity exercise. The higher O2 that we observed during perimaximal exercise when it was preceded by priming exercise was almost certainly associated with an increased muscle blood flow. Krustrup et al. (32) reported that the significant increase in thigh O2 beyond 2 min in the second of two bouts of supramaximal supine knee-extension exercise was associated with a significant increase in thigh blood flow and no further change in muscle O2 extraction. However, this relationship does not prove cause and effect, because an increased blood flow would be required to meet the increased O2 demand if, for example, more muscle fibers were recruited in the second bout. Interestingly, in our study, the higher O2 at the end of exercise when it was preceded by the priming exercise was attained, despite no significant difference in HR and no clear improvement in muscle oxygenation at the same point in time (Figs. 2 and 3). It, therefore, remains unclear whether the higher muscle blood flow observed during high-intensity exercise when it is preceded by a bout of high-intensity priming exercise is a cause or a consequence of the increased absolute O2 attained.
In the present study, the time to exhaustion during perimaximal exercise was reduced by 19% when it was preceded by multiple-sprint exercise. In contrast, our laboratory (26) has recently reported that the performance of prior heavy exercise resulted in a significant extension of time to exhaustion during subsequent perimaximal exercise. The most likely explanation for this difference in the effect of prior exercise on the tolerance to perimaximal exercise is the intensity of the priming bout. In our laboratory's previous study, the priming bout involved 6 min of constant-work-rate exercise at 80% O2 peak, which, following 10-min recovery, resulted in a blood [lactate] of 2.6 mM immediately before the onset of perimaximal exercise. In the present study, the priming exercise involved three bouts of 30-s maximal sprinting, and, despite a longer recovery period of 15 min, the blood [lactate] immediately before the onset of perimaximal exercise was 7.7 mM. It is apparent that the extent to which prior exercise can enhance or impair performance during subsequent perimaximal exercise is dependent on the extent to which acid-base balance (or some related factor) is altered (26). However, despite the different effects on exercise tolerance in this and our previous study, we have consistently observed that a significantly higher (end-exercise) O2 peak is attained, with no significant difference in the rate of adaptation of O2, when exhaustive perimaximal exercise is preceded by priming exercise. One additional novel observation from the present study was that the oxygen deficit at the end of exercise (i.e., MRT x increase in O2 at end exercise above baseline) was not significantly different between the first and second bouts of perimaximal exercise (MAX1: 1.76 ± 0.50 liters vs. MAX2: 1.78 ± 0.32 liters), despite significant differences in the time to exhaustion and the O2 peak attained. These data indicate that exercise of this type might be terminated when the "anaerobic capacity" (comprising the energy derived from phosphocreatine depletion and anaerobic glycolysis along with stored O2) becomes exhausted.
In summary, we have shown that prior multiple-sprint exercise that resulted in significant lactic acidemia and increased muscle oxygenation did not alter the p during subsequent perimaximal exercise. These data suggest that the p is not limited by O2 availability, even in the transition to exercise with a O2 requirement O2 peak, at least in young healthy subjects performing upright cycle exercise. However, the gain of the primary component of O2 was significantly increased by the performance of prior multiple-sprint exercise. Prior sprint exercise, therefore, resulted in the projection of O2 toward a higher amplitude but with the same (presumably intracellularly limited) time constant. The physiological mechanism(s) responsible for both the higher projected gain and the higher O2 actually attained at the end of exercise (despite a shorter time to fatigue) when perimaximal exercise is preceded by sprint exercise is presently obscure and is worthy of further research attention.
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REFERENCES |
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) and when preceded by multiple-sprint exercise (
). Shown are the final minute of cycling at 20 W followed by an abrupt transition to perimaximal exercise that was continued to exhaustion. Note the significantly higher HR at the onset and throughout exercise except for at the point of fatigue. EE, end exercise. Values are means ± SD. Significantly different: *P < 0.05 and **P < 0.01.
