Effects Of Acute Oral Glucose Or Fructose Ingestion On Thermoregulatory Responses During Passive Heating

Abstract

BACKGROUND: It has been reported that acute hyperglycemia inhibits the rise in body core temperature and enhances cutaneous vasodilation during exercise in the heat. However, the effects of acute hyperglycemia on thermoregulatory responses to passive heating at rest remain unclear. Insulin is known to inhibit vasodilation by peripheral mechanisms and induce body core temperature rise by central mechanisms, therefore we further assessed the effects of insulin secretion to glucose ingestion by comparing the responses with fructose ingestion. PURPOSE: To test the hypotheses that hyperglycemia induced by oral glucose ingestion modifies thermoregulatory responses during passive heating at rest and that these responses are associated with insulin secretion. METHODS: Study 1: Eight healthy young men performed two trials. Subjects rested in a sitting position in an artificial climate chamber controlled at 28°C of Ta and 40% of RH during each trial. After 10 min baseline measurement, subjects drank glucose solution (GLU; water 300 ml + glucose 75 g) or water (CNT; water 300ml). Twenty min after drinking, subjects put their lower leg into hot water controlled at 42°C for 60 min. During the experiment, blood glucose concentration (BG), oxygen uptake (VO2), esophageal temperature (Tes), mean skin temperature (Tsk), heart rate (HR), blood pressure (BP), sweat rate (SR) and cutaneous vascular conductance (CVC) at chest and forearm, and total sweat rate (TSR) were measured. Study 2: Three healthy young men performed two trials. Subjects followed the same protocol as study 1, but drank glucose (GLU; water 300 ml + glucose 75 g) or fructose solution (FRU; water 300 ml + fructose 75g). RESULTS: Study 1: BG was significantly higher in GLU than CNT throughout heating. Forearm SR and TSR (GLU: 301 ± 28g, CNT: 328 ± 30g, mean ± SE, P < 0.05) were lower in GLU than CNT. Tes threshold for forearm sweating was relatively higher (P = 0.08) in GLU than CNT. Differnce in Tes threshold for forearm sweating (R = 0.96) and TSR (R = 0.78) between GLU and CNT were correlated with BG (both, P < 0.05). HR and systolic BP (both, P < 0.05) were higher in GLU than CNT, while there were no significant differences in VO2, Tes, Tsk, CVC at both sites, and chest SR between trials. Study 2: Tes, HR, and TSR (GLU: 340 ± 39 g, FRU: 441 ± 58 g, mean ± SE) were lower in GLU than FRU. CONCLUSIONS: Acute hyperglycemia induced by oral glucose ingestion inhibits sweating responses but has no effect on cutaneous vascular responses during passive heating at rest, which might be an effect of insulin secretion to glucose ingestion.