Elevated Core Temperature Research Articles

The Autophagic Response to Passive and Exercise‐induced Increases in Body Core Temperature in Young Adults

Autophagy is an essential cellular survival mechanism that involves the degradation and recycling of aged or damaged organelles and protein aggregates to maintain cellular homeostasis. While autophagic dysfunction occurs with aging and is associated with many disease‐related pathologies, methods to modulate autophagic activity remain poorly understood in the context of human physiology. Recently, we demonstrated that autophagy is activated in an intensity‐dependent manner during both exercise and passive heat stress, however it is unknown if the autophagic response to elevations in body core temperature (Tcore) during passive heat exposure are comparable to those elicited through exercise. Therefore, we sought to assess the autophagic response to an elevated state of hyperthermia associated with intense exercise and compare responses to a similar rate and magnitude of increase in Tcore elicited through warm water immersion (WI). We evaluated the hypothesis that autophagic stimulation would occur during both exercise and WI, although responses would be greater during the exercise bout. To assess this hypothesis, 6 young men (mean [SD] 23 [3] years) performed 30 min of intense (70% of maximal oxygen consumption (VO2max)) semi‐recumbent cycling. On a separate day (at least 72h after the exercise bout), the same participants were immersed in warm water (up to the clavicle) for 30 min, with the water temperature adjusted to elicit the same relative increase in Tcore (as estimated by rectal temperature) as was achieved during the prior exercise session. Given Tcore during WI was matched to the prior exercise bout, all WI trials were conducted after the exercise session. Autophagic activity was assessed in peripheral blood mononuclear cells prior to, immediately post‐exercise or WI, and following a seated recovery (3 and 6h). Western blot was used to assess changes in autophagy via microtubule‐associated light chain 3 beta (LC3‐II) and normalized to β‐actin (expressed as relative fold change to the respective baseline). Area under the curve was used to assess the Tcore response between conditions and protein data were analyzed via a two‐way repeated measures ANOVA with Fisher’s LSD (α=0.05). A similar average relative increase in Tcore was observed during the exercise and WI bouts (0.65 [0.21]°C vs 0.61 [0.19]°C, respectively; p=0.80) with a return to baseline within 3h in both conditions. In response to 30‐min of exercise, LC3‐II significantly increased immediately after exercise (1.69 [0.12]; p<0.01) and remained elevated above baseline at 3h (1.51 [0.23]; p<0.01) and 6h (1.38 [0.16]; p<0.01). A similar pattern of response was observed following WI (1.86 [0.77]; p=0.04), however, LC3‐II returned to pre‐WI levels within the first 3h of recovery. Our preliminary findings show similar increases in autophagy following a similar elevation in core temperature associated induced by exercise and WI. However, the autophagic response only remained elevated after exercise, likely caused by exercise‐associated metabolic perturbations. Further research is warranted to delineate the underlying pathways of autophagic activation during these different thermal stressors.

Calcium‐activated Chloride Channel TMEM16A/ANO1 Does Not Mediate the Regulation of Sweating and Cutaneous Vasodilation in Humans In Vivo

The regulation of human body temperature during a heat stress is dependent on the activation of the heat loss responses of cutaneous vasodilation and eccrine sweating. While significant advancements have been made in our understanding of the mechanisms governing their regulation, new potential modifiers such as transmembrane member 16A (TMEM16A), a Ca2+‐activated Cl‐ channel also known as anoctamin 1 (ANO1), continue to be identified. In vitro and animal studies suggest a role for TMEM16A in the regulation of sweat secretion and vascular tone. For example, Ca2+ induced Cl‐current was abolished in TMEM16A deficit, but not BEST2 deficit, NCL‐SG3 human eccrine sweat gland cell lines. Further, animal models showed the activation of TMEM16A on vascular smooth muscle cells blunts vasodilation. However, direct evidence supporting a role of TMEM16 in mediating cutaneous vasodilation as well as eccrine sweating in humans in vivo remains to be established. Therefore, we evaluated the hypothesis that TMEM16A mediates the regulation of sweating and cutaneous vasodilation during a whole‐body heat stress in young adults.Twelve young (24 ± 2 years) adults (6 females) underwent a whole‐body heat stress induced by a water‐perfused suit to raise core temperature 1.1±0.1ºC above baseline resting levels. Sweat rate (ventilated capsule) and cutaneous vascular conductance (assessed as skin blood flow/mean arterial pressure and normalised to maximal conductance achieved via simultaneous local skin heating to 44°C and administration of sodium nitroprusside) were assessed at four skin sites on the forearm treated with 1) lactated Ringers (control), 2) 5 % dimethyl sulfoxide serving as a vehicle control, 3) 1 mM T16Ainh‐A01 (a TMEM16A blocker) or 4) 2 mM benzbromarone (another TMEM16A blocker). All drugs were administered continuously via intradermal microdialysis.Sweat rate increased as heating continued at all skin sites (P < 0.001 for a main effect of heating stage). Neither the main effect of treatment site nor the interaction between treatment site and heating stage was significant (both P ≥ 0.318). Cutaneous vascular conductance increased in parallel to elevations in core temperature (P < 0.001 for a main effect of heating stage). Although no main effect of treatment site was observed (P = 0.109), a significant interaction between heating stage and treatment site was measured (P < 0.001). Post‐hoc analysis revealed that cutaneous vascular conductance at the DMSO‐treated site was higher than the control site at baseline (P = 0.047). By contrast, cutaneous vascular conductance at moderate elevations in core temperature (i.e., ≥0.4‐0.8 °C) was greater at the control site relative to the DMSO‐treated site (all P ≤ 0.013). Importantly, no differences were measured in cutaneous vascular conductance between the DMSO‐treated site and TMEM16A blocker‐treated sites (all P ≥ 0.073).Taken together, our findings demonstrate for the first time that TMEM16A does not contribute to the regulation of sweating and cutaneous vasodilation during whole‐body heating in young adults in vivo.

Menstrual Cycle Modulates the Contribution of Dry Heat Loss to Total Heat Loss During Exercise in Warm‐Dry Conditions in Young, Recreationally Active Females: Preliminary Findings

The mid‐luteal phase of the menstrual cycle is characterized by an upward shift in basal body core temperature secondary to elevated circulating estradiol and progesterone levels as compared to the early‐follicular phase. This elevation in body core temperature, perhaps together with increased estradiol‐mediated cutaneous vasodilation, may increase convective and radiative (dry) heat loss by improving core‐to‐skin heat transfer. This increase in dry heat loss may, in turn, reduce the need for sweat secretion (evaporative heat loss) without necessarily altering the relative contribution of these avenues to total heat exchange. Thus, the purpose of this study was to evaluate the hypothesis that females in the mid‐luteal phase would exhibit a greater contribution of dry heat loss to total heat loss as compared to the early‐follicular phase during exercise in warm‐dry conditions.Seven young, recreationally active, ovulating females (3 using hormonal intrauterine devices, mean (SD), 24 (3) years, V̇O2peak 40.5 (3.4) mL kg‐1 min‐1) completed two 45‐min bouts of semi‐recumbent cycling at a low (175 W m‐2; ~40% V̇O2peak) and high (275 W m‐2; ~65% V̇O2peak) rate of metabolic heat production, interspersed by 15‐min rest, in warm‐dry conditions (30.0 (0.2) °C, (25 (9) % relative humidity) in the early‐follicular (cycle days 2‐6) and mid‐luteal phase (days 19‐23). Metabolic heat production and dry and evaporative heat loss were measured via indirect and direct calorimetry, respectively. The contribution of dry heat loss was expressed as a percentage of total heat loss. Body core temperature (esophageal, n=6) and mean skin temperature (8 sites) were measured continuously. Averages of the final 5‐min of exercise in each heat load were compared between phases using dependent, two‐tailed t‐tests.As anticipated, resting body core temperature in the mid‐luteal phase was 0.2 °C [95% CI: 0.1, 0.3] higher than in the early‐follicular phase (p<0.001). Core temperature remained 0.2 °C [0.1, 0.5] higher at the low heat load (37.8 (0.2) vs. 37.6 (0.3) °C, p<0.01), but initial differences in core temperature were not observed in the high heat load (38.4 (0.3) vs. 38.3 (0.4) °C, p=0.83). Skin temperature and core‐to‐skin gradient were similar between phases throughout (all p≥0.21). Total heat loss was not different between phases at the low (162 (8) vs. 162 (13) W m‐2, p=0.93) or high (255 (10) vs. 252 (7) W m‐2, p=0.39) heat loads. However, the contribution of dry heat loss to total heat loss was 3% [1, 4] greater in the mid‐luteal phase at the low heat load (20 (8) vs. 17 (9) %, p<0.01). This difference was not observed at the high heat load (12 (8) vs. 10 (9) %, p=0.16).In this preliminary analysis, females in the mid‐luteal phase exhibited a higher body core temperature and greater contribution of dry heat loss to total heat loss at low exercise‐induced heat loads in warm‐dry conditions. However, these differences were not observed at higher heat loads. These data provide novel mechanistic insight into the shifts in the contribution of the main avenues of heat loss in ovulating females across the menstrual cycle.

Heat Stress More Negatively Impacts Cardiac Muscle Mitochondria in Female Versus Male Pigs

With continued trends toward more frequent and more severe heat events there is a greater risk of environment‐induced heat stress (HS). How persistently elevated core temperatures impacts body tissues remains largely unknown. Our preliminary evidence indicates HS may negatively impact cardiac tissue and that biological sex may play a role in HS‐mediated pathology. To further test the hypothesis that cardiac muscle mitochondria are more negatively impacted by HS in females than in males, samples were isolated from the left ventricle (LV) of the heart from 3‐month‐old castrated male and prepubertal female pigs that were exposed to thermoneutral (TN) conditions (n = 4 per sex) or HS conditions for 24 h at 37°C (HS; n = 6 per sex). Samples were analyzed for citrate synthase (CS) and cytochrome c oxidase (COX) activities, and for mitochondrial oxidative phosphorylation (P) and electron transfer (E) capacities via high resolution respirometry. Data were analyzed by mixed linear models in SAS v9.4 with treatment, sex, and treatment × sex as fixed effects. A traditional marker of mitochondrial volume density, CS activity, tended to be greater in TN males compared to HS males (P = 0.08) but was unaffected by HS in female pigs. Conversely, intrinsic (relative to CS activity) mitochondrial function, as measured by COX activity, was greater in TN females than HS females (P = 0.04) and within HS, males maintained greater intrinsic mitochondrial function than females (P = 0.02). Both integrative (relative to tissue wet weight) and intrinsic mitochondrial leak respiration were greater in HS than TN pigs (P = 0.03) but the contribution of leak to total E (flux control ratio; FCRLEAK) tended to be greater in males than females (P = 0.07). Conversely, both integrative and intrinsic maximal E (ECI+II) tended to be greater in female than male pigs (P = 0.08) indicating a greater degree of excess electron transfer capacity in females. The contribution of complex I‐supported P (PCI) to total E (FCRPCI) tended to be greater in TN compared to HS pigs regardless of sex (P = 0.09) and the contribution of maximal P to E (FCRPCI+II) was greater in TN females compared to HS females (P = 0.05). This resulted in the FCRPCI+IIbeing greater in males compared to females in the HS condition (P = 0.01), suggesting greater coupling of oxidative phosphorylation and electron transfer in cardiac mitochondria in males during 24 h of HS. These results suggest that HS may negatively impact cardiac muscle mitochondria in female pigs compared to males. Moreover, these data indicate that persistent HS has deleterious consequences for the myocardium and may represent an additional health concern caused by global climate trends. This project was supported by USDA NIFA Award #2020‐68014‐31954.

Exertional heat stroke-related rhabdomyolysis recurring twice in a 12-year-old boy athlete

Exertional heat stroke (EHS) is a life-threatening entity characterized by elevated core temperature with potential for multiorgan dysfunction. EHS-related rhabdomyolysis usually occurs in the early phase. We report a boy athlete with EHS-related rhabdomyolysis, which recurred 15 and 79 days after the initial event. This case indicates that EHS can cause recurrences of rhabdomyolysis along with persistent symptoms, which could hamper the return to daily activity. Children with EHS, particularly athletes, may be at risk for recurrent rhabdomyolysis.

The impact of elevated body core temperature on critical power as determined by a 3-min all-out test.

Critical power (CP) delineates the heavy and severe exercise intensity domains, and sustained work rates above CP result in an inexorable progression of oxygen uptake to a maximal value and, subsequently, the limit of exercise tolerance. The finite work capacity above CP, W', is defined by the curvature constant of the power-duration relationship. Heavy or severe exercise in a hot environment generates additional challenges related to the rise in body core temperature (Tc) that may impact CP and W'. The purpose of this study was to determine the effect of elevated Tc on CP and W'. CP and W' were estimated by end-test power (EP; mean of final 30 s) and work above end-test power (WEP), respectively, from 3-min "all-out" tests performed on a cycle ergometer. Volunteers (n = 8, 4 female) performed the 3-min tests during a familiarization visit and two experimental visits (thermoneutral vs. hot, randomized crossover design). Before experimental 3-min tests, the subjects were immersed in water (thermoneutral: 36°C for 30 min; hot: 40.5°C until Tc was ≥38.5°C). Mean Tc was significantly greater in the hot condition than in the thermoneutral condition (38.5 ± 0.0°C vs. 37.4 ± 0.2°C; means ± SD, P < 0.01). All 3-min tests were performed in an environmental chamber [thermoneutral: 18°C, 45% relative humidity (RH); hot: 38 °C, 40% RH]. EP was similar between thermoneutral (239 ± 57 W) and hot (234 ± 66 W; P = 0.55) conditions. WEP was similar between thermoneutral (10.9 ± 3.0 kJ) and hot conditions (9.3 ± 3.6; P = 0.19). These results suggest that elevated Tc has no significant impact on EP or WEP.NEW & NOTEWORTHY The parameters of the power-duration relationship (critical power and W') estimated by a 3-min all-out test were not altered by elevated body core temperature as compared with a thermoneutral condition.

Sex-based differences in body core temperature response across repeat work bouts in the heat

ObjectiveTo investigate the effects of repeated work bouts in the heat on peak body core temperature and to explore sex-based differences in body core temperature responses. MethodsFourteen males and fifteen females performed four work bouts (two heavy and two moderate, alternating) in 32.5 °C Wet Bulb Globe Temperature (WBGT), each separated by 30-min seated rest in 28.0 °C WBGT. Participants wore a military combat uniform with body armour and helmet (10 kg load) during the work bouts, removing the vest and helmet during recovery periods. ResultsBody core temperature elevation over time was faster in the first compared with subsequent work bouts of each intensity. Body core temperature elevation was similar between males and females during the first heavy work bout, then remained significantly lower in females for the reminder of the trial. ConclusionsContrary to the assumed progressive elevation in strain, but in agreement with recent literature, a gradual reduction in heat storage in subsequent exercise bouts prevented a cumulative increase in heat strain in the conditions tested.

Material Interactions in Severe Accidents – Benchmarking the MELCOR V2.2 Eutectics Model for a BWR-3 MARK-I Station Blackout: Part I – Single Case Analysis

In this analysis, the two material interaction models available in the MELCOR code are benchmarked for a severe accident at a BWR under representative Fukushima Daiichi boundary conditions. This part of the benchmark investigates the impact of each material interaction model on accident progression through a detailed single case analysis. It is found that the eutectics model simulation exhibits more rapid accident progression for the duration of the accident. The slower accident progression exhibited by the interactive materials model simulation, however, allows for a greater degree of core material oxidation and hydrogen generation to occur, as well as elevated core temperatures during the ex-vessel accident phase. The eutectics model simulation exhibits more significant degradation of core components during the late in-vessel accident phase – more debris forms and relocates to the lower plenum before lower head failure. The larger debris bed observed in the eutectics model simulation also reaches higher temperatures, presenting a more significant thermal challenge to the lower head until its failure. At the end of the simulated accident scenario, however, core damage is comparable between both simulations due to significant core degradation that occurs during the ex-vessel phase in the interactive materials model simulation. A key difference between the two models’ performance is the maximum temperatures that can be reached in the core and therefore the maximum ΔT between any two components. When implementing the interactive materials model, users have the option to modify the liquefaction temperature of the ZrO2-interactive and UO2-interactive materials as a way to mimic early fuel rod failure due to material interactions. Through modification of the liquefaction of high melting point materials with significant mass, users may inadvertently limit maximum core temperatures for fuel, cladding, and debris components.

NLRP3 ablation enhances tolerance in heat stroke pathology by inhibiting IL-1\u03b2-mediated neuroinflammation

BackgroundPatients with prior illness are more vulnerable to heat stroke-induced injury, but the underlying mechanism is unknown. Recent studies suggested that NLRP3 inflammasome played an important role in the pathophysiology of heat stroke.MethodsIn this study, we used a classic animal heat stroke model. Prior infection was mimicked by using lipopolysaccharide (LPS) or lipoteichoic acid (LTA) injection before heat stroke (LPS/LTA 1 mg/kg). Mice survival analysis curve and core temperature (TC) elevation curve were produced. NLRP3 inflammasome activation was measured by using real-time PCR and Western blot. Mice hypothalamus was dissected and neuroinflammation level was measured. To further demonstrate the role of NLRP3 inflammasome, Nlrp3 knockout mice were used. In addition, IL-1β neutralizing antibody was injected to test potential therapeutic effect on heat stroke.ResultsPrior infection simulated by LPS/LTA injection resulted in latent inflammation status presented by high levels of cytokines in peripheral serum. However, LPS/LTA failed to cause any change in animal survival rate or body temperature. In the absence of LPS/LTA, heat treatment induced heat stroke and animal death without significant systemic or neuroinflammation. Despite a decreased level of IL-1β in hypothalamus, Nlrp3 knockout mice demonstrated no survival advantage under mere heat exposure. In animals with prior infection, their heat tolerance was severely impaired and NLRP3 inflammasome induced neuroinflammation was detected. The use of Nlrp3 knockout mice enhanced heat tolerance and alleviated heat stroke-induced death by reducing mice hypothalamus IL-1β production with prior infection condition. Furthermore, IL-1β neutralizing antibody injection significantly extended endotoxemic mice survival under heat stroke.ConclusionsBased on the above results, NLRP3/IL-1β induced neuroinflammation might be an important mechanistic factor in heat stroke pathology, especially with prior infection. IL-1β may serve as a biomarker for heat stroke severity and potential therapeutic method.

Acute Kidney Injury Risk is Exacerbated During Prolonged Exposure to Uncompensable Heat

Recent predictions indicate that extreme heat events will soon approach or exceed a wet bulb temperature of 35°C, which is considered the limit of thermal compensability in humans during resting conditions. Exposure to extreme heat events increases the risk of acute kidney injury (AKI), which is largely of renal tubular etiology and contributed to by elevations in core temperature and the development of dehydration. The effects of prolonged resting exposure to extreme heat that approaches of exceeds the limits of thermal compensability on AKI risk in humans is unknown. Therefore, we tested the hypothesis that AKI risk is elevated to a greater extent during an eight hour resting exposure to uncompensable heat stress, compared to compensable heat stress. Methods Fifteen healthy males (age: 23 ± 3 y; height: 179 ± 9 cm; weight 84.5 ± 18.4 kg) participated in resting exposures for 8 h in three warm (32°C, 33°C, 35°C dry bulb temperature) and extremely humid (>95% relative humidity) environments. Wet bulb temperatures differed between the three trials (31.6 ± 0.5°C, 32.1 ± 0.4°C, and 34.4 ± 0.5°C) resulting in two compensable (32°C, 33°C) and one uncompensable (35°C) environment, respectively. Core body temperature and body mass were measured every hour. Insulin-like growth factor-binding protein 7 [IGFBP7] and tissue inhibitor of metalloproteinase 2 [TIMP-2] were measured from urine samples collected at 0, 4 and 8 h of exposure. The product of IGFBP7 and TIMP-2 [IGFBP7xTIMP-2] provided an index of AKI risk, which is consistent with the FDA approved interpretation. IGFBP7 and TIMP-2 on their own provide an indication of proximal and distal tubular injury, respectively. Data are presented as an absolute change from 0 h as mean ± SD. Results Core temperature, body mass, IGFBP7, and TIMP-2 were not different at 0 h (all p>0.05). Core temperature increased over time in all trials (p<0.01). Changes in core temperature did not differ between the 32°C (0.6 ± 0.3°C) and 33°C (0.7 ± 0.3°C) trials (p=0.68), but was higher in the 35°C trial at 8 h (1.4 ± 0.4°C) compared to the 32°C and 33°C trials (p<0.01). Body mass decreased over time in all three trials (p<0.01). At 8 h, the change in body mass was not different between the 32°C (-1.4 ± 0.4%) and 33°C (-1.6 ± 0.7%) trials (p=0.68), but the reduction in body mass was greater in the 35°C trial (-1.9 ± 0.5%) compared to the 32°C trial (p=0.01). Urinary IGFBP7 increased over time in all trials (p<0.01). The increase in urinary IGFBP7 at 8 h differed between the 35°C (930 ± 749 ng/dL) and 32°C (337 ± 207 ng/dL) trials (p=0.04), but not the 33°C trial (373 ± 197 ng/dL; p=0.06). Similarly, urinary TIMP-2 increased over time in all three trials (p<0.01) and was greater at 8 h in the 35°C (21 ± 11 ng/dL) trial compared to the 32°C trial (9 ± 6 ng/dL; p=0.01). Finally, the increase in [IGFBP7xTIMP-2]was markedly greater at 8 h in the 35°C trial (868 ± 756 ng/dL2) compared to the 32°C (8 ± 9 ng/dL2; p<0.01) and 33°C (22 ± 26 ng/dL2; p<0.01) trials. Conclusion AKI risk is exacerbated during prolonged resting exposures to uncompensable heat stress, compared to compensable conditions, which is contributed to by injury in both the proximal and distal tubules.

Target Temperature Control in Patients with Burns

Severe burns lead to a persistent hypermetabolic response of the organism with significantly increased resting energy turnover, multi-organ dysfunction, muscle breakdown and increased risk of infection. Elevated core and skin temperatures are characteristic. A further increase in the metabolic rate can be triggered by heat losses, for which these patients are particularly predisposed due to high heat dissipation via evaporation of moisture and impairment of the thermoregulatory and insulating properties of the burnt skin. This is especially true in all treatment situations with exposure to large, uncovered skin surfaces, such as primary care, dressing changes in the intensive care unit and surgery with extensive sterile operating field. It has been shown that hypothermia is associated with numerous risks for the burn patient. Consistent heat management with measurement of the core body temperature and application of external and internal heat protection measures is recommended. Traditionally, an increase in room temperature is used here. However, this effective measure is limited by the resilience of the intensive care practitioners and the surgeons. To avoid perioperative hypothermia, strict surgical planning with limitation of the duration of surgery and close intraoperative communication about the risk of hypothermia are of particular importance.The differentiation between accepted temperature increase and infectious fever is often only possible by the inclusion of further examination findings. The criterion for sepsis is a temperature above 39 °C or below 36.5 °C.

Influence of a Patent Foramen Ovale on Heart Rate‐Core Temperature Relationship at Rest and During Exercise in Young, Healthy Men

During both passive and active heat stress, there is a relationship between increases in core temperature (Tcore) and the heart rate (HR) response. As Tcore rises, HR increases as a result of sympathetic nervous system stimulation and due to the direct effects of temperature on the sinoatrial node. Young, healthy men with a patent foramen ovale (PFO+) have a higher Tcore at rest and during exercise so they may have altered thermoregulatory (Tcore) and cardiovascular (HR) coupling compared to those without a PFO (PFO-). We aimed to test two hypotheses: 1) That there is a relationship between inter-individual values for HR and Tcore at rest and during exercise and 2) The presence of a PFO alters the HR-Tcore inter-individual relationship at rest and during exercise. Thirty male subjects free of cardiometabolic and respiratory diseases (ages 19-36) participated in the study (15 PFO+/15 PFO-) and performed a graded exercise protocol that included cycling at exercise intensities of 50% (154 ± 22 W) and 90% (277 ± 40 W) of VO2max. HR and Tcore (esophageal probe) were measured at rest and continuously during the exercise test. Linear regression analyses were performed to determine the relationships between Tcore and HR at rest and at 50% and 90% of VO2max as a main group and in both PFO- and PFO+ subgroups. Absolute workload was not different at 50% and 90% VO2max between PFO+ and PFO- groups (p > 0.05). A positive relationship between Tcore and HR was seen at rest (r = 0.45, p < 0.05), 50% (r = 0.50, p < 0.05), and 90% (r = 0.44, p < 0.05) VO2max for combined group data. PFO+ subjects had higher resting HR (66 ± 8 vs 58 ± 9 bpm, p < 0.05) and Tcore (36.67 ± 0.23 vs 36.41 ± 0.28°C, p < 0.05) vs PFO- subjects; no group differences were seen during exercise (p > 0.05 for both intensities). A positive relationship existed between individual values for resting Tcore and HR in PFO+ (r = 0.66, p < 0.05) but not in PFO- subjects. In PFO+ subjects, there was no relationship between the two variables during exercise. In PFO- subjects, there was a positive relationship between Tcore and HR at 50% (r = 0.65, p < 0.05) and 90% (r = 0.54, p < 0.05) VO2max. Our data are consistent with the idea that there are differences in thermoregulatory and/or cardiovascular coupling between PFO+ and PFO- subjects at rest and during exercise. A possible explanation is that PFO+ subjects may have higher levels of inflammatory markers (interleukins, TNFα, etc), leading to elevated core temperatures at rest, thus contributing to the greater variability in the HR-Tcore responses during exercise.

Heat Stress Management in the Military: Wet-Bulb Globe Temperature Offsets for Modern Body Armor Systems.

The aim of this study was to model the effect of body armor coverage on body core temperature elevation and wet-bulb globe temperature (WBGT) offset. Heat stress is a critical factor influencing the health and safety of military populations. Work duration limits can be imposed to mitigate the risk of exertional heat illness and are derived based on the environmental conditions (WBGT). Traditionally a 3°C offset to WBGT is recommended when wearing body armor; however, modern body armor systems provide a range of coverage options, which may influence thermal strain imposed on the wearer. The biophysical properties of four military clothing ensembles of increasing ballistic protection coverage were measured on a heated sweating manikin in accordance with standard international criteria. Body core temperature elevation during light, moderate, and heavy work was modeled in environmental conditions from 16°C to 34°C WBGT using the heat strain decision aid. Increasing ballistic protection resulted in shorter work durations to reach a critical core temperature limit of 38.5°C. Environmental conditions, armor coverage, and work intensity had a significant influence on WBGT offset. Contrary to the traditional recommendation, the required WBGT offset was &gt;3°C in temperate conditions (&lt;27°C WBGT), particularly for moderate and heavy work. In contrast, a lower WBGT offset could be applied during light work and moderate work in low levels of coverage. Correct WBGT offsets are important for enabling adequate risk management strategies for mitigating risks of exertional heat illness.

T6 Burn Survivors Can Perform Mild/moderate-intensity Exercise in Thermoneutral Conditions Without a Risk of Excessive Elevations in Core Body Temperature

Abstract Introduction Burned skin excision and subsequent grafting removes sweat glands, which impairs thermoregulation. Consequently, exercise prescribed for rehabilitation may expose individuals with burn injuries to a greater risk of hyperthermia, depending on exercise duration, intensity, and environmental temperature. Little is known regarding the risk of hyperthermia in adult burn survivors performing mild/moderate-intensity exercise under thermoneutral environmental conditions, i.e. conditions similar to the rehabilitation clinic and/or the gym. This project tested the hypothesis that burn survivors, across a wide range of percent total body surface area (%TBSA) burned, can participate in mild/moderate-intensity exercise in a thermoneutral environment without excessive elevations in core body temperature. Methods Twenty-eight well-healed burn survivors with low (23±5%TBSA; N=10), moderate (42±7%TBSA; N=9), and high (60±8%TBSA; N=9) sized burn injuries performed 60 minutes of cycle ergometry exercise (72±15 Watts, oxygen uptake rate of 1.25±0.21 L/min equivalent to 4.5±0.2 METs) in a 25°C and 23% relative humidity environment. Absolute gastrointestinal temperatures (Tcore) and changes in gastrointestinal temperatures (ΔTcore) were obtained at 15-minute increments throughout the exercise bout. A participant with an absolute Tcore of greater than 38.5°C, and/or a ΔTcore of &amp;gt;1.5°C, at any time point during the trial was categorized as being at risk for hyperthermia. Results Sixty minutes of exercise increased Tcore in all groups (Low: 0.72±0.21°C; Moderate: 0.42±0.22°C; High: 0.77±0.25°C, all P&amp;lt; 0.01 from pre-exercise baseline), resulting in similar absolute Tcore values of upon exercise termination (Low: 37.87±0.24°C; Moderate: 37.56±0.34°C; High: 37.76±0.47°C, P=0.19). Importantly, no participant was categorized as being at risk for hyperthermia, based upon the aforementioned criteria. Conclusions These data indicate that individuals with substantial %TBSA burned can exercise at a mild/moderate intensity for 60 minutes in thermoneutral environmental conditions without a risk of excessive elevations in body core temperature.

ADGRA1 negatively regulates energy expenditure and thermogenesis through both sympathetic nervous system and hypothalamus\u2013pituitary\u2013thyroid axis in male mice

Adhesion G protein-coupled receptor A1 (ADGRA1, also known as GPR123) belongs to the G protein-coupled receptors (GPCRs) family and is well conserved in the vertebrate lineage. However, the structure of ADGRA1 is unique and its physiological function remains unknown. Previous studies have shown that Adgra1 is predominantly expressed in the central nervous system (CNS), indicating its important role in the transduction of neural signals. The aim of this study is to investigate the central function of Adgra1 in vivo and clarify its physiological significance by establishing an Adgra1-deficient mouse (Adgra1−/−) model. The results show that Adgra1−/− male mice exhibit decreased body weight with normal food intake and locomotion, shrinkage of body mass, increased lipolysis, and hypermetabolic activity. Meanwhile, mutant male mice present elevated core temperature coupled with resistance to hypothermia upon cold stimulus. Further studies show that tyrosine hydroxylase (TH) and β3-adrenergic receptor (β3-AR), indicators of sympathetic nerve excitability, are activated as well as their downstream molecules including uncoupling protein 1 (UCP1), coactivator 1 alpha (PGC1-α) in brown adipose tissue (BAT), and hormone-sensitive lipase (HSL) in white adipose tissue (WAT). In addition, mutant male mice have higher levels of serum T3, T4, accompanied by increased mRNAs of hypothalamus–pituitary–thyroid axis. Finally, Adgra1−/− male mice present abnormal activation of PI3K/AKT/GSK3β and MEK/ERK pathways in hypothalamus. Overexpression of ADGRA1 in Neuro2A cell line appears to suppress these two signaling pathways. In contrast, Adgra1−/− female mice show comparable body weight along with normal metabolic process to their sex-matched controls. Collectively, ADGRA1 is a negative regulator of sympathetic nervous system (SNS) and hypothalamus–pituitary–thyroid axis by regulating PI3K/AKT/GSK3β and MEK/ERK pathways in hypothalamus of male mice, suggesting an important role of ADGRA1 in maintaining metabolic homeostasis including energy expenditure and thermogenic balance.

Perceived Thermal Response of Stone Quarry Workers in Hot Environment

Introduction: Impact of heat on health of workers goes unrecognized by the virtue of the indispensable fact that every individual has varied perception and tolerance capacity. The present study determine the physiological signs with perceived subjective responses under the thermal stress.Materials and Methods: The study was spread on open field stone quarry workers (N = 934) during the summer (May to June), post monsoon (September to October), and winter (December to January).Results: In the summer months, dry bulb temperature range from 36.1 to 43.2°C and the distribution of Wet Bulb Globe temperature (WBGT) outdoor values were outlier-prone than normal distribution indicated heat vulnerability. The environmental effect on weighted average skin temperature (Tsk) local segmental Tsk and deep body temperature (Tcr) were greater than the effects that might be attributed to work severity. The tolerance time level in summer months (65 ± 13 min at WBGT 35 ± 2.3°C) was less than in other two season. About 85% of workers in summer, 68% in post monsoon and 79% in winter recorded working heart rate greater than 90 beats/min. Physiological and subjective responses to heat stress indicated that during summer month the workers complained of excessive sweating (93.5%), feeling of thirst/dry mouth (88.7%), elevated Core temperature (Tcr) (58.7%) and decreased working capacity (75.6%). The observation found that around 14% workers were vulnerable to heat stress and the workers had no knowledge to mitigate the heat related illnesses.Discussion and Conclusions: The stone quarry work as compared to other outdoor workers have environmental adversaries which becomes confounding variables in the study of such occupations. There was significant difference (p &amp;lt; 0.001) as far as the physiological and thermoregulatory responses were concerned in three different months of investigation.

Impact of elevated core temperature on cognition in hot environments within a military context.

PurposeCognition can be impaired during exercise in the heat, potentially contributing to military casualties. To our knowledge, the independent role of elevated core temperature during exercise has not been determined. The aim of the current study was to evaluate effects of elevated core temperature on cognition during physically encumbering, heated exercise, and to determine whether the perceptual cooling effects of menthol preserves cognition.MethodsEight participants complete three trials in randomised order: one normothermic (CON) and two with elevated (38.5°C) core temperature, induced by prior immersion in neutral versus hot water The CON trial and one hot trial (HOT) used a water mouth-rinse following each cognitive task of the trial, (HOT) while the other used a menthol mouth-rinse (MENT). Participants walked in humid heat (33°C, 75% relative humidity) in military clothing, completing a cognitive battery of reaction time, perceptual processing, working memory, executive function, cognitive flexibility, vigilance, and declarative memory.ResultsNo differences in cognitive performance were observed between any conditions. Near-infrared spectroscopy showed greater oxygenated haemoglobin tissue content in HOT and MENT compared to CON (ΔO2Hb-deO2Hb: 2.3 ± 4.5 µM, p < .024), and lower deoxygenated haemoglobin in MENT than in CON or HOT (p = .017), suggesting higher brain metabolism during the more stressful conditions.ConclusionModerately elevated core (38.5°C) and skin temperature does not appear to impair cognitive performance during exercise despite mildly elevated cerebral metabolism. The effects of menthol remain undetermined due to the lack of heat-mediated cognitive impairment.

Guidelines of the Polish Society of Anaesthesiology and Intensive Therapy regarding prevention of inadvertent intraoperative hypothermia.

Core body temperature is strictly regulated (± 0.2 °C) and coordinated at the level of central nervous system located in the hypothalamus via several protective effector mechanisms that prevent overcooling and overheating. The central regulation permits both circadian and monthly variations of even 1°C; under normal conditions, however, the activation of effective protective mechanisms prevents even the slightest overcooling and core temperature elevation at any moment of the day.

Feasibility of continuous fever monitoring using wearable devices

Elevated core temperature constitutes an important biomarker for COVID-19 infection; however, no standards currently exist to monitor fever using wearable peripheral temperature sensors. Evidence that sensors could be used to develop fever monitoring capabilities would enable large-scale health-monitoring research and provide high-temporal resolution data on fever responses across heterogeneous populations. We launched the TemPredict study in March of 2020 to capture continuous physiological data, including peripheral temperature, from a commercially available wearable device during the novel coronavirus pandemic. We coupled these data with symptom reports and COVID-19 diagnosis data. Here we report findings from the first 50 subjects who reported COVID-19 infections. These cases provide the first evidence that illness-associated elevations in peripheral temperature are observable using wearable devices and correlate with self-reported fever. Our analyses support the hypothesis that wearable sensors can detect illnesses in the absence of symptom recognition. Finally, these data support the hypothesis that prediction of illness onset is possible using continuously generated physiological data collected by wearable sensors. Our findings should encourage further research into the role of wearable sensors in public health efforts aimed at illness detection, and underscore the importance of integrating temperature sensors into commercially available wearables.

Body temperature and physical performance responses are not maintained at the time of pitch-entry when typical substitute-specific match-day practices are adopted before simulated soccer match-play

ObjectivesTo profile performance and physiological responses to typical patterns of match-day activity for second-half soccer substitutes. DesignDescriptive. MethodsFollowing a warm-up, 13 male team sports players underwent ∼85min of rest, punctuated with five min rewarm-ups at ∼25, ∼50, and ∼70min, before ∼30min of simulated soccer match-play. Countermovement jump performance (jump height, peak power output), alongside 15m sprints, were assessed post-warm-up, and pre- and post-simulated match-play. Core temperature, heart rate, ratings of perceived exertion, and blood glucose and lactate concentrations were measured throughout. ResultsWarm-up-induced core temperature elevations (∼2.3%, +0.85°C; p<0.001) were maintained until after the first rewarm-up. Thereafter, core temperature was reduced from post-warm-up values until pre-simulated match-play (∼1.6%, −0.60°C; p<0.001), where values were similar to pre-warm-up (37.07±0.24°C, p=0.981). Simulated match-play increased core temperature progressively (p≤0.05) but values remained lower than post-warm-up (∼5min; p=0.002) until ∼10min into exercise. From post-warm-up to pre-simulated match-play, sprint times (∼3.9%, +0.10s, p=0.003), jump height (∼9.4%, −3.1cm; p=0.017), and peak power output (∼7.2%, −296W; p<0.001) worsened. Despite increased ratings of perceived exertion and elevated blood lactate concentrations (p≤0.05), sprint times were maintained throughout exercise, whereas peak power increased (∼7.8%, +294W; p=0.006) pre- to post-exercise. ConclusionsAt the point of simulated pitch-entry, body temperature and physical performance responses were not maintained from warm-up cessation despite typical substitute-specific match-day practices being employed in thermoneutral conditions. Evidence of performance-limiting fatigue was absent during ∼30min of simulated match-play. These data question the efficacy of practices typically implemented by substitutes before pitch-entry.