Endocrinology and Metabolism

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

Gregory J. Crowther, William F. Kemper, Michael F. Carey, Kevin E. Conley


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 be1) 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


  • This research was supported by National Institute of Arthritis and Musculoskeletal and Skin Diseases Grants AR-42928 and AR-45184. G. J. Crowther and W. F. Kemper were recipients of National Science Foundation predoctoral fellowships.

  • Portions of this work have been previously presented in abstract form (8).

  • Current address for M. F. Carey: Exercise Metabolism Unit, Victoria University, Footscray 3011, Australia.

  • Address for reprint requests and other correspondence: K. E. Conley, Dept. of Radiology, Box 357115, Univ. of Washington Medical Center, Seattle, WA 98195-7115 (E-mail:kconley{at}u.washington.edu).

  • The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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