Open AccessEffect 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
Author(s) -
Fan JuiLin,
Bourdillon Nicolas,
Kayser Bengt
Publication year - 2013
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.1002/phy2.66
Subject(s) - hypocapnia , medicine , cerebral blood flow , oxygenation , hypoxia (environmental) , anesthesia , hyperventilation , cardiology , acidosis , chemistry , hypercapnia , oxygen , organic chemistry
Abstract 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 ( MCA v; 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 MCA v and lowered cerebral O 2 Hb, cerebral DO 2 , and muscle O 2 Hb ( P < 0.001). CO 2 clamping elevated PETCO 2 and MCA v 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.