Cutaneous vasodilatation responses synchronize with sweat expulsions

To examine whether cutaneous active vasodilatation is mediated by sudomotor nerve fibres we recorded cutaneous blood flow and sweat rates continuously with laser-Doppler flowmetry and capacitance hygrometry, respectively, from the dorsal and plantar aspects of the foot in 11 male subjects at varying ambient temperatures (T _a) between 22 and 40°C (relative humidity 40%). In a warmer environment (T _a 29–40°C), predominant responses of the blood flow curve from the sole of the foot were transient depressions (negative blood flow responses, NBR), whereas those from the dorsal foot were transient increases (positive blood flow responses, PBR). The PBR on the dorsal foot occurred spontaneously or in response to mental or sensory stimuli, and when PBR did not fuse with each other the rate of PBR was linearly related to tympanic temperature. When dorsal foot sweating was continuous, PBR on the dorsal foot almost entirely synchronized with sweat expulsion. When dorsal foot sweating was intermittent PBR sometimes occurred on the dorsal foot without corresponding sweat expulsions, but these PBR showed a complete correspondence with subthreshold sweat expulsion seen on a methacholine-treated area. The amplitude and the duration of PBR showed a significant linear relationship with the amplitude and the duration of the corresponding sweat expulsion. In a thermoneutral or cooler environment (T _a 22–29°C), PBR occurred on the sole of the foot when mental or sensory stimuli elicited sweating in that area. Thus, PBR occurred when and where sweating appeared. Atropine failed to abolish PBR on the dorsal foot. Blockade of the peroneal nerve eliminated both PBR and NBR on the dorsal foot. The results indicate that an active vasodilatation mechanism is present on the sole of the foot as well as on the dorsal foot, and thus suggest that active vasodilatation is closely related to sudomotor nerve activation.     

Pilocarpine-induced sweat gland function in individuals with multiple sclerosis.

This investigation tested the hypothesis that cholinergic sweat function of individuals with multiple sclerosis (MS) (MS-Con; n = 10) is diminished relative to matched healthy control subjects (Con; n = 10). In addition, cholinergic sweat function was determined before and after 15 wk of aerobic training in a subgroup of individuals with MS (MS-Ex; n = 7). Cholinergic sweating responses were assessed via pilocarpine iontophoresis on ventral forearm skin. A collection disk placed over the stimulated area collected sweat for 15 min. Sweat rate (SR) was calculated by dividing sweat collector volume by collection area and time. Iodine-treated paper was applied to the stimulated area to measure number of activated sweat glands (ASG). Sweat gland output (SGO) was calculated by dividing SR by density of glands under the collector. Sweat gland function was determined in MS-Ex to test the hypothesis that exercise training would increase sweating responses. No differences in ASG were observed between MS-Con and Con. SR and SGO in MS-Con [0.18 mg.cm(-2).min(-1) (SD 0.08); 1.74 microg.gland(-1).min(-1) (SD 0.79), respectively] were significantly lower (P < or = 0.05) than in Con [0.27 mg.cm(-2).min(-1) (SD 0.10); 2.43 microg.gland(-1).min(-1) (SD 0.69)]. Aerobic exercise training significantly (P < or = 0.05) increased peak aerobic capacity in MS-Ex [1.86 (SD 0.75) vs. 2.10 (SD 0.67) l/min] with no changes in ASG, SR, and SGO. Sweat gland function in individuals with MS is impaired relative to healthy controls. Fifteen weeks of aerobic training did not increase stimulated sweating responses in individuals with MS. Diminished peripheral sweating responses may be a consequence of impairments in autonomic control of sudomotor function.     

Compensatory hyperhidrosis following thoracic sympathectomy: a biophysical rationale

A side-effect of endoscopic thoracic sympathectomy (ETS) is compensatory hyperhidrosis (CH), characterized by excessive sweating from skin areas with intact sudomotor function. The physiological mechanism of CH is unknown, but may represent an augmented local sweat rate from skin areas with uninterrupted sympathetic innervation based on evaporative heat balance requirements. For a given combination of activity and climate, the same absolute amount of evaporation (if any) is needed to balance the rate of metabolic heat production both pre- and post-ETS. However, the rate of local sweating per unit of skin surface area with intact sudomotor activity must be greater post-ETS as evaporation must be derived from a smaller skin surface area. Under conditions with high evaporative requirements, greater degradations in sweating efficiency associated with an increased dripping of sweat should also occur post-ETS, further pronouncing the sweat rate required for heat balance. In conclusion, in addition to the potential role of psychological stimuli for increased sudomotor activity, the existence of CH post-ETS can be described by the interplay between fundamental thermoregulatory physiology and altered heat balance biophysics and does not require a postoperative alteration in physiological control.     

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.     

Different responses in skin and muscle sympathetic nerve activity to static muscle contraction

We microneurographically recorded the traffic of sympathetic nerves leading to foot volar skin activity (SSA) and leg skeletal muscle activity (MSA) during isometric handgrip and simultaneously determined sweat rate by the ventilated capsule method and skin blood flow by laser-Doppler flowmetry in the innervating area of SSA. SSA increased abruptly and was almost constant during handgrip, accompanied by an increase in sweat rate, whereas skin blood flow showed no significant change during the handgrip. MSA showed a time-dependent increase during the course of handgrip. During arterial occlusion of the working forearm after handgrip, SSA decayed to the precontraction control level, whereas MSA remained at a higher level than during control. During involuntary biceps muscle contraction induced by electrical stimulation, both SSA and MSA increased. The results suggest that the SSA response during voluntary handgrip, which was demonstrated to contain mainly sudomotor activity, might be influenced by central command and input from peripheral mechanoreceptors but be influenced little by input from muscle chemoreceptors.     

Influence of hydrothermal ambient conditions on sweat evaporation efficiency]

Sweat efficiency is defined as the ratio between evaporative and sweat rates. The work was carried out on two resting subjects acclimatised to humid heat. Body sweat rate and rate of sweat loss by dripping were recorded separately by continuous weighing. Evaporation from the skin was obtained by the difference between the two weight loss curves. The subjects were exposed for 75 minutes to increases in humidity levels as constant air temperatures (42, 44, 46, or 48 degrees C). The amplitude of the increases was successively equal to 7.5, 15.0, 22.5 or 50.0 mb of water vapor pressure. During the 75 minutes preceding each increase the water vapor pressure of the air was maintained at 20.0 mb. 1. Sweat efficiency decreases prior to complete wetting of the skin surface. The inter-individual mean value of the wetted skin area threshold over which sweat efficiency is less than 1 is around 60%. 2. Sweat efficiency is linearly related to the reciprocal of the required wetted skin area (see article). These results are compared with those of other authors. The differences observed are explained in terms of physiological or physical variables involved in the sweat rate control or in the evaporative sweat loss. These include wetness of skin, posture, activity of subjects and the velocity of air over the skin surface.     

Mechanisms underlying the age-related decrement in the human sweating response

To examine the mechanisms underlying the age-related decrement in the ability to sweat, seven older (64-76 years) and seven younger (20-24 years) men participated in a 60-min sweating test. The test consisted of placing the subject's lower legs in a water bath at 42 degrees C while sitting in a controlled environment of 35 degrees C ambient temperature and 45% relative humidity. The rectal (Trc) and skin temperatures, local sweating rates (m(sw): on the forehead, chest, back, forearm and thigh) and the frequency of sweat expulsion (f(sw)) were measured during the test. No group difference was observed in the mean body temperature (Tb) throughout the passive heating, although the older men had a higher Tre and a lower mean skin temperature during the last half of the 60-min test. There were no group differences in the Tb threshold for sweating, although the time to the onset of sweating tended to be longer for the older men regardless of body site. The m(sw) increased gradually for approximately 35 min after the start of heat exposure in the older men and for 30 min in the younger men and then reached a steady state. During the first half of the test, the older men had a significantly lower m(sw) at all sites. During the last half of the test, only m(sw) on the thigh was significantly lower in the older men than in the younger men. There was no group difference in the slope of f(sw) versus Tb (an indicator of the change in the central sudomotor response to thermal input). The slope of m(sw) versus f(sw) (an indicator of the change in peripheral activity in response to central sudomotor changes) was significantly lower on the thigh in the older men, but there were no differences for the other sites. These results suggest that in older men the lower thigh m(sw) observed during the last half of the heat test was possibly due to age-related modifications of peripheral mechanisms involving the sweat glands and surrounding tissues. It was not due to a change in the central drive to sudomotor function. Furthermore, the sluggish m(sw) responses in the older men appear to have been related to age-related modifications of the sensitivity of thermoreceptors in various body regions to thermal stimuli. They may also involve lower sweat glands' sensitivity to cholinergic stimulus or sluggish vasodilatation, and do not reflect age-related changes in the central drive.     

Humid heat acclimation does not elicit a preferential sweat redistribution toward the limbs

We tested the hypothesis that local sweat rates would not display a systematic postadaptation redistribution toward the limbs after humid heat acclimation. Eleven nonadapted males were acclimated over 3 wk (16 exposures), cycling 90 min/day, 6 days/wk (40 degrees C, 60% relative humidity), using the controlled-hyperthermia acclimation technique, in which work rate was modified to achieve and maintain a target core temperature (38.5 degrees C). Local sudomotor adaptation (forehead, chest, scapula, forearm, thigh) and onset thresholds were studied during constant work intensity heat stress tests (39.8 degrees C, 59.2% relative humidity) conducted on days 1, 8, and 22 of acclimation. The mean body temperature (Tb) at which sweating commenced (threshold) was reduced on days 8 and 22 (P < 0.05), and these displacements paralleled the resting thermoneutral Tb shift, such that the Tb change to elicit sweating remained constant from days 1 to 22. Whole body sweat rate increased significantly from 0.87 +/- 0.06 l/h on day 1 to 1.09 +/- 0.08 and 1.16 +/- 0.11 l/h on days 8 and 22, respectively. However, not all skin regions exhibited equivalent relative sweat rate elevations from day 1 to day 22. The relative increase in forearm sweat rate (117 +/- 31%) exceeded that at the forehead (47 +/- 18%; P < 0.05) and thigh (42 +/- 16%; P < 0.05), while the chest sweat rate elevation (106 +/- 29%) also exceeded the thigh (P < 0.05). Two unique postacclimation observations arose from this project. First, reduced sweat thresholds appeared to be primarily related to a lower resting Tb, and more dependent on Tb change. Second, our data did not support the hypothesis of a generalized and preferential trunk-to-limb sweat redistribution after heat acclimation.     

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.     

Contribution of central versus sweat gland mechanisms to the seasonal change of sweating function in young sedentary males and females

In summer and winter, young, sedentary male (N = 5) and female (N = 7) subjects were exposed to heat in a climate chamber in which ambient temperature (Ta) was raised continuously from 30 to 42°C at a rate of 0.1°C min⁻¹ at a relative humidity of 40%. Sweat rates (SR) were measured continuously on forearm, chest and forehead together with tympanic temperature (Tty), mean skin temperature ( [`T] s ) \left( {\overline {\hbox{T}} {\hbox{s}}} \right) and mean body temperature ( [`T] b ) \left( {\overline {\hbox{T}} {\hbox{b}}} \right) . The rate of sweat expulsions (Fsw) was obtained as an indicator of central sudomotor activity. Tty and ( [`T] b ) \left( {\overline {\hbox{T}} {\hbox{b}}} \right) were significantly lower during summer compared with winter in males; SR was not significantly different between summer and winter in males, but was significantly higher during summer in females; SR during winter was higher in males compared with females. The regression line relating Fsw to ( [`T] b ) \left( {\overline {\hbox{T}} {\hbox{b}}} \right) shifted significantly from winter to summer in males and females, but the magnitude of the shift was not significantly different between the two subject groups. The regression line relating SR to Fsw was steepened significantly from winter to summer in males and females, and the change in the slope was significantly greater in females than in males. Females showed a lower slope in winter and a similar slope in summer compared to males. It was concluded that sweating function was improved during summer mediated by central sudomotor and sweat gland mechanisms in males and females, and, although the change of sweat gland function from winter to summer was greater in females as compared with males, the level of increased sweat gland function during summer was similar between the two subject groups.     

Prolonged head-down tilt exposure reduces maximal cutaneous vasodilator and sweating capacity in humans.

Cutaneous vasodilation and sweat rate are reduced during a thermal challenge after simulated and actual microgravity exposure. The effects of microgravity exposure on cutaneous vasodilator capacity and on sweat gland function are unknown. The purpose of this study was to test the hypothesis that simulated microgravity exposure, using the 6 degrees head-down tilt (HDT) bed rest model, reduces maximal forearm cutaneous vascular conductance (FVC) and sweat gland function and that exercise during HDT preserves these responses. To test these hypotheses, 20 subjects were exposed to 14 days of strict HDT bed rest. Twelve of those subjects exercised (supine cycle ergometry) at 75% of pre-bed rest heart rate maximum for 90 min/day throughout HDT bed rest. Before and after HDT bed rest, maximal FVC was measured, via plethysmography, by heating the entire forearm to 42 degrees C for 45 min. Sweat gland function was assessed by administering 1 x 10(-6) to 2 M acetylcholine (9 doses) via intradermal microdialysis while simultaneously monitoring sweat rate over the microdialysis membranes. In the nonexercise group, maximal FVC and maximal stimulated sweat rate were significantly reduced after HDT bed rest. In contrast, these responses were unchanged in the exercise group. These data suggest that 14 days of simulated microgravity exposure, using the HDT bed rest model, reduces cutaneous vasodilator and sweating capacity, whereas aerobic exercise training during HDT bed rest preserves these responses.     

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.     

Influence of training on sweating responses during submaximal exercise in horses.

Sweating responses were examined in five horses during a standardized exercise test (SET) in hot conditions (32-34 degrees C, 45-55% relative humidity) during 8 wk of exercise training (5 days/wk) in moderate conditions (19-21 degrees C, 45-55% relative humidity). SETs consisting of 7 km at 50% maximal O(2) consumption, determined 1 wk before training day (TD) 0, were completed on a treadmill set at a 6 degrees incline on TD0, 14, 28, 42, and 56. Mean maximal O(2) consumption, measured 2 days before each SET, increased 19% [TD0 to 42: 135 +/- 5 (SE) to 161 +/- 4 ml. kg(-1). min(-1)]. Peak sweating rate (SR) during exercise increased on TD14, 28, 42, and 56 compared with TD0, whereas SRs and sweat losses in recovery decreased by TD28. By TD56, end-exercise rectal and pulmonary artery temperature decreased by 0.9 +/- 0.1 and 1.2 +/- 0.1 degrees C, respectively, and mean change in body mass during the SET decreased by 23% (TD0: 10.1 +/- 0.9; TD56: 7.7 +/- 0.3 kg). Sweat Na(+) concentration during exercise decreased, whereas sweat K(+) concentration increased, and values for Cl(-) concentration in sweat were unchanged. Moderate-intensity training in cool conditions resulted in a 1.6-fold increase in sweating sensitivity evident by 4 wk and a 0.7 +/- 0.1 degrees C decrease in sweating threshold after 8 wk during exercise in hot, dry conditions. Altered sweating responses contributed to improved heat dissipation during exercise and a lower end-exercise core temperature. Despite higher SRs for a given core temperature during exercise, decreases in recovery SRs result in an overall reduction in sweat fluid losses but no change in total sweat ion losses after training.     

Sweat gland density and response during high-intensity exercise in athletes with spinal cord injuries

Sweat production is crucial for thermoregulation. However, sweating can be problematic for individuals with spinal cord injuries (SCI), as they display a blunting of sudomotor and vasomotor responses below the level of the injury. Sweat gland density and eccrine gland metabolism in SCI are not well understood. Consequently, this study examined sweat lactate (S-LA) (reflective of sweat gland metabolism), active sweat gland density (SGD), and sweat output per gland (S/G) in 7 SCI athletes and 8 able-bodied (AB) controls matched for arm ergometry VO₂peak. A sweat collection device was positioned on the upper scapular and medial calf of each subject just prior to the beginning of the trial, with iodine sweat gland density patches positioned on the upper scapular and medial calf. Participants were tested on a ramp protocol (7 min per stage, 20 W increase per stage) in a common exercise environment (21±1°C, 45-65% relative humidity). An independent t-test revealed lower (p<0.05) SGD (upper scapular) for SCI (22.3 ±14.8 glands · cm⁻²) vs. AB. (41.0 ± 8.1 glands · cm⁻²). However, there was no significant difference for S/G between groups. S-LA was significantly greater (p<0.05) during the second exercise stage for SCI (11.5±10.9 mmol · l⁻¹) vs. AB (26.8±11.07 mmol · l⁻¹). These findings suggest that SCI athletes had less active sweat glands compared to the AB group, but the sweat response was similar (SLA, S/G) between AB and SCI athletes. The results suggest similar interglandular metabolic activity irrespective of overall sweat rate.     

Influence of beta-adrenergic blockade on the control of sweating in humans

To evaluate the role of beta-adrenergic receptors in the control of human sweating, we studied six subjects during 40 min of cycle-ergometer exercise (60% maximal O2 consumption) at 22 degrees C 2 h after oral administration of placebo or nonselective beta-blockade (BB, 80 mg propranolol). Internal temperature (esophageal temperature, Tes), mean skin temperature (Tsk), local chest temperature (Tch), and local chest sweat rate (msw) were continuously recorded. The control of sweating was best described by the slope of the linear relationship between msw and Tes and the threshold Tes for the onset of sweating. The slope of the msw-Tes relationship decreased 27% (P less than 0.01), from 1.80 to 1.30 mg X cm-2 X min-1 X degree C-1 during BB. The Tes threshold for sweating (36.8 degrees C) was not altered as the result of BB. These data suggest that BB modified the control of sweating via some peripheral interaction. Since Tsk was significantly (P less than 0.05) reduced during BB exercise, from a control value of 32.8 to 32.2 degrees C, we evaluated the influence of the reduction in local skin temperature (Tsk) in the altered control of sweating. Reductions in Tch accounted for only 45% of the decrease in the slope of the msw-Tes relationship during BB. Since evaporative heat loss requirement during exercise with BB, as estimated from the energy balance equation, was also reduced 18%, compared with control exercise, we concluded that during BB the reduction in sweating at any Tes is the consequence of both a decrease in local Tsk and a direct effect on sweat gland.     

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.     

Equine sweating responses to submaximal exercise during 21 days of heat acclimation.

This study examined sweating responses in six exercise-trained horses during 21 consecutive days (4 h/day) of exposure to, and daily exercise in, hot humid conditions (32-34 degrees C, 80-85% relative humidity). On days 0, 3, 7, 14, and 21, horses completed a standardized exercise test on a treadmill (6 degrees incline) at a speed eliciting 50% of maximal O(2) uptake until a pulmonary artery temperature of 41.5 degrees C was attained. Sweat was collected at rest, every 5 min during exercise, and during 1 h of standing recovery for measurement of ion composition (Na(+), K(+), and Cl(-)) and sweating rate (SR). There was no change in the mean time to reach a pulmonary artery temperature of 41.5 degrees C (range 19.09 +/- 1.41 min on day 0 to 20.92 +/- 1.98 min on day 3). Peak SR during exercise (ml. m(-2). min(-1)) increased on day 7 (57.5 +/- 5. 0) but was not different on day 21 (48.0 +/- 4.7) compared with day 0 (52.0 +/- 3.4). Heat acclimation resulted in a 17% decline in SR during recovery and decreases in body mass and sweat fluid losses during the standardized exercise test of 25 and 22%, respectively, by day 21. By day 21, there was also a 10% decrease in mean sweat Na(+) concentration for a given SR during exercise and recovery; this contributed to an approximately 26% decrease in calculated total sweat ion losses (3,112 +/- 114 mmol on day 0 vs. 2,295 +/- 107 mmol on day 21). By day 21, there was a decrease in sweating threshold ( approximately 1 degrees C) but no change in sweat sensitivity. It is concluded that horses responded to 21 days of acclimation to, and exercise in, hot humid conditions with a reduction in sweat ion losses attributed to decreases in sweat Na(+) concentration and SR during recovery.     

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.     

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.