We have recently proposed that the pulmonary oxygen uptake (V˙O2) kinetics is a crucial determinant of severe-intensity exercise performance (i.e., exercise performed above the critical power, CP; for review, see Burnley and Jones ). It is our contention that the kinetics of V˙O2 interacts with the finite capacity for substrate-level phosphorylation (derived from phosphocreatine (PCr) hydrolysis and glycolysis leading to the formation of lactate) and the prevailing peak V˙O2 (V˙O2peak) to determine the tolerable duration of supra-CP exercise. The V˙O2 slow component does not stabilize above CP, and its trajectory steepens as power output is increased beyond CP (33). As a result, V˙O2peak is attained more rapidly at higher work rates in the severe-intensity domain, with exhaustion occurring soon thereafter. By extension, the kinetics of V˙O2 interacting with the V˙O2peak may determine the curvature of the power-duration relationship (the W′ parameter, with CP being the asymptote). These proposals suggest that altering the V˙O2 kinetics, V˙O2peak, and/or the capacity for substrate-level phosphorylation would predictably alter the time to exhaustion (Tlim) and hence one or both of the parameters of the power-duration relationship (for examples, see Burnley and Jones ).
When repeated bouts of heavy- or severe-intensity exercise are performed (the former representing work rates performed between the gas exchange threshold (GET) and CP), the kinetics of V˙O2 in response to the second bout of exercise is substantially altered (20). The "priming" effect was first described as a "speeding" of the overall V˙O2 kinetics (17,26). Later studies demonstrated that this overall speeding could be attributed to a reduction in the amplitude of the V˙O2 slow component, with the time constant of the primary component being unaffected (3,6,8,10,24,34). When recovery duration is sufficient to restore baseline V˙O2, it has been consistently demonstrated that the amplitude of the primary component is increased after priming (i.e., priming increases the anticipated steady-state V˙O2) (6,8,16,31). However, other studies have demonstrated faster primary kinetics in the primed state (13,32,35). Thus, primed V˙O2 kinetics is characterized by an increase in the primary V˙O2 amplitude, a reduction in the V˙O2 slow component, and, on occasion, a speeding of the primary kinetics (20).
In the primed state, the increase in the aerobic contribution early in exercise, coupled with a delay in the attainment of V˙O2peak consequent to a reduced V˙O2 slow component (should the primary V˙O2 amplitude project to a submaximal value), can influence exercise performance. Priming exercise in the heavy- and/or severe-intensity domain followed by sufficient recovery (>9-10 min) has been shown to increase Tlim by 10%-60% (1,11,22) and increase mean power output during short-term high-intensity performance by 2%-5% (7,30). Jones et al. (22) showed that this enhancement of exercise tolerance was associated with a tendency for W′ to be increased, whereas more recently, Miura et al. (27) reported that priming increased the CP. In contrast, severe-intensity priming followed by a brief recovery period (14,15) or prior sprint exercise (18,39) has been shown to reduce subsequent exercise tolerance, reflected in a reduction in the W′ parameter with no change in the CP (14,15,18). More prolonged recovery reduces (14) or even eliminates (37) these negative effects on exercise tolerance and the parameters of the power-duration relationship.
Despite intensive study in recent years, the influence of priming exercise intensity on the kinetics of V˙O2 and the parameters of the power-duration relationship remains equivocal. This may be because most investigators using a power output equal to GET plus 50% of the difference (Δ) between V˙O2 and GET to induce a priming effect (10,22,27). Although this work rate typically produces a priming effect, it has the unfortunate characteristic of being near CP. Hence, subjects within these studies may not be exercising exclusively in the heavy- or severe-intensity domain. Furthermore, there seems to be little agreement between those studies in which the priming was performed above or below 50% Δ: Bailey et al. (1) observed no priming effects and no effect on Tlim after exercise at 40% Δ, whereas severe-intensity priming (at 70% Δ) increased Tlim for recovery durations >9 min. In contrast, Ferguson et al. (14) observed a reduction in performance, and W′, 15 min after severe-intensity priming. The present study was therefore designed to investigate the effects of priming intensity with specific reference to the critical power on the kinetics of V˙O2, the Tlim, and the parameters of the power-duration relationship.
The purpose of the present study was to test two hypotheses: First, that priming exercise performed exclusively in the heavy-intensity domain (<CP) followed by 10 min of recovery would increase the primary V˙O2 amplitude, reduce the amplitude and trajectory of the V˙O2 slow component, and increase Tlim during subsequent bouts of severe-intensity exercise. This, in turn, would alter the power-duration relationship by increasing the W′ parameter. Second, priming exercise performed exclusively in the severe-intensity domain (>CP) followed by 10 min of recovery would increase the primary V˙O2 amplitude, reduce the amplitude and trajectory of the V˙O2 slow component, but would have no effect on the Tlim. As a result, we predicted that prior severe-intensity exercise would have no effect on the power-duration relationship. Ten minutes of recovery was chosen owing to previous work showing consistent priming and performance effects using this recovery period (10,22).
Ten healthy trained male cyclists (age = 31 ± 8 yr, height = 181 ± 6 cm, body mass = 77.2 ± 11.3 kg) volunteered to participate in this study and provided written informed consent. Ethical approval of the experimental design was obtained from the ethics committee of Aberystwyth University before the commencement of this study. All procedures were conducted in accordance with the Declaration of Helsinki. Subjects were instructed to arrive for testing in a rested (no strenuous exercise in the preceding 24 h) and hydrated state. They were instructed to refrain from consuming alcohol for 24 h before each test and to avoid consuming food and caffeine in the 3 h before each test.
Subjects reported to the laboratory on 13 occasions during a 4-wk period. The first visit was used to collect all demographic and anthropometric data and to perform an incremental ramp test to determine the GET and V˙O2peak. These data were then used to calculate a range of work rates for all subsequent exhaustive tests. An initial "control" condition series of four exhaustive trials was performed on separate days (visits 2-5) to define the power-duration relationship and to identify work rates for the prior heavy and prior severe priming bouts. After these initial five trials, all subjects repeated the same four work rates, preceded by a bout of prior heavy or severe exercise and a 10-min "recovery"period, each performed on separate days (visits 6-13). Pulmonary V˙O2 was measured throughout each trial, blood (lactate) was determined before and after exercise, and Tlim was recorded to the nearest second.
Determination of GET and V˙O2peak.
All exercise tests were performed on an electrically braked cycle ergometer (Lode Excalibur Sport, Groningen, The Netherlands), which was calibrated according to the manufacturer's instructions. The subjects' GET and V˙O2peak were established using a ramp test. The subjects adjusted the seat and handlebar positions for comfort, and measurements were recorded for use in all subsequent tests. The subjects self-selected a cadence of 80-100 rpm and were instructed to maintain this cadence throughout all exercise tests. During the ramp test, the subjects first performed 3 min of "unloaded" pedaling, followed by an increase in work rate of 30 W·min−1 until volitional exhaustion (operationally defined as a fall in cadence of >10 rpm despite strong verbal encouragement). Throughout this test, V˙O2 was measured on a breath-by-breath basis with the data reduced to 5-s averages for analysis. The V˙O2peak was determined as the highest average V˙O2 during a 30-s period. The GET was estimated using the V-slope method (5). To account for the time lag in the increase in V˙O2 to the increase in the external work rate during incremental exercise, the work rate corresponding to GET was reduced by two-thirds of the ramp rate.
Determination of the power-duration relationship.
To determine the parameters of the power-duration relationship, subjects performed constant-work-rate exercise to exhaustion at GET plus 60%, 70%, or 80% of the difference (Δ) between GET and V˙O2peak and 100% of the work rate achieved at the end of the ramp test (WRpeak). These trials were performed in a randomized order on separate days and were chosen to elicit a range of time to exhaustion between 2 and 15 min (19). Each trial was preceded by 3 min of unloaded "baseline" pedaling after which the work rate was increased in a "square-wave" fashion to the desired work rate. Subjects were instructed to maintain their desired cadence for as long as possible with the test being terminated when the cadence fell by >10 rpm and could not be increased despite strong verbal encouragement, with Tlim being recorded to the nearest second. Blood [lactate] was measured both at rest before each test and immediately on exhaustion. Pulmonary gas exchange was recorded breath-by-breath throughout each test (see Measurements section). The subjects were not informed of the work rates imposed or of the outcome of the tests until they had completed all experimentation.
Prior exercise protocol.
After the establishment of the control power-duration relationship, the priming work rates were calculated. Prior heavy exercise was calculated as GET plus 50% of the difference between GET and CP, whereas the prior severe exercise work rate was derived by linear regression as a power output, which could be maintained for 8 min (P = [W′ / 480] + CP) (15). Both the prior heavy and prior severe priming bouts were maintained for 6 min. At 6 min, subjects were allowed to "spin down" against zero resistance for 1 min and then rested passively for 6 min before remounting the ergometer and performing 3 min of unloaded pedaling. After this 3-min period, one of the four severe intensity work rates was immediately imposed, and the subjects again exercised to exhaustion as described above. One minute before and immediately after these exercise bouts, a fingertip capillary blood sample was taken to determine blood [lactate]. Subjects repeated this process on separate days and in a randomized order until all experimental trials were completed.
Throughout all tests, subjects wore a nose clip and a mouthpiece (dead space, 90 mL) containing an impeller turbine for the measurement of volume (resistance 0.75 mm Hg·L−1·s−1 at 15 L·s−1) and a port for the capillary line (Jaeger Triple V). Inspired and expired gas concentrations were continuously sampled via the capillary line at 100 Hz using paramagnetic O2 and infrared CO2 analyzers (Jaeger Oxycon Pro, Hoechberg, Germany). The analyzers were calibrated with gases of known concentration before each test, and a 3-L calibration syringe was used to calibrate the turbine volume transducer (Hans Rudolph, Kansas City, MO). The volume and concentration signals were time-aligned by accounting for gas transit and analyzer rise time during the calibration process, and V˙O2, carbon dioxide output (V˙CO2), and minute ventilation (V˙E) were calculated breath-by-breath using standard formulae (4). Capillary whole blood was collected into Microvette cb300 Lithium-Heparin capillary tubes (Sarstedt, Nümbrecht, Germany) 1 min before and immediately after each constant-load exercise trial to exhaustion, and blood [lactate] was determined enzymatically using an automated analyzer (YSI 2300 Stat Plus, Yellow Springs, OH).
The V˙O2 responses to each exercise test to exhaustion were filtered to remove errant breaths because of coughs and swallowing before being linearly interpolated to provide one value per second. Iterative nonlinear regression was used to characterize the primary V˙O2 response by removing the first 20 s of data (to eliminate the phase 1 component) and then fitting from 20 s to 2 min a monoexponential function of the form:
where V˙O2(t) is the V˙O2 at time t; V˙O2(b) is the baseline V˙O2 measured in the 60 s preceding the transition in work rate; and AP, TDP, and τP are the amplitude, time delay, and the time constant of the primary (phase 2) response, respectively (8,32). The amplitude of the slow component was determined by subtracting the primary amplitude from the peak V˙O2 measured during the test, and the rate of increase in V˙O2 during this phase (i.e., the slow component trajectory [L·min−2]) was estimated using the following equation:
To estimate the parameters of the power-duration relationship, external work output (W) was plotted against Tlim. Linear regression was used to provide parameter estimates for both CP and W′, using the work-time model (28,29):
Time to exhaustion, power-duration relationship parameter estimates, and parameters derived from the modeling of the V˙O2, and blood (lactate) data were analyzed using one- or two-way (intensity × condition) ANOVAs with repeated measures, as appropriate. Where differences were observed between conditions, 95% paired-samples confidence intervals (CI) were used to determine at which specific intensities (60%, 70%, 80% Δ, or 100% peak work rate) the differences occurred. Significance was accepted at P < 0.05 and when 95% paired-samples CI did not include zero. Results are reported as mean ± SD.
During the ramp exercise, test subjects achieved a peak power output at the limit of tolerance of 411 ± 48 W, and a V˙O2peak of 4.36 ± 0.41 L·min−1 (57 ± 8 mL·kg−1·min−1). The GET occurred at 2.38 ± 0.63 L·min−1 and was achieved at 163 ± 56 W. The work rates calculated for the heavy- and severe-intensity priming bouts were 225 ± 52 W (25% ± 1% Δ) and 319 ± 46 W (63% ± 2% Δ), respectively. The work rates for the exhaustive exercise tests were: 60% Δ, 311 ± 50 W; 70% Δ, 336 ± 49 W; 80% Δ, 361 ± 49 W; and 100% WRpeak, 411 ± 48 W.
The blood (lactate) measured at baseline was similar between work rates within conditions but significantly different between conditions. The blood [lactate] before the control trials was 0.9 ± 0.3 mM. Blood lactate was significantly elevated at all work rates after prior heavy exercise (to 1.8 ± 0.5 mM) and to a considerably greater extent after prior severe exercise (to 6.4 ± 1.4 mM; F = 141.65, P < 0.001). There was no significant difference in the blood [lactate] at the end of exhaustive exercise in each experimental condition (9.6 ± 1.4 mM after the control trials, 9.4 ± 1.3 mM after prior heavy priming, and 10.0 ± 1.4 mM after prior severe priming).
Table 1 presents the V˙O2 responses to the various trials to exhaustion after heavy priming. Compared with the control condition, heavy priming had no effect on the baseline V˙O2 (Table 1) or the time constant of the primary response for any of the subsequent bouts (F = 1.06, P = 0.37). However, the primary amplitude was significantly increased during the 70% Δ and 100% WRpeak trials (F = 15.27, P < 0.001; 95% CI: 70% Δ = 0.06-0.43 L·min−1, 100% WRpeak = 0.05-0.40 L·min−1), and when the amplitude was expressed in absolute terms (baseline V˙O2 + AP), the amplitude was significantly increased at 60% and 70% Δ and 100% WRpeak (F = 42.31, P < 0.001; Table 1). The 95% CI associated with the parameter estimates of the primary time constant were 5.2 ± 0.7 s across all conditions and with the primary amplitude was 0.08 ± 0.01 L·min−1 across all conditions. After heavy priming exercise, the V˙O2 slow component was reduced (F = 15.13, P < 0.001), with this difference being significant at 60% Δ only (95% CI = −0.35 to −0.04 L·min−1). The trajectory of the V˙O2 slow component was also significantly reduced at 60% and 70% Δ after priming exercise (F = 10.01, P = 0.002; Table 1). The V˙O2peak was significantly increased after priming at 70% Δ (F = 10.76, P = 0.001; 95% CI = 0.03-0.22 L·min−1), 80% Δ (95% CI = 0.05-0.42 L·min−1), and 100% WRpeak (95% CI = 0.15-0.42 L·min−1; Table 1). An example of these V˙O2 responses is presented in Figures 1A, B.
There was a significant main effect of heavy priming on time to exhaustion (F = 7.29, P = 0.005), and post hoc analysis revealed that exercise tolerance was significantly increased at 70% Δ (95% CI = 3-108 s) and 100% WRpeak (95% CI = 5-36 s). As shown in Table 2, there was no effect of heavy priming on the critical power (control vs heavy priming, 284 ± 47 vs 283 ± 44 W; 95% CI = −7 to 5 W), whereas the W′ was significantly increased (16.0 ± 4.8 vs 18.7 ± 4.8 kJ, 95% CI = 0.3-5.2 kJ). An example of the power-duration relationship in a subject demonstrating improved exercise tolerance after heavy priming is shown in Figure 1C.
The V˙O2 responses to severe-intensity exercise after severe priming exercise are presented in Table 1. Severe-intensity priming significantly increased the baseline V˙O2 at 70% Δ and 100% WRpeak (F = 4.95, P = 0.02). The primary time constant was not altered after severe-intensity priming, but the primary amplitude was significantly increased at 60%, 70%, and 80% Δ (F = 15.27, P < 0.001). The absolute primary amplitude was significantly increased at all work rates after severe-intensity priming exercise (Table 1). The V˙O2 slow component was significantly reduced by severe-intensity priming exercise at 60% (95% CI = −0.43 to −0.14 L·min−1) and 70% Δ (95% CI = −0.42 to −0.16 L·min−1; Table 1), and this was also reflected in a reduction in the slow component trajectory at these work rates (95% CI: 60% Δ = −0.03 to −0.01 L·min−2, 70% Δ = −0.14 to −0.07 L·min−2; Figs. 1D, E). Finally, the V˙O2peak at 70% and 80% Δ and 100% WRpeak was significantly increased by previous severe-intensity exercise (95% CI: 70% Δ = 0.12-0.41 L·min−1, 80% Δ = 0.03-0.27 L·min−1, 100% WRpeak = 0.18-0.44 L·min−1).
The time to exhaustion during severe-intensity exercise was not significantly affected by severe-intensity priming exercise (Table 1). The parameters of the power-duration relationship were unaffected by severe-intensity priming exercise (CP: 284 ± 47 vs 275 ± 45 W, 95% CI = −19 to 2 W; W′: 16.0 ± 4.8 vs 16.7 ± 4.7 kJ, 95% CI = −1.4 to 3.9 kJ; Table 2). The CIs associated with the parameter estimates of the power-duration relationship were 30 ± 19 W for the critical power and 10.5 ± 10.0 kJ for the W′across all conditions.
The present study demonstrated that prior exercise performed exclusively in the heavy-intensity domain, which led to a modest increase in blood [lactate], primed the V˙O2 kinetics and increased Tlim during subsequent severe-intensity exercise. The enhancement in exercise tolerance was attributable to a significant increase in the curvature constant of the power-duration relationship (W′), with no change in the critical power. Prior exercise performed exclusively in the severe-intensity domain, which resulted in a substantial increase in blood (lactate), also primed the V˙O2 kinetics but had no effect on Tlim or the parameters of the power-duration relationship.
Prior heavy-intensity exercise resulted in primed V˙O2 kinetics during subsequent severe-intensity exercise: the primary V˙O2 amplitude was increased with no change in the primary time constant, and the slow component amplitude and trajectory was reduced (Table 1). These responses have been demonstrated repeatedly in the past (3,6-8,10,16,24,26,31,34), with other reports suggesting that the primary time constant is reduced after priming exercise (13,32,35). The increased V˙O2 response in the first 2-3 min of exercise has been demonstrated to enhance exercise performance (1,7,11,22,27,30). In the present study, Tlim was increased by ∼19% after heavy-intensity priming exercise, which was statistically significant at 70% Δ and 100% WRpeak (Table 1). The increased Tlim was associated with an increase in the W′ of ∼2.7 kJ or ∼17%, supporting the previous work of Jones et al. (22), who observed that W′ tended to increase after priming at 50% Δ and the same 10-min recovery duration as used in the present experiments. Heavy-intensity priming exercise did not alter the CP, which is consistent with previous evidence (22) but not with the more recent study of Miura et al. (27), who observed an increase in CP of ∼8 W after priming exercise at 50% Δ. Thus, although several reports have shown improved exercise tolerance after heavy priming exercise and that this could be due to either an increase in the CP or the W′, the present results provide the first evidence that priming performed exclusively in the heavy-intensity domain can significantly increase the W′ without altering the CP.
The physiological determinants of the W′ and, by extension, the determinants of Tlim during severe-intensity exercise are unclear (21). We have recently suggested that the tolerable duration of severe-intensity exercise may depend on three interrelated factors, namely, the amount of energy available from substrate-level phosphorylation, the V˙O2 kinetics, and the V˙O2peak (9). Severe-intensity exercise requires an obligatory energetic contribution from substrate-level phosphorylation, which is itself limited by the depletion of its constituents (chiefly PCr) and/or the accumulation of metabolites such as H+ and inorganic phosphate (23,36). The kinetics of V˙O2 dictates the rate of energy supply from substrate-level phosphorylation during both the primary phase and as the V˙O2 slow component develops (evidenced by the existence of a PCr slow component) (23,32), whereas the V˙O2peak limits the development of the V˙O2 kinetics (9). In this context, the results of the present study could be interpreted in the following way: heavy-intensity priming exercise increased the aerobic contribution to early exercise and reduces the amplitude and trajectory of the V˙O2 slow component. In addition, heavy-intensity priming exercise increased the V˙O2peak, providing a greater scope for the V˙O2 response. Because prior heavy exercise does not lead to progressive PCr depletion or metabolite accumulation (23), the capacity for substrate-level phosphorylation should be completely intact 10 min after heavy-intensity priming exercise. Thus, the primed V˙O2 kinetics may have served to reduce the rate of substrate-level phosphorylation and delay the attainment of V˙O2peak, which may have resulted in the increase in Tlim and therefore the W′.
Severe-intensity priming exercise resulted in a substantial baseline blood [lactate] elevation (to ∼6-7 mM); an increase in the primary V˙O2 amplitude at 60%, 70%, and 80% Δ (of ∼270 mL·min−1); and a reduced V˙O2 slow component amplitude and trajectory at 60% and 70% Δ (Table 1). Despite these priming effects, and in stark contrast to heavy-intensity priming exercise, these responses were associated with no change in Tlim or the parameters of the power-duration relationship. Previous studies have demonstrated that prior exercise resulting in substantial baseline blood [lactate] elevation (typically >5 mM) is associated with either no significant change in exercise performance (7,25) or a significant decrease in Tlim (1,14,15,39). In this study, severe-intensity priming tended to reduce the CP with no change in the W′ (Table 2), although this tendency for CP to fall can be attributed to substantial reductions in CP in two subjects, with the remainder showing little change. Previous studies investigating severe-intensity prior exercise have suggested that the CP is unaffected but that the W′ is reduced (14,15). The latter effect was not observed in the present study, although the same work rate has been shown to substantially deplete W′ when measured after 2 min of recovery (15). It is possible that the capacity for substrate-level phosphorylation was reduced after the severe-intensity priming and the 10-min recovery period, but this reduction was balanced by the priming effects on the V˙O2 kinetics. Although speculative, this might explain why no measurable changes in performance or the parameters of the power-duration relationship were observed after severe-intensity priming exercise in the present study.
The design of the present experiments (priming exercise followed by 10 min of recovery) followed from our earlier work shows robust effects on the V˙O2 response and of substantial enhancements in exercise performance after 10 min of recovery (10,22). However, priming effects have been observed after at least 30-45 min of recovery (8), whereas the recovery of the muscle high-energy phosphates and pH typically requires <20 min (e.g., Baker et al. ). Furthermore, Bailey et al. (1) have recently reported that the greatest positive priming effect (measured as time to exhaustion at 80% Δ) occurred 20 min after 6 min of priming at 70% Δ. These investigators also showed that the V˙O2 response and performance were unaffected by priming exercise at 40% Δ followed by 3, 9, or 20 min of recovery, in contrast with the present study. For comparison, our priming intensities were ∼25% Δ and ∼63% Δ. Although an essential feature of experimental design was the strict assignment of heavy- and severe-intensity priming, our choice of these priming work rates and 10-min recovery duration was unlikely to optimize the performance effects. The heavy-intensity priming bouts produced relatively modest priming effects on the V˙O2 response that led to a significant increase in Tlim at 70% Δ and 100% WRpeak only, whereas the 10-min recovery may have been too short to allow the priming effects to outweigh the fatiguing effects of severe-intensity priming. The relationship between the priming effects on the V˙O2 kinetics and exercise tolerance therefore seems to rest on something of a "knife edge" when intermediate recovery durations (6-15 min) are used, with increased (1,10,11,22,27), decreased (14,15,39), and unaltered performance (10,25) (present study) all having been observed. More prolonged recovery intervals (≥20 min) may produce more consistent performance effects, although only if the priming is of severe intensity (1).
One intriguing feature of the present results was that the improvement in time to exhaustion at 70% Δ after heavy priming exercise was not associated with a significant reduction in the amplitude of the V˙O2 slow component but was instead occasioned by a reduced V˙O2 slow component trajectory. This suggests that a reduced V˙O2 slow component amplitude per se is not a prerequisite for enhanced exercise performance after priming exercise. Also, a reduced V˙O2 slow component after priming exercise is not necessarily associated with performance enhancement either (1,11,25) (present study). That said, it is important to note that the interpretation of the V˙O2 slow component amplitude during exhaustive severe-intensity exercise is not straightforward because its amplitude depends on the primary amplitude and on the V˙O2peak. If the primary amplitude is increased and the V˙O2peak does not change, the V˙O2 slow component amplitude must decrease, even if this is of no mechanistic significance. This is effectively illustrated by the data presented in Table 1 and Figure 1: the amplitude of the V˙O2 slow component systematically decreases with increasing power output, whereas the trajectory increases. For severe-intensity work rates, the trajectory of the V˙O2 slow component is probably the more meaningful parameter because it does not depend on the value of the primary amplitude or the V˙O2peak (9). However, quantifying the V˙O2 slow component using its trajectory during severe-intensity exercise carries with it the implicit assumption that the increase in V˙O2 during this phase is linear. Although the V˙O2 slow component can, on occasion, be described as a linear function of time (e.g., Casaburi et al. [12[), the consensus seems to favor some form of nonlinear increase as exercise progresses (e.g., Whipp et al. ). Consequently, the trajectory data reported herein should be considered an index, only, of the rate at which the V˙O2 slow component develops throughout the duration of exhaustive exercise.
Because of the nature of the present experiments, the methods contain several limitations. First, the control power-duration relationship had to be established before the priming bouts were conducted. This was necessary to partition the priming work rates into the heavy- and severe-intensity domains, although this may have resulted in an order effect for time to exhaustion in the control versus primed conditions. However, the order of the primed bouts (heavy and severe) was randomized, and the performance effects were distinct (see above). Second, we were unable to repeat each trial to enhance the signal-to-noise ratio of the V˙O2 responses. As a result, the confidence in the parameter estimates was lower than is typically the case for studies of V˙O2 kinetics. However, the CI associated with the primary amplitude was smaller than the increase reported, and we are therefore confident that this effect is real. Third, because of the number of exhaustive trials involved in these experiments (13 per subject), we were unable to perform additional trials if the CIs associated with the parameters of the power-duration relationship were large. As a result, the confidence in the parameter estimates was typically poor, representing ∼11% of the critical power and ∼66% of the W′, limiting the possibility of detecting meaningful changes in these parameters.
In summary, prior heavy exercise increased the primary V˙O2 amplitude and increased the tolerable duration of severe-intensity exercise performed after 10 min of recovery. This was associated with a significant increase in the W′. Prior severe exercise also primed the V˙O2 response but had no significant effect on exercise tolerance, the CP, or the W′. Thus, despite similar priming effects on the V˙O2 kinetics after prior heavy- and severe-intensity exercise, the effect on exercise performance was positive after prior heavy-intensity priming and neutral after prior severe-intensity priming and a recovery period of 10 min. The present results are consistent with the concept that when the V˙O2 kinetics is primed in the absence of muscle fatigue, the amount of work that can be performed above the CP is increased.
No sources of external funding were received for this work.
The authors report no conflict of interest.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
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