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1 Department of Human Physiology, Institute of Exercise and Sport Sciences and Departments of 2 Infection Diseases and 3 Anesthesia, Rigshospitalet, University of Copenhagen; Denmark
The development of
hyperthermia during prolonged exercise in humans is associated with
various changes in the brain, but it is not known whether 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, either when subjects remained normothermic (core
temperature = 37.9°C; control) or when severe hyperthermia had
developed (core temperature = 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 with control at
the end of exercise (43 ± 4 vs. 51 ± 4 ml · 100 g
1 · min1; P < 0.05). Concomitant with the reduction in gCBF, there was a
proportionally larger increase in the arteriovenous differences for
oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared with control. The
hyperthermia-induced lowering of gCBF did not alter cerebral lactate
release. The hyperthermia-induced reduction in exercise cerebral blood
flow seems to relate to a concomitant 18% lowering of arterial carbon
dioxide tension, whereas the higher cerebral metabolic rate of oxygen
may be ascribed to a Q10 (temperature) effect
and/or the level of cerebral neuronal activity associated with
increased exertion.
brain; cardiac output; heat stress
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