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Ambient temperature below which pigs should not be continuously showered in lairage.

Showering pigs with cold water during preslaughter lairage is thought to be useful in reducing the body temperature of hot, easily stressed animals. However, showering when the ambient temperature is too low could chill them too severely. To assess the effects of showering and to determine a temperature below which pigs should not be showered, pigs from one source, passing through a commercial slaughterhouse lairage, were split into two groups of approximately 50 each, showered and unshowered, on 10 days with a range of ambient temperatures. The pigs' behaviour and any damage to their skin were recorded, various measures of body temperature were taken before and after showering, and blood taken at slaughter was analysed for plasma creatine kinase, cortisol and lactate. Showering prevented the usual reduction in activity observed in pigs in lairage at high ambient temperatures. On the basis of the reduction in their flank temperature during showering, it is recommended that pigs should not be showered continuously if the temperature inside or outside the lairage falls below 5 degrees C, and showering should cease if they are seen to be shivering.

Abattoirs↗

Insulin response in rats acutely exposed to cold.

To examine the role of insulin during shivering thermogenesis, rats (unacclimatized) were exposed to 4 degrees C for 24 h and compared with control rats kept at 25 degrees C. Cold exposure lowered plasma insulin levels by one half, despite unchanged plasma glucose concentrations. Adrenodemedullation 2 weeks prior to cold exposure partially restored the ability of cold rats' plasma insulin levels to respond to a glucose load, unless it was accompanied by a subcutaneous injection of epinephrine. When additional normal rats were cold stressed and injected immediately after exposure with an alpha-adrenergic blocking agent (phentolamine), an intravenous glucose challenge caused a mean peak insulin value that was 50% higher than that of untreated controls, while the glucose level was less elevated. The results suggest that cold depresses blood insulin levels through activation of the sympathetic adrenal system, an effect most likely mediated by alpha-adrenergic inhibition of the pancreatic insulin response.

Adrenal Medulla↗

Threshold dissociation of thermoregulatory effector responses in febrile rabbits.

When the core temperature stabilizes at a hyperthermic level after iv injection of lipopolysaccharide (LPS), the threshold core temperature for cutaneous vasoconstriction (Thcv) is significantly increased in hot and neutral environments, while the threshold core temperature for shivering (Thsh) is not significantly altered in hot or cold environments but is significantly reduced at thermoneutrality. This type of dissociated threshold alterations of thermoregulatory effector responses seems to be typical for the febrile response of rabbits to LPS. Because the same threshold dissociation can be demonstrated after icv injection of LPS, the systemic and the central effects of LPS in the generation of fever seem to be mediated by identical mechanisms. Prostaglandins of the E series (PGE), one of the mediators considered as important in fever generation, cause parallel increases in Thcv and Thsh when injected icv. This indicates that the mode of action of PGE on the central targets producing hyperthermia differs from that of the ensemble of mediators involved in the generation of LPS fever in rabbits. In rabbits pretreated with aspirin, the threshold dissociation after iv LPS injection still occurs. This indicates that factors other than PGE play an important role in the generation of the threshold dissociation of thermoregulatory effector responses, which is typical for LPS fever. These data indicate also that the states of activity of the thermoregulatory effectors involved in the febrile responses can be altered individually and that the activities of these effectors during LPS fever are quite different from their activities in the control state.

Animals↗

Thermogenesis during rest and exercise in cold air.

Nine non-cold-acclimated subjects (5 female, 4 male, mean age 22.5 years) were studied to determine whether nonshivering thermogenesis contributes to cold-induced metabolic heat production during rest (50 min standing) and exercise (40 min treadmill walking) in 5 degrees C. Propranolol was administered orally (females, 60 mg, 1.12 mg.kg-1; males, 80 mg, 0.96 mg.kg-1) to block nonshivering thermogenesis. Measurements were taken at both 25 degrees C, 13.1 Torr (water vapor pressure; 1 Torr = 133.3 Pa) and 5 degrees C, 3.6 Torr, with sessions randomly assigned to be drug-neutral (DN), drug-cold (DC), placebo-neutral (PN), and placebo-cold (PC). Body core temperature was not different between any of the experimental conditions. Mean body temperature (5 degrees C, 32.2 +/- 0.20 degrees C (+/- SEM); 25 degrees C, 35.3 +/- 0.20 degrees C) and mean skin temperature (5 degrees C, 22.4 +/- 0.70 degrees C; 25 degrees C, 31.4 +/- 0.60 degrees C) were lower (p < 0.05) in the 5 degrees C than 25 degrees C environment (rest, exercise, drug (D), placebo (P), combined); while shivering (EMG) was higher (16.5 +/- 3.9% above baseline) at 5 degrees C than 25 degrees C (15 +/- 2.1% below baseline) (p < 0.05). The greater VO2 in 5 degrees C compared with 25 degrees C for the same condition is the thermoregulatory VO2 (TVO2). TVO2 (mL.min-1) was lower (p < 0.05) on the D (mean = 189.5 +/- 17.7) than on the P (mean = 238.1 +/- 20.2) during rest and during exercise (D, 206.1 +/- 63.7; P, 338.4 +/- 46.7). The EMG was 21% above baseline in the DC, and 12% above baseline for PC (p > 0.05). These results suggest a nonshivering component to heat production during acute cold exposure, which can be blocked with propranolol.

Adolescent↗

Bacteremia-induced changes in pituitary hormone release and effect of naloxone.

Acute bacteremia in sheep caused a surge of plasma beta-endorphin/beta-lipotropin (beta-EP/beta-LPH) associated with shivering behavior, tachycardia, hyperthermia, hemoconcentration, and decreased respiration rate. The surge of plasma beta-EP/beta-LPH was immediately followed by increases (P less than 0.05) in plasma prolactin and growth hormone (GH) concentrations and a depression (P less than 0.05) of plasma luteinizing hormone. These changes in pituitary hormone release were consistent with opioid-induced changes described in the literature. To examine possible opioid mediation, naloxone (2.5 mg X kg-1 X h-1) was continuously infused intravenously from 3 h before to 3 h after induction of an E. coli bacteremia. With the exception of plasma GH, naloxone failed to alter any of the hormonal or clinical parameters associated with bacteremia. For plasma GH, naloxone delayed (P less than 0.01) the increase but did not attenuate its magnitude, suggesting that an opioid mechanism may influence the timing of the pituitary GH release resulting from bacteremia. In general, opioid mechanisms sensitive to the present dosage of naloxone do not appear to mediate bacteremia-induced changes in hormonal or clinical parameters.

Animals↗

Two daily glucagon injections induce nonshivering thermogenesis in Muscovy ducklings.

In 6-wk-old chronically glucagon-treated (GT) ducklings, the calorigenic effect of intraperitoneal test injection of glucagon was measured at 25 and 4 degrees C ambient temperature (Ta). At 25 degrees C Ta, the increase in metabolic rate (MR) due to test injection of glucagon (360 micrograms/kg) reached 5.3 W/kg (i.e., 98% above the saline control value) in GT ducklings and only 1.7 W/kg (i.e., 29% above the control value) in control (TN) ducklings. After the injection, GT ducklings developed a hyperthermia, reaching 2.4 degrees C, accompanied by intense panting, whereas thermal body temperature did not change in TN ducklings. At 4 degrees C Ta for the same dose of glucagon, no significant change in MR was observed in GT ducklings during 180 min of exposure, whereas a 25% decrease in MR occurred in the same conditions in TN ducklings. In the cold, glucagon injection inhibited shivering in both groups of ducklings but thermogenesis was not suppressed in GT ducklings, showing a true nonshivering thermogenesis in these birds. This nonshivering thermogenesis was estimated to be 3 W/kg (i.e., 55% above resting MR). Such changes produced by chronic glucagon treatment resemble the artificial cold acclimation of rats chronically treated by norepinephrine.

Animals↗

Baroreflexive depression of oxygen consumption in the squirrel monkey at 10 degrees C.

Unanesthetized squirrel monkeys exposed to an ambient temperature of 10 degrees C showed elevations in total body oxygen consumption (VO2), arterial blood pressure (BP), and heart rate (HR) above values recorded at 28 degrees C. Further elevation of BP in the cold by intravenous infusion of phenylephrine was accompanied by immediate reduction in VO2, inhibition of shivering, and decrease in rectal temperature, as well as immediate reduction in HR. The magnitude of reduction in VO2 correlated with the magnitude of the concomitant baroreflexive bradycardia. When the pressor effects of phenylephrine were opposed by administration of diazoxide or phentolamine, the inhibitory effects of phenylephrine on both HR and VO2 were abolished. In animals previously subjected to bilateral sinoaortic denervation, both the bradycardia and depression in oxygen consumption normally associated with BP elevation were markedly reduced. These results suggest that elevation of blood pressuere can inhibit the thermoregulatory increase in total body oxygen consumption normally produced by cold exposure, and that this inhibition, like the concomitant bradycardia, is probably mediated via the sinoaortic baroreceptors.

Animals↗

Spinal cord, hypothalamic, and air temperature: interaction with arousal states in the marmot.

Yellow-bellied marmots, Marmota flaviventris, prepared with U-shaped thermodes in the epidural space of the thoracic vertebral canal, a thermode in the preoptic hypothalamus, and cortical surface and hippocampal electrodes, were used to investigate the interaction of arousal states with temperature regulation. It was found that arousal state of the animal influences the thermoregulatory responses initiated in either the spinal cord or hypothalamus. Further, changes in ambient temperature affected both the gain and the threshold of these responses. The interaction of the hypothalamus and spinal cord was not an additive function, however the threshold for shivering of each could be altered by temperature manipulation of the other. Future studies in modeling of temperature regulation should consider the contributions of temperature receptors of the spinal cord and the arousal state of the animal during the stimulation period.

Animals↗

Some aspects of temperature regulation in newborn harp seal pups.

Harp seals are born on the drifting ice of the North Atlantic Ocean during arctic winter when temperatures of -20 degrees C, occasionally in combination with wind of 10 m/s, might prevail for days. At birth the pups lack subcutaneous blubber and the wet infantile fur has a conductance value of 30.0 W . m-2 . degrees C-1, as compared with only 2.0 W . m-2 . degrees C-1 when dry. While still wet immediately after birth the pups are nevertheless able to retain body core temperature by shivering. This activity leads to reduction of muscle fat and glycogen stores. Nonshivering thermogenesis commences in thermogenic adipose tissue by virtue of loosely coupled mitochondria. Thermogenic adipose tissue is found at birth both as a subcutaneous layer along the back and as internal deposits around venous plexuses in the neck, on the pericardium, on the kidneys, and the abdominal walls. After about 3 days of suckling the subcutaneous adipose tissue loses its thermogenic function being gradually transformed into blubber, whereas the internal deposits persist at least until the pups venture into water at the age of 3-4 wk.

Adipose Tissue↗

Effect of 5-hydroxytryptamine and acetylcholine on the energy budget of chickens.

Intraventricular injections of 5-hydroxytryptamine-HCl (258 nmol) or acetylcholine-HCl (550 nmol) in the chicken caused body temperature to rise at 35 degrees C ambient, a result of decreased evaporative heat loss due to bradypnea. At 10 and 20 degrees C ambient, neither drug affected body temperature. Although these drugs decreased physical activity or shivering or both at 10 and 20 degrees C, metabolic heat production was not depressed enough to alter body temperature significantly. Heart rate decreased simultaneously with decreased activity at 20 degrees C. This study is the first to inject 5-hydroxytryptamine as a salt of HCl, instead of creatinine sulfate, as is commonly used. It is suggested that some of the differences reported herein, compared to other studies, are due to the type of salt used. It is postulated that either 5-hydroxytryptamine or acetylcholine, rather than norepinephrine, may be an important neurotransmitter in the neural pathways for thermoregulation in chickens, even though their action on thermoregulation is minor compared with norepinephrine.

Acetylcholine↗

Nonshivering thermogenesis and adaptation to fasting in king penguin chicks.

The ability to develop nonshivering thermogenesis (NST) and the effect of fasting on thermogenic response to cold were studied in winter-acclimatized king penguin chicks. Metabolic rate (MR) and integrated electrical muscle activity were measured at different ambient temperatures. In cold-acclimatized (5 degrees C) fed chicks, shivering threshold temperature (STT) was 9.4 degrees C lower than lower critical temperature (LCT), indicating that NST (0.7 W/kg) occurs at moderate cold, whereas in control chicks fed and reared at 25 degrees C for 3 wk, LCT and STT were similar. Chicks reared in the cold and fasting for 3 wk or 4-5 mo (natural winter fast) developed an NST of 0.8 and 2.4 W/kg, respectively, despite the fast. In fasting chicks, the intercept of the metabolic curve with the abscissa at zero MR was far below body temperature, contrasting with the classic model for heat loss. Their low LCT indicates the capacity of a large reduction in convective conductance characteristic of diving animals and allows energy sparing in moderate cold. Below LCT, conductance reincreases progressively, leading to a steeper than expected slope of the metabolic curve and allowing preservation of a threshold temperature in the shell. These results show for the first time in a wild young bird the development of NST after cold acclimatization. Further, at the temperature of cold acclimatization, an energy-sparing mechanism is shown in response to long-term fast adaptation.

Acclimatization↗

Thermoregulatory responses of the inbred heat-tolerant FOK rat to cold.

The responses of inbred heat-tolerant FOK rats to cold were compared with those of Wistar King A/H (WKAH) and Std:Wistar (WSTR) strains. The fall of colonic temperature during cold exposure was unexpectedly smaller in FOK than in other groups, but the onset of shivering was delayed in FOK. Norepinephrine (NE)-induced in vivo oxygen consumption and the mitochondrial uncoupling protein 1 level of brown adipose tissue (BAT) were not different among the groups, but the cold-induced increases in in vivo oxygen consumption as well as plasma glycerol and free fatty acids were higher in FOK than in other groups. In vitro NE-induced oxygen consumption of BAT was less in FOK than WSTR, but not WKAH. The magnitude of the NE-induced increase in blood flow through BAT was higher in FOK than in other groups. These results suggest that FOK paradoxically have a high capacity for nonshivering thermogenesis in spite of their high capacity for heat tolerance, probably due to an increased lipid utilization and improved circulation of BAT.

Adaptation, Physiological↗

Adaptive modifications in the thermoregulatory system of long-distance runners.

In seven long-distance runners (42 km or more) the thermoregulatory responses to acute external cooling and heating, under resting conditions, were recorded and compared with those in physically untrained controls. Sweating as well as shivering thresholds were significantly decreased in the runners when compared either in terms of mean body temperature (Tb) or esophageal temperature (Tes); Tb and Tes were reduced in the runners at rest under thermoneutral conditions. Moreover, cold sensation in the runners occurred at lower Tb. The runners thus behaved as if the "set point" of their thermoregulatory system had been reset to a lower level. As for the sweating threshold, the shift is quantitatively comparable to that found in heat adaptation. The described modifications in long-distance runners would prolong the time period until a dangerous body temperature-one of the important limiting factors in physical endurance-is reached during heavy exercise.

Adolescent↗

Physical fitness and thermoregulatory reactions in a cold environment in men.

The relationship between the physical fitness level (maximal O2 consumption, VO2max) and thermoregulatory reactions was studied in 17 adult males submitted to an acute cold exposure. Standard cold tests were performed in nude subjects, lying for 2 h in a climatic chamber at three ambient air temperatures (10, 5, and 1 degrees C). The level of physical fitness conditioned the intensity of thermoregulatory reactions to cold. For all subjects, there was a direct relationship between physical fitness and 1) metabolic heat production, 2) level of mean skin temperature (Tsk), 3) level of skin conductance, and 4) level of Tsk at the onset of shivering. The predominance of thermogenic or insulative reactions depended on the intensity of the cold stress: insulative reactions were preferential at 10 degrees C, or even at 5 degrees C, whereas colder ambient temperature (1 degree C) triggered metabolic heat production abilities, which were closely related to the subject's physical fitness level. Fit subjects have more efficient thermoregulatory abilities against cold stress than unfit subjects, certainly because of an improved sensitivity of the thermoregulatory system.

Adipose Tissue↗

Plasma glucose and insulin responses to oral and intravenous glucose in cold-exposed humans.

Although glucose tolerance and skeletal muscle glucose uptake are markedly improved by cold exposure in animals, little is known about such responses in humans. This study used two variations of a glucose tolerance test (GTT) to investigate changes in carbohydrate metabolism in healthy males during nude exposure to cold. In experiment 1, an oral GTT was performed in the cold and in the warm (3 h at 10 or 29 degrees C). To bypass the gastrointestinal tract, and to suppress hepatic glucose output, a second experiment was carried out as described above, using an intravenous GTT. Even though cold exposure raised metabolic rate greater than 2.5 times, plasma glucose and insulin responses to an oral GTT remained unaltered. In contrast, cold exposure reduced the entire plasma glucose profile as a function of time during the intravenous GTT (P less than 0.05), as plasma glucose was returned to basal levels within 1 h in comparison to a full 2 h in the warm, despite low insulin levels. The results of the intravenous GTT demonstrate that even with low insulin levels, carbohydrate metabolism is increased in cold-exposed males. This effect could be masked in the oral GTT by gastrointestinal factors and a high hepatic glucose output. Cold exposure may enhance insulin sensitivity and/or responsiveness for glucose uptake, mainly in shivering skeletal muscles.

Administration, Oral↗

Hypoxia similarly impairs metabolic responses to cutaneous and core cold stimuli in conscious rats.

Cold exposure elicits several thermoregulatory responses, including an increased metabolic heat production from shivering and nonshivering thermogenesis. The increased metabolism can be in response to body core and/or body cutaneous cooling. Hypoxic hypoxia has been shown to attenuate the metabolic response to cutaneous cooling. We measured metabolic heat production in adult conscious rats during independent cutaneous and core cooling, during normoxia and hypoxia, to 1) test the hypothesis that hypoxia suppresses the metabolic response to independent core cooling and 2) determine whether hypoxia acts preferentially on the response to cutaneous or core cooling. The animals were studied in a temperature-controlled metabolic chamber, and body core temperature was controlled by an abdominal heat exchange coil. Ambient temperature was varied (10, 19, and 28 degrees C) while core temperature was clamped at 37 degrees C or core temperature was varied (33, 35, and 37 degrees C) at a stable ambient temperature of 28 degrees C. Our data indicate that although the sensitivity of the metabolic response to core cooling is about five to six times that to cutaneous cooling. Hypoxia similarly attenuates thermoregulatory responses to both stimuli.

Animals↗

Thermoregulatory responses to cold transients: effects of menstrual cycle in resting women.

Effects of the menstrual cycle on heat loss and heat production (M) and core and skin temperature responses to cold were studied in six unacclimatized female nonsmokers (18-29 yr of age). Each woman, resting supine, was exposed to a cold transient (ambient temperature = mean radiant temperature = 20 to -5 degrees C at -0.32 degrees C/min, relative humidity = 50 +/- 2%, wind speed = 1 m/s) in the follicular (F) phase (days 2-6) and midluteal (L) phase (days 19-23) of her menstrual cycle. Clothed in each of two ensembles with different thermal resistances, women performed multiple experiments in the F and L phases. Thermal resistance was 0.2 and 0.4 m2 . K . W-1 for ensembles A and B, respectively. Esophageal temperature (Tes), mean weighted skin temperature (Tsk), finger temperature (Tfing), and area-weighted heat flux were recorded continuously. Rate of heat debt (-S) and integrated mean body temperature (Tb,i) were calculated by partitional calorimetry throughout the cold ramp. Extensive peripheral vasoconstriction in the F phase during early periods of the ramp elevated Tes above thermoneutral levels. Shivering thermogenesis (DeltaM = M - Mbasal, W /m2) was highly correlated with declines in Tsk and Tfing (P <0.0001). There was a reduced slope in M as a function of Tb,i in the L phase with ensembles A (P < 0.02) and B (P < 0.01). Heat flux was higher and -S was less in the L phases with ensemble A (P < 0.05). An analytic model revealed that Tsk and Tes contribute as additive inputs and Tfing has a multiplicative effect on the total control of DeltaM during cold transients (R2 = 0.9). Endogenous hormonal levels at each menstrual cycle phase, core temperature and Tsk inputs, vascular responses, and variations in body heat balance must be considered in quantifying thermoregulatory responses in women during cold stress.

Adult↗

Thermoregulation during cold exposure: effects of prior exercise.

This study examined whether acute exercise would impair the body's capability to maintain thermal balance during a subsequent cold exposure. Ten men rested for 2 h during a standardized cold-air test (4.6 degrees C) after two treatments: 1) 60 min of cycle exercise (Ex) at 55% peak O(2) uptake and 2) passive heating (Heat). Ex was performed during a 35 degrees C water immersion (WI), and Heat was conducted during a 38.2 degrees C WI. The duration of Heat was individually adjusted (mean = 53 min) so that rectal temperature was similar at the end of WI in both Ex (38.2 degrees C) and Heat (38.1 degrees C). During the cold-air test after Ex, relative to Heat 1) rectal temperature was lower (P < 0.05) from minutes 40-120, 2) mean weighted heat flow was higher (P < 0.05), 3) insulation was lower (P < 0.05), and 4) metabolic heat production was not different. These results suggest that prior physical exercise may predispose a person to greater heat loss and to experience a larger decline in core temperature when subsequently exposed to cold air. The combination of exercise intensity and duration studied in these experiments did not fatigue the shivering response to cold exposure.

Adult↗