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Purpose: The aim of this study is to explore the physiological vascular adaptation to exposure to high altitude and to test the hypothesis that its impairment might play a role in the pathophysiology of acute mountain sickness (AMS). Methods: 34 healthy volunteers (age 38±11years, 13 women) were studied at the sea-level and after passive ascent to 3842 m (Aguille du Midi, France). Blood pressure (BP), O2 saturation (SO2), endothelial function (flow-mediated dilation, FMD), carotid distensibility coefficient (DC), carotid-femoral pulse wave velocity (PWV), peak systolic velocity in the middle cerebral artery (MCA-PSV) were performed at sea level (T0) and after 4-h hypobaric hypoxia (T1). AMS was defined as a Lake-Louise Score>5 after 24-h hypobaric hypoxia (T2). Results: At T2 12 individuals developed AMS (AMS+). AMS+ had a greater SO2 worsening at T1 as compared to AMS- (AMS+: 97.2±1.2 to 79.3±5.8%; AMS-: 97.3±1.2 to 83.1 ± 5.7%, p=0.03), with similar heart rate increase and unchanged BP. FMD was significantly reduced in AMS+ (5.75±3.01 to 3.27±1.87%, p=0.04), but not in AMS- (4.74±2.47 to 4.02±2.36%). Mean carotid diameter was increased at T1 in both groups. DC tended to be increased in AMS- but not in AMS+, while PWV was unchanged. MCA-PSV was increased in AMS-, but not in AMS+. Conclusions: In healthy asymptomatic individuals exposed to high altitude, conduit artery endothelial function is preserved in the cerebral district vasodilatation, increased elasticity and blood flow occurs. This compensatory response is early blunted in AMS+, before symptoms onset, thus suggesting a pathogenetic role.