There is controversy concerning the factor(s) that limit the rate at which pulmonary oxygen uptake (Î{special}J{special}) rises following the onset of exercise, with some groups favouring an intra-muscular metabolic inertia (e.g. Grassi et al. 1998) and others favouring an O₂ availability limitation (e.g. Hughson et al. 2001). The metabolic acidosis caused by the performance of prior heavy exercise results in enhanced vasodilatation and blood flow during subsequent exercise, and thus the prior exercise model represents a good test of whether muscle perfusion limits Î{special}J{special} kinetics following the onset of exercise. We therefore hypothesised that prior multiple-sprint exercise would reduce the time constant for the phase II Î{special}J{special} kinetics during subsequent supra-maximal intensity exercise (where there is evidence that O₂ availability may be compromised; Grassi et al. 2000).

Seven healthy males (age 20-33 yrs) gave written informed consent to participate in this study which was approved by the Manchester Metropolitan University Ethics Committee. On two separate occasions, the subjects performed square wave transitions from unloaded cycling to a work rate equivalent to ~105 % Î{special}J{special} peak following no prior exercise (control, C) and 12 min after the last bout of repeated sprint exercise (3 X 30 s maximal cycle ergometer sprints separated by 5 min rest, PSE). Pulmonary gas exchange was measured breath-by-breath and Î{special}J{special} kinetics were determined from the averaged response to each condition. The data were analysed using paired t tests and are expressed as the mean ± S.E.M. Statistical significance was accepted at P < 0.05.

Following the sprint exercise bouts, both pre-test heart rate (C: 98 ± 4 vs. PSE: 127 ± 4 b min^-1; P < 0.01) and pre-test blood [lactate] (C: 1.3 ± 0.1 vs. PSE: 7.7 ± 0.3 mM; P < 0.01) were significantly elevated. Near infra red spectroscopy also indicated a marked elevation in muscle oxygenation in PSE compared to C. However, despite indirect evidence that muscle blood flow and O₂ availability were enhanced, the phase II time constant was not significantly affected by prior sprint exercise (C: 33.8 ± 2.1 vs. PSE: 33.2 ± 2.9 s). The asymptotic gain of the fundamental Î{special}J{special} response (change in Î{special}J{special}/change in work rate) (C: 8.1 ± 0.4 vs. PSE: 9.0 ± 0.3 ml min^-1.W^-1; P < 0.05), and the end-exercise Î{special}J{special} (C: 3.28 ± 0.15 vs. PSE: 3.53 ± 0.18 L min^-1; P < 0.01) were significantly elevated following sprint exercise. The performance of prior sprint exercise does not influence the time constant for the rise in Î{special}J{special} following the onset of subsequent supra-maximal exercise but does result in an increased asymptotic gain of the fundamental Î{special}J{special} response.

These data are consistent with the interpretation that the time constant for the rise in Î{special}J{special} following the onset of exercise is not limited by O₂ availability even in the transition to supra-maximal work rates (cf. Bangsbo et al. 2000). The cause of the higher initial ‘target amplitude’ for Î{special}J{special} following sprint exercise is unclear but may indicate that the gain of the fundamental Î{special}J{special} response is itself sensitive to O₂ availability or or to changes in muscle fibre recruitment.