Effects of cold and capsaicin desensitization on prostaglandin E hypothermia in rats

Intraperitoneal injection of prostaglandin E1 (PGE) produces a transient hypothermia in rats that lasts 1-2 h. Rats exposed to an ambient temperature (Ta) of 26 degrees C displayed a decrease in rectal temperature (Tre) of 0.95 +/- 0.12 degrees C (SE) after injection with PGE (100 micrograms/kg ip). Hypothermia was produced mainly by heat losses, as indicated by increases in tail blood flow. At Ta of 4 degrees C, PGE produced a comparable fall in Tre of 1.00 +/- 0.14 degrees C. However, in the cold the hypothermia was caused solely by decreases in heat production. These results indicate that the PGE-induced hypothermia is not the result of a peripheral vasodilation induced by the direct action of PGE on the tail vascular smooth muscle but is a central nervous system-mediated response of the thermoregulatory system induced by PGE within the peritoneal cavity. Capsaicin injected subcutaneously induces a transient hypothermia in rats because of stimulation of the warm receptors. If administered peripherally in sufficient amounts, it is reputed to impair peripheral warm receptors so that they become desensitized to the hypothermic effects of capsaicin. We measured PGE-induced hypothermias in rats both before and after capsaicin desensitization at Ta of 26 degrees C. Before desensitization the hypothermia was -1.14 +/- 0.12 degrees C, whereas after capsaicin treatment the PGE-induced hypothermia was -0.34 +/- 0.17 degrees C. The biological effects of capsaicin are diverse; however, based on current thinking about the thermoregulatory effects of capsaicin desensitization, our results indicate that peripheral warm receptor pathways are in some manner implicated in the hypothermia induced by intraperitoneal PGE.     

Heat debt as an index for cold adaptation in men

Several types of cold adaptation in men have been described in the literature (metabolic, insulative, hypothermic). The aim of this study is to show that the decrease of heat debt can be considered as a new index for cold adaptation. Ten male subjects were acclimated by water immersions (temperature 10-15 degrees C, 4 immersions/wk over 2 mo). Thermoregulatory responses before and after acclimation were tested by a standard cold test in a climatic chamber for 2 h at rest [dry bulb temperature (Tdb): 10 degrees C; relative humidity (rh): 25%]. After adaptation, four thermoregulatory modifications were observed: an increase in the delay for the onset of shivering (32.7 +/- 7.99 instead of 14.1 +/- 5.25 min); a decrease of body temperature levels for the onset of shivering [rectal temperature (Tre): 37.06 +/- 0.08 instead of 37.31 +/- 0.06 degrees C; mean skin temperature (Tsk): 24.83 +/- 0.56 instead of 26.86 +/- 0.46 degrees C; mean body temperature (Tb): 33.03 +/- 0.20 instead of 34.16 +/- 0.37 degrees C); a lower level of body temperatures in thermoneutrality (Tre = 37.16 +/- 0.08 instead of 37.39 +/- 0.06 degrees C; Tsk = 31.29 +/- 0.21 instead of 32.01 +/- 0.22 degrees C; Tb = 35.92 +/- 0.08 instead of 36.22 +/- 0.05 degrees C); a decrease of heat debt calculated from the difference between heat gains and heat losses (5.66 +/- 0.08 instead of 8.33 +/- 0.38 kJ/kg). The different types of cold adaptation observed are related to the physical characteristics of the subjects (percent body fat content) and the level of physical fitness (VO2max).(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of skeletal muscle glycogen on passive rewarming after hypothermia

To examine the influence of muscle glycogen on the thermal responses to passive rewarming subsequent to mild hypothermia, eight subjects completed two cold-water immersions (18 degrees C), followed by 75 min of passive rewarming (24 degrees C air, resting in blanket). The experiments followed several days of different exercise-diet regimens eliciting either low (LMG; 141.0 +/- 10.5 mmol.kg.dry wt-1) or normal (NMG; 526.2 +/- 44.2 mmol.kg.dry wt-1) prewarming muscle glycogen levels. Cold-water immersion was performed for 180 min or to a rectal temperature (Tre) of 35.5 degrees C. In four subjects (group A, body fat = 20 +/- 1%), postimmersion Tre was similar to preimmersion Tre for both trials (36.73 +/- 0.18 vs. 37.26 +/- 0.18 degrees C, respectively). Passive rewarming in group A resulted in an increase in Tre of only 0.13 +/- 0.08 degrees C. Conversely, initial rewarming Tre for the other four subjects (group B, body fat = 12 +/- 1%) averaged 35.50 +/- 0.05 degrees C for both trials. Rewarming increased Tre similarly in group B during both LMG (0.76 +/- 0.25 degrees C) and NMG (0.89 +/- 0.13 degrees C). Afterdrop responses, evident only in those individuals whose body core cooled during immersion (group B), were not different between LMG and NMG. These data support the contention that Tre responses during passive rewarming are related to body insulation. Furthermore these results indicate that low muscle glycogen levels do not impair rewarming time nor alter after-drop responses during passive rewarming after mild-to-moderate hypothermia.     

Radio frequency (13.56 MHz) energy enhances recovery from mild hypothermia

The rate of warming after hypothermia depends on the method of rewarming. This study compared the effectiveness of radio frequency (RF) energy against hot (41 degrees C) water immersion (HW) and an insulated cocoon (IC) for rewarming hypothermic men. Six men fasted overnight and were rewarmed for 1 h after attaining a 0.5 degree C reduction in rectal temperature (Tre). Tre and esophageal (Tes) temperature were recorded every 5 min with nonmetallic thermal probes. The base-line value for Tre and Tes just before rewarming was subtracted from each 5 min Tre and Tes during rewarming to give delta Tre and delta Tes. The 12 delta Tes values were averaged for each individual and were compared using analysis of variance. The average delta Tes for RF (1.15 +/- 0.22 degrees C/h) was faster (P less than 0.001) than either IC (0.37 +/- 0.16 degrees C/h) or HW (0.18 +/- 0.09 degree C/h). The present study shows the superiority of RF energy for rewarming mildly hypothermic men.     

Changes in thermal insulation during underwater exercise in Korean female wet-suit divers

The present work was undertaken to examine the effect of wet suits on the pattern of heat exchange during immersion in cold water. Four Korean women divers wearing wet suits were immersed to the neck in water of critical temperature (Tcw) while resting for 3 h or exercising (2-3 met on a bicycle ergometer) for 2 h. During immersion both rectal (Tre) and skin temperatures and O2 consumption (VO2) were measured, from which heat production (M = 4.83 VO2), skin heat loss (Hsk = 0.92 M +/- heat store change based on delta Tre), and thermal insulation were calculated. The average Tcw of the subjects with wet suits was 16.5 +/- 1.2 degrees C (SE), which was 12.3 degrees C lower than that of the same subjects with swim suits (28.8 +/- 0.4 degrees C). During the 3rd h of immersion, Tre and mean skin temperatures (Tsk) averaged 37.3 +/- 0.1 and 28.0 +/- 0.5 degrees C, and skin heat loss per unit surface area 42.3 +/- 2.66 kcal X m-2 X h. The calculated body insulation [Ibody = Tre - Tsk/Hsk] and the total shell insulation [Itotal = (Tre - TW)/Hsk] were 0.23 +/- 0.02 and 0.5 +/- 0.04 degrees C X kcal-1 X m2 X h, respectively. During immersion exercise, both Itotal and Ibody declined exponentially as the exercise intensity increased. Surprisingly, the insulation due to wet suit (Isuit = Itotal - Ibody) also decreased with exercise intensity, from 0.28 degrees C X kcal-1 X m2 X h at rest to 0.12 degrees C X kcal-1 X m2 X h at exercise levels of 2-3 met.(ABSTRACT TRUNCATED AT 250 WORDS)     

A second postcooling afterdrop: more evidence for a convective mechanism.

An attempt was made to demonstrate the importance of increased perfusion of cold tissue in core temperature afterdrop. Five male subjects were cooled twice in water (8 degrees C) for 53-80 min. They were then rewarmed by one of two methods (shivering thermogenesis or treadmill exercise) for another 40-65 min, after which they entered a warm bath (40 degrees C). Esophageal temperature (Tes) as well as thigh and calf muscle temperatures at three depths (1.5, 3.0, and 4.5 cm) were measured. Cold water immersion was terminated at Tes varying between 33.0 and 34.5 degrees C. For each subject this temperature was similar in both trials. The initial core temperature afterdrop was 58% greater during exercise (mean +/- SE, 0.65 +/- 0.10 degrees C) than shivering (0.41 +/- 0.06 degrees C) (P < 0.005). Within the first 5 min after subjects entered the warm bath the initial rate of rewarming (previously established during shivering or exercise, approximately 0.07 degrees C/min) decreased. The attenuation was 0.088 +/- 0.03 degrees C/min (P < 0.025) after shivering and 0.062 +/- 0.022 degrees C/min (P < 0.025) after exercise. In 4 of 10 trials (2 after shivering and 2 after exercise) a second afterdrop occurred during this period. We suggest that increased perfusion of cold tissue is one probable mechanism responsible for attenuation or reversal of the initial rewarming rate. These results have important implications for treatment of hypothermia victims, even when treatment commences long after removal from cold water.     

Effect of thermal history on the rat's response to varying environmental temperature

After acclimating individually housed male rats to temperatures of either 24.5 +/- 0.1 or 29.2 +/- 0.1 degrees C for 14 days, randomly paired animals from each group were acutely exposed (3 h) in series to experimental temperatures between 18.0 and 34.5 degrees C in a controlled environment room. Relative humidity of 50 +/- 0.3% and a 12-h light-dark photoperiod (light from 0900 to 2100 h) were maintained. Metabolic rate (MR) and evaporative water loss (EWL) were-measured using an open-flow system; thermistors were used to measure the rectal (Tre) and tail skin (Tts) temperatures. MR was relatively constant over a temperature range of 22.2 to 27.0 degrees C for rats acclimated to 24.5 degrees C and 20.0 to 29.2 degrees C for rats acclimated to 29.2 degrees C. Above and below these ranges, MR for both groups was significantly (P less than 0.05) elevated. At their respective acclimation temperatures, the absolute Tre and Tts of 29.2 degrees C rats were maintained at an elevated level compared with 24.5 degrees C rats. Although EWL for both groups was relatively constant between 18.0 and 27.0 degrees C, 24.5 degrees C rats displayed higher EWL changes at most environmental temperatures above 27.0 degrees C. At 34.5 degrees C, 29.2 degrees C rats dissipated 26% more metabolic heat by evaporation compared with 24.5 degrees C rats. These data suggest that acclimation temperatures of rats affected the thermoneutral zone and alter the set-point temperature around which thermal responses are regulated.     

Comparison of thermal responses between rest and leg exercise in water

This study examined both the thermal and metabolic responses of individuals in cool (30 degrees C, n = 9) and cold (18 degrees C, n = 7; 20 degrees C, n = 2) water. Male volunteers were immersed up to the neck for 1 h during both seated rest (R) and leg exercise (LE). In 30 degrees C water, metabolic rate (M) remained unchanged over time during both R (115 W, 60 min) and LE (528 W, 60 min). Mean skin temperature (Tsk) declined (P less than 0.05) over 1 h during R, while Tsk was unchanged during LE. Rectal (Tre) and esophageal (Tes) temperatures decreased (P less than 0.05) during R (delta Tre, -0.5 degrees C; delta Tes, -0.3 degrees C) and increased (P less than 0.05) during LE (delta Tre, 0.4 degrees C; Tsk, 0.4 degrees C). M, Tsk, Tre, and Tes were higher (P less than 0.05) during LE compared with R. In cool water, all regional heat flows (leg, chest, and arm) were generally greater (P less than 0.05) during LE than R. In cold water, M increased (P less than 0.05) over 1 h during R but remained unchanged during LE. Tre decreased (P less than 0.05) during R (delta Tre, -0.8 degrees C) but was unchanged during LE. Tes declined (P less than 0.05) during R (delta Tes, -0.4 degrees C) but increased (P less than 0.05) during LE (delta Tes, 0.2 degrees C). M, Tre, and Tes were higher (P less than 0.05), whereas Tsk was not different during LE compared with R at 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Development of deep hypothermia in rats with limited motor activity

Changes of the main organism functions (breathing frequency, heart rate and shivering) were investigated under hypothermia in two groups of rats. Animals of the first group were fixed rigidly on the special platform with fixing of head and limbs, and those of the second one--the rats, were placed in a punched cylindrical chamber, inside which they could move freely forward and back. In 2.5-3.0 hours after anaesthesia the rats were placed in a refrigerator (-5 degrees C) until they stop breathing. Cessation of breathing of the first group rats occurred in 1.7 +/- 0.3 hours from the beginning of cooling at body temperature 17.3 +/- 0.6 degrees C and the brain temperature 15.7 +/- 0.5 degrees C. In the second group, a prolonged activation of the frequency of breathing, heart rate and intensity of electrical activity of muscles during 2.5-3.0 hours, was observed. Only in 4.5-5.0 hours, the breathing stopped at rectal temperature 12.3 +/- 1.1 degrees C and the brain temperature 12.9 +/- 0.9 degrees C. In these animals, the time of survival in the cold environment increased considerably and the temperature thresholds of the termination of breathing were lowered. Thus, the activation in the thermo-regulative muscle tone and in shivering muscles provides the most effective resistance against cooling of rats, reducing a surface of heat, dissipation and keeping the temperature of internal areas of body.     

Shivering and cardiorespiratory responses during normocapnic hypoxia in the pigeon

To study the inhibitory effect of hypoxia on the cold defense mechanism, pigeons were exposed at low ambient temperature (5 degrees C) to various inhaled gas mixtures: normoxia [0.21 fractional concentration of O2 (FIO2)], hypoxia (0.07 FIO2), and normocapnic hypoxia (0.07 FIO2 + 0.045 FICO2). Electromyographic (EMG) activity indicative of shivering thermogenesis was inhibited during hypoxia, and body temperature (Tre) fell by 0.09 degrees C/min. Respiratory frequency (f) and minute ventilation (VE) increased by 143 and 135%, respectively, compared with normoxia, but tidal volume (VT) was not changed. PO2, PCO2, and O2 contents in the arterial and mixed venous blood were decreased and pH was enhanced. During normocapnic hypoxia, shivering EMG was present at approximately 50% of the normoxic intensity; Tre fell by only 0.04 degrees C/min. Arterial and mixed venous PCO2 and pH were the same as during normoxia, but VE increased by 430% because of twofold increases in both f and VT. During normocapnic hypoxia, arterial PO2 and O2 content were higher than during hypoxia alone. We conclude that the persistence of shivering during normocapnic hypoxia is due to maintenance of critical levels of arterial PO2 and O2 content.     

Inhibition of shivering in hypothermic seals during diving

The mammalian response to hypothermia is increased metabolic heat production, usually by way of muscular activity, such as shivering. Seals, however, have been reported to respond to diving with hypothermia, which in other mammals under other circumstances would have elicited vigorous shivering. In the diving situation, shivering could be counterproductive, because it obviously would increase oxygen consumption and therefore reduce diving capacity. We have measured the electromyographic (EMG) activity of three different muscles and the rectal and brain temperature of hooded seals (Cystophora cristata) while they were exposed to low ambient temperatures in a climatic chamber and while they performed a series of experimental dives in cold water. In air, the seals had a normal mammalian shivering response to cold. Muscles were recruited in a sequential manner until body temperature stopped dropping. Shivering was initiated when rectal temperature fell below 35.3 +/- 0.6 degrees C (n = 6). In the hypothermic diving seal, however, the EMG activity in all of the muscles that had been shivering vigorously before submergence was much reduced, or stopped altogether, whereas it increased again upon emergence but was again reduced if diving was repeated. We conclude that shivering is inhibited during diving to allow a decrease in body temperature whereby oxygen consumption is decreased and diving capacity is extended.     

Thermoregulatory model for immersion of humans in cold water

The mathematical models of thermoregulation of Stolwijk and Hardy, and Montgomery were used to develop a model suitable for the simulation of human physiological responses to cold-water immersion. Data were obtained from experiments where 13 healthy male volunteers were totally immersed under resting and nude conditions for 1 h in water temperatures of 20 and 28 degrees C. At these temperatures, the mean measured rectal temperature (Tre) fell by approximately 0.9 and 0.5 degrees C, respectively, yet mean measured metabolic rate (M) rose by approximately 275 and 90 W for the low body fat group (n = 7) and 195 and 45 W for the moderate body fat group (n = 6). To predict the observed Tre and M values, the present model 1) included thermal inputs for shivering from the skin independent of their inclusion with the central temperature to account for the observed initial rapid rise in M, 2) determined a thermally neutral body temperature profile such that the measured and predicted initial values of Tre and M were matched, 3) confined the initial shivering to the trunk region to avoid an overly large predicted initial rate of rectal cooling, and 4) calculated the steady-state convective heat loss by assuming a zero heat storage in the skin compartment to circumvent the acute sensitivity to the small skin-water temperature difference when using conventional methods. The last three modifications are unique to thermoregulatory modeling.     

Effects of restraint stress on catecholamine concentrations in the glandular stomach of rats

Restraint stress is known to induce gastric ulcers in rats. Peripheral sympathetic activity and catecholamines are involved in the pathogenesis of these gastric ulcers. The aim of the present study was to evaluate the effects of restraint on mucosal and muscle catecholamine concentrations in the glandular stomach of rats. In unrestrained rats, noradrenaline concentration was higher in the muscle than in the mucosa of the glandular stomach (629 +/- 106 vs 18 +/- 3 pg/mg and 217 +/- 37 vs 18 +/- 8 pg/mg, respectively in the corpus and the antrum, p less than 0.01). This can be explained by the existence of an abundant noradrenergic innervation in the muscle layer. After 20 hours of restraint, adrenaline and noradrenaline concentrations were significantly decreased in adrenals, in comparison with unrestrained animals (255 +/- 53 vs 638 +/- 160 ng/mg and 113 +/- 17 vs 198 +/- 37 ng/mg, respectively for adrenaline and noradrenaline, p less than 0.05). In the glandular stomach, noradrenaline and adrenaline concentrations in restrained rats were not significantly different from those in unrestrained rats. However, adrenaline concentrations in the muscle of restrained rats were higher than in the mucosa. Moreover, restraint induced a significant decrease in dopamine concentration in the antral mucosa (from 100 +/- 12 pg/mg in unrestrained rats to 15 +/- 5 pg/mg in restrained rats), suggesting that a depletion in dopamine in the antral mucosa could be one of the pathogenetic factors involved in antral gastric stress-induced ulcers in rats.     

Muscle glycogen utilization during shivering thermogenesis in humans

The purpose of the present study was to clarify the importance of skeletal muscle glycogen as a fuel for shivering thermogenesis in humans during cold-water immersion. Fourteen seminude subjects were immersed to the shoulders in 18 degrees C water for 90 min or until rectal temperature (Tre) decreased to 35.5 degrees C. Biopsies from the vastus lateralis muscle and venous blood samples were obtained before and immediately after the immersion. Metabolic rate increased during the immersion to 3.5 +/- 0.3 (SE) times resting values, whereas Tre decreased by 0.9 degrees C to approximately 35.8 degrees C at the end of the immersion. Intramuscular glycogen concentration in the vastus lateralis decreased from 410 +/- 15 to 332 +/- 18 mmol glucose/kg dry muscle, with each subject showing a decrease (P less than 0.001). Plasma volume decreased (P less than 0.001) markedly during the immersion (-24 +/- 1%). After correcting for this decrease, blood lactate and plasma glycerol levels increased by 60 (P less than 0.05) and 38% (P less than 0.01), respectively, whereas plasma glucose levels were reduced by 20% after the immersion (P less than 0.001). The mean expiratory exchange ratio showed a biphasic pattern, increasing initially during the first 30 min of the immersion from 0.80 +/- 0.06 to 0.85 +/- 0.05 (P less than 0.01) and decreasing thereafter toward basal values. The results demonstrate clearly that intramuscular glycogen reserves are used as a metabolic substrate to fuel intensive thermogenic shivering activity of human skeletal muscle.     

Effect of locomotor respiratory coupling on respiratory evaporative heat loss in the sheep.

During galloping, many animals display 1:1 coupling of breaths and strides. Locomotor respiratory coupling (LRC) may limit respiratory evaporative heat loss (REHL) by constraining respiratory frequency (f). Five sheep were exercised twice each, according to a five-step protocol: 5 min at the walk, 5 min at the trot (trot1), 10 min at the gallop, 5 min at the trot (trot2), and 5 min at the walk. Rectal temperature (T(re)), stride frequency, f, REHL, and arterial CO(2) tension and pH were measured at each step. Tidal volume (VT) was calculated. LRC was observed only during galloping. The coupling ratio remained at 1:1 while VT increased continuously during galloping, causing REHL to increase from 2.9 +/- 0.2 (SE) W/kg at the end of trot1 to a peak of 5.3 +/- 0.3 W/kg. T(re) rose from 39.0 +/- 0.1 degrees C preexercise to 40.2 +/- 0.2 degrees C at the end of galloping. At the gallop-trot2 transition, VT fell and f rose, despite a continued rise in T(re). Arterial CO(2) tension fell from 36.5 +/- 1.1 Torr preexercise to 31.8 +/- 1.4 Torr by the end of trot1 and then further to 21.5 +/- 1.2 Torr by the end of galloping, resulting in alkalosis. In conclusion, LRC did not prevent increases in REHL in sheep because VT increased. The increased VT caused hypocapnia and presumably elevated the cost of breathing.     

Development of hypothermia in rats at increase of [Ca2+] in the blood

In rats, data on influence of i. v. administration of calcium chloride on the level of [Ca2+] in the blood and on process of oppression ofthermoregulatory and respiratory functions in rats in hypothermia. 0.18 or 0.135 mmol Ca2+ on the 3rd minute from beginning of the administration increased [Ca2+] in the blood from 1.01 +/- 0.03 to 2.56 +/- 0.08 mM (or 2.27 +/- 0.06 mM). Then [Ca2+] was reduced gradually, in 20 minutes from administration, solution of CaCh [Ca2+] exceeded the initial level by 20-30 %. The increase of concentration of ionized calcium in the rat blood strengthened the cold oppression of breathing and cold shivering as compared with the control (administration of physiological solution). Arrest of breathing in rats after administration of CaCl2 solution occurred at higher rectal temperatures (21 +/- 0.03 degrees C) as compared with control experiments (18 +/- 0.4 degrees C), p < 0.05. It is suggested that increase of [Ca2+] in the blood strengthens effects of cold in the form of oppression of thermoregulatory and respiratory functions.     

Glucose, glycogen, and insulin responses in the hypothermic rat

The rat appears to be unable to utilize glucose during hypothermia. The objective of this study was to examine carbohydrate homeostasis during induction, hypothermia, and rewarming phases. Groups of normothermic animals were euthanized to serve as time controls for comparison. Hypothermia (15 degrees C) was produced by exposure to helox (80% helium:20% oxygen) at 0 +/- 1 degree C. Hyperglycemia was noted during the induction process (169 +/- 8 in control vs 326 +/- 49 mg/dl). Serum glucose increased further during 4 hr of hypothermia, but following rewarming (Tre of 33 +/- 1 degrees C) was reduced (153 +/- 16 mg/dl) significantly (P less than 0.05). Serum insulin was depressed during hypothermic induction (from 48 +/- 4 in controls to 19 +/- 3 microU/ml in hypothermic rats) and increased only slightly during the arousal process, remaining significantly lower than in normothermic subjects. Initial hepatic, skeletal muscle, and cardiac glycogen concentrations were reduced 34, 68, and 75%, respectively, during hypothermic induction. While liver glycogen decreased further during 4 hr of hypothermia, skeletal and cardiac stores increased markedly. During rewarming, hepatic glycogen was markedly decreased, while skeletal and cardiac stores were maintained. These data suggest that hyperglycemia in the hypothermic rat can be accounted for by glycogenolysis and hypoinsulinemia. In addition, this study indicates repletion of skeletal and cardiac muscle glycogen during maintained hypothermia and sparing of muscle glycogen during rewarming.     

Behavioral thermoregulation by hypoxic rats.

To address whether a shift in hypothalamic thermal setpoint might be a significant factor in induction of hypoxic hypothermia, behavioral thermoregulation was examined in 7 female Sprague-Dawley rats implanted with radiotelethermometers for deep body temperature (Tb) measurement in a thermocline during normoxia (PO2 = 125 torr) and hypoxia (PO2 = 60 torr). Normoxic rats (TNox) selected a mean ambient temperature of 19.7 +/- 1.4 (SE) degrees C and maintained Tb at 37.0 +/- 0.2 degrees C. Hypoxic rats selected a significantly higher ambient temperature (THox = 28.6 +/- 2.2 degrees C) but maintained Tb significantly lower at 35.5 +/- 0.3 degrees C. Without a thermal gradient (ambient temperature = 25 degrees C), Tb during hypoxia was 35.4 +/- 0.4 degrees C. The maintenance of a lower body temperature during hypoxia through behavioral thermoregulation despite having warmer temperatures available supports the hypothesis that the thermoregulatory setpoint of hypoxic rats is shifted to promote thermoregulation at a lower Tb, effectively reducing oxygen demand when oxygen supply is limited.     

Thermoregulatory responses to cold water at different times of day.

This study examined how time of day affects thermoregulation during cold-water immersion (CWI). It was hypothesized that the shivering and vasoconstrictor responses to CWI would differ at 0700 vs. 1500 because of lower initial core temperatures (T(core)) at 0700. Nine men were immersed (20 degrees C, 2 h) at 0700 and 1500 on 2 days. No differences (P > 0.05) between times were observed for metabolic heat production (M, 150 W. m(-2)), heat flow (250 W. m(-2)), mean skin temperature (T(sk), 21 degrees C), and the mean body temperature-change in M (DeltaM) relationship. Rectal temperature (T(re)) was higher (P < 0.05) before (Delta = 0.4 degrees C) and throughout CWI during 1500. The change in T(re) was greater (P < 0. 05) at 1500 (-1.4 degrees C) vs. 0700 (-1.2 degrees C), likely because of the higher T(re)-T(sk) gradient (0.3 degrees C) at 1500. These data indicate that shivering and vasoconstriction are not affected by time of day. These observations raise the possibility that CWI may increase the risk of hypothermia in the early morning because of a lower initial T(core).     

Thermoregulatory responses to exercise in dehydrated dogs

Measurements of rectal temperature (Tre), water lost by evaporation (Eresp) and drooling, cardiac output (CO), and common carotid blood flow (CCBF) were made in dogs (mean hydrated wt 31.0 +/- 1.5 kg) running for 1 h on a level treadmill at 7.5 km/h at an ambient temperature of 25 degrees C. Each animal was studied when it was hydrated ad libitum and when it had been dehydrated by removal of drinking water until 9-10% of the initial body weight had been lost. Dehydrated exercising animals had significantly higher Tre and lower rates of Eresp, CO, and CCBF. Tre and Eresp were measured in seven animals. Average Tre during running was 39.11 +/- 0.10 degrees C in hydrated and 39.80 +/- 0.25 degrees C in dehydrated animals (P less than 0.01). Average Eresp during running was 3.9 +/- 0.3 g/min in hydrated animals and 2.3 +/- 0.3 g/min in dehydrated animals (P less than 0.01). Average CO during exercise, measured in five animals, was 11.1 +/- 0.7 1/min in the hydrated state and 8.6 +/- 0.5 1/min in the dehydrated state (P less than 0.01). Unilateral CCBF during exercise, measured in four animals, was 602 +/- 40 ml/min in the hydrated state and 418 +/- 22 ml/min in the dehydrated state (P less than 0.01). Water lost by drooling in seven exercising animals was 41.5 +/- 11 g/h when they were hydrated and 0.6 +/- 0.4 g/h when they were dehydrated. It is concluded that dehydrated dogs doing mild exercise can save water by reducing Eresp and regulating body temperature above hydrated levels.(ABSTRACT TRUNCATED AT 250 WORDS)