Document Detail

Control of glycolysis in contracting skeletal muscle. II. Turning it off.
MedLine Citation:
PMID:  11739086     Owner:  NLM     Status:  MEDLINE    
Glycolytic flux in muscle declines rapidly after exercise stops, indicating that muscle activation is a key controller of glycolysis. The mechanism underlying this control could be 1) a Ca(2+)-mediated modulation of glycogenolysis, which supplies substrate (hexose phosphates, HP) to the glycolytic pathway, or 2) a direct effect on glycolytic enzymes. To distinguish between these possibilities, HP levels were raised by voluntary 1-Hz exercise, and glycolytic flux was measured after the exercise ceased. Glycolytic H(+) and ATP production were quantified from changes in muscle pH, phosphocreatine concentration, and P(i) concentration as measured by 31P magnetic resonance spectroscopy. Substrate (HP) and metabolite (P(i), ADP, and AMP) levels remained high when exercise stopped because of the occlusion of blood flow with a pressure cuff. Glycolytic flux declined to basal levels within approximately 20 s of the end of exercise despite elevated levels of HP and metabolites. Therefore, this flux does not subside because of insufficient HP substrate; rather, glycolysis is controlled independently of glycogenolytic HP production. We conclude that the inactivation of glycolysis after exercise reflects the cessation of contractile activity and is mediated within the glycolytic pathway rather than via the control of glycogen breakdown.
Gregory J Crowther; William F Kemper; Michael F Carey; Kevin E Conley
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  282     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2002 Jan 
Date Detail:
Created Date:  2001-12-12     Completed Date:  2002-01-16     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E74-9     Citation Subset:  IM; S    
Department of Physiology and Biophysics, University of Washington Medical Center, Seattle, Washington 98195-7115, USA.
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MeSH Terms
Adenosine Triphosphate / metabolism
Exercise / physiology
Glycolysis / physiology*
Hexoses / metabolism
Hydrogen / metabolism
Hydrogen-Ion Concentration
Magnetic Resonance Spectroscopy
Middle Aged
Models, Biological
Muscle Contraction / physiology*
Muscle, Skeletal / physiology*
Phosphates / metabolism
Phosphorus / metabolism
Grant Support
Reg. No./Substance:
0/Hexoses; 0/Phosphates; 1333-74-0/Hydrogen; 56-65-5/Adenosine Triphosphate; 67-07-2/Phosphocreatine; 7723-14-0/Phosphorus

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