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.     

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.     

Effects of mode of exercise recovery on thermoregulatory and cardiovascular responses.

To identify the effects of exercise recovery mode on cutaneous vascular conductance (CVC) and sweat rate, eight healthy adults performed two 15-min bouts of upright cycle ergometry at 60% of maximal heart rate followed by either inactive or active (loadless pedaling) recovery. An index of CVC was calculated from the ratio of laser-Doppler flux to mean arterial pressure. CVC was then expressed as a percentage of maximum (%max) as determined from local heating. At 3 min postexercise, CVC was greater during active recovery (chest: 40 +/- 3, forearm: 48 +/- 3%max) compared with during inactive recovery (chest: 21 +/- 2, forearm: 25 +/- 4%max); all P < 0.05. Moreover, at the same time point sweat rate was greater during active recovery (chest: 0.47 +/- 0.10, forearm: 0.46 +/- 0.10 mg x cm(-2) x min(-1)) compared with during inactive recovery (chest: 0.28 +/- 0.10, forearm: 0.14 +/- 0.20 mg x cm(-2) x min(-1)); all P < 0.05. Mean arterial blood pressure, esophageal temperature, and skin temperature were not different between recovery modes. These data suggest that skin blood flow and sweat rate during recovery from exercise may be modulated by nonthermoregulatory mechanisms and that sustained elevations in skin blood flow and sweat rate during mild active recovery may be important for postexertional heat dissipation.     

Dynamics of sweating in men and women during passive heating

The dynamics of sweating was investigated at rest in 8 men and 8 women. Electrical skin resistance (ESR), rectal temperature (Tre) and mean skin temperature (Tsk) were measured in subjects exposed to 40 degrees C environmental temperature, 30% relative air humidity, and 1 m X s-1 air flow. Sweat rate was computed from continuous measurement of the whole body weight loss. It was found that increases in Tre, Tsk and mean body temperature (Tb) were higher in women than in men by 0.16, 0.38 and 0.21 degrees C, but only the difference in delta Tb was significant (p less than 0.05). The dynamics of sweating in men and women respectively, was as follows: delay (td) 7.8 and 18.1 min (p less than 0.01), time constant (tau) 7.5 and 8.8 min (N.S.), inertia time (ti) 15.3 and 26.9 min (p less than 0.002), and total body weight loss 153 and 111 g X m-2 X h-1 (p less than 0.001). Dynamic parameters of ESR did not differ significantly between men and women. Inertia times of ESR and sweat rate correlated in men (r = 0.93, p less than 0.001), and in women (r = 0.76, p less than 0.02). In men, delta Tre correlated with inertia time of sweat rate (r = 0.81, p less than 0.01) as well as with the inertia time of ESR (r = 0.83, p less than 0.001). No relation was found between delta Tre and the dynamics of sweating in women. It is concluded that the dynamics of sweating plays a decisive role in limiting delta Tre in men under dry heat exposure. The later onset of sweating in women does not influence the rectal temperature increase significantly. In women, delta Tre is probably limited by a complex interaction of sweating, skin blood flow increase, and metabolic rate decrease.     

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 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.     

Mean body temperature does not modulate eccrine sweat rate during upright tilt.

Conflicting reports exist about the role of baroreflexes in efferent control of eccrine sweat rate. These conflicting reports may be due to differing mean body temperatures between studies. The purpose of this project was to test the hypothesis that mean body temperature modulates the effect of head-up tilt on sweat rate and skin sympathetic nerve activity (SSNA). To address this question, mean body temperature (0.9.internal temperature + 0.1.mean skin temperature), SSNA (microneurography of peroneal nerve, n = 8), and sweat rate (from an area innervated by the peroneal nerve and from two forearm sites, one perfused with neostigmine to augment sweating at lower mean body temperatures and the second with the vehicle, n = 12) were measured in 13 subjects during multiple 30 degrees head-up tilts during whole body heating. At the end of the heat stress, mean body temperature (36.8 +/- 0.1 to 38.0 +/- 0.1 degrees C) and sweat rate at all sites were significantly elevated. No significant correlations were observed between mean body temperature and the change in SSNA during head-up tilt (r = 0.07; P = 0.62), sweating within the innervated area (r = 0.06; P = 0.56), sweating at the neostigmine treated site (r = 0.04; P = 0.69), or sweating at the control site (r = 0.01; P = 0.94). Also, for each tilt throughout the heat stress, there were no significant differences in sweat rate (final tilt sweat rates were 0.69 +/- 0.11 and 0.68 +/- 0.11 mg.cm(-2).min(-1) within the innervated area; 1.04 +/- 0.16 and 1.06 +/- 0.16 mg.cm(-2).min(-1) at the neostigmine-treated site; and 0.85 +/- 0.15 and 0.85 +/- 0.15 mg.cm(-2).min(-1) at the control site, for supine and tilt, respectively). Hence, these data indicate that mean body temperature does not modulate eccrine sweat rate during baroreceptor unloading induced via 30 degrees head-up tilt.     

Role of nitric oxide in methacholine-induced sweating and vasodilation in human skin.

The purpose of this study was to determine whether the nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) demonstrates significant muscarinic-receptor antagonism during methacholine (MCh)-stimulated sweating in human forearm skin. Three intradermal microdialysis probes were placed in the skin of eight healthy adults (4 men and 4 women). MCh in the range of 0.033-243 mM in nine steps was perfused through a microdialysis probe with and without the presence of the nitric oxide synthase inhibitor L-NAME (10 mM) or the L-arginine analog NG-monomethyl-L-arginine (L-NMMA; 10 mM). Local sweat rate (sweat rate) and skin blood flow (laser-Doppler velocimetry) were measured directly over each microdialysis probe. We observed similar resting sweat rates at MCh only, MCh and L-NAME, and MCh and L-NMMA sites averaging 0.175 +/- 0.029, 0.186 +/- 0.034, and 0.139 +/- 0.027 mg x min(-1) x cm(-2), respectively. Peak sweat rate (0.46 +/- 0.11, 0.56 +/- 0.16, and 0.53 +/- 0.16. mg x min(-1) x cm(-2)) was also similar among all three sites. MCh produced a sigmoid-shape dose-response curve and 50% of the maximal attainable response (0.42 +/- 0.14 mM for MCh only) was shifted rightward shift in the presence of L-NAME or L-NMMA (2.88 +/- 0.79 and 3.91 +/- 1.14 mM, respectively; P < 0.05). These results indicate that nitric oxide acts to augment MCh-stimulated sweat gland function in human skin. In addition, L-NAME consistently blunted the MCh-induced vasodilation, whereas L-NMMA did not. These data support the hypothesis that muscarinic-induced dilation in cutaneous blood vessels is not mediated by nitric oxide production and that the role of L-NAME in attenuating acetylcholine-induced vasodilation may be due to its potential to act as a muscarinic-receptor antagonist.     

Neural control and mechanisms of eccrine sweating during heat stress and exercise.

In humans, evaporative heat loss from eccrine sweat glands is critical for thermoregulation during exercise and/or exposure to hot environmental conditions, particularly when environmental temperature is greater than skin temperature. Since the time of the ancient Greeks, the significance of sweating has been recognized, whereas our understanding of the mechanisms and controllers of sweating has largely developed during the past century. This review initially focuses on the basic mechanisms of eccrine sweat secretion during heat stress and/or exercise along with a review of the primary controllers of thermoregulatory sweating (i.e., internal and skin temperatures). This is followed by a review of key nonthermal factors associated with prolonged heat stress and exercise that have been proposed to modulate the sweating response. Finally, mechanisms pertaining to the effects of heat acclimation and microgravity exposure are presented.     

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.     

Long Distance Runners Present Upregulated Sweating Responses than Sedentary Counterparts

Relatively few studies have investigated peripheral sweating mechanisms of long-distance runners. The aim of this study was to compare peripheral sweating mechanisms in male long-distance runners, and sedentary counterparts. Thirty six subjects, including 20 sedentary controls and 16 long-distance runners (with 7–12 years of athletic training, average 9.2±2.1 years) were observed. Quantitative sudomotor axon reflex testing (QSART) with iontophoresis (2 mA for 5 min) and 10% acetylcholine (ACh) were performed to determine axon reflex-mediated and directly activated (DIR, muscarinic receptor) sweating. Sweat onset time, sweat rate, number of activated sweat glands, sweat output per gland and skin temperature were measured at rest while maximum oxygen uptake (VO₂max) were measured during maximal cycling. Sweat rate, activated sweat glands, sweat output per gland, skin temperature and VO₂max were significantly higher in the trained runners than in the sedentary controls. Sweat onset time was significantly shorter for the runners. In the group of long-distance runners, significant correlations were found between VO₂max and sweat onset time (r² = 0.543, P<0.01, n = 16), DIR sweat rate (r² = 0.584, P<0.001, n = 16), sweat output per gland (r² = 0.539, P<0.01, n = 16). There was no correlation between VO₂max and activated sweat glands. These findings suggest that habitual long-distance running results in upregulation of the peripheral sweating mechanisms in humans. Additional research is needed to determine the molecular mechanism underlying these changes. These findings complement the existing sweating data in long-distance runners.     

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.     

Physiological adjustments of young men to five-hour desert walks.

Seven young men undertook a desert walk of 30 km at a rate of 100 m/min. Six finished; the seventh stopped after 24 km. Each satisfied his thirst with cool tap water each hour. Periodic observations included metabolic rate, blood pressure, heart rate, rectal and skin temperature, body weight, and volume of water drunk. Hand sweat was collected each hour and body sweat residues on the skin were collected at the end of the walk. Subjective reports revealed portents of breakdown: aching muscles, painful joints, hot or blistered feet, hunger, and boredom. Cardiovascular adjustment and temperature regulation maintained tolerable conditions. The volumes of water evaporated by the 5-h walkers were about the same. Wet bulb temperatures were below 25 degrees C; all sweat evaporated and was available for temperature regulation. The volume of water drawn from body reserves was closely correlated with concentration of chloride in body sweat; the volume of water that satisfied thirst maintained osmotic pressure.     

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.     

Comparison of thermoregulatory responses to heat between Malaysian and Japanese males during leg immersion

The objective of this study was to investigate thermoregulatory responses to heat in tropical (Malaysian) and temperate (Japanese) natives, during 60 min of passive heating. Ten Japanese (mean ages: 20.8 ± 0.9 years) and ten Malaysian males (mean ages: 22.3 ± 1.6 years) with matched morphological characteristics and physical fitness participated in this study. Passive heating was induced through leg immersion in hot water (42°C) for 60 min under conditions of 28°C air temperature and 50% RH. Local sweat rate on the forehead and thigh were significantly lower in Malaysians during leg immersion, but no significant differences in total sweat rate were observed between Malaysians (86.3 ± 11.8 g m⁻² h⁻¹) and Japanese (83.2 ± 6.4  g m⁻² h⁻¹) after leg immersion. In addition, Malaysians displayed a smaller rise in rectal temperature (0.3 ± 0.1°C) than Japanese (0.7 ± 0.1°C) during leg immersion, with a greater increase in hand skin temperature. Skin blood flow was significantly lower on the forehead and forearm in Malaysians during leg immersion. No significant different in mean skin temperature during leg immersion was observed between the two groups. These findings indicated that regional differences in body sweating distribution might exist between Malaysians and Japanese during heat exposure, with more uniform distribution of local sweat rate over the whole body among tropical Malaysians. Altogether, Malaysians appear to display enhanced efficiency of thermal sweating and thermoregulatory responses in dissipating heat loss during heat loading. Thermoregulatory differences between tropical and temperate natives in this study can be interpreted as a result of heat adaptations to physiological function.     

Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women.

The purpose of the study was to examine the effect of 1) active (loadless pedaling), 2) passive (assisted pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), cutaneous vascular conductance (CVC), and sweat rate during recovery after 15 min of dynamic exercise in women. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, CVC, and sweating during exercise recovery. Ten female subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 20 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (Tsk), esophageal temperature (Tes), skin blood flow, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, 15, and 20 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active recovery mode, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining MAP. Sweat rate was different among all modes after 12 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the inactive mode (P < 0.05). No differences in either Tes or Tsk were observed among conditions. The results indicate that CVC can be modulated by central command and possibly cardiopulmonary baroreceptors in women. However, differences in sweat rate may be influenced by factors such as central command, mechanoreceptor stimulation, or cardiopulmonary baroreceptors.     

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.     

Active recovery attenuates the fall in sweat rate but not cutaneous vascular conductance after supine exercise.

The purpose of this study was to identify whether baroreceptor unloading was responsible for less efficient heat loss responses (i.e., skin blood flow and sweat rate) previously reported during inactive compared with active recovery after upright cycle exercise (Carter R III, Wilson TE, Watenpaugh DE, Smith ML, and Crandall CG. J Appl Physiol 93: 1918-1929, 2002). Eight healthy adults performed two 15-min bouts of supine cycle exercise followed by inactive or active (no-load pedaling) supine recovery. Core temperature (T(core)), mean skin temperature (T(sk)), heart rate, mean arterial blood pressure (MAP), thoracic impedance, central venous pressure (n = 4), cutaneous vascular conductance (CVC; laser-Doppler flux/MAP expressed as percentage of maximal vasodilation), and sweat rate were measured throughout exercise and during 5 min of recovery. Exercise bouts were similar in power output, heart rate, T(core), and T(sk). Baroreceptor loading and thermal status were similar during trials because MAP (90 +/- 4, 88 +/- 4 mmHg), thoracic impedance (29 +/- 1, 28 +/- 2 Omega), central venous pressure (5 +/- 1, 4 +/- 1 mmHg), T(core) (37.5 +/- 0.1, 37.5 +/- 0.1 degrees C), and T(sk) (34.1 +/- 0.3, 34.2 +/- 0.2 degrees C) were not significantly different at 3 min of recovery between active and inactive recoveries, respectively; all P > 0.05. At 3 min of recovery, chest CVC was not significantly different between active (25 +/- 6% of maximum) and inactive (28 +/- 6% of maximum; P > 0.05) recovery. In contrast, at this time point, chest sweat rate was higher during active (0.45 +/- 0.16 mg.cm(-2).min(-1)) compared with inactive (0.34 +/- 0.19 mg.cm(-2).min(-1); P < 0.05) recovery. After exercise CVC and sweat rate are differentially controlled, with CVC being primarily influenced by baroreceptor loading status while sweat rate is influenced by other factors.     

Experiment studies on sweating for exercise prescription: total body sweat rate in relation to work load in physically trained adult males

This study was designed to examine whether or not the total body sweat rate can be used as a practical index for prescribing exercise. The sweat rate was experimentally studied in relation to factors such as intensity of exercise, the secretory capacity of sweating mechanism, and body temperature. After determining the maximum sweating rate on the whole body surface, regarded as the secretory capacity of the sweating mechanism, each physically trained subject was made to pedal a bicycle ergometer for 60 min at each of several kinds of mechanical work rates under fixed hot climatic conditions in summer. Total body sweat rate, rectal temperature, and RMR were measured during the experiment. The sweat secreting index (SSI), which is ratio of total body sweat rate to maximum sweat rate, was calculated, and was presumed to indicate the functioning rate of sweat secretory capacity. The total body sweat rate responded to factors such as RMR, SSI, and rectal temperature with a high correlation coefficient. From these results it was concluded that the total body sweat rate can be used as a practical index for prescribing exercise.