The effect of α1-adrenergic blockade on post-exercise brachial artery flow-mediated dilatation at sea-level and high-altitude

Abstract

We examined the hypotheses that 1) at rest, endothelial function would be impaired at high-altitude compared to sea-level, 2) endothelial function would be reduced to a greater extent at sea-level compared to high-altitude after maximal exercise, and 3) reductions in endothelial function following moderate-intensity exercise at both sea-level and high-altitude are mediated via an α₁-adrenergic pathway. In a double-blinded, counter-balanced, randomized and placebo-controlled design, nine healthy participants performed a maximal-exercise test, and two 30-min sessions of semi-recumbent cycling exercise at 50% peak Watt following either placebo or α₁-adrenergic blockade (prazosin; 0.05mg kg ⁻¹). These experiments were completed at both sea-level (344m) and high-altitude (3800m). Blood pressure (finger photoplethysmography), heart rate (electrocardiogram), oxygen saturation (pulse oximetry), and brachial artery blood flow and shear rate (ultrasound) were recorded prior to, during, and following exercise. Endothelial function assessed by brachial artery flow-mediated dilatation (FMD) was measured prior to, immediately following, and 60-min post-exercise. Our findings were: 1) at rest, FMD remained unchanged between sea-level and high-altitude (placebo P = 0.287; prazosin: P = 0.110); 2) FMD remained unchanged after maximal exercise at sea-level and high-altitude (P = 0.244); 3) the 2.9 ± 0.8% (P = 0.043) reduction in FMD immediately after moderate-intensity exercise at sea-level was abolished via α₁-adrenergic blockade. Conversely, at high-altitude, FMD was unaltered following moderate-intensity exercise, and administration of α₁-adrenergic blockade elevated FMD (P = 0.032). Our results suggest endothelial function is differentially affected by exercise when exposed to hypobaric hypoxia. These findings have implications for understanding the chronic impacts of hypoxemia on exercise, and the interactions between the α₁-adrenergic pathway and endothelial function.

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