Brain glycogen supercompensation following exhaustive exercise
Article first published online: 6 JAN 2012
© 2011 The Authors. Journal compilation © 2011 The Physiological Society
The Journal of Physiology
Volume 590, Issue 3, pages 607–616, February 2012
How to Cite
Matsui, T., Ishikawa, T., Ito, H., Okamoto, M., Inoue, K., Lee, M.-c., Fujikawa, T., Ichitani, Y., Kawanaka, K. and Soya, H. (2012), Brain glycogen supercompensation following exhaustive exercise. The Journal of Physiology, 590: 607–616. doi: 10.1113/jphysiol.2011.217919
- Issue published online: 27 JAN 2012
- Article first published online: 6 JAN 2012
- Accepted manuscript online: 9 NOV 2011 11:50PM EST
- (Received 7 September 2011; accepted after revision 4 November 2011; first published online 7 November 2011)
Non-technical summary Exercise training elicits an increase in the basal level of muscular glycogen. This happens when glycogen recovers to above its basal level (supercompensation) after it decreases with acute exercise. Although untested, it is hypothesized that, similar to that of skeletal muscle, brain glycogen supercompensation occurs after acute exhaustive exercise. We provide evidence that exhaustive exercise induces glycogen supercompensation not only in skeletal muscles, but also in the brain. Furthermore, we observed exercise training-induced increases in basal glycogen levels in the cortex and hippocampus, which are involved in motor control and cognitive function. This suggests that, like skeletal muscles, the brain adapts metabolically, probably to meet the increased energy demands of exercise training.
Abstract Brain glycogen localized in astrocytes, a critical energy source for neurons, decreases during prolonged exhaustive exercise with hypoglycaemia. However, it is uncertain whether exhaustive exercise induces glycogen supercompensation in the brain as in skeletal muscle. To explore this question, we exercised adult male rats to exhaustion at moderate intensity (20 m min−1) by treadmill, and quantified glycogen levels in several brain loci and skeletal muscles using a high-power (10 kW) microwave irradiation method as a gold standard. Skeletal muscle glycogen was depleted by 82–90% with exhaustive exercise, and supercompensated by 43–46% at 24 h after exercise. Brain glycogen levels decreased by 50–64% with exhaustive exercise, and supercompensated by 29–63% (whole brain 46%, cortex 60%, hippocampus 33%, hypothalamus 29%, cerebellum 63% and brainstem 49%) at 6 h after exercise. The brain glycogen supercompensation rates after exercise positively correlated with their decrease rates during exercise. We also observed that cortical and hippocampal glycogen supercompensation were sustained until 24 h after exercise (long-lasting supercompensation), and their basal glycogen levels increased with 4 weeks of exercise training (60 min day−1 at 20 m min−1). These results support the hypothesis that, like the effect in skeletal muscles, glycogen supercompensation also occurs in the brain following exhaustive exercise, and the extent of supercompensation is dependent on that of glycogen decrease during exercise across brain regions. However, supercompensation in the brain preceded that of skeletal muscles. Further, the long-lasting supercompensation of the cortex and hippocampus is probably a prerequisite for their training adaptation (increased basal levels), probably to meet the increased energy demands of the brain in exercising animals.