A bout of aerobic exercise in the heat increases carbohydrate use but does not enhance the disposal of an oral glucose load, in healthy active individuals.

We investigated if a bout of exercise in a hot environment (HEAT) would reduce the postprandial hyperglycemia induced by glucose ingestion. The hypothesis was that HEAT stimulating glycogen use would increase the disposal of the ingested glucose (i.e., OGTT; 75 g of glucose). Separated by at least 1 week, nine young-healthy individuals underwent three trials after an overnight fast in a randomized order. Two trials included 50 min of pedaling at 58±5% VO2MAX either in a thermoneutral (21±1ºC; NEUTRAL) or in a hot environment (33±1ºC; HEAT) eliciting similar energy expenditure (503±101 kcals). These two trials were compared to a no-exercise trial (NO EXER). Twenty min after exercise (or rest), subjects underwent an OGTT, while carbohydrate oxidation (CHOxid, using indirect calorimetry) plasma blood glucose, insulin concentrations (i.e., [glucose], [insulin]), and double tracer glucose kinetics ([U- 13 C] glucose ingestion and [6,6-2 H2 ] glucose infusion) were monitored for 120 min. At rest, [glucose], [insulin], and rates of appearance/disappearance of glucose in plasma (glucose Ra/Rd) were similar among trials. During exercise, heart rate, tympanic temperature, [glucose], glycogen oxidation, and total CHOxid were higher during HEAT than NEUTRAL (i.e., 149±35 vs 124±31 µmol·kg-1 ·min-1 , p=0.010). However, during the following OGTT glucose Rd was similar in HEAT and NEUTRAL (i.e., 25.1±3.6 vs 25.2±5.3 µmol·kg-1 ·min-1 , p=0.981). Insulin sensitivity (i.e., ISIMATSUDA ) only improved in NEUTRAL compared to NO EXER (10.1±4.6 vs 8.8±3.7 a.u.; p=0.044). In summary, stimulating carbohydrate use with exercise in a hot environment does not improve postprandial plasma glucose disposal or insulin sensitivity in a subsequent OGTT.