Control of fructose 2,6-diphosphate in muscle of exercising fasted rats.

This study examined the role of epinephrine in controlling intramuscular signals that may accelerate lactate production in less active muscles during exercise. Sham-operated (sham) or adrenodemedullated (ADM) rats were fasted 24 h and then were killed at rest or after running for 15 or 30 min on a treadmill (21 m/min, 15% grade). One-half of the ADM rats were infused with epinephrine (6 micrograms/h) intravenously (jugular catheter) during exercise. ADM rats exhibited lower blood glucose, blood lactate, white quadriceps muscle content of lactate, glucose 6-phosphate, fructose 6-phosphate, and adenosine 3',5'-cyclic monophosphate (cAMP) during exercise than did sham rats or epinephrine-infused ADM rats. The white quadriceps muscle contents of fructose 2,6-diphosphate (F-2,6-P2) and glucose 1,6-diphosphate (G-1,6-P2) (allosteric activators of glycolysis) were at least two times as high in sham rats and in epinephrine-infused rats as in ADM rats during exercise. We conclude that the exercise-induced rise in epinephrine is responsible for the acceleration of glycolysis in less active muscle during exercise. This effect is likely mediated by epinephrine-induced increases in cAMP, F-2,6-P2, and G-1,6-P2.