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ABSTRACT The thermosensory system is relevant to both the conceptualization and treatment of depression. There is evidence that depression is associated with changes in thermoregulatory functioning, and that thermosensory pathways can be recruited to influence affect and reduce depressive symptoms. In this study, we investigated the relationship between severity of depressive symptoms and changes to measures of subjective experiences associated with thermoregulatory processes as well as the relationship between severity of depressive symptoms and affective responses to warm stimuli, specifically frequency of warmth-seeking behavior. Participants (N = 529) completed measures of depressive symptoms, subjective experiences associated with thermoregulatory processes (i.e., perceived sweating and preferred ambient temperature) and frequency of warmth-seeking behavior (e.g., long hot baths, saunas, etc.). We demonstrate that, controlling for age and gender, greater severity of depressive symptoms is associated with greater perceived sweating and lower preferred ambient temperature. Furthermore, we demonstrate that greater severity of depressive symptoms is associated with more frequent warmth-seeking behavior, and that something other than thermal preference (i.e., stated preference for warmer temperature) is driving this behavior. These data highlight the importance of incorporating the thermoregulatory system in our conceptualization of the pathophysiology of depression and support the potential to recruit thermosensory pathways to target depressive symptoms.

Endothermic animals, including humans, generate metabolic heat to maintain a stable internal temperature, enabling activity in cold environments but at the cost of requiring substantial food as an energy source.Consequently, during the winter, when temperatures are low and food scarcity is challenging, some endotherms voluntarily enter a hypoactive metabolic state known as torpor to survive by conserving energy.Animals that enter torpor reduce their body temperature and lower their heart rate and respiration to a fraction of the normal levels, from half to just a few percent.Torpor is classified by its duration into "hibernation" and "daily torpor" (diurnal hypometabolism).The definition of hibernation is entering torpor for a period ranging from several days to weeks during the winter season, while daily torpor is defined as torpor that ends within 24 hours.Over 200 animal species, including birds and rodents, are known to enter torpor.However, the mechanisms underlying the regulation of torpor and hibernation remain largely elusive.When fasted in a cold environment, mice temporarily reduce their body temperature and basal metabolism, entering daily torpor.Before the drop in body temperature, a decrease in oxygen consumption and carbon dioxide production can be observed, indicating that mice in torpor suppress thermogenesis.During torpor, mice take a curled-up posture and constrict blood vessels near the body surface, including the limbs and tail.Thus, it can be inferred that mice physiologically suppress heat production and dissipation during torpor to conserve energy.The use of laboratory mice, widely employed in experimental biology, as a model for torpor enables expediting the investigation into the mechanisms underlying torpor.The central nervous system, especially the several nucleus in hypothalamus, is believed to converge internal nutritional status, environmental temperature, and circadian rhythms to regulate the onset, duration, and termination of torpor.However, the detailed neural underpinnings of these processes had long needed to be clarified.In recent years, with the vast advancement of techniques for manipulating neural activity such as optogenetics, chemogenetics, and the creation of transgenic animals, researchers, including us, have started uncovering some of the neural circuits that control torpor [1][2][3][4][5].In this paper, we will introduce our latest findings related to the hypothalamic mechanisms controlling torpor and provide an overview of the future challenges and prospects in the field.To comprehensively identify the neuronal circuits controlling torpor, we performed a whole-brain screen for torpor-activated neurons with optically clear, intact brain volume imaging [1].As a result, we found that the antero-preoptic area (anterodorsal preoptic area and anteroventral preoptic area), medial preoptic area (MPA), paraventricular nucleus, and dorsomedial hypothalamus (DMH) were all strongly activated before and during torpor.These findings align with the previous studies that show the preoptic areas [2] and the DMH [3,4] are implicated in the regulation of torpor.Following genetic silencing of the activity of Vgat-expressing GABAergic neurons in the DMH or Trpm2-expressing neurons in the MPA led to the absence of significant body temperature reductions during torpor, indicating the essential role of these neurons in thermoregulation during torpor.

ABSTRACT This study aimed to investigate seasonal heat acclimatization in active adolescents following summer. Fifteen (5 females) active adolescents (14.6 ± 1.0 y) completed a 45-min heat response test (HRT) walking at 60% V ˙ O2peak in 40°C and 30% relative humidity before and after summer (i.e. November 2022 and March 2023). During the HRT, gastro-intestinal temperature (Tgi), skin temperature (Tsk), heart rate, local sweat rate (LSR) and whole-body sweat loss (WBSL) were recorded. Carbon monoxide rebreathing and dual-energy X-ray absorptiometry scans determined resting hematological measures and body composition. Participants completed physical activity (PA) diaries and wore an accelerometer for two one-week periods (pre- and post-summer). Daytime wet-bulb globe temperature (WBGT) was calculated for each summer day. Data are presented as posterior mean and 90% credible intervals. Participants reported 7 ± 4 h·wk−1 of outdoor PA, and daytime WBGT was 21.2 ± 4.6°C. Following summer, resting Tgi and heart rate were reduced by 0.2°C [−0.3, −0.1; probability of direction = 99%] and 7 beats·min−1 [−10, −3; 100%], respectively. During the HRT, there was an earlier onset of sweating (−0.2°C [−0.3, −0.0; 98%]), an attenuated rise of Tgi (0.2°C [−0.5, 0.0; 92%]) and mean Tsk changed by −0.2°C [−0.5, 0.1; 86%]. There was minimal evidence for heat adaptations in LSR or WBSL, hematological parameters or perceptual measures. This is the first study to demonstrate seasonal heat adaptations in active adolescents. Reductions in resting Tgi and exercising Tsk and a lower Tgi at the onset of sweating were associated with a smaller rise in Tgi during the HRT following summer.

ABSTRACT Utilizing metadata from existing exertional and exertional-heat stress studies, the study aimed to determine if the exercise-associated increase in core body temperature can predict the change in exercise-induced gastrointestinal syndrome (EIGS) biomarkers and exercise-associated gastrointestinal symptoms (Ex-GIS). Endurance-trained individuals completed 2 h of running exercise in temperate (21.2-30.0°C) to hot (35.0-37.2°C) ambient conditions (n = 132 trials). Blood samples were collected pre- and post-exercise to determine the change in gastrointestinal integrity biomarkers and systemic inflammatory cytokines. Physiological and thermoregulatory strain variables were assessed every 10–15 min during exercise. The strength of the linear relationship between maximal (M-Tre) and change (Δ Tre) in rectal temperature and EIGS variables was determined via Spearman’s rank correlation coefficients. While the strength of prediction was determined via simple and multiple linear regression analyses dependent on screened EIGS and Ex-GIS confounding factors. Significant positive correlations between Tre maximum (M-Tre) and change (Δ Tre) with I-FABP (rs = 0.434, p < 0.001; and rs = 0.305, p < 0.001; respectively), sCD14 (rs = 0.358, p < 0.001; and rs = 0.362, p < 0.001), systemic inflammatory response profile (SIR-Profile) (p < 0.001), and total Ex-GIS (p < 0.05) were observed. M-Tre and Δ Tre significantly predicted (adjusted R2) magnitude of change in I-FABP (R2(2,123)=0.164, p < 0.001; and R2(2,119)=0.058, p = 0.011; respectively), sCD14 (R2(2,81)=0.249, p < 0.001; and R2(2,77)=0.214, p < 0.001), SIR-Profile (p < 0.001), and total Ex-GIS (p < 0.05). Strong to weak correlations were observed between M-Tre and Δ Tre with plasma concentrations of I-FABP, sCD14, SIR-Profile, and Ex-GIS in response to exercise. M-Tre and Δ Tre can predict the magnitude of these EIGS variables and Ex-GIS in response to exercise.

ABSTRACT This study investigated the seasonal effects that working outdoors had on various parameters in mining industry workers over the course of a work-shift. Workers (n = 27) were assessed in summer (33.3 ± 4.2°C, 38 ± 18% RH; n = 13, age = 46 ± 14 y, BMI = 29.1 ± 5.7 kg/m2) and winter (23.6 ± 5.1°C, 39 ± 20% RH; n = 14, age = 44 ± 12 y, BMI = 31.2 ± 4.1 kg/m2). Core temperature and heart-rate were measured continuously (analyzed at five time points), while perceptual measures, cognitive and manual dexterity performance were assessed at various times over an 11-h shift at the start of a 14-day swing. Hydration was assessed (urine specific gravity) pre- and post-shift. Working memory was impaired in summer compared to winter (−10%; p = 0.039), however did not change throughout the shift. Processing efficiency was significantly reduced at 12 pm (−12%; p = 0.005) and 5 pm (−21%; p < 0.001) compared to 9 am, irrespective of season (p > 0.05). Manual dexterity (dominant-hand) improved over the shift (+13%, p = 0.002), but was not different between seasons. Perceived fatigue had no main effect of season or shift. Core temperature, heart-rate, thermal sensation and rating of perceived exertion increased throughout the shift, with only core temperature and thermal sensation showing a seasonal effect (summer: +0.33°C, +18%, respectively; p < 0.002). Notably, 23% of workers in summer and 64% in winter started work significantly dehydrated, with 54% and 64% in summer and winter, respectively, finishing work with significant to serious dehydration. Impairment in working memory in summer combined with high levels of dehydration over the work-shift reinforces the need for workplace education on the importance of hydration and risk of occupation heat stress. Abbreviations: Core temperature: Tc; Fly-in fly-out: FIFO; Ratings of perceived exertion: RPE; Relative humidity: RH; Urinary specific gravity: USG; Wet bulb globe temperature: WBGT.

ABSTRACT Thermal safety guidelines with upper thresholds aim to protect athletes’ health, yet evidence-based sport-specific thresholds remain unestablished. Experimenting with athletes in severely hot conditions raises ethical concerns, so we used a thermo-physiological model to validate the thresholds of guidelines for outdoor sports. First, the reproducibility of the joint system thermoregulation model (JOS-3) of core temperature has been validated for 18 sports experiments (n = 213) and 11 general exercise experiments (n = 121) using the Bland – Altman analysis. Then, core temperatures were predicted using the JOS-3 in conditions corresponding to the upper thresholds, and if the 90th–99.7th percentile core temperature value (corresponding to 0.3%–10% of the participants) exceeded 40°C, the thresholds were judged as potentially hazardous. Finally, we proposed revisions for sports with potentially hazardous thresholds. As a result, the JOS-3 could simulate core temperature increases in most experiments (27/29) for six sports and general exercises with an accuracy of 0.5°C. The current upper thresholds for marathons, triathlons, and football are potentially hazardous. Suggested revisions, based on specified percentiles, include: Football: revise from wet bulb globe temperature (WBGT) 32°C to 29–31°C or not revise. Marathon: revise from WBGT 28°C to 24–27°C. Triathlon: revise from WBGT 32.2°C to 23–26°C. If conducting sports events under the revised upper thresholds proves difficult, taking measures for a possible high incidence of heat illness becomes crucial, such as placing additional medical resources, assisting heat acclimatization and cooling strategies for participants, and rule changes such as shorter match times and increased breaks.

ABSTRACT This study systematically reviewed the literature reporting the changes in rats’ core body temperature (TCORE) induced by either incremental- or constant-speed running to fatigue or exhaustion. In addition, multiple linear regression analyses were used to determine the factors contributing to the TCORE values attained when exercise was interrupted. Four databases (EMBASE, PubMed, SPORTDiscus, and Web of Science) were searched in October 2021, and this search was updated in August 2022. Seventy-two studies (n = 1,538 rats) were included in the systematic review. These studies described heterogeneous experimental conditions; for example, the ambient temperature ranged from 5 to 40°C. The rats quit exercising with TCORE values varying more than 8°C among studies, with the lowest and highest values corresponding to 34.9°C and 43.4°C, respectively. Multiple linear regression analyses indicated that the ambient temperature (p < 0.001), initial TCORE (p < 0.001), distance traveled (p < 0.001; only incremental exercises), and running speed and duration (p < 0.001; only constant exercises) contributed significantly to explaining the variance in the TCORE at the end of the exercise. In conclusion, rats subjected to treadmill running exhibit heterogeneous TCORE when fatigued or exhausted. Moreover, it is not possible to determine a narrow range of TCORE associated with exercise cessation in hyperthermic rats. Ambient temperature, initial TCORE, and physical performance-related variables are the best predictors of TCORE at fatigue or exhaustion. From a broader perspective, this systematic review provides relevant information for selecting appropriate methods in future studies designed to investigate exercise thermoregulation in rats.

ABSTRACT A paradoxical heat sensation (PHS) is the misperception of warmth when the skin is cooled. PHS is uncommon in healthy individuals but common in patients with neuropathy and is associated with reduced thermal sensitivity. Identifying conditions that contribute to PHS may indirectly help us understand why some patients experience PHS. We hypothesized that pre-warming increased the number of PHS and that pre-cooling had minimal effect on PHS. We tested 100 healthy participants’ thermal sensitivity on the dorsum of their feet by measuring detection and pain thresholds to cold and warm stimuli and PHS. PHS was measured using the thermal sensory limen (TSL) procedure from the quantitative sensory testing protocol of the German Research Network on Neuropathic Pain and by using a modified TSL protocol (mTSL). In the mTSL we examined the participants’ thermal detection and PHS after pre-warming of 38°C and 44°C and pre-cooling of 26°C and 20°C. Compared to a baseline condition, the number of PHS responders was significantly increased after pre-cooling (20°C: RR = 1.9 (1.1; 3.3), p = 0.023 and 26°C: RR = 1.9 (1.2; 3.2), p = 0.017), but not significantly after pre-warming (38°C: RR = 1.5 (0.86; 2.8), p = 0.21 and 44°C: RR = 1.7 (.995; 2.9), p = 0.078). Pre-warming and pre-cooling increased the detection threshold of both cold and warm temperatures. We discussed these findings in relation to thermal sensory mechanisms and possible PHS mechanisms. In conclusion, PHS and thermosensation are closely related and pre-cooling can induce PHS responses in healthy individuals.