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Am J Physiol Endocrinol Metab 282: E74-E79, 2002;
0193-1849/02 $5.00
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Vol. 282, Issue 1, E74-E79, January 2002

Control of glycolysis in contracting skeletal muscle. II. Turning it off

Gregory J. Crowther1, William F. Kemper1, Michael F. Carey2, and Kevin E. Conley1,2,3

Departments of 2 Radiology, 1 Physiology and Biophysics, and 3 Bioengineering, University of Washington Medical Center, Seattle, Washington 98195-7115

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 Ca2+-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 Pi concentration as measured by 31P magnetic resonance spectroscopy. Substrate (HP) and metabolite (Pi, 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 ~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.

metabolic flux control; muscle energetics; human tibialis anterior


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