Effect of hypoxia on the dynamic response of hyperaemia in the contracting human calf muscle

New Findings "¢"‚What is the central question of this study? The effect of hypoxia on the dynamic response of muscle hyperaemia during exercise is not known. "¢"‚What is the main finding and its importance? Demonstrates that the effect of hypoxia on muscle hyperaemia is very rapid, occurring within the first 2-3 contractions of exercise and before the conventional oxygen-dependent processes would exert their effects. Although systemic hypoxia increases the muscle hyperaemic response during 'steady-state' exercise, its effect on the dynamic characteristics of this response is not clear. In the present study, we first established that hypoxia increases the steady-state hyperaemic response at low workloads during calf exercise. To study dynamic aspects of this response, eight subjects performed eight exercise trials while breathing a normoxic (fractional inspired O2= 0.2094) or hypoxic gas mixture (fractional inspired O2= 0.105). Subjects performed intermittent contractions (1 s) of the calf muscle at 20% maximal voluntary contraction, and the leg blood flow (LBF), leg vascular conductance (LVC) and EMG activities of the triceps surae muscles were measured during each contraction-relaxation period (3 s). The LBF and LVC responses were averaged for each subject and fitted using a four-phase, exponential growth and decay function. Hypoxia evoked significant increases in the change in LBF (15%) and LVC (23%) from the start to the end of exercise, as well as the amplitude of the rapid growth phase of LBF and LVC (21%). Similar, but non-significant, effects on the amplitude of the slow growth phase of LBF (P= 0.08) and LVC (P= 0.10) were observed. By contrast, hypoxia had no effect on temporal parameters of these growth phases, parameters defining the decay phases or EMG activities. These results suggest that the effect of hypoxia on exercise hyperaemia is targeted at the rapid and perhaps the slow growth phase of the response, and is not mediated by a change in the level of muscle activation.