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J Appl Physiol (March 1, 2002). doi:10.1152/japplphysiol.00049.2002
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Articles in PresS, published online ahead of print March 1, 2002
J Appl Physiol, 10.1152/jap.00049.2002
Submitted on January 18, 2002
Accepted on February 22, 2002

Effects of hyperthermia on the cerebral blood flow and metabolism during prolonged exercise in humans

Lars Nybo1*, Kirsten Moller2, Stefanos Volianitis3, Bodil Nielsen1, and Niels Sechen3

1 Department of Human Physiology, University of Copenhagen, Institute of Exercise and Sport Sciences, Copenhagen, Denmark
2 Department of Infection Diseases, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark
3 Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

* To whom correspondence should be addressed. E-mail: lnnielsen{at}aki.ku.dk.

The development of hyperthermia during prolonged exercise in humans is associated with various changes in the brain, but it is not known if the cerebral metabolism or the global cerebral blood flow (gCBF) is affected. Eight endurance-trained subjects completed two exercise bouts on a cycle ergometer. The gCBF and cerebral metabolic rates of oxygen, glucose and lactate were determined with the Kety-Schmidt technique after 15 min of exercise when core temperature was similar across trials, and at the end of exercise, when subjects either remained normothermic (Tcore = 37.9°C; control) or when severe hyperthermia had developed (Tcore = 39.5°C; hyperthermia). The gCBF was similar after 15 min in the two trials and it remained stable throughout control. In contrast, during hyperthermia gCBF decreased by 18 % and was therefore lower in hyperthermia compared to control at the end of exercise (43 ± 4 vs. 51 ± 4 ml (100g)-1 min-1; P<0.05). Concomitant with the reduction in gCBF, there was a proportionally larger increase in the arterio-venous differences for oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared to control. The hyperthermia-induced lowering of gCBF did not alter cerebral lactate release. The hyperthermia-induced reduction in exercise CBF seems to relate to a concomitant 18 % lowering of PaCO2, while the higher cerebral metabolic rate of oxygen may be ascribed to a Q10 effect and/or the level of cerebral neuronal activity associated with increased exertion.




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