Abstract
High altitude exposure typically reduces endothelial function, and this is modulated by hemoconcentration resulting from plasma volume contraction. However, the specific impact of hypobaric hypoxia, independent of external factors (e.g. cold, varying altitudes, exercise, diet, dehydration) on endothelial function is unknown. We examined the temporal changes in blood viscosity, shear stress and endothelial function and the impact of plasma volume expansion (PVX) during exposure to hypobaric hypoxia while controlling for external factors. Eleven healthy males (25±4 years; mean±SD) completed two four-day chamber visits (normoxia [NX] and hypobaric hypoxia [HH; equivalent altitude: 3500m]) in a cross-over design. Endothelial function was assessed via flow-mediated dilation in response to transient (reactive hyperemia; RH-FMD) and sustained (progressive handgrip exercise; SS-FMD) increases in shear stress prior to entering and after 1h, 6h, 12h, 48h and 96h in the chamber. During HH, endothelial function was also measured on the last day after PVX to pre-exposure levels (1140±320 ml balanced crystalloid solution). Blood viscosity and arterial shear stress increased on the first day during HH compared to NX and remained elevated at 48h and 96h (P<0.005). RH-FMD did not differ during HH compared to NX and was unaffected by PVX despite reductions in blood viscosity (P<0.05). The stimulus-response slope of increases in shear stress to vasodilation during SS-FMD was preserved in HH and increased by 44±73% following PVX (P=0.023). These findings suggest that endothelial function is maintained in HH when other stressors are absent and that PVX improves endothelial function in a shear stress stimulus-specific manner.