Effect of physical training on peripheral sweat production

1988 ◽  
Vol 65 (2) ◽  
pp. 811-814 ◽  
Author(s):  
M. J. Buono ◽  
N. T. Sjoholm
Keyword(s):  
Physical Training ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Secretory Activity ◽  
Sweat Glands ◽  
Trained Subjects ◽  
Peripheral Mechanism ◽  
Sweat Production ◽  
Sedentary Women

The purpose of this study was to determine the in vivo secretory activity of sweat glands from sedentary and trained subjects. Peripheral sweat production was determined using pilocarpine iontophoresis in 40 volunteers (10 sedentary men, 10 endurance-trained men, 10 sedentary women, 10 endurance-trained women). Peripheral sweat rate was significantly (P less than 0.05) greater in trained men [6.9 +/- 0.6 (SE) g.m2.min-1] and women (6.1 +/- 0.7) compared with sedentary men (3.1 +/- 0.5) and women (2.5 +/- 0.4). Furthermore, peripheral sweat rate was significantly correlated (r = 0.73) with maximal O2 uptake. The above two findings would suggest that physical training improves the secretory activity of the human sweat gland. Such a result supports previous findings that have suggested that the potentiation in sweating seen after training is achieved via a peripheral mechanism. In addition, several gender-related differences were found in the sudorific response of men and women. Specifically, women have a significantly greater sweat gland density, whereas men have a greater sweat production per gland.

Individual variations in structure and function of human eccrine sweat gland

1983 ◽  
Vol 245 (2) ◽  
pp. R203-R208 ◽  
Author(s):  
K. Sato ◽  
F. Sato
Keyword(s):  
Sweat Gland ◽  
Sweat Rate ◽  
Unit Length ◽  
Secretory Activity ◽  
Eccrine Sweat Gland ◽  
Sweat Glands ◽  
And Function ◽  
Eccrine Sweat

The mechanisms underlying variations in perspiration rate at the glandular level are still poorly understood. Human eccrine sweat glands were dissected from the back of 12 adults, cannulated, and stimulated in vitro with methacholine (Mch). The maximal sweat rate and pKA for Mch determined from the dose-response curve for each individual were compared with the anatomic dimensions of the isolated secretory tubules. There was significant correlation between Mch sensitivity (pKA) and the size of the sweat gland, sweat rate per gland, sweat rate per unit length of the secretory tubule, and sweat rate per unit glandular volume. The sweat glands from individuals judged to be poor sweaters exhibited smaller size, lower secretory activity both in vivo and in vitro, and decreased Mch sensitivity compared with glands from physically fit individuals. We conclude that the increased Mch sensitivity and glandular hypertrophy are the two important features of functionally active sweat glands and infer that these parameters could improve as a result of acclimatization to physical exercise and/or heat.

scholarly journals Is active sweating during heat acclimation required for improvements in peripheral sweat gland function?

2009 ◽  
Vol 297 (4) ◽  
pp. R1082-R1085 ◽  
Author(s):  
Michael J. Buono ◽  
Travis R. Numan ◽  
Ryan M. Claros ◽  
Stephanie K. Brodine ◽  
Fred W. Kolkhorst
Keyword(s):  
Sweat Gland ◽  
Sweat Rate ◽  
Heat Acclimation ◽  
Whole Body ◽  
Moderate Intensity ◽  
Sweat Glands ◽  
Exercise Heart Rate ◽  
Sweat Production ◽  
Gland Function ◽  
Pilocarpine Iontophoresis

We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35°C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 ± 22 vs. 138 ± 17 beats/min; P = 0.0001) and rectal temperature (38.2 ± 0.3 vs. 37.9 ± 0.3°C; P = 0.0003) and increased whole body sweat rate (0.70 ± 0.29 vs. 1.06 ± 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days ( P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 ± 0.20 vs. 0.66 ± 0.22 mg·cm−2·min−1). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 ± 0.21 mg·cm−2·min−1 ( P = 0.021) but decreased 52% to 0.32 ± 0.18 mg·cm−2·min−1 ( P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.

scholarly journals Role of Bradykinin Type 2 Receptors in Human Sweat Secretion: Translational Evidence Does Not Support a Functional Relationship

2021 ◽  
Vol 34 (3) ◽  
pp. 162-166
Author(s):  
Thad E. Wilson ◽  
Seetharam Narra ◽  
Kristen Metzler-Wilson ◽  
Artur Schneider ◽  
Kelsey A. Bullens ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Potential Therapeutic Target ◽  
Sweat Secretion ◽  
Hoe 140 ◽  
A Current

Bradykinin increases skin blood flow via a cGMP mechanism but its role in sweating in vivo is unclear. There is a current need to translate cell culture and nonhuman paw pad studies into in vivo human preparations to test for therapeutic viability for disorders affecting sweat glands. Protocol 1: physiological sweating was induced in 10 healthy subjects via perfusing warm (46–48°C) water through a tube-lined suit while bradykinin type 2 receptor (B2R) antagonist (HOE-140; 40 μM) and only the vehicle (lactated Ringer’s) were perfused intradermally via microdialysis. Heat stress increased sweat rate (HOE-140 = +0.79 ± 0.12 and vehicle = +0.64 ± 0.10 mg/cm<sup>2</sup>/min), but no differences were noted with B2R antagonism. Protocol 2: pharmacological sweating was induced in 6 healthy subjects via intradermally perfusing pilocarpine (1.67 mg/mL) followed by the same B2R antagonist approach. Pilocarpine increased sweating (HOE-140 = +0.38 ± 0.16 and vehicle = +0.32 ± 0.12 mg/cm<sup>2</sup>/min); again no differences were observed with B2R antagonism. Last, 5 additional subjects were recruited for various control experiments which identified that a functional dose of HOE-140 was utilized and it was not sudorific during normothermic conditions. These data indicate B2R antagonists do not modulate physiologically or pharmacologically induced eccrine secretion volumes. Thus, B2R agonist/antagonist development as a potential therapeutic target for hypo- and hyperhidrosis appears unwarranted.

scholarly journals Role of bradykinin type 2 receptors in human sweat secretion: translational evidence does not support a functional relationship

2020 ◽  
Author(s):  
Thad E. Wilson ◽  
Seetharam Narra ◽  
Kristen Metzler-Wilson ◽  
Artur Schneider ◽  
Kelsey A. Bullens ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Potential Therapeutic Target ◽  
Sweat Secretion ◽  
Hoe 140 ◽  
A Current

AbstractBradykinin increases skin blood flow via a cGMP mechanism but its role in sweating in vivo is unclear. There is a current need to translate cell culture and non-human paw pad studies into in vivo human preparations to test for therapeutic viability for disorders affecting sweat glands. Protocol 1: physiological sweating was induced in 10 healthy subjects via perfusing warm (46-48°C) water through a tube-lined suit while bradykinin type 2 receptor (B2R) antagonist (HOE-140; 40 μM) and only the vehicle (lactated Ringer’s) were perfused intradermally via microdialysis. Heat stress increased sweat rate (HOE-140 = +0.79±0.12 and vehicle = +0.64±0.10 mg/cm2/min), but no differences were noted with B2R antagonism. Protocol 2: pharmacological sweating was induced in 6 healthy subjects via intradermally perfusing pilocarpine (1.67 mg/ml) followed by the same B2R antagonist approach. Pilocarpine increased sweating (HOE-140 = +0.38±0.16 and vehicle = +0.32±0.12 mg/cm2/min); again no differences were observed with B2R antagonism. Lastly, 5 additional subjects were recruited for various control experiments which identified that a functional dose of HOE-140 was utilized and it was not sudorific during normothermic conditions. These data indicate B2R antagonists do not modulate physiologically-or pharmacologically-induced eccrine secretion volumes. Thus, B2R agonist/antagonist development as a potential therapeutic target for hypo- and hyperhidrosis appears unwarranted.

scholarly journals Evidence for β-adrenergic modulation of sweating during incremental exercise in habitually trained males

2017 ◽  
Vol 123 (1) ◽  
pp. 182-189 ◽  
Author(s):  
Tatsuro Amano ◽  
Yosuke Shitara ◽  
Naoto Fujii ◽  
Yoshimitsu Inoue ◽  
Narihiko Kondo
Keyword(s):  
Relative Intensity ◽  
Sweat Rate ◽  
Absolute Intensity ◽  
Control Site ◽  
Incremental Exercise ◽  
Saline Control ◽  
Maximum Workload ◽  
Sweat Production ◽  
Adrenergic Mechanism

The aim of the present study was to determine the β-adrenergic contribution to sweating during incremental exercise in habitually trained males. Nine habitually trained and 11 untrained males performed incremental cycling until exhaustion (20 W/min). Bilateral forearm sweat rates (ventilated capsule) were measured at two skin sites that were transdermally administered via iontophoresis with either 1% propranolol (Propranolol, a nonselective β-adrenergic receptor antagonist) or saline (Control). The sweat rate was evaluated as a function of both relative (percentage of maximum workload) and absolute exercise intensities. The sweat rate at the Propranolol site was lower than the control during exercise at 80 (0.57 ± 0.21 and 0.45 ± 0.19 mg·cm−2·min−1 for Control and Propranolol, respectively) and 90% (0.74 ± 0.22 and 0.65 ± 0.17 mg·cm−2·min−1, respectively) of maximum workload in trained males (all P < 0.05). By contrast, no between-site differences in sweat rates were observed in untrained counterparts (all P > 0.05). At the same absolute intensity, higher sweat rates on the control site were observed in trained males relative to the untrained during exercise at 160 (0.23 ± 0.20 and 0.04 ± 0.05 mg·cm−2·min−1 for trained and untrained, respectively) and 180 W (0.40 ± 0.20 and 0.13 ± 0.13 mg·cm−2·min−1, respectively) (all P < 0.05), whereas this between-group difference was not observed at the Propranolol site (all P > 0.05). We show that the β-adrenergic mechanism does modulate sweating during exercise at a submaximal high relative intensity in habitually trained males. The β-adrenergic mechanism may in part contribute to the greater sweat production in habitually trained males than in untrained counterparts during exercise. NEW & NOTEWORTHY We demonstrated for the first time that the β-adrenergic mechanism does modulate sweating (i.e., β-adrenergic sweating) during exercise using a localized β-adrenoceptor blockade in humans in vivo. β-Adrenergic sweating was evident in habitually trained individuals during exercise at a submaximal high relative intensity (80–90% maximal work). This observation advances our understanding of human thermoregulation during exercise and of the mechanism that underlies sweat gland adaptation to habitual exercise training.

Cysteine proteinase inhibitor in eccrine sweat is derived from sweat gland

1991 ◽  
Vol 260 (2) ◽  
pp. R314-R320 ◽  
Author(s):  
H. Yokozeki ◽  
T. Hibino ◽  
T. Takemura ◽  
K. Sato
Keyword(s):  
Liquid Chromatography ◽  
Molecular Mass ◽  
Sweat Gland ◽  
Proteinase Inhibitors ◽  
Sweat Rate ◽  
Cysteine Proteinase ◽  
Sweat Glands ◽  
Cysteine Proteinase Inhibitor ◽  
Eccrine Sweat

Although cysteine proteinases have been reported to be present in human eccrine sweat, their endogenous inhibitors, cysteine proteinase inhibitors (CPIs), have remained unstudied. We now present evidence that CPIs are indeed a true ingredient of human eccrine sweat. Sweat induced in sauna was collected over a Vaseline barrier placed on the skin to minimize epidermal contamination. The absence of major epidermal contamination of the sweat was further ensured by monitoring an epidermal marker, high-molecular-mass aminopeptidase. Sweat CPI was purified sequentially by chromatography with Sephacryl S-200, carboxymethylated papain-Sepharose, and anion-exchange Mono Q fast-protein liquid chromatography columns. Sweat CPI has a molecular mass of approximately 15 kDa, is stable for temperature (up to 80 degrees C) and pH (from 3 to 10), and inhibits papain, ficin, and sweat cathepsin B- and H-like enzymes. Sweat CPI may be of sweat gland origin because 1) the rate of CPI output in sweat (CPI concentration x sweat rate) is constant over 45 min; 2) antibody against epidermal CPI, which cross-reacts with sweat CPI, localized immunoreactivity in the sweat duct; 3) CPI activity was present in the glandular extracts of control and methacholine-stimulated (for 1 h in vitro) human sweat glands; and 4) the peaks of CPI activity in the glandular extract and sweat CPI were both eluted (by high-pressure liquid chromatography) at around 15 kDa. Sweat CPI may be very similar to epidermal CPI (which belongs to the stefin family of CPIs) because of many shared characteristics. The identity and function of sweat CPI remain to be studied.

Pilocarpine-induced sweat gland function in individuals with multiple sclerosis

2005 ◽  
Vol 98 (5) ◽  
pp. 1740-1744 ◽  
Author(s):  
Scott L. Davis ◽  
Thad E. Wilson ◽  
Jamie M. Vener ◽  
Craig G. Crandall ◽  
Jack H. Petajan ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Exercise Training ◽  
Sweat Gland ◽  
Aerobic Training ◽  
Sweat Rate ◽  
Aerobic Exercise Training ◽  
Sweat Glands ◽  
Sudomotor Function ◽  
Sweat Function ◽  
Gland Function

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 μg·gland−1·min−1 (SD 0.79), respectively] were significantly lower ( P ≤ 0.05) than in Con [0.27 mg·cm−2·min−1 (SD 0.10); 2.43 μg·gland−1·min−1 (SD 0.69)]. Aerobic exercise training significantly ( P ≤ 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.

Local inhibition of carbonic anhydrase does not decrease sweat rate

2018 ◽  
Vol 30 (1) ◽  
pp. 47-50 ◽  
Author(s):  
Jeff Moore ◽  
Sarah Northway ◽  
Nicole Wells ◽  
Emily Woolf ◽  
Michael J. Buono
Keyword(s):  
Carbonic Anhydrase ◽  
Healthy Subjects ◽  
Sweat Rate ◽  
Sweat Glands ◽  
Local Administration ◽  
Distilled Water ◽  
Local Inhibition ◽  
Sweat Production ◽  
Transdermal Iontophoresis ◽  
Eccrine Sweat Glands

Abstract Background: The purpose of this study was to measure sweat rate during exercise in the heat after directly inhibiting carbonic anhydrase (CA) in eccrine sweat glands via transdermal iontophoresis of acetazolamide. It was hypothesized that if CA was important for sweat production, local administration of acetazolamide, without the confounding systemic effects of dehydration typically associated with past studies, would have a significant effect on sweat rate during exercise. Methods: Ten healthy subjects volunteered to exercise in the heat following acetazolamide or distilled water iontophoresis on the forearm. Results: The distilled water iontophoresis site had a mean sweat rate during exercise in the heat of 0.59±0.31 μL/cm2/min, while the acetazolamide iontophoresis site had a mean sweat rate of 0.63±0.36 μL/cm2/min (p>0.05). Conclusions: The most important finding of the current study was that iontophoresis of acetazolamide did not significantly decrease sweat rate during exercise in the heat. Such results suggest that in past studies it was systemic dehydration, and not CA inhibition at the level of the sweat gland, that caused the reported decreased sweat rate.

TEA-sensitive K+ channels and human eccrine sweat gland output

2019 ◽  
Vol 127 (4) ◽  
pp. 921-929 ◽  
Author(s):  
Gary W. Mack ◽  
Benjamin S. Smith ◽  
Benjamin Rowland
Keyword(s):  
Electrical Stimulation ◽  
Epithelial Cells ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Stimulus Frequency ◽  
Extracellular Fluid ◽  
Response Curves ◽  
Stimulus Response ◽  
Sweat Production ◽  
Eccrine Sweat

Cholinergic-activated sweating depends on an influx of Ca2+ from extracellular fluid. It is thought that the opening of K+ channels on secretory epithelial cells facilitates Ca2+ entry. We examined the hypothesis that tetraethylammonium (TEA)-sensitive K+ channels participate in sweat production. We used a pre-post experimental design and initiated cholinergic-mediated sweating with intradermal electrical stimulation, monitored local sweat rate (SR) with a small sweat capsule mounted on the skin, and delivered 50 mM TEA via intradermal microdialysis. Local SR was activated by intradermal stimulation frequencies of 0.2–64 Hz, and we generated a sigmoid-shaped stimulus-response curve by plotting the area under the SR-time curve versus log10 stimulus frequency. Peak local SR was reduced from 0.372 ± 0.331 to 0.226 ± 0.190 mg·min−1·cm−2 ( P = 0.0001) during application of 50 mM TEA, whereas the EC50 and Hill slopes were not altered. The global sigmoid-shaped stimulus-response curves for control and 50 mM TEA were significantly different ( P < 0.0001), and the plateau region was significantly reduced ( P = 0.0023) with the TEA treatment. The effect of TEA on peak local SR was similar in male and female subjects. However, we did note a small effect of sex on the shape of the stimulus-response curves during intradermal electrical stimulation. Overall, these data support the hypothesis that cholinergic control of sweat gland activity is modulated by the presence of TEA-sensitive K+ channels in human sweat gland epithelial cells. NEW & NOTEWORTHY The contribution of various potassium channels to the process of cholinergic-mediated human eccrine sweat production is unclear. Using a novel model for cholinergic-mediated sweating in humans, we provide evidence that tetraethylammonium-sensitive K+ channels (KCa1.1 and Kv channels) contribute to eccrine sweat production.

Effect of local acetylcholinesterase inhibition on sweat rate in humans

2001 ◽  
Vol 90 (3) ◽  
pp. 757-762 ◽  
Author(s):  
Manabu Shibasaki ◽  
Craig G. Crandall
Keyword(s):  
Sweat Rate ◽  
Ringer Solution ◽  
Control Site ◽  
Acetylcholinesterase Inhibition ◽  
Whole Body ◽  
Sweat Glands ◽  
Ache Inhibitor ◽  
Temperature Threshold ◽  
Treated Site

ACh is the neurotransmitter responsible for increasing sweat rate (SR) in humans. Because ACh is rapidly hydrolyzed by acetylcholinesterase (AChE), it is possible that AChE contributes to the modulation of SR. Thus the primary purpose of this project was to identify whether AChE around human sweat glands is capable of modulating SR during local application of various concentrations of ACh in vivo, as well as during a heat stress. In seven subjects, two microdialysis probes were placed in the intradermal space of the forearm. One probe was perfused with the AChE inhibitor neostigmine (10 μM); the adjacent membrane was perfused with the vehicle (Ringer solution). SR over both membranes was monitored via capacitance hygrometry during microdialysis administration of various concentrations of ACh (1 × 10−7–2 M) and during whole body heating. SR was significantly greater at the neostigmine-treated site than at the control site during administration of lower concentrations of ACh (1 × 10−7–1 × 10−3 M, P < 0.05), but not during administration of higher concentrations of ACh (1 × 10−2–2 M, P > 0.05). Moreover, the core temperature threshold for the onset of sweating at the neostigmine-treated site was significantly reduced relative to that at the control site. However, no differences in SR were observed between sites after 35 min of whole body heating. These results suggest that AChE is capable of modulating SR when ACh concentrations are low to moderate (i.e., when sudomotor activity is low) but is less effective in governing SR after SR has increased substantially.

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