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Vizcardo-Galindo, Gustavo

University of British Columbia

High altitude trekking alters upper limb hemodynamics and reduces brachial artery vascular function in lowlanders. However, whether these changes are reversible with the correction of hypoxia is unknown. We investigated the impact of 15 minutes of oxygen supplementation (O₂) on brachial artery hemodynamics, reactive hyperemia (microvascular function) and flow-mediated dilation (FMD; endothelial function). Healthy male participants (aged 21-42 years) were examined prior to and with O₂ at 3440m (day 4 at high altitude; n=7), 4371m (day 7; n=7), and 5050m (day 10; n=12) using Duplex ultrasound. At 3440m, O₂ decreased brachial artery diameter (-5±5%; P=0.04), baseline blood flow (-44±15%; P<0.001), oxygen delivery (-39±16 P<0.001) and peak reactive hyperemia (-8±8%; P=0.02). Although at 3440m O₂ elevated FMD (P=0.04), this was attributed to the reduction in baseline diameter (allometrically-scaled FMD, P=0.145). Only antegrade shear stress was reduced by O₂ at 4371m (P=0.026). However, at 5050m, a reduction in brachial artery blood flow (-17±22%; P=0.03), but not oxygen delivery, diameter, reactive hyperemia or FMD occurred with O₂. Collectively, these findings suggest that O₂ causes vasoconstriction in the upper limb along the arterial tree (conduit and resistance arteries), limiting oxygen delivery and reactive hyperemia during early trekking at high altitude. With prolonged, more severe high-altitude exposure, O₂ reduces blood flow in the upper limb without compromising oxygen delivery, reactive hyperemia or FMD. Therefore, supplemental oxygen appears to have differential impacts on vascular function that are modulated by the duration and severity of high-altitude exposure.

Text

2023-01-16

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/83646

Health and Exercise Sciences

University of British Columbia

UBCO

http://creativecommons.org/licenses/by-nc-nd/4.0/