Glucoregulatory responses to intense exercise performed in the postprandial state

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 I) little evidence for increased intestinal absorptio n of glucose during exercise exists, and 2) intravenous glucose does not pr event it. We investigated IE in 10 PA and 8 PP fit, lean, young males who h ad exercised for 15 min at >84% maximum O-2 uptake, starting 3 h after a 41 2-kcal mixed meal. The meal induced a small rise in glycemia with sustained insulin and glucagon increases. Preexercise glucose total R-a and utilizat ion (R-d) were equal and similar to 130% of the PA level. Exercise hypergly cemia in PP was delayed and diminished and, in early recovery, was of short er 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 sign ificantly correlated. Exercise glucagon, insulin, and glucagon-to-insulin r esponses 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 o f recovery in PP (P = 0.001). Therefore, the total R-a response to IE is pr eserved despite the possibility of prior PP suppression of endogenous R-a a nd is consistent with catecholamine mediation. Post-IE hyperglycemia is red uced in the postprandial state.