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Mitochondrial oxidative phosphorylation, which modulates resynthesis of PCr, depends in part on the availability of O2 for the mitochondria in working muscle. Particularly during intense exercise, the induced lower O2 availability due to hypoxic condition by inadequate blood flow affects mitochondrial oxidative phosphorylation. However, there are few studies which have reported the relationship between mitochondrial stimuli and oxygen diffusion rate from capillary to mitochondria in skeletal muscle (muscle rDO2) during varying-workload exercise including under severe acidosis conditions in humans. The purpose of this study was to investigate the relationship between muscle PCr, rDO2, and muscle deoxygenation in humans during incremental dynamic exercise. Twelve healthy, nonsmoking male subjects participated in this study. The subjects performed incremental dynamic handgrip exercise until exhaustion. Muscle PCr during exercise was evaluated using 31-phosphorus magnetic resonance spectroscopy. Muscle deoxygenation level was monitored using near-infrared spectroscopy, and muscle rDO2 was determined by the rate of muscle deoxygenation during temporary arterial occlusion immediately after the end of each exercise stage. Muscle PCr level subsequently decreased with higher workloads, and muscle rDO2 above 10%MVC significantly increased from the resting, and was constant with higher workloads. Muscle deoxygenation level was also significantly greater above 10%MVC, and gradually increased with higher workloads. These results suggest that muscle rDO2 is limited at higher workloads, although mitochondrial stimuli are increased. The constant muscle rDO2 with higher workloads may be caused by reduced O2 gradient from capillary to mitochondria.
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