Acute ingestion of Ibuprofen does not influence the release of IL-6 or improve self-paced exercise in the heat despite altering cortical activity.

The present study tested the hypothesis that ingesting 800 mg Ibuprofen prior to self-paced cycling at a fixed rating of perceived exertion (RPE) improves performance by attenuating the release of Interleukin (IL)-6 and its signalling molecules, whilst simultaneously modulating cortical activity and cerebral oxygenation to the brain. Eight healthy, recreationally active males ingested 800 mg Ibuprofen or a placebo ~ 1 h prior to performing fixed RPE cycling for 60 min in 35 °C and 60% relative humidity at an intensity of hard to very hard (RPE = 16) with intermittent maximal (RPE = 20) sprints every 10 min. Power output (PO), core and mean skin temperatures (Tc, Tsk), respectively, and heart rate (HR) were measured continuously. Electroencephalography (EEG) recordings at the frontal (Fz), motor (Cz) and Parietal (Pz) areas (90 s) were collected every 5 min. IL-6, soluble glycoprotein receptor (sgp130) and IL-6 receptor (R) were collected at pre-, 30 min and immediately post-exercise. Mean PO, HR, Tc and Tsk, and RPE were not different between trials (P ≥ 0.33). At end-exercise, the change in IL-6, sgp130 and sIL-6R was not different between trials (P ≥ 0.12). The increase in α and ß activity did not differ in any cortices between trials (P ≥ 0.07); however, there was a significant reduction in α/ß activity in the Ibuprofen compared to placebo trials at all sites (P ≤ 0.05). Ingesting a maximal, over-the-counter dose of Ibuprofen prior to exercise in the heat does not attenuate the release of IL-6, nor improve performance, but may influence cortical activity evidenced by a greater reduction in α/ß activity.

The effect of cooling garments to improve physical function in people with multiple sclerosis: A systematic review and meta-analysis.

BACKGROUND: There is strong evidence for the benefits of exercise for people with Multiple Sclerosis (MS), however, up to 80% of people with MS report experiencing exacerbated symptoms with elevated body temperatures. A range of cooling garments to assist people with MS manage symptoms of heat sensitivity have been investigated. Therefore, the aim of this systematic review was to assess the effect of cooling garments to improve physical function in people with MS, and to determine any associated physiological and perceptual responses. METHOD: A systematic review adhering to the PRISMA guidelines was performed. The eligibility criteria required investigations to have conducted a randomized controlled trial or cross-over study to assess the effect of a cooling garment to improve physical function, or a related physiological or perceptual measure, in people with MS. RESULTS: Thirteen empirical studies were identified, compromising of acute cross-over designs (61.5%), longitudinal parallel group designs (23.1%) or a combination of both (15.4%). The studies included 384 participants with MS with an expanded disability status scale range of 1-7.5. Garments included liquid-perfused cooling vests/tops/hoods (50.0%), phase-change cooling vests (38.9%), a cooling thigh-cuff (5.6%) and a palm cooling device (5.6%). The cooling garments were effective at improving walking capacity and functional mobility, and some studies demonstrated improvements in muscular strength and balance, but not manual dexterity. The garments also resulted in improved core temperature, skin temperature, thermal sensation and subjective fatigue. Improvements occurred in temperate and warm conditions, and both with and without an exercise stimulus. DISCUSSION: Cooling garments can improve physical function for people with MS. Since none of the cooling garments caused harm, and no particular cooling garment could be identified as being superior, people with MS should experiment with different cooling garments to determine their preference, and industry should focus on cooling garments that are effective, accessible and user-friendly.

Metabolic and inflammatory health in SARS-CoV-2 and the potential role for habitual exercise in reducing disease severity.

INTRODUCTION: The rapid emergence and spread of SARS-CoV-2 in late 2019 has infected millions of people worldwide with significant morbidity and mortality with various responses from health authorities to limit the spread of the virus. Although population-wide inoculation is preferred, currently, there is large variation and disparity in the acquisition, development, and deployment of vaccination programs in many countries. Even with availability of a vaccine, achieving herd immunity does not guarantee against reinfection from SARS-CoV-2. Emerging evidence indicates that vaccines do not eliminate infection but protect against severe disease and potential hospitalisation. Therefore, additional strategies which strengthen the immune system should be strongly considered to assist in reducing the overall health care burden and stem the rate of infection. There is now substantial evidence that SARS-CoV-2 disease severity and death are linked to existing comorbidities such as cardiovascular disease, obesity, and metabolic disorders. PURPOSE: In this review, we discuss the potential medium-to-long-term strategy of habitual exercise and its relationship to targeted comorbidities and underlying inflammation as a protective mechanism against SARS-CoV-2 disease severity. CONCLUSION: We conclude that engagement in habitual physical activity and exercise could be a strategy to mitigate the development of comorbidities and improve the response of the immune system, potentially reducing the risk of symptoms and life-threatening complications if infected.

Heat Safety in the Workplace: Modified Delphi Consensus to Establish Strategies and Resources to Protect the US Workers.

The purpose of this consensus document was to develop feasible, evidence-based occupational heat safety recommendations to protect the US workers that experience heat stress. Heat safety recommendations were created to protect worker health and to avoid productivity losses associated with occupational heat stress. Recommendations were tailored to be utilized by safety managers, industrial hygienists, and the employers who bear responsibility for implementing heat safety plans. An interdisciplinary roundtable comprised of 51 experts was assembled to create a narrative review summarizing current data and gaps in knowledge within eight heat safety topics: (a) heat hygiene, (b) hydration, (c) heat acclimatization, (d) environmental monitoring, (e) physiological monitoring, (f) body cooling, (g) textiles and personal protective gear, and (h) emergency action plan implementation. The consensus-based recommendations for each topic were created using the Delphi method and evaluated based on scientific evidence, feasibility, and clarity. The current document presents 40 occupational heat safety recommendations across all eight topics. Establishing these recommendations will help organizations and employers create effective heat safety plans for their workplaces, address factors that limit the implementation of heat safety best-practices and protect worker health and productivity.

Voluntary Cooling during Exercise Is Augmented in People with Multiple Sclerosis Who Experience Heat Sensitivity.

INTRODUCTION: We tested the hypothesis that people with multiple sclerosis (MS) who experience heat sensitivity voluntarily engage in cool-seeking behavior during exercise to a greater extent than healthy controls. METHODS: In a 27.0°C ± 0.2°C, 41% ± 2% RH environment, seven participants with relapsing-remitting MS who exhibited heat sensitivity and seven healthy controls completed two randomized trials cycling for 40 min (EX) at 3.5 W·kg-1 metabolic heat production, followed by 30 min recovery (REC). In one trial, participants were restricted from engaging in cooling (CON). In the other trial, participants voluntarily pressed a button to receive 2 min of ~2°C water perfusing a top (COOL). Mean skin and core temperatures and mean skin wettedness were recorded continuously. Total time in cooling provided an index of cool-seeking behavior. RPE, total symptom scores (MS only), and subjective fatigue (MS only) were recorded every 10 min. RESULTS: Core temperature (+0.5°C ± 0.1°C) and skin wettedness (+0.53 ± 0.02 a.u.) increased but were not different between groups or trials at end exercise (P = 0.196) or end recovery (P = 0.342). Mean skin temperature was reduced in COOL compared with CON at end exercise (P ≤ 0.002), with no differences between groups (P ≥ 0.532). MS spent more total time in cooling during EX (MS, 13 ± 3 min; healthy, 7 ± 4 min; P < 0.001) but not REC (MS, 2 ± 1 min; healthy, 0 ± 1 min; P = 0.496). RPE was greater at end exercise in MS (P = 0.001). Total symptom scores increased during exercise (P = 0.005) but was not different between trials (P = 0.321), whereas subjective fatigue was not attenuated in the cooling trial (P = 0.065). CONCLUSION: Voluntary cooling is augmented in MS but does not consistently mitigate perceptions of heat-related symptoms or subjective fatigue.

The requirement for physical effort reduces voluntary cooling behavior during heat exposure in humans.

We tested the hypothesis that cool-seeking behavior during heat exposure is attenuated when physical effort is required. Twelve healthy adults (mean(SD), 24(4) years, four women) underwent three experimental trials during two hours of exposure to 41(1) °C, 20(0)% relative humidity in which subjects undertook intermittent exercise alternating between seated rest and cycling exercise at ~4 metabolic equivalents every 15 min. In all trials, subjects wore a water perfused suit top. In the control trial (Control), no water perfused the suit. In the other trials, subjects were freely able to perfuse 2.1(0.2) °C water through the suit. In one cooling trial, subjects received two minutes of cooling by pressing a button (Button). The other cooling trial permitted cooling by engaging in isometric handgrip exercise at 15% of maximal grip strength (Handgrip), with cooling maintained throughout the duration the required force was produced or until two minutes elapsed. In both Button and Handgrip, a one-minute washout proceeded cooling. Core temperature increased over time in all trials (P<0.01) and there were no differences between trials (P = 0.32). Mean skin temperature at the end of heat exposure was lowest in Button [34.2(1.5) °C] compared to Handgrip [35.6(0.8) °C, P = 0.03] and Control [36.9(0.7) °C, P<0.01]. The total number of behaviors [8(3) vs. 10(5), P = 0.04] and cumulative cooling time [850(323) vs. 1230(616) seconds, P = 0.02] were lower in Handgrip compared to Button. These data indicate that when physical effort is required, the incidence and duration of cooling behavior during heat exposure is attenuated compared to when behaving requires minimal physical effort.

Increased skin wetness independently augments cool-seeking behaviour during passive heat stress.

KEY POINTS: Skin wetness occurring secondary to the build-up of sweat on the skin provokes thermal discomfort, the precursor to engaging in cool-seeking behaviour. Associative evidence indicates that skin wetness stimulates cool-seeking behaviour to a greater extent than increases in core and mean skin temperatures. The independent contribution of skin wetness to cool-seeking behaviour during heat stress has never been established. We demonstrate that skin wetness augments cool-seeking behaviour during passive heat stress independently of differential increases in skin temperature and core temperature. We also identify that perceptions of skin wetness were not elevated despite increases in actual skin wetness. These data support the proposition that afferent signalling from skin wetness enhances the desire to engage in cool-seeking behaviour during passive heat stress. ABSTRACT: This study tested the hypothesis that elevations in skin wetness augments cool-seeking behaviour during passive heat stress. Twelve subjects (6 females, age: 24 ± 2 y) donned a water-perfused suit circulating 34 °C water and completed two trials resting supine in a 28.5 ± 0.4 °C environment. The trials involved a 20 min baseline period (26 ± 3% relative humidity (RH)), 60 min while ambient humidity was maintained at 26±3% RH (LOW) or increased to 67 ± 5% RH (HIGH), followed by 60 min passive heat stress (HS) where the water temperature in the suit was incrementally increased to 50 °C. Subjects were able to seek cooling when their neck was thermally uncomfortable by pressing a button. Each button press initiated 30 s of -20 °C fluid perfusing through a custom-made device secured against the skin on the dorsal neck. Mean skin (Tskin ) and core (Tcore ) temperatures, mean skin wetness (Wskin ) and neck device temperature (Tdevice ) were measured continuously. Cool-seeking behaviour was determined from total time receiving cooling (TTcool ) and cumulative button presses. Tskin and Tcore increased during HS (P < 0.01) but were not different between conditions (P ≥ 0.11). Wskin was elevated in HIGH vs. LOW during HS (60 min: by + 0.06 ± 0.07 a.u., P ≤ 0.04). Tdevice was lower in HIGH vs. LOW at 40-50 min of HS (P ≤ 0.01). TTcool was greater for HIGH (330 ± 172 s) vs. LOW (225 ± 167 s, P < 0.01), while the number of cumulative button presses was greater from 40-60 min in HS for HIGH vs. LOW (P ≤ 0.04). Increased skin wetness amplifies the engagement in cool-seeking behaviour during passive heat stress.

High-fructose corn syrup-sweetened soft drink consumption increases vascular resistance in the kidneys at rest and during sympathetic activation.

We first tested the hypothesis that consuming a high-fructose corn syrup (HFCS)-sweetened soft drink augments kidney vasoconstriction to sympathetic stimulation compared with water (study 1). In a second study, we examined the mechanisms underlying these observations (study 2). In study 1, 13 healthy adults completed a cold pressor test, a sympathoexcitatory maneuver, before (preconsumption) and 30 min after drinking 500 mL of decarbonated HFCS-sweetened soft drink or water (postconsumption). In study 2, venous blood samples were obtained in 12 healthy adults before and 30 min after consumption of 500 mL water or soft drinks matched for caffeine content and taste, which were either artificially sweetened (Diet trial), sucrose-sweetened (Sucrose trial), or sweetened with HFCS (HFCS trial). In both study 1 and study 2, vascular resistance was calculated as mean arterial pressure divided by blood velocity, which was measured via Doppler ultrasound in renal and segmental arteries. In study 1, HFCS consumption increased vascular resistance in the segmental artery at rest (by 0.5 ± 0.6 mmHg·cm-1·s-1, P = 0.01) and during the cold pressor test (average change: 0.5 ± 1.0 mmHg·cm-1·s-1, main effect: P = 0.05). In study 2, segmental artery vascular resistance increased in the HFCS trial (by 0.8 ± 0.7 mmHg·cm-1·s-1, P = 0.02) but not in the other trials. Increases in serum uric acid were greater in the HFCS trial (0.3 ± 0.4 mg/dL, P ≤ 0.04) compared with the Water and Diet trials, and serum copeptin increased in the HFCS trial (by 0.8 ± 1.0 pmol/L, P = 0.06). These findings indicate that HFCS acutely increases vascular resistance in the kidneys, independent of caffeine content and beverage osmolality, which likely occurs via simultaneous elevations in circulating uric acid and vasopressin.

Both hyperthermia and dehydration during physical work in the heat contribute to the risk of acute kidney injury.

Occupational heat stress increases the risk of acute kidney injury (AKI) and kidney disease. This study tested the hypothesis that attenuating the magnitude of hyperthermia (i.e., increase in core temperature) and/or dehydration during prolonged physical work in the heat attenuates increases in AKI biomarkers. Thirteen healthy adults (3 women, 23 ± 2 yr) exercised for 2 h in a 39.7 ± 0.6°C, 32 ± 3% relative-humidity environmental chamber. In four trials, subjects received water to remain euhydrated (Water), continuous upper-body cooling (Cooling), a combination of both (Water + Cooling), or no intervention (Control). The magnitude of hyperthermia (increased core temperature of 1.9 ± 0.3°C; P < 0.01) and dehydration (percent loss of body mass of -2.4 ± 0.5%; P < 0.01) were greatest in the Control group. There were greater increases in the urinary biomarkers of AKI in the Control trial: albumin (increase of 13 ± 11 µg/mL; P ≤ 0.05 compared with other trials), neutrophil gelatinase-associated lipocalin (NGAL) (increase of 16 ± 14 ng/dL, P ≤ 0.05 compared with Cooling and Water + Cooling groups), and insulin-like growth factor-binding protein 7 (IGFBP7) (increase of 227 ± 190 ng/mL; P ≤ 0.05 compared with other trials). Increases in IGFBP7 in the Control trial persisted after correcting for urine production/concentration. There were no differences in the AKI biomarker tissue inhibitor of metalloproteinase 2 (TIMP-2) between trials (P ≥ 0.11). Our findings indicate that the risk of AKI is highest with greater magnitudes of hyperthermia and dehydration during physical work in the heat. Additionally, the differential findings between IGFBP7 (preferentially secreted in proximal tubules) and TIMP-2 (distal tubules) suggest the proximal tubules as the location of potential renal injury.NEW & NOTEWORTHY We demonstrate that the risk for acute kidney injury (AKI) is higher in humans with greater magnitudes of hyperthermia and dehydration during physical work in the heat and that alleviating the hyperthermia and/or limiting dehydration equally reduce the risk of AKI. The biomarker panel employed in this study suggests the proximal tubules as the location of potential renal injury.

Thermal Behavior Augments Heat Loss Following Low Intensity Exercise.

We tested the hypothesis that thermal behavior alleviates thermal discomfort and accelerates core temperature recovery following low intensity exercise. Methods: In a 27 0 C, 48 6% relative humidity environment, 12 healthy subjects (six females) completed 60 min of exercise followed by 90 min of seated recovery on two occasions. Subjects wore a suit top perfusing 34 ± 0 °C water during exercise. In the control trial, this water continually perfused throughout recovery. In the behavior trial, the upper body was maintained thermally comfortable by pressing a button to receive cool water (3 2 °C) perfusing through the top for 2 min per button press. Results: Physiological variables (core temperature, p ≥ 0.18; mean skin temperature, p = 0.99; skin wettedness, p ≥ 0.09; forearm skin blood flow, p = 0.29 and local axilla sweat rate, p = 0.99) did not differ between trials during exercise. Following exercise, mean skin temperature decreased in the behavior trial in the first 10 min (by -0.5 0.7 °C, p < 0.01) and upper body skin temperature was reduced until 70 min into recovery (by 1.8 1.4 °C, p < 0.05). Core temperature recovered to pre-exercise levels 17 31 min faster (p = 0.02) in the behavior trial. There were no differences in skin blood flow or local sweat rate between conditions during recovery (p ≥ 0.05). Whole-body thermal discomfort was reduced (by -0.4 0.5 a.u.) in the behavior trial compared to the control trial within the first 20 min of recovery (p ≤ 0.02). Thermal behavior via upper body cooling resulted in augmented cumulative heat loss within the first 30 min of recovery (Behavior: 288 92 kJ; Control: 160 44 kJ, p = 0.02). Conclusions: Engaging in thermal behavior that results in large reductions in mean skin temperature following exercise accelerates the recovery of core temperature and alleviates thermal discomfort by promoting heat loss.

Renal and segmental artery hemodynamics during whole body passive heating and cooling recovery.

High environmental temperatures are associated with increased risk of acute kidney injury, which may be related to reductions in renal blood flow. The susceptibility of the kidneys may be increased because of heat stress-induced changes in renal vascular resistance (RVR) to sympathetic activation. We tested the hypotheses that, compared with normothermia, increases in RVR during the cold pressor test (CPT, a sympathoexcitatory maneuver) are attenuated during passive heating and exacerbated after cooling recovery. Twenty-four healthy adults (22 ± 2 yr; 12 women, 12 men) completed CPTs at normothermic baseline, after passive heating to a rise in core temperature of ~1.2°C, and after cooling recovery when core temperature returned to ~0.2°C above normothermic baseline. Blood velocity was measured by Doppler ultrasound in the distal segment of the right renal artery (Renal, n = 24 during thermal stress, n = 12 during CPTs) or the middle portion of a segmental artery (Segmental, n = 12). RVR was calculated as mean arterial pressure divided by renal or segmental blood velocity. RVR increased at the end of CPT during normothermic baseline in both arteries (Renal: by 1.0 ± 1.0 mmHg·cm-1·s, Segmental: by 2.2 ± 1.2 mmHg·cm-1·s, P ≤ 0.03), and these increases were abolished with passive heating (P ≥ 0.76). At the end of cooling recovery, RVR in both arteries to the CPT was restored to that of normothermic baseline (P ≤ 0.17). These data show that increases in RVR to sympathetic activation during passive heating are attenuated and return to that of normothermic baseline after cooling recovery.NEW & NOTEWORTHY Our data indicate that increases in renal vascular resistance to the cold pressor test (i.e., sympathetic activation) are attenuated during passive heating, but at the end of cooling recovery this response returns to that of normothermic baseline. Importantly, hemodynamic responses were assessed in arteries going to (renal artery) and within (segmental artery) the kidney, which has not been previously examined in the same study during thermal and/or sympathetic stressors.

Thermal behavior alleviates thermal discomfort during steady-state exercise without affecting whole body heat loss.

We tested the hypothesis that thermal behavior resulting in reductions in mean skin temperature alleviates thermal discomfort and mitigates the rise in core temperature during light-intensity exercise. In a 27 ± 0°C, 48 ± 6% relative humidity environment, 12 healthy subjects (6 men, 6 women) completed 60 min of recumbent cycling. In both trials, subjects wore a water-perfused suit top continually perfusing 34 ± 0°C water. In the behavior trial, subjects maintained their upper body thermally comfortable by pressing a button to perfuse cool water (2.2 ± 0.5°C) through the top for 2 min per button press. Metabolic heat production (control: 404 ± 52 W, behavior: 397 ± 65 W; P = 0.44) was similar between trials. Mean skin temperature was reduced in the behavior trial (by -2.1 ± 1.8°C, P < 0.01) because of voluntary reductions in water-perfused top temperature (P < 0.01). Whole body (P = 0.02) and local sweat rates were lower in the behavior trial (P ≤ 0.05). Absolute core temperature was similar (P ≥ 0.30); however, the change in core temperature was greater in the behavior trial after 40 min of exercise (P ≤ 0.03). Partitional calorimetry did not reveal any differences in cumulative heat storage (control: 554 ± 229, behavior: 544 ± 283 kJ; P = 0.90). Thermal behavior alleviated whole body thermal discomfort during exercise (by -1.17 ± 0.40 arbitrary units, P < 0.01). Despite lower evaporative cooling in the behavior trial, similar heat loss was achieved by voluntarily employing convective cooling. Therefore, thermal behavior resulting in large reductions in skin temperature is effective at alleviating thermal discomfort during exercise without affecting whole body heat loss.NEW & NOTEWORTHY This study aimed to determine the effectiveness of thermal behavior in maintaining thermal comfort during exercise by allowing subjects to voluntarily cool their torso and upper limbs with 2°C water throughout a light-intensity exercise protocol. We show that voluntary cooling of the upper body alleviates thermal discomfort while maintaining heat balance through convective rather than evaporative means of heat loss.

Exercise intensity independently modulates thermal behavior during exercise recovery but not during exercise.

We tested the hypothesis that thermal behavior is greater during and after high- compared with moderate-intensity exercise. In a 27°C, 20% relative humidity environment, 20 participants (10 women, 10 men) cycled for 30 min at moderate [53% (SD 6) peak oxygen uptake (V̇o2peak) or high [78% (SD 6) V̇o2peak] intensity, followed by 120 min of recovery. Mean skin and core temperatures and mean skin wettedness were recorded continuously. Participants maintained thermally comfortable neck temperatures with a custom-made neck device. Neck device temperature provided an index of thermal behavior. The weighted average of mean skin and core temperatures and mean skin wettedness provided an indication of the afferent stimulus to thermally behave. Mean skin and core temperatures were greater at end-exercise in high intensity (P < 0.01). Core temperature remained elevated in high intensity until 70 min of recovery (P = 0.03). Mean skin wettedness and the afferent stimulus were greater at 10-20 min of exercise in high intensity (P ≤ 0.03) and remained elevated until 60 min of recovery (P < 0.01). Neck device temperature was lower during exercise in high versus moderate intensity (P ≤ 0.02). There was a strong relation between the afferent stimulus and neck device temperature during exercise (high: R2 = 0.82, P < 0.01; moderate: R2 = 0.95, P < 0.01) and recovery (high: R2 = 0.97, P < 0.01; moderate: R2 = 0.93, P < 0.01). During exercise, slope (P = 0.49) and y-intercept (P = 0.91) did not differ between intensities. In contrast, slope was steeper (P < 0.01) and y-intercept was higher (P < 0.01) during recovery from high-intensity exercise. Thermal behavior is greater during high-intensity exercise because of the greater stimulus to behave. The withdrawal of thermal behavior is augmented after high-intensity exercise. NEW & NOTEWORTHY This is the first study to determine the effects of exercise intensity on thermal behavior. We show that exercise intensity does not independently modulate thermal behavior during exercise but is dependent on the magnitude of afferent stimuli. In contrast, the withdrawal of thermal behavior after high-intensity exercise is augmented. This may be a consequence of an attenuated perceptual response to afferent stimuli, which may be due to processes underlying postexercise hypoalgesia.

Regulation of Body Temperature by Autonomic and Behavioral Thermoeffectors.

Thermoregulation is accomplished via autonomic and behavioral responses. Autonomic responses may influence decisions to behaviorally thermoregulate. For instance, in addition to changes in body temperature, skin wettedness and involuntary muscle contraction, which occur subsequent to sweating and shivering, likely modulate thermal behavior. This autonomic-behavioral interaction provides the rationale for our hypothesis that thermoregulatory behavior decreases the requirement for autonomic responses.

Thermal Behavior Differs between Males and Females during Exercise and Recovery.

INTRODUCTION: This study tested the hypothesis that females rely on thermal behavior to a greater extent during and after exercise, relative to males. METHODS: In a 24°C ± 1°C; (45% ± 10% RH) environment, 10 males (M) and 10 females (F) (22 ± 2 yr) cycled for 60 min (metabolic heat production: M, 117 ± 18 W·m; F, 129 ± 21 W·m), followed by 60-min recovery. Mean skin and core temperatures, skin blood flow and local sweat rates were measured continually. Subjects controlled the temperature of their dorsal neck to perceived thermal comfort using a custom-made device. Neck device temperature provided an index of thermal behavior and mean body temperature provided an index of the stimulus for thermal behavior. Data were analyzed for total area under the curve for exercise and recovery time points. To further isolate the effect of exercise on thermal behavior during recovery, data were also analyzed the minute mean body temperature returned to preexercise levels within a subject. RESULTS: There were no sex differences in metabolic heat production (P = 0.71) or body temperatures (P ≥ 0.10) during exercise. Area under the curve for neck device temperature during exercise was greater for F (-98.4°C·min ± 33.6°C·min vs -64.5°C·min ± 47.8°C·min, P = 0.04), but did not differ during recovery (F, 86.8°C·min ± 37.8°C·min; M, 65.6°C·min ± 35.9°C·min; P = 0.11). In M, mean skin (P = 0.90), core (P = 0.70) and neck device (P = 0.99) temperatures had recovered by the time that mean body temperature had returned to preexercise levels. However, in F, neck device temperature (P = 0.04) was reduced while core temperature remained elevated (P < 0.01). CONCLUSIONS: Females use thermal behavior during exercise to a greater extent than M. During recovery, thermal behavior may compensate for elevated core temperatures in F despite mean body temperatures returning to preexercise levels.

Skin wettedness is an important contributor to thermal behavior during exercise and recovery.

We tested the hypothesis that mean skin wettedness contributes to thermal behavior to a greater extent than core and mean skin temperatures. In a 27.0 ± 1.0°C environment, 16 young participants (8 females) cycled for 30 min at 281 ± 51 W·m2, followed by 120 min of seated recovery. Mean skin and core temperatures and mean skin wettedness were recorded continuously. Participants maintained a thermally comfortable neck temperature throughout the protocol using a custom-made device. Neck device temperature provided an index of thermal behavior. Linear regression was performed using individual minute data with mean skin wettedness and core and mean skin temperatures as independent variables and neck device temperature as the dependent variable. Standarized ß-coefficients were used to determine relative contributions to thermal behavior. Mean skin temperature differed from preexercise (32.6 ± 0.5°C) to 10 min into exercise (32.3 ± 0.6°C, P < 0.01). Core temperature increased from 37.1 ± 0.3°C preexercise to 37.7 ± 0.4°C by end exercise ( P < 0.01) and remained elevated through 30 min of recovery (37.2 ± 0.3°C, P < 0.01). Mean skin wettedness increased from preexercise [0.14 ± 0.03 arbitrary units (AU)] to 20 min into exercise (0.43 ± 0.09 AU, P < 0.01) and remained elevated through 80 min of recovery (0.18 ± 0.06 AU, P ≤ 0.05). Neck device temperature decreased from 26.4 ± 1.6°C preexercise to 18.5 ± 8.7°C 10 min into exercise ( P = 0.03) and remained depressed through 20 min of recovery (14.4 ± 11.2°C, P < 0.01). Mean skin wettedness (52 ± 24%) provided a greater contribution to thermal behavior compared with core (22 ± 22%, P = 0.06) and mean skin (26 ± 16%, P = 0.04) temperatures. Skin wettedness is an important contributing factor to thermal behavior during exercise and recovery.

The motivation to behaviorally thermoregulate during passive heat exposure in humans is dependent on the magnitude of increases in skin temperature.

We tested the hypothesis that the motivation to behaviorally thermoregulate in humans is dependent on the magnitude of changes in mean skin temperature. Ten healthy subjects (22 ±â€¯3 y, 5 females) underwent 60 min of seated rest in a 32±1 °C or 42±1 °C environment (20% relative humidity). Trials were completed in a counterbalanced order. The motivation to behaviorally thermoregulate was measured using an operant behavior task on a fixed ratio schedule, in which subjects received thermal reinforcement after clicking a button 100 times. The reinforcer was 30 s of cooling on the dorsal aspect of the neck. The motivation to behave was defined as the cumulative number of button clicks over time and behavioral thermoregulation was defined as the change in neck skin temperature. Mean skin temperature was higher throughout the 42 °C versus the 32 °C trial (at 60 min: 36.3±0.5 °C vs. 34.5±0.5 °C, P < .01) and core temperature became higher in this trial 40 min into heat exposure (at 60 min: 37.2±0.2 °C vs. 37.1±0.1 °C, P ≤ .04), but did not differ from pre- heat exposure (P = .81). Neck skin temperature was lower in the 42 °C compared to the 32 °C trial starting at 30 min (33.7±0.8 °C vs. 35.3±0.5°C, P < .01), which was maintained thereafter (P ≤ .04). Cumulative responding for thermal reinforcement was greater in the 42 °C trial compared to the 32 °C trial at 20 min (180±155 clicks vs. 0±0 clicks, P < .01), which persisted thereafter (P < .01). These data indicate that the motivation to behaviorally thermoregulate during passive heat exposure in humans is dependent on the magnitude of increases in skin temperature.