AENDO May 41/5

Kreisman, Stuart H., Anthony Manzon, Sharon J. Nessim, José A. Morais, Réjeanne Gougeon, Simon J. Fisher, Mladen Vranic, and Errol B. Marliss. Glucoregulatory responses to intense exercise performed in the postprandial state. Am J Physiol Endocrinol Metab 278: E786–E793, 2000.—A sevento eightfold increment in hepatic glucose production (endogenous Ra) occurs in postabsorptive (PA) intense exercise (IE). A similar response is likely present in the postprandial (PP) state, when most such exercise is performed, because 1) little evidence for increased intestinal absorption of glucose during exercise exists, and 2) intravenous glucose does not prevent it. We investigated IE in 10 PA and 8 PP fit, lean, young males who had exercised for 15 min at .84% maximum O2 uptake, starting 3 h after a 412-kcal mixed meal. The meal induced a small rise in glycemia with sustained insulin and glucagon increases. Preexercise glucose total Ra and utilization (Rd) were equal and ,130% of the PA level. Exercise hyperglycemia in PP was delayed and diminished and, in early recovery, was of shorter duration and lesser magnitude (P 5 0.042). Peak catecholamine (12to 16-fold increase) and Ra (PP: 11.5 6 1.4, PA: 13.8 6 1.4 mg·kg21 · min21) responses did not differ, and their responses during exercise were significantly correlated. Exercise glucagon, insulin, and glucagon-to-insulin responses were small or not significant. Rd reached the same peak (PP: 8.0 6 0.6, PA: 9.3 6 0.8 mg·kg21 ·min21) but was greater at 20–120 min of recovery in PP (P 5 0.001). Therefore, the total Ra response to IE is preserved despite the possibility of prior PP suppression of endogenous Ra and is consistent with catecholamine mediation. Post-IE hyperglycemia is reduced in the postprandial state.