Sweat Rate Research Articles

Realtime Monitoring of Local Sweat Rate Kinetics during Constant-Load Exercise Using Perspiration-Meter with Airflow Compensation System.

Epidermal wearable sweat biomarker sensing technologies are likely affected by sweat rate because of the dilution effect and limited measurement methods. However, there is a dearth of reports on the local sweat rate (LSR) monitored in real-time during exercise. This explorative study investigated the feasibility of real-time LSR monitoring and clarified LSR kinetics on the forehead and upper arm during constant-load exercise using a perspiration meter with an airflow compensation system. This observational cross-sectional study included 18 recreationally trained males (mean age, 20.6 ± 0.8 years). LSR on the forehead and upper arm (mg/cm2/min) were measured during a constant-load exercise test at 25% of their pre-evaluated peak power until exhaustion. The LSR kinetics had two inflection points, with a gradual decrease in the incremental slope for each section. After the second flexion point, the LSR slope slightly decreased and was maintained until exhaustion. However, the degree of change varied among the participants. Although the ratio of forehead LSR to upper arm LSR tended to decrease gradually over time, there was little change in this ratio after a second flexion point of LSR in both. These findings suggest possible differences in LSR control between the forehead and upper arm during constant-load exercise to prolonged exhaustion.

Gas‐Permeable Highly Sensitive Nanomesh Humidity Sensor for Continuous Measurement of Skin Humidity

AbstractOn‐skin humidity sensors can be used to measure the sweat rate on the human skin surface. However, it is challenging to realize a precise, long‐term skin humidity measurement. The main challenge is to develop an on‐skin humidity sensor that has gas permeability, high sensitivity, and flexibility simultaneously. Porous materials and electrodes can enhance the properties of the humidity sensor for fulfilling continuous monitoring. Herein, a humidity sensor composed of nanomesh Au electrodes and nanomesh humidity‐sensitive materials, is reported. The porous structure makes the sensor flexible and gas permeable, increases the surface area, and leads to high sensitivity. The sensor has a high sensitivity of 640 000% in the relative‐humidity range of over 40–100%, together with a gas permeability similar to that of an open environment. The gas permeability suppresses the skin inflammation, endows natural evaporation of sweat, and brings an identical condition with bare skin. To evaluate the utility of the nanomesh sensor, on‐skin humidity measurements are performed, and the humidity change due to sweating after exercise is recorded.

Fluid Balance and Thermoregulatory Responses during Wheelchair Basketball Games in Hot vs. Temperate Conditions.

The impaired vaso- and sudomotor functions limit sweat capacity in individuals with a spinal cord injury (SCI) and might increase the risk for heat-related illness and decreased performance, especially in hot conditions (HOT). This study investigated the differences in fluid balance and thermal responses between wheelchair basketball (WCB) games in HOT and temperate conditions (TMP). Eleven male WCB athletes (39.8 y, 82.8 kg) with SCI (lesion level C5-L4) participated, five in HOT (31 °C) and eight in TMP games (21 °C). Fluid balance, sweat rate, body core temperature, distance, velocity and thermal sensation were assessed. The relative change in body mass was higher in the HOT group (median: −0.35%, interquartile-range: 0.15%, p = 0.02) compared to TMP (+0.11%, 0.35%) group. The sweat rate was significantly higher in the HOT group (0.93 L/h, 0.58 L/h, p = 0.02) compared to the TMP groups (0.48 L/h, 0.19 L/h). Body core temperature increased significantly higher in the TMP group (1.05 °C, 0.15 °C, p = 0.01) compared to the HOT group (0.8 °C, 0.4 °C). The mean velocity (HOT: 1.12 m/s, 0.11 m/s, TMP: 1.07 m/s, 0.08 m/s, p = 0.54) did not differ between the games. The WCB game in HOT leads to significantly higher sweat rate and loss in body mass compared to TMP. Even relative body mass loss was less than 2%. Athletes thus have to be supported with enough fluid, especially during games in HOT.

Wireless Wearable Electrochemical Sensing Platform with Zero-Power Osmotic Sweat Extraction for Continuous Lactate Monitoring.

Wearable and wireless monitoring of biomarkers such as lactate in sweat can provide a deeper understanding of a subject's metabolic stressors, cardiovascular health, and physiological response to exercise. However, the state-of-the-art wearable and wireless electrochemical systems rely on active sweat released either via high-exertion exercise, electrical stimulation (such as iontophoresis requiring electrical power), or chemical stimulation (such as by delivering pilocarpine or carbachol inside skin), to extract sweat under low-perspiring conditions such as at rest. Here, we present a continuous sweat lactate monitoring platform combining a hydrogel for osmotic sweat extraction, with a paper microfluidic channel for facilitating sweat transport and management, a screen-printed electrochemical lactate sensor, and a custom-built wireless wearable potentiostat system. Osmosis enables zero-electrical power sweat extraction at rest, while continuous evaporation at the end of a paper channel allows long-term sensing from fresh sweat. The positioning of the lactate sensors provides near-instantaneous sensing at low sweat volume, and the custom-designed potentiostat supports continuous monitoring with ultra-low power consumption. For a proof of concept, the prototype system was evaluated for continuous measurement of sweat lactate across a range of physiological activities with changing lactate concentrations and sweat rates: for 2 h at the resting state, 1 h during medium-intensity exercise, and 30 min during high-intensity exercise. Overall, this wearable system holds the potential of providing comprehensive and long-term continuous analysis of sweat lactate trends in the human body during rest and under exercising conditions.

Do E2 and P4 contribute to the explained variance in core temperature response for trained women during exertional heat stress when metabolic rates are very high?

PurposeWomen remain underrepresented in the exercise thermoregulation literature despite their participation in leisure-time and occupational physical activity in heat-stressful environments continuing to increase. Here, we determined the relative contribution of the primary ovarian hormones (estrogen [E2] and progesterone [P4]) alongside other morphological (e.g., body mass), physiological (e.g., sweat rates), functional (e.g., aerobic fitness) and environmental (e.g., vapor pressure) factors in explaining the individual variation in core temperature responses for trained women working at very high metabolic rates, specifically peak core temperature (Tpeak) and work output (mean power output).MethodsThirty-six trained women (32 ± 9 year, 53 ± 9 ml·kg−1·min−1), distinguished by intra-participant (early follicular and mid-luteal phases) or inter-participant (ovulatory vs. anovulatory vs. oral contraceptive pill user) differences in their endogenous E2 and P4 concentrations, completed a self-paced 30-min cycling work trial in warm–dry (2.2 ± 0.2 kPa, 34.1 ± 0.2 °C, 41.4 ± 3.4% RH) and/or warm–humid (3.4 ± 0.1 kPa, 30.2 ± 1.2 °C, 79.8 ± 3.7% RH) conditions that yielded 115 separate trials. Stepwise linear regression was used to explain the variance of the dependent variables.ResultsModels were able to account for 60% of the variance in Tpeak (overline{R }2: 41% core temperature at the start of work trial, overline{R }2: 15% power output, overline{R }2: 4% [E2]) and 44% of the variance in mean power output (overline{R }2: 35% peak aerobic power, overline{R }2: 9% perceived exertion).ConclusionE2 contributes a small amount toward the core temperature response in trained women, whereby starting core temperature and peak aerobic power explain the greatest variance in Tpeak and work output, respectively.

Personalized Hydration Requirements of Runners.

This study sought to (a)estimate how the duration of running influences sweat losses and contributes to the daily fluid requirement, and (b)empirically estimate the drinking rates required to prevent significant dehydration (≥2% body weight as body water). Individual sweating data and running duration were obtained from male (n = 83) and female (n = 36) runners (n = 146 total observations) performing under highly heterogeneous conditions and over a range of exercise durations (33-280min). Running <60min/day increased daily fluid needs by a factor of 1.3, whereas running >60min/day increased the daily fluid need by a factor of 1.9-2.3. Running <60min/day generally required no fluid intake to prevent significant dehydration before run completion (31/35 runners). In contrast, running >60min/day required more than 50% replacement of sweating rates to prevent the same (65/111 runners). Overall sweat losses ranged from ∼0.2 to ∼5.0L/day, whereas the drinking rates required to prevent significant dehydration ranged from 0 to 1.4L/hr. The characterization of sweat losses, sweat rate, and required drinking among runners in this study indicate wide individual variability that warrants personalized hydration practices, particularly when running is prolonged (>60min) and performance is important. This study may serve as a useful guidepost for sports dietitians when planning and communicating fluid needs to athletes, as well as complement guidance related to both personalized programmed and thirst-driven drinking strategies.

TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation in humans in vivo.

What is the central question of this study? Do transmembrane member 16A (TMEM16A) blockers modulate the activation of heat loss responses of sweating and cutaneous vasodilatation? What are the main finding and its importance? Relative to the vehicle control site, TMEM16A blockers T16Ainh-A01 and benzbromarone had no effect on sweat rate or cutaneous vascular conductance during whole-body heating inducing a 1.1±0.1°C increase in core temperature above baseline resting levels. These results suggest that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heat stress. Animal and in vitro studies suggest that transmembrane member 16A (TMEM16A), a Ca2+ -activated Cl- channel, contributes to regulating eccrine sweating. However, direct evidence supporting this possibility in humans is lacking. We assessed the hypothesis that TMEM16A blockers attenuate sweating during whole-body heating in humans. Additionally, we assessed the associated changes in the heat loss response of cutaneous vasodilatation to determine if a functional role of TMEM16A may exist. Twelve young (24±2years) adults (six females) underwent whole-body heating using a water-perfused suit to raise core temperature 1.1±0.1°C above baseline. Sweat rate and cutaneous vascular conductance (normalized to maximal conductance via administration of sodium nitroprusside) were evaluated continuously at four forearm skin sites treated continuously by intradermal microdialysis with (1) lactated Ringer's solution (control), (2) 5% dimethyl sulfoxide (DMSO) serving as a vehicle control, or (3) TMEM16A blockers 1mM T16Ainh-A01 or 2mM benzbromarone dissolved in 5% DMSO solution. All drugs were administered continuously via intradermal microdialysis. Whole-body heating increased core temperature progressively and this was paralleled by an increase in sweat rate and cutaneous vascular conductance at all skin sites. However, sweat rate (all P>0.318) and cutaneous vascular conductance (all P≥0.073) did not differ between the vehicle control site relative to the TMEM16A blocker-treated sites. Collectively, our findings indicate that TMEM16A blockers T16Ainh-A01 and benzbromarone do not modulate the regulation of sweating and cutaneous vasodilatation during whole-body heating in young adults in vivo.

Influence of sex and biological maturation on the sudomotor response to exercise-heat stress: are girls disadvantaged?

Both adult females and children have been reported to have a lower sweating capacity and thus reduced evaporative heat loss potential that may increase their susceptibility to exertional hyperthermia in the heat. Compared with males, females have a lower maximal sweat rate and thus a theoretically lower maximum skin wettedness due to a lower sweat output per gland. Similarly, children have been suggested to be disadvantaged in high ambient temperatures due to a lower sweat production and therefore reduced evaporative capacity, despite modifications of heat transfer due to physical attributes and possible evaporative efficiency. The reported reductions in the sudomotor activity of females and children suggest a lower sweating capacity in girls. However, because of the complexities of isolating sex and maturation from the confounding effects of morphological differences (e.g., body surface area-to-mass ratio) and metabolic heat production, limited evidence exists supporting whether children, and, more specifically, girls are at a thermoregulatory disadvantage. Furthermore, a limited number of child-adult comparison studies involve females and very few studies have directly compared regional and whole body sudomotor activity between boys and girls. This minireview highlights the exercise-induced sudomotor response of females and children, summarizes previous research investigating the sudomotor response to exercise in girls, and suggests important areas for further research.

The effect of acute intradermal administration of ascorbate on heat loss responses in older adults with uncomplicated controlled hypertension.

What is the central question of this study? Does acute intradermal administration of the antioxidant ascorbate augment local forearm cutaneous vasodilatation and sweating via nitric oxide synthase (NOS)-dependent mechanisms during exercise-heat stress in older adults with uncomplicated controlled hypertension? What is the main finding and its importance? Relative to the control site, ascorbate had no effect on forearm cutaneous vascular conductance (CVC) and sweat rate, although CVC was reduced with NOS inhibition in older adults with hypertension. Acute local administration of ascorbate to forearm skin does not modulate heat loss responses during exercise-heat stress in older adults with hypertension. Nitric oxide synthase (NOS) contributes to the heat loss responses of cutaneous vasodilatation and sweating during exercise. However, the contribution of NOS may be attenuated in individuals with uncomplicated, controlled hypertension due to elevated oxidative stress, which can reduce NO bioavailability. We evaluated the hypothesis that the acute local intradermal administration of the antioxidant ascorbate would enhance cutaneous vasodilatation and sweating via NOS-dependent mechanisms during an exercise-heat stress in adults with hypertension. Habitually active adults who were normotensive (n=14, 7 females, 62±4years) or had uncomplicated, controlled hypertension (n=13, 6 females, 62±5years) performed 30min of moderate-intensity (50% of their pre-determined peak oxygen uptake) semi-recumbent cycling in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance (CVC) and sweat rate were assessed at four forearm skin sites continuously perfused with (1) lactated Ringer solution (Control), (2) 10mM antioxidant ascorbate, (3) 10mMNG -nitro-l-arginine methyl ester (l-NAME), a non-selective NOS inhibitor, or (4) a combination of ascorbate and l-NAME. Relative to Control, no effect of ascorbate was observed on CVC or sweating in either group (P=0.619). However, l-NAME reduced CVC relative to Control in both groups (P≤0.038). No effect of any treatment on sweating was observed (P≥0.306). Thus, acute local administration of ascorbate to forearm skin does not enhance the activation of heat loss responses of cutaneous vasodilatation and sweating in older adults, and those with hypertension during an exercise-heat stress.

Responses to a 5-Day Sport-Specific Heat Acclimatization Camp in Elite Female Rugby Sevens Athletes.

To describe the physiological (resting core temperature, exercising heart rate, and sweat rate) and psychophysical (rating of perceived exertion, thermal sensation, and thermal comfort) responses to a short-term heat acclimatization (HA) training camp in elite female rugby sevens athletes. Nineteen professional female rugby sevens athletes participated in a 5-day HA camp in Darwin, Australia (training average: 32.2°C and 58% relative humidity). Training involved normal team practice prescribed by appropriate staff. Markers of physiological and psychophysical adaptations to HA were collected at various stages during the camp. Partial eta-squared effect sizes (from linear mixed-effects models), rank-biserial correlations (from Freidman tests), and P values were used to assess changes across the protocol. Resting core temperature did not significantly change. Exercising heart rate showed a large and significant reduction from day 1 to day 5 (175 [13] vs 171 [12]beats·min-1), as did sweat rate (1.1 [0.3] vs 1.0 [0.2]L·h-1). Thermal sensation showed a large and significant reduction between day 1 and day 5 (median [interquartile range] = 5 [5-5.5] vs 4.5 [4-5]). Changes in rating of perceived exertion and thermal comfort were unclear. Beneficial cardiovascular adaptations were observed simultaneously across a full squad of elite female rugby sevens players (without expensive facilities/equipment or modifying training content). However, beneficial changes in resting core temperature, sweat rate, and thermal/effort perceptions likely require a greater thermal impulse. These data contribute to the development of evidence-informed practice for minimal effective HA doses in female team-sport athletes, who are underrepresented in the current research.

Dehydration Rate and a Novel Model to Aid Search and Relief for Undocumented Border Crossers in the Sonoran Desert

There has been a proliferation of geographic literature exploring the fatal effects of immigration policy since the early 2000s. Studies have used geographic information systems (GIS) and predictive modeling to explore potential relationships between border protection infrastructure, environment, and migrant death. Although some studies have used GIS to determine the probable effects of heat stress, none have included the potential perspiration as a limiting factor to pedestrian travel in an arid environment during daylight hours. Heat exposure is the leading cause of mortality for migrants in the desert regions of the U.S.–Mexico border, and humans rely on water to regulate temperature. For a more systematic methodology and higher precision, we calculated the maximum distances a person could walk in Arizona’s Sonoran Desert accounting for sweat rate. The locations of recovered human remains (RHR) correlate with water usage and increased difficulty of pedestrian travel. Further, our results showed at higher precision a significant correlation of mortality and spatial rates of dehydration and demonstrate that sweat rate is a better predictor of RHR location than heat or slope alone and will be more informative for search and relief operations in the region.

Modelling sodium requirements of athletes across a variety of exercise scenarios – Identifying when to test and target, or season to taste

ABSTRACT Evidence suggests the focus for sodium replacement during exercise should be maintenance of plasma sodium concentration ([Na+]plasma) for any given total body water (TBW) volume. The sodium intake to achieve stable [Na+]plasma given known fluid and electrolyte intakes and losses can be mathematically estimated. Therefore the aim of this investigation was to model sodium requirements of athletes during exercise, observing the influence of sweat rate, exercise duration, body mass, baseline [Na+]plasma and sweat potassium [K+]sweat, and relevance to competition (soccer, elite marathon, and 160 km ultramarathon running). Models were constructed across a range of sweat sodium concentrations ([Na+]sweat) (20–80 mmol·L−1), sweat rates (0.5–2.5 L·h−1) and fluid replacement (10–90% of losses). In the competition-specific scenarios, fluid replacement was calculated to achieve 2% TBW losses. Sodium requirements were driven by fluid replacement (% of losses) and [Na+]sweat, with minimal or no influence of other variables. Replacing sodium was unnecessary in all realistic scenarios modelled for a soccer match and elite marathon. In contrast, the 160 km ultramarathon required ≥47% sodium replacement when [Na+]sweat was ≥40 mmol·L−1 and >80% of fluid losses were replaced. In conclusion, sodium requirements to maintain stable [Na+]plasma during exercise depend on both the proportion of fluid losses replaced, and [Na+]sweat. Only when prolonged exercise is coupled with aggressive fluid replacement (>80%) and whole body [Na+]sweat ≥40 mmol·L−1 does sweat composition testing and significant, targeted sodium replacement appear necessary. Highlights Modelling sodium intake requirements with sodium and fluid intake expressed as a proportion of losses, allows robust models to be constructed that are not influenced by sweat rate, exercise duration, body mass, and only to a minor extent by baseline plasma sodium and sweat potassium. When applied to specific sporting scenarios, targeted sodium replacement, and therefore sweat composition testing, appears unnecessary in all realistic scenarios modelled for a soccer match or elite marathon race. Athletes can therefore choose sodium intake according to taste preferences rather than physiological need. During a 160 km ultramarathon, targeted sodium replacement may be necessary because fluid replacement needs are greater as a proportion of losses. However the required quantity remains <50% of losses unless sweat rate is ≥1.5 L·hr−1, sweat sodium is ≥40 mmol·L−1, and fluid replacement is ≥90% of losses. The modelling technique described could be utilised by researchers to personalise sodium replacement in intervention studies for each participant, or by practitioners to either estimate the likely sodium needs of athletes during exercise, or to decide when sweat composition testing is or is not likely to be useful.

Rapid chloride and bicarbonate determination by capillary electrophoresis for confirmatory testing of cystic fibrosis infants with volume-limited sweat specimens

Objectives Cystic fibrosis (CF) is a debilitating genetic disorder that benefits from early detection. CF diagnosis relies on measuring elevated sweat chloride that is difficult in neonates with low sweat rates. We introduce a new method for sweat chloride determination from volume-limited specimens, and explore the potential utility of sweat bicarbonate in neonatal CF screening.Methods A rapid assay (< 5 min) was developed to analyze chloride and bicarbonate using capillary electrophoresis with indirect UV detection (CE-iUV). Pilocarpine-stimulated sweat samples from screen-positive CF infants were collected at two hospital sites, including confirmed CF (n = 12), CF screen-positive inconclusive diagnosis (n = 4), and unaffected non-CF cases (n = 37). All sweat chloride samples were analyzed by a coulometric titrator and CE-iUV, and the viability to measure acid-labile bicarbonate was also evaluated.Results Stability studies revealed that bicarbonate can be reliably assessed in sweat if acidification and heating were avoided. Method validation demonstrated that sweat chloride and bicarbonate were quantified with acceptable accuracy (recovery of 102%), precision (CV = 3.7%) and detection limits (∼ 0.1 mM). An inter-laboratory comparison confirmed a mean bias of 6.5% (n = 53) for sweat chloride determination by CE-iUV relative to a commercial chloridometer. However, sweat bicarbonate did not discriminate between CF and non-CF infants (AUC = 0.623, p = 0.215) unlike chloride (AUC = 1.00, p = 3.00 × 10−7).Conclusions CE-iUV offers a robust method for sweat chloride testing from presumptive CF infants that may reduce testing failure rates. However, sweat bicarbonate does not have clinical value in newborn CF diagnosis.

An unconventional vertical fluidic-controlled wearable platform for synchronously detecting sweat rate and electrolyte concentration

Epidermal microfluidic devices with long microchannels have been developed for continuous sweat analysis, which are crucial to assess personal hydration status and underlying health conditions. However, the flow resistance in long channels and the ionic concentration variation significantly affect the accuracy of both the sweat rate and electrolyte concentration measurements. Herein, we present a novel fluidic-controlled wearable platform for synchronously dropwise-detecting the sweat rate and total electrolyte concentration. The unconventional platform consisting of a vertically shortened channel, a pair of embedded electrodes and an absorption layer, is designed to minimize the flow resistance and transform sweat fluidics into uniform micro-droplets for chronological and dropwise detection. Real-time sweat conductance is decoupled from a square-wave-like curve, where the sweat rate and electrolyte concentration can be derived from the interval time and peak value, respectively. Flexible and wearable band devices are demonstrated to show their potential application for hydration status assessment during exercises.

Flexible nanostructured CuO thin film: A promising candidate for wearable real-time sweat rate monitoring devices

Hydration level monitoring ensures clinically convenient instructions for preventive medicine and disease diagnostics. This paper aims to develop a wearable metal-oxide based sensor for monitoring hydration levels using flexible nanostructured copper oxide (CuO) thin film. Nanostructured CuO thin films were designed and fabricated on flexible cellulose acetate (CA) substrates via the successive ionic layer adsorption and reaction (SILAR) method. The obtained CuO films vigorously adhered to the CA substrate, and the resulting coated substrates were efficiently flexible to be used as wearable hydration level monitoring systems to realize big data collection of human health. The sensing response of the CuO-based flexible sensors is heavily improved by optimizing the growth process.

Heat Acclimation in Females Does Not Limit Aerobic Exercise Training Outcomes.

Recent aerobic exercise training in the heat has reported blunted aerobic power improvements and reduced mitochondrial-related gene expression in men. It is unclear if this heat-induced blunting of the training response exists in females. The purpose of the present study was to determine the impact of 60 min of cycling in the heat over three weeks on thermoregulation, gene expression, and aerobic capacity in females. Untrained females (n = 22; 24 ± 4yoa) were assigned to three weeks of aerobic training in either 20 °C (n = 12) or 33 °C (n = 10; 40%RH). Maximal aerobic capacity (39.5 ± 6.5 to 41.5 ± 6.2 mL·kg−1·min−1, p = 0.021, ηp2 = 0.240, 95% CI [0.315, 3.388]) and peak aerobic power (191.0 ± 33.0 to 206.7 ± 27.2 W, p < 0.001, ηp2 = 0.531, 95% CI [8.734, 22.383]) increased, while the absolute-intensity trial (50%VO2peak) HR decreased (152 ± 15 to 140 ± 13 b·min−1, p < 0.001, ηp2 = 0.691, 95% CI [15.925, 8.353]), but they were not different between temperatures (p = 0.440, p = 0.955, p = 0.341, respectively). Independent of temperature, Day 22 tolerance trial skin temperatures decreased from Day 1 (p = 0.006, ηp2 = 0.319, 95% CI [1.408, 0.266), but training did not influence core temperature (p = 0.598). Average sweat rates were higher in the 33 °C group vs. the 20 °C group (p = 0.008, ηp2 = 0.303, 95% CI [67.9, 394.9]) but did not change due to training (p = 0.571). Pre-training PGC-1α mRNA increased 4h-post-exercise (5.29 ± 0.70 fold change, p < 0.001), was lower post-training (2.69 ± 0.22 fold change, p = 0.004), and was not different between temperatures (p = 0.455). While training induced some diminished transcriptional stimulus, generally the training temperature had little effect on genes related to mitochondrial biogenesis, mitophagy, and metabolic enzymes. These female participants increased aerobic fitness and maintained an exercise-induced PGC-1α mRNA response in the heat equal to that of room temperature conditions, contrasting with the blunted responses previously observed in men.

Can Finnish Sauna Bathing Induce Heat Acclimation in Adults with Stable Coronary Artery Disease?

IntroductionExtreme heat is associated with a greater risk of mortality that particularly affects older adults with cardiovascular disease (CVD). Regular heat exposure induces an adaptation of thermoregulatory mechanisms (acclimation) that may alleviate thermal and/or cardiac strain during subsequent heat exposure. However, limited research has examined practical heat acclimation protocols that could be recommended to vulnerable populations, such as adults with CVD. The objective of this study was to test the hypothesis that 8 weeks of Finnish sauna bathing reduces core temperature and heart rate and increases sweating during heat exposure.Method14 participants (11 men/3 women, 63 ± 5 years, 28.7 ± 3.8 kg/m2) with stable coronary artery disease participated in an 8‐week Finnish sauna intervention (4 sessions/week, 20 to 30 min/session, at ~80°C, 20% humidity). Core temperature (ingestible telemetric pill), heart rate (Polar watch), and sweat rate (change in nude body weight) were measured during the first and last sauna sessions.ResultsResting core temperature prior to the first sauna session was 37.4 ± 0.4°C, compared to 37.1 ± 0.3°C prior to the last session (p= 0.04). Core temperature at the end of sauna bathing did not differ between the first (37.77 ±0.34°C) and the last (37.59 ± 0.31°C, p=0.20) sessions. Heart rate at the end of sauna bathing was greater during the last (90 ± 17 bpm) compared to first (85 ± 16 bpm, p=0.13) sessions. Sweat rate was greater during the last sauna session (first session: 8.6 ± 5.9 mL/min vs. last session: 5.1 ± 3.0 mL/min, p&lt;0.01).ConclusionEight weeks of Finnish sauna bathing reduces resting core temperature and increases sweat rate during heat exposure in adults with stable coronary artery disease. However, these adaptations did not translate into reduced thermal and cardiac strain during heat exposure.

Elevations in sweat sodium concentration following ischemia‐reperfusion injury during heat stress

INTRODUCTIONAcute kidney injury is a major cause of excess hospitalizations during heat waves. The etiology of this acute kidney injury is likely contributed to by renal ischemia‐reperfusion (IR) injury. Renal IR injury results in damage to the renal tubules and a subsequent impairment in sodium reabsorption. Fractional excretion of sodium is often used as an indirect marker of damage to the renal tubules and increases of &gt;1% reflect ischemic acute kidney injury. Mechanistic studies, which are limited to rodent IR models, have reported that impairments in sodium reabsorption following ischemic acute kidney injury are mediated by a reduction in active transporters for sodium reabsorption in the renal tubules. However, similar in vivo studies are not possible in humans. The eccrine sweat glands have been proposed as a model of the nephrons given the anatomical and physiological similarities (e.g., sodium reabsorption).PURPOSETest the hypothesis that sweat sodium concentrations are elevated following IR injury during passive heat stress.METHODSFifteen healthy adults (10 women; age: 25±3 y; body mass index: 23.7±3.5 kg·m‐2) completed a cross‐body design experiment consisting of ~160 min of passive heat stress (core body temperature: +1.5±0.2°C) utilizing a suit perfused with 50°C water. At 60 min of whole‐body heating, one upper arm (randomized) was occluded (220 mmHg) for 20 min followed by reperfusion. Sweat was collected from the ventral aspect of each forearm via an absorbent patch (~77 cm2) pre‐ and post‐IR for 24±4 and 30±6 min, respectively. Sweat sodium concentration (mmol·L‐1) was measured in duplicate via electrolyte analyzer (EasyLyte® Plus). Local sweat rate was measured on the distal aspect of the dorsal forearm continuously via hygrometry (mL·min‐1·cm‐2). Comparisons were made between the experimental (IR) and control arms. Data are reported as mean±SD.RESULTSLocal sweat rate increased during whole‐body passive heating (p&lt;0.001) and was not different between the experimental and control arms at any timepoint except during ischemia (0.45±0.53 vs.1.31±0.43 mL·min‐1·cm‐2, respectively; p&lt;0.001). Sweat sodium concentration did not change from pre‐ to post‐IR in the control arm (pre: 54.9±32.2 mmol·L‐1 and post: 58.7±25.6 mmol·L‐1; p=0.99), but increased from pre‐ to post‐IR in the experimental arm (pre: 48.4±23.3 mmol·L‐1 and post: 63.8±30.9 mmol·L‐1; p=0.02). Furthermore, the change from pre‐IR in sweat sodium concentration was different between experimental and control arms post‐IR (+12.5±14.70 mmol·L‐1 versus ‐0.3±20.5 mmol·L‐1, respectively; p=0.05).CONCLUSIONIn support of our hypothesis, sweat sodium concentration was elevated following IR injury and does not appear to be mediated by alterations in sweat rate. These observations are in‐line with rodent renal IR models demonstrating impaired sodium reabsorption. While these findings appear to support the use of eccrine sweat glands as a model, further testing is required to verify its use to understand impaired sodium handling following IR injury in humans.

Critical Environmental Limits for Young, Healthy Adults (PSU HEAT)

The average temperature of the Earth has been steadily increasing for decades and is expected to continue increasing throughout the 21st century. Along with the increase in average global temperatures, the frequency, duration, and severity of heat waves have increased. Thus, there is a critical need for research targeted at understanding the specific environmental conditions associated with increased risk of heat‐ and humidity‐related morbidity and mortality.PurposeTo establish critical environmental limits for healthy young adults at two metabolic rates that reflect activities of daily living and light activity. We hypothesized that critical environmental limits would be shifted toward lower combinations of temperature and humidity at higher compared to lower rates of metabolic heat production.MethodsTwenty‐five (12M/13F; 24 ± 4 yrs) subjects were exposed to progressive heat stress in an environmental chamber at two rates of metabolic heat production chosen to represent minimal activity (MinAct) or light ambulation (LightAmb). Progressive heat stress comprised either (1) constant dry‐bulb temperature (Tdb; 36, 38, or 40 °C) and increasing ambient water vapor pressure (Pa; Pcrit trials), or (2) constant Pa (12, 16, or 20 mmHg) and increasing Tdb (Tcrit trials). Chamber Tdb and Pa, and subject gastrointestinal temperature (Tgi), were continuously monitored throughout each trial. After a 30‐min equilibration period, progressive heat stress superseded until subject heat balance could no longer be maintained and a clear rise in Tgi was observed. Each subject was tested during MinAct and LightAmb in 2 or 3 randomized environmental conditions, for a total of 4–6 trials per participant.ResultsBy design, oxygen consumption (V̇O2: 0.46 ± 0.10 vs. 0.80 ± 0.16 L/min; 1.8 ± 0.3 vs. 3.2 ± 0.3 METs), metabolic heat production (82.9 ± 12.5 vs. 133.3 ± 14.8), and sweat rate (142.8 ± 80.2 vs. 230.8 ± 84.9) were lower for MinAct compared to LightAmb (all p &lt; 0.0001). There were no differences in these variables (p ≥ 0.05) among environmental conditions for either MinAct or LightAmb intensities. Higher metabolic heat production (p &lt; 0.001) during LightAmb compared to MinAct trials resulted in significantly lower critical environmental limits across all Pcrit and Tcrit conditions (all p &lt; 0.001).ConclusionsThese data are the first to define critical environmental limits for the maintenance of heat balance in healthy young adults during minimal to light physical activity reflecting activities of daily living and light household tasks. By establishing critical environmental limits in a young, healthy population, the findings of this study will be used as a benchmark for future studies in aged and other vulnerable populations, and can be used to develop guidelines, policy decisions, and evidence‐based alert communications to minimize adverse impacts of extreme heat events.

Voluntary drinking prevents dehydration when following occupational heat stress recommendations

INTRODUCTIONFederal and local entities issue guidance that aims to maintain core temperature (TC) below 38.0°C in unacclimated workers exposed to heat. These heat stress recommendations prescribe work‐rest ratios as a function of wet bulb globe temperature (WBGT) and metabolic heat production (Hprod). Hydration recommendations are less nuanced and suggest drinking 237 mL of a cool sport drink every 15‐20 min for work in the heat exceeding 2 h. This drinking regimen is based on the premise that ad libitum drinking during heat exposure results in dehydration [defined as &gt;2% body mass loss (BML)] due to inadequate drinking. To our knowledge, this hydration guidance has not been examined under heat stress recommendation compliant scenarios. Thus, it is unknown if ad libitumdrinking results in dehydration during recommendation compliant work in the heat.PURPOSETest the hypothesis that ad libitum drinking during heat stress recommendation compliant work in the heat will result in &gt;2% BML.METHODSSix, healthy, unacclimated, euhydrated subjects (2 women; 27±5 y) completed four trials consisting of 4 h (half a workday) of exposure to WBGTs of 23.9±0.2°C (A), 26.3±0.9°C (B), 28.4±0.1°C (C), 29.2±0.7°C (D). Subjects walked on a treadmill evoking a Hprod of 481±95 W, which is the average Hprod for outdoor workers in the U.S. NIOSH‐compliant work‐rest ratios were prescribed as a function of WBGT and Hprod [work:rest per hour (in min) ‐ A: 60:0, B: 45:15, C: 30:30, D: 15:45] and subjects were provided 237 mL of a cool (10±4°C) flavor preferred sport drink (Gatorade) every 15 min and drank ad libitum. BML was determined from changes in nude body mass and correction for fluid intake and urine loss provided an estimate of sweat rate. TC (telemetry pill) is reported as an average over the trial and as the percent of time TC exceeded 38.0°C (Time &gt;38). Thirst perception (1 = not thirsty, 9 = very, very thirsty) is reported as an average over the trial. Data are presented as mean±SD (parametric) or median (interquartile range) (nonparametric).RESULTSAverage TC was higher in Trial A (37.8±0.4°C; p=0.05) and Trial B (37.6±0.3°C; p=0.03) versus Trial D (37.3±0.4°C) but did not differ between the other trials (p≥0.20). Time &gt;38 did not differ between trials (A: 24 (5,43)%, B: 6 (0,5)%, C: 0 (0,5)%, D: 0 (0,0)%; p=0.17). Sweat rate was higher in Trial A (0.5±0.1 L/h) versus Trial D (0.4±0.1 L/h; p=0.05) but did not differ between any other trials (p≥0.12). Thirst perception (A: 2±1 a.u., B: 2±0 a.u, C: 2±1 a.u, D: 2±0 a.u; p=0.20) and fluid intake (A: 1.6±0.6 L, B: 1.5±0.5 L, C: 1.7±0.5 L, D: 1.6±0.7 L; p=0.88) did not differ between trials. BML did not differ between trials (A: ‐0.9±0.9%, B: ‐0.8±0.6%, C: ‐0.5±0.4%, D: ‐0.3±0.6%; p=0.24). One subject in one trial lost &gt;2% body mass (Trial A: ‐2.7%).CONCLUSIONAd libitumdrinking during recommendation compliant work in the heat rarely resulted in dehydration. Modification of work‐rest ratios across a range of WBGTs while working at a fixed Hprod mostly maintained TC &lt;38.0°C when ad libitumdrinking was permitted. Thus, absolute fluid prescription may not be necessary to prevent dehydration if adhering to occupational heat stress recommendations and cool fluids are readily available.