Ventilatory effects of 8 h of isocapnic hypoxia with and without β-blockade in humans

This study investigated whether changing sympathetic activity, acting via β-receptors, might induce the progressive ventilatory changes observed in response to prolonged hypoxia. The responses of 10 human subjects to four 8-h protocols were compared:1) isocapnic hypoxia (end-tidal$P{O}_2$ = 50 Torr) plus 80-mg doses of oral propranolol; 2) isocapnic hypoxia, as in protocol 1, with oral placebo; 3) air breathing with propranolol; and 4) air breathing with placebo. Exposures were conducted in a chamber designed to maintain end-tidal gases constant by computer control. Ventilation (V˙e) was measured at regular intervals throughout. Additionally, the subjects’ ventilatory hypoxic sensitivity and their residual V˙e during hyperoxia (5 min) were assessed at 0, 4, and 8 h by using a dynamic end-tidal forcing technique. β-Blockade did not significantly alter either the rise in V˙e seen during 8 h of isocapnic hypoxia or the changes observed in the acute hypoxic ventilatory response and residual V˙e in hyperoxia over that period. The results do not provide evidence that changes in sympathetic activity acting via β-receptors play a role in the mediation of ventilatory changes observed during 8 h of isocapnic hypoxia.