Abstract

Previously, we found resting metabolic rate increased at high altitude but the mechanism and consequences of this increase were unclear. We sought to test the role of beta-sympathetic activation for increasing metabolic rate and the contribution of an increase in metabolic rate to raising total ventilation at altitude. Following baseline studies at sea level, two groups of six healthy male subjects received either placebo or propranolol (80 mg/8 h) for 3 days prior to ascent to Pikes Peak (4300 m) where treatment was continued for 15 days. O 2 consumption increased in placebo-treated subjects with a rise of 20 ± 5% ( X ± SEM) on day 1 and no change 0 ± 7% in propranolol-treated subjects (difference between groups, P < 0.05). The increase in total ventilation upon ascent was 28 ± 2% in the placebo group vs 9 ± 7% in the propranolol group ( P < 0.05) and was correlated with metabolic rate in individual subjects. Decreasing end-tidal P CO 2 , taken as an index of ventilatory acclimization, was similar in both groups. Thus, beta-sympathetic activation appears to increase metabolic rate upon ascent to high altitude and lead to a proportionate elevation in total ventilation but does not alter ventilatory acclimization.

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