Literature DB >> 15142684

Cerebral perturbations provoked by prolonged exercise.

Lars Nybo1, Niels H Secher.   

Abstract

This review addresses cerebral metabolic and neurohumoral alterations during prolonged exercise in humans with special focus on associations with fatigue. Global energy turnover in the brain is unaltered by the transition from rest to moderately intense exercise, apparently because exercise-induced activation of some brain regions including cortical motor areas is compensated for by reduced activity in other regions of the brain. However, strenuous exercise is associated with cerebral metabolic and neurohumoral alterations that may relate to central fatigue. Fatigue should be acknowledged as a complex phenomenon influenced by both peripheral and central factors. However, failure to drive the motorneurons adequately as a consequence of neurophysiological alterations seems to play a dominant role under some circumstances. During exercise with hyperthermia excessive accumulation of heat in the brain due to impeded heat removal by the cerebral circulation may elevate the brain temperature to >40 degrees C and impair the ability to sustain maximal motor activation. Also, when prolonged exercise results in hypoglycaemia, perceived exertion increases at the same time as the cerebral glucose uptake becomes low, and centrally mediated fatigue appears to arise as the cerebral energy turnover becomes restricted by the availability of substrates for the brain. Changes in serotonergic activity, inhibitory feed-back from the exercising muscles, elevated ammonia levels, and alterations in regional dopaminergic activity may also contribute to the impaired voluntary activation of the motorneurons after prolonged and strenuous exercise. Furthermore, central fatigue may involve depletion of cerebral glycogen stores, as signified by the observation that following exhaustive exercise the cerebral glucose uptake increases out of proportion to that of oxygen. In summary, prolonged exercise may induce homeostatic disturbances within the central nervous system (CNS) that subsequently attenuates motor activation. Therefore, strenuous exercise is a challenge not only to the cardiorespiratory and locomotive systems but also to the brain. Copyright 2004 Elsevier Ltd

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Year:  2004        PMID: 15142684     DOI: 10.1016/j.pneurobio.2004.03.005

Source DB:  PubMed          Journal:  Prog Neurobiol        ISSN: 0301-0082            Impact factor:   11.685


  90 in total

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Review 2.  Non-thermal modification of heat-loss responses during exercise in humans.

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4.  Cerebral ammonia uptake and accumulation during prolonged exercise in humans.

Authors:  Lars Nybo; Mads K Dalsgaard; Adam Steensberg; Kirsten Møller; Niels H Secher
Journal:  J Physiol       Date:  2004-12-20       Impact factor: 5.182

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6.  Acute dopamine/noradrenaline reuptake inhibition enhances human exercise performance in warm, but not temperate conditions.

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Review 7.  Exercise-induced homeostatic perturbations provoked by singles tennis match play with reference to development of fatigue.

Authors:  Alberto Mendez-Villanueva; Jaime Fernandez-Fernandez; David Bishop
Journal:  Br J Sports Med       Date:  2007-11       Impact factor: 13.800

8.  Environmental heat stress, hyperammonemia and nucleotide metabolism during intermittent exercise.

Authors:  Magni Mohr; Peter Rasmussen; Barry Drust; Bodil Nielsen; Lars Nybo
Journal:  Eur J Appl Physiol       Date:  2006-02-17       Impact factor: 3.078

9.  Astrocytic glycogen-derived lactate fuels the brain during exhaustive exercise to maintain endurance capacity.

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