Effect of end‐tidal CO2 clamping on cerebrovascular function, oxygenation, and performance during 15‐km time trial cycling in severe normobaric hypoxia: the role of cerebral O2 delivery

Physiological Reports

Jui-Lin Fan¹  Nicolas Bourdillon¹ 

[1] Institute of Sports Sciences, Faculty of Biology and Medicine, University of Lausanne, Lausanne, Switzerland

关键词: CO2 clamping;    exercise;    hypoxia;    ventilatory control;   

DOI  :  10.1002/phy2.66

来源: Wiley

【 摘 要 】

Abstract

During heavy exercise, hyperventilation-induced hypocapnia leads to cerebral vasoconstriction, resulting in a reduction in cerebral blood flow (CBF). A reduction in CBF would impair cerebral O₂ delivery and potentially account for reduced exercise performance in hypoxia. We tested the hypothesis that end-tidal Pco₂ (PETCO₂) clamping in hypoxic exercise would prevent the hypocapnia-induced reduction in CBF during heavy exercise, thus improving exercise performance. We measured PETCO₂, middle cerebral artery velocity (MCAv; index of CBF), prefrontal cerebral cortex oxygenation (cerebral O₂Hb; index of cerebral oxygenation), cerebral O₂ delivery (DO₂), and leg muscle oxygenation (muscle O₂Hb) in 10 healthy men (age 27 ± 7 years; VO₂max 63.3 ± 6.6 mL/kg/min; mean ± SD) during simulated 15-km time trial cycling (TT) in normoxia and hypoxia (FIO₂ = 0.10) with and without CO₂ clamping. During exercise, hypoxia elevated MCAv and lowered cerebral O₂Hb, cerebral DO₂, and muscle O₂Hb (P < 0.001). CO₂ clamping elevated PETCO₂ and MCAv during exercise in both normoxic and hypoxic conditions (P < 0.001 and P = 0.024), but had no effect on either cerebral and muscle O₂Hb (P = 0.118 and P = 0.124). Nevertheless, CO₂ clamping elevated cerebral DO₂ during TT in both normoxic and hypoxic conditions (P < 0.001). CO₂ clamping restored cerebral DO₂ to normoxic values during TT in hypoxia and tended to have a greater effect on TT performance in hypoxia compared to normoxia (P = 0.097). However, post hoc analysis revealed no effect of CO₂ clamping on TT performance either in normoxia (P = 0.588) or in hypoxia (P = 0.108). Our findings confirm that the hyperventilation-induced hypocapnia and the subsequent drop in cerebral oxygenation are unlikely to be the cause of the reduced endurance exercise performance in hypoxia.

【 授权许可】

CC BY   
© 2013 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society.

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