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The human body constantly exchanges heat with the environment. Temperature regulation is a homeostatic feedback control system that ensures deep body temperature is maintained within narrow limits despite wide variations in environmental conditions and activity-related elevations in metabolic heat production. Extensive research has been performed to study the physiological regulation of deep body temperature. This review focuses on healthy and disordered human temperature regulation during heat stress. Central to this discussion is the notion that various morphological features, intrinsic factors, diseases, and injuries independently and interactively influence deep body temperature during exercise and/or exposure to hot ambient temperatures. The first sections review fundamental aspects of the human heat stress response, including the biophysical principles governing heat balance and the autonomic control of heat loss thermoeffectors. Next, we discuss the effects of different intrinsic factors (morphology, heat adaptation, biological sex, and age), diseases (neurological, cardiovascular, metabolic, and genetic), and injuries (spinal cord injury, deep burns, and heat stroke), with emphasis on the mechanisms by which these factors enhance or disturb the regulation of deep body temperature during heat stress. We conclude with key unanswered questions in this field of research.

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.)

New Findings: What is the central question of this study? Does attenuated skin blood flow diminish sweating and reduce the critical environmental limit for heat balance, which indicates maximal heat loss potential, during severe heat stress? What is the main finding and its importance? Isosmotic hypovolaemia attenuated skin blood flow by ∼20% but did not result in different sweating rates, mean skin temperatures or critical environmental limits for heat balance compared with control and volume-infusion treatments, suggesting that the lower levels of skin blood flow commonly observed in aged and diseased populations may not diminish maximal whole-body heat dissipation. Attenuated skin blood flow (SkBF) is often assumed to impair core temperature (T c ) regulation. Profound pharmacologically induced reductions in SkBF (∼85%) lead to impaired sweating, but whether the smaller attenuations in SkBF (∼20%) more often associated with ageing and certain diseases lead to decrements in sweating and maximal heat loss potential is unknown. Seven healthy men (28 ± 4 years old) completed a 30 min equilibration period at 41°C and a vapour pressure (P a ) of 2.57 kPa followed by incremental steps in P a of 0.17 kPa every 6 min to 5.95 kPa. Differences in heat loss potential were assessed by identifying the critical vapour pressure (P crit ) at which an upward inflection in T c occurred. The following three separate treatments elicited changes in plasma volume to achieve three distinct levels of SkBF: control (CON); diuretic-induced isosmotic dehydration to lower SkBF (DEH); and continuous saline infusion to maintain SkBF (SAL). The T c , mean skin temperature (T sk ), heart rate, mean laser-Doppler flux (forearm and thigh; LDF mean ), mean local sweat rate (forearm and thigh; LSR mean ) and metabolic rate were measured. In DEH, a 14.2 ± 5.7% lower plasma volume resulted in a ∼20% lower LDF mean in perfusion units (PU) (DEH, 139 ± 23 PU; CON, 176 ± 22 PU; and SAL, 186 ± 22 PU; P = 0.034). However, LSR mean and whole-body sweat losses were unaffected by treatment throughout (P > 0.482). The P crit for T c was similar between treatments (CON, 5.05 ± 0.30 kPa; DEH, 4.93 ± 0.16 kPa; and SAL, 5.12 ± 0.10 kPa; P = 0.166). Furthermore, no differences were observed in the skin-air temperature gradient, metabolic rate or changes in T c (P > 0.197). In conclusion, a ∼20% reduction in SkBF alters neither sweat rate nor the upper limit for heat loss from the skin during non-encapsulated passive heat stress., (© 2016 The Authors. Experimental Physiology © 2016 The Physiological Society.)

Humans maintain a relatively constant core temperature through the dynamic balance between endogenous heat production and heat dissipation to the surrounding environment. In response to metabolic or environmental disturbances to heat balance, the autonomic nervous system initiates cutaneous vasodilation and eccrine sweating to facilitate higher rates of dry (primarily convection and radiation) and evaporative transfer from the body surface; however, absolute heat losses are ultimately governed by the properties of the skin and the environment. Over the duration of a heat exposure, the cumulative imbalance between heat production and heat dissipation leads to body heat storage, but the consequent change in core temperature, which has implications for health and safety in occupational and athletic settings particularly among certain clinical populations, involves a complex interaction between changes in body heat content and the body's morphological characteristics (mass, surface area, and tissue composition) that collectively determine the body's thermal inertia. The aim of this review is to highlight the biophysical aspects of human core temperature regulation by outlining the principles of human energy exchange and examining the influence of body morphology during exercise and environmental heat stress. An understanding of the biophysical factors influencing core temperature will enable researchers and practitioners to better identify and treat individuals/populations most vulnerable to heat illness and injury during exercise and extreme heat events. Further, appropriate guidelines may be developed to optimize health, safety, and work performance during heat stress., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Individual variation in the thermoregulatory responses to exercise is notoriously large. Although aerobic fitness (V̇o2 max) and body fatness are traditionally considered important predictors of individual core temperature and sweating responses, recent evidence indicates potentially important and independent roles for biophysical factors. Using stepwise regression, we examined the proportion of individual variability in rectal temperature changes (ΔTre), whole body sweat loss (WBSL), and steady-state local sweat rate (LSRss) independently described by 1) biophysical factors associated with metabolic heat production (Hprod) and evaporative heat balance requirements (Ereq) relative to body size and 2) factors independently related to V̇o2 max and body fatness. In a total of 69 trials, 28 males of wide-ranging morphological traits and V̇o2 max values cycled at workloads corresponding to a range of absolute Hprod (410-898 W) and relative intensities (32.2-82.0% V̇o2 max) for 60 min in 24.8 ± 0.7°C and 33.4 ± 12.2% relative humidity. Hprod (in W/kg total body mass) alone described ∼50% of the variability in ΔTre (adjusted to r(2) = 0.496; P < 0.001), whereas surface area-to-mass ratio and body fat percentage (BF%) explained an additional 4.3 and 2.3% of variability, respectively. For WBSL, Ereq (in W) alone explained ∼71% of variance (adjusted to r(2) = 0.713, P < 0.001), and the inclusion of BF% explained an additional 1.3%. Similarly, Ereq (in W/m(2)) correlated significantly with LSRss (adjusted to r(2) = 0.603, P < 0.001), whereas %V̇o2 max described an additional ∼4% of total variance. In conclusion, biophysical parameters related to Hprod, Ereq, and body size explain 54-71% of the individual variability in ΔTre, WBSL, and LSRss, and only 1-4% of additional variance is explained by factors related to fitness or fatness., (Copyright © 2015 the American Physiological Society.)

Two studies were performed to 1) characterize changes in local sweat rate (LSR) following fluid ingestion of different temperatures during exercise, and 2) identify the potential location of thermoreceptors along the gastrointestinal tract that independently modify sudomotor activity. In study 1, 12 men cycled at 50% Vo2peak for 75 min while ingesting 3.2 ml/kg of 1.5°C, 37°C, or 50°C fluid 5 min before exercise; and after 15, 30, and 45-min of exercise. In study 2, 8 men cycled at 50% Vo2peak for 75 min while 3.2 ml/kg of 1.5°C or 50°C fluid was delivered directly into the stomach via a nasogastric tube (NG trials) or was mouth-swilled only (SW trials) after 15, 30, and 45 min of exercise. Rectal (Tre), aural canal (Tau), and mean skin temperature (Tsk); and LSR on the forehead, upper-back, and forearm were measured. In study 1, Tre, Tau, and Tsk were identical between trials, but after each ingestion, LSR was significantly suppressed at all sites with 1.5°C fluid and was elevated with 50°C fluid compared with 37°C fluid (P < 0.001). The peak difference in mean LSR between 1.5°C and 50°C fluid after ingestion was 0.29 ± 0.06 mg·min(-1)·cm(-2). In study 2, LSR was similar between 1.5°C and 50°C fluids with SW trials (P = 0.738), but lower at all sites with 1.5°C fluid in NG trials (P < 0.001) despite no concurrent differences in Tre, Tau, and Tsk. These data demonstrate that 1) LSR is transiently altered by cold and warm fluid ingestion despite similar core and skin temperatures; and 2) thermoreceptors that independently and acutely modulate sudomotor output during fluid ingestion probably reside within the abdominal area, but not the mouth.

This study assessed the accuracy of the technical absorbent (TA) method for measuring local sweat rate (LSR) relative to the well-established ventilated capsule (VC) method during steady-state and nonsteady-state sweating using large and small sample surface areas on the forearm and midback. Forty participants (38 males and two females) cycled at 60% peak oxygen consumption for 75 min in either a temperate [22.3 ± 0.9°C, 32 ± 17% relative humidity (RH)] or warm (32.5 ± 0.8°C, 29 ± 7% RH) environment. Simultaneous bilateral comparisons of 5-min LSR measurements using the TA and VC methods were performed for the back and forearm after 10, 30, 50, and 70 min. LSR values, measured using the TA method, were highly correlated with the VC method at all time points, irrespective of sample surface area and body region (all P < 0.001). On average, ≈ 79% of the variability observed in LSR measured with the VC method was described by the TA method. The mean difference in absolute LSR using the TA method (TA-VC with 95% confidence intervals) was -0.23 [-0.30,-0.16], -0.11 [-0.21,0.00], -0.03 [-0.14,+0.08], and +0.02 [-0.07,+0.11] mg · cm(-2) · min(-1) after 10, 30, 50, and 70 min of exercise, respectively. Duplicate LSR measurements within each method during steady-state sweating were highly correlated (TA: r = 0.96, P < 0.001, n = 20; VC: r = 0.97, P < 0.001, n = 20) with a mean bias of +0.07 ± 0.14 and +0.01 ± 0.10 mg · cm(-2) · min(-1) for TA and VC methods, respectively. The mean smallest detectable difference in LSR was 0.12 and 0.05 mg · min(-1) · cm(-2) for TA and VC methods, respectively. These data support the TA method as a reliable alternative for measuring the rate of sweat appearance on the skin surface.

The present study investigated the influence of maximal oxygen uptake (V(O2 max)) on local steady-state sudomotor responses to exercise, independently of evaporative requirements for heat balance (E(req)). Eleven fit (F; (V(O2 max))61.9 ± 6.0 ml kg(-1) min(-1)) and 10 unfit men (UF; (V(O2 max)) 40.4 ± 3.8 ml kg(-1) min(-1)) cycled for 60 min at an air temperature of 24.5 ± 0.8°C and ambient humidity of 0.9 ± 0.3 kPa at a set metabolic heat production per unit surface area, producing the same E(req) in all participants (BAL trial) and, in a second trial, at 60% of (V(O2 max)). During the BAL trial, absolute power (F 107 ± 2 and UF 102 ± 2 W; P = 0.126), E(req) (F 175 ± 5 and UF 176 ± 9 W m(-2); P = 0.855), steady-state whole-body sweat rate (F 0.44 ± 0.02 and UF 0.47 ± 0.02 mg cm(-2) min(-1); P = 0.385) and local sweat rate on the arm (F 0.29 ± 0.03 and UF 0.35 ± 0.03 mg cm(-2) min(-1); P = 0.129) were not different between groups; however, local sweat rate on the forehead in UF (1.67 ± 0.20 mg cm(-2) min(-1)) was almost double (P = 0.002) that of F (0.87 ± 0.11 mg cm(-2) min(-1)). Heart rate, ratings of perceived exertion and relative exercise intensity were also significantly greater in UF (P < 0.05). There was a trend towards an elevated minute ventilation in UF (P = 0.052), while end-tidal P(CO2) was significantly lower in UF (P = 0.028). At 60% (V(O2 max)), absolute power (F 174 ± 6 and UF 110 ± 5 W; P < 0.001), E(req) (F 291 ± 14 and UF 190 ± 17 W m(-2); P < 0.001), steady-state whole-body sweat rate (F 0.84 ± 0.05 and UF 0.53 ± 0.03 mg cm(-2) min(-1); P < 0.001) and local sweat rate on the arm (F 0.75 ± 0.04 and UF 0.35 ± 0.03 mg cm(-2) min(-1); P < 0.001) and on the forehead (F 2.92 ± 0.42 and UF 1.68 ± 0.23 mg cm(-2) min(-1); P = 0.022) were all significantly greater in F compared with UF. Heart rate and ratings of perceived exertion were similar at all time points (P > 0.05). Significantly greater minute ventilation (P < 0.001) and end-tidal P (CO2) responses (P = 0.017) were found in F. In conclusion, aerobic fitness alters local sweating on the forehead, but not the forearm, independently of evaporative requirements for heat balance, and may be the result of differential control of sweating in these skin areas associated with the relative intensity of exercise.

The independent influence of peak oxygen uptake (Vo(₂ peak)) on changes in thermoregulatory responses during exercise in a neutral climate has not been previously isolated because of complex interactions between Vo(₂ peak), metabolic heat production (H(prod)), body mass, and body surface area (BSA). It was hypothesized that Vo(₂ peak) does not independently alter changes in core temperature and sweating during exercise. Fourteen males, 7 high (HI) Vo(₂ peak): 60.1 ± 4.5 ml·kg⁻¹·min⁻¹; 7 low (LO) Vo(₂ peak): 40.3 ± 2.9 ml·kg⁻¹·min⁻¹ matched for body mass (HI: 78.2 ± 6.1 kg; LO: 78.7 ± 7.1 kg) and BSA (HI: 1.97 ± 0.08 m²; LO: 1.94 ± 0.08 m²), cycled for 60-min at 1) a fixed heat production (FHP trial) and 2) a relative exercise intensity of 60% Vo(₂ peak) (REL trial) at 24.8 ± 0.6°C, 26 ± 10% RH. In the FHP trial, H(prod) was similar between the HI (542 ± 38 W, 7.0 ± 0.6 W/kg or 275 ± 25 W/m²) and LO (535 ± 39 W, 6.9 ± 0.9 W/kg or 277 ± 29 W/m²) groups, while changes in rectal (T(re): HI: 0.87 ± 0.15°C, LO: 0.87 ± 0.18°C, P = 1.00) and aural canal (T(au): HI: 0.70 ± 0.12°C, LO: 0.74 ± 0.21°C, P = 0.65) temperature, whole-body sweat loss (WBSL) (HI: 434 ± 80 ml, LO: 440 ± 41 ml; P = 0.86), and steady-state local sweating (LSR(back)) (P = 0.40) were all similar despite relative exercise intensity being different (HI: 39.7 ± 4.2%, LO: 57.6 ± 8.0% Vo(2 peak); P = 0.001). At 60% Vo(2 peak), H(prod) was greater in the HI (834 ± 77 W, 10.7 ± 1.3 W/kg or 423 ± 44 W/m²) compared with LO (600 ± 90 W, 7.7 ± 1.4 W/kg or 310 ± 50 W/m²) group (all P < 0.001), as were changes in T(re) (HI: 1.43 ± 0.28°C, LO: 0.89 ± 0.19°C; P = 0.001) and T(au) (HI: 1.11 ± 0.21°C, LO: 0.66 ± 0.14°C; P < 0.001), and WBSL between 0 and 15, 15 and 30, 30 and 45, and 45 and 60 min (all P < 0.01), and LSR(back) (P = 0.02). The absolute esophageal temperature (T(es)) onset for sudomotor activity was ∼0.3°C lower (P < 0.05) in the HI group, but the change in T(es) from preexercise values before sweating onset was similar between groups. Sudomotor thermosensitivity during exercise were similar in both FHP (P = 0.22) and REL (P = 0.77) trials. In conclusion, changes in core temperature and sweating during exercise in a neutral climate are determined by H(prod), mass, and BSA, not Vo(₂ peak).

This study sought to assess the within-subject influence of acute hypoxia on exercise-induced changes in core temperature and sweating. Eight participants [1.75 (0.06) m, 70.2 (6.8) kg, 25 (4) yr, 54 (8) ml·kg−1·min−1] completed 45 min of cycling, once in normoxia (NORM; FIO2 = 0.21) and twice in hypoxia (HYP1/HYP2; FIO2= 0.13) at 34.4(0.2)°C, 46(3)% RH. These trials were designed to elicit 1) two distinctly different %V̇o2peak [NORM: 45 (8)% and HYP1: 62 (7)%] at the same heat production (Hprod) [NORM: 6.7 (0.6) W/kg and HYP1: 7.0 (0.5) W/kg]; and 2) the same %V̇o2peak [NORM: 45 (8)% and HYP2: 48 (5)%] with different Hprod [NORM: 6.7 (0.6) W/kg and HYP2: 5.5 (0.6) W/kg]. At a fixed %V̇o2peak, changes in rectal temperature (ΔTre) and changes in esophageal temperature (ΔTes) were greater at end-exercise in NORM [ΔTre: 0.76 (0.19)°C; ΔTes: 0.64 (0.22)°C] compared with HYP2 [ΔTre: 0.56 (0.22)°C, P < 0.01; ΔTes: 0.42 (0.21)°C, P < 0.01]. As a result of a greater Hprod (P < 0.01) in normoxia, and therefore evaporative heat balance requirements, to maintain a similar %V̇o2peak compared with hypoxia, mean local sweat rates (LSR) from the forearm, upper back, and forehead were greater (all P < 0.01) in NORM [1.10 (0.20) mg·cm−2·min−1] compared with HYP2 [0.71 (0.19) mg·cm−2·min−1]. However, at a fixed Hprod, ΔTre [0.75 (0.24)°C; P = 0.77] and ΔTes [0.63 (0.29)°C; P = 0.69] were not different in HYP1, compared with NORM. Likewise, mean LSR [1.11 (0.20) mg·cm−2·min−1] was not different (P = 0.84) in HYP1 compared with NORM. These data demonstrate, using a within-subjects design, that hypoxia does not independently influence thermoregulatory responses. Additionally, further evidence is provided to support that metabolic heat production, irrespective of %V̇o2peak, determines changes in core temperature and sweating during exercise. NEW & NOTEWORTHY Using a within-subject design, hypoxia does not independently alter core temperature and sweating during exercise at a fixed rate of heat production. These findings also further contribute to the development of a methodological framework for assessing differences in thermoregulatory responses to exercise between various populations and individuals. Using the combined environmental stressors of heat and hypoxia we conclusively demonstrate that exercise intensity relative to aerobic capacity (i.e., %V̇o2max) does not influence changes in thermoregulatory responses. [ABSTRACT FROM AUTHOR]

A side-effect of endoscopic thoracic sympathectomy (ETS) is compensatory hyperhidrosis (CH), characterized by excessive sweating from skin areas with intact sudomotor function. The physiological mechanism of CH is unknown, but may represent an augmented local sweat rate from skin areas with uninterrupted sympathetic innervation based on evaporative heat balance requirements. For a given combination of activity and climate, the same absolute amount of evaporation (if any) is needed to balance the rate of metabolic heat production both pre- and post-ETS. However, the rate of local sweating per unit of skin surface area with intact sudomotor activity must be greater post-ETS as evaporation must be derived from a smaller skin surface area. Under conditions with high evaporative requirements, greater degradations in sweating efficiency associated with an increased dripping of sweat should also occur post-ETS, further pronouncing the sweat rate required for heat balance. In conclusion, in addition to the potential role of psychological stimuli for increased sudomotor activity, the existence of CH post-ETS can be described by the interplay between fundamental thermoregulatory physiology and altered heat balance biophysics and does not require a postoperative alteration in physiological control. [ABSTRACT FROM AUTHOR]