The brain at work: A cerebral metabolic manifestation of central fatigue?
Article first published online: 29 MAR 2007
Copyright © 2007 Wiley-Liss, Inc.
Journal of Neuroscience Research
Special Issue: Brain Energy Metabolism: Integrating molecular, cellular and metabolic aspects of neuron-glial interactions
Volume 85, Issue 15, pages 3334–3339, 15 November 2007
How to Cite
Dalsgaard, M. K. and Secher, N. H. (2007), The brain at work: A cerebral metabolic manifestation of central fatigue?. J. Neurosci. Res., 85: 3334–3339. doi: 10.1002/jnr.21274
- Issue published online: 23 OCT 2007
- Article first published online: 29 MAR 2007
- Manuscript Accepted: 12 JAN 2007
- Manuscript Revised: 8 JAN 2007
- Manuscript Received: 31 OCT 2006
- muscle fiber types;
- neuromuscular blockade
Central fatigue refers to circumstances in which strength appears to be limited by the ability of the central nervous system to recruit motoneurons. Central fatigue manifests when the effort to contract skeletal muscles is intense and, thus, is aggravated when exercise is performed under stress, whereas it becomes attenuated following training. Central fatigue has not been explained, but the cerebral metabolic response to intense exercise, as to other modalities of cerebral activation, is a reduction in its “metabolic ratio” (MR), i.e., the brain's uptake of oxygen relative to that of carbohydrate. At rest the MR is close to 6 but during intense whole-body exercise it decreases to less than 3, with the uptake of lactate becoming as important as that of glucose. It remains debated what underlies this apparent inability of the brain to oxidize the carbohydrate taken up, but it may approach ∼10 mmol glucose equivalents. In the case of exercise, a concomitant uptake of ammonium for formation of amino acids may account for only ∼10% of this “extra” carbohydrate taken up. Also, accumulation of intermediates in metabolic pathways and compartmentalization of metabolism between astrocytes and neurons are avenues that have to be explored. Depletion of glycogen stores and subsequent supercompensation during periods of low neuronal activity may not only play a role but also link brain metabolism to its function. © 2007 Wiley-Liss, Inc.