Nybo Lars, Møller Kirsten, Volianitis Stefanos, Nielsen Bodil, Secher Niels H
Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Denmark.
J Appl Physiol (1985). 2002 Jul;93(1):58-64. doi: 10.1152/japplphysiol.00049.2002.
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 degrees C; control) or when severe hyperthermia had developed (core temperature = 39.5 degrees 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). min(-1); 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 Q(10) (temperature) effect and/or the level of cerebral neuronal activity associated with increased exertion.
人类长时间运动期间体温过高的发展与大脑的各种变化有关,但尚不清楚脑代谢或全脑血流量(gCBF)是否受到影响。八名耐力训练的受试者在自行车测力计上完成了两次运动试验。在运动15分钟后,当各试验的核心温度相似时,以及在运动结束时,当受试者保持正常体温(核心温度 = 37.9摄氏度;对照组)或出现严重体温过高(核心温度 = 39.5摄氏度;体温过高组)时,采用Kety-Schmidt技术测定gCBF以及氧、葡萄糖和乳酸的脑代谢率。两次试验在15分钟后的gCBF相似,且在整个对照组期间保持稳定。相比之下,在体温过高期间,gCBF下降了18%,因此在运动结束时,体温过高组的gCBF低于对照组(43±4 vs. 51±4 ml·100 g⁻¹·min⁻¹;P<0.05)。与gCBF降低相伴的是,氧和葡萄糖的动静脉差值有更大比例的增加,因此在体温过高试验结束时,脑代谢率高于对照组。体温过高引起的gCBF降低并未改变脑乳酸释放。体温过高引起的运动脑血流量减少似乎与动脉二氧化碳张力同时降低18%有关,而较高的脑氧代谢率可能归因于Q₁₀(温度)效应和/或与运动增加相关的脑神经元活动水平。