Whole-body Sweat Loss Research Articles

Dietary nitrate supplementation does not influence thermoregulatory or cardiovascular strain in older individuals during severe ambient heat stress.

What is the central question of this study? Does dietary nitrate supplementation with beetroot juice attenuate thermoregulatory and cardiovascular strain in older adults during severe heat stress? What is the main finding and its importance? A 7-day nitrate supplementation regimen lowered resting mean arterial pressure in thermoneutral conditions. During heat stress, core and mean skin temperatures, vasodilatory responses, sweat loss, heart rate and left ventricular function were unchanged, and mean arterial pressure was only transiently reduced, post-supplementation. These data suggest nitrate supplementation with beetroot juice does not mitigate thermoregulatory or cardiovascular strain in heat-stressed older individuals. This study tested the hypothesis that dietary nitrate supplementation with concentrated beetroot juice attenuates thermoregulatory and cardiovascular strain in older individuals during environmental heat stress. Nine healthy older individuals (six females, three males; aged 67±5years) were exposed to 42.5±0.1°C and 34.0±0.5% relative humidity conditions for 120min before (CON) and after 7days of dietary nitrate supplementation with concentrated beetroot juice (BRJ; 280ml, ∼16.8mmol of nitrate daily). Core and skin temperatures, body mass changes (indicative of whole-body sweat loss), skin blood flow and cutaneous vascular conductance, forearm blood flow and vascular conductance, heart rate, arterial blood pressures and indices of cardiac function were measured. The 7-day beetroot juice regimen increased plasma nitrate/nitrite levels from 27.4±15.2 to 477.0±102.5μmoll-1 (P<0.01) and lowered resting mean arterial pressure from 90±7 to 83±10mmHg at baseline under thermoneutral conditions (P=0.02). However, during subsequent heat stress, no differences in core and skin temperatures, skin blood flow and vascular conductance, forearm blood flow and vascular conductance, whole-body sweat loss, heart rate, and echocardiographic indices of systolic function and diastolic filling were evident following nitrate supplementation (all P>0.05). Mean arterial pressure was lower in BRJ vs. CON during heat stress (treatment-by-time interaction: P=0.02). Overall, these findings suggest that dietary nitrate supplementation with concentrated beetroot juice does not attenuate thermoregulatory or cardiovascular strain in older individuals exposed to severe ambient heat stress.

The Impact Of Short-Term Hot Water Immersion On Heat Acclimation And Thermotolerance

BACKGROUND: Environmental heat stress increases physiological strain during exercise in non-acclimated individuals. Heat acclimation (HA) protocols are often used as countermeasures to preserve physiological function during exercise in the heat. Passive heat strategies could be a potential method of HA that reduces excess physical exertion prior to activity or relocation. PURPOSE: To determine the effect of hot water immersion (HWI) on heat acclimation and thermotolerance. METHODS: 6 males (Age: 23.8 ± 1.5; VO2max: 45.0 ± 7.5 mL/kg/min.) participated in a crossover, counterbalanced study with a four-week washout between conditions. Heat stress tests (HST) were performed PRE and POST acclimation sessions and consisted of 45 min of cycling at 50% of VO2max in 40 °C, 40% RH. Acclimation sessions were either three consecutive bouts of HWI or traditional heat-exercise training (TRAD). HWI sessions consisted of 40 min of submersion at 40 °C. TRAD sessions consisted of 40 min of cycling at 50% VO2max in 40 °C, 40% RH. Core body temperature (Tcore), heart rate (HR), rate of perceived exertion (RPE), and thermal sensation (TSS) were recorded during HSTs. Blood was drawn PRE and POST HST to determine change in plasma volume. Nude body mass was recorded before and after HSTs to calculate whole body sweat loss (WBSL). Tcore and HR were used to calculate physiological strain index (PSI). RESULTS: HWI decreased average HR (PRE: 158 ± 7; POST: 149 ± 7; p = < 0.05), peak HR (176 ± 7; 164 ± 5; p = < 0.05), and end exercise RPE (15.3 ± 1.8; 13.2 ± 1.9; p = < 0.05). HWI had no significant effect on resting TCore (37.2 ± 0.4; 36.8 ± 0.3; p = 0.66), end exercise TCore (38.7 ± 0.4; 38.4 ± 0.3; p = 0.20), PSI (7.8 ± 1.1; 7.0 ± 0.8; p = 0.56), or TSS (10.8 ± 1.0; 9.5 ± 1.2; p = 0.09). TRAD resulted in no significant changes in average HR (PRE: 153 ± 11; POST: 149 ± 11; p = 0.82), peak HR (170 ± 9; 165 ± 10; p = 0.51), end exercise RPE (15.1 ± 1.2; 13.3 ± 2.0; p = 0.87), PSI (9.3 ± 2.1; 8.6 ± 1.4; p = 0.73), or TSS (10.5 ± 0.8; 10.7 ± 1.5; p = 0.77). Plasma volume expansion (%) was observed in both groups (HWI: 6.6 ± 6.4; TRAD: 4.3 ± 2.0; p = 0.41). CONCLUSION: Three consecutive HWI sessions are effective in lowering HR during submaximal exercise in the heat. Compared to heat-exercise exposures, HWI is a method in which to more rapidly elicit a HA phenotype.

No Relation Between Short-term Sodium Intake And Whole Body Sweat Sodium Concentration During Exercise-heat Stress

Research has been limited and mixed with regards to the effect of normal, short-term dietary sodium (Na) intake on sweat Na concentration ([Na]) and total sweat Na losses during exercise. PURPOSE: To determine the relation between dietary Na intake during exercise and up to 48-h before exercise on whole-body (WB) sweat [Na] and total sweat Na loss during 90 min of moderate-intensity cycling in the heat. METHODS: Forty-nine recreational athletes (34 men, 15 women; 34 ± 4 years; 75 ± 12 kg) cycled for 90 min at 78 ± 5% HRmax in the heat (320C, 25-50% RH). The WB washdown technique was used to collect sweat electrolytes during exercise and ion chromatography analysis was used to determine sweat [Na]. Total sweat Na loss was the product of WB sweat [Na] and WB sweat loss. Subjects were instructed to consume their normal diet before their trials. Upon arriving to the lab, each subject turned in a diet log, which included specific portion sizes and brand/type for all foods, fluids, and dietary supplements consumed in the previous 48 h. The investigators reviewed the diet logs for completeness with the subjects. Na intake was determined by Registered Dietitians using a computer based dietary analysis tool. Na intake during the trial was determined from the volume of 6% carbohydrate electrolyte (38 mmol/L Na) solution consumed ad libitum. Pearson correlation analysis was used to determine the relation between Na intake versus WB sweat [Na] and total sweat Na loss. Data are shown as mean ± SD. RESULTS: WB sweat [Na] was 41.1 ± 15.6 mmol/L and total sweat Na losses were 60.9 ± 35.3 mmol. Na intake during exercise, 24-h and 48-h before exercise were 32.4 ± 18.0 mmol, 188 ± 102 mmol, and 350 ± 159 mmol. There were no significant correlations between dietary Na intake and WB sweat [Na] (r = -0.002 to 0.02, p=0.90-0.99) or total sweat Na losses (r = 0.07 to 0.19, p=0.20-0.61) for any of the comparisons. CONCLUSION: There were no correlations between normal dietary Na intake during and up to 48 h before exercise versus WB sweat [Na] or total sweat Na losses. These results suggest that short-term Na intake does not play a significant role in explaining the inter-individual differences in WB sweat Na during exercise.

Normobaric hypoxia does not alter the critical environmental limits for thermal balance during exercise‐heat stress

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

Impaired Thermoregulatory Function during Dynamic Exercise in Multiple Sclerosis.

Impairments in sudomotor function during passive whole-body heating have been reported in multiple sclerosis (MS), a demyelinating disease of the CNS that disrupts autonomic function. However, the capability of the thermoregulatory system to control body temperature during exercise has never been assessed in MS. Thus, the aim of the present study was to test the hypothesis that thermoregulatory function is impaired in MS patients compared with healthy controls (CON) exercising at similar rates of metabolic heat production. Sweating and skin blood flow responses were compared between 12 individuals diagnosed with relapsing-remitting MS (9 females, 3 males) and 12 sex-, age-, mass-, and BSA-matched CON during a single bout of cycling exercise (rate of metabolic heat production: ∼4.5 W·kg) for 60 min in a climate-controlled room (25°C, 30% RH). Individuals with MS exhibited an attenuated increase in cumulative whole-body sweat loss after 30 min (MS, 72 ± 51 g; CON, 104 ± 37 g; P = 0.04) and 60 min (MS, 209 ± 94 g; CON, 285 ± 62 g; P = 0.02), as well as lower sweating thermosensitivity (MS, 0.49 ± 0.26 mg·cm·min·°C; CON, 0.86 ± 0.30 mg·cm·min·°C; P = 0.049). Despite evidence for thermoregulatory dysfunction, there were no differences between MS and CON in esophageal or rectal temperatures at 30- or 60-min time points (P > 0.05). Cutaneous vasculature responses were also not different in MS compared with CON (P > 0.05). Taken together, MS blunts sweating responses during exercise while cutaneous vasculature responses are preserved. Altered mechanisms of body temperature regulation in persons with MS may lead to temporary worsening of disease symptoms and limit exercise tolerance under more thermally challenging conditions.

Exercise intensity effects on total sweat electrolyte losses and regional vs. whole-body sweat [Na+], [Cl\u2212], and [K+

PurposeTo quantify total sweat electrolyte losses at two relative exercise intensities and determine the effect of workload on the relation between regional (REG) and whole body (WB) sweat electrolyte concentrations.MethodsEleven recreational athletes (7 men, 4 women; 71.5 ± 8.4 kg) completed two randomized trials cycling (30 °C, 44% rh) for 90 min at 45% (LOW) and 65% (MOD) of VO2max in a plastic isolation chamber to determine WB sweat [Na+] and [Cl−] using the washdown technique. REG sweat [Na+] and [Cl−] were measured at 11 REG sites using absorbent patches. Total sweat electrolyte losses were the product of WB sweat loss (WBSL) and WB sweat electrolyte concentrations.ResultsWBSL (0.86 ± 0.15 vs. 1.27 ± 0.24 L), WB sweat [Na+] (32.6 ± 14.3 vs. 52.7 ± 14.6 mmol/L), WB sweat [Cl−] (29.8 ± 13.6 vs. 52.5 ± 15.6 mmol/L), total sweat Na+ loss (659 ± 340 vs. 1565 ± 590 mg), and total sweat Cl− loss (931 ± 494 vs. 2378 ± 853 mg) increased significantly (p < 0.05) from LOW to MOD. REG sweat [Na+] and [Cl−] increased from LOW to MOD at all sites except thigh and calf. Intensity had a significant effect on the regression model predicting WB from REG at the ventral wrist, lower back, thigh, and calf for sweat [Na+] and [Cl−].ConclusionTotal sweat Na+ and Cl− losses increased by ~ 150% with increased exercise intensity. Regression equations can be used to predict WB sweat [Na+] and [Cl−] from some REG sites (e.g., dorsal forearm) irrespective of intensity (between 45 and 65% VO2max), but other sites (especially ventral wrist, lower back, thigh, and calf) require separate prediction equations accounting for workload.

Circadian Rhythm Does Not Alter the Sweating Response to Exercise in Thermoneutral and Warm Ambient Temperatures

The present study sought to determine whether the diurnal fluctuation in core temperature alters the sweating response to exercise in thermoneutral (23°C) and warm (33°C) environments. Six healthy males exercised on a semi‐recumbent ergometer at a fixed evaporative requirement for heat balance (200W/m2) for 60 min at two different times of day and two ambient temperatures matched for absolute humidity (1.3 kPa); i) 0800h/23°C, ii) 0800h/33°C, iii) 1600h/23°C, and iv) 1600h/33°C. Esophageal temperature (Tes), mean body temperature (Tb), local sweat rate (LSR) measured at the arm and upper back, and whole body sweat loss (WBSL) were measured. Resting absolute Tes was higher at 1600h compared to 0800h at 23°C (0800h: 36.7±0.2°C, 1600h: 36.9±0.2°C; P=0.04) and 33°C (0800h: 36.6±0.2°C, 1600h 36.9±0.2°C; P=0.005). Similarly, end‐exercise (steady‐state) absolute Tes was higher at 1600h relative to 0800h at 23°C (0800h: 37.4±0.2°C, 1600h: 37.6±0.2°C; P=0.04) and 33°C (0800h: 37.0±0.2°C, 1600h 37.2±0.2°C; P=0.01). However the change in Tes was similar irrespective of the time of day at both 23°C (0800h: 0.7±0.1°C, 1600h: 0.7±0.2°C; P=0.37) and 33°C (0800h: 0.4±0.1°C, 1600h: 0.3±0.1°C; P=0.35). Further, mean steady‐state LSR of arm and back after 60 min of exercise was similar irrespective of time at both 23°C (0800h: 0.66±0.06 mg/cm2/min, 1600h: 0.65±0.13 mg/cm2/min; P=0.74) and 33°C (0800h: 0.62±0.11 mg/cm2/min, 1600 h: 0.58±0.11 mg/cm2/min, P=0.50). Likewise, WBSL at steady‐state (46 to 60 min) was similar between morning and afternoon trials at 23°C (0800h: 156±28 g, 1600h: 162±36 g; P=0.38) and 33°C (0800h: 147±29 g, 1600h: 158±34 g, P=0.55). While sweating commenced prior to exercise in 33°C, the onset threshold for sweating occurred at a higher Tb at 1600h compared to 800h at 23°C (0800h: 35.6±0.1°C, 1600h 35.9±0.2°C; P=0.03), however the change in Tb was similar at 23°C regardless of time of day (0800h: 0.14±0.07°C, 1600h 0.17±0.12°C; P=0.47). Lastly, sudomotor thermosensitivity (LSR‐Tb) was similar at both 23°C (0800h: 0.80±0.26 mg/cm2/min/°C, 1600h: 0.82±0.30 mg/cm2/min/°C; P=0.80) and 33°C (0800h: 0.81±0.18 mg/cm2/min, 1600h: 0.90±0.40 mg/cm2/min, P=0.87). Taken together, preliminary data suggests the difference in absolute core temperature (~0.3°C) associated with diurnal fluctuation does not alter the sweating response at a fixed evaporative requirement for heat balance in both thermoneutral and warm conditions.Support or Funding InformationN.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.

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.

Decreased thermal sweating of central sudomotor mechanism in African and Korean men.

Tropical natives sweat less and preserve more body fluid than temperate natives, tolerating heat stress. However, the mechanisms involved in such sweating reduction have not been fully elucidated. We examined the sudomotor responses of men of African (n = 36) and Korean (n = 41) ancestry during hot water (43 °C) leg immersion (central sudomotor response). Correlations between mean body temperature, basal metabolic rate (BMR), and sweat rate were also examined. All procedures were done in an automated climate chamber. Local skin temperatures and BMR were measured and mean body temperature was calculated. Sweating activities which include evaporative loss rate, sweat onset time, sweat rate, sweat volume, and whole-body sweat loss volume were examined. In the heat load test, Africans showed lower mean body and local skin temperatures than Koreans before and after heating. Before and after heating, BMR declined significantly in Africans, while that of Koreans declined less. Local sweat onset time increased more in Africans than in Koreans. Local evaporative loss rate, local sweat volume, local sweat rate, and whole body sweat loss volume were reduced in Africans compared with Koreans. There were positive associations of mean body temperature and resting BMR with mean sweat rate. In conclusion, we observed a larger reduction of sudomotor activity in tropical Africans than in temperate Koreans, which was associated with their lower mean body temperature and lower resting BMR.

Age Modulates Physiological Responses during Fan Use under Extreme Heat and Humidity.

We examined the effect of electric fan use on cardiovascular and thermoregulatory responses of nine young (26 ± 3 yr) and nine aged (68 ± 4 yr) adults exposed to extreme heat and humidity. While resting at a temperature of 42°C, relative humidity increased from 30% to 70% in 2% increments every 5 min. On randomized days, the protocol was repeated without or with fan use. HR, core (Tcore) and mean skin (Tsk) temperatures were measured continuously. Whole-body sweat loss was measured from changes in nude body weight. Other measures of cardiovascular (cardiac output), thermoregulatory (local cutaneous and forearm vascular conductance, local sweat rate), and perceptual (thermal and thirst sensations) responses were also examined. When averaged over the entire protocol, fan use resulted in a small reduction of HR (-2 bpm, 95% confidence interval [CI], -8 to 3), and slightly greater Tcore (+0.05°C; 95% CI, -0.13 to 0.23) and Tsk (+0.03°C; 95% CI, -0.36 to 0.42) in young adults. In contrast, fan use resulted in greater HR (+5 bpm; 95% CI, 0-10), Tcore (+0.20°C; 95% CI, 0.00-0.41), and Tsk (+0.47°C; 95% CI, 0.18-0.76) in aged adults. A greater whole-body sweat loss during fan use was observed in young (+0.2 kg; 95% CI, -0.2 to 0.6) but not aged (0.0 kg; 95% CI, -0.2 to 0.2) adults. Greater local sweat rate and cutaneous vascular conductance were observed with fan use in aged adults. Other measures of cardiovascular, thermoregulatory, and perceptual responses were unaffected by fan use in both groups. During extreme heat and humidity, fan use elevates physiological strain in aged, but not young, adults.

CORP: Improving the status quo for measuring whole body sweat losses.

The measurement of whole body sweat losses (WBSL) is important to the study of body heat balance, body water balance, establishing guidelines for water and electrolyte consumption, and the study of metabolism and health. In principal, WBSL is measured by an acute change in body mass (ΔBM) in response to a thermoregulatory sweating stimulus. In this Cores of Reproducibility in Physiology (CORP) review, we revisit several basic, but rarely discussed, assumptions important to WBSL research, including the common equivalences: mass = weight = water = sweat. Sources of large potential measurement errors are also discussed, as are best practices for avoiding them. The goal of this CORP review is to ultimately improve the accuracy, reproducibility, and application of WBSL research.

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.

Does attenuated skin blood flow lower sweat rate and the critical environmental limit for heat balance during severe heat exposure?

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

Effect of stride frequency on thermoregulatory responses during endurance running in distance runners

Changing stride frequency may influence oxygen uptake and heart rate during running as a function of running economy and central command. This study investigated the influence of stride frequency manipulation on thermoregulatory responses during endurance running. Seven healthy endurance runners ran on a treadmill at a velocity of 15km/h for 60min in a controlled environmental chamber (ambient temperature 27°C and relative humidity 50%), and stride frequency was manipulated. Stride frequency was intermittently manipulated by increasing and decreasing frequency by 10% from the pre-determined preferred frequency. These periods of increase or decrease were separated by free frequency running in the order of free stride frequency, stride frequency manipulation (increase or decrease), free stride frequency, and stride frequency manipulation (increase or decrease) for 15min each. The increased and decreased stride frequencies were 110% and 91% of the free running frequency, respectively (196±6, 162±5, and 178±5steps/min, respectively, P<0.01). Compared to the control, stride frequency manipulation did not affect rectal temperature, heart rate, or the rate of perceived exhaustion during running. Whole-body sweat loss increased significantly when stride frequency was manipulated (1.48±0.11 and 1.57±0.11kg for control and manipulated stride frequencies, respectively, P<0.05), but stride frequency had a small effect on sweat loss overall (Cohen's d=0.31). A higher mean skin temperature was also observed under mixed frequency conditions compared to that in the control (P<0.05). While the precise mechanisms underlying these changes remain unknown (e.g. running economy or central command), our results suggest that manipulation of stride frequency does not have a large effect on sweat loss or other physiological variables, but does increase mean skin temperature during endurance running.

Physiologic and performance effects of sago supplementation before and during cycling in a warm-humid environment

ABSTRACTThe present study determined whether 0.8g/kg bodyweight sago ingested before (Pre-Sago) or during (Dur-Sago) exercise under warm-humid conditions (30 ± 2°C, 78 ± 3 % RH; 20 km·h−1 frontal airflow) conferred a performance and/or physiological benefit compared to a control (Control) condition. Eight trained, male cyclists/triathletes (45 ± 4 y, VO2peak: 65 ± 10 ml·kg−1·min−1, peak aerobic power: 397 ± 71 W) completed 3 15-min time-trials (∼75% VO2peak) pre-loaded with 45 min of steady-state (∼55% VO2peak) cycling following > 24 h standardization of training and diet. Measures of work completed, rectal and mean skin temperatures, heart rate, expiratory gases and venous blood samples were taken. Compared to Control, Pre-Sago resulted in a smaller rise in rectal temperature (0.3 ± 0.5°C) while heart rate increased to a greater extent (6 ± 13 beats·min−1) during exercise (both P < 0.05), however, compared to Control time-trial performance remained unaffected (Pre-Sago: −0.5 ± 4.0%, P > 0.05). During exercise, plasma glucose concentrations were maintained higher for Dur-Sago than Control (P < 0.05), however substrate oxidation rates remained similar (P > 0.05). Dur-Sago also resulted in a higher plasma sodium concentration (2 ± 2 mmol·l1) and lower whole-body sweat loss (544 ± 636 g) and, therefore, reduced plasma volume contraction (all P < 0.05). Heart rate increased to a greater extent (5 ± 13 beats·min−1) during Dur-Sago, yet compared to Control time-trial performance remained unaffected (+0.9 ± 2.3%, P > 0.05). Uniquely, these results indicate that during exercise heat stress feeding sago can result in some ‘beneficial’ physiological responses, however these do not translate to changes in exercise performance when performed in a post-prandial state.

Ice Slurry Ingestion Leads to a Lower Net Heat Loss during Exercise in the Heat.

To compare the reductions in evaporative heat loss from the skin (Esk) to internal heat loss (Hfluid) induced by ice slurry (ICE) ingestion relative to 37 °C fluid and the accompanying body temperature and local thermoeffector responses during exercise in warm, dry conditions (33.5 °C ± 1.4 °C; 23.7% ± 2.6% relative humidity [RH]). Nine men cycled at approximately 55% VO2peak for 75 min and ingested 3.2 mL · kg(-1) aliquots of 37 °C fluid or ICE after 15, 30, and 45 min of exercise. Metabolic heat production (M-W), rectal temperature (Tre), mean skin temperature (Tsk), whole-body sweat loss (WBSL), local sweat rate (LSR), and skin blood flow (SkBF) were measured throughout. Net heat loss (HLnet) and heat storage (S) were estimated using partitional calorimetry. Relative to the 37 °C trial, M-W was similar (P = 0.81) with ICE ingestion; however, the 200 ± 20 kJ greater Hfluid (P < 0.001) with ICE ingestion was overcompensated by a 381 ± 199-kJ lower Esk (P < 0.001). Net heat loss (HLnet) was consequently 131 ± 120 kJ lower (P = 0.01) and S was greater (P = 0.05) with ICE ingestion compared with 37 °C fluid ingestion. Concurrently, LSR and WBSL were lower by 0.16 ± 0.14 mg · min(-1) · cm(-2) (P < 0.01) and 191 ± 122 g (P < 0.001), respectively, and SkBF tended to be lower (P = 0.06) by 5.4%maxAU ± 13.4%maxAU in the ICE trial. Changes in Tre and Tsk were similar throughout exercise with ICE compared to 37 °C fluid ingestion. Relative to 37 °C, ICE ingestion caused disproportionately greater reductions in Esk relative to Hfluid, resulting in a lower HLnet and greater S. Mechanistically, LSR and possibly SkBF were suppressed independently of Tre or Tsk, reaffirming the concept of human abdominal thermoreception. From a heat balance perspective, recommendations for ICE ingestion during exercise in warm, dry conditions should be reconsidered.

Aerobic fitness and body fatness describe minimal variability in the thermoregulatory responses to exercise after accounting for heat production and body size

Aerobic fitness (VO2max) and body fatness have been regularly suggested as important determinants of core temperature and sweating responses to exercise [3,5], but recent studies suggest that biophysical factors related to heat production (Hprod), total body mass (TBM), and body surface area (BSA), predominantly influence rectal temperature changes (ΔTre) and sweating [1,2,4]. The present study tested the hypotheses that (i) individual variation in ΔTre, whole-body sweat loss (WBSL), and steady-state local sweat rate (LSRss) is determined primarily by Hprod (W.kg-1 TBM), evaporation required for heat balance (Ereq, W), and Ereq (W.m-2), respectively, and (ii) factors related to VO2max and body fat percentage (BF%) contribute minimally to the residual variance in these responses.

Explained variance in the thermoregulatory responses to exercise: the independent roles of biophysical and fitness/fatness-related factors.

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

Acute acetaminophen ingestion does not alter core temperature or sweating during exercise in hot-humid conditions.

Acute acetaminophen (ACT) ingestion has been reported to reduce thermal strain during cycling in the heat. In this study, nine active participants ingested 20 mg of ACT per kg of total body mass (ACT) or a placebo (PLA), 60 min prior to cycling at a fixed rate of metabolic heat production (ACT: 8.3 ± 0.3 W/kg; PLA: 8.5 ± 0.5 W/kg), which was equivalent to 55 ± 6% VO2max , for 60 min at 34.5 ± 0.1 °C, 52 ± 1% relative humidity. Resting rectal temperature (Tre ; ACT: 36.70 ± 0.17 °C; PLA: 36.80 ± 0.16 °C, P = 0.24), esophageal temperature (Tes ; ACT: 36.54 ± 0.22 °C; PLA: 36.61 ± 0.17 °C, P = 0.50) and mean skin temperature (Tsk ; ACT: 34.00 ± 0.14 °C; PLA: 33.96 ± 0.20 °C, P = 0.70) were all similar among conditions. At end-exercise, no differences in ΔTre (ACT: 1.12 ± 0.15 °C; PLA: 1.11 ± 0.21 °C, P = 0.92), ΔTes (ACT: 0.90 ± 0.28 °C; PLA: 0.88 ± 0.23 °C, P = 0.84), ΔTsk (ACT: 0.80 ± 0.39 °C; PLA: 0.70 ± 0.46 °C, P = 0.63), mean local sweat rate (ACT: 1.02 ± 0.15 mg/cm(2) /min; PLA: 1.02 ± 0.13 mg/cm(2) /min, P = 0.98) and whole-body sweat loss (ACT: 663 ± 83 g; PLA: 663 ± 77 g, P = 0.995) were evident. Furthermore, ratings of perceived exertion and thermal sensation and thermal comfort were not different between ACT and PLA conditions. In conclusion, ACT ingested 60 min prior to moderate intensity exercise in hot-humid conditions does not alter physiologic thermoregulatory control nor perceived strain.

Characterizing Individual Variability In The Core Temperature And Sweating Responses To Exercise

To normalize the influence of heat production (Hprod) and body morphology on thermoregulatory responses to exercise, between-groups comparisons of rectal temperature changes (ΔTre), whole-body sweat loss (WBSL), and steady-state local sweat rate (LSRss) should be performed at intensities that elicit same Hprod per kilogram of total body mass (W/kg), absolute evaporative requirement for heat balance (Ereq; W), and Ereq per square meter of body surface area (BSA; W/m2), respectively. However, it is unknown how well these parameters, and others related to aerobic fitness and morphology, explain individual variability in the aforementioned thermoregulatory responses. PURPOSE: To determine the contribution of various biophysical and physiological factors to the explained variance in the ΔTre, WBSL, and LSRss responses to exercise in compensable conditions. METHODS: A cohort of 37 subjects, heterogeneous for maximum oxygen uptake (VO2max) and body morphology, completed multiple trials consisting of 60 min of exercise in temperate conditions (25°C, 33% RH, 1.2 m/s air velocity) at intensities corresponding to a range of target absolute Hprod (410-918 W) and relative intensities (32.2-82.0% of VO2max). Metabolic rate, rectal and skin temperatures, and forearm LSR were measured continuously; WBSL was estimated from changes in body mass. RESULTS: Individual characteristics and experimental data were normally distributed. Individual variation in ΔTre was correlated with Hprod in W/kg (β = 0.673, P < 0.001) and body mass (β = −0.190, P = 0.027) with an adjusted R2 of 0.535 (P < 0.001). Additionally, only Ereq in W (β = 0.858, P < 0.001) correlated with WBSL (adjusted R2 = 0.732, P < 0.001), and only Ereq in W/m2 (β = 0.634, P < 0.001) correlated with LSRss (adjusted R2 = 0.631, P < 0.001). Factors related to body composition and aerobic fitness did not correlate with the residual variance. CONCLUSION: These data show that investigators must first consider factors related to Hprod, Ereq, body mass, and BSA when examining possible physiological differences in the core temperature and thermoregulatory sweating responses to exercise. Supported by NSERC Discovery Grant #386143-2010