Pulmonary vascular response to air-breathing exercise in humans following an 8-h exposure to hypoxia

This study is concerned with the pulmonary vasculature in euoxia after preconditioning with 8 h of hypoxia. The particular question we ask is whether the pulmonary vasculature will dilate normally with exercise or retain some degree of vasoconstriction, as has previously been reported in studies involving longer exposures to the hypoxia of high altitude. Ten subjects were studied on two separate days. On one day, subjects were exposed to 8 h of isocapnic hypoxia (end-tidal PO2PO2 55 Torr) and on the other day to 8 h of euoxia as a control. Before and after each exposure, subjects undertook 20 min of exercise at an intensity to elevate heart rate (HR) by ∼30 bpm. During this period, Doppler echocardiography was used to assess the maximum pressure gradient during systole across the tricuspid valve (ΔPmax) as an index of pulmonary arterial pressure. Following 8-h hypoxia, but not control, ΔPmax increased by ∼2 mmHg with the subjects breathing air at rest (ANOVA, P < 0.02). Under control conditions, exercise at ∼30 bpm above resting HR increased ΔPmax by 9.9 ± 1.3 mmHg (mean ± SE). Following 8-h hypoxia, but not control, this sensitivity of ΔPmax to exercise increased by ∼35% to 13.4 ± 2.1 mmHg (P < 0.05). We conclude that prior conditioning with 8 h of hypoxia impairs the ability of the pulmonary vasculature to dilate normally during exercise.