Exercise which elicits a metabolic acidaemia has been shown to reduce substrate-level phosphorylation (Rossiter et al. 2001) and speed the overall V_O2 kinetics (Gerbino et al. 1996; Burnley et al. 2000) during subsequent high-intensity exercise. It has been proposed that these effects may predispose to increase exercise tolerance (Gerbino et al. 1996; Rossiter et al. 2001). The purpose of this study was therefore to test the hypothesis that prior heavy exercise increases time to exhaustion during subsequent peri-maximal exercise.

Seven healthy males (27 ± 3 years; 78.4 ± 0.7 kg; means ± S.D.) volunteered to participate in this study which was approved by the institutional ethics committee. The subjects first completed a ramp exercise test on an electrically braked cycle ergometer to determine the gas exchange threshold (GET) andV_O2,max. Subsequently, the subjects performed square wave transitions from unloaded cycling to power outputs equivalent to 100, 110 and 120 %V_O2,max following no prior exercise (control, C) and 10 min after a 6 min bout of heavy exercise (HE) at 50 % Δ (half-way between the GET andV_O2,max). Four subjects also performed the peri-maximal exercise bouts 10 min after a moderate intensity exercise bout (ME; ~12 min at 80 % GET). For all trials, the time to ‘exhaustion’ was recorded to the nearest second, where ‘exhaustion’ was defined as a fall in self-selected pedal rate of > 5 rev min^-1. A blood sample was taken from the fingertip immediately before and after each trial for the determination of blood [lactate]. Differences between the C and HE conditions were analysed with paired t tests and are reported as means ± S.E.M.

Blood [lactate] was higher at the onset of the peri-maximal exercise bouts when they were preceded by HE (C: ~ 1.1 vs. HE: ~2.5 mM; P < 0.01) but there was no significant difference in blood [lactate] at end-exercise. Time to exhaustion was increased by prior HE at 100 % (C: 386 ± 92 vs. HE: 613 ± 161 s), 110 % (C: 218 ± 26 vs. HE: 284 ± 47 s), and 120 % (C: 139 ± 18 vs. HE: 180 ± 29 s)V_O2,max (all P < 0.01). Prior ME, which did not increase blood [lactate], did not affect time to exhaustion nor the time course of the V_O2 response during exercise (n = 4). At 100 %V_O2,max, V_O2 was not significantly different between C and the prior HE condition either at 1 min into exercise (C: 3.04 ± 0.09 vs. HE: 3.14 ± 0.14 l min^-1) or at exhaustion (C: 3.89 ± 0.08 vs. HE: 3.88 ± 0.13 l min^-1). At 110 %V_O2,max, V_O2 was significantly higher at 1 min into exercise following prior HE (C: 3.11 ± 0.14 vs. HE: 3.42 ± 0.16 l min^-1; P < 0.05) but there was no significant difference at exhaustion (C: 3.89 ± 0.08 vs. HE: 3.90 ± 0.12 l min^-1). At 120 %V_O2,max, V_O2 was significantly higher following prior HE both at 1 min into exercise (C: 3.25 ± 0.12 vs. HE: 3.67 ± 0.15 l min^-1; P < 0.01) and at exhaustion (C: 3.60 ± 0.08 vs. HE: 3.95 ± 0.12 l min^-1; P < 0.01).

These results indicate that prior heavy exercise which increases blood [lactate] to 2-3 mM results in an increased time to exhaustion during subsequent peri-maximal exercise. Prior heavy (but not moderate) exercise therefore appears to enhance the aerobic contribution to energy turnover in subsequent high-intensity exercise and retard the rate at which fatigue develops. However, the characteristics of the prior work rate, exercise duration and recovery period that optimise this effect remain to be determined.