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Hypocapnia during hypoxic exercise and its impact on cerebral oxygenation, ventilation and maximal whole body O(2) uptake


Siebenmann, Christoph; Sørensen, Henrik; Jacobs, Robert A; Haider, Thomas; Rasmussen, Peter; Lundby, Carsten (2013). Hypocapnia during hypoxic exercise and its impact on cerebral oxygenation, ventilation and maximal whole body O(2) uptake. Respiratory Physiology & Neurobiology, 185(2):461-467.

Abstract

With hypoxic exposure ventilation is elevated through the hypoxic ventilatory response. We tested the hypothesis that the resulting hypocapnia reduces maximal exercise capacity by decreasing (i) cerebral blood flow and oxygenation and (ii) the ventilatory drive. Eight subjects performed two incremental exercise tests at 3454m altitude in a blinded manner. In one trial end-tidal [Formula: see text] was clamped to 40mmHg by CO(2)-supplementation. Mean blood flow velocity in the middle cerebral artery (MCAv(mean)) was determined by trans-cranial Doppler sonography and cerebral oxygenation by near infra-red spectroscopy. Without CO(2)-supplementation, [Formula: see text] decreased to 30±3mmHg (P<0.0001 vs isocapnic trial). Although CO(2)-supplementation increased MCAv(mean) by 17±14% (P<0.0001) and attenuated the decrease in cerebral oxygenation (-4.7±0.9% vs -5.4±0.9%; P=0.002) this did not affect maximal O(2)-uptake. Clamping [Formula: see text] increased ventilation during submaximal but not during maximal exercise (P=0.99). We conclude that although hypocapnia promotes a decrease in MCAv(mean) and cerebral oxygenation, this does not limit maximal O(2)-uptake. Furthermore, hypocapnia does not restrict ventilation during maximal hypoxic exercise.

Abstract

With hypoxic exposure ventilation is elevated through the hypoxic ventilatory response. We tested the hypothesis that the resulting hypocapnia reduces maximal exercise capacity by decreasing (i) cerebral blood flow and oxygenation and (ii) the ventilatory drive. Eight subjects performed two incremental exercise tests at 3454m altitude in a blinded manner. In one trial end-tidal [Formula: see text] was clamped to 40mmHg by CO(2)-supplementation. Mean blood flow velocity in the middle cerebral artery (MCAv(mean)) was determined by trans-cranial Doppler sonography and cerebral oxygenation by near infra-red spectroscopy. Without CO(2)-supplementation, [Formula: see text] decreased to 30±3mmHg (P<0.0001 vs isocapnic trial). Although CO(2)-supplementation increased MCAv(mean) by 17±14% (P<0.0001) and attenuated the decrease in cerebral oxygenation (-4.7±0.9% vs -5.4±0.9%; P=0.002) this did not affect maximal O(2)-uptake. Clamping [Formula: see text] increased ventilation during submaximal but not during maximal exercise (P=0.99). We conclude that although hypocapnia promotes a decrease in MCAv(mean) and cerebral oxygenation, this does not limit maximal O(2)-uptake. Furthermore, hypocapnia does not restrict ventilation during maximal hypoxic exercise.

Citations

13 citations in Web of Science®
17 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Center for Integrative Human Physiology
05 Vetsuisse Faculty > Institute of Veterinary Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2013
Deposited On:14 Dec 2012 16:18
Last Modified:05 Apr 2016 16:05
Publisher:Elsevier
ISSN:1569-9048
Publisher DOI:https://doi.org/10.1016/j.resp.2012.08.012
PubMed ID:22922610

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