Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 282, Issue 1, Pages E74-E79Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.2002.282.1.E74
Keywords
metabolic flux control; muscle energetics; human tibialis anterior
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Funding
- NIAMS NIH HHS [AR-42928, AR-45184] Funding Source: Medline
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR045184] Funding Source: NIH RePORTER
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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 P-i concentration as measured by P-31 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 similar to 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.
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