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1 Department of Anesthesia, The Copenhagen Muscle Research Center, Rigshospitalet, Copenhagen, Denmark
2 Internal Medicine, Cardiovascular Research Institute Amsterdam, Academic Medical Center, Amsterdam, Netherlands
* To whom correspondence should be addressed. E-mail: nhsecher{at}rh.regionh.dk.
During exercise the Kety-Schmidt determined cerebral blood flow (CBF) does not change because the jugular vein is collapsed in the upright position. In contrast, when CBF is evaluated by 133Xenon clearance, by flow in the internal carotid artery, or by flow velocity in basal cerebral arteries, a ~25% increase is detected with a parallel increase in metabolism. During activation an increase in cerebral oxygen supply is required because there is no capillary recruitment within the brain and increased metabolism becomes dependent on an enhanced gradient for oxygen diffusion. During maximal whole body exercise, however, cerebral oxygenation decreases because of eventual arterial desaturation and marked hyperventilation-related hypocapnia of consequence for CBF. Reduced cerebral oxygenation affects recruitment of motor units and supplemental oxygen enhances cerebral oxygenation and work capacity without effects on muscle oxygenation. Also the work of breathing and the increasing temperature of the brain during exercise are of importance for the development of so-called central fatigue. During prolonged exercise the perceived exertion is related to accumulation of ammonia in the brain and data support that glycogen depletion in astrocytes limits the ability of the brain to accelerate its metabolism during activation. The release of interleukin 6 from the brain when exercise is prolonged may represent a signaling pathway in matching the metabolic response of the brain. Preliminary data suggest a coupling between the circulatory and metabolic perturbations in the brain during strenuous exercise and the ability of the brain to access slow twitch muscle fiber populations.
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