This study investigated whether changing sympathetic activity, acting via b
eta-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 Po-2 = 50 Torr
) plus 80-mg doses of oral propranolol; 2) isocapnic hypoxia, as in protoco
l 1, with oral placebo; 3) air breathing with propranolol; and 4) air breat
hing with placebo. Exposures were conducted in a chamber designed to mainta
in end-tidal gases constant by computer control. Ventilation ((V) over dot(
E)) was measured at regular intervals throughout. Additionally, the subject
s' ventilatory hypoxic sensitivity and their residual (V) over dot(E) durin
g hyperoxia (5 min) were assessed at 0, 4, and 8 h by using a dynamic end-t
idal forcing technique. beta-Blockade did not significantly alter either th
e rise in (V) over dot(E) seen during 8 h of isocapnic hypoxia or the chang
es observed in the acute hypoxic ventilatory response and residual (V) over
dot(E) in hyperoxia over that period. The results do not provide evidence
that changes in sympathetic activity acting via beta-receptors play a role
in the mediation of ventilatory changes observed during 8 h of isocapnic hy
poxia.