• Christoph Siebenmann, Henrik Sørensen, Robert A Jacobs, Thomas Haider, Peter Rasmussen, and Carsten Lundby.
• Zurich Centre for Integrative Human Physiology, Zurich, Switzerland.
• Respir Physiol Neurobiol. 2013 Jan 15;185(2):461-7.

AbstractWith 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 3454 m altitude in a blinded manner. In one trial end-tidal [Formula: see text] was clamped to 40 mmHg 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 ± 3 mmHg (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.Copyright © 2012 Elsevier B.V. All rights reserved.

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