Document Detail


Brain glycogen supercompensation following exhaustive exercise.
MedLine Citation:
PMID:  22063629     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Takashi Matsui; Taro Ishikawa; Hitoshi Ito; Masahiro Okamoto; Koshiro Inoue; Min-Chul Lee; Takahiko Fujikawa; Yukio Ichitani; Kentaro Kawanaka; Hideaki Soya
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-11-07
Journal Detail:
Title:  The Journal of physiology     Volume:  590     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-02-02     Completed Date:  2012-06-21     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  607-16     Citation Subset:  IM    
Affiliation:
Laboratory of Exercise Biochemistry & Neuroendocrinology, Institute for Health and Sports Sciences, University of Tsukuba, 1-1-1 Tennoudai, Tsukuba 305-8574, Ibaraki, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Glucose / analysis
Brain / physiology*
Citrate (si)-Synthase / metabolism
Glycogen / physiology*
Insulin / blood
Lactic Acid / blood
Liver / physiology
Male
Microwaves
Muscle, Skeletal / physiology
Physical Conditioning, Animal / physiology*
Rats
Rats, Wistar
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Insulin; 50-21-5/Lactic Acid; 9005-79-2/Glycogen; EC 2.3.3.1/Citrate (si)-Synthase
Comments/Corrections
Comment In:
J Physiol. 2012 Mar 1;590(Pt 5):1013   [PMID:  22399816 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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