Influences of overall thermal balance on local inputs for drive of evaporation in men

Three kinds of experiments were carried out in a climatic chamber: experiments with warm load on the whole body at 36 degrees C (4 subjects); experiments at 36 degrees C with reduction of thermal load (28 degrees C) on the left leg (right leg at 36 degrees C) (8 subjects); and experiments at 36 degrees C with antisymmetric thermal load on the legs of 44 degrees C (right leg) and 28 degrees C (left leg), which resulted in additional thermal loads of +/- 30 W/leg (8 subjects). The additional thermal loads, which were applied via two climatic boxes, produced measurable effects on sweat rate when applied to one leg only. In comparison to the experiment 1, experiment 2 brought about a significant reduction of local evaporation on the left leg. With antisymmetric thermal loads on both legs (experiment 3), which did not influence the overall thermal balance, there was no significant influence on local evaporation, although significant changes of local temperatures were measured. It is suggested that the well-known regulatory models, declaring local, mean skin, and core temperatures as local evaporation drive should be supplemented with an important additional feature: local control of evaporation by local skin temperature may be blocked by an overall thermal balance.     

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.     

Temperature and sweating responses in one-legged and two-legged exercise.

In looking at the thermoregulatory responses resulting from symmetrical or asymmetrical exercise, this paper has focused on the effect of local skin temperature (Tsk,local) on local sweat rates (msw,local) during one-legged (W1) and two-legged (W2) exercise on an ergocycle. Five subjects underwent four 3-h tests at 36 degrees C, each consisting of six 25-min exercise periods alternating with 5-min rest periods. The subjects performed W1 and W2 at 45 and 90 W, respectively, either dehydrated or rehydrated. Body temperatures and total sweat rate were measured as well as four msw,local (on chest and thighs), assessed from sweat capsules under which Tsk,local was maintained at predetermined levels (37.0 degrees C and 35.5 degrees C). The combinations of Tsk,local levels, capsule locations, exercise intensity and hydration level chosen in our protocol led to the following results. The hydration level affected rectal temperature but not total or msw,local. No specific effect of muscle activity was found; msw,local on thighs of resting and working legs were similar. The msw,local were only influenced by exercise intensity, msw,local being more elevated during the higher intensity. No significant effect of Tsk,local on msw,local was found, whatever the experimental condition and/or the location. It was concluded that local thermal effects on msw,local could have been masked by the strong central drive for sweating which has been found to exist in subjects exercising in a warm environment.     

Thermoregulatory adjustments during continuous heat exposure

Body temperature regulation was studied in 6 male subjects during an acclimation procedure involving uninterrupted heat exposure for 5 successive days and nights in a hot dry environment (ambient temperature = 35 degrees C, dew-point temperature = 7 degrees C; air velocity = 0.2 m.s-1). Data were obtained at rest and during exercise (relative mechanical workload = 35% VO2max). At rest, hourly measurements were made of oesophageal and 4 local skin temperatures, to allow the calculation of mean skin temperature, and of body motility and heart rate. During the working periods these measurements were made at 5 min intervals. Hourly whole-body weight loss was measured at rest on a sensitive platform scale while in the working condition just before starting and immediately after completing the bicycle exercise. The results show that, in both exercise and at rest, the successive heat exposures increased the sweat gland output during the first 3 days. Afterwards, sweat rate decreased without any corresponding change in body temperature. For the fixed workload, the sweat rate decline was associated with a decrease in circulatory strain. Adjustments in both sweating and circulatory mechanisms occur in the first 3 days of continuous heat exposure. The overall sweat rate decline could involve a redistribution of the regional sweating rates which enhances the sweat gland activities of skin areas with maximal evaporative efficiencies.     

Differential heating of trunk and extremities. Effects on thermoregulation mechanisms

Experiments in which the whole human body was heated or cooled are compared with others in which one extremity (arm or leg) was simultaneously cooled or heated. With a warm load on the rest of the body resulting in general sweating, a cold load on one extremity did not evoke local shivering; with general body cooling, heating one limb did not stop the shivering. Skin temperatures of the other parts of the body were not influenced by warming or cooling one extremity. Evaporative heat loss was influenced by local, mean skin and core temperature, whereas shivering did not depend on local temperature, and vasomotor control seemed to be controlled predominantly by central temperatures. A cold load on an extremity during whole body heating in most cases induced an oscillatory behaviour of core temperature and of the evaporative heat loss from the body and the extremity. It is assumed that local, mean skin and core temperatures influence the three autonomous effector systems to very different degree.     

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)     

Leg skin temperature and thigh sweat output: possible central influence of local thermal inputs

To demonstrate whether or not the skin temperature of one lower limb can have an influence on the sweat rate of the contralateral leg, the two legs of five subjects were exposed inside leg-chambers to specific local thermal conditions while sweat rates were measured on both limbs. Three experiments (C I,II,III) of 3 h were carried out: each included two phases A and B. During A, the right leg was not ventilated, while the left leg was (C I) or was not (C II–III) ventilated. During B, the legs were either removed from the leg-chambers (C I) or ventilated inside the chambers at differently controlled levels of leg skin temperature (C II–III). At all times, sweat capsules on both legs measured the sweat rates of local areas of the thigh which were also temperature-controlled. Results showed that, at constant or slightly increased mean skin and core temperatures, the sweat output of one leg could be decreased at constant (C II) or higher local skin temperature (C III) probably due to a decrease in the temperature of the opposite leg. This finding is interpreted as a consequence of a central negative effect, originating from contralateral thermal inputs.     

Active cutaneous vasodilation in resting humans during mild heat stress.

The role of skin temperature in reflex control of the active cutaneous vasodilator system was examined in six subjects during mild graded heat stress imposed by perfusing water at 34, 36, 38, and 40 degrees C through a tube-lined garment. Skin sympathetic nerve activity (SSNA) was recorded from the peroneal nerve with microneurography. While monitoring esophageal, mean skin, and local skin temperatures, we recorded skin blood flow at bretylium-treated and untreated skin sites by using laser-Doppler velocimetry and local sweat rate by using capacitance hygrometry on the dorsal foot. Cutaneous vascular conductance (CVC) was calculated by dividing skin blood flow by mean arterial pressure. Mild heat stress increased mean skin temperature by 0.2 or 0.3 degrees C every stage, but esophageal and local skin temperature did not change during the first three stages. CVC at the bretylium tosylate-treated site (CVC(BT)) and sweat expulsion number increased at 38 and 40 degrees C compared with 34 degrees C (P < 0.05); however, CVC at the untreated site did not change. SSNA increased at 40 degrees C (P < 0.05, different from 34 degrees C). However, SSNA burst amplitude increased (P < 0.05), whereas SSNA burst duration decreased (P < 0.05), at the same time as we observed the increase in CVC(BT) and sweat expulsion number. These data support the hypothesis that the active vasodilator system is activated by changes in mean skin temperature, even at normal core temperature, and illustrate the intricate competition between active vasodilator and the vasoconstrictor system for control of skin blood flow during mild heat stress.     

Thermoregulatory responses to intermittent exercise are influenced by knit structure of underwear

The purpose of this study was to evaluate the role of knit structure in underwear on thermoregulatory responses. Underwear manufactured from 100% polypropylene fibres in five different knit structures (1-by-1 rib, fleece, fishnet, interlock, double-layer rib) was evaluated. All five underwear prototypes were tested as part of a prototype clothing system. Measured on a thermal manikin these clothing systems had total thermal resistances of 0.243, 0.268, 0.256, 0.248 and 0.250 m2.K.W-1, respectively (including a value for the thermal resistance of the ambient environment of 0.104 m2.K.W-1). Human testing was done on eight male subjects and took place at ambient temperature (Ta) = 5 degrees C, dew point temperature (Tdp) = -3.5 degrees C and air velocity (Va) = 0.32 m.s-1. The test comprised a repeated bout of 40-min cycle exercise (315 W.m-2; 52%, SD 4.9% maximal oxygen uptake) followed by 20 min of rest (62 W.m-2). The oxygen uptake, heart rate, oesophageal temperature, skin temperature, Ta, Tdp at the skin and in the ambient air, onset of sweating, evaporation rate, non-evaporated sweat accumulated in the clothing and total evaporative loss of mass were measured. Skin wettedness was calculated. The differences in knit structure of the underwear in the clothing systems resulted in significant differences in mean skin temperature, local and average skin wettedness, non-evaporated and evaporated sweat during the course of the intermittent exercise test. No differences were observed over this period in the core temperature measurements.     

Human exposure to 2450 MHz CW energy at levels outside the IEEE C95.1 standard does not increase core temperature

Permission was received from the Brooks AFB Institutional Review Board and the AF Surgeon General's Office to exceed the peak power density (PD = 35 mW/cm(2)) we had previously studied during partial body exposure of human volunteers at 2450 MHz. Two additional peak PD were tested (50 and 70 mW/cm(2)). The higher of these PD (normalized peak local SAR = 15.4 W/kg) is well outside the IEEE C95.1 guidelines for partial body exposure, as is the estimated whole body SAR approximately 1.0 W/kg. Seven volunteers (four males, three females) were tested at each PD in three ambient temperatures (T(a) = 24, 28, and 31 degrees C) under our standard protocol (30 min baseline, 45 min RF exposure, 10 min baseline). The thermophysiological data (esophageal and six skin temperatures, metabolic heat production, local sweat rate, and local skin blood flow) were combined with comparable data at PD = 0, 27, and 35 mW/cm(2) from our 1999 study to generate response functions across PD. No change in esophageal temperature or metabolic heat production was recorded at any PD in any T(a). At PD = 70 mW/cm(2), skin temperature on the upper back (irradiated directly) increased 4.0 degrees C in T(a) = 24 degrees C, 2.6 degrees C in T(a) = 28 degrees C, and 1.8 degrees C in T(a) = 31 degrees C. These differences were primarily due to the increase in local sweat rate, which was greatest in T(a) = 31 degrees C. Also at PD = 70 mW/cm(2), local skin blood flow on the back increased 65% over baseline levels in T(a) = 31 degrees C, but only 40% in T(a) = 24 degrees C. Although T(a) becomes an important variable when RF exposure exceeds the C95.1 partial body exposure limits, vigorous heat loss responses of blood flow and sweating maintain thermal homeostasis efficiently. It is also clear that strong sensations of heat and thermal discomfort will motivate a timely retreat from a strong RF field, long before these physiological responses are exhausted. Published 2001 Wiley-Liss, Inc.     

Thermophysiological consequences of whole body resonant RF exposure (100 MHz) in human volunteers

Thermophysiological responses of heat production and heat loss were measured in seven adult volunteers (six males and one female, aged 31-74 years) during 45 min dorsal exposures of the whole body to 100 MHz continuous wave (CW) radio frequency (RF) energy. Three power densities (PD) (average PD = 4, 6, and 8 mW/cm(2); whole body specific absorption rate [SAR] = 0.068 [W/kg]/[mW/cm(2)]) were tested in each of three ambient temperatures (T(a) = 24, 28, and 31 degrees C), as well as in T(a) controls (no RF). A standardized protocol (30 min baseline, 45 min RF or sham exposure, 10 min baseline) was used. Measured responses included esophageal and seven skin temperatures, metabolic heat production, local sweat rate, and local skin blood flow. No changes in metabolic heat production occurred under any test condition. Unlike published results of similar exposures at 450 and 2450 MHz, local skin temperatures, even those on the back that were irradiated directly, changed little or not at all during 100 MHz exposures. The sole exception was the temperature of the ankle skin, which increased by 3-4 degrees C in some subjects at PD = 8 mW/cm(2). During the 45 min RF exposure, esophageal temperature showed modest changes (range = -0.15 to 0.13 degrees C) and never exceeded 37.2 degrees C. Thermoregulation was principally controlled by appropriate increases in evaporative heat loss (sweating) and, to a lesser extent, by changes in skin blood flow. Because of the deep penetration of RF energy at this frequency, effectively bypassing the skin, these changes must have been stimulated by thermal receptors deep in the body rather than those located in the skin.     

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.     

Thermographic studies on patterns of skin temperature after exercise.

In six subjects thermograms of the thighs and the forearms were taken before, during and after 10 min ergometer exercise at 100 W at an ambient temperature of 23 degrees C. During exercise, an intra-individually constant and reproducible skin temperature pattern with local temperature differences exceeding 3 degrees C evolved. Reactions after external local cooling or after occlusion of blood flow and measurements with a laser Doppler-flowmeter showed dispersed convective heat transport to be the source of this irregular pattern. Temperature differences of 3.6 degrees C and deviations of blood flow in the skin microcirculation of 300% within a distance of a few centimetres reduce the value of single-spot measurements of skin temperature with reference to the whole extremity.     

Partial-body exposure of human volunteers to 2450 MHz pulsed or CW fields provokes similar thermoregulatory responses

Many reports describe data showing that continuous wave (CW) and pulsed (PW) radiofrequency (RF) fields, at the same frequency and average power density (PD), yield similar response changes in the exposed organism. During whole-body exposure of squirrel monkeys at 2450 MHz CW and PW fields, heat production and heat loss responses were nearly identical. To explore this question in humans, we exposed two different groups of volunteers to 2450 MHz CW (two females, five males) and PW (65 micros pulse width, 10(4) pps; three females, three males) RF fields. We measured thermophysiological responses of heat production and heat loss (esophageal and six skin temperatures, metabolic heat production, local skin blood flow, and local sweat rate) under a standardized protocol (30 min baseline, 45 min RF or sham exposure, 10 min baseline), conducted in three ambient temperatures (T(a) = 24, 28, and 31 degrees C). At each T(a), average PDs studied were 0, 27, and 35 mW/cm2 (Specific absorption rate (SAR) = 0, 5.94, and 7.7 W/kg). Mean data for each group showed minimal changes in core temperature and metabolic heat production for all test conditions and no reliable differences between CW and PW exposure. Local skin temperatures showed similar trends for CW and PW exposure that were PD-dependent; only the skin temperature of the upper back (facing the antenna) showed a reliably greater increase (P =.005) during PW exposure than during CW exposure. Local sweat rate and skin blood flow were both T(a)- and PD-dependent and showed greater variability than other measures between CW and PW exposures; this variability was attributable primarily to the characteristics of the two subject groups. With one noted exception, no clear evidence for a differential response to CW and PW fields was found.     

Thermophysiological responses of human volunteers to whole body RF exposure at 220 MHz

Since 1994, our research has demonstrated how thermophysiological responses are mobilized in human volunteers exposed to three radio frequencies, 100, 450, and 2450 MHz. A significant gap in this frequency range is now filled by the present study, conducted at 220 MHz. Thermoregulatory responses of heat loss and heat production were measured in six adult volunteers (five males, one female, aged 24-63 years) during 45 min whole body dorsal exposures to 220 MHz radio frequency (RF) energy. Three power densities (PD = 9, 12, and 15 mW/cm(2) [1 mW/cm(2) = 10 W/m(2)], whole body average normalized specific absorption rate [SAR] = 0.045 [W/kg]/[mW/cm(2)] = 0.0045 [W/kg]/[W/m(2)]) were tested at each of three ambient temperatures (T(a) = 24, 28, and 31 degrees C) plus T(a) controls (no RF). Measured responses included esophageal (T(esoph)) and seven skin temperatures (T(sk)), metabolic rate (M), local sweat rate, and local skin blood flow (SkBF). Derived measures included heart rate (HR), respiration rate, and total evaporative water loss (EWL). Finite difference-time domain (FDTD) modeling of a seated 70 kg human exposed to 220 MHz predicted six localized "hot spots" at which local temperatures were also measured. No changes in M occurred under any test condition, while T(esoph) showed small changes (< or =0.35 degrees C) but never exceeded 37.3 degrees C. As with similar exposures at 100 MHz, local T(sk) changed little and modest increases in SkBF were recorded. At 220 MHz, vigorous sweating occurred at PD = 12 and 15 mW/cm(2), with sweating levels higher than those observed for equivalent PD at 100 MHz. Predicted "hot spots" were confirmed by local temperature measurements. The FDTD model showed the local SAR in deep neural tissues that harbor temperature-sensitive neurons (e.g., brainstem, spinal cord) to be greater at 220 than at 100 MHz. Human exposure at both 220 and 100 MHz results in far less skin heating than occurs during exposure at 450 MHz. However, the exposed subjects thermoregulate efficiently because of increased heat loss responses, particularly sweating. It is clear that these responses are controlled by neural signals from thermosensors deep in the brainstem and spinal cord, rather than those in the skin.     

Enhanced protein synthetic capacity in Atlantic cod (Gadus morhua) is associated with temperature-induced compensatory growth

Atlantic cod (Gadus morhua) were held either at seasonal ambient temperatures (-0.3 to 11 degrees C) or at a relatively constant control temperature (8-11 degrees C) to investigate aspects of protein synthesis during a period of compensatory growth. Protein synthesis rate, total RNA, and RNA-specific protein synthesis rate were determined in white muscle and liver when ambient temperatures were -0.3, 4.5, and 11 degrees C in February, June, and July, respectively. To allow for comparisons between treatment temperatures, fish were also acutely transferred to a comparable assay temperature in February and June. Over the transition from 4.5 to 11 degrees C (June to July), the ambient-held cod had a significant increase in size and a substantially higher growth rate relative to control-held fish over the same period, consistent with cold-induced compensatory growth. During the onset of this enhanced growth, in June when ambient temperature was approximately 4.5 degrees C, ambient-held fish elevated their capacity for protein synthesis in the white muscle and liver via elevation of the RNA content. When ambient temperature reached the same point as for the control fish (11 degrees C), the rate of white muscle protein synthesis remained higher in the ambient-held vs. that in the control-held fish, a process facilitated by elevated RNA content and greater RNA-specific rate of protein synthesis. In the liver, all measured characteristics of protein synthesis were the same for ambient and control fish in July. The latter suggests that compensatory growth may be in part explained by improved efficiency of protein synthesis.     

Effects of thyrotropin releasing hormone on human sudomotor and cutaneous vasomotor activities

At an ambient temperature of 34-41 degrees C (rh = 40%) forearm sweat rates were measured by capacitance hygrometry in 9 male volunteers. Thyrotropin releasing hormone (TRH) was infused intravenously at 0.1 mg.min-1 for 20 to 30 min. Sweat rate increased rapidly within a minute after initiation of TRH infusion, decreased rapidly after the peak sweat rate was attained in 2-5 min of TRH infusion, and then levelled off in 6-10 min near the level before TRH infusion. Core temperature (Tre, Tty) started to decline at the time of the peak sweat rate and levelled off almost coincidentally with the levelling off in sweat rate. Average values for the rate of sweat expulsions (Fsw), sweat rate and mean body temperature (Tb) were obtained from the data of the last 10 min period of TRH infusion. The regression line for the relationship of Fsw to Tb shifted during the TRH infusion to the left of the line for the control; that of sweat rate to Fsw hardly shifted. At an ambient temperature of 24-27 degrees C TRH produced vasodilation as evidenced by an increase in skin blood flow (measured by means of thermal distribution), an increase in amplitude of the photoelectric plethysmogram and an elevation of skin temperature in the finger tips. It is suggested that TRH may act, either directly or indirectly, on the central thermoregulatory mechanism (or on the thermoreceptive mechanism) to lower the reference temperature for heat dissipation.     

Body heat balance in man subjected to endogenous and exogenous heat load

The body heat balance, measured by a thermometric method, was investigated in humans subjected to endogenous and exogenous heat load. The purpose of the present study was to test the concept of heat exchange by a servomechanism in human thermoregulation. Two series of experiments were performed on male volunteers. In series I 15 subjects performed physical exercise (50% VO2 max) for 60 min at a constant ambient temperature of 25 degrees C. In series II 16 subjects rested in a climatic chamber where the ambient temperature was elevated over 30 min from 22 to 42 degrees C and kept stable at this level during the subsequent 60 min. It was found that in both series of experiments the sweating rate followed an exponential curve exhibiting an inertial course. Heat was stored in the body mainly at the beginning of experiment. In series I the net body heat load of 125 W/m2 was equalized by sweat evaporation, beginning after 40 min of the exercise. In series II the net body heat load of 80 W/m2 was equalized in the same way, starting after 35 min of the constant high ambient temperature. In both series of experiments the amount of heat stored in the body calculated from the body heat balance was quite close to the amount of heat calculated from the calorimetric equation. It is concluded, that under the present experimental conditions, heat loss from the body by sweat evaporation seems to be a regulated variable in the human thermoregulatory system. The observed increase in rectal temperature may result from an inertial course of the sweating reaction.     

Functional differentiation of thermoregulation, with particular references to seasonal variation of whole body sweat rate of exercising man

We investigated the seasonal variation of sweating response during exercise. Four adult healthy men repeated a moderate bicycle exercise (60 watts) in a climatic chamber of an ambient temperature of 30 degrees C (relative humidity, 45%) in winter, spring, summer, and fall. In summer, sweat rate immediately increased as soon as the exercise started, whereas in winter in a few minutes. The mean sweat rate during exercise was significantly different between winter and summer. The transient reduction of the Tsk was observed at the beginning of the exercise in winter. The Tsk decreased in proportion to increasing of sweat rate in each season. Significantly negative correlations were found between sweat rate and the rate of change of Tsk during exercise in each season. The slope and intercept of regression line were significantly different between winter and summer. The index of sweating was made available for the relative value, changing rate against annual mean value of total sweat loss (delta SR, %). The relative value rather than the absolute value (i.e., expressed as g.m-2.h-1) corrected well with skin temperature. It is suggested that the present results may reflect adapted changes in the thermoregulatory mechanisms to seasonal acclimatization. Moreover, the fall in skin temperature during exercise may be not due to increased evaporative cooling, but may be the result of vasoconstriction probably caused by non-thermal factors.