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Thermal comfort in an office impacts physical health, stress, and productivity. Humidity affects thermal comfort; however, the underlying mechanism remains unclear. This study assessed the influence of humidity on body temperature, thermal comfort, stress, and their relationship in working individuals. Thirteen participants performed three sets of 20-min calculation tasks followed by a 10-min rest in 26 °C or 33 °C with relative humidity (RH) of 30 % or 60 %. Core body temperature (T core ), mean skin surface temperature (T skin ), and electrocardiogram were continuously recorded. Subjective thermal sensations and comfort were assessed with visual analog scales. Stress level was estimated based on α-amylase activity and immunoglobulin A level in saliva and heart rate variability. Mean T skin and T core elevated at 33 °C with 60 % RH, where warm sensation and thermal discomfort also increased. Heart rate variability reflecting parasympathetic nerve activity decreased. There was a negative linear relationship between weighted body temperature and thermal comfort. However, thermal discomfort was augmented at a given weighted body temperature at 60 % RH. Thus, under indoor working conditions, high humidity may augment thermal discomfort and become a stress factor. Increases in T skin and T core are involved in the mechanism, alongside other factors., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have influenced the work reported in this study., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

We evaluated the reliability of a newly developed wearable ear canal thermometer based on three different experiments, in which ear canal and rectal temperature (T ear and T rec , respectively) were simultaneously monitored. In Experiment 1, participants sat at 28 °C and 50% relative humidity (RH), during which fanning or 41 °C lower legs water immersion was conducted. In Experiment 2, participants conducted a 70-min treadmill exercise (4 km/h, 0.5% slope) at 35 °C and 50% RH with intermittent fanning. In Experiment 3, participants completed a 20 min treadmill exercise (6 km/h, 5% slope) at 35 °C and 65% RH. Bland-Altman analysis for T ear and T rec showed the difference of - 0.2-0.3 °C and the limit of agreement of the mean ± 0.3-0.6 °C. The intraclass correlation coefficient was 0.44-0.83. The results may suggest that the ear canal thermometer is useful to assess core body temperature in sports and/or labor fields., (© 2023. The Author(s).)

Background: The aims of this study were to (1) evaluate whether recently introduced methods of measuring axillary temperature are reliable, (2) examine if individuals know their baseline body temperature based on an actual measurement, and (3) assess the factors affecting axillary temperature and reevaluate the meaning of the axillary temperature., Methods: Subjects were healthy young men and women (n = 76 and n = 65, respectively). Three measurements were obtained: (1) axillary temperature using a digital thermometer in a predictive mode requiring 10 s (T ax-10 s ), (2) axillary temperature using a digital thermometer in a standard mode requiring 10 min (T ax-10 min ), and (3) tympanic membrane temperature continuously measured by infrared thermometry (T ty ). The subjects answered questions about eating and exercise habits, sleep and menstrual cycles, and thermoregulation and reported what they believed their regular body temperature to be (T reg )., Results: T reg , T ax-10 s , T ax-10 min , and T ty were 36.2 ± 0.4, 36.4 ± 0.5, 36.5 ± 0.4, and 36.8 ± 0.3 °C (mean ± SD), respectively. There were correlations between T ty and T ax-10 min , T ty and T ax-10 s , and T ax-10 min and T ax-10 s (r = .62, r = .46, and r = .59, respectively, P < .001), but not between T reg and T ax-10 s (r = .11, P = .20). A lower T ax-10 s was associated with smaller body mass indices and irregular menstrual cycles., Conclusions: Modern devices for measuring axillary temperature may have changed the range of body temperature that is recognized as normal. Core body temperature variations estimated by tympanic measurements were smaller than those estimated by axillary measurements. This variation of axillary temperature may be due to changes in the measurement methods introduced by modern devices and techniques. However, axillary temperature values correlated well with those of tympanic measurements, suggesting that the technique may reliably report an individual's state of health. It is important for individuals to know their baseline axillary temperature to evaluate subsequent temperature measurements as normal or abnormal. Moreover, axillary temperature variations may, in part, reflect fat mass and changes due to the menstrual cycle.

We assessed the relationship between core temperature (Tc) and sleep rhythms in mice, and examined the effects of ambient temperature and fasting. Tc, electroencephalograms (EEG), electromyograms (EMG), and spontaneous activity in male ICR mice (n=9) were measured by telemetry for 3 days under a 12:12h dark-light cycle. Mice were fed or fasted at an ambient temperature (Ta) of 27°C or 20°C for the final 30h of the experiment. The vigilance state was categorized into a wake state, rapid-eye movement (REM) sleep, and non-REM (NREM) sleep, and the total sleep time (TST) was assessed. Relationships between Tc and TST, NREM periods, and REM sleep were estimated using Pearson's correlation coefficient. During cold exposure, Tc decreased during the dark and light phases, and TST and the periods of NREM and REM sleep decreased during the dark phase. Throughout the fasting period, Tc also decreased during the dark and light phases. Furthermore, the decrease in Tc was augmented when fasting and cold were combined. TST and NREM sleep periods decreased in the light and dark phases, respectively, whereas REM sleep periods decreased in both phases. Negative linear correlations (r=-0.884 to -0.987) were observed between Tc and TST, NREM sleep periods, and REM sleep periods, except for Tc and REM sleep periods where fasting and cold conditions were combined. The correlations between sleep and Tc rhythms were well maintained during cold exposure and fasting. However, when cold and fasting were combined, REM sleep and Tc rhythms were desynchronized., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Rats place their tails underneath their body trunks when cold (tail-hiding behavior). The aim of the present study was to determine whether this behavior is necessary to maintain body temperature. Male Wistar rats were divided into 'fed' and '42-h fasting' groups. A one-piece tail holder (8.4 cm in length) that prevented the tail-hiding behavior or a three-piece tail holder (2.8 cm in length) that allowed for the tail-hiding behavior was attached to the tails of the rats. The rats were exposed to 27°C for 180 min or to 20°C for 90 min followed by 15°C for 90 min with continuous body temperature and oxygen consumption measurements. Body temperature decreased by -1.0 ± 0.1°C at 15°C only in the rats that prevented tail-hiding behavior of the 42-h fasting group, and oxygen consumption increased at 15°C in all animals. Oxygen consumption was not different between the rats that prevented tail-hiding behavior and the rats that allowed the behavior in the fed and 42-h fasting groups under ambient conditions. These results show that the tail-hiding behavior is involved in thermoregulation in the cold in fasting rats.

We evaluated the effect of plasma hyperosmolality on behavioral thermoregulation in mice, using a new experimental system. The system consisted of Plexiglas box (dimensions: 50×12×19 cm) with five computer-controlled Peltier boards (dimensions: 10×10 cm) at the bottom. Experiments were conducted in two different settings of the system. An operant behavior setting: each board was first set to 39°C, and the right-end board was changed to 20°C for 1 min when a mouse moved to a specific position. A temperature mosaic setting: each board was randomly set to 15°C, 22°C, 28°C, 35°C, or 39°C with a 6-min interval, but each board temperature was different from the others at a given time point. Mice were injected subcutaneous (s.c.) isotonic or hypertonic saline (154 mM (IS group) or 2,500 mM (HS group), 10 ml/kg body wt), and exposed to either setting for 90 min. In the operant setting, the HS group showed fewer operant behavior counts than the IS group (11±5 and 25±4 counts, respectively; P<0.05) with greater increase in body temperature (1.6±0.4°C vs. 0.0±0.2°C, respectively; P<0.05). In the mosaic setting, the HS group selected the board temperature of 35°C more frequently than the other temperatures (P<0.05) with the same increase in body temperature. These results may suggest that plasma hyperosmolality modulates behavioral thermoregulatory response to heat and induce regulated hyperthermia., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Thermogenesis in the brown adipose tissue (BAT) is activated by the stimulation of the ventromedial hypothalamic nucleus (VMH). Local warming of the preoptic area (PO) suppresses this response. Injection of the GABA(A) receptor antagonist bicuculline into the caudal periaqueductal gray (cPAG), where excitatory neurons for BAT thermogenesis are located, did not influence the suppressive effect of PO warming. On the other hand, after bicuculline injection into the raphé pallidus, where excitatory neurons for BAT thermogenesis are also located, VMH stimulation produced BAT thermogenesis even during PO warming. The present results suggest that the inhibitory signal from the PO reaches the raphé pallidus and not the cPAG for the control of BAT thermogenesis.

The criptochrome genes (Cry1 and Cry2) are involved in the molecular mechanism that controls the circadian clock, and mice lacking these genes ([Cry1.sup.-/-]/ [Cry2.sup.-/-]) are behaviorally arrhythmic. It has been speculated that the circadian clock modulates the characteristics of thermoregulation, resulting in body temperature ([T.sub.b]) rhythm. However, there is no direct evidence proving this speculation. We show here that Tb and heat production in [Cry1.sup.-/-]/[Cry2.sup.-/-] mice are arrhythmic under constant darkness. In contrast, both rhythms occur under a light-dark cycle and/or periodical food restriction linked with spontaneous activity and/or eating, although they are not robust as those in wild-type mice. The relationship between heat production and [T.sub.b] in [Cry1.sup.-/-]/[Cry2.sup.-/-] mice is linear and identical under any conditions, indicating that their [T.sub.b] rhythm is determined by heat production rhythm associated with activity and eating. However, [T.sub.b] in wild-type mice is maintained at a relatively higher level in the active phase than the inactive phase regardless of the heat production level. These results indicate that the thermoregulatory responses are modulated according to the circadian phase, and the Cry genes are involved in this mechanism. circadian clock; thermoregulation; metabolism

We evaluated cold sensation at rest and in response to exercise-induced changes in core and skin temperatures in cold-sensitive exercise trained females. Fifty-eight trained young females were screened by a questionnaire, selecting cold-sensitive (Cold-sensitive, n = 7) and non-cold-sensitive (Control, n = 7) individuals. Participants rested in a room at 29.5°C for ~100 min after which ambient temperature was reduced to 23.5°C where they remained resting for 60 min. Participants then performed 30-min of moderate intensity cycling (50% peak oxygen uptake) followed by a 60-min recovery. Core and mean skin temperatures and cold sensation over the whole-body and extremities (fingers and toes) were assessed throughout. Resting core temperature was lower in the Cold-sensitive relative to Control group (36.4 ± 0.3 vs. 36.7 ± 0.2°C). Core temperature increased to similar levels at end-exercise (~37.2°C) and gradually returned to near preexercise rest levels at the end of recovery (>36.6°C). Whole-body cold sensation was greater in the Cold-sensitive relative to Control group during resting at a room temperature of 23.5°C only without a difference in mean skin temperature between groups. In contrast, cold sensation of the extremities was greater in the Cold-sensitive group prior to, during and following exercise albeit this was not paralleled by differences in mean extremity skin temperature. We show that young trained females who are sensitive to cold exhibit augmented whole-body cold sensation during rest under temperate ambient conditions. However, this response is diminished during and following exercise. In contrast, cold sensation of extremities is augmented during resting that persists during and following exercise. [ABSTRACT FROM AUTHOR]

Fasted mice show torpor-like hypothermia in the cold in their inactive phase. The aim of the present study was to elucidate whether leptin and/or ghrelin are involved in this reaction and to identify its neurophysiological mechanisms. In ob/ ob mice, which lack leptin, metabolic heat production (oxygen consumption, V o2) was suppressed in 20°C cold in both the light and dark phases, resulting in hypothermia. When wild-type mice received a systemic injection of 8 µg ghrelin in the early light phase, followed by a 2 -h cold exposure to 10°C, their core body temperature (Tb) decreased by 1.7°C, and they displayed a less marked increase in V o2 compared with vehicle -injected mice. However, ghrelin injection in the early dark phase resulted in the maintenance of Tb and increased V o2 in the mice, which was similar to the result observed in the vehicle-injected mice. The number of doubly labeled neurons with cFos and neuropeptide Y (NPY) in the suprachiasmatic nucleus was greater in the light phase in the ghrelin-injected mice, which may suggest that ghrelin activates NPY neurons. On the contrary, in the paraventricular nucleus, the counts became greater only when they were exposed to the cold in the dark phase. These results indicate that ghrelin plays an important role in inducing time-dependent changes in thermoregulation in the cold via hypothalamic pathways. (Author correspondence: ) [ABSTRACT FROM AUTHOR]

Systemic salt loading has been reported to facilitate operant heat-escape/cold-seeking behavior. In the present study, we hypothesized that the median preoptic nucleus (MnPO) would be involved in this mechanism. Rats were divided into two groups (n = 6 each): one group had the MnPO lesion with ibotenic acid (4.0 μg) and the other was the vehicle control. After subcutaneous injection (10 ml/kg) of either isotonic- (154 mM) or hypertonic-saline (2,500 mM), each rat was placed in a behavior box, where the ambient temperature was changed to 26°C, 35°C, and 40°C every 1 h. The position of a rat in the box and the body core temperature (Tcore) were monitored. A rat could trigger 0°C air for 45 s in the 35°C and 40°C heat when moved in a specific area in the box (operant behavior). In the control group, counts of the operant behavior were greater (P < 0.05) in the hypertonic- than in the isotonic-saline injection (17 ± 2 and 10 ± 2 at 35°C, 24 ± 2 and 18 ± 1 at 40°C). Tcore remained unchanged throughout the exposure, although the level was lower (P < 0.05) in the hypertonic- than in the isotonic-saline trial (36.6 ± 0.2°C and 37.4 ± 0.1°C at 26°C and 36.9 ± 0.2°C and 37.4 ± 0.1°C at 40°C, respectively). However, in the MnPO-lesion group, counts of the behavior were similar between the hypertonic- and isotonic-saline injection trials (10 ± 2 and 8 ± 1 at 35°C, and 17 ± 1 and 16 ± 1 at 40°C, respectively). Tcore increased (P < 0.05) in the heat in both trials (36.8 ± 0.1°C and 37.4 ± 0.1°C at 26°C and 37.4 ± 0.2°C and 37.8 ± 0.2°C at 40°C in the hypertonic- and isotonic-saline injection trials, respectively). These results may suggest that, at least in part, the MnPO is involved in the facilitation of heat-escape/cold-seeking behavior during osmotic stimulation. [ABSTRACT FROM AUTHOR]

Elucidates the role of the exercise-induced increase in plasma osmolality (P[sub osmol]) in the regulation of cutaneous vasodilation (CVD) during exercise. Relationship between the change in esophageal temperature required to elicit CVD and P[sub osmol] during light and moderate exercise and passive body heating; Body core temperature threshold for CVD.

Rats place their tails underneath their bodies in the cold (tail-hiding behavior), which is a behavioral indicator of thermoregulation. The aim of the present study was to elucidate the effect of estradiol (E 2 ) on tail-hiding behavior and neural activity assessed by immunohistochemistry. Ovariectomized rats were implanted with a silastic tube with or without E 2 underneath the dorsal skin (E 2 (−) and E 2 (+) groups), and exposed to 27 °C, 16 °C, and 10 °C for 2 h with continuous body temperature (T b ), tail skin temperature (T tail ), and behavioral measurements. cFos immunoreactive (cFos-IR) cells in the insula, secondary somatosensory cortex, medial preoptic nucleus, parastrial nucleus, amygdala, and lateral parabrachial nucleus were counted. T b and T tail were not different between the E 2 (−) and E 2 (+) groups. At 16 °C, the duration and the onset of tail-hiding behavior in the E 2 (+) group were greater than that in the E 2 (−) group. The number of cFos-IR cells in the insula of the E 2 (−) group was greater than that of the E 2 (+) group in rats kept at 16 °C. E 2 might modulate tail-hiding behavior of female rats at 16 °C, and the insula may be involved in the response. [ABSTRACT FROM AUTHOR]

It has been speculated that the control of core temperature is modulated by physiological demands. We could not prove the modulation because we did not have a good method to evaluate the control. In the present study, the control of core temperature in mice was assessed by exposing them to various ambient temperatures ( T a ), and the influence of circadian rhythm and feeding condition was evaluated. Male ICR mice ( n =20) were placed in a box where T a was increased or decreased from 27 °C to 40 °C or to −4 °C (0.15 °C/min) at 0800 and 2000 (daytime and nighttime, respectively). Intra-abdominal temperature ( T core ) was monitored by telemetry. The relationship between T core and T a was assessed. The range of T a where T core was relatively stable (range of normothermia, RNT) and T core corresponding to the RNT median (regulated T core ) were estimated by model analysis. In fed mice, the regression slope within the RNT was smaller in the nighttime than in the daytime (0.02 and 0.06, respectively), and the regulated T core was higher in the nighttime than in the daytime (37.5 °C and 36.0 °C, respectively). In the fasted mice, the slope remained unchanged, and the regulated T core decreased in the nighttime (0.05 and 35.9 °C, respectively), while the slopes in the daytime became greater (0.13). Without the estimating individual thermoregulatory response such as metabolic heat production and skin vasodilation, the analysis of the T a – T core relationship could describe the character of the core temperature control. The present results show that the character of the system changes depending on time of day and feeding conditions. [ABSTRACT FROM AUTHOR]

Abstract: The present study examined the effect of the central administration of estrogen on responses to the cold. Estrogen or cholesterol was applied locally to the medial preoptic nucleus (MPO) or dorsomedial hypothalamic nucleus (DMH) of the hypothalamus in free-moving ovariectomized rats. Forty-eight hours after the application, rats had 2-h exposure at 10 or 25°C. Body temperature (T b) and the tail surface temperature (T tail) were continuously measured by telemetry and thermography, respectively. The change of T b at 10°C from the 25°C baseline was higher in the estrogen application in the MPO than that in the cholesterol application; however, such difference was not observed in the DMH application. The uncoupling 1 protein mRNA level in the interscapular brown adipose tissue involved in non-shivering thermogenesis was not different between the estrogen and cholesterol applications in the MPO and DMH. T tail decreased in the cold, which was greater after the estrogen application in the MPO than after the cholesterol application. These results show that estrogen affects the MPO in female rats, changing T b in the cold. Moreover, suppression of heat loss from the tail may be involved in the mechanism. [Copyright &y& Elsevier]

Abstract: We investigated the effects of alcohol on thermoregulatory responses and thermal sensations during mild heat exposure in humans. Eight healthy men participated in this study. Experiments were conducted twice for each subject at a room temperature of 33°C. After a 30-min resting period, the subject drank either 15% alcohol (alcohol session) at a dose of 0.36g/kg body weight or equal volume of water (control session). Skin blood flow and chest sweat rate in the alcohol session significantly increased over those in controls 10min after drinking. Deep body temperature in the alcohol session started to decrease 20min after the onset of sweating and eventually fell 0.3°C lower than in the controls. Whole body hot sensation transiently increased after alcohol drinking, whereas it changed little after water drinking. The increased “hot” sensation would presumably cause cool-seeking behavior, if permitted. Thus, alcohol influences thermoregulation so that body core temperature is lowered not only by automatic mechanisms (sweating and skin vasodilation) but also behaviorally. These results suggest that decreases in body temperature after alcohol drinking are not secondary to skin vasodilation, a well-known effect of alcohol, but rather result from a decrease in the regulated body temperature evidenced by the coordinated modulation of various effectors of thermoregulation and sensation. [Copyright &y& Elsevier]

Regional activation of the brain was studied in humans using functional magnetic resonance imaging during whole body cooling that produced thermal comfort/discomfort. Eight normal male subjects lay in a sleeping bag through which air was blown, exposing subjects to cold air (8°C) for 22 min. Each subject scored their degree of thermal comfort and discomfort every min. As the subjects reported more discomfort the blood oxygen level dependent response in the bilateral amygdala increased. There was no activation in the thalamus, somatosensory, cingulate, or insula cortices. This result suggests that the amygdala plays a role in the genesis of thermal discomfort due to cold. [Copyright &y& Elsevier]

Recently we found that food-deprived rats kept under a light–dark cycle showed a progressive reduction in body temperature during the light phase on each subsequent day while body temperature in the dark phase did not differ from baseline values. In this study, we investigated the effect of lesioning the hypothalamic suprachiasmatic nucleus (SCN) on body temperature modulation by food deprivation. In the SCN-lesioned rats in which daily rhythms of body temperature and activity were abolished, body temperature was unchanged by food deprivation. We also examined the effect of food deprivation on the daily changes in Fos expression in the SCN. Under normal fed conditions the number of SCN cells expressing Fos is high during the day and low at night. Food deprivation attenuated the amplitude of this daily change in Fos expression in the SCN. This tendency was prominent in the dorsal part of the SCN, while the ventral part showed no effect of food deprivation. These findings suggest that the SCN plays some role in body temperature modulation due to food deprivation. [Copyright &y& Elsevier]