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1 Department of Exercise and Sport Science, Manchester Metropolitan University, Alsager, Cheshire, United Kingdom
2 Department of Movement and Sports Sciences, Ghent University, Ghent, Belgium
3 Department of Kinesiology, Kansas State University, Manhattan, Kansas, USA
* To whom correspondence should be addressed. E-mail: a.m.jones{at}mmu.ac.uk.
We hypothesised that the metabolic acidosis resulting from the performance of multiple sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (VO2) kinetics during subsequent peri-maximal intensity constant work rate exercise, if O2 availability represented a limitation to VO2 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 pre-determined VO2 peak, separated by 3 x 30 s maximal sprint cycling and 15 min recovery. Blood [lactate] (mean ±S.D. MAX1: 1.3 ± 0.4 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, peri-maximal exercise when it was preceded by multiple sprint exercise. Near infra-red spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when peri-maximal exercise was preceded by multiple sprint exercise. However, the time constant describing the primary component (i.e. phase II) increase in VO2 was not significantly different between the two conditions (MAX1: 33.8 ± 5.5 vs. MAX2: 33.2 ± 7.7 s). Rather, the asymptotic 'gain' of the primary VO2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 ± 0.9 vs. MAX2: 9.0 ± 0.7 ml.min-1.W-1; P<0.05), such that VO2 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 VO2 response but does increase the amplitude to which VO2 may rise following the onset of peri-maximal intensity cycle exercise.
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