Sympathoadrenal responses to cold and ketamine anesthesia in the rhesus monkey

The effect of cold exposure on the sympathoadrenal system in primates was studied with and without ketamine anesthesia in eight adult rhesus monkeys. Each monkey was placed in a primate chair at a thermoneutral temperature (25 degrees C) for 1 h (control) followed by cold exposure (12 degrees C) for 3 h or placed in a circulating water bath (28 degrees C) to induce a decrease in core temperature (Tre) to 35 and 33 degrees C. Plasma catecholamines were analyzed by high-pressure liquid chromatography with electrochemical detection (60-65% recovery, coefficient of variation = 15%). The 3-h cold exposure was associated with a 175% increase above control levels of norepinephrine (NE) and a 100% increase in epinephrine (E). Decreases were evident in Tre (0.5 degree C), mean skin temperature (Tsk, 5.5 degrees C), and mean body temperature (Tb, 2.0 degrees C). Continuous infusion of ketamine (0.65 mg . kg-1 . min-1) resulted in no change in the plasma levels of NE and E from the control levels. Tre, Tsk, and Tb all showed greater declines with the addition of ketamine infusion to the cold exposure. Water exposure (28 degrees C) under ketamine anesthesia resulted in a drop in Tre to 33 degrees C within 1 h. Plasma levels of NE and E were unchanged from control values at Tre of 35 and 33 degrees C. The data suggest that the administration of ketamine abolished both the thermoregulatory response and the catecholamine response to acute cold exposure.     

Effect of cold exposure on the concentration of triglyceride in the liver of the rat

The aim of the present study was to examine an effect of cold exposure on the concentration of triglycerides (TG) in the rat's liver. The rats were divided into the following groups: control, fed with oil, treated with hydrocortisone, fed with oil and treated with hydrocortisone, treated with noradrenaline. The rats exposed to cold were kept in wire cages (one rat in one cage) in the cold room at temperature +2 degrees C. They had free access to food (pellet diet for rodents) and water. In the control group the exposure to cold increased mildly (though significantly) the TG concentration after 1 and 3 h and had no effect after 2 and 24 h. It did not affect the concentration of plasma free fatty acids (FFA). At room temperature feeding with oil (2 ml/100 g of body weight) alone, and combined with hydrocortisone treatment (5 mg/100 g of body weight) as well as treatment with noradrenaline (0.1 mg/100 g of body weight) had no effect on the liver TG concentration, although the concentration of plasma FFA was increased. Exposure to cold for 3 h increased markedly the liver TG concentration in each of those groups. It is concluded that exposure to cold elicits a mechanism, which in the presence of elevated plasma FFA concentration induces accumulation of TG in the liver.     

Influences of age and gender on human thermoregulatory responses to cold exposures

To delineate age- and gender-related differences in physiological responses to cold exposure, men and women between the ages of 20 and 29 yr and 51 and 72 yr, wearing minimal clothing, were exposed at rest for 2 h to 28, 20, 15, and 10 degrees C room temperatures with 40% relative humidity. During the coldest exposure, the rates of increase in metabolic rate (W X m-2 or ml X kg lean body mass-1 X min-1 were similar for all groups. However, older women (n = 7) may have benefited from a larger (P less than 0.05) early metabolic (M) increase (40% within 15 min) than young men (18%) (n = 10), young women (5%) (n = 10), or older men (5%) (n = 10). A similar rapid M response in older women occurred during the 15 degrees C exposure. During all cold exposures, older women maintained constant rectal temperature (Tre) and young women maintained Tre only during the 20 degrees C exposures, whereas Tre of the men declined during all cold exposures (P less than 0.01). Changes in Tre and mean skin temperature (Ts) during cold exposure were largely related to body fat, although age and surface area/mass modified the changes in men. The data suggest that older men are more susceptible to cold ambients than younger people, since they did not prevent a further decline in their initially relatively low Tre. Despite greater insulation from body fat, the older women maintained a constant Tre at greater metabolic cost than men or younger women.     

Thermoregulatory responses of young and older men to cold exposure.

Nine young (20-25 years) and ten older (60-71 years) men, matched for body fatness and surface area:mass ratio, underwent cold tests in summer and winter. The cold tests consisted of a 60-min exposure, wearing only swimming trunks, to an air temperature of 17 degrees C (both seasons) and 12 degrees C (winter only). Rectal (Tre) and mean skin (Tsk) temperatures, metabolic heat production (M), systolic (BPs) and diastolic (BPd) blood pressures and heart rate (fc) were measured. During the equilibrium period (28 degrees C air temperature) there were no age-related differences in Tre, Tsk, BPs, BPd, or fc regardless of season, although M of the older men was significantly lower (P < 0.003). The decrease in Tre and Tsk (due to the marked decrease in six of the older men) and the increase in BPs and BPd were significantly greater (P < 0.004) for the older men during all the cold exposures. The rate of increase in M was significantly greater (P < 0.01) for the older group when exposed to 12 degrees C in winter and 17 degrees C in summer (due to the marked increase in four of the older men). This trend was not apparent during the 17 degrees C exposure in winter. There was no age-related difference in fc during the exposures. Significant decreases in Tre and Tsk and increases in M, BPs and BPd during the 12 degrees C exposure were observed for the older group (P < 0.003) compared to their responses during the 17 degrees C exposure in winter. In contrast, Tre, M, BPs in the young group were not affected as much by the colder environment. It was concluded that older men have more variable responses and some appear more or less responsive to mild and moderate cold air than young men.     

Substrate preference in aminophylline-stimulated thermogenesis

The present study investigated the suitability of different substrates on aminophylline (AMPY)-induced thermogenesis in rats during cold exposure. Feeding of distilled water 60 min prior to cold exposure in two-day fasted rats resulted in the lowest total heat production and final body temperature in both saline- and AMPY-treated groups. Feeding of 5 ml Intralipid (2 Kcal/ml), a triglyceride mixture, did not improve thermogenesis beyond the control levels. However, feeding of isocaloric substitutes of sucrose elevated significantly the total thermogenesis by 7.9% and 7.4% and final body temperature by 2.23 and 1.61 degrees C, respectively, in saline- and AMPY-treated groups. The increase in thermogenesis by sucrose is not due to its thermic effect. It is concluded that sucrose, in combination with AMPY, may be of value in improving resistance to cold.     

The physiological strain index applied to heat-stressed rats.

A physiological strain index (PSI) based on heart rate (HR) and rectal temperature (Tre) was recently suggested to evaluate exercise-heat stress in humans. The purpose of this study was to adjust PSI for rats and to evaluate this index at different levels of heat acclimation and training. The corrections of HR and Tre to modify the index for rats are as follows: PSI = 5 (Tre t - Tre 0). (41.5 - Tre 0)-1 + 5 (HRt - HR0). (550 - HR0)-1, where HRt and Tre t are simultaneous measurements taken at any time during the exposure and HR0 and Tre 0 are the initial measurements. The adjusted PSI was applied to five groups (n = 11-14 per group) of acclimated rats (control and 2, 5, 10, and 30 days) exposed for 70 min to a hot climate [40 degrees C, 20% relative humidity (RH)]. A separate database representing two groups of acclimated or trained rats was also used and involved 20 min of low-intensity exercise (O2 consumption approximately 50 ml. min-1. kg-1) at three different climates: normothermic (24 degrees C, 40% RH), hot-wet (35 degrees C, 70% RH), and hot-dry (40 degrees C, 20% RH). In normothermia, rats also performed moderate exercise (O2 consumption approximately 60 ml. min-1. kg-1). The adjusted PSI differentiated among acclimation levels and significantly discriminated among all exposures during low-intensity exercise (P < 0.05). Furthermore, this index was able to assess the individual roles played by heat acclimation and exercise training.     

Effect of ambient temperature on protein breakdown during prolonged exercise

Male subjects (n = 8) cycled for 90 min in 5, 20, and 30 degrees C environments. Rectal (Tre), chest, and thigh temperatures, O2 consumption (VO2), respiratory exchange ratio (R), and venous concentrations of glucose, free fatty acids (FFA), urea N, lactic acid (LA), norepinephrine (NE), epinephrine (E), and cortisol (C) were measured before, during, and after exercise. Urea N excretion was measured in 72 h of nonexercise, in 72 h of exercise (exercise day + 2 post-exercise days) urine samples, and in exercise sweat. Calculated 72-h protein utilization (means +/- SE) was significantly greater (P less than 0.05) for the 5 (86.9 +/- 27.1 g) and 20 (82.9 +/- 22.7 g) compared with 30 degrees C (34.01 +/- 19.1 g) trial. Regardless of ambient temperature exercise increased the venous concentration of C, E, and NE. These catabolic hormones were greatest in 5, lowest in 20, and intermediate in 30 degrees C. Exercise Tre and VO2 were greatest in the 30 degrees C environment. Venous FFA concentration was significantly higher and R significantly lower in 5 vs. 20 or 30 degrees C, and venous LA concentration was significantly greater in 30 vs. 20 or 5 degrees C. Although these results indicate that exercise protein breakdown is affected by ambient temperatures, the mechanism of action is not due solely to circulating NE, E, and C. Differences in venous FFA and LA across environmental temperatures suggest that alterations in carbohydrate and fat metabolism may have contributed to the observed variable protein utilization.     

Acute cold exposure and the metabolism of glucose and some of its precursors in the liver of the fed and fasted sheep.

Measurements of total body oxygen consumption, visceral and hepatic blood flow, oxygen consumption, exchanges of amino acids, lactate, pyruvate and glucose were made on sheep fed 3--6 h or 21 h before the experiment and exposed for 3 h to a neutral environment (15 degrees C) or a cold environment (0.5 to 4 degrees C with clipped coat and wind speed 2 m.s-1). Recent feeding significantly increasedd the total oxygen consumption and the oxygen consumption of the viscera and liver. No general release of amino acids from the viscera or uptake by the liver after feeding was detected although the arterial plasma concentration of essential amino acids did increase significantly after feeding. The plasma concentration of most non-essential amino acids also increased except that of glycine, which decreased significantly. Cold exposure increased the total oxygen consumption and reduced the respiratory quotient significantly. Release of amino acids from the viscera was stimulated by cold exposure. There was a variable increase in the hepatic uptake of lactate and alanine when the sheep were fasted and cold-exposed. The liver's glucose output doubled and the blood (arterial) glucose concentration significantly increased in the cold.     

Thermoregulation in the cold after physical training at different ambient air temperatures

Since human thermoregulation at rest is altered by cold exposure, it was hypothesized that physical training under cold conditions would alter thermoregulation. Three groups (n = 8) of male subjects (mean age 24.3 +/- 0.9 years) were evaluated: group T (interval training at 21 degrees C), group CT (interval training at 1 degrees C), and group C (no training, equivalent exposure to 1 degrees C). Each group was submitted, before and after 4 weeks of interval training (5 d/week), to a cold air test at rest (SCAT) (dry bulb temperature (Tdb) = 1 degrees C) for a 2-h period for evaluation of the thermoregulatory responses. During SCAT, after the training/acclimation period, group T exhibited a higher rectal temperature (Tre) (P < 0.05) without significant change in mean skin temperature (Tsk) whereas metabolic heat production (M) was higher at the beginning of the SCAT (P < 0.05). For group CT, no thermoregulatory change was observed. Group C showed a lower Tre (P < 0.05) without significant change in either Tsk or in M, suggesting the development of a hypothermic general cold adaptation. This study showed, first, that the cold thermoregulatory responses induced by an interval training differed following the climatic conditions of the training and, second, that this training performed in the cold prevented the development of a general cold adaptation.     

Role of the sympathetic nervous system in cold-induced hypertension in rats

Hypertension develops in rats exposed chronically to cold [6 +/- 2 degrees C (SE)] and includes both an elevation of mean arterial pressure and cardiac hypertrophy. Previous studies suggest that cold-exposed animals, at least initially, have a large sustained increase in the activity of their sympathetic nervous system, suggesting a failure of the baroreceptor system to provide sufficient negative feedback to the central nervous system. The present study was designed to investigate whether alterations in the activity of the sympathetic nervous system, including the baroreceptor reflex, occur during exposure to cold and whether they contribute to cold-induced hypertension. Twenty male rats were prepared with indwelling catheters in the femoral artery and vein. Ten of the rats were exposed to cold (6 +/- 2 degrees C) chronically, while the remaining 10 were kept at 26 +/- 2 degrees C. Withdrawal of arterial blood samples (less than 5 ml/kg), measurement of direct arterial pressures, and measurement of baroreflex function were carried out at 0800 h at intervals throughout the experiment. Norepinephrine and epinephrine concentrations in plasma were also determined at intervals throughout the experiment. Systolic, diastolic, and mean blood pressures of cold-exposed rats were increased to levels significantly above those of controls. The sensitivity of the baroreflex (delta heart period/delta mean arterial pressure) was decreased in the cold-treated group. The concentration of norepinephrine in plasma increased after 24 h of exposure to cold and remained elevated throughout the experiment, whereas the concentration of epinephrine in plasma increased initially but returned to control levels after 19 days of exposure to cold.(ABSTRACT TRUNCATED AT 250 WORDS)     

Body temperature and plasma prolactin and norepinephrine relationships during exercise in a warm environment: effect of dehydration

The effects of euhydration (Eh) and light (Dh1) and moderate (Dh2) dehydrations on plasma prolactin (PRL) levels were studied in 5 young male volunteers at rest and during exercise to exhaustion (50% of VO2max) in a warm environment (Tdb = 35 degrees C, rh = 20-30%). Light and moderate dehydrations (loss of 1.1 and 1.8% body respectively) were obtained before exercise by controlled hyperthermia. Compared to Eh, time for exhaustion was reduced in Dh1 and Dh2 (p less than 0.01) and rectal temperature (Tre) rose faster in Dh2 (p less than 0.05). Both venous plasma PRL and norepinephrine (NE) increased during exercise at any hydration level (p less than 0.05). Plasma PRL reached higher values after 40 and 60 min in Dh2 and Dh1 (p less than 0.05). Plasma NE values were higher in Dh2 at rest and at the 40th min during exercise (p less than 0.05). Plasma PRL was linearly correlated to Tre and plasma NE (p less than 0.001) but unrelated to plasma volume variation and osmolality. Our results provide further evidence for the major effect of body temperature in exercise-induced PRL changes. Moreover, the plasma PRL-NE relationship suggests that these changes may result from central noradrenergic activation.     

Plasma catecholamine concentrations in normotensive rats of different strains and in spontaneously hypertensive rats under basal conditions and during cold exposure

Under basal conditions, the levels of circulating norepinephrine (NE) and epinephrine (E) were higher in normotensive Wistar rats of different origins than in Sprague-Dawley rats. Since the decline of ³H-NE concentration in the plasma after i.v. injection was similar in Wistar and in Sprague-Dawley rats, the higher levels of endogenous NE in the former strain probably reflect greater NE release from sympathetic nerve terminals. In normotensive Sprague-Dawley and Wistar rats, plasma NE rose to various extents during cold exposure (4°C), depending on the basal plasma NE levels. Compared with normotensive Wistar Kyoto rats (WKY), spontaneously hypertensive rats (SHR) had similar basal plasma E and NE concentrations, similar rates of ³H-NE disappearance, but more rapid increases to higher values of plasma NE during cold exposure. It is concluded that the basal rate of peripheral catecholamine release does not seem to be the main determining factor for arterial blood pressure in the various rat strains and that the sympathetic neuronal system of SHR is more responsive to cold exposure than that of WKY rats.     

Control of heat-induced cutaneous vasodilatation in relation to age

Well matched unacclimatised older (age 55-68, 4 women, 2 men) and younger (age 19-30, 4 women, 2 men) subjects performed 75 min cycle exercise (approximately 40% VO2max) in a hot environment (37 degrees C, 60% rh). Rectal temperature (Tre), mean skin temperature (Tsk), arm blood flow (ABF, strain gauge plethysmography), and cardiac output (Q, CO2 rebreathing) were measured to examine age-related differences in heat-induced vasodilatation. Tre and Tsk rose to the same extent in each group during the exposure. There was no significant intergroup difference in sweat rate (older: 332 +/- 43 ml.m-2.h-1, younger: 435 +/- 49 ml.m-2.h-1; mean +/- SEM). However, the older subjects responded to exercise in the heat with a lower ABF response which could be attributed to a lower Q for the same exercise intensity. The slope of the ABF-Tre relationship was attenuated in the older subjects (9.3 +/- 1.3 vs 17.9 +/- 3.3 ml.100 ml-1.min-1.degrees C-1, p less than 0.05), but the Tre threshold for vasodilatation was about 37.0 degrees C for both groups. These results suggest an altered control of skin vasodilatation during exercise in the heat in older individuals. This attenuated ABF response appears to be unrelated to VO2max, and may reflect an age-related change in thermoregulatory cardiovascular function.     

Thermal adjustment to cold-water exposure in resting men and women

Thermoregulatory responses were studied in 10 men and 8 women at rest in air and during 1-h immersion in water at 20, 24, and 28 degrees C. For men of high body fat (27.6%), rectal temperature (Tre) and oxygen consumption (VO2) were maintained at air values at all water temperatures (Tw). For men of average (16.8%) and low (9.2%) fat the change in Tre (delta Tre) was inversely related to body fat at all Tw with VO2 increasing to 1.07 l X min-1 for a -1.6 degrees C delta Tre for lean men. For women of average (25.2%) and low (18.5%) fat Tre decreased steadily during immersion at all Tw. The greatest changes occurred at 20 degrees C with little differences in delta Tre and VO2 noted between these groups of women. In comparison with males of similar percent fat, Tre dropped to a greater extent (P less than 0.05) in females at 20 and 24 degrees C. Stated somewhat differently, lean women with twice the percentage of fat have similar delta Tre as lean men at all Tw. For delta Tre greater than -1.0 degree C men showed significantly greater (P less than 0.05) thermogenesis compared with women. The differences in thermoregulation between men and women during cold stress at rest may be due partly to the sensitivity of the thermogenic response as well as the significant differences in lean body weight and surface area-to-mass ratio between the sexes.     

Metabolic effects of exposure to hypoxia plus cold at rest and during exercise in humans

To determine effects on metabolic responses, subjects were exposed to four environmental conditions for 90 min at rest followed by 30 min of exercise: breathing room air with an ambient temperature of 25 degrees C (NN); breathing room air with an ambient temperature of 8 degrees C (NC); hypoxia (induced by breathing 12% O2 in N2) with a neutral temperature (HN); and hypoxia in the cold (HC). Hypoxia increased heart rate (HR), systolic blood pressure (SBP), pulmonary ventilation (VE), respiratory exchange ratio (R), blood lactate, and perceived exertion during exercise while depressing rectal temperature (Tre) and O2 uptake (VO2). Cold exposure elevated SBP, diastolic blood pressure (DBP), VE, VO2, blood glucose, and blood glycerol but decreased HR, Tre, and R. Shivering and DBP were higher and Tre was lower in HC compared with NC. HR, SBP, VE, R, and lactate tended to be higher in HC compared with NC, whereas VO2 and blood glycerol tended to be depressed. These results suggest that cold exposure during hypoxia results in an increased reliance on shivering for thermogenesis at rest whereas, during exercise, heat loss is accelerated.     

Acute blood biochemical alterations in response to marathon running.

Adrenal-sympathico function, blood carbohydrates and lipids, and water and electrolyte balance were studied in six highly trained male marathon runners prior to and after running a marathon (26.2 miles; 42.2 km) and on control days corresponding to the above times. Fluid intake was not sufficient to maintain body weight, the runners losing approximately 2.8 kg. Estimated plasma volume losses (161 ml, 4.4%) indicated that most of the fluid loss was extravascular. Tre rose an average 2.4 degrees C and a significant negative correlation between running time and rise in Tre was observed. Glucose, fatty acids, glycerol, hemoglobin, and plasma proteins were significantly elevated after the race. Small but statistically significant increments in lactate and pyruvate were also observed. Alterations in adrenal-sympathico function were indicated by increased levels of cortisol, epinephrine, and norepinephrine.     

Human cold air habituation is independent of thyroxine and thyrotropin.

Thyroxine (T4) is required in species possessing brown adipose tissue (BAT) for the maintenance of cold tolerance and adaptation. In humans, who possess negligible quantities of BAT, the importance of T4 has not been demonstrated. We studied the effects of decreased serum T4 and thyrotropin (TSH) on human cold habituation after repeated cold air exposures. Eight men (T3+) received a single daily dose of triiodothyronine (T3; 30 micrograms/day), and another eight men (T3-) received a placebo. All 16 normal thyroid men underwent a standardized cold air test (SCAT) under basal conditions in January and again in March after eighty 30-min 4.4 degrees C air exposures (10/wk). Measurements of basal metabolic rate (BMR), O2 consumption (VO2), mean arterial pressure (MAP), plasma norepinephrine (NE), serum TSH, free and total T4, and free and total T3 were repeated before and after 8 wk of exposure. TSH, free T4, and total T4 were 50% lower for T3+ than for T3- subjects. Total and free T3 were not different between groups. BMR was unchanged after habituation, whereas the cold-stimulated VO2, MAP, and NE were significantly reduced for all subjects in March. The relationship between VO2 and NE (r2 = 0.44, P less than 0.001) during the initial SCAT was unchanged with habituation. We suggest that human cold habituation is independent of major changes in circulating T4 and TSH.     

Energy balance and diabetes. The effects of cold exposure, exercise training, and diet composition on glucose tolerance and glucose metabolism in rat peripheral tissues

The effects of cold exposure, exercise training, and diet (high fat versus high carbohydrate) on glucose tolerance and glucose metabolism in rat peripheral tissues will be briefly reviewed. Stimulation of energy expenditure by cold exposure (4 degrees C) or exercise training generally leads to decreased plasma insulin levels and to an improvement in glucose tolerance, suggesting that insulin action on peripheral tissues is increased when energy expenditure is stimulated. On the contrary, feeding high-fat diets to sedentary rats living in the warm (25 degrees C) induces hyperinsulinemia and insulin resistance resulting in a marked deterioration of glucose tolerance. Nevertheless, cold exposure reverses the diabetogenic effects of high-fat feeding, demonstrating that nutrition-induced insulin resistance is amplified in sedentary animals living at temperatures close to thermoneutrality. Radioactive tracer studies of 2-deoxyglucose uptake in peripheral tissues revealed that cold exposure synergistically potentiates the effects of insulin on glucose uptake in skeletal muscles as well as in white and brown adipose tissues. However, more recent data showed that cold exposure improves glucose tolerance and stimulates glucose uptake in starved animals (ie., in the virtual absence of circulating insulin) nearly by the same order of magnitude as in fed animals. It is therefore concluded that cold exposure, and possibly also exercise, improve glucose tolerance and stimulate glucose uptake in peripheral tissues primarily by enhancing glucose oxidation via insulin-independent pathways, and secondarily by increasing the responsiveness of peripheral tissues to insulin.     

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)     

Effect of the exposure to chronic-intermittent cold on the thyrotropin and thyroid hormones in the rat

Rats exposed to acute cold (4 degrees C for 2 h), chronic cold (4 degrees C), and chronic-intermittent cold (4 degrees C for 2 h daily) were killed after 1, 2, 3, 4, and 10 days of cold exposure. The control group was maintained at 25 degrees C. In each animal, the plasma concentration of thyrotropine (THS), triiodothyronine (T3), and thyroxine (T4) was determined by radioimmunoassay. At the initial time of exposure, elevations in TSH, T3, and T4 were observed in the rats in each experimental group. However, on the 10th day, in rats exposed to chronic-intermittent cold, TSH, T3, and T4 decreased to values lower than the control values. In animals exposed to acute cold as well as to chronic cold no differences were found, with respect to the controls, in TSH and T4. In rats exposed to acute cold for 10 days, the T3 value was lower than the control value; however, in animals exposed to chronic cold, T3 was same as that in the controls. The results indicate that, in the rat, exposure to chronic-intermittent cold produces an inhibition in the secretion of TSH and thyroid hormones.