Control of sweating during the human menstrual cycle

Thermoregulatory responses were studied in seven women during two separate experimental protocols in the follicular (F, days 4-7) phase and during the luteal (L, days 19-22) phase of the menstrual cycle. Continuous measurements of esophageal temperature (Tes), mean skin temperature (Tsk), oxygen uptake and forearm sweating (ms) were made during all experiments. Protocol I involved both passive heat exposure (3 h) and cycle exercise at approximately 80% VO2 peak during which the environmental chamber was controlled at Ta = 50.0 degrees C, rh = 14% (Pw = 1.7 kPa). In protocol II subjects were tested during thirty-five minutes of exercise at approximately 85% VO2 peak at Ta = 35 degrees C and rh = 25% (Pw = 1.4 kPa). The normal L increase in resting Tes (approximately 0.3 degrees C) occurred in all seven subjects. Tsk was higher during L than F in all experiments conducted at 50 degrees C. During exercise and passive heat exposure, the Tes threshold for sweating was higher in L, with no change in the thermosensitivity (slope) of ms to Tes between menstrual cycle phases. This rightward or upward shift in Tes threshold for initiation of sweating averaged 0.5 degrees C for all experiments. The data indicate the luteal phase modulation in the control of sweating in healthy women is also apparent during severe exercise and/or heat stress.     

The relative influence of physical fitness, acclimatization state, anthropometric measures and gender on individual reactions to heat stress

An experiment was set up to quantify the relative influence of fitness, acclimatization, gender and anthropometric measures on physiological responses to heat stress. For this purpose, 12 male and 12 female subjects were exposed to a neutral [ambient temperature (Ta) 21 degrees C, relative humidity (r.h. 50%)], a warm, humid (Ta 34 degrees C, r.h. 80%) and a hot, dry (Ta 45 degrees C, r.h. 20%) climate at rest and at two exercise intensities [25%, and 45% maximal O2 intake (VO2max)], seated seminude in a net chair behind a cycle ergometer. Their physiological responses were recorded and the data submitted to a multiple regression analysis. It was shown that for the variance in heat storage, the percentage of body fat and the surface to mass ratio had relatively the largest influence of all the individual parameters, followed by VO2max and the sweat rate versus increase in core temperature (total r2 = 92%). For the skin temperature variation, the relative influence of individual parameters (sweat gain, VO2max) was small. For body core temperatures, individual parameters had a large influence. The largest effect was due to the percentage of fat and the surface to mass ratio, followed by the sweating setpoint and, finally, VO2max (total r2 = 54%-70%). For the variance in heart rate the VO2max was the most relevant parameter, followed by the setpoint of the sweat rate:rectal temperature relationship (total r2 = 88%). Blood pressure and skin blood flow predictions were also shown to improve by the addition of individual characteristics to the model.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of cerebrospinal fluid hyperosmolality on sweating in the heat-stressed patas monkey

Dehydration increases the osmolality of body fluids and decreases the rate of sweating during thermal stress. By localizing osmotic stimuli to central nervous system tissues, this study assessed the role of central stimulation on sweating in a heat-stressed nonhuman primate. Lenperone-tranquilized patas monkeys (Erythrocebus patas n = 5), exposed to 41 +/- 2 degrees C, were monitored for calf sweat rate, rectal and mean skin temperatures, oxygen consumption, and heart rate during infusions (255-413 microliters) of hypertonic artificial cerebrospinal fluid (ACSF) into the third cerebral ventricle. ACSF made hypertonic with NaCl to yield osmolalities of 800 and 1,000 mosmol/kgH2O significantly decreased sweat rate compared with control ACSF (285 mosmol/kgH2O), achieving maximal reductions during infusion of 37 and 53%, respectively. Rectal temperature significantly increased during the recovery period, reaching elevations of 0.69 and 0.72 degrees C, respectively, at 20 min postinfusion. In contrast, ACSF made hypertonic with sucrose (800 mosmol/kgH2O) failed to change sweat rate or rectal temperature during infusion in three animals. Thus, intracerebroventricular infusions of hypertonic ACSF mimicked dehydration-induced effects on thermoregulation. The reduction in heat loss during infusion appeared to depend on an elevation in cerebrospinal fluid [Na+] and not osmolality per se.     

Exercise thermoregulation after prolonged wakefulness

The effect of 33 h of wakefulness on the control of forearm cutaneous blood flow and forearm sweating during exercise was studied in three men and three women. Subjects exercised for 30 min at 60% peak O2 consumption while seated behind a cycle ergometer (Ta = 35 degrees C, Pw = 1.0 kPa). We measured esophageal temperature (Tes), mean skin temperature, and arm sweating continuously and forearm blood flow (FBF) as an index of skin blood flow, twice each minute by venous occlusion plethysmography. During steady-state exercise, Tes was unchanged by sleep loss. The sensitivity of FBF to Tes was depressed an average of 30% (P less than 0.05) after 33 h of wakefulness with a slight decrease (-0.15 degrees C, P less than 0.05) in the core temperature threshold for vasodilatory onset. Sleep loss did not alter the Tes at which the onset of sweating occurred; however, sensitivity of arm sweating to Tes tended to be lower but was not significant. Arm skin temperature was not different between control and sleep loss experiments. Reflex cutaneous vasodilation during exercise appeared to be reduced by both central and local factors after 33 h of wakefulness.     

Comparison in men of physiological responses to exercise of increasing intensity at low and moderate ambient temperatures

In six male subjects the sweating thresholds, heart rate (fc), as well as the metabolic responses to exercise of different intensities [40%, 60% and 80% maximal oxygen uptake (VO2max)], were compared at ambient temperatures (Ta) of 5 degrees C (LT) and 24 degrees C (MT). Each period of exercise was preceded by a rest period at the same temperature. In LT experiments, the subjects rested until shivering occurred and in MT experiments the rest period was made to be of exactly equivalent length. Oxygen uptake (VO2) at the end of each rest period was higher in LT than MT (P less than 0.05). During 20-min exercise at 40% VO2max performed in the cold no sweating was recorded, while at higher exercise intensities sweating occurred at similar rectal temperatures (Tre) but at lower mean skin (Tsk) and mean body temperatures (Tb) in LT than MT experiments (P less than 0.001). The exercise induced VO2 increase was greater only at the end of the light (40% VO2max) exercise in the cold in comparison with MT (P less than 0.001). Both fc and blood lactate concentration [1a]b were lower at the end of LT than MT for moderate (60% VO2max) and heavy (80% VO2max) exercises. It was concluded that the sweating threshold during exercise in the cold environment had shifted towards lower Tb and Tsk. It was also found that subjects exposed to cold possessed a potentially greater ability to exercise at moderate and high intensities than those at 24 degrees C since the increases in Tre, fc and [1a]b were lower at the lower Ta.     

Effects of apomorphine on thermoregulatory responses of rats to different ambient temperatures.

Either systemic or central administration of apomorphine produced dose-related decreases in rectal temperature at ambient temperatures (Ta) of 8 and 22 degrees C in rats. At Ta = 8 degrees C, the hypothermia was brought about by a decrease in metabolic rate (M). At Ta = 22 degrees C, the hypothermia was due to an increase in mean skin temperature, an increase in respiratory evaporative heat loss (Eres) and a decrease in M. This increased mean skin temperature was due to increased tail and foot skin temperatures. However, at Ta = 29 degrees C, apomorphine produced increased rectal temperatures due to increased M and decreased Eres. Moreover, the apomorphine-induced hypothermia or hyperthermia was antagonized by either haloperidol or 6-hydroxydopamine, but not by 5,6-dihydroxytryptamine. The data indicate that apomorphine acts on dopamine neurons within brain, with both pre- and post-synaptic sites of action, to influence body temperature.     

Sweat gland response to local heating during sleep in man

In order to assess whether the fluctuations in the sweating response occurring during sleep are related to changes in central drive or in peripheral sweat gland reactivity, 4 healthy male subjects spent 6 non-consecutive nights in a climatic chamber. Air temperature was 25 degrees C, dew-point temperature was 10 degrees C and air velocity was 0.3 m X s-1, while wall temperature was either 38 degrees C, 46 degrees C or 48.7 degrees C giving 3 levels of operative temperature (To = 30, 33 or 34 degrees C). During the whole night, 2 local sweating rates on the right and the left sides of the upper chest were continuously recorded from 12 cm2 area capsules using a dew-point hygrometer technique, while applying local thermal clamps, a constant 2 degrees C difference in local skin temperatures being imposed between the two symmetrical skin areas. Continuous measurements were made of rectal temperature, 10 local skin temperatures, 2 EEGs, 2 EOGs, 1 EMG and 1 ECG. Results show that the multiplicative relationship between the peripheral influence of local skin temperature and the central drive for sweating described in waking subjects, is still valid in sleeping subjects. No peripheral change appears in sweat gland reactivity between the different sleep stages. Changes in the sensitivity of the thermoregulatory system occurring during sleep cannot be explained by a local factor acting at the sweat gland level.     

Core temperature "null zone".

An experimental protocol was designed to investigate whether human core temperature is regulated at a "set point" or whether there is a neutral zone between the core thresholds for shivering thermogenesis and sweating. Nine male subjects exercised on an underwater cycle ergometer at a work rate equivalent to 50% of their maximum work rate. Throughout an initial 2-min rest period, the 20-min exercise protocol, and the 100-min recovery period, subjects remained immersed to the chin in water maintained at 28 degrees C. On completion of the exercise, the rate of forehead sweating (Esw) decayed from a mean peak value of 7.7 +/- 4.2 (SD) to 0.6 +/- 0.3 g.m-2.min-1, which corresponds to the rate of passive transpiration, at core temperatures of 37.42 +/- 0.29 and 37.39 +/- 0.48 degrees C, as measured in the esophagus (Tes) and rectum (Tre), respectively. Oxygen uptake (VO2) decreased rapidly from an exercising level of 2.11 +/- 0.25 to 0.46 +/- 0.09 l/min within 4 min of the recovery period. Thereafter, VO2 remained stable for approximately 20 min, eventually increased with progressive cooling of the core region, and was elevated above the median resting values determined between 15 and 20 min at Tes = 36.84 +/- 0.38 degrees C and Tre = 36.80 +/- 0.39 degrees C. These results indicate that the core temperatures at which sweating ceases and shivering commences are significantly different (P less than 0.001) regardless of whether core temperature is measured within the esophagus or rectum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of the menstrual cycle on the sweating response measured by direct calorimetry in women exposed to warm environmental conditions

The whole body sweating response was measured at rest in eight women during the follicular (F) and the luteal (L) phases of the menstrual cycle. Subjects were exposed for 30-min to neutral (N) environmental conditions [ambient temperature (Ta) 28 degrees C] and then for 90-min to warm (W) environmental conditions (Ta, 35 degrees C) in a direct calorimeter. At the end of the N exposure, tympanic temperature (Tty) was 0.18 (SEM 0.06) degrees C higher in the L than in the F phase (P less than 0.05), whereas mean skin temperature (Tsk) was unchanged. During W exposure, the time to the onset of sweating as well as the concomitant increase in body heat content were similar in both phases. At the onset of sweating, the tympanic threshold temperature (Tty,thresh) was higher in the L phase [37.18 (SEM 0.08) degrees C] than in the F phase [36.95 (SEM 0.07) degrees C; P less than 0.01]. The magnitude of the shift in Tty,thresh [0.23 (SEM 0.07) degrees C] was similar to the L-F difference in Tty observed at the end of the N exposure. The mean skin threshold temperature was not statistically different between the two phases. The slope of the relationship between sweating rate and Tty was similar in F and L. It was concluded that the internal set point temperature of resting women exposed to warm environmental conditions shifted to a higher value during the L phase compared to the F phase of the menstrual cycle; and that the magnitude of the shift corresponded to the difference in internal temperature observed in neutral environmental conditions between the two phases.     

Ambient temperature affects glabrous skin vasculature and sweating responses to mental task in humans

We compared responses in heart rate (HR), mean blood pressure (MAP), sweating rate (SR), sweating expulsion (SwE), and skin vascular conductance (VC) to mental task among different ambient temperature (Ta) conditions, i.e., 12, 16, 20, and 24 degrees C. Seven subjects (27+/-5 yrs, 64+/-14 kg) underwent a 2-min color word conflict test (CWT) after 2 mins of baseline data acquisition following a 20-min resting period. All subjects wore long sleeve shirts and long pants. The skin blood flow was measured with a laser Doppler probe on the left index finger pulp to calculate skin VC, and the SR and sweating expulsion (SwE) were measured with a ventilated capsule on the left thenar. CWT significantly increased the HR and MAP, while there was no significant effect of Ta on the magnitudes of these responses. CWT significantly decreased the skin VC when the Ta was 24 degrees C, whereas it significantly increased the skin VC when the Ta was 12 or 16 degrees C. CWT significantly increased SR and SwE in all Ta conditions, and the SwE was greater in warmer conditions. These findings suggest that different ambient temperatures induce different responses in finger skin vasculature to mental task, implying the independent response of cutaneous vasomotor tone and sweat glands in glabrous skin to mental task.     

Effects of modafinil on heat thermoregulatory responses in humans at rest

The effects of modafinil on heat thermoregulatory responses were studied in 10 male subjects submitted to a sweating test after taking 200 mg of modafinil or placebo. Sweating tests were performed in a hot climatic chamber (45 degrees C, relative humidity <15%, wind speed = 0.8 m x s(-1), duration 1.5 h). Body temperatures (rectal (Tre) and 10 skin temperatures (Tsk)), sweat rate, and metabolic heat production (M) were studied as well as heart rate (HR). Results showed that modafinil induced at the end of the sweating test higher body temperatures increases (0.50 +/- 0.04 versus 0.24 +/- 0.05 degrees C (P < 0.01) for deltaTre and 3.64 +/- 0.16 versus 3.32 +/- 0.16 degrees C (P < 0.05) for deltaTsk (mean skin temperature)) and a decrease in sweating rate throughout the heat exposure (P < 0.05) without change in M, leading to a higher body heat storage (P < 0.05). AHR was also increased, especially at the end of the sweating test (17.95 +/- 1.49 versus 12.52 +/- 1.24 beats/min (P < 0.01)). In conclusion, modafinil induced a slight hyperthermic effect during passive dry heat exposure related to a lower sweat rate, probably by its action on the central nervous system, and this could impair heat tolerance.     

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

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

Local sweating responses of different body areas in dehydration-hydration experiments

Five subjects performed intermittent exercise on a bicycle ergometer (25 min work, 5 min rest cycles for 2 hours, and 20 min work, 10 min rest cycles for a further hour) in a hot environment (air and wall temperatures = 36 degrees C; dew-point temperature = 10 degrees C; air velocity = 0.6 m.s-1). The relative mechanical work load was of 70 W (30% of the maximal aerobic capacity). Seven experimental tests were carried out in order to induce a plasma hypovolemia associated with either a plasma hypo- or hyperosmolarity. The preexercise level of body hydration was also manipulated by giving a diuretic, or by ingestion of 500 ml of isotonic electrolyte sucrose solution before the start of exercise. Continuous measurements were made of rectal and mean skin temperatures. The sweating responses of the chest and of the thigh (over the active muscles of the leg) were monitored from 4 sweat collection capsules highly ventilated. On each of these body areas, the local skin temperatures under one of the 2 capsules was kept at a constant level (37 degrees C). The effects of the level of body hydration on the sweating response only appear when a high local thermal clamp is imposed beneath the capsule. This local effect is particularly strong over the active muscles of the thigh. The influence of the preexercise hydration appears during dehydration tests. This effect is not significant when fluid is given to the subject during the exercise. The change in the sensitivity of the thermoregulatory system is more strongly associated with plasma osmolarity than hypovolemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mean skin temperature in warm humid climates

Mean skin temperature (Tsk) was measured in 24 subjects during experiments in a climatic chamber. Three conditions of ambient temperature (Ta = 25.6 degrees, 28.9 degrees and 32.2 degrees C), and three of humidity (relative humidity = 50%, 70% and 90%) were studied. A relationship was established by a linear regression technique. It is valid in the 24 degree-34 degree C range, for air velocity = 0.2 m.s-1, clothing insulation = 0.077 degrees C.m2.w-1 (0.5 clo), metabolic rate = 64 w.m-2 (1.1 met) and radiant temperature = air temperature. In these conditions Tsk = 28.125 + 0.021 Pw + 0.210 Ta (Pw: ambient water vapour pressure in mb). It shows a small humidity influence. The influences of sex, transition from one condition to the next, and air velocity were also studied. Measurements in Africa confirmed the small influence of humidity. Ethnic life-style differences indicated that a high precision in Tsk determination is difficult to achieve.     

Thermoregulatory responses of the immature rat following repeated postnatal exposures to 2,450-MHz microwaves

This study was designed to determine the changes that occur in the thermoregulatory ability of the immature rat repeatedly exposed to low-level microwave radiation. Beginning at 6-7 days of age, previously untreated rats were exposed to 2,450-MHz continuous-wave microwaves at a power density of 5 mW/cm2 for 10 days (4 h/day). Microwave and sham (control) exposures were conducted at ambient temperatures (Ta) which represent different levels of cold stress for the immature rat (ie, "exposure" Ta = 20 and 30 degrees C). Physiological tests were conducted at 5-6 and 16-17 days of age, in the absence of microwaves, to determine pre- and postexposure responses, respectively. Measurements of metabolic rate, colonic temperature, and tail skin temperature were made at "test" Ta = 25.0, 30.0, 32.5, and 35.0 degrees C. Mean growth rates were lower for rats exposed to Ta = 20 degrees C than for those exposed to Ta = 30 degrees C, but microwave exposure exerted no effect at either exposure Ta. Metabolic rates and body temperatures of all exposure groups were similar to values for untreated animals at test Ta of 32.5 degrees C and 35.0 degrees C. Colonic temperatures of rats repeatedly exposed to sham or microwave conditions at exposure Ta = 20 degrees C or to sham conditions at exposure Ta = 30 degrees C were approximately 1 degrees C below the level for untreated animals at test Ta of 25.0 degrees C and 30.0 degrees C. However, when the exposure Ta was warmer, rats exhibited a higher colonic temperature at these cold test Ta, indicating that the effectiveness of low-level microwave treatment to alter thermoregulatory responses depends on the magnitude of the cold stress.     

Human temperature regulation during narcosis induced by inhalation of 30% nitrous oxide.

The study investigated the effect of inhalation of 30% nitrous oxide (N2O) on temperature regulation in humans. Seven male subjects were immersed to the neck in 28 degrees C water on two separate occasions. They exercised at a rate equivalent to 50% of their maximum work rate on an underwater cycle ergometer for 20 min and remained immersed for an additional 100 min after the exercise. In one trial (AIR) the subjects inspired compressed air, and in the other trial (N2O) they inspired a gas mixture containing N2O (20.93% O2-30% N2O-49.07% N2). Sweating, measured at the forehead, and shivering thermogenesis, as reflected by O2 uptake, were monitored throughout the 100-min recovery period. The threshold core temperatures at which sweating was extinguished and shivering was initiated were established relative to resting preexercise levels. Neither the magnitude of the sweating response nor the core threshold at which it was extinguished was significantly affected by the inhalation of N2O. In contrast, shivering thermogenesis was both significantly reduced during the N2O condition and initiated at significantly lower core temperatures [change in esophageal temperature (delta T(es)) = -0.98 +/- 0.33 degrees C and change in rectal temperature (delta T(re)) = -1.26 degrees C] during the N2O than during the AIR condition (delta T(es) = -0.36 +/- 0.31 degrees C and delta T(re) = -0.44 +/- 0.22 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)     

Evaluation of vapor permeation through garments during exercise

Five males [age 28 +/- 8 yr; maximum O2 uptake (VO2max) 50 +/- 6 ml O2 . kg-1 . min-1; body wt 70 +/- 3 kg; DuBois surface area 1.85 +/- 0.02 m2] exercised on a cycle ergometer, placed on a Potter scale, at 31% VO2max for up to 2 h at an ambient temperature (Ta) of 25 degrees C and a dew-point temperature of 15 degrees C. Air movement was varied from still air to 0.4 and 2 m/s. Each subject, in separate runs, wore a track suit (TS ensemble) of 60% polyester-40% cotton (effective clo = 0.5); a Gortex parka (GOR ensemble), covering a sweat shirt and bottom of TS (effective clo = 1.4); or the TS ensemble covered by polyethylene overgarment (POG ensemble). Esophageal, skin temperature (Tsk) at eight sites, and heart rate were continuously recorded. Dew-point sensors recorded temperatures under the garments at ambient and chest (windward site) and midscapular sites. Local skin wettedness (loc w) and ratio of evaporative heat loss (Esk) to maximum evaporative capacity were determined. An observed average effective permeation (Pe, W . m-2 . Torr-1) was calculated as Esk/loc w (Ps,sk - Pw), where w is the average of chest and back loc w and (Ps,sk - Pw) is the gradient of skin saturation vapor pressure at Tsk and Ta. Additionally, the local effective evaporative coefficient was determined for chest and back sites by Esk/(Ps,dpl - Pw). The GOR ensemble produced an almost as high a Pe as the TS ensemble (82-86% of Pe with TS in still air and 0.4- and 2-m/s conditions). Direct dew-point recording offers an easy practical dimension to the study of efficacy of latent heat loss and skin wettedness properties through garments.     

Water loss distribution in exercising men under hot conditions

Dynamics of sweating and water loss distribution were studied in 7 exercising men under thermoneutral conditions (Ta, 25 degrees C; Tw, 24 degrees C and RH, 54%) and during moderate heat exposure (Ta, 30 degrees C; Tw, 30 degrees C; RH, 54%). The subjects performed bicycle exercise at intensity of 50% V O2 max. Dynamics of sweating was greater after heat exposure (delay in onset of sweating 3.6 and 1.4 min, p less than 0.05; time constant 10.1 and 7.3 min, p less than 0.02). The dynamics of sweating was related to the net body heat load (r = -0.80, p less than 0.001). Sweat evaporation from the skin (Esk) was significantly higher in heat exposed exercising subjects while dripping sweat (mdrip) did not differ significantly. Water loss distribution in relation to total water loss during control exercise was as follows: (Ediff + Eres) 14.8% (Esk) 59.6%; and (mdrip) 25.6%. During exercise under heat exposure (Ediff + Eres) was 12.1%; (Esk) was 67.5%; and (mdrip) was 20.4%. It is concluded that moderate heat exposure accelerate sweating reaction but does not change significantly water loss distribution in exercising subjects. Dripping sweat seems to be an attribute of sweating not only in hot humid conditions but also under temperate temperature and air humidity.     

Thermal, metabolic, and cardiovascular responses to various degrees of cold stress.

The metabolic, thermal, and cardiovascular responses of two male Caucasians to 1 2 h exposure to ambient temperature ranging between 28 degrees C and 5 degrees C were studied and related to the respective ambient temperatures. The metabolic heat production increased linearly with decreasing ambient temperature, where heat production (kcal times m- minus 2 times h- minus 1) = minus 2.79 Ta degrees C + 103.4, r = -0.97, P smaller than 0.001. During all exposures below 28 degrees C, the rate of decrease in mean skin temperature (Tsk) was found to be an exponential function dependent upon the ambient temperature (Ta) and the time of exposure. Reestablishment of Tsk steady state occurred at 90-120 min of exposure, and the time needed to attain steady state was linearly related to decreasing Ta. The net result was that a constant ratio of 1.5 of the external thermal gradient to the internal thermal gradient was obtained, and at all experimental temperatures, the whole body heat transfer coefficient remained constant. Cardiac output was inversely related to decreasing Ta, where cardiac output (Q) = minus 0.25 Ta degrees C + 14.0, r = minus 0.92, P smaller than 0.01. However, the primary reason for the increased Q, the stroke output, was also described as a third-order polynomial, although the increasing stroke volume throughout the Ta range (28-5 degrees C) was linearly related to decreasing ambients. The non-linear response of this parameter which occurred at 20 degrees C larger than or equal to Ta larger than or equal to 10 degrees C suggested that the organism's cardiac output response was an integration of the depressed heart rate response and the increasing stroke output at these temperatures.     

General and local cold adaptation after a ski journey in a severe arctic environment.

It is hypothesized that some of the variability in the conclusions of several human cold adaptation studies could be explained if not only were the changes in core and shell temperatures taken into account, before and after cold adaptation, but also the absolute temperatures and metabolic rate in both thermally neutral environments and in the cold. Such an approach was used in a group of volunteers before and after a ski journey (3 weeks at -20 to -30 degrees C) across Greenland. Eight subjects were submitted to cold tests (Tdb = 1 degree C, r.h. = 40%, wind speed = 0.8 m.s-1) for 2 hours. Thermoregulatory changes were also monitored in a neutral environment (Tdb = 30 degrees C). In the neutral environment, the arctic journey increased metabolic rate (11.2%; P less than 0.05) and mean skin temperature [Tsk: 33.5 (SEM 0.2) degrees C vs 32.9 (SEM 0.2) degrees C, P less than 0.05]. During the cold test, the arctic journey was associated with a lower final rectal temperature [36.8 (SEM 0.2) degrees C vs 37.3 (SEM 0.2) degrees C, P less than 0.01], a lower final Tsk [20.7 (SEM 0.4) degrees C vs 21.2 (SEM 0.3) degrees C, P less than 0.01] with no change in metabolic heat production. These observations are indicative of an hypothermic insulative isometabolic general cold adaptation, which was associated with a local cold adaptation of the extremities, as shown by warmer foot temperatures [12.3 (SEM 0.9) degrees C vs 9.8 (SEM 0.9) degrees C, P less than 0.001].