Thermoregulation and thermal sensation during whole-body water immersion at different water temperatures in healthy individuals: A scoping review.

BACKGROUND: Severe thermal discomfort may increase risk of drowning due to hypothermia or hyperthermia from prolonged exposure to noxious water temperatures. The importance of using a behavioral thermoregulation model with thermal sensation may predict the thermal load that the human body receives when exposed to various immersive water conditions. However, there is no thermal sensation "gold standard" model specific for water immersion. This scoping review aims to present a comprehensive overview regarding human physiological and behavioral thermoregulation during whole-body water immersion and explore the feasibility for an accepted defined sensation scale for cold and hot water immersion. METHODS: A standard literary search was performed on PubMed, Google Scholar, and SCOPUS. The words "Water Immersion," "Thermoregulation," "Cardiovascular responses" were used either as independent searched terms and MeSH terms (Medical Subject Headings) or in combination with other text words. The inclusion criteria for clinical trials terms to thermoregulatory measurements (core or skin temperature), whole-body immersion, 18-60 years old and healthy individuals. The prementioned data were analyzed narratively to achieve the overall study objective. RESULTS: Twenty-three published articles fulfilled the review inclusion/exclusion criteria (with nine measured behavioral responses). Our outcomes illustrated a homogenous thermal sensation in a variety of water temperatures ranges, that was strongly associated with thermal balance, and observed different thermoregulatory responses. This scoping review highlights the impact of water immersion duration on human thermoneutral zone, thermal comfort zone, and thermal sensation. CONCLUSION: Our findings enlighten the significance of thermal sensation as a health indicator for establishing a behavioral thermal model applicable for water immersion. This scoping review provides insight for the needed development of subjective thermal model of thermal sensation in relation to human thermal physiology specific to immersive water temperature ranges within and outside the thermal neutral and comfort zone.

Six nights of sleep extension increases regional cerebral oxygenation without modifying cognitive performance at rest or following acute aerobic exercise.

Long sleep durations (≥540 min) are associated with poor cognitive performance in ageing adults, but the underlying cause is unclear. The aim of this study was to investigate the effect of extended sleep on cognitive performance and cerebral vascular function before and then after aerobic exercise. In all, 12 adults completed 6 nights of 8- (control) and 10+-h (sleep extension) time in bed in a randomised, crossover experiment. Sleep was measured using wrist actigraphy. On the last day of each time in bed protocol, participants performed three bouts of brisk walking. Sustained attention, spatial rotation ability, mental flexibility, and working memory were assessed, while prefrontal oxygen saturation index (ΔTSI) was measured using near-infrared spectroscopy. A two-way repeated-measures analysis of variance (time in bed × before/after exercise) was used for statistical analysis. Average sleep duration was longer following sleep extension as compared to control, at a mean (SD) of 551 (16) versus 428 (20) min (p < 0.001). Sleep extension did not alter cognitive performance as compared to control, but increased ΔTSI during tests of spatial rotation ability (main effect for time in bed, p = 0.03), mental flexibility (p = 0.04), and working memory (p < 0.01). Cognitive performance was improved (main effect for exercise, p < 0.05) following brisk walking for all cognitive domains except sustained attention with no interaction with time in bed. In summary, 6 nights of extended time in bed accompanied by long sleep durations does not impair cognitive performance at rest or alter the positive effect of acute aerobic exercise on cognition but may increase frontal cerebral oxygenation during cognitive functioning.

Sex difference in cerebral blood flow velocity during exercise hyperthermia.

INTRODUCTION: Cerebral blood flow and thermal perception during physical exercise under hyperthermia conditions in females are poorly understood. Because sex differences exist for blood pressure control, resting middle cerebral artery velocity (MCAVmean), and pain, we tested the hypothesis that females would have greater reductions in MCAvmean and increased thermal perceptual strain during exercise hyperthermia compared to males. METHODS: Twenty-two healthy active males and females completed 60 min of matched exercise metabolic heat production in a 1) control cool (24.0 ± 0.0 °C; 14.4 ± 3.4% Rh) and 2) hot (42.3 ± 0.3 °C; 28.4 ± 5.2% Rh) conditions in random order, separated by at least 3 days while MCAvmean, thermal comfort, and preference was obtained during the exercise. RESULTS: Compared to 36 °C mean body temperature (Mbt), as hyperthermia increased to 39 °C Mbt, females had a greater reduction in absolute (MCAvmean), and relative change (%Δ MCAvmean) and conductance (%Δ MCAvmean conductance) in MCAVmean compared to males (Interaction: Temperature x Sex, P ≤ 0.002). During exercise in cool conditions, absolute and conductance MCAvmean was maintained from rest through exercise; however, females had greater MCAVmean compared to males (Main effect: Sex, P < 0.0008). We also found disparities in females' perceptual thermal comfort and thermal preference. These differences may be associated with a greater reduction in partial pressure of end-tidal CO2, and different cardiovascular and blood pressure control to exercise under hyperthermia. CONCLUSIONS: In summary, females exercise cerebral blood flow velocity is reduced to a greater extent (25% vs 15%) and the initial reduction occurs at lower hyperthermia mean body temperatures (~38 °C vs ~39 °C) and are under greater thermal perceptual strain compared to males.

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.

Progressive dry to humid hyperthermia alters exercise cerebral blood flow.

INTRODUCTION: Exercising in hot conditions may increase the risk for exertional heat-related illness due to reduction in cerebral blood flow (CBF); however, the acute effect of exercise-induced changes on CBF during compensable and uncompensable heat stress remain unclear. We tested the hypothesis that exercising in hot dry and humid conditions would have different CBF responses. METHODS: Nine healthy active males completed a 30 min baseline rest then 60 min of low intensity self-paced exercise (12 rating of perceived exertion) in a 1) control compensable neutral dry (CN; 23.7 ±â€¯0.7 °C; 10.7 ±â€¯0.8%Rh) and 2) compensable hot dry (CH; 42.3 ±â€¯0.3 °C; 10.7 ±â€¯1.8%Rh) that progressively increased to an uncompensable hot humid (UCH; 42.3 ±â€¯0.3 °C; 55.2 ±â€¯7.7%Rh) environment in random order separated by at least 4 days. RESULTS: We observed that during CN environments from rest through 60 min of exercise, middle cerebral velocity (MCAvmean) and conductance (MCAvmean CVC) remained unchanged. In contrast, during CH, MCAvmean, MCAvmean CVC, and cardiac output (Q) increased and systemic vascular resistance (SVR) decreased. However, under UCH, MCAvmean, MCAvmean CVC, and Q was reduced. No difference in mean arterial pressure or ventilation was observed during any condition. Only during UCH, end-tidal PO2 increased and PCO2 decreased. The redistribution of blood to the skin for thermoregulation (heart rate, skin blood flow and sweat rate) remained higher during exercise in UCH environments. CONCLUSIONS: Collectively, exercise cerebral blood flow is altered by an integrative physiological manner that differs in CN, CH, and UCH environments. The control of CBF may be secondary to thermoregulatory control which may provide an explanation for the cause of exertional heat illness.

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.

Short-term metformin and exercise training effects on strength, aerobic capacity, glycemic control, and mitochondrial function in children with burn injury.

Severely burned children experience a chronic state of sympathetic nervous system activation that is associated with hypermetabolic/cardiac stress and muscle wasting. Metformin, a diabetes medication, helps control hyperglycemia in obese diabetic populations, and exercise has been shown to improve exercise strength and aerobic exercise capacity after severe burns. However, whether exercise improves glycemic control in burned children and whether combining exercise and metformin improves outcomes to a greater degree than exercise alone are unknown. We tested the hypothesis that a 6-wk exercise program combined with short-term metformin administration (E + M) improves aerobic and strength exercise capacity to a greater degree than exercise and placebo (E), while improving glucose tolerance and muscle metabolic function. We found that, before exercise training, the metformin group compared with the placebo group had attenuated mitochondrial respiration (pmol·s-1·mg-1) for each state: state 2 (-22.5 ± 3), state 3 (-42.4 ± 13), and oxphos (-58.9 ± 19) ( P ≤ 0.02, M vs. E + M group for each state). However, in the E + M group, exercise increased mitochondrial respiration in each state ( P ≤ 0.05), with respiration being comparable to that in the E group (each P > 0.05). In both groups, exercise induced comparable improvements in strength (change from preexercise, Δ1.6 ± 0.6 N-M·kgLBM) and V̇o2peak (Δ9 ± 7 mlO2·kgLBM) as well as fasting glucose (Δ19.3 ± 13 mg·dl) and glucose AUC (Δ3402 ± 3674 mg·dl-1·min-1), as measured by a 75-g OGTT (all P ≤ 0.03). Exercise reduced resting energy expenditure in E + M (Δ539 ± 480 kcal/24 h, P < 0.01) but not E subjects ( P = 0.68). Both groups exhibited reduced resting heart rate (Δ30 ± 23 beats/min, P ≤ 0.02). These data indicate that short-term metformin combined with exercise provides no further improvement beyond that of exercise alone for strength, exercise capacity, and glycemic control.

Cardiorespiratory Capacity and Strength Remain Attenuated in Children with Severe Burn Injuries at Over 3 Years Postburn.

OBJECTIVES: To compare physical capacity and body composition between children with burn injuries at approximately 4 years postburn and healthy, fit children. STUDY DESIGN: In this retrospective, case-control study, we analyzed the strength, aerobic capacity, and body composition of children with severe burn injuries (n = 40) at discharge, after completion of a 6- to 12-week rehabilitative exercise training program, and at 3-4 years postburn. Values were expressed as a relative percentage of those in age- and sex-matched children for comparison (n = 40 for discharge and postexercise; n = 40 for 3.5 years postburn). RESULTS: At discharge, lean body mass was 89% of that in children without burn injuries, and exercise rehabilitation restored this to 94% (P < .01). At 3.5 years postburn, lean body mass (94%), bone mineral content (89%), and bone mineral density (93%; each P ≤ .02) remained reduced, whereas total body fat was increased (148%, P = .01). Cardiorespiratory fitness remained lower in children with burn injuries both after exercise training (75%; P < .0001) and 3.5 years later (87%; P < .001). Peak torque (60%; P < .0001) and average power output (58%; P < .0001) were lower after discharge. Although exercise training improved these, they failed to reach levels achieved in healthy children without burns (83-84%; P < .0001) but were maintained at 85% and 82%, respectively, 3.5 years later (P < .0001). CONCLUSIONS: Although the benefits of rehabilitative exercise training on strength and cardiorespiratory capacity are maintained at almost 4 years postburn, they are not restored fully to the levels of healthy children. Although the underlying mechanism of this phenomenon remains elusive, these findings suggest that future development of continuous exercise rehabilitation interventions after discharge may further narrow the gap in relation to healthy adolescents.

ß-Adrenergic blockade does not impair the skin blood flow sensitivity to local heating in burned and nonburned skin under neutral and hot environments in children.

OBJECTIVE: We tested the hypothesis that propranolol, a drug given to burn patients to reduce hypermetabolism/cardiac stress, may inhibit heat dissipation by changing the sensitivity of skin blood flow (SkBF) to local heating under neutral and hot conditions. METHODS: In a randomized double-blind study, a placebo was given to eight burned children, while propranolol was given to 13 burned children with similar characteristics (mean±SD: 11.9±3 years, 147±20 cm, 45±23 kg, 56±12% Total body surface area burned). Nonburned children (n=13, 11.4±3 years, 152±15 cm, 52±13 kg) served as healthy controls. A progressive local heating protocol characterized SkBF responses in burned and unburned skin and nonburned control skin under the two environmental conditions (23 and 34°C) via laser Doppler flowmetry. RESULTS: Resting SkBF was greater in burned and unburned skin compared to the nonburned control (main effect: skin, P<.0001; 57±32 burned; 38±36 unburned vs 9±8 control %SkBFmax ). No difference was found for maximal SkBF capacity to local heating between groups. Additionally, dose-response curves for the sensitivity of SkBF to local heating were not different among burned or unburned skin, and nonburned control skin (EC50 , P>.05) under either condition. CONCLUSION: Therapeutic propranolol does not negatively affect SkBF under neutral or hot environmental conditions and further compromise temperature regulation in burned children.

Body Composition Changes in Severely Burned Children During ICU Hospitalization.

OBJECTIVES: Prolonged hospitalization due to burn injury results in physical inactivity and muscle weakness. However, how these changes are distributed among body parts is unknown. The aim of this study was to evaluate the degree of body composition changes in different anatomical regions during ICU hospitalization. DESIGN: Retrospective chart review. SETTING: Children's burn hospital. PATIENTS: Twenty-four severely burned children admitted to our institution between 2000 and 2015. INTERVENTIONS: All patients underwent a dual-energy x-ray absorptiometry within 2 weeks after injury and 2 weeks before discharge to determine body composition changes. No subject underwent anabolic intervention. We analyzed changes of bone mineral content, bone mineral density, total fat mass, total mass, and total lean mass of the entire body and specifically analyzed the changes between the upper and lower limbs. MEASUREMENTS AND MAIN RESULTS: In the 24 patients, age was 10 ± 5 years, total body surface area burned was 59% ± 17%, time between dual-energy x-ray absorptiometries was 34 ± 21 days, and length of stay was 39 ± 24 days. We found a significant (p < 0.001) average loss of 3% of lean mass in the whole body; this loss was significantly greater (p < 0.001) in the upper extremities (17%) than in the lower extremities (7%). We also observed a remodeling of the fat compartments, with a significant whole-body increase in fat mass (p < 0.001) that was greater in the truncal region (p < 0.0001) and in the lower limbs (p < 0.05). CONCLUSIONS: ICU hospitalization is associated with greater lean mass loss in the upper limbs of burned children. Mobilization programs should include early mobilization of upper limbs to restore upper extremity function.

Correlation Between PaO2/FIO2 and Peripheral Capillary Oxygenation/FIO2 in Burned Children With Smoke Inhalation Injury.

OBJECTIVES: Determine whether the peripheral capillary oxygenation/FIO2 ratio correlates with the PaO2/FIO2 ratio in burned children with smoke inhalation injury, with the goal of understanding if the peripheral capillary oxygenation/FIO2 ratio can serve as a surrogate for the PaO2/FIO2 ratio for the diagnosis of acute respiratory distress syndrome. DESIGN: Retrospective chart review. SETTING: Shriners Hospitals for Children-Galveston. PATIENTS: All burned children with smoke inhalation injury who were admitted from 1996 to 2014 and had simultaneously obtained peripheral capillary oxygenation, FIO2 and PaO2 measurements. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Two hundred seventy-three patients (63% male, 8 ± 5 yr, 53% ± 24% total body surface area burns) were analyzed. Peripheral capillary oxygenation/FIO2 ratios were divided into four subgroups based on peripheral capillary oxygenation values (≤ 100%, ≤ 98%, ≤ 95%, and ≤ 92%). Significance was accepted at r greater than 0.81. The r (number of matches) was 0.66 (23,072) for less than or equal to 100%, 0.87 (18,932) for less than or equal to 98%, 0.89 (7,056) for less than or equal to 95%, and 0.93 (4,229) for less than or equal to 92%. In the subgroup of patients who developed acute respiratory distress syndrome, r was 0.65 (8,357) for less than or equal to 100%, 0.89 (7,578) for less than or equal to 98%, 0.89 (4,115) for less than or equal to 95%, and 0.91 (2,288) less than or equal to 92%. CONCLUSIONS: PaO2/FIO2 and peripheral capillary oxygenation/FIO2 strongly correlate in burned children with smoke inhalation injury, with a peripheral capillary oxygenation of less than 92% providing the strongest correlation. Thus, peripheral capillary oxygenation/FIO2 ratio may be able to serve as surrogate for PaO2/FIO2, especially when titrating FIO2 to achieve a peripheral capillary oxygenation of 90-95% (i.e., in the acute respiratory distress syndrome range).

The change in metabolic heat production is a primary mediator of heat acclimation in adults.

PURPOSE: This study examined whether heat acclimation (HA) results in either predominate improvements in heat dissipation or reduced endogenous heat production via individual components of the human heat balance equation. METHODS: Twelve healthy inactive subjects (5 females, mean ± SD): age 28 ± 6y, 77.9 ± 2kg), completed a 10-day HA (42°C, 28% RH) hyperthermia clamp (90min/day exercise, ∆1.5°C in rectal temperature (Tre)) and control workload matched (CON: 23°C, 42% RH) protocols in a counterbalanced design separated by at least 2 mo. Pre-and post-HA were matched for external work rate (EXWR; day 1 and day 10 first 30min at 118 ± 29W, last 60min at 11 ± 5W); and metabolic heat production (Hprod; day 1 and day 9, first 30min at 296 ± 26Wm-2, last 60min 187 ± 33Wm-2). RESULTS: When Pre- and post- HA was matched for Hprod, there was no difference during the first 30 or last 60min of exercise for metabolic energy expenditure (MEE 363 ± 70/ 195 ± 32Wm-2), Hprod (296 ± 67/ 187 ± 33Wm-2) or Tre (∆2.1 ± 0.5°C). When pre- and post-HA was EXWR equivalent, HA significantly attenuated MEE during the first 30 and last 60min (303 ± 49/ 174 ± 35Wm-2), Hprod (241 ± 44/ 168 ± 33, W·m-2), and ∆Tre (∆1.3 ± 0.4°C) (each P < 0.0001). When ∆Tre, ∆Tsk, ∆Tb were each normalized per 100W Hprod, no differences were found for any pre-to post-HA comparison. Heat loss required (Ereq) to maintain steady state internal temperature (Ereq = 220 ± 32Wm-2), maximal capacity of the climate for evaporative heat loss (Emax = 266 ± 56Wm-2), evaporative heat loss from skin (Esk = 207 ± 38Wm-2) or skin wettedness (Ereq/Emax = 0.88 ± 0.23Wm-2) were not different among each condition during the last 60min. CONCLUSION: The mechanisms that underlie heat acclimation are not wholly attributed to heat dissipation enhancements per se, but are significantly influenced by metabolic heat production alterations under uncompensable heat stress environments.

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.

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.

Cognitive and perceptual responses during passive heat stress in younger and older adults.

We tested the hypothesis that attention, memory, and executive function are impaired to a greater extent in passively heat-stressed older adults than in passively heat-stressed younger adults. In a randomized, crossover design, 15 older (age: 69 ± 5 yr) and 14 younger (age: 30 ± 4 yr) healthy subjects underwent passive heat stress and time control trials. Cognitive tests (outcomes: accuracy and reaction time) from the CANTAB battery evaluated attention [rapid visual processing (RVP), choice reaction time (CRT)], memory [spatial span (SSP), pattern recognition memory (PRM)], and executive function [one touch stockings of Cambridge (OTS)]. Testing was undertaken on two occasions during each trial, at baseline and after internal temperature had increased by 1.0 ± 0.2°C or after a time control period. For tests that measured attention, reaction time during RVP and CRT was slower (P ≤ 0.01) in the older group. During heat stress, RVP reaction time improved (P < 0.01) in both groups. Heat stress had no effect (P ≥ 0.09) on RVP or CRT accuracy in either group. For tests that measured memory, accuracy on SSP and PRM was lower (P < 0.01) in the older group, but there was no effect of heat stress (P ≥ 0.14). For tests that measured executive function, overall, accuracy on OTS was lower, and reaction time was slower in the older group (P ≤ 0.05). Reaction time generally improved during heat stress, but there was no effect of heat stress on accuracy in either group. These data indicate that moderate increases in body temperature during passive heat stress do not differentially compromise cognitive function in younger and older adults.

Fluid restriction during exercise in the heat reduces tolerance to progressive central hypovolaemia.

NEW FINDINGS: What is the central question of this study? Interactions between dehydration, as occurs during exercise in the heat without fluid replacement, and hyperthermia on the ability to tolerate central hypovolaemia are unknown. What is the main finding and its importance? We show that inadequate fluid intake during exercise in the heat can impair tolerance to central hypovolaemia even when it elicits only mild dehydration. These findings suggest that hydration during physical work in the heat has important military and occupational relevance for protection against the adverse effects of a subsequent haemorrhagic injury. This study tested the hypothesis that dehydration induced via exercise in the heat impairs tolerance to central hypovolaemia. Eleven male subjects (32 ± 7 years old, 81.5 ± 11.1 kg) walked (O2 uptake 1.7 ± 0.4 l min(-1) ) in a 40°C, 30% relative humidity environment on three occasions, as follows: (i) subjects walked for 90 min, drinking water to offset sweat loss (Hydrated, n = 11); (ii) water intake was restricted, and exercise was terminated when intestinal temperature increased to the same level as in the Hydrated trial (Isothermic Dehydrated, n = 11); and (iii) water intake was restricted, and exercise duration was 90 min (Time Match Dehydrated, n = 9). For each trial, tolerance to central hypovolaemia was determined following exercise via progressive lower body negative pressure and quantified as time to presyncope. Increases in intestinal temperature prior to lower body negative pressure were not different (P = 0.91) between Hydrated (1.1 ± 0.4°C) and Isothermic Dehydrated trials (1.1 ± 0.4°C), but both were lower than in the Time Match Dehydrated trial (1.7 ± 0.5°C, P < 0.01). Prior to lower body negative pressure, body weight was unchanged in the Hydrated trial (-0.1 ± 0.2%), but was reduced in Isothermic Dehydrated (-0.9 ± 0.4%) and further so in Time Match Dehydrated trial (-1.9 ± 0.6%, all P < 0.01). Time to presyncope was greater in Hydrated (14.7 ± 3.2 min) compared with Isothermic Dehydrated (11.9 ± 3.3 min, P < 0.01) and Time Match Dehydrated trials (10.2 ± 1.6 min, P = 0.03), which were not different (P = 0.19). These data indicate that inadequate fluid intake during exercise in the heat reduces tolerance to central hypovolaemia independent of increases in body temperature.

Tissue oxygen saturation during hyperthermic progressive central hypovolemia.

During normothermia, a reduction in near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (So2) is an indicator of central hypovolemia. Hyperthermia increases skin blood flow and reduces tolerance to central hypovolemia, both of which may alter the interpretation of tissue So2 during central hypovolemia. This study tested the hypothesis that maximal reductions in tissue So2 would be similar throughout normothermic and hyperthermic central hypovolemia to presyncope. Ten healthy males (means ± SD; 32 ± 5 yr) underwent central hypovolemia via progressive lower-body negative pressure (LBNP) to presyncope during normothermia (skin temperature ≈34°C) and hyperthermia (+1.2 ± 0.1°C increase in internal temperature via a water-perfused suit, skin temperature ≈39°C). NIRS-derived forearm (flexor digitorum profundus) tissue So2 was measured throughout and analyzed as the absolute change from pre-LBNP. Hyperthermia reduced (P < 0.001) LBNP tolerance by 49 ± 33% (from 16.7 ± 7.9 to 7.2 ± 3.9 min). Pre-LBNP, tissue So2 was similar (P = 0.654) between normothermia (74 ± 5%) and hyperthermia (73 ± 7%). Tissue So2 decreased (P < 0.001) throughout LBNP, but the reduction from pre-LBNP to presyncope was greater during normothermia (-10 ± 6%) than during hyperthermia (-6 ± 5%; P = 0.041). Contrary to our hypothesis, these findings indicate that hyperthermia is associated with a smaller maximal reduction in tissue So2 during central hypovolemia to presyncope.

Key Exercise Concepts in the Rehabilitation from Severe Burns.

This article presents information on the benefits of exercise in counteracting the detrimental effects of bed rest, and/or severe burns. Exercise is key for maintaining physical function, lean body mass, metabolic recovery, and psychosocial health after major burn injuries. The details of an exercise training program conducted in severely burned persons are presented, as well as information on the importance of proper regulation of body temperature during exercise or physical activity. The sections on exercise and thermoregulation are followed by a section on the role of exercise in scarring and contractures. Finally, gaps in the current knowledge of exercise, thermoregulation, and contractures are presented.

Uneven terrain affects metabolic cost and gait in simulated complex lunar surfaces.

Objective. Upcoming missions of the National Aeronautics and Space Administration (NASA) to the Moon will include extensive human exploration of the lunar surface. Walking will be essential for many exploration tasks, and metabolic cost during ambulation on simulated complex lunar surfaces requires further characterization. In this study, ten healthy subjects (6 male and 4 female) participated in three simulated lunar terrain walking conditions at the NASA Johnson Space Center's planetary 'Rock Yard': (1) flat terrain, (2) flat terrain with obstacles, and (3) mixed terrain.Approach.Energy expenditure and gait were quantified with a wearable metabolic energy expenditure monitoring system and body-worn inertial measurement units (IMUs), respectively.Main results.It was found that participants walking on the mixed terrain, representing the highest workload condition, required significantly higher metabolic costs than in other terrain conditions (p< 0.001). Additionally, our novel IMU-based gait variables discriminated different terrains and identified changes in gait in simulated lunar terrain environments.Significance.Our results showed that the various surface irregularities and inconsistencies could cause additional physical effort while walking on the complex terrain. These findings provide insight into the effects of terrain on metabolic energy expenditure during simulated lunar extravehicular activities.

Sex Differences in Thermal Comfort, Perception, Feeling, Stress and Focus During Exercise Hyperthermia.

It is unclear whether men and women perceive thermal stress differently when changes in intestinal temperature (ΔTin) and metabolic heat production (MHprod) are matched between sexes during exercise hyperthermia. This study tested the hypothesis that females have enhanced sensitivity to comfort and perception of thermal stress during exercise hyperthermia in these conditions. We had 22 healthy active adults (11 males, 11 females; M age = 22.4 years, SD = 4.9; M height = 169 cm, SD = 7.6; M weight = 68.3 kg, SD = 13) exercise in random order, separated by at least three days at similar MHprod (M = 7.0 W/kg, SD = 1.5; p = 0.32) for 60 minutes on a cycle ergometer in cool (M = 24.00C, SD = 0.0; M = 14.4%Rh, SD = 3.6) and hot (M = 42.3°C, SD = 0.2; M = 10-60%Rh) environments with a progressive increase in humidity conditions. We measured ΔTin, and thermal stress indices for sensation (TS), comfort (TC), pleasantness (TP), and stickiness (S), feeling (FS scale), stress (visual analogue stress scale, VAS), focus (F) and felt arousal (FAS scale). We examined environmental conditions as wet bulb globe temperatures (WBGT). Males and females had similar increases in ΔTin (ME: WBGT; p < 0.0001), and both groups reported increased TS and TC and decreased TP (ME: WBGT, p ≤ 0.01). However, females reported that TS, TC, and TP, felt hotter overall, more uncomfortable, and more unpleasant, compared to males (ME: Sex; p < 0.04). Overall, females felt worse and were more stressed compared to males (ME: Sex; p ≤ 0.05). Females also reported greater internal focus as WBGT increased compared to males (I: WBGT × Sex; p < 0.003). Knowing that females perceive thermal stress during exercise hyperthermia to be hotter, more uncomfortable, more unpleasant, and more stressful compared to males can help coaches/trainers plan different exercise routines for exercisers of both sexes.