Abstract
The aim of this study was to characterize postprandial glucose flux after exercise in the fed versus overnight fasted state and to investigate the potential underlying mechanisms. In a randomized order, twelve men underwent breakfast-rest [(BR) 3 h semirecumbent], breakfast-exercise [(BE) 2 h semirecumbent before 60 min of cycling (50% peak power output)], and overnight fasted exercise [(FE) as per BE omitting breakfast] trials. An oral glucose tolerance test (OGTT) was completed after exercise (after rest on BR). Dual stable isotope tracers ([U-13C] glucose ingestion and [6,6-2H2] glucose infusion) and muscle biopsies were combined to assess postprandial plasma glucose kinetics and intramuscular signaling, respectively. Plasma intestinal fatty acid binding (I-FABP) concentrations were determined as a marker of intestinal damage. Breakfast before exercise increased postexercise plasma glucose disposal rates during the OGTT, from 44 g/120 min in FE {35 to 53 g/120 min [mean (normalized 95% confidence interval)] to 73 g/120 min in BE [55 to 90 g/120 min; P = 0.01]}. This higher plasma glucose disposal rate was, however, offset by increased plasma glucose appearance rates (principally OGTT-derived), resulting in a glycemic response that did not differ between BE and FE ( P = 0.11). Plasma I-FABP concentrations during exercise were 264 pg/ml (196 to 332 pg/ml) lower in BE versus FE ( P = 0.01). Breakfast before exercise increases postexercise postprandial plasma glucose disposal, which is offset (primarily) by increased appearance rates of orally ingested glucose. Therefore, metabolic responses to fed-state exercise cannot be readily inferred from studies conducted in a fasted state.
Highlights
Postprandial glycemia is a strong predictor of future mortality and morbidity
A main effect of the trial was detected for the plasma glucose RaTOTAL and glucose disappearance (Rd) during the oral glucose tolerance test (OGTT) (F ϭ 7.079, P ϭ 0.01), whereby the Rd was 45 g/120 min in BR (95% nCI: 36 to 62 g/120 min) versus 73 g/120 min in BE [(95% nCI: 55 to 90 g/120 min; P ϭ 0.09 vs. BR) and 44 g/120 min in FE (95% nCI: 35 to 53 g/120 min); P ϭ 0.01 vs. BE]
A main effect of trial was detected for RaTOTAL during the OGTT [(g/120 min); F ϭ 3.915, P ϭ 0.05], which was highest in BE (Fig. 2C)
Summary
Even in people without diabetes, those with greater blood glucose excursions after feeding are at an increased risk of cardiovascular disease [47, 48]. This glycemic response to food ingestion is dictated by blood glucose kinetics (i.e., the balance between the rates of glucose appearance into blood and glucose disposal from blood into peripheral tissues). Each bout of exercise potently stimulates postexercise insulin sensitivity and muscle glucose uptake [52]. Despite increases in blood glucose disposal rates, endurance-type exercise does not always reduce postprandial glucose excursions in the postexercise period [20, 54]. The finding that postprandial blood glucose concentrations are not lowered after exercise is because when exercise is performed (at least in the fasted state), the increase in postprandial blood glucose disposal after exercise can be offset—and even superseded— by increases in both endogenous and meal-derived blood glucose appearance rates [34, 54]
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