O2 extraction maintains O2 uptake during submaximal exercise with β-adrenergic blockade at 4,300 m

Whole body O-2 uptake ((V) over dot O-2) during maximal and submaximal exercise has been shown to be preserved in the setting of beta-adrenergic blockade at high altitude, despite marked reductions in heart rate during exercise. An increase in stroke volume at high altitude has been suggested as the mechanism that preserves systemic O-2 delivery (blood flow x arterial O-2 content) and thereby maintains (V) over dot O-2 at sea-level values. To test this hypothesis, we studied the effects of nonselective beta-adrenergic blockade on submaximal exercise performance in 11 normal men (26 +/- 1 yr)at sea level and on arrival and after 21 days at 4,300 m. Six subjects received propranolol (240 mg/day), and five subjects received placebo. At sea level, during submaximal exercise, cardiac output and O-2 delivery were significantly lower in propranolol- than in placebo-treated subjects. Increases in stroke volume and (V) over dot O-2 extraction were responsible for the maintenance of (V) over dto O-2. At 4,300 m, beta-adrenergic blockade had no significant effect on (V) over dot O-2, ventilation, alveolar PO2, and arterial blood gases during submaximal exercise. Despite increases in stroke volume, cardiac output and thereby O-2 delivery were still reduced in propranolol-treated subjects compared with subjects treated with placebo. Further reductions in already low levels of mixed venous Oz saturation were responsible for the maintenance of (V) over dot O-2 on arrival and after 21 days at 4,300 m in prppranolol-treated subjects. Despite similar workloads and Vet, propranolol-treated subjects exercised at greater perceived intensity than subjects given placebo at 4,300 m. The values for mixed venous O-2 saturation during submaximal exercise in propranolol-treated subjects at 4,300 m approached those reported at simulated altitudes >8,000 m. Thus beta-adrenergic blockade at 4,300 m results in significant reduction in O-2 delivery during submaximal exercise due to incomplete compensation by stroke volume for the reduction in exercise heart rate. Total body (V) over dot O-2 is maintained at a constant level by an interaction between mixed venous O-2 saturation, the arterial O-2-carrying capacity, and hemodynamics during exercise with acute and chronic hypoxia.