Hypoxia and the cardiovascular response to dynamic knee-extensor exercise

Hypoxia affects O-2 transport and aerobic exercise capacity. In two previous studies, conflicting results have been reported regarding whether O-2 delivery to the muscle is increased with hypoxia or whether there is a more efficient O-2 extraction to allow for compensation of the decreased O-2 availability at submaximal and maximal exercise. To reconcile this discrepancy, we measured limb blood flow (LBF), cardiac output, and O-2 uptake during two-legged knee-extensor exercise in eight healthy young men. They completed studies at rest, at two submaximal workloads, and at peak effort under normoxia (inspired O-2 fraction 0.21) and two levels of hypoxia (inspired O-2 fractions 0.16 and 0.11). During submaximal exercise, LBF increased in hypoxia and compensated for the decrement in arterial O-2 content. At peak effort, however, our subjects did not achieve a higher cardiac output or LBF. Thus O-2 delivery was not maintained and peak power output and leg O-2 uptake were reduced proportionately. These data are consistent then with the findings of an increased LBF to compensate for hypoxemia at submaximal exercise, but no such increase occurs at peak effort despite substantial cardiac capacity for an elevation in LBF.