The exponential models included amplitudes (Ap and As), time constants (τp and τs), and delay times (Tdp and Tds). Ap, τp, and Tdp describe the V̇O2 fundamental component, while As, τs, and Tds describe the V̇O2 slow component. A nonlinear least-square algorithm was used to determine the parameters of the best fitting curve. The mean-square amplitudes were used to evaluate whether the monoexponential or biexponential model provided the best fit to each data set. Owing to concerns over the relatively low signal/noise ratio with only one exercise transition in each condition, we chose to report only the mean response time for the primary phase of the response (TDp + τp).
Differences in time to exhaustion and physiological response between the perimaximal exercise bouts preceded by no prior exercise and those preceded by heavy-intensity prior exercise were tested for statistical significance using paired t-tests. Statistical significance was set at P < 0.05.
The mean (± SD) V̇O2peak of the participants was 50.3 ± 3.3 mL·kg−1·min−1, with GET occurring at 52 ± 12% of V̇O2peak. Heavy-intensity prior exercise was performed at 253 ± 51 W (N = 7). The work rates used in the exhaustive bouts were 322 ± 39, 357 ± 43, and 392 ± 48 W for the 100, 110, and 120% W-V̇O2peak conditions, respectively.
Time to exhaustion was significantly longer in all of the perimaximal bouts after heavy-intensity prior exercise compared with the control condition (Table 1 and Fig. 1). The CPwas not significantly affected by the performance of prior high-intensity exercise (control: 284 ± 35 vs heavy exercise: 289 ± 26 W), but the increase in W′ approached statistical significance (control: 15.5 ± 2.2 vs heavy exercise: 18.2 ± 3.5 kJ; P = 0.06), (Fig. 2). Heavy-intensity prior exercise caused a significant increase in blood [lactate], which was still present at the onset of the perimaximal exercise bouts (Table 1). However, no significant differences in blood [lactate] were observed at the termination of the perimaximal exercise bouts. Heart rate immediately before the onset of the perimaximal exercise bouts was significantly higher after prior heavy-intensity exercise compared with control (Table 1). This higher heart rate persisted throughout exercise and was still evident at the cessation of the exhaustive bouts, reaching significance at 110% and 120% W-V̇O2peak (P < 0.05).
Table 2 shows the V̇O2 responses to perimaximal exercise after no prior exercise and after heavy-intensity prior exercise. There was no significant difference in baseline V̇O2 at the onset of the perimaximal exercise bouts between the control and prior heavy-intensity exercise conditions. The V̇O2 kinetics in the primary adaptive phase (as given by the mean response time) were not significantly altered by the performance of prior heavy-intensity exercise. At 100% W-V̇O2peak, there was no significant difference in the V̇O2 at 1 min into exercise or at exhaustion. At 110% W-V̇O2peak, V̇O2 at 1 min into exercise was significantly higher than in the control condition (P < 0.05), but there was no significant difference in the V̇O2 at exhaustion. At 120% W-V̇O2peak, V̇O2 was significantly higher both at 1 min into exercise (P < 0.05) and at exhaustion (P < 0.05) compared with the control condition.
Consistent with our hypothesis, the results indicate that prior heavy-intensity exercise leads to a significant increase in time to exhaustion during subsequent perimaximal exercise. Previous research has demonstrated that prior high-intensity exercise results in an increased oxidative contribution to energy metabolism during subsequent high-intensity exercise, with a corresponding reduction in the oxygen deficit, as reflected in a reduced rate of substrate-level phosphorylation (1,6,23,24,29). There is direct evidence that muscle blood flow and O2 extraction are increased during high-intensity cycle exercise when it is preceded by a high-intensity warm-up (1,23). Furthermore, Rossiter et al. (29) reported that prior heavy leg extension exercise resulted in a 9% sparing of [PCr] over the first 2–3 min of an identical exercise bout performed 6 min later. Other groups have also shown that total anaerobic energy turnover is substantially reduced (by 25–45%) in the second of two high-intensity exercise bouts (1,11,23). The reduced lactate production and sparing of intramuscular [PCr] resulting from the increased muscle aerobic energy turnover might be expected to predispose to increased exercise tolerance (14), as indeed we found in the present study. This is because the point of exhaustion is often presumed to coincide with a depletion of intra-muscular phosphates to some critical value and/or the attainment of a critically low intracellular pH or high [lactate] (but see below) (12,15,27,28).
In the present study, the performance of prior heavy-intensity exercise led to a dramatic increase in the time to exhaustion during subsequent perimaximal exercise (29–59% compared with the control condition). Interestingly, however, prior heavy-intensity exercise did not cause a significant improvement in the CP but did influence the curvature constant of the power-time relationship, resulting in an increased W′ that approached statistical significance. It is likely that the difference in W′ would have reached statistical significance if our subject sample had been slightly larger, indicating that this is a real effect that is worthy of further investigation. The W′ is considered to represent a finite energy reserve comprising O2 stores (note that this would be relatively small), high-energy phosphates, and energy derived through anaerobic glycolysis (28). It is unclear, therefore, how the performance of heavy exercise might enhance the derivation of energy through predominantly O2-independent pathways (i.e., increase the “anaerobic capacity”) unless the effect of prior heavy-intensity exercise is to retard the rate at which metabolites that ultimately result in fatigue accumulate during subsequent exercise (see below).
It is important to point out that the performance of prior moderate-intensity exercise (i.e., “warm-up”) does not alter the V̇O2 or blood [lactate] response to subsequent exercise (10,14). Furthermore, moderate-intensity warm-up exercise does not appear to enhance performance during subsequent high-intensity endurance exercise (5,21). We have recently found that 12 min of prior moderate-intensity exercise, that would have resulted in a similar total energy expenditure to the prior heavy-intensity exercise bout performed in the present study, had a relatively small effect (+2–5%) on the time to exhaustion in subsequent perimaximal exercise bouts (Jones et al., unpublished observations, 2003). It has also been demonstrated that the elevation of muscle temperature by 2–3°C using hot packs or water baths (9,19,22) does not appreciably alter the V̇O2 or blood [lactate] response to subsequent exercise. Collectively, these results suggest that the extended time to exhaustion in the perimaximal bouts after prior heavy-intensity exercise was unlikely to be contingent on an increased muscle temperature.
Blood [lactate] was significantly elevated at the onset of the perimaximal exercise trials after prior heavy-intensity exercise (2.5 mM), and it might appear paradoxical that time to exhaustion was extended in the face of this residual acidosis. Both the lactate ion and the hydrogen ion have been shown to reduce force production in isolated muscle (15,27), and the accumulation of lactate and the reduction of pH during heavy exercise in humans is believed by many to be a major cause of muscle fatigue (13). However, many of the early studies that led to this view were conducted at unphysiologically low temperatures (17°C), and when these experiments are repeated at 37°C, the inhibitory effect of intracellular acidification on muscle contractility disappears (30). In an important recent study, Nielsen et al. (25) reported that the addition of 20-mM lactic acid to an isolated muscle preparation almost completely reversed the 75% loss of tetanic force caused by preincubation at an extra-cellular [K+] of 11 mM. These data indicate that, rather than causing fatigue, acidosis might protect against fatigue resulting from the loss of muscle K+ during exercise, at least in some situations. In the present study, it is therefore possible that the residual acidosis after prior heavy-intensity exercise served to preserve muscle function and retard the rate at which fatigue developed during the subsequent high-intensity exercise bouts.
It appears that the extent of the metabolic acidosis caused by prior exercise is important in determining the potential for performance enhancement (2,16,18). For example, Karlsson et al. (18) reported that prior exhaustive arm exercise that increased blood [lactate] to 10 mM resulted in a 31% reduction in the time to exhaustion in exhaustive leg cycle exercise performed 6 min later. More recently, Koppo and Bouckaert (21) reported that prior exercise at 90% V̇O2peak (as compared with 75% V̇O2peak in the present study), which resulted in a blood [lactate] of 6 mM, did not significantly alter time to exhaustion during subsequent exercise at 95% V̇O2peak. Also, Bishop et al. (5) reported that a continuous heavy-intensity warm-up at 75% V̇O2peak, which elevated blood [lactate] to 5.1 mM, did not improve performance in a 2-min all-out kayak ergometer test. It is possible that very-high-intensity prior exercise results in the accumulation of other fatiguing metabolites (e.g., Pi, H2PO4 −, ammonia) in muscle (30), or that more time is subsequently required for the restoration of extracellular [K+] (2). Therefore, differences in the rate of lactate clearance compared with the rate of clearance of other “fatiguing” metabolites and the speed with which the electrochemical gradient across the muscle membrane is restored may be important in determining the potential for performance enhancement. It may be that there is an optimal blood [lactate] of 2–3 mM that is required for performance enhancement because prior exercise that either results in no change in blood [lactate], or prior exercise and recovery combinations that result in large elevations in blood [lactate] of greater than 5 mM, does not enhance performance (5,18,21). Moderate-intensity warm-up exercise does not enhance the aerobic contribution to subsequent exercise (10,14), whereas severe-intensity warm-up exercise may not allow sufficient time for restoration of intramuscular high-energy phosphates and/or removal of fatiguing metabolites (e.g., Pi,H+, H2PO4 −, or extra-cellular K+) before the commencement of the criterion exercise challenge.
Although somewhat controversial, it appears that priming exercise does not result in a speeding of the V̇O2 kinetics over the primary adaptive phase of the response during subsequent cycle exercise but that V̇O2 projects to a greater initial amplitude with an unchanged time constant (3,7,8). In the present study, the overall primary V̇O2 kinetics expressed as the mean response time were not significantly affected by prior exercise; rather, V̇O2 appeared to project to and/or reach a higher V̇O2 in the perimaximal exercise bouts with a similar rate of response. Indeed, at 120% W-V̇O2peak, the increased time to exhaustion resulting from the performance of prior heavy-intensity exercise allowed V̇O2peak to be attained, whereas in the control condition exercise was terminated before V̇O2peak was reached (Fig. 3). As mentioned above, this suggests that the mechanism(s) causing fatigue in the control condition were in some way attenuated by the performance of prior high-intensity exercise.
The mechanisms responsible for the elevated V̇O2 throughout the transient phase of heavy exercise when it is preceded by a bout of heavy exercise are still debated, but these might feasibly include changes in O2 availability, enzyme activity, substrate availability, or motor unit recruitment (4,7,11,14). Gerbino et al. (14) suggested that the residual acidosis after a priming bout of heavy exercise might increase muscle vasodilation and result in more homogeneous muscle perfusion at exercise onset. For perimaximal exercise, at least, reduction of any heterogeneity in oxygen delivery to working muscle would be expected to increase V̇O2 and diminish Δ [lactate]. Alternatively, it is possible that changes in putative controllers of muscle respiration such as the phosphorylation potential, [PCr], NADH availability, and cytosolic [Ca2+] after prior heavy exercise might reduce any inherent inertia in the key enzymes controlling oxidative metabolism and result in either a reduced “lag” before muscle O2 consumption increases appreciably after the onset of subsequent exercise (4) or a more rapid adjustment to the “steady state” requirement. It is also known that prior exercise results in a stockpiling of acetyl groups, and it has been suggested that this greater availability of metabolic substrate might enhance mitochondrial ATP production (11). Finally, it has been suggested that the increased V̇O2 might be related to increased motor unit recruitment at the onset of exercise. Burnley et al. (7) reported that muscle iEMG was 19% higher at the onset of the second of two bouts of severe-intensity exercise and noted that the iEMG responses were qualitatively similar to the pulmonary V̇O2 responses in both bouts. Increased motor unit recruitment at the onset of heavy constant work rate exercise might be beneficial to performance because the metabolic strain on each fiber would be reduced.
In conclusion, the performance of prior high-intensity exercise resulted in a significant increase in time to exhaustion during subsequent perimaximal exercise at 100%, 110%, and 120% W-V̇O2peak despite, or perhaps because of, a significant elevation of blood [lactate] (to 2.5 mM) at exercise onset. The results of this study may have important implications for the preparation of athletes for competition and for the improvement of exercise tolerance in the elderly and in patient populations. The characteristics of the prior exercise intensity, exercise duration, exercise mode, and recovery period that optimize the ergogenic effect of prior heavy-intensity exercise remain to be determined. Elucidation of these characteristics, and examination of the effect of prior heavy-intensity exercise on performance both in athletes and in populations with compromised exercise tolerance, may be fruitful topics for future research.
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Keywords:©2003The American College of Sports Medicine
TIME TO EXHAUSTION; V̇O2 KINETICS; WARM-UP; FATIGUE