Exercise heat acclimation causes post-exercise hypotension and favorable improvements in lipid and immune profiles: A crossover randomized controlled trial.

BACKGROUND: Passive hyperthermic exposure causes an acute hypotensive response following the cessation of heat stress. Chronic heat stress is well documented in animal studies to instigate metabolic and lipid alterations. However, it is unknown if exercise-heat acclimation also causes favorable chronic blood pressure, lipid, and immune responses in humans. PURPOSE: This project tested the hypothesis that 10-day exercise-heat acclimation (HA) would cause greater post-exercise reductions in arterial blood pressure and favorable metabolic, lipid, and immune responses compared to 10-day exercise under neutral conditions (CON). METHODS: Thirteen healthy sedentary participants (8M/5F, 28 ±â€¯6y, 78 ±â€¯17 kg), completed a 10-day (90 min/day exercise bout) clamped hyperthermia HA (increase internal temperature 1.5 °C, in 42 °C, 28% Rh) and control (CON: 23 °C, 42% Rh) protocols in a counterbalanced design with a 2 month washout. Pre- and post-exercise HA/CON blood pressures were taken 1-h post-exercise on exercise days 1 and 10. Metabolic, lipid and immune panels were taken pre-post HA/CON. RESULTS: Exercise under heat stress had greater post-exercise hypotension (systolic; -6 mmHg, diastolic; -8 mmHg; and mean arterial pressure; -7 mmHg) on both days 1 and 10 compared to exercise under neutral conditions (main effect for condition, P ≤ 0.004). Only from pre-to-post HA, total cholesterol (168 ±â€¯19 to 157 ±â€¯15; P < 0.03) and triglycerides (137 ±â€¯45 to 111 ±â€¯30; P < 0.03) were reduced, while absolute lymphocytes (-26%), monocytes (-22%), and basophils (-49%) significantly decreased (each P ≤ 0.04). Relative values of neutrophils increased (18%) and lymphocytes decreased (-20%) only after HA (P ≤ 0.04). CONCLUSION: These data indicate that exercise in the heat (regardless of acclimation status) causes a profound post-exercise hypotensive response, while HA causes favorable lipid, and immune profile changes. Further examination of exercise-heat acclimation on vascular, metabolic, and immune responses will offer insight for benefits in other clinical populations with vascular, metabolic and immune dysfunction.

Hemostatic responses to exercise, dehydration, and simulated bleeding in heat-stressed humans.

Heat stress followed by an accompanying hemorrhagic challenge may influence hemostasis. We tested the hypothesis that hemostatic responses would be increased by passive heat stress, as well as exercise-induced heat stress, each with accompanying central hypovolemia to simulate a hemorrhagic insult. In aim 1, subjects were exposed to passive heating or normothermic time control, each followed by progressive lower-body negative pressure (LBNP) to presyncope. In aim 2 subjects exercised in hyperthermic environmental conditions, with and without accompanying dehydration, each also followed by progressive LBNP to presyncope. At baseline, pre-LBNP, and post-LBNP (<1, 30, and 60 min), hemostatic activity of venous blood was evaluated by plasma markers of hemostasis and thrombelastography. For aim 1, both hyperthermic and normothermic LBNP (H-LBNP and N-LBNP, respectively) resulted in higher levels of factor V, factor VIII, and von Willebrand factor antigen compared with the time control trial (all P < 0.05), but these responses were temperature independent. Hyperthermia increased fibrinolysis [clot lysis 30 min after the maximal amplitude reflecting clot strength (LY30)] to 5.1% post-LBNP compared with 1.5% (time control) and 2.7% in N-LBNP ( P = 0.05 for main effect). Hyperthermia also potentiated increased platelet counts post-LBNP as follows: 274 K/µl for H-LBNP, 246 K/µl for N-LBNP, and 196 K/µl for time control ( P < 0.05 for the interaction). For aim 2, hydration status associated with exercise in the heat did not affect the hemostatic activity, but fibrinolysis (LY30) was increased to 6-10% when subjects were dehydrated compared with an increase to 2-4% when hydrated ( P = 0.05 for treatment). Central hypovolemia via LBNP is a primary driver of hemostasis compared with hyperthermia and dehydration effects. However, hyperthermia does induce significant thrombocytosis and by itself causes an increase in clot lysis. Dehydration associated with exercise-induced heat stress increases clot lysis but does not affect exercise-activated or subsequent hypovolemia-activated hemostasis in hyperthermic humans. Clinical implications of these findings are that quickly restoring a hemorrhaging hypovolemic trauma patient with cold noncoagulant fluids (crystalloids) can have serious deleterious effects on the body's innate ability to form essential clots, and several factors can increase clot lysis, which should therefore be closely monitored.

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.

Omega-3 fatty acid supplementation combined with acute aerobic exercise does not alter the improved post-exercise insulin response in normoglycemic, inactive and overweight men.

PURPOSE: The aim of this study was to determine if omega-3 (n-3) supplementation combined with acute aerobic exercise would improve glucose and insulin responses in normoglycemic, inactive, overweight men. METHODS: In a random order, ten inactive and normoglycemic men (30.6 ± 10 years, 85.4 ± 11 kg, 26.7 ± 4 BMI) completed a rest (R) and exercise trial (EX) without n-3 supplementation. Following 42 days of n-3 supplementation, participants again completed a rest (R + n-3) and exercise trial (EX + n-3) with continued n-3 supplementation. The exercise trial consisted of 3 days of ~70 % VO2peak for 60 min/session. N-3 supplementation entailed 4.55 g/day of n-3 (EPA 2.45 g, DHA 1.61 g). A 75 g oral glucose tolerance (OGTT) test was administered 14-16 h after each trial. RESULTS: Relative to R (35,278 ± 9169 pmol/L), EX without n-3 reduced the incremental area under the curve for insulin (iAUCinsulin) during an OGTT by 21.3 % (27765 ± 4925 pmol/L, p = 0.018) and 20.6 % after the EX + n-3 trial (27,999 ± 8370 pmol/L; p = 0.007). In addition, EX (96 ± 21 pmol/L; p = 0.006) reduced C-peptide by 13.5 % when compared to R (111 ± 26 pmol/L). No difference was observed between R and n-3 trials for iAUCinsulin and iAUCC-peptide. Only EX improved insulin sensitivity index by 5.6 % (p = 0.02) when compared to R. CONCLUSIONS: These data suggest that n-3 supplementation does not add any additional benefit beyond the exercise induced insulin responses in inactive men. Furthermore, n-3 supplementation alone does not appear to impair insulin action in normoglycemic, inactive, overweight men.