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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...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
2013
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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 |
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author | Fan, Jui-Lin Bourdillon, Nicolas Kayser, Bengt |
author_facet | Fan, Jui-Lin Bourdillon, Nicolas Kayser, Bengt |
author_sort | Fan, Jui-Lin |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-3835019 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-38350192013-12-03 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 Fan, Jui-Lin Bourdillon, Nicolas Kayser, Bengt Physiol Rep Original Research 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. Blackwell Publishing Ltd 2013-08 2013-08-28 /pmc/articles/PMC3835019/ /pubmed/24303142 http://dx.doi.org/10.1002/phy2.66 Text en © 2013 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society http://creativecommons.org/licenses/by/2.5/ Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation. |
spellingShingle | Original Research Fan, Jui-Lin Bourdillon, Nicolas Kayser, Bengt 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 |
title | 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 |
title_full | 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 |
title_fullStr | 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 |
title_full_unstemmed | 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 |
title_short | 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 |
title_sort | 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 |
topic | Original Research |
url | 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 |
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