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Am J Physiol Endocrinol Metab 282: E67-E73, 2002;
0193-1849/02 $5.00
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Vol. 282, Issue 1, E67-E73, January 2002

Control of glycolysis in contracting skeletal muscle. I. Turning it on

Gregory J. Crowther1, Michael F. Carey2, William F. Kemper1, 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

Why does the onset of glycolytic flux in muscle lag the start of exercise? We tested the hypothesis that both elevated metabolite levels and muscle activity are required for flux to begin. Glycolytic flux was determined from changes in muscle pH, phosphocreatine concentration, and Pi concentration ([Pi]) as measured by 31P magnetic resonance spectroscopy. Eight subjects performed rapid ankle dorsiflexions to ~45% of maximal voluntary contraction force under ischemia at a rate of 1 contraction/s. Subjects completed two bouts of exercise separated by 1 min of ischemic rest. Glycolytic flux was activated by 27 s in the first bout, ceased during the ischemic rest period, and was activated more quickly in the second bout. Because the onset in both bouts occurred at approximately the same [Pi], ADP concentration, and AMP concentration, the activation of glycolysis appears to be related to the elevation of these metabolite concentrations. However, because no glycolytic flux occurred at rest, even when metabolite levels were high, both muscle activity and elevated metabolites are needed to turn on this pathway. We conclude that the delayed onset of glycolytic flux during exercise reflects the time needed to raise metabolites to flux-activating levels.

metabolic flux control; high-energy phosphates; human tibialis anterior


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