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. Issue 3 (28th August 2013)

• Record Type: Journal Article
• Authors: Fan, Jui‐Lin; Bourdillon, Nicolas; Kayser, Bengt
• Is Part Of: Physiological reports. Volume 1:Issue 3(2013:Aug.)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2013-08-28
• Subjects: Physiology -- Periodicals; 571
• DOI: 10.1002/phy2.66
• Languages: English
• ISSNs: 2051-817X

Abstract

<abstract abstract-type="main" id="phy266-abs-0001"> <title>Abstract</title> <p>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<sub>2</sub> delivery and potentially account for reduced exercise performance in hypoxia. We tested the hypothesis that end‐tidal <sc>Pco</sc><sub>2</sub> (PETCO<sub>2</sub>) clamping in hypoxic exercise would prevent the hypocapnia‐induced reduction in CBF during heavy exercise, thus improving exercise performance. We measured PETCO<sub>2</sub>, middle cerebral artery velocity (MCAv; index of CBF), prefrontal cerebral cortex oxygenation (cerebral O<sub>2</sub>Hb; index of cerebral oxygenation), cerebral O<sub>2</sub> delivery (DO<sub>2</sub>), and leg muscle oxygenation (muscle O<sub>2</sub>Hb) in 10 healthy men (age 27 ± 7 years; VO<sub>2</sub>max 63.3 ± 6.6 mL/kg/min; mean ± SD) during simulated 15‐km time trial cycling (TT) in normoxia and hypoxia (FIO<sub>2</sub> = 0.10) with and without CO<sub>2</sub> clamping. During exercise, hypoxia elevated MCAv and lowered cerebral O<sub>2</sub>Hb, cerebral DO<sub>2</sub>, and muscle O<sub>2</sub>Hb (<italic>P</italic> < 0.001). CO<sub>2</sub> clamping elevated PETCO<sub>2</sub> and MCAv during exercise in both normoxic and hypoxic conditions (<italic>P</italic> < 0.001 and <italic>P</italic> = 0.024), but had no effect on either cerebral and muscle O<sub>2</sub>Hb (<italic>P</italic> = 0.118 and <italic>P</italic> = 0.124). Nevertheless, CO<sub>2</sub> clamping elevated cerebral DO<sub>2</sub> during TT in both normoxic and hypoxic conditions (<italic>P</italic> < 0.001). CO<sub>2</sub> clamping restored cerebral DO<sub>2</sub> to normoxic values during TT in hypoxia and tended to have a greater effect on TT performance in hypoxia compared to normoxia (<italic>P</italic> = 0.097). However, post hoc analysis revealed no effect of CO<sub>2</sub> clamping on TT performance either in normoxia (<italic>P</italic> = 0.588) or in hypoxia (<italic>P</italic> = 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.</p> </abstract>