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Restoring heat stress‐associated reduction in middle cerebral artery velocity does not reduce fatigue in the heat
Author(s) -
Keiser S.,
Flück D.,
Stravs A.,
Hüppin F.,
Lundby C.
Publication year - 2015
Publication title -
scandinavian journal of medicine and science in sports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.575
H-Index - 115
eISSN - 1600-0838
pISSN - 0905-7188
DOI - 10.1111/sms.12345
Subject(s) - hyperventilation , medicine , oxygenation , anesthesia , heat stress , ventilation (architecture) , cardiology , zoology , thermodynamics , physics , biology
Heat‐induced hyperventilation may reduce Pa CO 2 and thereby cerebral perfusion and oxygenation and in turn exercise performance. To test this hypothesis, eight volunteers completed three incremental exercise tests to exhaustion: (a) 18 ° C ambient temperature ( CON ); (b) 38 ° C ( HEAT ); and (c) 38 ° C with addition of CO 2 to inspiration to prevent the hyperventilation‐induced reduction in Pa CO 2 ( HEAT + CO 2 ). In HEAT and HEAT + CO 2 , rectal temperature was elevated prior to the exercise tests by means of hot water submersion and was higher ( P < 0.05) than in CON . Compared with CON , ventilation was elevated ( P < 0.01), and hence, Pa CO 2 reduced in HEAT . This caused a reduction ( P < 0.05) in mean cerebral artery velocity ( MCAv mean ) from 68.6 ± 15.5 to 53.9 ± 10.0 cm/s, which was completely restored in HEAT + CO 2 (68.8 ± 5.8 cm/s). Cerebral oxygenation followed a similar pattern.V ˙ O 2 m a x was 4.6 ± 0.1 L /min in CON and decreased ( P < 0.05) to 4.1 ± 0.2 L /min in HEAT and remained reduced in HEAT + CO 2 (4.1 ± 0.2 L /min). Despite normalization of MCAv mean and cerebral oxygenation in HEAT + CO 2 , this did not improve exercise performance, and thus, the reduced MCAv mean in HEAT does not seem to limit exercise performance.