Large artery and cerebral pulsatile hemodynamics during high altitude sojourn.

High altitude sojourn elicits a unique challenge to the cerebrovascular system to compensate for hypoxemia. Exposure to hypoxia appears to decrease pulsatile cerebral blood flow. Yet, the mechanism remains unclear owing to competing vasoconstrictor and vasodilatory responses in the intra- and extra-cranial vasculature. This study examined changes in large artery and cerebral pulsatile hemodynamics, and the potential sex-specific responses, during high-altitude sojourn in 17 young, healthy adults. Nine females (23±4 yrs) and 8 males (24±4 yrs) underwent vascular assessments at 1,400 m and after a 6-day incremental ascent to 4,300 m. Carotid and middle cerebral artery pulsatility were measured via Doppler ultrasound. Aortic stiffness and carotid β-stiffness index were assessed via applanation tonometry and ultrasound, respectively. Pressure-flow and wave-power analyses were used to derive characteristic impedance and hydraulic power/energy parameters at the aorta, carotid, and MCA. Ascent from 1,400 to 4,300 m elicited increases in aortic, and decreases in carotid stiffness, as well as reductions in carotid and MCA pulsatility, and characteristic impedance of all vessels (p<0.05). Mean hydraulic energy increased at the carotid and MCA from 1,400 to 4,300 m (p<0.05), and medium to large effect sizes (η²=0.36-0.21) were observed for sex-by-altitude interaction terms indicating potential sex-specific changes in MCA pulsatility, characteristic impedance, and MCA hydraulic energy/power. These data suggest the potential for sex differences in the general reductions in cerebrovascular pulsatility with ascent to 4,300 m that likely stem from vasodilation-induced reductions in characteristic impedance and augmented cerebral blood flow.