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The present study assessed agreement between a wireless sweat rate monitor (KuduSmart® device) and the ventilated capsule (VC) technique for measuring: (i) minute-averaged local sweat rate (LSR), (ii) sweating onset, (iii) sudomotor thermosensitivity, and (iv) steady-state LSR, during passive heat stress and exercise. It was hypothesized that acceptable agreement with no bias would be observed between techniques for all assessed sweating characteristics. On two separate occasions for each intervention, participants were either passively heated by recirculating hot water (49 °C) through a tube-lined garment until rectal temperature increased 1 °C over baseline ( n  = 8), or a 60 min treadmill march at a fixed rate of heat production (∼500 W, n  = 9). LSR of the forearm was concurrently measured with a VC and the KuduSmart® device secured within ∼2 cm. Using a ratio scale Bland-Altman analysis with the VC as the reference, the KuduSmart® device demonstrated systematic bias and not acceptable agreement for minute-averaged LSR (1.17 [1.09, 1.27], CV = 44.5%), systematic bias and acceptable agreement for steady-state LSR (1.16 [1.09,1.23], CV = 19.5%), no bias and acceptable agreement for thermosensitivity (1.07 [0.99, 1.16], CV = 23.2%), and no bias and good agreement for sweating onset (1.00 [1.00, 1.00], CV = 11.1%). In total, ≥73% of all minute-averaged LSR observations with the KuduSmart ® device ( n  = 2743) were within an absolute error of <0.2 mg/cm 2 /min to the VC, the reference minimum detectable change in measurement error of a VC on the forearm. Collectively, the KuduSmart ® device may be a satisfactory solution for assessing the sweating response to heat stress where a VC is impractical., Competing Interests: The KuduSmart® device was provided at no cost to Dr. Nicholas Ravanelli from Crossbridge Scientific Ltd. Crossbridge Scientific Ltd was not involved in study design, data collection, analysis, interpretation of results, or manuscript preparation.

Human thermoregulatory control is often evaluated through the relationship between thermoeffector output and core or mean body temperature. In addition to providing a general indication of whether a variable of interest alters thermoregulatory control, this relationship is often used to determine how this alteration may occur. This latter interpretation relies upon two parameters of the thermoeffector output-body temperature relationship: the onset threshold and thermosensitivity. Traditionally, changes in the onset threshold and thermosensitivity are interpreted as "central" or "peripheral" modulation of thermoregulatory control, respectively. This mini-review revisits the origins of the thermoeffector output-body temperature relationship and its use to interpret "central" or "peripheral" modulation of thermoregulatory control. Against this background, we discuss the strengths and weaknesses of this approach and highlight that "central" thermoregulatory control reflects the neural control of body temperature whereas "peripheral" thermoregulatory control reflects properties specific to the thermoeffector organs. We highlight studies that employed more direct approaches to investigate the neural control of body temperature and peripheral properties of thermoeffector organs. We conclude by encouraging future investigations interested in studying thermoregulatory control to more directly investigate the component of the thermoeffector loop under investigation.heat; human; skin blood flow; sweat; thermoregulatory.

Introduction: Exercise thermoregulation studies typically control for time of day. The present study assessed whether circadian rhythm independently alters time-dependent changes in core temperature and sweating during exercise at a fixed rate of metabolic heat production (Hprod) during the wake period., Methods: Ten men (26 ± 2 yr, 76.6 ± 6.3 kg, 1.95 ± 0.10 m2) cycled for 60 min in three combinations of ambient temperature and Hprod (23°C-7.5 W·kg-1, 33°C-5.5 W·kg-1, and 33°C-7.5 W·kg-1) at two times of day (a.m.: 0800 h, p.m.: 1600 h). Rectal temperature (Tre), local sweat rate, and whole-body sweat losses were measured., Results: Absolute Tre was lower at baseline in a.m. versus p.m. for all three conditions (a.m.: 36.8°C ± 0.2°C, p.m.: 37.0°C ± 0.2°C, P < 0.01). The ΔTre was not altered by time of day (P > 0.22) and not different at 60 min between a.m. and p.m. for 23°C-7.5 W·kg-1 (a.m.: 0.83°C ± 0.14°C, p.m.: 0.75°C ± 0.20°C; P = 0.20), 33°C-5.5 W·kg-1 (a.m.: 0.51°C ± 0.14°C, p.m.: 0.47°C ± 0.14°C; P = 0.22), and 33°C-7.5 W·kg-1 (a.m.: 0.77°C ± 0.20°C, p.m.: 0.73°C ± 0.21°C; P = 0.80). The change in local sweat rate was unaffected by time of day (P > 0.16) and not different at 60 min in 23°C-7.5 W·kg-1 (a.m.: 0.67 ± 0.20 mg·cm-2·min-1, p.m.: 0.62 ± 0.21 mg·cm-2·min-1; P = 0.55), 33°C-5.5 W·kg-1 (a.m.: 0.59 ± 0.13 mg·cm-2·min-1, p.m.: 0.57 ± 0.12 mg·cm-2·min-1; P = 0.65), and 33°C-7.5 W·kg-1 (a.m.: 0.91 ± 0.19 mg·cm-2·min-1, p.m.: 0.84 ± 0.15 mg·cm-2·min-1; P = 0.33). Whole-body sweat loss was not different between a.m. and p.m. for 23°C-7.5 W·kg-1 (a.m.: 579 ± 72 g, p.m.: 579 ± 96 g; P = 0.99), 33°C-5.5 W·kg-1 (a.m.: 558 ± 48 g, p.m.: 555 ± 83 g; P = 0.89), and 33°C-7.5 W·kg-1 (a.m.: 796 ± 72 g, p.m.: 783 ± 75 g; P = 0.31)., Conclusions: The change in core temperature and sweating throughout a 60-min exercise bout in 23°C and 33°C were unaffected by circadian rhythm during the wake period when exercise intensity was prescribed to elicit comparable rates of Hprod, suggesting that scheduling thermoregulatory exercise trials for the same time of day is unnecessary., (Copyright © 2020 by the American College of Sports Medicine.)

New Findings: What is the central question of this study? Hypoxia reportedly does not impair thermoregulation during exercise in compensable heat stress conditions: does it have an impact on maximal heat dissipation and therefore the critical environmental limit for the physiological compensability of core temperature? What is the main finding and its importance? Although skin blood flow was higher in hypoxia, no differences in sweat rates or the critical environmental limit for the physiological compensability of core temperature - an indicator of maximal heat loss - were found compared to exercise in normoxia, indicating no influence of normobaric hypoxia on thermoregulatory capacity in warm conditions., Abstract: Altered control of skin blood flow (SkBF) in hypoxia does not impair thermoregulation during exercise in compensable conditions, but its impact on maximal heat dissipation is unknown. This study therefore sought to determine whether maximum heat loss is altered by hypoxia during exercise in warm conditions. On separate days, eight males exercised for 90 min at a fixed heat production of ∼500 W in normoxia (NORM) or normobaric hypoxia (HYP, F I O 2  = 0.13) in a 34°C environment. Ambient vapour pressure was maintained at 2.13 kPa for 45 min, after which it was raised 0.11 kPa every 7.5 min. The critical ambient vapour pressure at which oesophageal temperature inflected upward (P crit ) indicated that maximum heat dissipation had been reached. Neither local sweat rates on the upper arm, back and forehead (average NORM: 1.46 (0.15) vs. HYP: 1.41 (0.16) mg cm -2  min -1 ; P = 0.59) nor whole-body sweat losses (NORM: 1029 (137) g vs. HYP: 1025 (150) g; P = 0.95) were different between trials. Laser-Doppler flux values (LDF; arbitrary units), an index of SkBF, were not different between NORM and HYP on the forearm (P = 0.23) or back (P = 0.73); however, when normalized as a percentage of maximum, LDF values tended to be higher in HYP compared to NORM at the forearm (condition effect, P = 0.05) but not back (P = 0.19). Despite potentially greater SkBF in hypoxia, there was no difference in P crit between conditions (NORM: 3.67 (0.35) kPa; HYP: 3.46 (0.39) kPa; P = 0.22). These findings suggest that hypoxia does not independently alter thermoregulatory capacity during exercise in warm conditions., (© 2020 The Authors. Experimental Physiology © 2020 The Physiological Society.)

Key Points: When exercise was prescribed to elicit a fixed evaporative heat balance requirement (E req ), no differences in steady-state sweat rates were observed with different absolute oesophageal and/or skin temperatures, secondary to differences in time of the day (i.e. morning (AM) vs. afternoon (PM)) and ambient temperature (i.e. 23°C vs. 33°C). Exercise at a fixed metabolic heat production (H prod ), but a different E req (due to differences in air temperature), yielded higher steady-state sweat rates with a higher E req , irrespective of absolute oesophageal temperature. Circadian rhythm did not alter the change in core temperature prior to the onset for sudomotor activation, nor the thermosensitivity, resulting in similar cumulative whole-body sweat rates irrespective of time of day at a fixed E req . Collectively, these data indicate that during exercise in a compensable environment, steady-state sudomotor responses are influenced by E req rather than absolute core and skin temperatures, or H prod ., Abstract: The present study sought to determine whether absolute core temperature (modified via diurnal variation) and absolute skin temperature (modified by different air temperatures (T a )) alters the steady-state sweating response to exercise at a fixed evaporative heat balance requirement (E req ). Ten males exercised for 60 min on six occasions. Three T a /heat production (H prod ) combinations (23°C/525 W, 33°C/400 W, 33˚C/525 W) were completed in the morning (08.00 h, AM) and afternoon (16.00 h, PM), to yield: (1) the same E req (200 or 275 W·m -2 ) with different absolute core temperatures (AM vs. PM); (2) the same E req (200 W·m -2 ) with different skin temperatures (T a : 23˚C vs. 33˚C); (3) the same heat production (525 W) with different E req (200 vs. 275 W·m -2 ). Oesophageal temperature (T oes ), local sweat rate (LSR) on the arm and upper-back, and whole-body sweat rate (WBSR) were measured. Steady-state T oes was always higher in PM versus AM at an E req of 200 W·m -2 (23°C, P = 0.001; 33°C, P = 0.004) and 275 W·m -2 , (33°C, P = 0.001). However steady-state mean LSR (200 W·m -2 /23°C: P = 0.25; 200 W·m -2 /33°C: P = 0.86; 275 W·m -2 /33°C: P = 0.53) and WBSR (200 W·m -2 /23°C: P = 0.79; 200 W·m -2 /33°C: P = 0.48; 275W·m -2 /33°C: P = 0.32) were similar. When E req was matched (200 W·m -2 ) with different T a (23°C vs. 33°C), steady-state LSR (P > 0.17) and WBSR (P > 0.93) were similar despite different skin temperatures. For the same H prod (525 W) but different E req (200 vs. 275 W·m -2 ), mean LSR (P < 0.001), and WBSR (P < 0.001) were higher with a greater E req . Collectively, steady-state sweating during exercise is altered by E req but not T oes , skin temperature, or H prod ., (© 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society.)

Key Points: With the advent of more frequent extreme heat events, adaptability to hot environments will be crucial for the survival of many species, including humans. However, the mechanisms that mediate human heat adaptation have remained elusive. We tested the hypothesis that heat acclimation improves the neural control of body temperature. Skin sympathetic nerve activity, comprising the efferent neural signal that activates heat loss thermoeffectors, was measured in healthy adults exposed to passive heat stress before and after a 7 day heat acclimation protocol. Heat acclimation reduced the activation threshold for skin sympathetic nerve activity, leading to an earlier activation of cutaneous vasodilatation and sweat production. These findings demonstrate that heat acclimation improves the neural control of body temperature in humans., Abstract: Heat acclimation improves autonomic temperature regulation in humans. However, the mechanisms that mediate human heat adaptation remain poorly understood. The present study tested the hypothesis that heat acclimation improves the neural control of body temperature. Body temperatures, skin sympathetic nerve activity, cutaneous vasodilatation, and sweat production were measured in 14 healthy adults (nine men and five women, aged 27 ± 5 years) during passive heat stress performed before and after a 7 day heat acclimation protocol. Heat acclimation increased whole-body sweat rate [+0.54 L h -1 (0.32, 0.75), P < 0.01] and reduced resting core temperature [-0.29°C (-0.40, -0.18), P < 0.01]. During passive heat stress, the change in mean body temperature required to activate skin sympathetic nerve activity was reduced [-0.21°C (-0.34, -0.08), P < 0.01] following heat acclimation. The earlier activation of skin sympathetic nerve activity resulted in lower activation thresholds for cutaneous vasodilatation [-0.18°C (-0.35, -0.01), P = 0.04] and local sweat rate [-0.13°C (-0.24, -0.01), P = 0.03]. These results demonstrate that heat acclimation leads to an earlier activation of the neural efferent outflow that activates the heat loss thermoeffectors of cutaneous vasodilatation and sweating., (© 2020 The Authors. The Journal of Physiology © 2020 The Physiological Society.)

Purpose: To quantify how maximum skin wettedness (ωmax); that is, the determinant of the boundary between compensable and uncompensable heat stress, is altered by aerobic training in previously unfit individuals and further augmented by heat acclimation., Methods: Eight untrained individuals completed an 8-wk aerobic training program immediately followed by 8 d of hot/humid (38°C, 65%RH) heat acclimation. Participants completed a humidity ramp protocol pretraining (PRE-TRN), posttraining (POST-TRN), and after heat acclimation (POST-HA), involving treadmill marching at a heat production of 450 W for 105 min in 37.5°C, 2.0 kPa (35%RH). After attaining a steady-state esophageal temperature (Tes), humidity increased 0.04 kPa·min. An upward inflection in Tes indicated the upper limit of physiological compensability (Pcrit), which was then used to quantify ωmax. Local sweat rate, activated sweat gland density, and sweat gland output on the back and arm were simultaneously measured throughout., Results: Peak aerobic capacity increased POST-TRN by approximately 14% (PRE-TRN: 45.8 ± 11.8 mL·kg·min; POST-TRN: 52.0 ± 11.1 mL·kg·min, P < 0.001). ωmax values became progressively greater from PRE-TRN (0.72 ± 0.06) to POST-TRN (0.84 ± 0.08; P = 0.02), to POST-HA (0.95 ± 0.05; P = 0.03). These shifts in ωmax were facilitated by a progressively greater local sweat rate and activated sweat gland density from PRE-TRN (0.84 ± 0.21 mg·cm·min; 67 ± 20 glands per square centimeter) to POST-TRN (0.96 ± 0.21 mg·cm·min, P = 0.03; 86 ± 27 glands per square centimeter; P = 0.009), to POST-HA (1.15 ± 0.21 mg·cm·min; P < 0.001; 98 ± 35 glands per square centimeter; P < 0.001). No differences in sweat gland output were observed., Conclusions: A greater ωmax occurred after 8 wk of aerobic training, but ωmax was further augmented with heat acclimation, indicating only a partially increased heat loss capacity with training. These ωmax values may assist future predictions of heat stress risk in untrained/trained unacclimated individuals and trained heat-acclimated individuals.

Some studies have observed a functional relationship between sweating and skin blood flow. However, the implications of this relationship during physiologically relevant conditions remain unclear. We manipulated sudomotor activity through changes in sweating efficiency to determine if parallel changes in vasomotor activity are observed. Eight young men completed two trials at 36°C and two trials at 42°C. During these trials, air temperature remained constant while ambient vapor pressure increased from 1.6 to 5.6 kPa over 2 h. Forced airflow across the skin was used to create conditions of high (HiS eff ) or low (LoS eff ) sweating efficiency. Local sweat rate (LSR), local skin blood flow (SkBF), as well as mean skin and esophageal temperatures were measured continuously. It took longer for LSR to increase during HiS eff at 36°C (HiS eff : 99 ± 11 vs. LoS eff : 77 ± 11 min, P < 0.01) and 42°C (HiS eff : 72 ± 16 vs. LoS eff : 51 ± 15 min, P < 0.01). In general, an increase in LSR preceded the increase in SkBF when expressed as ambient vapor pressure and time for all conditions ( P < 0.05). However, both responses were activated at a similar change in mean body temperature (average across all trials, LSR: 0.26 ± 0.15 vs. SkBF: 0.30 ± 0.18°C, P = 0.26). These results demonstrate that altering the point at which LSR is initiated during heat exposure is paralleled by similar shifts for the increase in SkBF. However, local sweat production occurs before an increase in SkBF, suggesting that SkBF is not necessarily a prerequisite for sweating., (Copyright © 2017 the American Physiological Society.)

We sought to identify the appropriate exercise intensity for unbiased comparisons of changes in rectal temperature (ΔT re ) and local sweat rates (LSR) between groups unmatched for body size during uncompensable heat stress. Sixteen males vastly different in body morphology were separated into two equal groups [small (SM): 65.8 ± 6.2 kg, 1.8 ± 0.1 m 2 ; large (LG): 100.0 ± 13.1 kg, 2.3 ± 0.1 m 2 ], but matched for sudomotor thermosensitivity (SM: 1.3 ± 0.6; LG: 1.1 ± 0.4 mg·cm -2 ·min -1 ·°C -1 ). The maximum potential for evaporation (E max ) for each participant was assessed using an incremental humidity protocol. On separate occasions, participants then completed 60 min of cycling in a 35°C and 70% RH environment at (1) 50% of VO 2max , (2) a heat production (H prod ) of 520 W, (3) H prod relative to mass (6 W·kg -1 ), and (4) H prod relative to mass above E max (3 W·kg -1 >E max ). E max was similar between LG (347 ± 39 W, 154 ± 15 W·m -2 ) and SM (313 ± 63 W, 176 ± 34 W·m -2 , P  >   0.12). ΔT re was greater in SM compared to LG at 520 W (SM: 1.5 ± 0.5; LG 0.8 ± 0.3°C, P  <   0.001) and at 50% of VO 2max (SM: 1.4 ± 0.5; LG 0.9 ± 0.3°C, P  <   0.001). However, ΔT re was similar between groups when H prod was either 6 W·kg -1 (SM: 0.9 ± 0.3; LG 0.9 ± 0.2°C, P  =   0.98) and 3 W·kg -1 >E max (SM: 1.4 ± 0.5; LG 1.3 ± 0.4°C, P  =   0.99). LSR was similar between LG and SM irrespective of condition, suggesting maximum LSR was attained (SM: 1.10 ± 0.23; LG: 1.07 ± 0.35 mg·cm -2 ·min -1 , P  =   0.50). In conclusion, systematic differences in ΔT re and LSR between groups unmatched for body size during uncompensable heat stress can be avoided by a fixed H prod in W·kg -1 or W·kg -1 >E max ., (© 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)