Abstract

Orthostasis at sea level decreases brain tissue oxygenation and increases risk of syncope. High altitude reduces brain and peripheral muscle tissue oxygenation. This study determined the effect of short-term altitude acclimatization on cerebral and peripheral leg tissue oxygenation index (TOI) post-orthostasis. Seven lowlanders completed a supine-to-stand maneuver at sea level (450m) and for 3 consecutive days at high altitude (3776m). Cardiorespiratory measurements and near-infrared spectroscopy-derived oxygenation of the frontal lobe (cerebral TOI) and vastus lateralis (leg TOI) were measured at supine and 5-min post-orthostasis. After orthostasis at sea level, cerebral TOI decreased [mean Δ% (95% confidential interval): - 4.5%, (- 7.5, - 1.5), P < 0.001], whilst leg TOI was unchanged [- 4.6%, (- 10.9, 1.7), P = 0.42]. High altitude had no effect on cerebral TOI following orthostasis [days 1-3: - 2.3%, (- 5.3, 0.7); - 2.4%, (- 5.4, 0.6); - 2.1%, (- 5.1, 0.9), respectively, all P > 0.05], whereas leg TOI decreased [days 1-3: - 12.0%, (- 18.3, - 5.7); - 12.1%, (- 18.4, - 5.8); - 10.2%, (- 16.5, - 3.9), respectively, all P < 0.001]. This response did not differ with days spent at high altitude, despite evidence of cardiorespiratory acclimatization [increased peripheral oxygen saturation (supine: P = 0.01; stand: P = 0.02) and decreased end-tidal carbon dioxide (supine: P = 0.003; stand: P = 0.01)]. Cerebral oxygenation is preferentially maintained over leg oxygenation post-orthostasis at high altitude, suggesting different vascular regulation between cerebral and peripheral circulations. Short-term acclimatization to high altitude did not alter cerebral and leg oxygenation responses to orthostasis.

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