Chest Sweat Research Articles

Baroreceptor modulation of cutaneous vasodilator and sudomotor responses to thermal stress in humans.

1. The influence of baroreceptor unloading on cutaneous vasodilatation was investigated in ten human subjects during dynamic supine cycle ergometer exercise at 28 degrees C. Increases in forearm skin blood flow (venous occlusion plethysmography) and arterial blood pressure (non-invasive) were measured and used to calculate forearm vascular conductance while local chest sweating rate was measured by dew-point hygrometry. Subjects performed two similar exercise protocols with and without baroreceptor unloading induced by application of -40 mmHg lower body negative pressure (LBNP). The LBNP condition was reversed (i.e. either removed or applied) after 15 min while exercise continued for an additional 20 min. 2. During exercise without LBNP, the body core temperature threshold for vasodilatation (measured as oesophageal temperature, Tc) averaged 37.06 +/- 0.12 degrees C (+/- S.E.M.) and increased to 37.30 +/- 0.09 degrees C (P < 0.05) during exercise with LBNP. The rate of rise of forearm vascular conductance (FVC) per unit increase in Tc (an expression of thermal sensitivity) and peak FVC at 15 min was significantly attenuated during baroreceptor unloading. These effects were rapidly reversed when LBNP was turned off. 3. Baroreceptor unloading during the first 15 min of exercise attenuated the local chest sweating rate, which was also reversed when LBNP was removed. 4. The time course and quickness in which baroreceptor unloading modulated thermoregulatory control of skin blood flow and local chest sweat rate suggests that the interaction between these two homeostatic mechanisms is primarily neurally mediated. The ability of baroreceptor activity to modulate both control of skin blood flow and sweating suggests a common site of interaction, more proximal than the effector organs, and involving the active vasodilator system.

Local sweating responses during recovery sleep after sleep deprivation in humans.

Changes in the central control of sweating were investigated in five sleep-deprived subjects (kept awake for 40 h) during their recovery sleep under warm ambient conditions [operative temperature (T(o)) was either 35 or 38 degrees C]. Oesophageal (T(oes)) and mean skin (Tsk) temperatures, chest sweat rate (msw,ch), and concomitant electro-encephalographic data were recorded. Throughout the night at 35 or 38 degrees C T(o), msw,ch changes were measured at a constant local chest skin temperature (Tch) of 35.5 degrees C. The results showed that body temperatures (T(oes) and Tsk) of sleep-deprived subjects were influenced by thermal and hypnogogic conditions. The msw,ch levels correlated positively with T(oes) in the subjects studied during sleep stage 1-2 (light sleep: LS), sleep stage 3-4 (slow wave sleep: SWS) and rapid eye movement (REM) sleep. Contrary to what has been reported in normal sleep, firstly, the T(oes) threshold for sweating onset differed between REM sleep and both LS and SWS, and, secondly, the slopes of the msw,ch versus T(oes) relationships were unchanged between REM and non-REM (i.e. LS or SWS) sleep. The changes observed after sleep deprivation were hypothesized to be due to alterations in the functioning of the central nervous system controller.

Sweating and skin blood flow during exercise: effects of age and maximal oxygen uptake

Individuals greater than or equal to 60 yr of age are more susceptible to hyperthermia than younger people. However, the mechanisms involved remain unclear. To gain further insight, we examined the heat loss responses of 7 young (24-30 yr) and 13 older (58-74 yr) men during 20 min of cycle exercise [67.5% maximal O2 uptake (VO2max)] in a warm environment (30 degrees C, 55% relative humidity). Forearm blood flow (FBF) and chest sweat rate (SR) were plotted as a function of the weighted average of mean skin and esophageal temperatures [Tes(w)] during exercise. The sensitivity and threshold for each response were defined as the slope and Tes(w) at the onset of the response, respectively. When the young sedentary men were compared with a subgroup (n = 7) of the older physically active men with similar VO2max, the SR and FBF responses of the two groups did not differ significantly. However, when the young men were compared with a subgroup of older sedentary men with a similar maximal O2 pulse, the SR and FBF sensitivities were significantly reduced by 62 and 40%, respectively. These findings suggest that during a short exercise bout either 1) there is no primary effect of aging on heat loss responses but, rather, changes are associated with the age-related decrease in VO2max or 2) the decline in heat loss responses due to aging may be masked by repeated exercise training.

Responses to dehydration and rehydration during heat exposure in young and older men

Body temperature, plasma responses, and subjective ratings of thirst and hotness were studied in 5 older men (OM, 61-67 yr) and 6 younger men (YM, 21-29 yr) during 180-min thermal dehydration and subsequent 60-min rehydration (45 degrees C, 25% relative humidity). Rectal temperature (Tre) increased more rapidly and to a greater magnitude in OM, while average total body sweat rates and chest sweat rates were not significantly different. During dehydration, both OM and YM lost similar body weight (1.52 +/- 0.11 vs. 1.55 +/- 0.22%, mean +/- SE). However, in OM, plasma volume (Pv) decreased (-11.3 +/- 2.8 vs. -4.9 +/- 2.9%), and plasma osmolality (Posm) increased to a greater extent (+5.0 +/- 0.32 vs. 1.1 +/- 0.24 mosmol/kg) compared with YM. On rehydration, OM and YM similarly replaced water debt (46.6 +/- 4.9 vs. 49.0 +/- 3.0%). Within 30 min of drinking, YM had restored Pv and Posm, whereas OM showed slower responses, restoring Posm after 60 min and Pv only after a subsequent 30 min at 25 degrees C. Despite a higher Tre and greater change in Pv and Posm, OM rated themselves less thirsty and not significantly hotter than YM. These findings suggest that aging results in decreased ability to maintain Tre during heat stress and that the mechanisms comprise a combination of alterations in body fluid distribution and perception.

Effects of changing hypothalamic temperature on eccrine sweating in the patas monkey

Two male (10–13 kg) patas monkeys (Erythrocebus patas) were implanted with bilateral thermodes to control hypothalamic temperature. Animals were restrained in primate chairs and instrumented to yield hypothalamic (T HYPO), colonic (T c), and mean skin (T̄ SK) temperatures, chest sweat rate (m SW), and heart rate (HR). T HYPO was monitored using a thermocouple inserted to the tip of a non-perfused thermode; m SW was measured using resistance hygrometry. After the monkey equilibrated to a selected ambient temperature, four thermodes were perfused with water from a temperature-controlled bath. Increasing T HYPO from 37 to 41°C increased m sw from 0.05 to 0.30 mg.cm −2.min −1. Reducing T̄ SK shifted the T HYPO:m SW relationship to the right ( p<0.05) without significantly altering its slope. Activity-induced changes in HR, when T hypo was constant, caused fluctuations in ongoing sweating that closely tracked HR. We conclude that m SW in the patas monkey is controlled by both peripheral and central thermal inputs and nonthermal factors.

Sweating responses and body temperatures during nocturnal sleep in humans.

The changes in the central control of sweating were investigated in five sleeping subjects under neutral and warm conditions [operative temperature (To) = 30, 33, and 34 degrees C; dew-point temperature = 10 degrees C]. Esophageal (Tes) and mean skin (Tsk) temperatures, chest sweat rate (msw,1), and concomitant electroencephalographic data were recorded. Throughout the night, msw,1 was measured under a local thermal clamp of 38 degrees C. Results showed that the thermal environment exerted a strong influence on both the levels and the time patterns of body temperatures. Moreover, local sweating rate correlated positively with Tes, and this relationship varied according to sleep stages. For a given Tes level, there was a sleep stage-related gradation in msw,1 that was higher in slow-wave sleep (SWS) than in stage 1-2 and the lowest in rapid-eye-movement (REM) sleep. This is explained by a change in the excitability or the sensitivity of the thermoregulatory system. The msw,1 differences between stage 1-2 and SWS are accounted for by a decrease in the Tes threshold (Tset) for sweating while the slope of the msw,1-Tes relation remains unchanged. The lower msw,1 in REM sleep is explained by a lesser slope for the msw,1-Tes relation without any Tset change from stage 1-2.

Influence of menstrual cycle on thermoregulatory, metabolic, and heart rate responses to exercise at night.

Ten women [mean maximal O2 uptake (VO2max), 2.81 l X min-1] exercised for 15 min on a cycle ergometer in the middle of the luteal phase (L) and in the early follicular phase (F) of the menstrual cycle at the same constant work rates (mean 122 W) and an ambient temperature of 18 degrees C. Serum progesterone averaged 44.7 nmol X l-1 in L and 0.7 nmol X l-1 in F. After a 4-h resting period, exercise was performed between 3 and 4 A.M., when the L-F core temperature difference is maximal. Preexercise esophageal (Tes), tympanic (Tty), and rectal (Tre) temperatures averaged 0.6 degrees C higher in L. During exercise Tes, Tty, and Tre averaged 0.5 degrees C higher. The thresholds for chest sweating and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were elevated in L by an average of 0.47 degrees C, related to mean body temperature (Tb(es) = 0.87Tes + 0.13Tskin), Tes, Tty, or Tre. The above-threshold chest sweat rate and cutaneous heat clearances were also increased in L. The mean exercise heart rate was 170.0 beats X min-1 in L and 163.8 beats X min-1 in F. The mean exercise VO2 in L (2.21 l X min-1) was 5.2% higher than in F (2.10 l X min-1), the metabolic rate was increased in L by 5.6%, but the net efficiency was 5.3% lower. No significant L-F differences in the respiratory exchange ratio and postexercise plasma lactate were demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of menstrual cycle on shivering, skin blood flow, and sweating responses measured at night.

In 10 women, external cold and heat exposures were performed both in the middle of luteal phase (L) and in the early follicular phase (F) of the menstrual cycle. Serum progesterone concentrations in L and F averaged 46.0 and 0.9 nmol X l-1, respectively. The experiments took place between 3:00 and 4:30 A.M., when the L-F core temperature difference is maximal. At neutral ambient temperature, esophageal (Tes), tympanic (Tty), rectal (Tre), and mean skin (Tsk) temperatures averaged 0.59 degrees C higher in L than in F. The thresholds for shivering, chest sweating, and cutaneous vasodilation (heat clearance technique) at the thumb and forearm were increased in L by an average of 0.47 degrees C, related to mean body temperature [Tb(es) = 0.87Tes + 0.13 Tsk] and to Tes, Tty, Tre, or Tsk. The above-threshold chest sweat rate and cutaneous heat clearances at the thumb and forearm were also enhanced in L, when related to Tb(es) or time. The metabolic rate, arm blood flow, and heart rate at thermoneutral conditions were increased in L by 5.0%, 1.1 ml X 100 ml-1 X min-1, and 4.6 beats X min-1, respectively. The concomitant increase in threshold temperatures for all autonomic thermoregulatory responses in L supports the concept of a resetting of the set point underlying the basal body temperature elevation in L. The effects of the increased threshold temperatures are counteracted by enhanced heat loss responses.

Skin blood flow and sweating changes following exercise training and heat acclimation.

Eight subjects underwent an exercise training program (10 days at 75% VO2max for 1 h/day at 25 degrees C db/13 degrees C wb) and a heat-acclimation program (10 days at 50% VO2max for 1 h/day at 35 degrees C db/32 degrees C wb). The relations of chest sweat rate and of forearm blood flow to internal temperature were determined for each subject at a 25 degrees C ambient temperature before training, between training and acclimation, and following acclimation. Training shifted the vasodilation and sweating thresholds toward lower internal temperatures, and acclimation further lowered these thresholds. All threshold shifts were statistically significant (P less than 0.05). Training and acclimation both appeared to increase the slope of the sweating relation, but these effects were not statistically significant. Changes in the slope of the blood flow relation were small and inconsistent. Since arm blood flow is higher at any given internal temperature after acclimation, the lower blood flow which is reported to accompany heat acclimation must result from the lower body temperatures.