Whole-body Sweat Rate Research Articles

Predicting Hydration Status Using Machine Learning Models From Physiological and Sweat Biomarkers During Endurance Exercise: A Single Case Study.

Improper hydration routines can reduce athletic performance. Recent studies show that data from noninvasive biomarker recordings can help to evaluate the hydration status of subjects during endurance exercise. These studies are usually carried out on multiple subjects. In this work, we present the first study on predicting hydration status using machine learning models from single-subject experiments, which involve 32 exercise sessions of constant moderate intensity performed with and without fluid intake. During exercise, we measured four noninvasive physiological and sweat biomarkers including heart rate, core temperature, sweat sodium concentration, and whole-body sweat rate. Sweat sodium concentration was measured from six body regions using absorbent patches. We used three machine learning models to determine the percentage of body weight loss as an indicator of dehydration with these biomarkers and compared the prediction accuracy. The results on this single subject show that these models gave similar mean absolute errors, while in general the nonlinear models slightly outperformed the linear model in most of the experiments. The prediction accuracy of using the whole-body sweat rate or heart rate was higher than using core temperature or sweat sodium concentration. In addition, the model trained on the sweat sodium concentration collected from the arms gave slightly better accuracy than from the other five body regions. This exploratory work paves the way for the use of these machine learning models to develop personalized health monitoring together with emerging, noninvasive wearable sensor devices.

Heat acclimation does not negatively affect salivary immunoglobulin-A and self-reported illness symptoms and wellness in recreational athletes

ABSTRACT Heat acclimation (HA) protocols repeatedly expose individuals to heat stress. As HA is typically performed close to the pinnacle event, it is essential that the protocol does not compromise immune status, health, or wellbeing. The purpose of this study was to examine the effect of HA on resting salivary immunoglobulin-A (s-IgA) and salivary cortisol (s-cortisol), self-reported upper-respiratory tract symptoms, and self-reported wellness parameters. Seventeen participants (peak oxygen uptake 53.2 ± 9.0 mL·kg−1·min−1) completed a 10-day controlled-hyperthermia HA protocol, and a heat stress test both before (HST1) and after (HST2) HA (33°C, 65% relative humidity). Resting saliva samples were collected at HST1, day 3 and 7 of the HA protocol, HST2, and at 5 ± 1 days post-HA. Upper-respiratory tract symptom data were collected weekly from one week prior to HA until three weeks post HA, and wellness ratings were reported daily throughout HA. HA successfully induced physiological adaptations, with a lower end-exercise rectal temperature and heart rate and higher whole-body sweat rate at HST2 compared to HST1. In contrast, resting saliva flow rate, s-IgA concentration, s-cortisol concentration, and s-cortisol secretion rate remained unchanged (n = 11–14, P = 0.10–0.48). Resting s-IgA secretion rate increased by 39% from HST1 to HST2 (n = 14, P = 0.03). No changes were observed in self-reported upper respiratory tract symptoms and wellness ratings. In conclusion, controlled-hyperthermia HA did not negatively affect resting s-IgA and s-cortisol, self-reported upper-respiratory tract symptoms, and self-reported wellness parameters in recreational athletes.

Physiological Strain And Heat Storage In Different Hot Conditions Of Equivalent Wet Bulb Globe Temperature

Varying levels of ambient temperature and humidity differently affect heat storage (S) during walking, but the quantification of S at equivalent wet bulb globe temperature (WBGT) and affects on physiological strain have yet to be determined. PURPOSE: This investigation tested the hypothesis that varying hot environments of equal WBGT result in similar cumulative S but differing levels of cardiovascular strain and ventilatory regulation. METHODS: In a randomized crossover design, 12 subjects walked for 90 min on a treadmill in hot-dry (HD; 42.2 °C, 15% relative humidity (RH)) and warm-wet (WW; 30 °C, 80% RH) environments of equal WBGT (27.8 °C). Whole body sweat rate (WBSR) was determined by measuring body mass change. Ventilation (VE), respiratory rate (f), tidal volume (TV), respiratory exchange ratio (RER), and gas volumes (O2, CO2) were collected as 5-min averages, and core temperature (Tc, ingestible pill), heart rate (HR), and four-site mean skin temperature (Tsk) were recorded every 10 min. WBSR, S, evaporative heat loss (EHL), and dry heat gain (DHG) were assessed with paired t-tests and all other dependent variables with two-way analysis of variance (condition x time: 10, 50, 90 min). RESULTS: Tc (HD: 38.5 ± 0.5 °C; WW: 38.4 ± 0.4 °C, p = 0.38) and S (HD: 159 ± 235 W; WW: 359 ± 112 W, p = 0.06) increased during exercise (p < 0.01) and were not different between groups at min 90. Tsk (HD: 36.2 ± 0.9 °C; WW: 34.4 ± 0.7 °C, p < 0.01), HR (HD: 160 ± 19 bpm; WW: 154 ± 15 bpm, p = 0.03), and WBSR (HD: 15.1 ± 4.4 mL·min-1; WW: 10.0 ± 4.1 mL·min-1, p < 0.01) were greater in HD at min 90. Cumulative EHL (HD: 1203 ± 261 W; WW: 502 ± 126 W, p < 0.01) and DHG (HD: 221 ± 69 W; WW: -260 ± 72 W, p < 0.01) were higher in HD. VE (HD: 38.1 ± 9.8 L·min-1; WW: 37.6 ± 10.5 L·min-1, p = 0.64), its components f and TV (p = 0.12; p = 0.66, respectively), RER (HD: 0.86 ± 0.04; WW: 0.83 ± 0.04, p = 0.21) and the ventilatory equivalents for CO2 (HD: 34.6 ± 5.5 VE·VCO2-1; WW: 34.7 ± 4.3 VE·VCO2-1, p = 0.95) and O2 (HD: 29.9 ± 5.3 VE·VO2-1; WW: 28.8 ± 3.3 VE·VO2-1, p = 0.29) were not different at min 90 between trials nor when VE, VE·VCO2-1, and VE·VO2-1 were adjusted for change in Tc (p = 0.59; p = 0.26; p = 0.49, respectively). CONCLUSIONS: Different hot conditions of equal WBGT elicit similar increases in Tc, S, and ventilation, but higher cardiovascular strain was observed in HD compared to WW during walking in the heat.

Thermoregulation is not impaired in breast cancer survivors during moderate-intensity exercise performed in warm and hot environments.

This study aimed to assess how female breast cancer survivors (BCS) respond physiologically, hematologically, and perceptually to exercise under heat stress compared to females with no history of breast cancer (CON). Twenty‐one females (9 BCS and 12 CON [age; 54 ± 7 years, stature; 167 ± 6 cm, body mass; 68.1 ± 7.62 kg, and body fat; 30.9 ± 3.8%]) completed a warm (25℃, 50% relative humidity, RH) and hot (35℃, 50%RH) trial in a repeated‐measures crossover design. Trials consisted of 30 min of rest, 30 min of walking at 4 metabolic equivalents, and a 6‐minute walk test (6MWT). Physiological measurements (core temperature (T re), skin temperature (T skin), heart rate (HR), and sweat analysis) and perceptual rating scales (ratings of perceived exertion, thermal sensation [whole body and localized], and thermal comfort) were taken at 5‐ and 10‐min intervals throughout, respectively. Venous blood samples were taken before and after to assess; IL‐6, IL‐10, CRP, IFN‐γ, and TGF‐β1. All physiological markers were higher during the 35 versus 25℃ trial; T re (~0.25℃, p = 0.002), T skin (~3.8℃, p < 0.001), HR (~12 beats·min−1, p = 0.023), and whole‐body sweat rate (~0.4 L·hr−1, p < 0.001), with no difference observed between groups in either condition (p > 0.05). Both groups covered a greater 6MWT distance in 25 versus 35℃ (by ~200 m; p = 0.003). Nevertheless, the control group covered more distance than BCS, regardless of environmental temperature (by ~400 m, p = 0.03). Thermoregulation was not disadvantaged in BCS compared to controls during moderate‐intensity exercise under heat stress. However, self‐paced exercise performance was reduced for BCS regardless of environmental temperature.

Individual characteristics associated with the magnitude of heat acclimation adaptations

PurposeThe magnitude of heat acclimation (HA) adaptations varies largely among individuals, but it remains unclear what factors influence this variability. This study compared individual characteristics related to fitness status and body dimensions of low-, medium-, and high responders to HA.MethodsTwenty-four participants (9 female, 15 male; maximum oxygen uptake [dot{{V}}O2peak,kg] 52 ± 9 mL kg−1 min−1) completed 10 daily controlled-hyperthermia HA sessions. Adaptations were evaluated by heat stress tests (HST; 35 min cycling 1.5 W kg−1; 33 °C, 65% relative humidity) pre- and post-HA. Low-, medium-, and high responder groups were determined based on tertiles (n = 8) of individual adaptations for resting rectal temperature (Tre), exercise-induced Tre rise (ΔTre), whole-body sweat rate (WBSR), and heart rate (HR).ResultsBody dimensions (p > 0.3) and dot{{V}}O2peak,kg (p > 0.052) did not differentiate low-, medium-, and high responders for resting Tre or ΔTre. High WBSR responders had a larger body mass and lower body surface area-to-mass ratio than low responders (83.0 ± 9.3 vs 67.5 ± 7.3 kg; 249 ± 12 vs 274 ± 15 cm2 kg−1, respectively; p < 0.005). Conversely, high HR responders had a smaller body mass than low responders (69.2 ± 6.8 vs 83.4 ± 9.4 kg; p = 0.02). dot{{V}}O2peak,kg did not differ among levels of responsiveness for WBSR and HR (p > 0.3).ConclusionIndividual body dimensions influenced the magnitude of sudomotor and cardiovascular adaptive responses, but did not differentiate Tre adaptations to HA. The influence of dot{{V}}O2peak,kg on the magnitude of adaptations was limited.

Independent Influence of Skin Temperature on Whole-Body Sweat Rate.

It is often assumed that a person with a higher mean skin temperature (Tsk) will sweat more during exercise. However, it has not yet been demonstrated whether Tsk describes any individual variability in whole-body sweat rate (WBSR) independently of the evaporative requirement for heat balance (Ereq). One hundred forty bouts of 2-h treadmill walking completed by a pool of 21 participants (23 ± 4 yr, 174 ± 8 cm, 76 ± 11 kg, 1.9 ± 0.2 m) under up to nine conditions were analyzed. Trials employed varying rates of metabolic heat production (Hprod; 197-813 W), and environmental conditions (15°C, 20°C, 25°C, 30°C; all 50% relative humidity), yielding a wide range of Ereq (86-684 W) and Tsk values (26.9°C-34.4°C). The individual variation observed in WBSR was best described using Ereq (in watts; R = 0.784) as a sole descriptor, relative to Ereq (in watts per meter squared; R = 0.735), Hprod (in watts; R = 0.639), Hprod (in watts per meter squared; R = 0.584), ambient air temperature (Ta) (R = 0.263), and Tsk (R = 0.077; all, P < 0.001). A multiple stepwise linear regression included only Ereq (in watts; adjusted R = 0.784), with Tsk not significantly correlating with the residual variance (P = 0.285), independently of Ereq (in watts). Hprod (in watts) had similar predictive strength to Ereq (in watts) at a fixed air temperature, explaining only 5.2% at 30°C, 4.9% at 25°C, 2.7% at 20°C, and 0.5% at 15°C (all, P < 0.001) less variance in WBSR compared with Ereq. However, when data from all ambient temperatures were pooled, Hprod alone was a markedly worse predictor of WBSR than Ereq (R = 0.639 vs 0.784; P < 0.001). Ereq (in watts) explained approximately four-fifths of the individual variation in WBSR over a range of ambient temperatures and exercise intensities, whereas Tsk did not explain any residual variance independently of Ereq.

Effectiveness of skin-heating using a water-perfused suit as passive and post-exercise heat acclimation strategies.

The purpose of the present study was to evaluate the effectiveness of passive and post-exercise heat acclimation strategies through directly heating the skin with a water-perfused suit. Nineteen young males participated in the heat acclimation (HA) protocols for 10 days, which were conducted at an air temperature of 33oC with 60%RH. The exercise-only condition (N=6) conducted 1-h treadmill walking (6km·h-1) followed by 1-h rest. The post-exercise passive-heating condition (N=6) wore the suit (inflow water temperature 44.2oC) for 1-h after 1-h walking. The passive-heating condition (N=7) donned the suit for 2h. Heat tolerance tests (leg immersion in 42oC water for 60min) were conducted before and after the training to evaluate changes due to the 10-day intervention. Reflecting that suit-wearing for 10 days as both passive and post-exercise HA strategies can effectively induce adaptive changes, significant interaction effects appeared in: increase or decrease in mean skin temperature (P<0.05) and elevation in whole-body sweat rate (P<0.05). Reduction in rectal temperature (P<0.05) and blood pressure (P<0.05) were found most prominently in the passive-heating condition. These results indicate that this new method of heat acclimation training, donning a skin-heating water-perfused suit, can generate thermoregulatory benefits. The passive HA intervention could be applied to individuals for whom doing exercise regularly are not feasible.

Aluminium salt-based antiperspirant coated prosthesis liners do not suppress local sweating during moderate intensity exercise in hot and temperate conditions

ObjectiveTo determine whether coating prosthesis liners with a 5% aluminium zirconium tetrachlorohydrate antiperspirant solution (AZCH) reduces local sweating on the thigh. DesignDouble-blinded counter-balanced crossover design MethodsFourteen able-bodied participants (age: 28±5 y; body mass: 73.9±7.9kg, height: 1.73±0.09m; peak oxygen consumption [VO2peak]: 50.7±9.1 mlO2⋅kg−1⋅min−1) simultaneously wore a prosthesis liner on each leg, one treated with AZCH and one untreated, for four days prior to running at 50% of VO2peak for 60min in a temperate (23.7±0.7°C and 42.2±2.6% relative humidity) or hot (34.0±1.6°C and 40.8±6.1% relative humidity) environment. Rectal temperature (Tre) and whole-body sweat rates (WBSR) were measured to characterize thermal strain. Local sweat rate (LSR) was measured bilaterally underneath the liners, continuously, and heat-activated-sweat gland density (HASGD) was measured bilaterally every 15min. ResultsIn temperate condition, the mean change in Tre was 1.2±0.4°C and WBSR was 723±129g⋅h−1, whereas in the hot condition, change in Tre was 1.2±0.5°C and WBSR was 911±231g⋅h−1. In the temperate condition, AZCH treatment did not alter LSR (treated: 0.50±0.17 mg·cm–2min–1, untreated: 0.50±0.17 mg·cm–2min–1; P=0.87) or HASGD (treated: 54±14 glands·cm–2, untreated 55±14 glands·cm–2; P=0.38). In the hot condition, AZCH treatment paradoxically increased LSR (treated: 0.88±0.38 mg·cm–2min–1, untreated: 0.74±0.28 mg·cm–2min–1; P=0.04) but not HASGD (treated: 52±17 glands·cm–2, untreated: 48±19 glands·cm–2; P=0.77). ConclusionThese results indicate coating prosthesis liners with 5% AZCH is ineffective at reducing local sweating.

Steady-state sweating during exercise is determined by the evaporative requirement for heat balance independently of absolute core and skin temperatures.

When exercise was prescribed to elicit a fixed evaporative heat balance requirement (Ereq ), 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 (Hprod ), but a different Ereq (due to differences in air temperature), yielded higher steady-state sweat rates with a higher Ereq , 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 Ereq . Collectively, these data indicate that during exercise in a compensable environment, steady-state sudomotor responses are influenced by Ereq rather than absolute core and skin temperatures, or Hprod . The present study sought to determine whether absolute core temperature (modified via diurnal variation) and absolute skin temperature (modified by different air temperatures (Ta )) alters the steady-state sweating response to exercise at a fixed evaporative heat balance requirement (Ereq ). Ten males exercised for 60min on six occasions. Three Ta /heat production (Hprod ) combinations (23°C/525W, 33°C/400W, 33˚C/525W) were completed in the morning (08.00h, AM) and afternoon (16.00h, PM), to yield: (1) the same Ereq (200 or 275W·m-2 ) with different absolute core temperatures (AM vs. PM); (2) the same Ereq (200W·m-2 ) with different skin temperatures (Ta : 23˚C vs. 33˚C); (3) the same heat production (525W) with different Ereq (200 vs. 275W·m-2 ). Oesophageal temperature (Toes ), local sweat rate (LSR) on the arm and upper-back, and whole-body sweat rate (WBSR) were measured. Steady-state Toes was always higher in PM versus AM at an Ereq of 200W·m-2 (23°C, P=0.001; 33°C, P=0.004) and 275W·m-2 , (33°C, P=0.001). However steady-state mean LSR (200W·m-2 /23°C: P=0.25; 200W·m-2 /33°C: P=0.86; 275W·m-2 /33°C: P=0.53) and WBSR (200W·m-2 /23°C: P=0.79; 200W·m-2 /33°C: P=0.48; 275W·m-2 /33°C: P=0.32) were similar. When Ereq was matched (200W·m-2 ) with different Ta (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 Hprod (525 W) but different Ereq (200 vs. 275W·m-2 ), mean LSR (P<0.001), and WBSR (P<0.001) were higher with a greater Ereq . Collectively, steady-state sweating during exercise is altered by Ereq but not Toes , skin temperature, or Hprod .

Adaptive changes in physiological and perceptual responses during 10-day heat acclimation training using a water-perfused suit

BackgroundWhile active heat acclimation strategies have been robustly explored, not many studies highlighted passive heat acclimation strategies. Particularly, little evidence demonstrated advantages of utilizing a water-perfused suit as a passive heating strategy. This study aimed to explore heat adaptive changes in physiological and perceptual responses during 10-day heat acclimation training using a water-perfused suit.MethodsNineteen young males were divided into three experimental groups: exercise condition (N = 6, HAEXE, 1-h exercise at 6 km h−1 followed by 1-h rest in a sitting position), exercise and passive heating condition (N = 6, HAEXE+SUIT, 1-h exercise at 6 km h−1 followed 1-h passive heating in a sitting position), and passive heating condition (N = 7, HASUIT, 2-h passive heating in a sitting position). All heating programs were conducted for 10 consecutive days in a climatic chamber maintained at 33 °C with 60% relative humidity. The passive heating was conducted using a newly developed water-perfused suit with 44 °C water.ResultsGreater whole-body sweat rate and alleviated perceptual strain were found in HASUIT and HAEXE+SUIT after 5 and/or 10 days (P < 0.05) but not in the exercise-only condition (HAEXE). Lower rectal temperature and heart rate were found in all conditions after the training (P < 0.05). Heat adaptive changes appeared earlier in HASUIT except for sweat responses.ConclusionsFor heat acclimation in hot humid environments, passive and post-exercise heat acclimation training using the suit (water inflow temperature 44 °C) were more effective than the mild exercise (1-h walking at 6 km h−1). This form of passive heating (HASUIT) may be an especially effective strategy for the elderly and the disabled who are not able to exercise in hot environments.

No thermoregulatory or ergogenic effect of dietary nitrate among physically inactive males, exercising above gas exchange threshold in hot and dry conditions

The aim of this study was to determine the effect of five days dietary nitrate (NO3 −) consumption on exercise tolerance and thermoregulation during cycling in hot, dry conditions. In a double-blind, randomised crossover design, 11 healthy males participated in an exercise tolerance test (Tlim) in the heat (35°C, 28% relative humidity), cycling above the thermoneutral gas exchange threshold, after five days of dietary supplementation, with either NO3 –rich beetroot juice (BR; ∼ 9.2 mmol NO3 −) or placebo (PLA). Changes in plasma [NO3 −] and nitrite [NO2 −], core and mean skin temperatures, mean local and whole-body sweat rates, heart rate, perceptual ratings and pulmonary gas exchange were measured during exercise, alongside calorimetric estimations of thermal balance. Mean arterial pressures (MAP) were recorded pre-Tlim. There were no differences in Tlim between conditions (BR = 22.8 ± 8.1 min; Placebo = 20.7 ± 7.9 min) (P = 0.184), despite increases in plasma [NO3 −] and [NO2 −] (P < 0.001) and a 3.8% reduction in resting MAP (P = 0.004) in the BR condition. There were no other differences in thermoregulatory, cardio-metabolic, perceptual or calorimetric responses to the Tlim between conditions (P > 0.05). Dietary NO3 − supplementation had no effect on exercise tolerance or thermoregulation in hot, dry conditions, despite reductions in resting MAP and increases in plasma [NO3 −] and [NO2 −]. Healthy, yet physically inactive individuals with no known impairments in vasodilatory and sudomotor function do not appear to require BR for ergogenic or thermolytic effects during exercise in the heat.

Core Temperature and Sweating in Men and Women During a 15-km Race in Cool Conditions.

Studies often assess the impact of sex on the relation between core body temperature (CBT), whole-body sweat rate (WBSR), and heat production during exercise in laboratory settings, but less is known in free-living conditions. Therefore, the authors compared the relation between CBT, WBSR, and heat production between sexes in a 15-km race under cool conditions. During 3 editions of the Seven Hills Run (Nijmegen, the Netherlands) with similar ambient conditions (8-12°C, 80-95% relative humidity), CBT and WBSR were measured among 375 participants (52% male) before and immediately after the 15-km race. Heat production was estimated using initial body mass and mean running speed, assuming negligible external work. Men finished the race in 76 (12) minutes and women in 83 (13) minutes (P < .001, effect size [ES] = 0.55). Absolute heat production was higher in men than in women (1185 [163]W vs 867 [122]W, respectively, P < .001, ES = 1.47), even after normalizing to body mass (15.0 [2.2]W/kg vs 13.8 [1.9]W/kg, P < .001, ES = 0.56). Finish CBT did not differ between men and women (39.2°C [0.7°C] vs 39.2°C [0.7°C], P = .71, ES = 0.04). Men demonstrated a greater increase in CBT (1.5°C [0.8°C] vs 1.3°C [0.7°C], respectively, P = .013, ES = 0.31); the sex difference remains after correcting for heat production (P = .004). WBSR was larger in men (18.0 [6.9]g/min) than in women (11.4 [4.7]g/min; P < .001, ES = 0.97). A weak correlation between WBSR and heat production was found irrespective of sex (R2 = .395, P < .001). WBSR was associated with heat production, irrespective of sex, during a self-paced 15-km running race in cool environmental conditions. Men had a higher ΔCBT than women.

Improved neural control of body temperature following heat acclimation in humans.

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 7day 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. 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 14healthy adults (nine men and five women, aged 27±5 years) during passive heat stress performed before and after a 7day heat acclimation protocol. Heat acclimation increased whole-body sweat rate [+0.54Lh-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.

Thermoregulatory adaptations with progressive heat acclimation are predominantly evident in uncompensable, but not compensable, conditions.

This study assessed whether, notwithstanding lower resting absolute core temperatures, alterations in time-dependent changes in thermoregulatory responses following partial and complete heat acclimation (HA) are only evident during uncompensable heat stress. Eight untrained individuals underwent 8 wk of aerobic training (i.e., partial HA) followed by 6 days of HA in 38°C/65% relative humidity (RH) (i.e., complete HA). On separate days, esophageal temperature (Tes), arm (LSRarm), and back (LSRback) sweat rate, and whole body sweat rate (WBSR) were measured during a 45-min compensable (37°C/30% RH) and 60-min uncompensable (37°C/60% RH) heat stress trial pre-training (PRE-TRN), post-training (POST-TRN), and post-heat acclimation (POST-HA). For compensable heat stress trials, resting Tes was lower POST-TRN (36.74 ± 0.27°C, P = 0.05) and POST-HA (36.60 ± 0.27°C, P = 0.001) compared with PRE-TRN (36.99 ± 0.19°C); however, ΔTes was similar in all trials (PRE-TRN:0.40 ± 0.23°C; POST-TRN:0.42 ± 0.20°C; POST-HA:0.43 ± 0.12°C, P = 0.97). While LSRback was unaltered by HA (P = 0.94), end-exercise LSRarm was higher POST-TRN (0.70 ± 0.14 mg·cm-2·min-1, P < 0.001) and POST-HA (0.75 ± 0.16 mg·cm-2·min-1, P < 0.001) compared with PRE-TRN (0.61 ± 0.15 mg·cm-2·min-1). Despite matched evaporative heat balance requirements, steady-state WBSR (31st-45th min) was greater POST-TRN (12.7 ± 1.0 g/min, P = 0.02) and POST-HA (12.9 ± 0.8 g/min, P = 0.004), compared with PRE-TRN (11.7 ± 0.9 g/min). For uncompensable heat stress trials, resting Tes was lower POST-TRN (36.77 ± 0.22°C, P = 0.05) and POST-HA (36.62 ± 0.15°C, P = 0.03) compared with PRE-TRN (36.86 ± 0.24°C). But ΔTes was smaller POST-TRN (0.77 ± 0.19°C, P = 0.05) and POST-HA (0.75 ± 0.15°C, P = 0.04) compared with PRE-TRN (1.10 ± 0.32°C). LSRback and LSRarm increased with HA (P < 0.007), supporting the greater WBSR with HA (POST-TRN:14.4 ± 2.4 g/min, P < 0.001; POST-HA:16.8 ± 2.8 g/min, P < 0.001) compared with PRE-TRN (12.7 ± 3.2 g/min). In conclusion, the thermal benefits of HA are primarily evident when conditions challenge the physiological capacity to dissipate heat.NEW & NOTEWORTHY We demonstrate that neither partial nor complete heat acclimation alters the change in core temperature during compensable heat stress compared with an unacclimated state, despite a marginally greater whole body sweat rate. However, the greater local and whole body sweat rate with partial and complete heat acclimation reduced the rise in core temperature during 60 min of uncompensable heat stress compared with an unacclimated state, suggesting the improvements in heat dissipation associated with heat acclimation are best observed when the upper physiological limits for evaporative heat loss are challenged.

Intermittent sprint performance in the heat is not altered by augmenting thermal perception via L-menthol or capsaicin mouth rinses

PurposeCooling sensations elicited by mouth rinsing with L-menthol have been reported as ergogenic. Presently, responses to L-menthol mouth rinsing during intermittent sprint performance (ISP) in the heat are unknown and the impact of increased thermal perception on ISP via capsaicin has also not been quantified. This experiment aimed to identify whether eliciting cooling/warming sensations via L-menthol/capsaicin would alter ISP in the heat.MethodFourteen participants (mass = 72 ± 9 kg, dot {V}{{text{O}}_{2{text{peak}}}} = 3.30 ± 0.90 L min−1), undertook four experimental trials, involving 40 min of ISP in hot conditions (40.2 ± 0.6 °C, 42 ± 2% R.H.) with mouth rinsing (25 mL, 6 s) at the protocol onset, and every 10 min thereafter. Cooling (0.01% L-menthol; MEN), warming (0.2% capsaicin; CAP), placebo (0.3 sham-CHO; PLA), and control (water; CON) mouth rinses were utilized. Performance was quantified via power (PP) and work done (WD) during sprints. Heart rate (HR), core (Trec) and skin (Tskin) temperature, perceived exertion (RPE), thermal sensation (Tsens), and comfort (Tcom) were measured at 10 min intervals. Sweat rate (whole-body sweat rate) was calculated from ∆mass.ResultPP reduced over time (P < 0.05); however, no change was observed between trials for PP or WD (P > 0.05). Tcom increased over time and was lower in MEN (2.7 ± 1.1; P < 0.05) with no difference between CAP (3.1 ± 1.2), PLA (3.2 ± 1.3) and CON (3.1 ± 1.3). RPE, Tsens HR, Trec, and Tskin increased over time (P < 0.05) with no between trial differences (P > 0.05).ConclusionDespite improved thermal comfort via L-menthol, ISP did not improve. Capsaicin did not alter thermal perception or ISP. The reduction in ISP over time in hot conditions is not influenced by thermal perception.

Heart Failure Modulates Thermoregulatory Control Independently Of Differences In Physical Characteristics And Metabolic Heat Production

PURPOSE: Heart failure (HF) patients appear to exhibit altered thermoregulatory responses during exercise in the heat. However, the extent to which these responses are altered due to physiological impairments independently of biophysical factors associated with differences in metabolic heat production (Hprod), evaporative heat balance requirements (Ereq) and/or body size, is presently unclear. Therefore, we examined thermoregulatory responses in 10 HF and 10 age-matched controls (CON) similar in body size during exercise at a fixed rate of Hprod, and thus Ereq, in a 30°C environment. METHODS: Rectal temperature (Trec), local sweat rate (LSR), and cutaneous vascular conductance (CVC) were measured during 60-min of cycle ergometry. Whole-body sweat rate (WBSR) was estimated from pre-post nude body weight corrected for fluid intake. Hprod and Ereq, as well as dry heat loss (Hdry) and evaporative heat loss from the skin (Esk) ─ assuming all secreted sweat evaporated, were calculated using partitional calorimetry. RESULTS: Despite exercising at the same rate of Hprod (HF: 338±43; CON: 323±31W, p=0.25), Trec was greater (p<0.01) in HF (0.81±0.16°C) than CON (0.49±0.27°C). In keeping with a similar Ereq (HF: 285±40; CON: 274±28W, p=0.35), no differences in WBSR (HF: 0.45±0.11; CON: 0.41±0.07L/h, p=0.38) or LSR (HF: 0.96±0.17; CON: 0.79±0.15mg/cm2/min, p=0.50) were observed between groups. Similarly, Hdry was comparable between groups (HF: 22.9±3.2; CON: 20.4±5.0W, p=0.14). Consequently, the cumulative body heat storage was similar between groups (HF: 154±106; CON: 196±174kJ, p=0.44). Furthermore, CVC was lower in HF than CON (HF: 0.83±0.42; CON: 2.10±0.79au/mmHg, p<0.01). CONCLUSIONS: Collectively, these findings demonstrate that HF patients exhibit an impaired skin blood flow response, but no differences in sweating. Given that HF had similar body heat storage to CON at the same Hprod, their greater rise in core temperature can be attributed to a less uniform internal distribution of heat between the body core and periphery.

The Sweating and Core Temperature Response to Compensable and Uncompensable Heat Stress Following Heat Acclimation

While a greater maximal sweat rate following heat acclimation has been suggested to mitigate the rise in core temperature during uncompensable heat stress, it remains unclear whether heat acclimation will alter the core temperature response to compensable heat stress wherein heat balance is attainable. Thus, the primary aim of the present study was to evaluate the influence of complete heat acclimation on sweating and core temperature response to exercise in a compensable and uncompensable environment. A total of 8 (6 males, 2 females) unacclimated individuals were recruited. On separate days, participants exercised at a fixed rate of heat production (450 W) for 45‐mins of compensable heat stress (CHS; 37°C, 30% RH) and 60‐min of uncompressible heat stress (UCHS; 37°C, 60% RH) before and after heat acclimation. Core temperature [esophageal (Tes) and rectal (Tre)], local sweat rate of the arm (LSRarm) and back (LSRback), and whole body sweat loss (WBSL) were measured during experimental trials. Heat acclimation included an 8‐wk aerobic training intervention followed by 10 consecutive days of up to 90 minutes of treadmill walking in hot and humid conditions (38°C, 65% RH). Prior to CHS or UCHS, resting absolute Tes and Tre were lower following heat acclimation (Tes: 36.6±0.2°C; Tre: 36.8±0.1°C) relative to unacclimated (Tes: 36.9±0.2°C, P=0.002; Tre: 37.1±0.2°C, P=0.003). During CHS, the change in Tes and Tre were similar following heat acclimation (ΔTes: 0.4±0.1°C; ΔTre: 0.7±0.1°C) compared to unacclimated (ΔTes: 0.4±0.2°C, P=0.72; ΔTre: 0.7±0.1°C, P=0.61). Cumulative WBSL during CHS was marginally greater with acclimation (557±40 g) relative to unacclimated (494±59 g, P=0.01). Despite no difference in LSRback following 45‐min of CHS with or without heat acclimation (P=0.94), stead‐state LSRarm was slightly higher with acclimation (0.75±0.16 mg/cm2/min) compared to unacclimated (0.61±0.15 mg/cm2/min, P&lt;0.001). In contrast, the change in Tes and Tre during UCHS was significantly smaller following heat acclimation (ΔTes: 0.7±0.2°C; ΔTre: 0.9±0.2°C) relative to an unacclimated state (ΔTes: 1.1±0.3°C, P=0.04; ΔTre: 1.1±0.2°C, P&lt;0.001). WBSL was far greater during UCHS post‐heat acclimation (913±126 g) in comparison to prior to acclimation (671±83 g, P&lt;0.001). Further, end‐exercise LSRback and LSRarm were higher post‐heat acclimation (LSRback: 1.48±0.28 mg/cm2/min; LSRarm: 1.20±0.33 mg/cm2/min) relative to pre‐acclimation (LSRback: 1.21±0.26, P&lt;0.001; LSRarm: 0.91±0.26 mg/cm2/min, P&lt;0.001) during UCHS. Taken together, the core temperature response to compensable heat stress is similar irrespective of acclimation status, despite marginal greater whole‐body sweat rates. However, the large increases local and whole body sweat rate following heat acclimation clearly mitigated the rise in core temperature during uncompensable heat stress.Support or Funding InformationThis research was supported by a Discovery Grant from the Natural Sciences and Engineering Research Council (NSERC) of Canada (#386143‐2010, held by O.J.). N.R. was supported by an NSERC Postgraduate Scholarship‐Doctoral and a University of Ottawa Excellence Scholarship.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Thermoeffector Responses at a Fixed Rate of Heat Production in Heart Failure Patients.

Heart failure (HF) patients seem to exhibit altered thermoregulatory responses during exercise in the heat. However, the extent to which these responses are altered due to physiological impairments independently of biophysical factors associated with differences in metabolic heat production (Hprod), evaporative heat balance requirements (Ereq), and/or body size is presently unclear. Therefore, we examined thermoregulatory responses in 10 HF patients and 10 age-matched controls (CON) similar in body size during exercise at a fixed rate of Hprod and therefore Ereq in a 30°C environment. Rectal temperature, local sweat rate, and cutaneous vascular conductance were measured throughout 60 min of cycle ergometry. Whole-body sweat rate was estimated from pre-post nude body weight corrected for fluid intake. Despite exercising at the same rate of Hprod (HF, 338 ± 43 W; CON, 323 ± 31 W; P = 0.25), the rise in rectal temperature was greater (P < 0.01) in HF (0.81°C ± 0.16°C) than in CON (0.49°C ± 0.27°C). In keeping with a similar Ereq (HF, 285 ± 40 W; CON, 274 ± 28 W; P = 0.35), no differences in whole-body sweat rate (HF, 0.45 ± 0.11 L·h; CON, 0.41 ± 0.07 L·h; P = 0.38) or local sweat rate (HF, 0.96 ± 0.17 mg·cm·min; CON, 0.79 ± 0.15 mg·cm·min; P = 0.50) were observed between groups. However, the rise in cutaneous vascular conductance was lower in HF than in CON (HF, 0.83 ± 0.42 au·mm Hg; CON, 2.10 ± 0.79 au·mm Hg; P < 0.01). In addition, the cumulative body heat storage estimated from partitional calorimetry was similar between groups (HF, 154 ± 106 kJ; CON, 196 ± 174 kJ; P = 0.44). Collectively, these findings demonstrate that HF patients exhibit a blunted skin blood flow response, but no differences in sweating. Given that HF patients had similar body heat storage to that of CON at the same Hprod, their greater rise in core temperature can be attributed to a less uniform internal distribution of heat between the body core and periphery.

The Influence Of Aerobic Training On Maximum Skin Wettedness And Its Effects During Uncompensable Heat Stress

PURPOSE: The purpose of the present experiment was to quantify how maximum skin wettedness (ωmax) is altered by aerobic training, and compare it to what is achieved following heat acclimation (HA). METHODS: Eight sedentary individuals (6 males, 2 females) participated in an 8-week aerobic training regime followed by a 9-day heat acclimation (HA) protocol. Participants completed on separate days, i) a treadmill humidity ramp protocol trial to assess ωmax; and ii) a 60-min treadmill march (450 W of heat production) in an uncompensable environment: 38°C, 60% RH, on three separate occasions: pre-training (PRE-T), post-training (POST-T), and post-heat acclimation (POST-HA); The change in rectal (ΔTre), and mean skin temperature (Tsk) were recorded. Whole body sweat loss (WBSL) was calculated as the change in nude body mass and sweating efficiency (Seff) was derived by dividing the sweating required to achieve ωmax (with 100% evaporation) by the actual whole-body sweat rate between the 30th and 60th minute of exercise. RESULTS: Aerobic training increased aerobic capacity by ∼14% (PRE-T: 45.8±11.8 ml/kg/min; POST-T: 52.0±11.1 ml/kg/min, P<0.001). In the humidity ramp trial, ωmax was lower PRE-T (0.75±0.07) compared to POST-T (0.87±0.12, P=0.01) and POST-HA (1.00±0.00, P=0.001), and POST-T was lower than POST-HA (P=0.04). In the UC trial, ΔTre was greater PRE-T (1.13±0.16°C) compared to POST-T (0.96±0.13°C, P<0.001) and POST-HA (0.96±0.20°C, P<0.001). PRE-T Tsk was higher after 60-min (38.0±0.4°C) compared to POST-T (37.2±0.9°C, P<0.001) and POST-HA (37.1±0.4°C, P<0.001). WBSL was significantly greater POST-HA (913±126 g) compared to POST-T (794±78 g; P=0.002) and PRE-T (671±83 g, P<0.001), however Seff was similar throughout (PRE-T: 67±10%; POST-T: 68±11%; POST-HA: 66±8%). CONCLUSIONS: Aerobic training and HA independently increase ωmax without altering Seff. A graded reduction in thermal strain during uncompensable heat stress is observed from PRE-T to POST-T, and to POST-HA.

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

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.