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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.

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 (Ta), and the influence of circadian rhythm and feeding condition was evaluated. Male ICR mice (n=20) were placed in a box where Ta 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 (Tcore) was monitored by telemetry. The relationship between Tcore and Ta was assessed. The range of Ta where Tcore was relatively stable (range of normothermia, RNT) and Tcore corresponding to the RNT median (regulated Tcore) 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 Tcore 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 Tcore 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 Ta-Tcore 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.

Cold defense mechanisms in mice are attenuated in the light phase during fasting, resulting in hypothermia. The present study examined whether specific neurons and areas in the SCN are related to the response. Mice were fasted over 47h or remained fed, during which they were placed at 20 or 27°C for 3h in the light or dark phases. Body temperature (Tb) was monitored. After the exposure, immunoreactive (IR) cells of cFos, arginine vasopressin (AVP), and vasoactive intestinal polypeptide (VIP) in the SCN were assessed. Tb at 20°C during fasting was lower in the light phase than in the dark phase. Both AVP/cFos-IR and VIP/cFos-IR cells increased when mice were at 20°C during fasting in the light phase. Such increase was observed in the central part of the SCN. These responses in the SCN may be related to the hypothermia in the light phase.

Some animals have mechanisms that selectively cool the brain during hyperthermia. However, it remains controversial if humans have the mechanism. In the present study, we investigated the effect of...

Although the posterior part of the hypothalamus has long been considered important for thermoregulatory shivering, it is unknown whether the neurons there or the passing fibers are implicated in the response. Exposure of urethane-anesthetized rats to cold (15-21 degrees C) elicits shivering. An injection of muscimol (0.5 mM), a GABA(A) receptor agonist, into the medial part of the hypothalamus, including the dorsomedial and posterior nuclei, suppressed the cold-induced shivering. This result suggests that neurons having an excitatory effect on shivering are in this region of the hypothalamus.

We tested the hypothesis that an elevation in albumin synthetic rate contributes to increased plasma albumin content during exercise-induced hypervolemia. Albumin synthetic rate was measured in seven healthy subjects at 1–5 and 21–22 h after 72 min of intense (85% peak oxygen consumption rate) intermittent exercise and after 5 h recovery in either upright (Up) or supine (Sup) postures. Deuterated phenylalanine (d5-Phe) was administrated by a primed-constant infusion method, and fractional synthetic rate (FSR) and absolute synthetic rate (ASR) of albumin were calculated from the enrichment of d5-Phe in plasma albumin, determined by gas chromatography-mass spectrometry. FSR of albumin in Up increased significantly ( P < 0.05) from 4.9 ± 0.9%/day at control to 7.3 ± 0.9%/day at 22 h of recovery. ASR of albumin increased from 87.9 ± 17.0 to 141.1 ± 16.6 mg albumin ⋅ kg body wt− 1 ⋅ day− 1. In contrast, FSR and ASR of albumin were unchanged in Sup (3.9 ± 0.4 to 4.0 ± 1.4%/day and 74.2 ± 8.9 to 85.3 ± 23.9 mg albumin ⋅ kg body wt− 1 ⋅ day− 1at control and 22 h of recovery, respectively). Increased albumin synthesis after upright intense exercise contributes to the expansion of greater albumin content and its maintenance. We conclude that stimuli related to posture are critical in modulating the drive for albumin synthesis after intense exercise.

We examined the hypothesis that activation of the muscle metaboreflex during dynamic exercise would augment influences tending to cause a rise in arginine vasopressin, plasma renin activity, and catecholamines during dynamic exercise in humans. Ten healthy adults performed 30 min of supine cycle ergometer exercise at ∼50% of peak oxygen consumption with or without moderate muscle metaboreflex activation by application of 35 mmHg lower body positive pressure (LBPP). Application of LBPP during the first 15 or last 15 min of exercise increased mean arterial blood pressure, plasma lactate concentration, and minute ventilation, indicating an activation of the muscle metaboreflex. These changes were rapidly reversed when LBPP was removed. During exercise at this intensity, LBPP augmented the release of arginine vasopressin and catecholamines but not of plasma renin activity. These results suggest that, although in humans hormonal responses are induced by moderate activation of the muscle metaboreflex during dynamic exercise, the thresholds for these responses may not be uniform among the various glands and hormones.

To test the hypothesis that exercise-induced hypervolemia is a posture-dependent process, we measured plasma volume, plasma albumin content, and renal function in seven healthy subjects for 22 h after single upright (Up) or supine (Sup) intense (85% peak oxygen consumption rate) exercise. This posture was maintained for 5 h after exercise. Plasma volume decreased during exercise but returned to control levels by 5 h of recovery in both postures. By 22 h of recovery, plasma volume increased 2.4 ± 0.8 ml/kg in Up but decreased 2.1 ± 0.8 ml/kg in Sup. The plasma volume expansion in Up was accompanied by an increase in plasma albumin content (0.11 ± 0.04 g/kg; P < 0.05). Plasma albumin content was unchanged in Sup. Urine volume and sodium clearance were lower in Up than Sup ( P < 0.05) by 5 h of recovery. These data suggest that increased plasma albumin content contributes to the acute phase of exercise-induced hypervolemia. More importantly, the mechanism by which exercise influences the distribution of albumin between extra- and intravascular stores after exercise is altered by posture and is unknown. We speculate that factors associated with postural changes (e.g., central venous pressure) modify the increase in plasma albumin content and the plasma volume expansion after exercise.

To clarify whether an increase in urinary sodium (Na) excretion during cold-air exposure is attenuated in trained athletes, we analyzed the urinary and hormonal responses to cold-air exposure at 15 degrees C in trained (TR, n = 9) and untrained men (UT, n = 9). During 15 degrees C exposure in the UT group, the urinary Na excretion (UNaV), fractional excretion of Na and urinary Na to K ratio (UNa/K) increased significantly (p

Dear Editor-in Chief,The Challenge Article “Temperature receptors in cutaneous nerve endings are thermostat molecules that induce thermoregulatory behaviors against thermal load” by Dr. Shigeo Koba...

The aim of the study was to assess if autonomic thermoregulation and thermal perception in women exposed to cold are different during follicular and luteal phases of the menstrual cycle. Although c...

We tested the hypothesis that cardiovascular responses to lower body positive pressure (LBPP) would be dependent on the posture of the subject and also on the background condition (rest or exercise). We measured heart rate (HR), mean arterial blood pressure (MAP), and cardiac stroke volume in eight subjects at rest and during cycle ergometer exercise (76 +/- 3 W) with and without LBPP (25, 50, and 75 mmHg) in the supine and upright positions. At rest, the increase in MAP was proportional to the increase in LBPP and was greater in the supine (6 +/- 2, 15 +/- 3, and 26 +/- 3 mmHg) than in the upright (2 +/- 3, 9 +/- 3, and 17 +/- 3 mmHg) position. During dynamic exercise, the increases in MAP evoked by 25, 50, and 75 mmHg LBPP were greater in the supine (13 +/- 2, 28 +/- 3, and 40 +/- 3 mmHg) than in the upright (7 +/- 3, 12 +/- 3, and 25 +/- 3 mmHg) position. We conclude that the systemic pressure response to LBPP is clearly dependent on the body position, with the larger pressure responses being associated with the supine position both at rest and during dynamic leg exercise.

We studied the difference of thermoregulatory responses between trained male athletes (TR, n = 9) and untrained men (UT, n = 7) during 60 min of cold exposure (15 degrees C) without shivering, and examined the effects of physical fitness and body fat on these responses. Mean skin temperature (Tsk), esophageal temperature (Tes), and skin conductance (Kb) were similar between TR and UT, and heat production (M) for TR increased significantly during exposure at 15 degrees C. The M at 15 degrees C correlated positively with maximal oxygen uptake and negatively with body fat (%BF), but not with Tes. The Kb correlated negatively with Tes and positively with Tsk. The %BF also correlated negatively with Kb and Tsk during exposure at 15 degrees C, and the slope of %BF vs. Tsk relationship was significantly steeper in TR than in UT. These results suggest that (1) body temperature is maintained by the reduction of skin conductance, and (2) heat insulation independent of body fat is enhanced in trained athletes during cold exposure without shivering.

To clarify the relationship between aerobic power (VO2max), blood volume (BV), and thermoregulatory responses to exercise-heat stress, we analyzed the cross-sectional relationship between the resting BV, plasma volume (PV), erythrocyte volume (EV), VO2max, forearm blood flow (FBF), and sweating responses during exercise in a hot environment (31 degrees C, 50% relative humidity). Twelve college-aged male subjects with a mean maximal oxygen uptake of 48 (range 42-59) mL.kg-1.min-1, a mean PV of 54 (range 42-72) mL.kg-1, a mean EV of 31 (range 23-43) mL.kg-1, and a mean BV of 85 (range 67-115) mL.kg-1 (measured by the Evans Blue dye dilution method) performed three sessions of 20-min cycle exercise at two levels of intensity (40% and 60% VO2max). The BV, PV and EV correlated positively with peak FBF (r = 0.596-0.711, P < 0.05), the increase of FBF in response to a unit rise in esophageal temperature (Tes; peak delta FBF/peak delta Tes) (r = 0.592-0.656, P < 0.05) and with total sweat loss (TSL) (r = 0.599-0.634, P < 0.05) during the exercise. The VO2max correlated with TSL during exercise at 40% VO2max (r = 0.578, P < 0.05), but not with peak FBF and peak delta FBF/peak delta Tes. The VO2max per lean body mass also showed a significant positive correlation with BV (r = 0.769, P < 0.01), PV (r = 0.706, P < 0.05), and with EV (r = 0.841, P < 0.001). The peak delta FBF/peak delta Tes was correlated positively with peak FBF (r = 0.597-0.830, P < 0.05-0.01) and negatively with peak Tes (r = 0.641-0.769, P < 0.05-0.01) during the exercise at the two levels. However, the chest sweat rate (CSR), TSL, and the increase of CSR in response to a unit rise in Tes (peak delta CSR/peak delta Tes) showed no correlation with peak Tes during the exercise at the two levels. These findings suggest that 1) heat dissipation responses during exercise were related more to blood volume than aerobic power and 2) skin blood flow was related more to body temperature than sweating responses during exercise under mild heat stress.

To analyze drinking mechanisms in seawater teleosts, seawater-adapted eels were used as a model system. When the intestine of the eel was perfused with iso-osmotic mannitol, the eels drank sea water. However, when the perfusion medium was switched to iso-osmotic NaCl, seawater drinking was depressed. This depression was observed even after blocking NaCl absorption across the intestine by replacement of the perfusate with choline chloride or by treatment with furosemide, an inhibitor of NaCl and water absorption across the eel intestine. Furthermore, depression of drinking rate preceded an increase in urine flow by over 1 h. These results indicate that this depression is not due to a recovery of blood volume and suggest that intestinal Cl− itself inhibits drinking. Direct action of luminal Cl− on drinking behavior was further supported by the observation that perfusion with iso-osmotic NMDG–HCl, Tris–HCl, choline chloride and RbCl all inhibited seawater drinking. When NaCl in the perfusion medium was replaced with sodium acetate, sodium butyrate, sodium methylsulfate or NaSCN, the drinking rate was enhanced threefold, suggesting that Na+ itself stimulates drinking in the absence of Cl−. In the present study, concentrations of Na+ and Cl− in the swallowed fluid were also measured simultaneously. As the drinking rate was enhanced, the Na+ and Cl− concentrations in the gastrointestinal fluid were increased. On the basis of these results, it seems possible that high concentrations of Cl− in the intestine reduce the drinking rate, thus lowering esophageal Cl− concentration due to desalination of the ingested sea water. When Cl− concentration in the intestine falls below a certain level, Na+ will stimulate seawater drinking again.

In a previous study, we investigated the contribution of the surface of the face, chest, abdomen, and thigh to thermal comfort by applying local temperature stimulation during whole-body exposure to mild heat or cold. In hot conditions, humans prefer a cool face, and in cold they prefer a warm abdomen. In this study, we extended investigation of regional differences in thermal comfort to the neck, hand, soles, abdomen (Experiment 1), the upper and lower back, upper arm, and abdomen (Experiment 2). The methodology was similar to that used in the previous study. To compare the results of each experiment, we utilized the abdomen as the reference area in these experiments. Thermal comfort feelings were not particularly strong for the limbs and extremities, in spite of the fact that changes in skin temperature induced by local temperature stimulation of the limbs and extremities were always larger than changes that were induced in the more proximal body parts. For the trunk areas, a significant difference in thermal comfort was not observed among the abdomen, and upper and lower back. An exception involved local cooling during whole-body mild cold exposure, wherein the most dominant preference was for a warmer temperature of the abdomen. As for the neck and abdomen, clear differences were observed during local cooling, while no significant difference was observed during local warming. We combined the results for the current and the previous study, and characterized regional differences in thermal comfort and thermal preference for the whole-body surface.

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.

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 degrees 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 degrees C from the 25 degrees 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.

We would like to emphasize about the system involved with homeostatic maintenance of body temperature. First, the primary mission of the thermoregulatory system is to defend core temperature (T (core)) against changes in ambient temperature (T (a)), the most frequently encountered disturbance for the system. T (a) should be treated as a feedforward input to the system, which has not been adequately recognized by thermal physiologists. Second, homeostatic demands from outside the thermoregulatory system may require or produce an altered T (core), such as fever (demand from the immune system). There are also conditions where some thermoregulatory effectors might be better not recruited due to demands from other homeostatic systems, such as during dehydration or fasting. Third, many experiments have supported the original assertion of Satinoff that multiple thermoregulatory effectors are controlled by different and relatively independent neuronal circuits. However, it would also be of value to be able to characterize strictly regulatory properties of the entire system by providing a clear definition for the level of regulation. Based on the assumption that T (core) is the regulated variable of the thermoregulatory system, regulated T (core) is defined as the T (core) that pertains within the range of normothermic T (a) (Gordon in temperature and toxicology: an integrative, comparative, and environmental approach, CRC Press, Boca Raton, 2005), i.e., the T (a) range in which an animal maintains a stable T (core). The proposed approach would facilitate the categorization and evaluation of how normal biological alterations, physiological stressors, and pathological conditions modify temperature regulation. In any case, of overriding importance is to recognize the means by which an alteration in T (core) (and modification of associated effector activities) increases the overall viability of the organism.

Hypohydration caused by exercise in the heat attenuates autonomic thermoregulation such as sweating and skin blood flow in humans. In contrast, it remains unknown if behavioral thermoregulation is modulated during hypohydration. We assume that thermal unpleasantness could drive the behavioral response, and would also be modulated during hypohydration. Nine healthy young men participated in the present study. Body and skin temperatures were monitored. Ratings of thermal sensation and pleasantness were conducted. After approximately 45 min rest at 27 degrees C, they performed 50-min cycling exercise, which was at the level of 40% of heart rate range at 35 degrees C (hypohydration trial) or at the level of 10% of heart rate range at 23 degrees C (control trial), respectively. Subjects returned to the rest at 27 degrees C, and the ambient temperature was then changed from 22 to 38 degrees C. Body weight decreased by 0.9+/-0.1% immediately after exercise in the hypohydration trial and 0.3+/-0.1% in the control trial. In the cold, no significant difference in thermal sensation or pleasantness was observed between trials. There was no significant difference in thermal pleasantness between trials in the heat, although thermal sensation in the heat (32.5-36 degrees C) was significantly lower in the hypohydration trial than in the control trial. In addition, laser Doppler flow of the skin and sweat rate were attenuated in the heat in the hypohydration trial. These results may indicate that mild hypohydration after exercise in the heat has no influence on behavioral responses to the heat.

The circadian rhythm of body temperature (T(b)) is a well-known phenomenon. However, it is unknown how the circadian system including the suprachiasmatic nucleus (SCN) and clock genes affects thermoregulation. Food deprivation in mice induces a greater reduction of T(b) particularly in the light phase. We examined the role of Clock, one of key clock genes and the SCN during induced hypothermia. At 20 degrees C with fasting, mice increased their metabolic heat production in the dark phase and maintained T(b), whereas in the light phase, heat production was less, resulting in hypothermia. Under these conditions, neuronal activity in the SCN, assessed by cFos expression, increased only in the light phase. However, such differences in thermoregulatory and neural responses between the phases in Clock mutant mice were less marked. The neural network between the SCN and paraventricular nucleus appeared to be important in hypothermia. These findings suggest that the circadian system per se is influenced by both the feeding condition and environmental temperature and that it modulates thermoregulation.

The circadian rhythm of body temperature (Tb) is a well-known phenomenon. However, it is unknown how the circadian system affects thermoregulation. Food deprivation in mice induces a greater reduction of Tb particularly in the light phase. We examined the role of the clock gene and the suprachiasmatic nucleus (SCN) during induced hypothermia. At 20C with fasting, mice increased their metabolic heat production in the dark phase and maintained T~b~, whereas in the light phase, heat production was less, resulting in hypothermia. Under these conditions, neuronal activity in the SCN, assessed by cFos expression, increased only in the light phase. The differences between the phases in Clock mutant mice were less marked. The neural network between the SCN and paraventricular nucleus appeared to be important in hypothermia. These findings suggest that the circadian system per se is influenced by both the feeding condition and environmental temperature and that it modulates thermoregulation.

Sensations evoked by thermal stimulation (temperature-related sensations) can be divided into two categories, “temperature sensation” and “thermal comfort.” Although several studies have investigated regional differences in temperature sensation, less is known about the sensitivity differences in thermal comfort for the various body regions. In the present study, we examined regional differences in temperature-related sensations with special attention to thermal comfort. Healthy male subjects sitting in an environment of mild heat or cold were locally cooled or warmed with water-perfused stimulators. Areas stimulated were the face, chest, abdomen, and thigh. Temperature sensation and thermal comfort of the stimulated areas were reported by the subjects, as was whole body thermal comfort. During mild heat exposure, facial cooling was most comfortable and facial warming was most uncomfortable. On the other hand, during mild cold exposure, neither warming nor cooling of the face had a major effect. The chest and abdomen had characteristics opposite to those of the face. Local warming of the chest and abdomen did produce a strong comfort sensation during whole body cold exposure. The thermal comfort seen in this study suggests that if given the chance, humans would preferentially cool the head in the heat, and they would maintain the warmth of the trunk areas in the cold. The qualitative differences seen in thermal comfort for the various areas cannot be explained solely by the density or properties of the peripheral thermal receptors and thus must reflect processing mechanisms in the central nervous system.

We investigated the effects of alcohol on thermoregulatory responses and thermal sensations during cold exposure in humans. Eight healthy men (mean age 22.3+/-0.7 year) participated in this study. Experiments were conducted twice for each subject at a room temperature of 18 degrees C. After a 30-min resting period, the subject drank either 15% alcohol at a dose of 0.36 g/kg body weight (alcohol session) or an equal volume of distilled water (control session), and remained in a sitting position for another 60 min. Mean skin temperature continued to decrease and was similar in control and alcohol sessions. Metabolic rate was lower in the alcohol session, but the difference did not affect core temperature, which decreased in a similar manner in both alcohol and control sessions (from 36.9+/-0.1 degrees C to 36.6+/-0.1 degrees C). Whole body sensations of cold and thermal discomfort became successively stronger in the control session, whereas these sensations were both greatly diminished after drinking alcohol. In a previous study we performed in the heat, using a similar protocol, alcohol produced a definite, coordinated effect on all autonomic and sentient heat loss effectors. In the current study in the cold, as compared to responses in the heat, alcohol intake was followed by lesser alterations in autonomic effector responses, but increased changes in sensations of temperature and thermal discomfort. Overall, our results indicate that although alcohol influences thermoregulation in the cold as well as in the heat, detailed aspects of the influence are quite different.

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 mug) 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 degrees C, 35 degrees C, and 40 degrees C every 1 h. The position of a rat in the box and the body core temperature (T(core)) were monitored. A rat could trigger 0 degrees C air for 45 s in the 35 degrees C and 40 degrees 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 degrees C, 24 +/- 2 and 18 +/- 1 at 40 degrees C). T(core) 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 degrees C and 37.4 +/- 0.1 degrees C at 26 degrees C and 36.9 +/- 0.2 degrees C and 37.4 +/- 0.1 degrees C at 40 degrees 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 degrees C, and 17 +/- 1 and 16 +/- 1 at 40 degrees C, respectively). T(core) increased (P < 0.05) in the heat in both trials (36.8 +/- 0.1 degrees C and 37.4 +/- 0.1 degrees C at 26 degrees C and 37.4 +/- 0.2 degrees C and 37.8 +/- 0.2 degrees C at 40 degrees 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.

Homeothermic animals regulate body temperature by autonomic and behavioral thermoeffector responses. The regulation is conducted mainly in the brain. Especially, the preoptic area (PO) in the hypothalamus plays a key role. The PO has abundant warm-sensitive neurons, sending excitatory signals to the brain regions involved in heat loss mechanisms, and inhibitory signals to those involved in heat production mechanisms. The sympathetic fibers determine tail blood flow in rats, which is an effective heat loss process. Some areas in the midbrain and medulla are involved in the control of tail blood flow. Recent study also showed that the hypothalamus is involved in heat escape behavior in rats. However, our knowledge about behavioral regulation is limited. The central mechanism for thermal comfort and discomfort, which induce various behavioral responses, should be clarified. In the heat, dehydration affects both autonomic and behavioral thermoregulation by non-thermoregulatory factors such as high Na+ concentration. The PO seems to be closely involved in these responses. The knowledge about the central mechanisms involved in thermoregulation is important to improve industrial health, e.g. preventing accidents associated with the heat or organizing more comfortable working environment.

We report a new system for monitoring sensations of many body parts as well as comprehensively showing the distribution of overall skin temperature (T(sk)) and temperature-related sensations. The system consists of a console with 52 levers to report temperature-related sensations and software that facilitates the visualization of the distribution of T(sk) and temperature-related sensations by displaying them on a model of the human body. The system's utility was demonstrated with a physiological experiment involving three males and three females. They were exposed to step changes of ambient temperature from 23 degrees C to 33 degrees C. We measured T(sk) at 50 points, and the subjects concurrently provided estimates of local temperature sensation and thermal comfort/discomfort at 25 loci. This system greatly facilitates the perception and analysis of spatial relationships and differences in temperature and sensation in various areas of the body.

Sensations evoked by innocuous thermal stimulation can be divided into two categories. One is “temperature sensation” in a narrow sense, which is directed towards an object outside the body. The other is the “thermal comfort/discomfort” of the body that is important for thermoregulation. We recently reported rCBF changes in the amygdala which correlated with thermal comfort during whole body cooling (Kanosue et al., 2000). In the present study we investigated the region of brain that is activated by local thermal stimulation of the hand. Eight healthy subjects were recruited and gave written informed consent to participate in the study. Warm (39°C) or cold (25°C) stimuli was applied to the right or left hand for 30 s by using a water circulating tube that covered the whole hand. Each subject reported the magnitude of the stimulus intensity of temperature sensation using a scale from 1 (very cold) to 9 (very hot). All subjects reported hot or cold sensations and not pain. We examined the correlation between the rating scores and regional activity over the entire brain with a 3 Tesla MR imagers (VP, General Electrics, Milwaukee, US). Activation was observed in the contralateral secondary somatosensory cortex in response to both warm and cold stimulation of the hand. No activation was observed in the amygdala. This suggests that temperature sensation and thermal comfort might be generated by completely different structures of the brain.

In homeothermic animals, body core temperature (Tcore) is regulated by both autonomic and behavioural processes. However, it is well known that during a heat exposure in dehydrated animals both processes are modulated by an increase in plasma solute concentration, e.g. Na+, and/or a decrease in blood volume. The two factors attenuate both evaporative and non-evaporative heat loss mechanisms, e.g. saliva secretion and tail blood flow in rats, and panting and skin blood flow in dogs (Baker & Doris, 1982; Horowitz & Nadel, 1984; Baker & Dawson, 1985; Horowitz & Meiri, 1985; Nakajima et al. 1998). This attenuation of heat loss mechanisms would be important in preserving body fluid and preventing an excessive blood distribution to the periphery; however animals may lose their body temperature homeostasis. In contrast, it was reported that operant heat-escape/cold-seeking behaviour increased after subcutaneous (S.C.) hypertonic-saline injection in rats (Nagashima et al. 2001; Konishi et al. 2002) and pigeons (Brummermann & Rautenberg, 1989). These results may indicate that behavioural thermoregulatory processes are activated by an increase in plasma solutes, i.e. elevation of plasma osmolality and/or Na+ concentration, compensating the attenuation of the autonomic heat loss mechanisms. Dehydration has been reported to decrease the resting metabolic rate (MR) in rats (Horowitz & Samueloff, 1989) and camels (Schroter et al. 1987). We also reported that, in rats, Tcore decreased by 0.9 °C after S.C. hypertonic-saline injection in a thermoneutral condition at 26 °C (Nagashima et al. 2001; Konishi et al. 2002). These responses may prevent Tcore from reaching a critical level in a hot environment. However, animals also become dehydrated in a cold environment due to cold-induced diuresis, blunted thirst, increased respiratory water loss, or low availability of food and water (Fregly, 1982; Allen & Gellai, 1993). Therefore, the reductions of MR and Tcore might be critical for animals during a cold exposure. However, it remains uncertain whether dehydration and/or salt loading (systemic hypertonic-saline injection) also have influences on autonomic and behavioural thermoregulatory responses to the cold. In the present study, we evaluated the effects of S.C. hypertonic-saline injection on metabolic heat production and cold-escape/warm-seeking behaviour during consecutive 20 and 10 °C cold exposure in rats. The behavioural response was assessed using the operant behaviour system that our laboratory has previously reported (Chen et al. 1998). We hypothesized that, after the hypertonic-saline injection, (1) MR during the cold exposure would be attenuated; and (2) Tcore would decrease; however (3) when the operant cold-escape/warm-seeking behaviour was available, the rats would be able to maintain Tcore by increasing the behaviour.

To investigate the mechanism involved in the reduction of body core temperature (Tcore) during fasting in rats, which is selective in the light phase, we measured Tcore, surface temperature, and oxygen consumption rate in fed control animals and in fasted animals on day 3 of fasting and day 4 of recovery at an ambient temperature (Ta) of 23°C by biotelemetry, infrared thermography, and indirect calorimetry, respectively. On the fasting day, 1) Tcore in the light phase decreased ( P < 0.05) from the control; however, Tcore in the dark phase was unchanged, 2) tail temperature fell from the control ( P < 0.05, from 30.7 ± 0.1 to 23.9 ± 0.1°C in the dark phase and from 29.4 ± 0.1 to 25.2 ± 0.2°C in the light phase), 3) oxygen consumption rate decreased from the control ( P < 0.05, from 24.37 ± 1.06 to 16.24 ± 0.69 ml · min−1 · kg body wt−0.75 in the dark phase and from 18.91 ± 0.64 to 14.00 ± 0.41 ml · min−1 · kg body wt−0.75 in the light phase). All these values returned to the control levels on the recovery day. The results suggest that, in the fasting condition, Tcore in the dark phase was maintained by suppression of the heat loss mechanism, despite the reduction of metabolic heat production. In contrast, the response was weakened in the light phase, decreasing Tcore greatly. Moreover, the change in the regulation of tail blood flow was a likely mechanism to suppress heat loss.

The preoptic area (POA) occupies a crucial position among the structures participating in thermoregulation, but we know little about its efferent projections for controlling various effector responses. In this study, we used an immunohistochemical analysis of Fos expression during local warming of the preoptic area. To avoid the effects of anesthesia or stress, which are known to elicit Fos induction in various brain regions, we used a novel thermode specifically designed for chronic warming of discrete brain structures in freely moving rats. At an ambient temperature of 22 degrees C, local POA warming increased Fos immunoreactivity in the supraoptic nucleus (SON) and the periaqueductal gray matter (PAG). Exposure of animals to an ambient temperature of 5 degrees C induced Fos immunoreactivity in the magnocellular paraventricular nucleus (mPVN) and the dorsomedial region of the hypothalamus (DMH). Concurrent warming of the POA suppressed Fos expression in these areas. These findings suggest that thermal information from the preoptic area sends excitatory signals to the SON and the PAG, and inhibitory signals to the mPVN and the DMH.

We tested the hypothesis that renal tubular Na+ reabsorption increased during the first 24 h of exercise-induced plasma volume expansion. Renal function was assessed 1 day after no-exercise control (C) or intermittent cycle ergometer exercise (Ex, 85% of peak O2 uptake) for 2 h before and 3 h after saline loading (12.5 ml/kg over 30 min) in seven subjects. Ex reduced renal blood flow ( p-aminohippurate clearance) compared with C (0.83 ± 0.12 vs. 1.49 ± 0.24 l/min, P < 0.05) but did not influence glomerular filtration rates (97 ± 10 ml/min, inulin clearance). Fractional tubular reabsorption of Na+ in the proximal tubules was higher in Ex than in C ( P < 0.05). Saline loading decreased fractional tubular reabsorption of Na+ from 99.1 ± 0.1 to 98.7 ± 0.1% ( P < 0.05) in C but not in Ex (99.3 ± 0.1 to 99.4 ± 0.1%). Saline loading reduced plasma renin activity and plasma arginine vasopressin levels in C and Ex, although the magnitude of decrease was greater in C ( P < 0.05). These results indicate that, during the acute phase of exercise-induced plasma volume expansion, increased tubular Na+ reabsorption is directed primarily to the proximal tubules and is associated with a decrease in renal blood flow. In addition, saline infusion caused a smaller reduction in fluid-regulating hormones in Ex. The attenuated volume-regulatory response acts to preserve distal tubular Na+ reabsorption during saline infusion 24 h after exercise.

We examined the effect of hypertonic saline injection on heat-escape/cold-seeking behavior in desalivated rats. Rats were exposed to 40°C heat after normal (154 mM NaCl, control) or hypertonic saline (2,500 mM NaCl) injection (1 ml/100 g body wt). The rats received a 0°C air for 30 s when they entered a specific area in an experimental box. Core temperature (Tc) surpassed 40°C in both conditions when 0°C air was not available. Hypertonic saline injection produced a lower baseline Tcthan control [36.9 ± 0.2 and 37.9 ± 0.2°C (means ± SE), P < 0.05] and a greater number of 0°C air rewards during the 2-h heat with lower Tc at the end (48 ± 1 and 34 ± 2, 37.6 ± 0.1, and 37.3 ± 0.1°C in the control and hypertonic saline injection trial, respectively, P < 0.05, n = 6). However, Tc was similar (37.7 ± 0.2 and 37.6 ± 0.4°C in the control and hypertonic saline injection trial, n = 5) when 0°C air was automatically and intermittently (35 times) given during the heat. Rats augment heat-defense mechanisms in response to osmotic stress by lowering the baseline Tc and increasing heat-escape/cold-seeking behavior.

The body temperature of homeothermic animals is regulated by systems that utilize multiple behavioral and autonomic effector responses. In the last few years, new approaches have brought us new information and new ideas about neuronal interconnections in the thermoregulatory network. Studies utilizing chemical stimulation of the preoptic area revealed both heat loss and production responses are controlled by warm-sensitive neurons. These neurons send excitatory efferent signals for the heat loss and inhibitory efferent signals for the heat production. The warm-sensitive neurons are separated and work independently to control these two opposing responses. Recent electrophysiological analysis have identified some neurons sending axons directly to the spinal cord for thermoregulatory effector control. Included are midbrain reticulospinal neurons for shivering and premotor neurons in the medulla oblongata for skin vasomotor control. As for the afferent side of the thermoregulatory network, the vagus nerve is recently paid much attention, which would convey signals for peripheral infection to the brain and be responsible for the induction of fever. The vagus nerve may also participate in thermoregulation in afebrile conditions, because some substances such as cholecyctokinin and leptin activate the vagus nerve. Although the functional role for this response is still obscure, the vagus may transfer nutritional and/or metabolic signals to the brain, affecting metabolism and body temperature.

The body temperature of homeothermic animals is regulated by systems that utilize multiple behavioral and autonomic effector responses. The thermoreceptors that provide inputs to the regulatory systems are distributed throughout the body. Although the regulatory aspects of this multiple input-output system are largely nervous, knowledge about the “neuronal circuit” for thermoregulation remained rather stagnant for several decades. However, the last few years have brought new approaches that have led to new information and new ideas about neuronal interconnections in the thermoregulatory network. This advance is especially true for efferent pathways from the preoptic area (PO). Recent studies utilizing chemical stimulation of the PO have revealed that not only heat loss but also heat production responses are controlled by PO warm-sensitive neurons. These neurons send excitatory efferent signals for heat loss and inhibitory efferent signals for heat production. The warm-sensitive neurons that control these two opposing responses are different and work independently. Recent electrophysiological analysis identified some neurons sending axons directly to the spinal cord for the control of thermoregulatory effectors. Included are midbrain reticulospinal neurons for shivering and premotor neurons in the medullary raphe nuclei for skin vasomotor control. Even though many neurons in the efferent pathways remain unidentified, recent advances in experimental techniques promise a much more detailed understanding of the neuronal circuit underlying thermoregulation in the near future.

To elucidate the role of increased plasma osmolality (Posmol), which occurs during exercise in the regulation of cutaneous vasodilation (CVD) during exercise, we determined the relationship between the change in esophageal temperature (ΔTes) required to elicit CVD (ΔTes threshold for CVD) and Posmol during light and moderate exercise (30 and 55% of peak oxygen consumption, respectively) and passive body heating. Then we compared the relationship with the data obtained in our previous study [A. Takamata, K. Nagashima, H. Nose, and T. Morimoto. Am. J. Physiol. 273 ( Regulatory Integrative Comp. Physiol.42): R197–R204, 1997], in which we determined the relationships during passive body heating following isotonic (0.9% NaCl) or hypertonic (2 or 3% NaCl) saline infusions in the same subjects. Posmol values at 5 min after the onset of exercise were 287.5 ± 0.9 mosmol/kgH2O during light exercise and 293.0 ± 1.2 mosmol/kgH2O during moderate exercise. Posmol just before passive body heating was 289.9 ± 1.4 mosmol/kgH2O. The ΔTes threshold for CVD was 0.09 ± 0.05°C during light exercise, 0.31 ± 0.09°C during moderate exercise, and 0.10 ± 0.05°C during passive body heating. The relationship between the ΔTes threshold for CVD and Posmol was shown to be on the same regression line both during exercise and during passive body heating with or without infusions [A. Takamata, K. Nagashima, H. Nose, and T. Morimoto. Am. J. Physiol. 273 ( Regulatory Integrative Comp. Physiol.42): R197–R204, 1997]. Our data suggest that the elevated body core temperature threshold for CVD during exercise could be the result of increased Posmol induced by exercise and is not due to reduced plasma volume or the intensity of the exercise itself.

The impact of posture on the immediate recovery of intravascular fluid and protein after intense exercise was determined in 14 volunteers. Forces which govern fluid and protein movement in muscle interstitial fluid pressure (PISF), interstitial colloid osmotic pressure (COPi), and plasma colloid osmotic pressure (COPp) were measured before and after exercise in the supine or upright position. During exercise, plasma volume (PV) decreased by 5.7 ± 0.7 and 7.0 ± 0.5 ml/kg body weight in the supine and upright posture, respectively. During recovery, PV returned to its baseline value within 30 min regardless of posture. PV fell below this level by 60 and 120 min in the supine and upright posture, respectively ( P < 0.05). Maintenance of PV in the upright position was associated with a decrease in systolic blood pressure, an increase in COPp (from 25 ± 1 to 27 ± 1 mmHg; P < 0.05), and an increase in PISF (from 5 ± 1 to 6 ± 2 mmHg), whereas COPi was unchanged. Increased PISFindicates that the hydrostatic pressure gradient favors fluid movement into the vascular space. However, retention of the recaptured fluid in the plasma is promoted only in the upright posture because of increased COPp.