Arterial O2 content and tension in regulation of cardiac output and leg blood flow during exercise in humans

Abstract

A universal O 2 sensor presumes that compensation for impaired O 2 delivery is triggered by low O 2 tension, but in humans, comparisons of compensatory responses to altered arterial O 2 content ([Formula: see text]) or tension ([Formula: see text]) have not been reported. To directly compare cardiac output (Q˙TOT) and leg blood flow (LBF) responses to a range of[Formula: see text] and[Formula: see text], seven healthy young men were studied during two-legged knee extension exercise with control hemoglobin concentration ([Hb] = 144.4 ± 4 g/l) and at least 1 wk later after isovolemic hemodilution ([Hb] = 115 ± 2 g/l). On each study day, subjects exercised twice at 30 W and on to voluntary exhaustion with an[Formula: see text] of 0.21 or 0.11. The interventions resulted in two conditions with matched[Formula: see text] but markedly different [Formula: see text] (hypoxia and anemia) and two conditions with matched[Formula: see text] and different[Formula: see text] (hypoxia and anemia + hypoxia). [Formula: see text] varied from 46 ± 3 Torr in hypoxia to 95 ± 3 Torr (range 37 to >100) in anemia ( P < 0.001), yet LBF at exercise was nearly identical. However, as[Formula: see text] dropped from 190 ± 5 ml/l in control to 132 ± 2 ml/l in anemia + hypoxia ( P < 0.001),Q˙TOT and LBF at 30 W rose to 12.8 ± 0.8 and 7.2 ± 0.3 l/min, respectively, values 23 and 47% above control ( P< 0.01). Thus regulation ofQ˙TOT, LBF, and arterial O 2 delivery to contracting intact human skeletal muscle is dependent for signaling primarily on[Formula: see text], not[Formula: see text]. This finding suggests that factors related to [Formula: see text]or [Hb] may play an important role in the regulation of blood flow during exercise in humans.