Glucoregulatory responses to intense exercise performed in the postprandial state

1 McGill Nutrition and Food Science Centre, Montreal, Quebec H3A 1A1; and 2 Departments of Physiology and Medicine, University of Toronto, Toronto, Ontario, Canada M5S 1A8 A seven- to eightfold increment in hepatic glucose production (endogenous R a ) 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 O 2 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 R a and utilization (R d ) 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 = 0.042). Peak catecholamine (12- to 16-fold increase) and R a (PP: 11.5 ± 1.4, PA: 13.8 ± 1.4 mg · kg 1 · min 1 ) 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. R d reached the same peak (PP: 8.0 ± 0.6, PA: 9.3 ± 0.8 mg · kg 1 · min 1 ) but was greater at 20-120 min of recovery in PP ( P = 0.001). Therefore, the total R a response to IE is preserved despite the possibility of prior PP suppression of endogenous R a and is consistent with catecholamine mediation. Post-IE hyperglycemia is reduced in the postprandial state. glucose turnover; postprandial exercise; catecholamines; insulin; glucagon