Shivering onset, metabolic response, and convective heat transfer during cold air exposure

The onset and intensity of shivering of various muscles during cold air exposure are quantified and related to increases in metabolic rate and convective heat loss. Thirteen male subjects resting in a supine position and wearing only shorts were exposed to 10 degrees C air (42% relative humidity and less than 0.4 m/s airflow) for 2 h. Measurements included surface electromyogram recordings at six muscle sites representing the trunk and limb regions of one side of the body, temperatures and heat fluxes at the same contralateral sites, and metabolic rate. The subjects were grouped according to lean (LEAN, n = 6) and average body fat (NORM, n = 7) content. While the rectal temperatures fluctuated slightly but not significantly during exposure, the skin temperature decreased greatly, more at the limb sites than at the trunk sites. Muscles of the trunk region began to shiver sooner and at a higher intensity than those of the limbs. The intensity of shivering and its increase over time of exposure were consistent with the increase in the convective heat transfer coefficient calculated from skin temperatures and heat fluxes. Both the onset of shivering and the magnitude of the increase in metabolic rate due to shivering were higher for the LEAN group than for the NORM group. A regression analysis indicates that, for a given decrease in mean skin temperature, the increase in metabolic rate due to shivering is attenuated by the square root of percent body fat. Thus the LEAN group shivered at higher intensity, resulting in higher increases in metabolic heat production and convective heat loss during cold air exposure than did the NORM group.     

Mechanism of action of physical antipyresis in the rat

To study the mechanism of action of physical antipyresis, core temperature was measured in two groups of rats in which heat loss was increased by cold exposure and by cooling an inferior cava heat exchanger, respectively, both before and after infection with Salmonella enteritidis. Cold exposure did not influence core temperature. On the other hand, cooling the heat exchanger caused a fall in core temperature of approximately 0.7 degree C, to 37 degrees C in normothermia and to 38.5 degrees C 24 h after the infection. These lower core temperatures were then regulated against any further increase in heat loss until the thermoregulatory metabolic capacity of the animals was exhausted and a hypothermia developed. It is concluded that in infectious fever the threshold temperature of shivering increases as much as core temperature. Furthermore it is suggested that physical antipyresis, such as sponging with tepid water, induces a moderate but regulated fall in temperature to about the threshold of shivering and that its efficacy may increase with ambient temperature.     

Control of sweating in man after work-induced thermal load and symmetrically applied cooling

To examine the compensatory effects of work-induced thermal load and symmetrically applied local cooling on local sweat rates, two kinds of experiment were carried out on eight male subjects in a climatic chamber: 1) Experiments at 36 degrees C ambient temperature with a work load of about 25 W by the right leg. 2) Experiments at 36 degrees C ambient temperature with a work load of about 25 W by the right leg as in 1., but with additional compensatory cooling of the left leg controlled throughout by heat balance calculations at 75-85 W, equal to the heat produced in the working leg, the necessary air temperature being dependent on local sweat rate. Work load without cooling brought about a significant increase in core temperatures, metabolism, heart rate and local sweat rates. With unchanged local skin temperatures local sweat rate increase was higher in the working leg. Therefore the existence of muscle thermoreceptors should be assumed, the afferent information from which is processed and weighted in a different way to that provided by skin receptors. Work load combined with additional cooling reduced local and mean skin temperatures and heart rate, but had no significant influence on core temperature or metabolism. However, local sweat rate was generally lower in both thighs, with a major reduction in the cooled leg confirming control of local sweat rate by local temperature.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of head skin temperature on tympanic and oral temperature in man.

Five subjects were sequentially heated and cooled in a double-climate chamber while mean skin temperature (except the head) and head skin temperature were separately varied. The tympanic membrane temperatures of these subjects were disproportionately influenced by changes in head skin temperature. By heating and cooling localized regions of the head, changes in tympanic membrane temperature that followed changes in skin temperature on the ipsilateral side of the head could be produced. During heating of the head, oral and tympanic membrane temperatures were influenced to a similar degree, while esophageal temperature remained essentially unaffected. However, under conditions in which the legs and feet were heated in a water bath, esophageal temperature showed more rapid changes than either tympanic membrane or oral temperature. These findings suggest that tympanic membrane temperature and, to a lesser degree, oral temperature may be affected by thermal exchange occurring between arteries and veins in the cervical and cephalic regions. In addition, the ability to influence selectively esophageal and tympanic membrane temperatures brings into question the arbitrary use of these measurements under widely different experimental conditions as estimates of core temperature.     

Thermal effects of whole head submersion in cold water on nonshivering humans.

This study isolated the effect of whole head submersion in cold water, on surface heat loss and body core cooling, when the confounding effect of shivering heat production was pharmacologically eliminated. Eight healthy male subjects were studied in 17 degrees C water under four conditions: the body was either insulated or uninsulated, with the head either above the water or completely submersed in each body-insulation subcondition. Shivering was abolished with buspirone (30 mg) and meperidine (2.5 mg/kg), and subjects breathed compressed air throughout all trials. Over the first 30 min of immersion, exposure of the head increased core cooling both in the body-insulated conditions (head out: 0.47 +/- 0.2 degrees C, head in: 0.77 +/- 0.2 degrees C; P < 0.05) and the body-exposed conditions (head out: 0.84 +/- 0.2 degrees C and head in: 1.17 +/- 0.5 degrees C; P < 0.02). Submersion of the head (7% of the body surface area) in the body-exposed conditions increased total heat loss by only 10%. In both body-exposed and body-insulated conditions, head submersion increased core cooling rate much more (average of 42%) than it increased total heat loss. This may be explained by a redistribution of blood flow in response to stimulation of thermosensitive and/or trigeminal receptors in the scalp, neck and face, where a given amount of heat loss would have a greater cooling effect on a smaller perfused body mass. In 17 degrees C water, the head does not contribute relatively more than the rest of the body to surface heat loss; however, a cold-induced reduction of perfused body mass may allow this small increase in heat loss to cause a relatively larger cooling of the body core.     

Thermal effects of dorsal head immersion in cold water on nonshivering humans.

Personal floatation devices maintain either a semirecumbent flotation posture with the head and upper chest out of the water or a horizontal flotation posture with the dorsal head and whole body immersed. The contribution of dorsal head and upper chest immersion to core cooling in cold water was isolated when the confounding effect of shivering heat production was inhibited with meperidine (Demerol, 2.5 mg/kg). Six male volunteers were immersed four times for up to 60 min, or until esophageal temperature = 34 degrees C. An insulated hoodless dry suit or two different personal floatation devices were used to create four conditions: 1) body insulated, head out; 2) body insulated, dorsal head immersed; 3) body exposed, head (and upper chest) out; and 4) body exposed, dorsal head (and upper chest) immersed. When the body was insulated, dorsal head immersion did not affect core cooling rate (1.1 degrees C/h) compared with head-out conditions (0.7 degrees C/h). When the body was exposed, however, the rate of core cooling increased by 40% from 3.6 degrees C/h with the head out to 5.0 degrees C/h with the dorsal head and upper chest immersed (P < 0.01). Heat loss from the dorsal head and upper chest was approximately proportional to the extra surface area that was immersed (approximately 10%). The exaggerated core cooling during dorsal head immersion (40% increase) may result from the extra heat loss affecting a smaller thermal core due to intense thermal stimulation of the body and head and resultant peripheral vasoconstriction. Dorsal head and upper chest immersion in cold water increases the rate of core cooling and decreases potential survival time.     

Thermal, cardiac and adrenergic responses to repeated local cooling

The aim of this study was to ascertain whether repeated local cooling induces the same or different adaptational responses as repeated whole body cooling. Repeated cooling of the legs (immersion into 12 degrees C water up to the knees for 30 min, 20 times during 4 weeks = local cold adaptation - LCA) attenuated the initial increase in heart rate and blood pressure currently observed in control subjects immersed in cold water up to the knees. After LCA the initial skin temperature decrease tended to be lower, indicating reduced vasoconstriction. Heart rate and systolic blood pressure appeared to be generally lower during rest and during the time course of cooling in LCA humans, when compared to controls. All these changes seem to indicate attenuation of the sympathetic tone. In contrast, the sustained skin temperature in different areas of the body (finger, palm, forearm, thigh, chest) appeared to be generally lower in LCA subjects than in controls (except for temperatures on the forehead). Plasma levels of catecholamines (measured 20 and 40 min after the onset of cooling) were also not influenced by local cold adaptation. Locally cold adapted subjects, when exposed to whole body cold water immersion test, showed no change in the threshold temperature for induction of cold thermogenesis. This indicates that the hypothermic type of cold adaptation, typically occurring after systemic cold adaptation, does not appear after local cold adaptation of the intensity used. It is concluded that in humans the cold adaptation due to repeated local cooling of legs induces different physiological changes than systemic cold adaptation.     

Consequences of partial body warming and cooling for the drives to local sweat rates

Climatic chamber experiments were carried out on young, healthy male students. The ambient temperature was 36 degrees C, while local warming of one extremity was compensated for by heatflow-equivalent cooling of the ipsilateral extremity by on-line calculation of the heat balance. When warming the arm and cooling the leg (type 1 experiments), a slight, but not statistically significant increase of local sweat rates at these extremities was recorded. However, when cooling the arm and warming the leg (type 2 experiments), both corresponding local sweat rates declined. The divergent results are interpreted in terms of previously reported different central weighting factors for skin temperatures as determined: (1) by the weighting for the area, or (2) by the weighting for the area and the sensitivity of the local sweat rate to warming and cooling. This means that the central processing of the mean skin temperature may be different for cooling and warming and that in both cases values can be different from recorded (area weighted) skin temperature. Calculating this modified mean skin temperature, we conclude that type 1 experiments may be interpreted by the hypothesis that the central regulator has a status very near an overall heat-balance, whereas type 2 experiments, although also carried out at heat-balance, may be centrally evaluated as predominant cooling. In these experiments again the central drives representing the whole body thermal state seem to override both the direct and centrally mediated local drives.     

Modulation of arterial baroreflex control of heart rate by skin cooling and heating in humans.

The purpose of this study was to examine the effects of skin cooling and heating on the heart rate (HR) control by the arterial baroreflex in humans. The subjects were 15 healthy men who underwent whole body thermal stress (esophageal temperatures, approximately 36.8 and approximately 37.0 degrees C; mean skin temperatures, approximately 26.4 and approximately 37.7 degrees C, in skin cooling and heating, respectively) produced by a cool or hot water-perfused suit during supine rest. The overall arterial baroreflex sensitivity in the HR control was calculated from spontaneous changes in beat-to-beat arterial pressure and HR during normothermic control and thermal stress periods. The carotid baroreflex sensitivity was evaluated from the maximum slope of the HR response to changes in carotid distending pressure, calculated as mean arterial pressure minus neck pressure. The overall arterial baroreflex sensitivity at existing arterial pressure increased during cooling (-1.32 +/- 0.25 vs. -2.13 +/- 0.20 beats. min(-1). mmHg(-1) in the control and cooling periods, respectively, P < 0.05), whereas it did not change significantly during heating (-1.39 +/- 0. 23 vs. -1.40 +/- 0.15 beats. min(-1). mmHg(-1) in the control and heating periods, respectively). Neither the cool nor heat loadings altered the carotid baroreflex sensitivity in the HR control. These results suggest that the sensitivity of HR control by the extracarotid (presumably aortic) baroreflex was augmented by whole body skin cooling, whereas the sensitivities of HR control by arterial baroreflex remain unchanged during mild whole body heating in humans.     

Heat balance precedes stabilization of body temperatures during cold water immersion.

Certain previous studies suggest, as hypothesized herein, that heat balance (i.e., when heat loss is matched by heat production) is attained before stabilization of body temperatures during cold exposure. This phenomenon is explained through a theoretical analysis of heat distribution in the body applied to an experiment involving cold water immersion. Six healthy and fit men (mean +/- SD of age = 37.5 +/- 6.5 yr, height = 1.79 +/- 0.07 m, mass = 81.8 +/- 9.5 kg, body fat = 17.3 +/- 4.2%, maximal O2 uptake = 46.9 +/- 5.5 l/min) were immersed in water ranging from 16.4 to 24.1 degrees C for up to 10 h. Core temperature (Tco) underwent an insignificant transient rise during the first hour of immersion, then declined steadily for several hours, although no subject's Tco reached 35 degrees C. Despite the continued decrease in Tco, shivering had reached a steady state of approximately 2 x resting metabolism. Heat debt peaked at 932 +/- 334 kJ after 2 h of immersion, indicating the attainment of heat balance, but unexpectedly proceeded to decline at approximately 48 kJ/h, indicating a recovery of mean body temperature. These observations were rationalized by introducing a third compartment of the body, comprising fat, connective tissue, muscle, and bone, between the core (viscera and vessels) and skin. Temperature change in this "mid region" can account for the incongruity between the body's heat debt and the changes in only the core and skin temperatures. The mid region temperature decreased by 3.7 +/- 1.1 degrees C at maximal heat debt and increased slowly thereafter. The reversal in heat debt might help explain why shivering drive failed to respond to a continued decrease in Tco, as shivering drive might be modulated by changes in body heat content.     

Exertion-induced fatigue and thermoregulation in the cold

Cold exposure facilitates body heat loss which can reduce body temperature, unless mitigated by enhanced heat conservation or increased heat production. When behavioral strategies inadequately defend body temperature, vasomotor and thermogenic responses are elicited, both of which are modulated if not mediated by sympathetic nervous activation. Both exercise and shivering increase metabolic heat production which helps offset body heat losses in the cold. However, exercise also increases peripheral blood flow, in turn facilitating heat loss, an effect that can persist for some time after exercise ceases. Whether exercise alleviates or exacerbates heat debt during cold exposure depends on the heat transfer coefficient of the environment, mode of activity and exercise intensity. Prolonged exhaustive exercise leading to energy substrate depletion could compromise maintenance of thermal balance in the cold simply by precluding continuation of further exercise and the associated thermogenesis. Hypoglycemia impairs shivering, but this appears to be centrally mediated, rather than a limitation to peripheral energy metabolism. Research is equivocal regarding the importance of muscle glycogen depletion in explaining shivering impairments. Recent research suggests that when acute exercise leads to fatigue without depleting energy stores, vasoconstrictor responses to cold are impaired, thus body heat conservation becomes degraded. Fatigue that was induced by chronic overexertion sustained over many weeks, appeared to delay the onset of shivering until body temperature fell lower than when subjects were rested, as well as impair vasoconstrictor responses. When heavy physical activity is coupled with underfeeding for prolonged periods, the resulting negative energy balance leads to loss of body mass, and the corresponding reduction in tissue insulation, in turn, compromises thermal balance by facilitating conductive transfer of body heat from core to shell. The possibility that impairments in thermoregulatory responses to cold associated with exertional fatigue are mediated by blunted sympathetic nervous responsiveness to cold is suggested by some experimental observations and merits further study.     

In vivo mechanisms of cutaneous vasodilation and vasoconstriction in humans during thermoregulatory challenges.

This review focuses on the neural and local mechanisms that have been demonstrated to effect cutaneous vasodilation and vasoconstriction in response to heat and cold stress in vivo in humans. First, our present understanding of the mechanisms by which sympathetic cholinergic nerves mediate cutaneous active vasodilation during reflex responses to whole body heating is discussed. These mechanisms include roles for cotransmission as well as nitric oxide (NO). Next, the mechanisms by which sympathetic noradrenergic nerves mediate cutaneous active vasoconstriction during whole body cooling are reviewed, including cotransmission by neuropeptide Y (NPY) acting through NPY Y1 receptors. Subsequently, current concepts for the mechanisms that effect local cutaneous vascular responses to direct skin warming are examined. These mechanisms include the roles of temperature-sensitive afferent neurons as well as NO in causing vasodilation during local heating of skin. This section is followed by a review of the mechanisms that cause local cutaneous vasoconstriction in response to direct cooling of the skin, including the dependence of these responses on intact sensory and sympathetic, noradrenergic innervation as well as roles for nonneural mechanisms. Finally, unresolved issues that warrant further research on mechanisms that control cutaneous vascular responses to heating and cooling are discussed.     

Local heating, but not indirect whole body heating, increases human skeletal muscle blood flow

For decades it was believed that direct and indirect heating (the latter of which elevates blood and core temperatures without directly heating the area being evaluated) increases skin but not skeletal muscle blood flow. Recent results, however, suggest that passive heating of the leg may increase muscle blood flow. Using the technique of positron-emission tomography, the present study tested the hypothesis that both direct and indirect heating increases muscle blood flow. Calf muscle and skin blood flows were evaluated from eight subjects during normothermic baseline, during local heating of the right calf [only the right calf was exposed to the heating source (water-perfused suit)], and during indirect whole body heat stress in which the left calf was not exposed to the heating source. Local heating increased intramuscular temperature of the right calf from 33.4 ± 1.0°C to 37.4 ± 0.8°C, without changing intestinal temperature. This stimulus increased muscle blood flow from 1.4 ± 0.5 to 2.3 ± 1.2 ml·100 g?1·min?1 (P < 0.05), whereas skin blood flow under the heating source increased from 0.7 ± 0.3 to 5.5 ± 1.5 ml·100 g?1·min?1 (P < 0.01). While whole body heat stress increased intestinal temperature by ～1°C, muscle blood flow in the calf that was not directly exposed to the water-perfused suit (i.e., indirect heating) did not increase during the whole body heat stress (normothermia: 1.6 ± 0.5 ml·100 g?1·min?1; heat stress: 1.7 ± 0.3 ml·100 g?1·min?1; P = 0.87). Whole body heating, however, reflexively increased calf skin blood flow (to 4.0 ± 1.5 ml·100 g?1·min?1) in the area not exposed to the water-perfused suit. These data show that local, but not indirect, heating increases calf skeletal muscle blood flow in humans. These results have important implications toward the reconsideration of previously accepted blood flow distribution during whole body heat stress.     

Skin and core temperature response to partial- and whole-body heating and cooling

1. Human subjects were exposed to partial- and whole-body heating and cooling in a controlled environmental chamber to quantify physiological and subjective responses to thermal asymmetries and transients.

2. Skin temperatures, core temperature, thermal sensation, and comfort responses were collected for 19 local body parts and for the whole body.

3. Core temperature increased in response to skin cooling and decreased in response to skin heating.

4. Hand and finger temperatures fluctuated significantly when the body was near a neutral thermal state.

5. When using a computer mouse in a cool environment, the skin temperature of the hand using the mouse was observed to be 2–3 °C lower than the unencumbered hand.     

The effect of dynamic exercise on resting cold thermoregulatory responses measured during water immersion

The purpose of this study was to evaluate the effect of exercise on the subsequent post-exercise thresholds for vasoconstriction and shivering measured during water immersion. On 2 separate days, seven subjects (six males and one female) were immersed in water (37.5 degrees C) that was subsequently cooled at a constant rate of approximately 6.5 degrees C x h(-1) until the thresholds for vasoconstriction and shivering were clearly established. Water temperature was then increased to 37.5 degrees C. Subjects remained immersed for approximately 20 min, after which they exited the water, were towel-dried and sat in room air (22 degrees C) until both esophageal temperature and mean skin temperature (Tsk) returned to near-baseline values. Subjects then either performed 15 min of cycle ergometry (at 65% maximal oxygen consumption) followed by 30 min of recovery (Exercise), or remained seated with no exercise for 45 min (Control). Subjects were then cooled again. The core temperature thresholds for both vasoconstriction and shivering increased significantly by 0.2 degrees C Post-Exercise (P < 0.05). Because the Tsk at the onset of vasoconstriction and shivering was different during Pre- and Post-Exercise Cooling, we compensated mathematically for changes in skin temperatures using the established linear cutaneous contribution of skin to the control of vasoconstriction and shivering (20%). The calculated core temperature threshold (at a designated skin temperature of 32.0 degrees C) for vasoconstriction increased significantly from 37.1 (0.3) degrees C to 37.5 ( 0.3) degrees C post-exercise (P < 0.05). Likewise, the shivering threshold increased from 36.2 (0.3) degrees C to 36.5 (0.3) degrees C post-exercise (P < 0.05). In contrast to the post-exercise increase in cold thermal response thresholds, sequential measurements demonstrated a time-dependent similarity in the Pre- and Post-Control thresholds for vasoconstriction and shivering. These data indicate that exercise has a prolonged effect on the post-exercise thresholds for both cold thermoregulatory responses.     

Voluntary muscle activation is impaired by core temperature rather than local muscle temperature.

Fatigue during hyperthermia may be due in part to a failure of the central nervous system to fully activate the working muscles. We investigated the effects of passive hyperthermia on maximal plantar flexor isometric torque (maximal isometric voluntary contraction) and voluntary activation to determine the roles of local skin temperature, core temperature, and peripheral muscle temperature in fatigue. Nine healthy subjects were passively heated from 37.2 to 39.5 degrees C (core temperature) and then cooled back down to 37.9 degrees C using a liquid-conditioning garment, with the right leg kept at a thermoneutral temperature throughout the protocol, whereas the left leg was allowed to heat and cool. Passive heating resulted in significant decreases in torque from [mean (SD)] 172 N x m (SD 39) to 160 N x m (SD 44) and in voluntary activation from 96% (SD 2) to 91% (SD 5) in the heated leg, and maximal isometric voluntary contraction decreased similarly from 178 N xm (SD 37) to 165 N x m (SD 38) and voluntary activation from 97% (SD 2) to 94% (SD 5) in the thermoneutral leg. The initiation of cooling, which produced a rapid decrease in skin temperature and cardiovascular strain [heart rate reserve decreased from 58% (SD 12) to 31% (SD 12)], did not immediately restore either torque or voluntary activation. However, when core temperature was lowered back to normal, torque and voluntary activation were restored to baseline values. It was concluded that an increase in core temperature is a factor responsible for reducing voluntary activation during brief voluntary isometric contractions and that temperature-induced changes in the contractile properties of muscle and local thermal afferent input from the skin do not contribute significantly to the decrement in torque.     

Effects of the menstrual cycle on muscle recruitment and oxidative fuel selection during cold exposure

Differences in core temperature and body heat content, generally observed between the luteal and follicular phase of the menstrual cycle, have been reported to modulate the thermogenic activity of cold-exposed women. However, it is unclear how this change in whole body shivering activity will influence fuel selection. The goal of this study was to quantify the effects of the menstrual cycle on muscle recruitment and oxidative fuel selection during low-intensity shivering. Electromyographic activity of eight large muscles was monitored while carbohydrate, lipid, and protein utilization was simultaneously quantified in the follicular and luteal phases of the menstrual cycle in nonacclimatized women shivering at a low intensity. The onset (～25 min), intensity (～15% of maximal voluntary contraction), and pattern (～6 shivering bursts/min) of the shivering response did not differ between menstrual cycle phases, regardless of differences in core temperature and hormone levels. This resulted in lipids remaining the predominant substrate, contributing 75% of total heat production, independent of menstrual phase. We conclude that hormone fluctuations inherent in the menstrual cycle do not affect mechanisms of substrate utilization in the cold. Whether the large contribution of lipids to total heat production in fuel selection confers a survival advantage remains to be established.     

Computer prediction of human thermoregulatory and temperature responses to a wide range of environmental conditions

A mathematical model for predicting human thermal and regulatory responses in cold, cool, neutral, warm, and hot environments has been developed and validated. The multi-segmental passive system, which models the dynamic heat transport within the body and the heat exchange between body parts and the environment, is discussed elsewhere. This paper is concerned with the development of the active system, which simulates the regulatory responses of shivering, sweating, and peripheral vasomotion of unacclimatised subjects. Following a comprehensive literature review, 26 independent experiments were selected that were designed to provoke each of these responses in different circumstances. Regression analysis revealed that skin and head core temperature affect regulatory responses in a non-linear fashion. A further signal, i.e. the rate of change of the mean skin temperature weighted by the skin temperature error signal, was identified as governing the dynamics of thermoregulatory processes in the cold. Verification and validation work was carried out using experimental data obtained from 90 exposures covering a range of steady and transient ambient temperatures between 5°C and 50°C and exercise intensities between 46 W/m² and 600 W/m². Good general agreement with measured data was obtained for regulatory responses, internal temperatures, and the mean and local skin temperatures of unacclimatised humans for the whole spectrum of climatic conditions and for different activity levels. Received: 20 November 2000 / Revised: 24 April 2001 / Accepted: 14 May 2001     

Thermal insulation and body temperature wearing a thermal swimsuit during water immersion

This study evaluated the effects of a thermal swimsuit on body temperatures, thermoregulatory responses and thermal insulation during 60 min water immersion at rest. Ten healthy male subjects wearing either thermal swimsuits or normal swimsuits were immersed in water (26 degrees C or 29 degrees C). Esophageal temperature, skin temperatures and oxygen consumption were measured during the experiments. Metabolic heat production was calculated from oxygen consumption. Heat loss from skin to the water was calculated from the metabolic heat production and the change in mean body temperature during water immersion. Total insulation and tissue insulation were estimated by dividing the temperature difference between the esophagus and the water or the esophagus and the skin with heat loss from the skin. Esophageal temperature with a thermal swimsuit was higher than that with a normal swimsuit at the end of immersion in both water temperature conditions (p<0.05). Oxygen consumption, metabolic heat production and heat loss from the skin were less with the thermal swimsuit than with a normal swimsuit in both water temperatures (p<0.05). Total insulation with the thermal swimsuit was higher than that with a normal swimsuit due to insulation of the suit at both water temperatures (p<0.05). Tissue insulation was similar in all four conditions, but significantly higher with the thermal swimsuit in both water temperature conditions (p<0.05), perhaps due to of the attenuation of shivering during immersion with a thermal swimsuit. A thermal swimsuit can increase total insulation and reduce heat loss from the skin. Therefore, subjects with thermal swimsuits can maintain higher body temperatures than with a normal swimsuit and reduce shivering thermo-genesis.     

Effect of rapid and slow cooling on thermoregulatory responses in hypertensive and normotensive rats after calcium administration

The effect of iontophoretic administration of calcium ions to skin in the area of cold stimulus application on the thermal thresholds and the magnitude of cold defense responses in normotensive Wistar and hypertensive ISIAH rats was studied. In thermoneutral conditions, administration of calciumions wos without effect on the measured thermoregulatory parameters. Under the effect of calcium, the thresholds of all the thermoregulatory responses to cooling (such as heat loss, oxygen consumption, shivering) are lowered and the values of heat loss and shivering thermogenesis are considerably increased. The effects of calcium on thermoregulatory responses depend on the rate of cooling. All changes are more expressive in hypertensive rats. The increased sensitivity of hypertensives to calcium suggests that change in their calcium metabolism may be a cause of the observed shifts in the thermoregulatory response to cold.