Function of human eccrine sweat glands during dynamic exercise and passive heat stress
Laboratory for Applied Human Physiology, Faculty of Human Development, Kobe University, Kobe 657-8501, Japan. Journal of Applied Physiology
(Impact Factor: 3.06).
The purpose of this study was to identify the pattern of change in the density of activated sweat glands (ASG) and sweat output per gland (SGO) during dynamic constant-workload exercise and passive heat stress. Eight male subjects (22.8 +/- 0.9 yr) exercised at a constant workload (117.5 +/- 4.8 W) and were also passively heated by lower-leg immersion into hot water of 42 degrees C under an ambient temperature of 25 degrees C and relative humidity of 50%. Esophageal temperature, mean skin temperature, sweating rate (SR), and heart rate were measured continuously during both trials. The number of ASG was determined every 4 min after the onset of sweating, whereas SGO was calculated by dividing SR by ASG. During both exercise and passive heating, SR increased abruptly during the first 8 min after onset of sweating, followed by a slower increase. Similarly for both protocols, the number of ASG increased rapidly during the first 8 min after the onset of sweating and then ceased to increase further (P > 0.05). Conversely, SGO increased linearly throughout both perturbations. Our results suggest that changes in forearm sweating rate rely on both ASG and SGO during the initial period of exercise and passive heating, whereas further increases in SR are dependent on increases in SGO.
Available from: PubMed Central
- "The number of activated sweat glands in the trained subjects was not significantly different from those in the controls, unlike sweat output per gland (P<0.001) between the trained and control subjects. Kondo et al.  suggested that changes in sweating rate rely on both activated sweat glands and sweat output per gland during the initial period of exercise stage when thermoregulation is passive, whereas further increases in sweating rate are dependent on increases in sweat output per gland. Therefore, the lack of a strong correlation between VO2max and activated sweat glands is not surprising. "
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ABSTRACT: 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.
Available from: ts-si.org
- "that these differences do not occur when the four groups perform at the same absolute exercise intensity. The increase in SR with increased exercise intensity and/or body temperature is controlled by increases in ASGs and/or SGO (Kondo et al. 1998, 2001). Kondo et al. (1998) reported that an increase in mean SR for five body sites (forehead, chest, back, forearm and thigh) occurred from 35 to 50% ˙ V O 2 max and depended on increases in ASGs and SGO, and the increase in SR from 50 to 65% ˙ V O 2 max was due only to an increase in SGO in untrained males ( ˙ V O 2 max ≈ 49.2 ml min −1 kg −1 ). "
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ABSTRACT: We assessed sex differences in the sweat gland response to changes in exercise intensity with respect to subjects' physical training status. In total, 37 subjects participated (10 trained and 10 untrained females, and 8 trained and 9 untrained males). Each subject cycled continuously at 35, 50 and 65% of their maximal O(2) uptake (V(O2max)) for 60 min at an ambient temperature of 30°C and a relative humidity of 45%. The mean local sweating rate (SR) on the forehead, chest, back, forearm and thigh was significantly greater in the trained subjects than in the untrained subjects of both sexes. The degree of the increase in SR with physical training was greater in males than in females at higher levels of exercise intensity. This increase in SR depended primarily on an increase in the sweat output per gland (SGO) in both sexes. However, control of the SR increase with increasing exercise intensity was altered by training in females, i.e. the increase in SR from exercise at 50 to 65% V(O2max) depended only on an increase in SGO in trained females and males and untrained males, but it depended on increases in activated sweat glands and the SGO in untrained females. It was concluded that training improved the sweating response, and a sex difference was observed in the degree of improvement in the sweating response due to physical training. This sex difference became more pronounced with increasing exercise intensity. A sex difference was observed in the control of sweating rate to an increase in exercise intensity, i.e. the maximal activated sweat gland responses of untrained females required a higher body temperature or work intensity than the other groups.
Available from: ncbi.nlm.nih.gov
- "The density and capacity of the sweat glands may differ from one body region to another (Sato and Sato, 1983; Shibasaki et al, 1997; Kondo et al, 1998). However, the forearm sweat glands have widely been used to approximate sweating activity of whole body (Wyndham et al, 1964; Wyndham, 1967; Chen & Elizondo, 1974; Ogawa et al, 1982; Kondo et al, 2001). "
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ABSTRACT: To determine the peripheral mechanisms involved in thermal sweating during the hot summers in July before acclimatization and after acclimatization in September, we evaluated the sweating response of healthy subjects (n=10) to acetylcholine (ACh), a primary neurotransmitter involved in peripheral sudomotor sensitivity. The quantitative sudomotor axon reflex test (QSART) measures sympathetic C fiber function after iontophoresed ACh evokes a measurable reliable sweat response. The QSART, at 2 mA for 5 min with 10% ACh, was applied to determine the directly activated (DIR) and axon reflex-mediated (AXR) sweating responses during ACh iontophoresis. The AXR sweat onset-time by the axon reflex was 1.50+/-0.32 min and 1.84+/-0.46 min before acclimatization in July and after acclimatization in September, respectively (p<0.01). The sweat volume of the AXR(1) [during 5 min 10% iontophoresis] by the axon reflex was 1.45+/-0.53 mg/cm(2) and 0.98+/-0.24 mg/cm(2) before acclimatization in July and after acclimatization in September, respectively (p<0.001). The sweat volume of the AXR(2) [during 5 min post-iontophoresis] by the axon reflex was 2.06+/-0.24 mg/cm(2) and 1.39+/-0.32 mg/cm(2) before and after acclimatization in July and September, respectively (p<0.001). The sweat volume of the DIR was 5.88+/-1.33 mg/cm(2) and 4.98+/-0.94 mg/cm(2) before and after acclimatization in July and September, respectively (p<0.01). These findings suggest that lower peripheral sudomotor responses of the ACh receptors are indicative of a blunted sympathetic nerve response to ACh during exposure to hot summer weather conditions.
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