Obese type 2 diabetics have a blunted hypotensive response to acute hyperthermia therapy that does not affect the perception of thermal stress or physiological strain compared to healthy adults.

PURPOSE: The objective of this study was to test the hypothesis that a hyperthermia-hypotensive challenge via whole body hot water immersion would alter the perception of hyperthermia and physiological strain in obese type 2 diabetics (T2DM) compared to healthy non-obese (HC) individuals. Additionally, we hypothesize that the mechanisms would be attributed to impaired blood pressure adjustments and afferent signals (via changes in internal and mean skin temperatures). METHODS: In random order, eleven obese T2DM (50±12y, 45±7% fat mass, 7.5±1.8% HbA1c) and nine similar aged (41±14y, P>0.05) HC non-obese (33±8% fat mass, P<0.01) non-diabetic (5.3±0.4% HbA1c, P<0.01) underwent a 60min bout of whole body passive hyperthermia followed by 60min of recovery or a 2h resting control condition. The perception of thermal sensation (TS, scale range: 1-13), calculated physiological strain (PSI), internal (Tre, rectal) and mean skin (Tsk) temperatures, heart rate (HR) and blood pressures (BP) were the primary dependent variables. RESULTS: Hyperthermia similarly increased Tre by 1.4±0.4°C, Tsk by 6.5±0.8°C and HR by 34±8bpm in both groups (P>0.5). Hyperthermia reduced diastolic BP (27% in T2DM and 33% in HC, P<0.05) and mean arterial BP (reduced by 15% in T2DM and by 19% in HC) relative to control conditions (P<0.05). The reduction of mean arterial BP area under the curve was attenuated in T2DM (12%) compared to HC (30%) (group×condition, P<0.01). TS and PSI during hyperthermia were not different between groups. Pearson product correlation reported strong correlations (r=0.69-0.89) with Tre and Tsk with TS in both populations. The linear stepwise regression analysis revealed similar relative contributions for Tre (~60%) and Tsk (~40%) on TS for both groups. CONCLUSIONS: These data indicate that obese T2DM with moderate metabolic control have an attenuated hyperthermia-hypotensive response that does not affect TS and PSI. This also may suggest behavioral thermoregulation is intact in this study group.

An acute bout of whole body passive hyperthermia increases plasma leptin, but does not alter glucose or insulin responses in obese type 2 diabetics and healthy adults.

Acute and chronic hyperthermic treatments in diabetic animal models repeatedly improve insulin sensitivity and glycemic control. Therefore, the purpose of this study was to test the hypothesis that an acute 1h bout of hyperthermic treatment improves glucose, insulin, and leptin responses to an oral glucose challenge (OGTT) in obese type 2 diabetics and healthy humans. Nine obese (45±7.1% fat mass) type 2 diabetics (T2DM: 50.1±12y, 7.5±1.8% HbA1c) absent of insulin therapy and nine similar aged (41.1±13.7y) healthy non-obese controls (HC: 33.4±7.8% fat mass, P<0.01; 5.3±0.4% HbA1c, P<0.01) participated. Using a randomized design, subjects underwent either a whole body passive hyperthermia treatment via head-out hot water immersion (1h resting in 39.4±0.4°C water) that increased internal temperature above baseline by ∆1.6±0.4°C or a control resting condition. Twenty-four hours post treatments, a 75g OGTT was administered to evaluate changes in plasma glucose, insulin, C-peptide, and leptin concentrations. Hyperthermia itself did not alter area under the curve for plasma glucose, insulin, or C-peptide during the OGTT in either group. Fasting absolute and normalized (kg·fat mass) plasma leptin was significantly increased (P<0.01) only after the hyperthermic exposure by 17% in T2DM and 24% in HC groups (P<0.001) when compared to the control condition. These data indicate that an acute hyperthermic treatment does not improve glucose tolerance 24h post treatment in moderate metabolic controlled obese T2DM or HC individuals.