Human sudomotor responses to heating and cooling upper-body skin surfaces: cutaneous thermal sensitivity

The influence of local skin temperature (T_skl) on the control of local and whole-body sweating was evaluated in eight healthy males. A water-perfusion garment (37 °C) and a climatic chamber (36.45 ± 0.78 °C; [±SD]; relative humidity 60.3 ± 1.6%) were used to raise and clamp skin and core temperatures. Warm and cool stimuli were applied to four upper-body skin regions (face, arm, forearm, hand) using perfusion patches (249.0 ± 0.2 cm²). Heating elevated, while cooling suppressed sweat rate (m˙_sw) locally, and at other skin surfaces. However, the tendency for T_skl manipulations to induce localized sweat responses was no more powerful than it was at stimulating sweating in non-treated regions (P > 0.05). Accordingly, neither thermal stimulus produced significantly greater local sudomotor influences than were elicited contralaterally (P > 0.05). No statistical support was found for the notion of inter-regional differences in upper-body cutaneous thermal sensitivity for sudomotor control, and, regardless of the stimulation site, whole-body sudomotor responses to localized thermal treatments were equivalent (P > 0.05).     

Sudomotor responses from glabrous and non-glabrous skin during cognitive and painful stimulations following passive heating

Aim: It is widely accepted that thermal and psychological sweating are independently controlled and respectively restricted to non‐glabrous (hairy) and glabrous skin. These assumptions were evaluated in six experiments conducted across eight body segments, in which 38 glabrous and non‐glabrous skin surfaces were investigated. Methods: Sweating was measured in 30 passively heated individuals using ventilated sweat capsules, with passive heating used to first establish steady‐state sweating, averaging 0.30 mg cm^?2 min^?1 (±0.03) across all sites, prior to the application of cognitive and painful stimuli. Results: These non‐thermal (psychological) stimulations significantly increased sweat secretion at more than 70% of the sites investigated [cognitive: 28 of 38 sites (P < 0.05); pain: 23 of 32 sites (P < 0.05)], eliciting peak sweat rates averaging 0.51 mg cm^?2 min^?1 (±0.05) and 0.47 mg cm^?2 min^?1 (±0.4 respectively) across all sites. Furthermore, non‐thermal sweating was evident from both the glabrous and non‐glabrous surfaces and occurred without mean body or local skin temperatures changes (P > 0.05). Indeed, neither thermal nor psychological sweating was restricted to discrete skin surfaces, and there were no consistent sudomotor differences between these two skin classifications. Finally, at no site was thermal sweating inhibited during a non‐thermal stimulation. Conclusion: These generalized sudomotor responses challenge the hypotheses that glabrous skin sweating is driven by psychological stimuli, and that thermal sweating is a phenomenon restricted to the non‐glabrous skin surfaces.     

Identification of sudomotor activity in cutaneous sympathetic nerves using sweat expulsion as the effector response

Summary In a warm environment at ambient temperatures between 25° and 38°C (relative humidity 50%–60%) the relationship between sympathetic activity in cutaneous nerves (SSA) and pulses of sweat expulsion was investigated in five young male subjects. The SSA was recorded from the peroneal nerve using a microelectrode. Sweat expulsion was identified on the sweat rate records obtained from skin areas on the dorsal side of the foot, for spontaneous sweating and drug-induced sweating, using capacitance hygrometry. Sweat expulsion was always preceded by bursts of SSA with latencies of 2.4–3.0 s. This temporal relationship between bursts of SSA and sweat expulsion was noted not only in various degrees of thermal sweating but also in the sweating evoked by arousal stimuli, or by painful electric stimulation. The amplitude of the sudomotor burst was linearly related to the maximal rate of increase of the corresponding sweat expulsion, the amplitude of the expulsion and the integrated amount of sweat produced for the duration of the expulsion. The results provide direct evidence that sweat expulsion reflects directly centrally-derived sudomotor activity.     

Neuro-effector characteristics of sweat glands in the human hand activated by irregular stimuli

Intraneural electrical stimulation of cutaneous fascicles in the median nerve was performed in 24 normal subjects and the effects on sweating within the innervation zone were monitored as changes of skin resistance and water vapour partial pressure (wvpp). The aims were: (1) to investigate the response variability between repeated stimulation sequences in the same skin site and between different sites and (2) to compare quantitative effects of regular and irregular stimulation on skin resistance and wvpp. Regional axillary anaesthesia of the brachial plexus eliminated spontaneous and reflex sympathetic activity. With repeated irregular stimulation sequences skin resistance responses from the same skin site varied only slightly between trials. Differences between response curves from two skin sites in the same subject or from different subjects were also small but significantly greater (P < 0.01) than differences between responses to repeated stimulation in the same site. Irregular stimulation with average frequencies of 0.49 Hz and 3.51 Hz gave greater resistance responses than if the same number of stimuli were delivered regularly (P < 0.01). The difference was most pronounced at 0.49 Hz. At an average frequency of 0.49 Hz the stimulation usually evoked no changes of wvpp whereas an average frequency of 3.51 Hz caused an increase of wvpp which was greater with irregular than with regular stimulation in all subjects. We conclude that: (1) sweat responses to sudomotor nerve traffic vary slightly due to local factors in the skin or the terminal nerve endings and (2) irregular sudomotor nerve traffic evokes more sweat than if the same impulses occur regularly.     

Neuro-effector characteristics of sweat glands in the human hand activated by irregular stimuli.

Intraneural electrical stimulation of cutaneous fascicles in the median nerve was performed in 24 normal subjects and the effects on sweating within the innervation zone were monitored as changes of skin resistance and water vapour partial pressure (wvpp). The aims were: (1) to investigate the response variability between repeated stimulation sequences in the same skin site and between different sites and (2) to compare quantitative effects of regular and irregular stimulation on skin resistance and wvpp. Regional axillary anaesthesia of the brachial plexus eliminated spontaneous and reflex sympathetic activity. With repeated irregular stimulation sequences skin resistance responses from the same skin site varied only slightly between trials. Differences between response curves from two skin sites in the same subject or from different subjects were also small but significantly greater (P < 0.01) than differences between responses to repeated stimulation in the same site. Irregular stimulation with average frequencies of 0.49 Hz and 3.51 Hz gave greater resistance responses than if the same number of stimuli were delivered regularly (P < 0.01). The difference was most pronounced at 0.49 Hz. At an average frequency of 0.49 Hz the stimulation usually evoked no changes of wvpp whereas an average frequency of 3.51 Hz caused an increase of wvpp which was greater with irregular than with regular stimulation in all subjects. We conclude that: (1) sweat responses to sudomotor nerve traffic vary slightly due to local factors in the skin or the terminal nerve endings and (2) irregular sudomotor nerve traffic evokes more sweat than if the same impulses occur regularly.     

Effect of skin temperature on the cholinergic sensitivity of the human eccrine sweat gland

Although sweat gland activity is directly controlled by the central nervous system, which detects changes in core body temperature, sweat glands can also be influenced by local cutaneous thermal conditions. OBJECTIVE: The present study sought to determine the effect of local skin temperature on pilocarpine-induced sweating within a range of typical skin temperatures. METHODS: Thirteen subjects (30 +/- 6 years; 172 +/- 11 cm; 72.8 +/- 11.0 kg) had forearm sweat rates measured at rest following pilocarpine iontophoresis at each of three skin temperatures in randomized order: warm (T(warm) = 37.1 +/- 0.9 degrees C), control (T(con) = 32.3 +/- 1.4 degrees C), and cool (T(cool) = 26.6 +/- 1.3 degrees C). T(skin) was raised and lowered with an electric heating pad and gel ice pack, respectively. Forearm T(skin) was measured with a skin temperature probe. Pilocarpine iontophoresis was used on an approximately 7 cm(2) area of the anterior forearm to stimulate localized sweating. Following stimulation, sweat was collected from the area for 15 min with a Macroduct Sweat Collection System. RESULTS: There was a higher sweat rate at T(warm) (p = 0.001) and T(con) (p = 0.006) compared to that at T(cool). However, there was no difference between the sweat rate at T(warm) and that at T(con) (p = 0.127). CONCLUSION: These results indicated that skin temperatures below approximately 32 degrees C affect local sweat production primarily by altering glandular sensitivity to the neurotransmitter, whereas skin temperatures above approximately 32 degrees C predominantly affect neurotransmitter release. Furthermore, sweat glands display maximal or near maximal cholinergic sensitivity at resting skin temperature in a thermoneutral environment.     

Temperature effects on neuronal membrane potentials and inward currents in rat hypothalamic tissue slices

Preoptic–anterior hypothalamic (PO/AH) neurones sense and regulate body temperature. Although controversial, it has been postulated that warm-induced depolarization determines neuronal thermosensitivity. Supporting this hypothesis, recent studies suggest that temperature-sensitive cationic channels (e.g. vanilloid receptor TRP channels) constitute the underlying mechanism of neuronal thermosensitivity. Moreover, earlier studies indicated that PO/AH neuronal warm sensitivity is due to depolarizing sodium currents that are sensitive to tetrodotoxin (TTX). To test these possibilities, intracellular recordings were made in rat hypothalamic tissue slices. Thermal effects on membrane potentials and currents were compared in PO/AH warm-sensitive, temperature-insensitive and silent neurones. All three types of neurones displayed slight depolarization during warming and hyperpolarization during cooling. There were no significant differences in membrane potential thermosensitivity for the different neuronal types. Voltage clamp recordings (at −92 mV) measured the thermal effects on persistent inward cationic currents. In all neurones, resting holding currents decreased during cooling and increased during warming, and there was no correlation between firing rate thermosensitivity and current thermosensitivity. To determine the thermosensitive contribution of persistent, TTX-sensitive currents, voltage clamp recordings were conducted in the presence of 0.5 μ m TTX. TTX decreased the current thermosensitivity in most neurones, but there were no resulting differences between the different neuronal types. The present study found no evidence of a resting ionic current that is unique to warm-sensitive neurones. This supports studies suggesting that neuronal thermosensitivity is controlled, not by resting currents, but rather by currents that determine rapid changes in membrane potential between successive action potentials.     

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°C while sitting in a controlled environment of 35°C ambient temperature and 45% relative humidity. The rectal (T _re) 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 (T¯ _b) throughout the passive heating, although the older men had a higher T _re and a lower mean skin temperature during the last half of the 60-min test. There were no group differences in the T¯ _b 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 T¯ _b (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.     

The reproducibility of closed-pouch sweat collection and thermoregulatory responses to exercise–heat stress

Seven active male subjects cycled for 60 min at 29.5 (0.8)% peak work rate on three separate occasions in a hot environmental condition [36.0 (0.1)°C, 60 (1)% relative humidity] in order to determine the reproducibility of a closed-pouch sweat collection technique for sweat composition at the scapula, forearm and thigh. To confirm that sweat composition was not influenced by between-trial variations in sudomotor drive, local sweat rate, whole-body sweat rate, heart rate (HR), rectal temperature (T_re) and mean skin temperature (T_sk) responses were also measured, consequently reproducibility was also established for these variables. Sweat composition did not differ among trials, with the mean coefficients of variation (CVs) for sweat [Na⁺], [K⁺] and pH being 10.4 (7.4)%, 8.1 (6.5)% and 1.3 (1.1)%, respectively. Local sweat rates did not differ among the three trials (P>0.05) although whole-body sweat rate was reduced in the third trial (P<0.05). The mean CVs were 11.0 (7.8)% and 4.7 (1.6)% for local and whole-body sweat rates, respectively. Between-trial differences were not evident for T_re, T_sk or HR with mean CVs of 0.3 (0.2)%, 0.7 (0.6)% and 3.9 (1.7)%, respectively, although HR tended to be greater in the first trial (P=0.08). It is proposed that moderate variations in sweat composition were influenced by variations in the local sweat rate, which were induced by application of the pouch.     

Effect of facial cooling during heat acclimation process on adaptive changes in sweating activity

On assumptions that tympanic temperature (Tty) reflects brain temperature and that the latter can be lowered by cooling of the face, effect of facial cooling during acclimation process on adaptive changes in sweating activity was examined, in comparison with the results of our previous studies on heat acclimation with controlled hyperthermia. Face fanning, by which Tty was clamped at approximately 37.1 degrees C, was combined with either of the following 9-day acclimation procedures: 90-min heating in a "Sauna box," keeping mean skin temperature slightly above 40 C, or 90-min exercise on a bicycle, clamping rectal temperature (Tre) at approximately 38 degrees C. Each procedure was imposed on the same four male subjects on different occasions, two of whom had participated in our previous experiments. Sweat tests, carried out before and immediately after the completion of the procedure, consisted of measurements of local sweat rates, whole body sweat rate, Tre, Tty, and skin temperatures on 5 areas, and of calculations of mean body temperature (Tb) and the rate of sweat expulsions (Fsw, as an indicator of central sudomotor activity). No or only a slight increase in sweating activity was observed following the acclimation procedures with face fanning, whereas similar procedures without face fanning had resulted in substantial enhancement of sweating activity in most of the cases, which had been attributed mainly to adaptive changes in central sudomotor activity (as indicated by a shift of the regression line relating Fsw to Tb). Similar results were obtained in an additional series of experiments, where the effects of 9-day 90-min exercise in heat, clamping Tre at approximately 38.2 degrees C, with and without facial cooling, were compared with each other in a subject. From the above results it is inferred that Tty reflects brain temperature and that enhancement of sweating activity induced by repeated heat load is strongly impeded, if not accompanied, by an elevation of brain temperature.     

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.     

The cholinergic blockade of both thermally and non-thermally induced human eccrine sweating

Thermally induced eccrine sweating is cholinergically mediated, but other neurotransmitters have been postulated for psychological (emotional) sweating. However, we hypothesized that such sweating is not noradrenergically driven in passively heated, resting humans. To test this, nine supine subjects were exposed to non-thermal stimuli (palmar pain, mental arithmetic and static exercise) known to evoke sweating. Trials consisted of the following four sequential phases: thermoneutral rest; passive heating to elevate (by ~1.0°C) and clamp mean body temperature and steady-state sweating (perfusion garment and footbath); an atropine sulphate infusion (0.04 mg kg(-1)) with thermal clamping sustained; and following clamp removal. Sudomotor responses from glabrous (hairless) and non-glabrous skin surfaces were measured simultaneously (precursor and discharged sweating). When thermoneutral, these non-thermal stimuli elicited significant sweating only from the palm (P < 0.05). Passive heating induced steady-state sweating ranging from 0.20 ± 0.04 (volar hand) to 1.40 ± 0.14 mg cm(-2) min(-1) (forehead), with each non-thermal stimulus provoking greater secretion (P < 0.05). Atropine suppressed thermal sweating, and it also eliminated the sudomotor responses to these non-thermal stimuli when body temperatures were prevented from rising (P > 0.05). However, when the thermal clamp was removed, core and skin temperatures became further elevated and sweating was restored (P < 0.05), indicating that the blockade had been overcome, presumably through elevated receptor competition. These observations establish the dependence of both thermal and non-thermal eccrine sweating from glabrous and non-glabrous surfaces on acetylcholine release, and challenge theories concerning the psychological modulation of sweating. Furthermore, no evidence existed for the significant participation of non-cholinergic neurotransmitters during any of these stimulations.     

Changes in eccrine sweating on the glabrous skin of the palm and finger during isometric exercise

Aim: The goals of this study were to investigate changes in the sweating and cutaneous vascular responses on the palm and the volar aspect of the index finger during sustained static exercise of increasing intensity and to determine whether the former can be attributed to altered sweat gland activity. Methods: Five male and five female subjects performed maximal voluntary handgrip contractions (MVC: right hand) for 60 s at 20, 35 and 50% MVC (ambient temperature 25 °C, relative humidity 50%). Results: The sweat rate and the number of activated sweat glands on the non‐exercised hand showed intensity‐dependent increases (P < 0.05). At 35 and 50% MVC, finger sweat secretion was significantly higher than on the palm, which was primarily associated with the number of activated sweat glands (P < 0.05). In addition, there was a marked simultaneous decrease in the cutaneous vascular conductance for the finger at 35 and 50% MVC (P < 0.05), but not for the palm. Conclusion: Our results suggest that a difference exists between intensity‐dependent increases of sudomotor responses within more than one glabrous skin site. Specifically, markedly greater sweating occurs on the volar finger than on the palmar surface during sustained static exercise. These differences in sweat rate mainly resulted from changes in the number of activated sweat glands. In addition, intra‐segment variations in cutaneous blood flow on the glabrous hand are shown.     

Neuronal nitric oxide synthase control mechanisms in the cutaneous vasculature of humans in vivo

The physiological roles of constituitively expressed nitric oxide synthase (NOS) isoforms in humans, in vivo , are unknown. Cutaneous vasodilatation during both central nervous system-mediated, thermoregulatory reflex responses to whole-body heat stress and during peripheral axon reflex-mediated, local responses to skin warming in humans depend on nitric oxide (NO) generation by constituitively expressed NOS of uncertain isoform. We hypothesized that neuronal NOS (nNOS, NOS I) effects cutaneous vasodilatation during whole-body heat stress, but not during local skin warming. We examined the effects of the nNOS inhibitor 7-nitroindazole (7-NI) administered by intradermal microdialysis on vasodilatation induced by whole-body heat stress or local skin warming. Skin blood flow (SkBF) was monitored by laser–Doppler flowmetry (LDF). Blood pressure (MAP) was monitored and cutaneous vascular conductance calculated (CVC = LDF/MAP). In protocol 1, whole-body heat stress was induced with water-perfused suits. In protocol 2, local skin warming was induced through local warming units at LDF sites. At the end of each protocol, 56 m m sodium nitroprusside was perfused at microdialysis sites to raise SkBF to maximal levels for data normalization. 7-NI significantly attenuated CVC increases during whole-body heat stress ( P < 0.05), but had no effect on CVC increases induced by local skin warming ( P > 0.05). These diametrically opposite effects of 7-NI on two NO-dependent processes verify selective nNOS antagonism, thus proving that the nNOS isoform affects NO increases and hence vasodilatation during centrally mediated, reflex responses to whole-body heat stress, but not during locally mediated, axon reflex responses to local skin warming. We conclude that the constituitively expressed nNOS isoform has distinct physiological roles in cardiovascular control mechanisms in humans, in vivo .     

Local sweating on the forehead, but not forearm, is influenced by aerobic fitness independently of heat balance requirements during exercise

The present study investigated the influence of maximal oxygen uptake (V(O2 max)) on local steady-state sudomotor responses to exercise, independently of evaporative requirements for heat balance (E(req)). Eleven fit (F; (V(O2 max))61.9 ± 6.0 ml kg(-1) min(-1)) and 10 unfit men (UF; (V(O2 max)) 40.4 ± 3.8 ml kg(-1) min(-1)) cycled for 60 min at an air temperature of 24.5 ± 0.8°C and ambient humidity of 0.9 ± 0.3 kPa at a set metabolic heat production per unit surface area, producing the same E(req) in all participants (BAL trial) and, in a second trial, at 60% of (V(O2 max)). During the BAL trial, absolute power (F 107 ± 2 and UF 102 ± 2 W; P = 0.126), E(req) (F 175 ± 5 and UF 176 ± 9 W m(-2); P = 0.855), steady-state whole-body sweat rate (F 0.44 ± 0.02 and UF 0.47 ± 0.02 mg cm(-2) min(-1); P = 0.385) and local sweat rate on the arm (F 0.29 ± 0.03 and UF 0.35 ± 0.03 mg cm(-2) min(-1); P = 0.129) were not different between groups; however, local sweat rate on the forehead in UF (1.67 ± 0.20 mg cm(-2) min(-1)) was almost double (P = 0.002) that of F (0.87 ± 0.11 mg cm(-2) min(-1)). Heart rate, ratings of perceived exertion and relative exercise intensity were also significantly greater in UF (P < 0.05). There was a trend towards an elevated minute ventilation in UF (P = 0.052), while end-tidal P(CO2) was significantly lower in UF (P = 0.028). At 60% (V(O2 max)), absolute power (F 174 ± 6 and UF 110 ± 5 W; P < 0.001), E(req) (F 291 ± 14 and UF 190 ± 17 W m(-2); P < 0.001), steady-state whole-body sweat rate (F 0.84 ± 0.05 and UF 0.53 ± 0.03 mg cm(-2) min(-1); P < 0.001) and local sweat rate on the arm (F 0.75 ± 0.04 and UF 0.35 ± 0.03 mg cm(-2) min(-1); P < 0.001) and on the forehead (F 2.92 ± 0.42 and UF 1.68 ± 0.23 mg cm(-2) min(-1); P = 0.022) were all significantly greater in F compared with UF. Heart rate and ratings of perceived exertion were similar at all time points (P > 0.05). Significantly greater minute ventilation (P < 0.001) and end-tidal P (CO2) responses (P = 0.017) were found in F. In conclusion, aerobic fitness alters local sweating on the forehead, but not the forearm, independently of evaporative requirements for heat balance, and may be the result of differential control of sweating in these skin areas associated with the relative intensity of exercise.     

Peripheral amplification of sweating – a role for calcitonin gene-related peptide

Neuropeptides are the mediators of neurogenic inflammation. Some pain disorders, e.g. complex regional pain syndromes, are characterized by increased neurogenic inflammation and by exaggerated sudomotor function. The aim of this study was to explore whether neuropeptides have a peripheral effect on human sweating. We investigated the effects of different concentrations of calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP) and substance P (SP) on acetylcholine-induced axon reflex sweating in healthy subjects (total n = 18). All substances were applied via dermal microdialysis. The experiments were done in a parallel setting: ACh alone and ACh combined with CGRP, VIP or SP in various concentrations were applied. Acetylcholine (10⁻² m ) always elicited a sweating response, neuropeptides alone did not. However, CGRP significantly enhanced ACh-induced sweating ( P < 0.01). Post hoc tests revealed that CGRP in physiological concentrations of 10⁻⁷–10⁻⁹ m was most effective. VIP at any concentration had no significant effect on axon reflex sweating. The duration of the sweating response ( P < 0.01), but not the amount of sweat, was reduced by SP. ACh-induced skin blood flow was significantly increased by CGRP ( P < 0.01), but unaltered by VIP and SP. The results indicate that CGRP amplifies axon reflex sweating in human skin.     

Contribution of skin thermal sensitivities of large body areas to sweating response

The thermal sensitivity of different parts of the body was investigated by heating large areas of the body surface while the mean skin temperature calculated from Hardy and DuBois ' formula (1938) was always kept constant. The right arm sweating responses recorded under a local thermal clamp were related to changes in segmental skin temperatures of the different parts of the body. The results show that: 1) the various local peripheral signals are projected into integrating structures in the central nervous system; 2) the thermal sensitivity is greater for the head-and-trunk area in comparison with other parts of the body. For resting nude subjects, the formula of Hardy and DuBois remains a pertinent way for evaluating the role of skin thermal signals in the central drive for sweating. The peripheral contribution to the central sweating drive depends only on the skin temperature change and on the size of the stimulated area.     

Effect of local cooling on sweating rate and cold sensation

Summary Subjects resting in a 39°C environment were stimulated in different skin regions with a water cooled thermode. This local cooling produced decreases in sweating rate measured at the thigh and increases in magnitude estimates of the cold sensation. The area of cold stimulation varied from 122 cm² to 384 cm². Sensitivity coefficients of the changes in sweating rate and magnitude estimate were corrected for differences in size of the area of stimulation and change in skin temperature and were normalized to the responses of the chest. The normalized coefficients showed the following relative sensitivities for changes in sweat rate and magnitude estimate respectively: forehead 3.3, 2.2; bach 1.2, 1.4; lower leg 1.1, 0.9; chest 1.0, 1.0; thigh 0.9, 1.0; abdomen 0.8, 0.8. Varying the area stimulated from 122 cm² to 384 cm² produced greater changes in the sweating response than in the magnitude estimate. Rate of skin cooling during the period of stimulation had more effect on the sweating response than on the magnitude estimate. We conclude that cooling different body regions produces generally equivalent changes in the sweat rate and sensation, with the forehead showing a much greater sensitivity per unit area and temperature decrease than other areas.     

Characteristics of central sudomotor mechanism estimated by frequency of sweat expulsions

Each of six male subjects was exposed during rest to at least ten different thermal environments (Ta, 22-44 degrees C; rh, 40%). Local sweat rates from both forearms were continuously recorded in a steady state of each exposure, using capacitance hygrometry. In the absence of spontaneous sweating, localized sweating was induced by intradermal administration of pilocarpine. Sweat expulsions synchronous at the two test areas were counted and their frequency (Fsw) was calculated. For each of additive and multiplicative combinations of Tcore (Tre, Tty) and Ts, the best combination for estimation of thermal input to the sudomotor center was determined using multiple regression analysis. Approximately 0.75Tre + 0.25Ts or 0.85Tty + 0.15Ts, and (Tre-36.33) (Ts-33.13) or (Tty-36.42) (Ts-32.24) were obtained for the additive and multiplicative combinations, respectively. The correlation coefficient (r) for the relationship of Fsw to the obtained best combination, either additive or multiplicative, and that of Fsw to Tb were almost comparable to each other. It is considered that Tb can be used as an approximation of thermal input and that the characteristics of frequency of sweat expulsion is a useful index for determining whether and how much the central sudomotor mechanism is involved in the change of sweat rate in response to various thermal and non-thermal stresses.