Endocrine response to acute cold exposure by lactating and non-lactating Norway rats

Plasma levels of corticosterone, prolactin and thyroxine (T4) were measured in lactating and non-lactating Norway rats at 22 degrees C and 4 degrees C. Acute cold exposure increased corticosterone secretion in all groups, although non-lactating female levels rose higher than those of mother rats. While prolactin levels are unaffected by acute cold exposure in non-lactating females, mothers with their litters had lower prolactin levels in the cold. T4 levels increased during cold exposure in lactating females, suggesting that the low T4 levels observed during lactation may not be due to lactational competition for available iodine.     

Hand immersion in cold water alleviating physiological strain and increasing tolerance to uncompensable heat stress

The current study examines the use of hand immersion in cold water to alleviate physiological strain caused by exercising in a hot climate while wearing NBC protective garments. Seventeen heat acclimated subjects wearing a semi-permeable NBC protective garment and a light bulletproof vest were exposed to a 125 min exercise-heat stress (35 degrees C, 50% RH; 5 km/h, 5% incline). The heat stress exposure routine included 5 min rest in the chamber followed by two 50:10 min work-rest cycles. During the control trial (CO), there was no intervention, whilst in the intervention condition the subjects immersed their hands and forearms in a 10 degrees C water bath (HI). The results demonstrated that hand immersion in cold water significantly reduced physiological strain. In the CO exposure during the first and second resting periods, the average rectal temperature (T (re)) practically did not decrease. With hand immersion, the mean (SD) T (re) decreased by 0.45 (0.05 degrees C) and 0.48 degrees C (0.06 degrees C) during the first and second rest periods respectively (P < 0.005). Significant decreases in skin temperature, sweat rate, heart rate, and heat storage was also noted in the HI vs. the CO trials. Tolerance time in the HI exposure were longer than in the CO exposure (only 12 subjects in the CO trial endured the entire heat exposure session, as opposed to all 17 subjects in the HI group). It is concluded that hand immersion in cold water for 10 min is an effective method for decreasing the physiological strain caused by exercising under heat stress while wearing NBC protective garments. The method is convenient, simple, and allows longer working periods in hot or contaminated areas with shorter resting periods.     

Metabolic reactions to changes in core and skin temperature in man.

The metabolic cold response, i.e. the increase in oxygen consumption above that for the given activity in a neutral environment, was measured in 7 subjects during cooling, resting or swimming in cold water (14, 16, 18, 20degrees C) and during rewarming in air (Ta 20, 30, 40degrees C), bicycling or resting. Esophageal temperatures varied between 38 and 34degrees C. Mean skin temperature was considered as equal to water temperature during cooling, and ranged between 25-35degrees C during rewarming in the different environments. Both central and peripheral cold stimulation induced metabolic cold responses. The skin temperature was the dominating factor in determining the response, especially in transient states. During rewarding a rising skin temperature suppressed the effects of even very low core temperatures.     

Plasma levels of endothelin-1 and atrial natriuretic peptide in men during a 2-hour stay in a cold room.

Male volunteers were exposed to +10 degrees C ambient temperature for 2 hours while they were sitting undressed. The levels of endothelin-1 and atrial natriuretic peptide were determined by radioimmunoassays. Control samples were obtained at thermoneutrality. The cold exposure resulted in lowering of the mean skin temperature (from 31.2 +/- 0.3 degrees C-22.6 +/- 2.5 degrees C, mean +/- SEM), which indicates that a marked vasoconstriction took place, as well as a decrease of the body heat content (by 11.2 +/- 0.7 kJ kg-1). However, plasma endothelin-1 levels did not change significantly during the exposure. Thus circulating endothelin-1 does not seem to be responsible for the vasoconstriction associated with cold air exposure. The plasma atrial natriuretic peptide levels exhibited a slight increase towards the end of the cold exposure. This finding is in accord with the notion that atrial natriuretic peptide might contribute to the diuresis frequently observed in the cold.     

Effects of central injection of biogenic amines during arousal from hibernation.

Simultaneous measurements of heat production (HP) and heat loss (HL) and brain and rectal temperatures were made in Richardon's ground squirrels (Spermophilus richardsonii) rewarming from hibernation at an ambient temperature of 6.0 +/- 0.5 degrees C. Calculations from HP and HL measurements from control animals showed that due to differential rewarming, there was a reduction of apparent specific heat of the animal to 0.59 cal/g. degrees C. This resulted in an energy saving of 30%. Three intracerebroventricular injections of 5-hydroxytryptamine (5-HT) of 56 microgram each at brain temperatures of 10, 20, and 30 degrees C caused initial suppression of HP and a greater overall HL, which resulted in a slower rate of arousal as compared to the controls. Injections of norepinephrine (NE) of 12.5 microgram each at similar brain temperatures caused a greater rate of HP, which resulted in a faster rate of arousal as compared to the controls. The respective actions of 5-HT and NE on thermoregulation during rewarming are similar to those in some euthermic hibernators and nonhibernating species. Our data indicated that these substances evoke thermoregulatory responses during arousal in much the same manner as during normothermia.     

Human face-only immersion in cold water reduces maximal apnoeic times and stimulates ventilation

In two studies, the cold shock and diving responses were investigated after human face immersion without prior hyperventilation to explore the mechanism(s) accounting for reductions in maximal apnoeic times (ATmax) at low water temperatures. In study 1, ATmax, heart rate (HR) and cutaneous blood cell velocity were measured in 13 non-apnoea-trained males during apnoeic face immersion in 0, 10, 20 and 33 degrees C water and room air (AIR). In study 2, six males were measured during non-apnoeic face immersion in 0, 10 and 33 degrees C water for ventilation (VE), respiratory exchange ratio (RER), HR and oxygen consumption (VO2), as well for end-tidal partial pressures of oxygen (PET,O2) and carbon dioxide (PET,CO2). Results indicated that the ATmax of 30.7 s (S.D. 7.1 s) at 0 degrees C (P < 0.001) and 48.2 s (S.D. 16.0 s) at 10 degrees C (P < 0.05) were significantly shorter than that of 58 s in AIR or 33 degrees C. During apnoea at 0, 10, 20 and 33 degrees C, both the deceleration of HR (P < 0.05) and peripheral vasoconstriction (P < 0.05), as well as the peak HR at 0 degrees C (P = 0.002) were significantly greater than in AIR. At 0 degrees C in comparison with 33 degrees C, non-apnoeic face immersions gave peaks in (P = 0.039), RER (P = 0.025), (P = 0.032) and HR (P = 0.011), as well as lower minimum values for (P = 0.033) and HR (P = 0.002). With as the covariate, ANCOVA showed that remained significantly greater (P = 0.003) at lower water temperatures. In conclusion, during face immersion at 10 degrees C and below, there is a non-metabolic, neurally mediated cold shock-like response that shortens apnoea, stimulates ventilation and predominates over the oxygen conserving effects of the dive response.     

Increased systolic blood pressure after mild cold and rewarming: relation to cold-induced thermogenesis and age

Aim: Higher winter mortality in elderly has been associated with augmented systolic blood pressure (SBP) response and with impaired defense of core temperature. Here we investigated whether the augmented SBP upon mild cold exposure remains after a rewarming period, and whether SBP changes are linked to thermoregulation. Therefore, we tested the following hypotheses: cold‐induced increase in SBP (1) remains augmented after rewarming in elderly compared to young adults (2) is related to non‐shivering thermogenesis (NST) upon mild cold (3) is related to vasoconstriction upon mild cold. Methods: Blood pressure, energy expenditure (EE), skin and core temperature, skin perfusion (abdomen, forearm, both sides of hand) and % body fat were measured in 12 young adults (Y) and 12 elderly (E). Supine subjects were exposed to a thermoneutral baseline 0.5 h (T_air = 30.1 °C), 1 h mild cold (T_air = 20.7 °C), 1 h rewarming (T_air = 34.8 °C) and 1 h baseline (T_air = 30.5 °C). Results: Upon mild cold only the young adults showed significant NST (Y: +2.5 ± 0.6 W m^?2, P < 0.05). No significant age effects in vasoconstriction were observed. After rewarming per cent change in SBP (%ΔSBP) remained significantly increased in both age groups and was augmented in elderly (Y: +5.0% ± 1.2% vs. E: +14.7% ± 3.1%, P < 0.05). Regression analysis revealed that %ΔSBP significantly related to ΔEE upon mild cold (P < 0.01, r² = 0.35) and in elderly also to %body fat (P < 0.02, r² = 0.57). Conclusion: Individual changes in SBP after rewarming correlate negatively to NST. Elderly did not show NST, which explains the greater SBP increase in this group. In elderly a relatively large %body fat protected against the adverse effects of mild cold.     

Effects of caffeine and high ambient temperature on haemodynamic and body temperature responses to dynamic exercise.

Caffeine can enhance mean arterial blood pressure (MAP) and attenuate forearm blood flow (FBF) and forearm vascular conductance (FVC) during exercise in thermal neutral conditions without altering body temperature. During exercise at higher ambient temperatures, where a greater transfer of heat from the body core to skin would be expected, caffeine-induced attenuation of FBF (i.e. cutaneous blood flow) could attenuate heat dissipation and increase body temperature (T(re)). We hypothesized that during exercise at an ambient temperature of 38 degrees C, caffeine increases MAP, and attenuates FBF and FVC such that T(re) is increased. Eleven caffeine-naive, active men, were studied at rest and during exercise after ingestion of a placebo or 6 mg kg(-1) of caffeine. MAP, heart rate (HR), FBF, FVC, T(re) skin temperature (T(sk)) and venous lactate concentrations (lactate) were assessed sequentially during rest at room temperature, after 45 min of exposure to an ambient temperature of 38 degrees C, and during 35 min of submaximal cycling. Heat exposure caused increases in MAP, FBF, FVC and T(sk) that were not altered by caffeine. HR, T(re), and lactate were unaffected. During exercise, only MAP (95 +/- 2 vs. 102 +/- 2 mmHg), HR (155 +/- 10 vs. 165 +/- 10 beats min(-1)), and lactate (2.0 +/- 0.4 vs. 2.3 +/- 0.4 mmol l(-1)) were increased by caffeine. These data indicate that increases in cutaneous blood flow during exercise in the heat are not reduced by caffeine. This may be because of activation of thermal reflexes that cause cutaneous vasodilation capable of offsetting caffeine-induced reductions in blood flow. Caffeine-induced increases in lactate, MAP and HR during exercise suggest that this drug and high ambient temperatures increase production of muscle metabolites that cause reflex cardiovascular responses.     

Face temperature and cardiorespiratory responses to wind in thermoneutral and cool subjects exposed to -10 degrees C

The effects of the thermal state of the body (slightly cool and neutral) and moderate wind speeds on face temperature, blood pressure, respiratory function and pain sensation during cold exposure were studied on eight healthy male subjects. They were dressed in cold-protective clothing and preconditioned at + 20 degrees C (TN) and -5 degrees C (CO) for 60 min, then exposed to -10 degrees C and 0 m x s(-1) (NoW), 1 (W1) and 5 (W5) m x s(-1) wind for 30 min. Thus, each individual was exposed six times. The exposure to wind entailed a combination of strong cooling of the bare face and mild body cooling. The forehead, cheek and nose temperatures decreased during cold exposure, and the decrease was greater at higher air velocities (P < 0.0001). All subjects reported pain sensations at 5 m x s(-1). At the end of exposure only the nose temperature was significantly lower in CO than in TN subjects; it was about 2 degrees C and reached 0 degrees C in two experiments. The systolic and diastolic blood pressure (SBP and DBP, respectively) increased significantly by 7.7 and 5.9 mmHg, respectively, during preconditioning at -5 degrees C, but did not change at + 20 degrees C. SBP and DBP increased during exposure to -10 degrees C in TN by approximately 9 mmHg. However, the total average increase of blood pressure (1-90 min) was similar in TN and CO (SBP 15 mmHg and DBP 13 mmHg). SBP and DBP increased more during exposure to 5 m x s(-1) at -10 degrees C than NoW. Blood pressure responses as observed in this study (SBP and DBP up to 51 and 45 mmHg, respectively) are potential health risks for hypertensive individuals and angina patients. Respiratory functions (FVC, FEV1) were reduced by about 3% by the cold (-5 and -10 degrees C) compared to pre-experiment values. Furthermore, the Wind Chill Index seems to underestimate the cooling power of 5 m x s(-1) at -10 degrees C of bare skin (e.g. face). Therefore it needs to be revised and we suggest that it is expanded to include risk levels for pain sensation.     

Metabolic cold acclimation after repetitive intermittent cold exposure in rat

Repetitive intermittent cold exposure (5 degrees C, 6 h/day, 4 weeks) (ICE) resulted in the same cold adaptability as assessed by an enhanced cold tolerance (less drop of colonic temperature at -5 degrees C) and nonshivering thermogenesis (NST) (greater noradrenaline-induced heat production) as that elicited by continuous cold exposure (5 degrees C, 4 weeks) (CA) in rats. Although shorter intermittent (5 degrees C, 2 h/day, 4 weeks) (ICE-2 hr) as well as shorter continuous (5 degrees C, 1 week) (CA-1 wk) cold exposure effected an improved cold adaptability, the magnitude of cold tolerance and NST was smaller as compared with that in CA and ICE. The cold deacclimation process as reflected on the decreased NST did not differ between CA and ICE. Food intake was less in ICE than CA, while increase in body weight during the acclimation period was greater in the former. Increase in adrenal weight was greater in CA than ICE, but plasma corticosterone level did not differ among warm controls (WC), CA, and ICE in resting state (after 18-20 h at warm control temperature of 25 degrees C). Weights of interscapular and dorsocervical brown adipose tissue (BAT) increased to the same degree in CA and ICE. Plasma glucagon level in resting state did not differ among groups, while BAT glucagon levels significantly increased in CA and ICE, but they were higher in dorsocervical site than interscapular site in all acclimated states. Acute cold exposure (-5 degrees C, 15 min) caused increases in plasma corticosterone, glucagon levels, and in BAT glucagon levels in all acclimated groups. The extent of increase was significantly less for plasma glucagon in CA, while plasma corticosterone increased similarly in all groups. These results indicate that repetitive short-term cold exposure could elicit the same cold adaptability as that induced by continuous exposure, but requiring only one-fourth of the time of continuous cold exposure. Moreover, it is suggested that glucagon is involved in both CA and ICE, but the same extent of cold adaptability can be obtained in the less energy-requiring and less stressful state in ICE.     

Metabolic Reactions to Changes in Core and Skin Temperature in Man

The metabolic cold response, i.e. the increase in oxygen consumption above that for the given activity in a neutral environment, was measured in 7 subjects during cooling, resting or swimming in cold water (14, 16, 18, 20°C) and during rewarming in air (T_a 20, 30, 40°C), bicycling or resting. Esophageal temperatures varied between 38 and 34°C. Mean skin temperature was considered as equal to water temperature during cooling, and ranged between 25–35°C during rewarming in the different environments. Both central and peripheral cold stimulation induced metabolic cold responses. The skin temperature was the dominating factor in determining the response, especially in transient states. During rewarming a rising skin temperature suppressed the effects of even very low core temperatures.     

Thermogenesis during ultrasonic vocalization by rat pups isolated in a warm environment: a thermographic analysis.

Ultrasonic vocalizations, emitted by rat pups when separated from their mother, littermates, and home cage, have been used as a measure of isolation distress. Recently, we demonstrated that cold exposure is the primary component of isolation that induces the vocalization. We were unable, however, to suppress all ultrasound production when transferring pups to a thermoneutral (35 degrees C) environment. Using an infrared thermography system that allows us to estimate noninvasively heat production by brown adipose tissue, we found that pups transferred from the home nest to a 35 degree C test chamber exhibited sizable levels of heat production while they were vocalizing. Moreover, both heat production and ultrasound emission decreased over the 15-min test. Next, we used extreme care to minimize thermal, and therefore respiratory, stimulation of pups before, during, and after the transfer procedure. We found that such precautions prevented both heat production and ultrasound emission following transfer. These results indicate that infant rats' thermal sensitivities are far greater than previously suspected.     

Hypothermia-induced respiratory arrest and recovery in neonatal rats

To examine the changes in breathing that occur during progressive hypothermia and rewarming in neonatal rats, we cooled and rewarmed rat pups during the first 6 days of life. During cooling, breathing stopped when rectal temperature (Tr) fell below 10.7+/-0.24 degrees C, and recovered spontaneously during rewarming when Tr reached 13.3+/-0.38 degrees C, regardless of age. During cooling, breathing frequency declined progressively, whereas tidal volume increased until Tr fell below 15 degrees C whence it declined to, but never below, normothermic levels. These data support suggestions that failure occurs at the level of the central rhythm generator for breathing and is not due to an inability to sustain the level of motor output. During rewarming, following respiratory arrest, the pattern of change was reversed, but with a significant thermal hysteresis, resulting in slower breathing and cardiac frequencies at any given rectal temperature during rewarming. There were no effects of age observed over the range studied on the changes in respiratory variables associated with hypothermia or rewarming. Breathing restarted spontaneously on rewarming with no evidence that gasping was required to initiate this process. The overall breathing pattern was episodic during the early stages of rewarming, however, suggesting that the respiratory rhythm is only periodically expressed during the initial stages of recovery from hypothermia.     

Behavioral thermoregulation in the squirrel monkey: adaptation processes during prolonged microwave exposure

During 10-min exposures to 2450-MHz microwaves at a power density of 6-8 m W/cm2, squirrel monkeys reliably select a cooler environment. Exposure duration, at power densities above and below this threshold, was the parameter investigated in these experiments. Monkeys were restrained in the far field of a horn antenna inside a 1.8 x 1.8 x 2.5 m anechoic chamber which was heated and cooled by forced convection. The animals learned to control the temperature of the circulating chamber air by selecting between cold (10-15 degrees C) and warm (50-55 degrees C) air sources. During the experiments, they were exposed to 12.4-cm (2450-MHz) continuous-wave microwaves for periods from 5 to 150 min. Microwave power densities explored were 4, 10, and 20 mW/cm2 which represent rates of whole-body energy absorption that range from approximately, .6 to 3.0 W/kg. No microwaves were present during 4-hr control experiments. The 4 mW/cm2 microwave exposure did not modify thermoregulatory behavior, no matter how long it lasted. The 10 and 20 mW/cm2 exposures stimulated the monkeys to select ambient temperatures 1.5 and 3.0 degrees C cooler than control levels, respectively. Except during the first microwave presentation of a series, or during the early minutes of a single long exposure, duration had no significant effect on selection of air temperature or on the body temperatures achieved thereby.     

Dopamine D2 receptor stimulation inhibits cold-initiated thermogenesis in brown adipose tissue in conscious rats

Dopamine D(2)-like receptor agonists cause hypothermia. We investigated whether inhibiting heat production by interscapular brown adipose tissue (iBAT), a major thermogenic organ in rats, contributes to hypothermia caused by dopamine D(2)-like receptor agonists. Temperature of iBAT and tail artery blood flow were measured in conscious rats. Activity in postganglionic sympathetic nerves supplying iBAT was assessed in anesthetized rats. Conscious rats were housed in a warm cage maintained at 26-28 degrees C and then transferred to a cold cage at 5-10 degrees C to induce iBAT thermogenesis. Cold exposure increased iBAT temperature (+0.7+/-0.1 degrees C, 30 min after transferring to the cold cage, P<0.01, n=54). The mixed dopamine D(2)/D(3) receptor agonist, 7-hydroxy-2-(di-n-propylamino)tetralin (7-OH-DPAT, 0.5 mg/kg s.c.) reversed the cold-induced increase in iBAT temperature (-2.8+/-0.2 degrees C at 30 min after 7-OH-DPAT treatment during cold exposure vs. +0.3+/-0.1 degrees C at 30 min after vehicle treatment during cold exposure, n=8). These temperature changes were blocked by pre-treatment with the D(2) receptor antagonists spiperone (20 microg/kg i.p.) and L-741,626 (2.5 mg/kg i.p.), but not by the selective D(3) receptor antagonist SB-277011A (10 mg/kg i.p.). Another mixed dopamine D(2)/D(3) receptor agonist, quinpirole (0.5 mg/kg s.c.) also reversed cold-induced iBAT thermogenesis, and this effect was also prevented by pre-treatment with spiperone, but not with a peripherally acting dopamine receptor antagonist, domperidone (2 mg/kg s.c.). Neither 7-OH-DPAT nor quinpirole reversed cutaneous vasoconstriction elicited by cold exposure. In anesthetized rats, quinpirole (0.5 mg/kg i.v.) abolished iBAT sympathetic nerve discharge elicited by cooling the trunk, and this change was reversed by spiperone (20 microg/kg i.v.). These results demonstrate that activation of CNS dopamine D(2) receptors inhibits sympathetically-mediated iBAT thermogenesis in response to cold exposure. Furthermore, they suggest that in rats hypothermia induced by dopamine D(2) receptor agonists in cold environments is mainly due to decreased heat production rather than to increased heat loss.     

Cold tolerance and metabolic heat production in male C57BL/6J mice at different times of day.

Nine-month-old male C57BL/6J mice were subjected to three-hour cold stress tests (partial restraint at 6 degrees C) at 9:00 a.m. or at 1:00 p.m. Tests were repeated three times at two-week intervals at the same time of day. Body temperature was measured by colonic thermoprobe, and metabolic heat production was measured by indirect calorimetry during each test. All mice showed habituation to repeated cold exposures (an improvement of cold tolerance across tests) due to an increase in metabolic heat production. The levels of metabolic heat production were similar during morning and afternoon testing; however, mice tested in the afternoon had consistently poorer cold tolerance, which indicated increased heat loss. Increased heat loss in mice of similar body weight and presumably similar body composition, suggests that there is less effective cold-induced skin vasoconstriction during the afternoon. We hypothesize that the compromised skin vasomotor response during the afternoon cold exposure results from competing effects of vasodilation due to local autoregulation stimulated by a circadian reduction of cardiac output during the sleep phase, and vasoconstriction due to the cold stress.     

Influence of moderate cold exposure on blood lactate during incremental exercise

Summary This study examined the effect of exposure of the whole body to moderate cold on blood lactate produced during incremental exercise. Nine subjects were tested in a climatic chamber, the room temperature being controlled either at 30°C or at 10°C. The protocol consisted of exercise increasing in intensity in 35 W increments every 3 min until exhaustion. Oxygen consumption (VO₂) was measured during the last minute of each exercise intensity. Blood samples were collected at rest and at exhaustion for the measurement of blood glucose, free fatty acid (FFA), noradrenaline (NA) and adrenaline (A) concentrations and, during the last 15 s of each exercise intensity, for the determination of blood lactate concentration [la^–]_b. TheVO₂ was identical under both environments. At 10°C, as compared to 30°C, the lactate anaerobic threshold (Th_{an, la} ^–) occurred at an exercise intensity 15 W higher and [Th_{an, la} ^–]_b was lower for submaximal intensities above the Th_{an, la} ^– Regardless of ambient temperature, glycaemia, A and NA concentrations were higher at exhaustion while FFA was unchanged. At exhaustion the NA concentration was greater at 10°C [15.60 (SEM 3.15) nmol·l^–1] than at 30°C [8.64 (SEM 2.37) nmol·l^–1]. We concluded that exposure to moderate cold influences the blood lactate produced during incremental exercise. These results suggested that vasoconstriction was partly responsible for the lower [la^–]_b observed for submaximal high intensities during severe cold exposure.     

Effect of body temperature on cold induced vasodilation

Cold-induced vasodilation (CIVD) is an acute increase in peripheral blood flow observed during cold exposures. It is hypothesized to protect against cold injuries, yet despite continuous research it remains an unexplained phenomenon. Contrary to the traditionally held view, we propose that CIVD is a thermoregulatory reflex mechanism contributing to heat loss. Ten adults (4 females; 23.8 +/- 2.0 years) randomly underwent three 130-min exposures to -20 degrees C incorporating a 10-min moderate exercise period at the 65th min, while wearing a liquid conditioning garment (LCG) and military arctic clothing. In the pre-warming condition, rectal temperature was increased by 0.5 degrees C via the LCG before the cold exposure. In the warming condition, participants regulated the LCG throughout the cold exposure to subjective comfort. In the control condition, the LCG was worn but was not operated either before or during the cold exposure. Results demonstrated that the majority of CIVD occurred during the warming condition when the thermometrically-estimated mean body temperature (T (b)) was at its highest. A thermoregulatory pattern was identified whereby CIVD occurred soon after T (b) increased past a threshold (~36.65 degrees C in warming and pre-warming; ~36.4 degrees C in control). When CIVD occurred, T (b) was reduced and CIVD ceased when T (b) fell below the threshold. These findings were independent of extremity temperature since CIVD episodes occurred at a large range of finger temperatures (7.2-33.5 degrees C). These observations were statistically confirmed by auto-regressive integrated moving average analysis (t = 9.602, P < 0.001). We conclude that CIVD is triggered by increased T (b) supporting the hypothesis that CIVD is a thermoregulatory mechanism contributing to heat loss.     

Lasting effect of infantile cold experience on cold tolerance in adult rats.

The effect of short and repetitive exposure to cold (5 degrees C, 4 hr/day for 2 weeks) from the birth up to the 14th day of newborn rats onthe thermal regulation in adulthood and on the tolerance to cold was investigated. After being exposed to cold, they were transferred to a room at 25 degrees C (N-CA). The control rats were raised at 25 degrees C (N-WA). An acute cold exposure test was performed by placing the animals in a room at 5 degrees C under urethane anesthesia. Electrical activity of neck muscles as an index of shivering was recorded. The colonic temperature fell at a significantly slower rate in N-CA rats with less shivering than in N-WA ones. Nonshivering thermogenesis tested by norepinephrine was significantly greater in N-CA rats than in N-WA ones. These results suggest that N-CA rats developed improved cold tolerance accompanied by greater nonshivering thermogenesis. Such a phenomenon in N-CA lasted for 18 weeks after the termination of cold exposure. Adult rats subjected to the same scheme of cold exposure (A-CA) (5 degrees C, 4 hr/day, 2 weeks) showed essentially the same results as seen in N-CA, but its improved cold tolerance and elevated nonshivering thermogenesis disappeared 4 weeks after the termination of cold exposure. Extirpation of interscapular brown adipose tissue immediately before the cold test did not appreciably affect the cold tolerance in N-CA and A-CA rats. The colonic temperature at the onset of shivering was significantly lower in N-CA as well as A-CA rats than in each of the corresponding control rats, indicating a shift of the shivering threshold to lower temperature values in the animals exposed intermittently to cold. These results indicate that an infantile experience with cold results in a greater and longer sustained ability to tolerate cold in adulthood, characterized by enhanced nonshivering thermogenesis.     

Fat metabolism and heat production in young rabbits

1. The rates of oxygen consumption were measured in 6-8-day-old rabbits at 34 and 15 degrees C after varying periods of starvation and cold exposure. At the start of the experiment the rabbits had been fasted for 24 hr. Eight rabbits were studied immediately, six after 24 and six after 48 hr in a cold environment (20 degrees C), and twelve after a further 48 hr in a warm environment (34 degrees C). All the animals had a similar increase in oxygen consumption during the final hour of cold exposure (15 degrees C).2. The rabbits kept at 20 degrees C lost 83% of the fat stored in their brown adipose tissue within 24 hr and a further 11% in the next 24 hr. The fat content of white adipose tissue had fallen by 75% at 48 hr. In contrast rabbits kept unfed at 34 degrees C had lost 47% of the fat in brown adipose tissue and 44% of the fat in white adipose tissue after 48 hr.3. In six rabbits subcutaneous thermocouples demonstrated that local heat production continued in brown adipose tissue after 48 hr cold exposure.4. In the rabbits kept at 34 degrees C the final cold exposure caused a large increase in the serum free fatty acid and glycerol concentrations. Much lower concentrations were found in rabbits kept at 20 degrees C.5. The results show that the fat stored in the brown adipose tissue of young rabbits exposed to cold is preferentially used for heat production. When this store of fat is exhausted, brown adipose tissue still produces heat presumably by oxidizing fat and glucose taken from the circulation.