During variable intensity exercise, excess muscle oxygen uptake during a repeated high-intensity workload is not explained by perfusion heterogeneity, suggesting it is derived from working muscle cells.
Suggests intracellular muscle factors drive excess VO2 in repeated high-intensity exercise; hypothesis-generating for VO2 regulation beyond perfusion.
The association between muscle oxygen uptake (VO(2)) and perfusion or perfusion heterogeneity (relative dispersion, RD) was studied in eight healthy male subjects during intermittent isometric (1 s on, 2 s off) one-legged knee-extension exercise at variable intensities using positron emission tomography and a-v blood sampling. Resistance during the first 6 min of exercise was 50% of maximal isometric voluntary contraction force (MVC) (HI-1), followed by 6 min at 10% MVC (LOW) and finishing with 6 min at 50% MVC (HI-2). Muscle perfusion and O(2) delivery during HI-1 (26 +/- 5 and 5.4 +/- 1.0 ml 100 g(-1) min(-1)) and HI-2 (28 +/- 4 and 5.8 +/- 0.7 ml 100 g(-1) min(-1)) were similar, but both were higher (P<0.01) than during LOW (15 +/- 3 and 3.0 +/- 0.6 ml 100 g(-1) min(-1)). Muscle VO(2) was also higher during both HI workloads (HI-1 3.3 +/- 0.4 and HI-2 4.1 +/- 0.6 ml 100 g(-1) min(-1)) than LOW (1.4 +/- 0.4 ml 100 g(-1) min(-1); P<0.01) and 25% higher during HI-2 than HI-1 (P<0.05). O(2) extraction was higher during HI workloads (HI-1 62 +/- 7 and HI-2 70 +/- 7%) than LOW (45 +/- 8%; P<0.01). O(2) extraction tended to be higher (P = 0.08) during HI-2 when compared to HI-1. Perfusion was less heterogeneous (P<0.05) during HI workloads when compared to LOW with no difference between HI workloads. Thus, during one-legged knee-extension exercise at variable intensities, skeletal muscle perfusion and O(2) delivery are unchanged between high-intensity workloads, whereas muscle VO(2) is increased during the second high-intensity workload. Perfusion heterogeneity cannot explain this discrepancy between O(2) delivery and uptake. We propose that the excess muscle VO(2) during the second high-intensity workload is derived from working muscle cells.
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Laaksonen et al. (2010) studied this question.
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