Sex differences in thermoeffector responses during exercise at fixed requirements for heat loss

2012 ◽  
Vol 113 (5) ◽  
pp. 746-757 ◽  
Author(s):  
Daniel Gagnon ◽  
Glen P. Kenny
Keyword(s):  
Sex Differences ◽  
Heat Loss ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Evaporative Heat Loss ◽  
Sudomotor Function ◽  
Thermal Chamber ◽  
Local Sweat Rate ◽  
Exercise Period ◽  
Paper Technique

To assess potential mechanisms responsible for the lower sudomotor thermosensitivity in women during exercise, we examined sex differences in sudomotor function and skin blood flow (SkBF) during exercise performed at progressive increases in the requirement for heat loss. Eight men and eight women cycled at rates of metabolic heat production of 200, 250, and 300 W/m2 of body surface area, with each rate being performed sequentially for 30 min. The protocol was performed in a direct calorimeter to measure evaporative heat loss (EHL) and in a thermal chamber to measure local sweat rate (LSR) (ventilated capsule), SkBF (laser-Doppler), sweat gland activation (modified iodine-paper technique), and sweat gland output (SGO) on the back, chest, and forearm. Despite a similar requirement for heat loss between the sexes, significantly lower increases in EHL and LSR were observed in women ( P ≤ 0.001). Sex differences in EHL and LSR were not consistently observed during the first and second exercise periods, whereas EHL (348 ± 13 vs. 307 ± 9 W/m2) and LSR on the back (1.61 ± 0.07 vs. 1.20 ± 0.09 mg·min−1·cm−2), chest (1.33 ± 0.06 vs. 1.08 ± 0.09 mg·min−1·cm−2), and forearm (1.53 ± 0.07 vs. 1.20 ± 0.06 mg·min−1·cm−2, men vs. women) became significantly greater in men during the last exercise period ( P < 0.05). At each site, differences in LSR were solely due to a greater SGO in men, as opposed to differences in sweat gland activation. In contrast, no sex differences in SkBF were observed throughout the exercise period. The present study demonstrates that sex differences in sudomotor function are only evidenced beyond a certain requirement for heat loss, solely through differences in SGO. In contrast, the lower EHL and LSR in women are not paralleled by a lower SkBF response.

Forearm cutaneous vascular and sudomotor responses to whole body passive heat stress in young smokers

2015 ◽  
Vol 309 (1) ◽  
pp. R36-R42 ◽  
Author(s):  
Nicole E. Moyen ◽  
Hannah M. Anderson ◽  
Jenna M. Burchfield ◽  
Matthew A. Tucker ◽  
Melina A. Gonzalez ◽  
...  
Keyword(s):  
Heat Stress ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Whole Body ◽  
Mean Body Temperature ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Local Sweat Rate ◽  
Vasomotor Activity ◽  
Young Smokers

The purpose of this study was to compare smokers and nonsmokers' sudomotor and cutaneous vascular responses to whole body passive heat stress. Nine regularly smoking (SMK: 29 ± 9 yr; 10 ± 6 cigarettes/day) and 13 nonsmoking (N-SMK: 27 ± 8 yr) males were passively heated until core temperature (TC) increased 1.5°C from baseline. Forearm local sweat rate (LSR) via ventilated capsule, sweat gland activation (SGA), sweat gland output (SGO), and cutaneous vasomotor activity via laser-Doppler flowmetry (CVC) were measured as mean body temperature increased (ΔTb) during passive heating using a water-perfused suit. Compared with N-SMK, SMK had a smaller ΔTb at the onset of sweating (0.52 ± 0.19 vs. 0.35 ± 0.14°C, respectively; P = 0.03) and cutaneous vasodilation (0.61 ± 0.21 vs. 0.31 ± 0.12°C, respectively; P < 0.01). Increases in LSR and CVC per °C ΔTb (i.e., sensitivity) were similar in N-SMK and SMK (LSR: 0.63 ± 0.21 vs. 0.60 ± 0.40 Δmg/cm2/min/°C ΔTb, respectively, P = 0.81; CVC: 82.5 ± 46.2 vs. 58.9 ± 23.3 Δ%max/°C ΔTb, respectively; P = 0.19). However, the plateau in LSR during whole body heating was higher in N-SMK vs. SMK (1.00 ± 0.13 vs. 0.79 ± 0.26 mg·cm−2·min−1; P = 0.03), which was likely a result of higher SGO (8.94 ± 3.99 vs. 5.94 ± 3.49 μg·gland−1·min−1, respectively; P = 0.08) and not number of SGA (104 ± 7 vs. 121 ± 9 glands/cm2, respectively; P = 0.58). During whole body passive heat stress, smokers had an earlier onset for forearm sweating and cutaneous vasodilation, but a lower local sweat rate that was likely due to lower sweat output per gland. These data provide insight into local (i.e., forearm) thermoregulatory responses of young smokers during uncompensatory whole body passive heat stress.

scholarly journals Blunted sweating does not alter the rise in core temperature in people with multiple sclerosis exercising in the heat

2020 ◽  
Author(s):  
Georgia K Chaseling ◽  
Davide Filingeri ◽  
Dustin R. Allen ◽  
Michael Barnett ◽  
Steve Vucic ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Heat Loss ◽  
Core Temperature ◽  
Heat Production ◽  
Sweat Rate ◽  
Onset Time ◽  
Local Sweat Rate ◽  
Temperature Heat ◽  
C 30 ◽  
Exercise Induced

Purpose: To determine whether thermoregulatory capacity is altered by MS during exercise in the heat. Methods: Sixteen MS (EDSS: 2.9±0.9; 47±8 y; 77.6±14.0 kg) and 14 healthy (CON) control participants (43±11 y; 78.6±17.0 kg) cycled at a heat production of 4 W.kg-1 for 60 minutes at 30˚C, 30%RH (WARM). A subset of 8 MS (EDSS: 2.6±0.5; 44±8 y; 82.3±18.2 kg) and 8 CON (44±12 y; 81.2±21.1 kg) also exercised at 35°C, 30%RH (HOT). Rectal (Tre), mean skin (Tsk) temperature, and local sweat rate on the upper-back (LSRback) and forearm (LSRarm), were measured. Results: All CON, yet only 9 of 16, and 7 of 8 MS participants completed 60 min of exercise in WARM and HOT trials, respectively. All MS participants unable to complete exercise stopped with ∆Tre between 0.2-0.5˚C. The time to reach a ∆Tre of 0.2˚C was similar (MS:28±15 min, CON: 32±18 min; P=0.51). For MS participants completing 60-min of exercise in WARM, ∆Tre (P=0.13), ∆Tsk (P=0.45), LSRback (P=0.69) and LSRarm (P=0.54) were similar to CON, but ΔTb (MS:0.16±0.13˚C, CON:0.07±0.06˚C; P=0.02) and onset time (MS:16±10 min, CON:8±5 min; P=0.02) for sweating were greater. Similarly, in HOT, ∆Tre (P=0.52), ∆Tsk (P=0.06), LSRback (P=0.59) and LSRarm (P=0.08) were similar, but ΔTb (MS: 0.19±0.16˚C, CON: 0.06±0.04˚C; P=0.04) and onset time (MS:13±7 min, CON:6±3 min; P=0.02) for sweating were greater with MS. Conclusion: Even at 35˚C, a delayed sweating onset didn't alter heat loss to sufficiently affect exercise-induced rises in core temperature. Heat intolerance with MS does not seem attributable to thermoregulatory impairments.

scholarly journals The effect of plasma osmolality and baroreceptor loading status on postexercise heat loss responses

2016 ◽  
Vol 310 (6) ◽  
pp. R522-R531 ◽  
Author(s):  
Gabrielle Paull ◽  
Sheila Dervis ◽  
Juliana Barrera-Ramirez ◽  
Ryan McGinn ◽  
Baies Haqani ◽  
...  
Keyword(s):  
Heat Loss ◽  
Regional Differences ◽  
Treadmill Exercise ◽  
Sweat Rate ◽  
Plasma Osmolality ◽  
Exercise Protocol ◽  
Natural Recovery ◽  
Doppler Flowmetry ◽  
Young Males ◽  
Local Sweat Rate

We examined the separate and combined effects of plasma osmolality and baroreceptor loading status on postexercise heat loss responses. Nine young males completed a 45-min treadmill exercise protocol at 58 ± 2% V̇o2 peak, followed by a 60-min recovery. On separate days, participants received 0.9% NaCl (ISO), 3.0% NaCl (HYP), or no infusion (natural recovery) throughout exercise. In two additional sessions (no infusion), lower-body negative (LBNP) or positive (LBPP) pressure was applied throughout the final 45 min of recovery. Local sweat rate (LSR; ventilated capsule: chest, forearm, upper back, forehead) and skin blood flow (SkBF; laser-Doppler flowmetry: forearm, upper back) were continuously measured. During HYP, upper back LSR was attenuated from end-exercise to 10 min of recovery by ∼0.35 ± 0.10 mg·min−1·cm−2 and during the last 20 min of recovery by ∼0.13 ± 0.03 mg·min−1·cm−2, while chest LSR was lower by 0.18 ± 0.06 mg·min−1·cm−2 at 50 min of recovery compared with natural recovery (all P < 0.05). Forearm and forehead LSRs were not affected by plasma hyperosmolality during HYP (all P > 0.28), which suggests regional differences in the osmotic modulation of postexercise LSR. Furthermore, LBPP application attenuated LSR by ∼0.07–0.28 mg·min−1·cm−2 during the last 30 min of recovery at all sites except the forehead compared with natural recovery (all P < 0.05). Relative to natural recovery, forearm and upper back SkBF were elevated during LBPP, ISO, and HYP by ∼6–10% by the end of recovery (all P < 0.05). We conclude that 1) hyperosmolality attenuates postexercise sweating heterogeneously among skin regions, and 2) baroreceptor loading modulates postexercise SkBF independently of changes in plasma osmolality without regional differences.

Local versus whole-body sweating adaptations following 14 days of traditional heat acclimation

2016 ◽  
Vol 41 (8) ◽  
pp. 816-824 ◽  
Author(s):  
Martin P. Poirier ◽  
Daniel Gagnon ◽  
Glen P. Kenny
Keyword(s):  
Sweat Gland ◽  
Sweat Rate ◽  
Recovery Period ◽  
Exercise Bout ◽  
Heat Acclimation ◽  
Whole Body ◽  
Regional Variability ◽  
Thermal Chamber ◽  
Local Measurements ◽  
Body Level

The purpose of this study was to examine if local changes in sweat rate following 14 days of heat acclimation reflect those that occur at the whole-body level. Both prior to and following a 14-day traditional heat acclimation protocol, 10 males exercised in the heat (35 °C, ∼20% relative humidity) at increasing rates of heat production equal to 300 (Ex1), 350 (Ex2), and 400 (Ex3) W·m−2. A 10-min recovery period followed Ex1, while a 20-min recovery period separated Ex2 and Ex3. The exercise protocol was performed in a direct calorimeter to measure whole-body sweat rate and, on a separate day, in a thermal chamber to measure local sweat rate (LSR), sweat gland activation (SGA), and sweat gland output (SGO) on the upper back, chest, and mid-anterior forearm. Post-acclimation, whole-body sweat rate was greater during each exercise bout (Ex1: 14.3 ± 0.9; Ex2: 17.3 ± 1.2; Ex3: 19.4 ± 1.3 g·min−1, all p ≤ 0.05) relative to pre-acclimation (Ex1: 13.1 ± 0.6; Ex2: 15.4 ± 0.8; Ex3: 16.5 ± 1.3 g·min−1). In contrast, only LSR on the forearm increased with acclimation, and this increase was only observed during Ex2 (Post: 1.32 ± 0.33 vs. Pre: 1.06 ± 0.22 mg·min−1·cm−2, p = 0.03) and Ex3 (Post: 1.47 ± 0.41 vs. Pre: 1.17 ± 0.23 mg·min−1·cm−2, p = 0.05). The greater forearm LSR post-acclimation was due to an increase in SGO, as no changes in SGA were observed. Overall, these data demonstrate marked regional variability in the effect of heat acclimation on LSR, such that not all local measurements of sweat rate reflect the improvements observed at the whole-body level.

Exercise-rest cycles do not alter local and whole body heat loss responses

2011 ◽  
Vol 300 (4) ◽  
pp. R958-R968 ◽  
Author(s):  
Daniel Gagnon ◽  
Glen P. Kenny
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Intermittent Exercise ◽  
Sweat Rate ◽  
Heat Content ◽  
Whole Body ◽  
Evaporative Heat Loss ◽  
Esophageal Temperature ◽  
Direct Calorimetry ◽  
Body Heat

Previous studies have suggested that greater core temperatures during intermittent exercise (Ex) are due to attenuated sweating [upper back sweat rate (SR)] and skin blood flow (SkBF) responses. We evaluated the hypothesis that heat loss is not altered during exercise-rest cycles (ER). Ten male participants randomly performed four 120-min trials: 1) 60-min Ex and 60-min recovery (60ER); 2) 3 × 20-min Ex separated by 20-min recoveries (20ER); 3) 6 × 10-min Ex separated by 10-min recoveries (10ER), or 4) 12 × 5-min Ex separated by 5-min recoveries (5ER). Exercise was performed at a workload of 130 W at 35°C. Whole body heat exchange was determined by direct calorimetry. Core temperature, SR (by ventilated capsule), and SkBF (by laser-doppler) were measured continuously. Evaporative heat loss (EHL) progressively increased with each ER, such that it was significantly greater ( P ≤ 0.05) at the end of the last compared with the first Ex for 5ER (299 ± 39 vs. 440 ± 41 W), 10ER (425 ± 51 vs. 519 ± 45 W), and 20ER (515 ± 63 vs. 575 ± 74 W). The slope of the EHL response against esophageal temperature significantly increased from the first to the last Ex within the 10ER (376 ± 56 vs. 445 ± 89 W/°C, P ≤ 0.05) and 20ER (535 ± 85 vs. 588 ± 28 W/°C, P ≤ 0.05) conditions, but not during 5ER (296 ± 96 W/°C vs. 278 ± 95 W/°C, P = 0.237). In contrast, the slope of the SkBF response against esophageal temperature did not significantly change from the first to the last Ex (5ER: 51 ± 23 vs. 54 ± 19%/°C, P = 0.848; 10ER: 53 ± 8 vs. 56 ± 21%/°C, P = 0.786; 20ER: 44 ± 20 vs. 50 ± 27%/°C, P = 0.432). Overall, no differences in body heat content and core temperature were observed. These results suggest that altered local and whole body heat loss responses do not explain the previously observed greater core temperatures during intermittent exercise.

Rate and composition of sweat fluid losses are unaltered by hypohydration during prolonged exercise in horses

1997 ◽  
Vol 83 (4) ◽  
pp. 1133-1143 ◽  
Author(s):  
Janene K. Kingston ◽  
Raymond J. Geor ◽  
Laura Jill McCutcheon
Keyword(s):  
Heat Loss ◽  
Prolonged Exercise ◽  
Sweat Rate ◽  
Ionic Composition ◽  
Evaporative Heat Loss ◽  
Uptake Pattern ◽  
K Concentration ◽  
Total Body ◽  
Low Intensity Exercise ◽  
Fluid Losses

Kingston, Janene K., Raymond J. Geor, and Laura Jill McCutcheon. Rate and composition of sweat fluid losses are unaltered by hypohydration during prolonged exercise in horses. J. Appl. Physiol. 83(4): 1133–1143, 1997.— Rate and ionic composition of sweat fluid losses and partitioning of evaporative heat loss into respiratory and cutaneous components were determined in six horses during three 15-km phases of exercise at ∼40% of maximal O2 uptake. Pattern of change in sweat rate (SR) and composition was similar during each phase. SR increased rapidly for the first 20 min of exercise but remained at ∼24–28 ml ⋅ m−2 ⋅ min−1during the remainder of each phase. Similarly, the concentrations of Na and Cl in sweat increased until 30 min of exercise but were unchanged thereafter. Sweat osmolality and concentrations of Na and Cl were positively correlated with SR. Sweat K concentration decreased during exercise but was not correlated with SR. Fluid losses were 33.8 ± 1.5 liters, resulting in decreases of ∼21% in plasma volume and ∼11% in total body water. The ∼6% hypohydration was not associated with an alteration in SR, sweat composition, or heat storage. Respiratory and cutaneous evaporative heat loss represented ∼23 and 70%, respectively, of the total heat dissipated, and the partitioning of heat loss was similar in each exercise phase. We conclude that SR and the relative proportions of respiratory and cutaneous evaporative heat loss are unchanged in horses during prolonged low-intensity exercise despite moderate hypohydration.

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.

scholarly journals Role of nitric oxide synthase in human sweat gland output

2020 ◽  
Vol 129 (2) ◽  
pp. 386-391
Author(s):  
Gary W. Mack
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Sweat Gland ◽  
Sweat Rate ◽  
Channel Blockade ◽  
Sweat Production ◽  
Local Sweat Rate ◽  
Oxide Synthase ◽  
Novel Model

The contribution of nitric oxide synthase (NOS) to the process of cholinergic-mediated human eccrine sweat production is unclear. Using a novel model for cholinergic-mediated sweating in humans, I demonstrate that blocking the NOS system led to a reduction in local sweat rate (LSR). This reduction in LSR was maintained in the presence of K+ channel blockade with tetraethylammonium.

Changes in serotonin contents in brain affect metabolic heat production of rabbits in cold

1978 ◽  
Vol 235 (1) ◽  
pp. R41-R47
Author(s):  
M. T. Lin ◽  
I. H. Pang ◽  
S. I. Chern ◽  
W. Y. Chia
Keyword(s):  
Blood Flow ◽  
Amino Acid ◽  
Heat Loss ◽  
Acid Decarboxylase ◽  
Evaporative Heat Loss ◽  
Decarboxylase Inhibitor ◽  
Ambient Temperatures ◽  
Amino Acid Decarboxylase ◽  
Metabolic Heat ◽  
Normal Limits

Elevating serotonin (5-HT) contents in brain with 5-hydroxytryptophan (5-HTP) reduced rectal temperature (Tre) in rabbits after peripheral decarboxylase inhibition with the aromatic-L-amino-acid decarboxylase inhibitor R04-4602 at two ambient temperatures (Ta), 2 and 22 degrees C. The hypothermia was brought about by both an increase in respiratory evaporative heat loss (Eres) and a decrease in metabolic rate (MR) in the cold. At a Ta of 22 degrees C, the hypothermia was achieved solely due to an increase in heat loss. Depleting brain contents of 5-HT with intraventricular, 5,7-dihydroxytryptamine (5,7-DHT) produced an increased Eres and ear blood flow even at Ta of 2 degrees C. Also, MR increased at all but the Ta of 32 degrees C. However, depleting the central and peripheral contents of 5-HT with p-chlorophenylalanine (pCPA) produced lower MR accompanied by lower Eres in the cold compared to the untreated control. Both groups of pCPA-treated and 5,7-DHT-treated animals maintained their Tre within normal limits. The data suggest that changes in 5-HT content in brain affects the MR of rabbits in the cold. Elevating brain content of 5-HT tends to depress the MR response to cold, while depleting brain content of 5-HT tends to enhance the MR response to cold.

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