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.

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.

Comparison of sweat rate during graded exercise and the local rate induced by pilocarpine.

Centrally stimulated sweat rate produced by graded exercise until exhaustion was compared to the local sweat rate induced by pilocarpine, often used as a sweating index for healthy individuals. Nine young male volunteers (22 +/- 4 years) were studied in temperate environment in two situations: at rest and during progressive exercise with 25 W increases every 2 min until exhaustion, on a cycle ergometer. In both situations, sweating was induced on the right forearm with 5 ml 0.5% pilocarpine hydrochloride applied by iontophoresis (1.5 mA, 5 min), with left forearm used as control. Local sweat rate was measured for 15 min at rest. During exercise, whole-body sweat rate was calculated from the body weight variation. Local sweat rate was measured from the time when heart rate reached 150 bpm until exhaustion and was collected using absorbent filter paper. Pharmacologically induced local sweat rate at rest (0.4 +/- 0.2 mg cm-2 min-1) and mean exercise-induced whole-body sweat rate (0.4 +/- 0.1 mg cm-2 min-1) were the same (P > 0.05) but were about five times smaller than local exercise-induced sweat rate (control = 2.1 +/- 1.4; pilocarpine = 2.7 +/- 1.2 mg cm-2 min-1), indicating different sudorific mechanisms. Both exercise-induced whole-body sweat rate (P < 0.05) and local sweat rate (P < 0.05) on control forearm correlated positively with pilocarpine-induced local sweat rate at rest. Assuming that exercise-induced sweating was a result of integrated physiological mechanisms, we suggest that local and whole-body sweat rate measured during graded exercise could be a better sweating index than pilocarpine.

Comparison of sweat rate during graded exercise and the local rate induced by pilocarpine

Centrally stimulated sweat rate produced by graded exercise until exhaustion was compared to the local sweat rate induced by pilocarpine, often used as a sweating index for healthy individuals. Nine young male volunteers (22 ± 4 years) were studied in temperate environment in two situations: at rest and during progressive exercise with 25 W increases every 2 min until exhaustion, on a cycle ergometer. In both situations, sweating was induced on the right forearm with 5 ml 0.5 percent pilocarpine hydrochloride applied by iontophoresis (1.5 mA, 5 min), with left forearm used as control. Local sweat rate was measured for 15 min at rest. During exercise, whole-body sweat rate was calculated from the body weight variation. Local sweat rate was measured from the time when heart rate reached 150 bpm until exhaustion and was collected using absorbent filter paper. Pharmacologically induced local sweat rate at rest (0.4 ± 0.2 mg cm-2 min-1) and mean exercise-induced whole-body sweat rate (0.4 ± 0.1 mg cm-2 min-1) were the same (P > 0.05) but were about five times smaller than local exercise-induced sweat rate (control = 2.1 ± 1.4; pilocarpine = 2.7 ± 1.2 mg cm-2 min-1), indicating different sudorific mechanisms. Both exercise-induced whole-body sweat rate (P < 0.05) and local sweat rate (P < 0.05) on control forearm correlated positively with pilocarpine-induced local sweat rate at rest. Assuming that exercise-induced sweating was a result of integrated physiological mechanisms, we suggest that local and whole-body sweat rate measured during graded exercise could be a better sweating index than pilocarpine.

Heat storage rate and acute fatigue in rats.

Thermal environmental stress can anticipate acute fatigue during exercise at a fixed intensity (%VO2max). Controversy exists about whether this anticipation is caused by the absolute internal temperature (Tint, degrees C), by the heat storage rate (HSR, cal/min) or by both mechanisms. The aim of the present study was to study acute fatigue (total exercise time, TET) during thermal stress by determining Tint and HSR from abdominal temperature. Thermal environmental stress was controlled in an environmental chamber and determined as wet bulb globe temperature ( degrees C), with three environmental temperatures being studied: cold (18 degrees C), thermoneutral (23.1 degrees C) or hot (29.4 degrees C). Six untrained male Wistar rats weighing 260-360 g were used. The animals were submitted to exercise at the same time of day in the three environments and at two treadmill velocities (21 and 24 m/min) until exhaustion. After implantation of a temperature sensor and treadmill adaptation, the animals were submitted to a Latin square experimental design using a 2 x 3 factorial scheme (velocity and environment), with the level of significance set at P<0.05. The results showed that the higher the velocity and the ambient temperature, the lower was the TET, with these two factors being independent. This result indicated that fatigue was independently affected by both the increase in exercise intensity and the thermal environmental stress. Fatigue developed at different Tint and HSR showed the best inverse relationship with TET. We conclude that HSR was the main anticipating factor of fatigue.

Heat storage rate and acute fatigue in rats

Thermal environmental stress can anticipate acute fatigue during exercise at a fixed intensity ( percentVO2max). Controversy exists about whether this anticipation is caused by the absolute internal temperature (Tint, ºC), by the heat storage rate (HSR, cal/min) or by both mechanisms. The aim of the present study was to study acute fatigue (total exercise time, TET) during thermal stress by determining Tint and HSR from abdominal temperature. Thermal environmental stress was controlled in an environmental chamber and determined as wet bulb globe temperature (ºC), with three environmental temperatures being studied: cold (18ºC), thermoneutral (23.1ºC) or hot (29.4ºC). Six untrained male Wistar rats weighing 260-360 g were used. The animals were submitted to exercise at the same time of day in the three environments and at two treadmill velocities (21 and 24 m/min) until exhaustion. After implantation of a temperature sensor and treadmill adaptation, the animals were submitted to a Latin square experimental design using a 2 x 3 factorial scheme (velocity and environment), with the level of significance set at P<0.05. The results showed that the higher the velocity and the ambient temperature, the lower was the TET, with these two factors being independent. This result indicated that fatigue was independently affected by both the increase in exercise intensity and the thermal environmental stress. Fatigue developed at different Tint and HSR showed the best inverse relationship with TET. We conclude that HSR was the main anticipating factor of fatigue