LAUSR

Myocardial oxygen delivery is primarily regulated through changes in vascular tone to match increased metabolic demands. In males, activation of the muscle metaboreflex during acute isocapnic hypoxia results in a paradoxical coronary vasoconstriction. Whether coronary blood velocity is reduced by metaboreflex activation following travel and/or adaptation to high-altitude is unknown. This study determined if the response of the coronary vasculature to muscle metaboreflex activation at low-altitude differs from acute (1/2 days) and prolonged (8/9 days) high-altitude. Healthy males (n=16) were recruited and performed isometric handgrip exercise (30 % max) followed by post-exercise circulatory occlusion (PECO) to isolate the muscle metaboreflex at low-altitude and following acute and prolonged high-altitude (3,800 m). Mean left anterior descending coronary artery blood velocity (LADvmean, transthoracic Doppler echocardiography), heart rate, mean arterial pressure (MAP), ventilation, and respired gases were assessed during baseline and PECO at all time-points. Coronary vascular conductance index (CVCi) was calculated as LADVmean/MAP. The change in LADvmean (acute altitude: -1.7 ± 3.9 cm/s, low-altitude: 2.6 ± 3.4 cm/s, P = 0.01) and CVCi (acute altitude: -0.05 ± 0.04 cm/s/mmHg, low-altitude: -0.01 ± 0.03 cm/s/mmHg, P = 0.005) induced by PECO differed significantly between acute high-altitude and low-altitude. The change in LADVmean and CVCi induced by PECO following prolonged high-altitude was not different from low-altitude. Our results suggest that coronary vasoconstriction with metaboreflex activation in males is greatest following acute ascent to high-altitude and restored to low-altitude levels following 8-9 days of acclimatization.