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Effect of end-tidal CO(2) clamping on cerebrovascular function, oxygenation, and performance during 15-km time trial cycling in severe normobaric hypoxia: the role of cerebral O(2) delivery

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 O(2) delivery and potentially account for reduced exercise performance in hypoxia. We tested the hypothesis t...

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Detalles Bibliográficos
Autores principales: Fan, Jui-Lin, Bourdillon, Nicolas, Kayser, Bengt
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835019/
https://www.ncbi.nlm.nih.gov/pubmed/24303142
http://dx.doi.org/10.1002/phy2.66
Descripción
Sumario: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 O(2) delivery and potentially account for reduced exercise performance in hypoxia. We tested the hypothesis that end-tidal Pco(2) (PETCO(2)) clamping in hypoxic exercise would prevent the hypocapnia-induced reduction in CBF during heavy exercise, thus improving exercise performance. We measured PETCO(2), middle cerebral artery velocity (MCAv; index of CBF), prefrontal cerebral cortex oxygenation (cerebral O(2)Hb; index of cerebral oxygenation), cerebral O(2) delivery (DO(2)), and leg muscle oxygenation (muscle O(2)Hb) in 10 healthy men (age 27 ± 7 years; VO(2)max 63.3 ± 6.6 mL/kg/min; mean ± SD) during simulated 15-km time trial cycling (TT) in normoxia and hypoxia (FIO(2) = 0.10) with and without CO(2) clamping. During exercise, hypoxia elevated MCAv and lowered cerebral O(2)Hb, cerebral DO(2), and muscle O(2)Hb (P < 0.001). CO(2) clamping elevated PETCO(2) 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 O(2)Hb (P = 0.118 and P = 0.124). Nevertheless, CO(2) clamping elevated cerebral DO(2) during TT in both normoxic and hypoxic conditions (P < 0.001). CO(2) clamping restored cerebral DO(2) 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 CO(2) 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.