Effects of acetazolamide on aerobic exercise capacity and pulmonary hemodynamics at high altitudes

Abstract

Aerobic exercise capacity is decreased at altitude because of combined decreases in arterial oxygenation and in cardiac output. Hypoxic pulmonary vasoconstriction could limit cardiac output in hypoxia. We tested the hypothesis that acetazolamide could improve exercise capacity at altitude by an increased arterial oxygenation and an inhibition of hypoxic pulmonary vasoconstriction. Resting and exercise pulmonary artery pressure (Ppa) and flow (Q) (Doppler echocardiography) and exercise capacity (cardiopulmonary exercise test) were determined at sea level, 10 days after arrival on the Bolivian altiplano, at Huayna Potosi (4,700 m), and again after the intake of 250 mg acetazolamide vs. a placebo three times a day for 24 h. Acetazolamide and placebo were administered double-blind and in a random sequence. Altitude shifted Ppa/Q plots to higher pressures and decreased maximum O2 consumption (V̇o2max). Acetazolamide had no effect on Ppa/Q plots but increased arterial O2 saturation at rest from 84 ± 5 to 90 ± 3% ( P < 0.05) and at exercise from 79 ± 6 to 83 ± 4% ( P < 0.05), and O2 consumption at the anaerobic threshold (V-slope method) from 21 ± 5 to 25 ± 5 ml·min−1·kg−1 ( P < 0.01). However, acetazolamide did not affect V̇o2max (from 31 ± 6 to 29 ± 7 ml·kg−1·min−1), and the maximum respiratory exchange ratio decreased from 1.2 ± 0.06 to 1.05 ± 0.03 ( P < 0.001). We conclude that acetazolamide does not affect maximum exercise capacity or pulmonary hemodynamics at high altitudes. Associated changes in the respiratory exchange ratio may be due to altered CO2 production kinetics.