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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 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 = 0.042). Peak
catecholamine (12- to 16-fold increase) and Ra (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. Rd 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 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.
glucose turnover; postprandial exercise; catecholamines; insulin; glucagon
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