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We tested the hypothesis that compliance with the National Institute for Occupational Safety and Health (NIOSH) heat stress recommendations will prevent reductions in glomerular filtration rate (GFR) across a range of wet-bulb globe temperatures (WBGTs) and work-rest ratios at a fixed work intensity. We also tested the hypothesis that noncompliance would result in a reduction in GFR compared with a work-rest matched compliant trial. Twelve healthy adults completed five trials (four NIOSH compliant and one noncompliant) that consisted of 4 h of exposure to a range of WBGTs. Subjects walked on a treadmill (heat production: approximately 430 W) and work-rest ratios (work/h: 60, 45, 30, and 15 min) were prescribed as a function of WBGT (24°C, 26.5°C, 28.5°C, 30°C, and 36°C), and subjects drank a sport drink ad libitum. Peak core temperature (TC) and percentage change in body weight (%ΔBW) were measured. Creatinine clearance measured pre- and postexposure provided a primary marker of GFR. Peak TC did not differ among NIOSH-compliant trials (P = 0.065) but differed between compliant versus noncompliant trials (P < 0.001). %ΔBW did not differ among NIOSH-compliant trials (P = 0.131) or between compliant versus noncompliant trials (P = 0.185). Creatinine clearance did not change or differ among compliant trials (P ≥ 0.079). Creatinine clearance did not change or differ between compliant versus noncompliant trials (P ≥ 0.661). Compliance with the NIOSH recommendations maintained GFR. Surprisingly, despite a greater heat strain in a noncompliant trial, GFR was maintained highlighting the potential relative importance of hydration. NEW & NOTEWORTHY: We highlight that glomerular filtration rate (GFR) is maintained during simulated occupational heat stress across a range of total work, work-rest ratios, and wet-bulb globe temperatures with ad libitum consumption of an electrolyte and sugar-containing sports drink. Compared with a work-rest matched compliant trial, noncompliance resulted in augmented heat strain but did not induce a reduction in GFR likely due to an increased relative fluid intake and robust fluid conservatory responses. [ABSTRACT FROM AUTHOR]

Occupational heat stress increases the risk of acute kidney injury (AKI). This study presents a secondary analysis to generate novel hypotheses for future studies by investigating the diagnostic accuracy of thermal, hydration, and heart rate assessments in discriminating positive AKI risk following physical work in the heat in unacclimatized individuals. Unacclimatized participants (n = 13, 3 women, age: ∼23 years) completed four trials involving 2 h of exercise in a 39.7 ± 0.6 °C, 32 ± 3% relative humidity environment that differed by experimental manipulation of hyperthermia (i.e., cooling intervention) and dehydration (i.e., water drinking). Diagnostic accuracy was assessed via receiver operating characteristic curve analysis. Positive AKI risk was identified when the product of concentrations insulin-like growth factor binding protein 7 and tissue inhibitor of metalloproteinase-2 [IGFBP7∙TIMP-2] exceeded 0.3 (ng∙mL−1)2∙1000−1. Peak absolute core temperature had the acceptable discriminatory ability (AUC = 0.71, p = 0.009), but a relatively large variance (AUC 95% CI: 0.57–0.86). Mean body temperature, urine specific gravity, urine osmolality, peak heart rate, and the peak percent of both maximum heart rate and heart rate reserve had poor discrimination (AUC = 0.66–0.69, p ≤ 0.051). Mean skin temperature, percent change in body mass and plasma volume, and serum sodium and osmolality had no discrimination (p ≥ 0.072). A peak increase in mean skin temperature of >4.7 °C had a positive likelihood ratio of 11.0 which suggests clinical significance. These data suggest that the absolute value of peak core temperature and the increase in mean skin temperature may be valuable to pursue in future studies as a biomarker for AKI risk in unacclimatized workers. [ABSTRACT FROM AUTHOR]

Men are likely at greater risk for heat-induced acute kidney injury compared with women, possibly due to differences in vascular control. We tested the hypothesis that the renal vasoconstrictor and vasodilator responses will be greater in younger women compared with men during passive heat stress. Twenty-five healthy adults [12 women (early follicular phase) and 13 men] completed two experimental visits, heat stress or normothermic time-control, assigned in a block-randomized crossover design. During heat stress, participants wore a water-perfused suit perfused with 50°C water. Core temperature was increased by ∼0.8°C in the first hour before commencing a 2-min cold pressor test (CPT). Core temperature remained clamped and at 1-h post-CPT, subjects ingested a whey protein shake (1.2 g of protein/kg body wt), and measurements were taken pre-, 75 min, and 150 min post-protein. Beat-to-beat blood pressure (Penaz method) was measured and segmental artery vascular resistance (VR, Doppler ultrasound) was calculated as segmental artery blood velocity ÷ mean arterial pressure. CPT-induced increases in segmental artery VR did not differ between trials (trial effect: P = 0.142) nor between men (heat stress: 1.5-±-1.0 mmHg/cm/s, normothermia: 1.4-±-1.0 mmHg/cm/s) and women (heat stress: 1.4-±-1.2 mmHg/cm/s, normothermia: 2.1-±-1.1 mmHg/cm/s) (group effect: P = 0.429). Reductions in segmental artery VR following oral protein loading did not differ between trials (trial effect: P = 0.080) nor between men (heat stress: −0.6-±-0.8 mmHg/cm/s, normothermia: −0.6-±-0.6 mmHg/cm/s) and women (heat stress: −0.5-±-0.5 mmHg/cm/s, normothermia: −1.1-±-0.6 mmHg/cm/s) (group effect: P = 0.204). Renal vasoconstrictor responses to the cold pressor test and vasodilator responses following an oral protein load during heat stress or normothermia do not differ between younger men and younger women in the early follicular phase of the menstrual cycle. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that women may be more at risk of becoming dehydrated during physical work in the heat in the early follicular phase (EF), compared with the late follicular (LF) and mid-luteal (ML) phases of the menstrual cycle when allowed free access to drink. Twelve healthy, eumenorrheic, unacclimated women (26 ± 5 yr) completed three trials (EF, LF, and ML phases) involving 4 h of exposure to 33.8 ± 0.8 °C, 54 ± 1% relative humidity. Each hour, participants walked on a treadmill for 30 min at a rate of metabolic heat production of 338 ± 9 W. Participants drank a cool, flavor-preferred non-caloric sport drink ad libitum. Nude body weight was measured pre- and post-exposure, and percent changes in body weight loss were interpreted as an index of changes in total body water. Total fluid intake and urine output were measured and sweat rate was estimated from changes in body mass corrected for fluid intake and urine output. Fluid intake was not different between phases (EF: 1,609 ± 919 mL; LF: 1,902 ± 799 mL; ML: 1,913 ± 671; P = 0.202). Total urine output (P = 0.543) nor sweat rate (P = 0.907) differed between phases. Percent changes in body mass were not different between phases (EF: -0.5 ± 0.9%; LF: -0.3 ± 0.9%; ML: -0.3 ± 0.7%; P = 0.417). This study demonstrates that the normal hormonal fluctuations that occur throughout the menstrual cycle do not alter fluid balance during physical work in the heat. [ABSTRACT FROM AUTHOR]

This study tested the hypothesis that, following exercise in the heat, motor task performance will be impaired when assessed simultaneously with a cognitive task. In a randomized, crossover and counterbalanced design, twelve healthy adults (23 ± 2 years, 5 women) completed four 10-minute exercise circuits involving upper and lower body exercise in a moderate (18.1 ± 1.7°C, 38 ± 10% relative humidity) and a hot (40.3 ± 1.1°C, 26 ± 5% relative humidity) environment. Experimental testing was completed in a temperate thermal environment before exercise (~25°C) and in either the moderate or hot environment following exercise. The 3 Back test (a test of working memory) was used as the cognitive task and postural sway was used as the motor task. Cognitive and motor task performance assessments were conducted both individually (solo) and simultaneously (dual). At the end of exercise, core temperature (by 0.4 ± 0.3°C, P < 0.001), heart rate (by 12 ± 18 bpm, P = 0.025), and mean skin temperature (by 7.6 ± 0.8°C, P < 0.001) were higher in the Hot trial compared to Moderate. During solo testing, postural sway increased from pre- to post-exercise in the Hot (P ≤ 0.028), but not the Moderate (P ≥ 0.261) trial. During dual testing, postural sway did not differ between trials (P ≥ 0.065) or over time (P ≥ 0.094). During solo testing, 3 Back performance did not differ between trials (P = 0.810) or over time (P = 0.707), but during dual testing 3 Back performance following exercise was reduced in the Hot compared to the Moderate trial (P = 0.028). Simultaneous assessment of motor and cognitive tasks reveals that motor performance is reduced following exercise in the heat. [ABSTRACT FROM AUTHOR]

Purpose: In a disabled submarine scenario, a pressurized rescue module (PRM) may be deployed to rescue survivors. If the PRM were to become disabled, conditions could become hot and humid exposing the occupants to heat stress. We tested the hypothesis that the rise in core temperature and fluid loss from sweating would increase with rising dry bulb temperature. Methods: Twelve males (age 22 ± 3 years; height 179 ± 7 cm; mass 77.4 ± 8.3 kg) completed this study. On three occasions, subjects were exposed to high humidity and either 28-, 32-, or 35°C for six hours in a dry hyperbaric chamber pressurized to 6.1 msw. Changes in core temperature (Tc) and body mass were recorded and linear regression lines fit to estimate the predicted rise in Tc and loss of fluid from sweating. Results: Heart rate was higher in the 35°C condition compared to the 28°C and 32°C conditions. Tc was higher in the 32°C condition compared to 28°C and higher in 35°C compared to the 28°C and 32°C conditions. Projected fluid loss in all of the tested conditions could exceed 6% of body mass after 24 hours of exposure endangering the health of sailors in a DISSUB or disabled PRM. A fluid intake of 1.0 to 3.5 L would be required to limit dehydration to 2% or 4% of initial mass depending upon condition. Conclusion: Prolonged exposure to 35°C conditions under pressure results in uncompensable heat stress. 32°C and 35°C exposures were compensable under these conditions but further research is required to elucidate the effect of increased ambient pressure on thermoregulation. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that thermal discomfort will be greater, mood will be worse, and physical symptoms of heat illness will be exacerbated with elevations in dry bulb temperature during exposure to >95% relative humidity disabled pressurized rescue module simulation. On three occasions, 15 healthy males (23 ± 3 years) sat in 32.1 ± 0.1°C, 33.1 ± 0.2°C or 35.0 ± 0.1°C, and 95 ± 2% relative humidity normobaric environments for eight hours. Thermal discomfort (visual analog scale), mood (profile of mood states), and physical symptoms of heat illness, ear-nose-throat, and muscle discomfort (environmental symptoms questionnaire) were assessed before and following each hour of exposure. Thermal discomfort was greater throughout the exposure in 35°C versus both 32°C and 33°C (p = 0.03) and did not differ between the latter conditions (p = 0.07). Mood worsened over time in all trials (p < 0.01) and was worse in 35°C compared to 32°C and 33°C after five hours of exposure (p = 0.05). Heat illness symptoms increased over time in all trials and was greater in 35°C versus 32°C and 33°C throughout the exposure (p = 0.04). Ear-nose-throat and muscle discomfort symptoms increased over time in all trials (p < 0.01) and were higher in 35°C versus 32°C and 33°C after the sixth hour of exposure (p = 0.02). In support of our hypothesis, mood was worse, physical symptoms of heat illness, and ear-nose-throat and muscle discomfort symptoms were exacerbated, and thermal discomfort was greater with elevations in dry bulb temperature during an eight-hour exposure to a >95% relative humidity disabled PRM simulation. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that, compared with normothermia, the increase in glomerular filtration rate (GFR) after an oral protein load (defined as the GFR reserve) is attenuated during moderate passive heat stress in young healthy adults. Sixteen participants (5 women; 26 ± 2 yr) completed two experimental visits, heat stress or a normothermic time-control, assigned in a block-randomized crossover design. During the heat stress trial, core temperature was increased by 0.6°C in the first hour before commencing a 2-min cold pressor test (CPT) to assess renal vasoconstrictor responses. One-hour post-CPT, subjects ingested a whey protein shake (1.2 g of protein/kg body wt), and measurements were taken pre-, 75, and 150 min postprotein. Segmental artery vascular resistance was calculated as the quotient of Doppler ultrasound-derived segmental artery blood velocity and mean arterial pressure and provided an estimate of renal vascular tone. GFR was estimated from creatinine clearance. The increase in segmental artery vascular resistance during the CPT was attenuated during heat stress (end CPT: 5.6 ± 0.9 vs. 4.7 ± 1.1 mmHg/cm/s, P = 0.024). However, the reduction in segmental artery vascular resistance in response to an oral protein load did not differ between heat stress (at 150 min: 1.9 ± 0.4 mmHg/cm/s) and normothermia (at 150 min: 1.8 ± 0.5 mmHg/cm/s; P = 0.979). The peak increase in creatinine clearance postprotein, independent of time, was attenuated during heat stress (+26 ± 19 vs. +16 ± 20 mL/ min, P = 0.013, n = 13). GFR reserve is diminished by mild passive heat stress. Moreover, renal vasoconstrictor responses are attenuated by mild passive heat stress, but renal vasodilator responses are maintained. [ABSTRACT FROM AUTHOR]

Wet bulb temperatures (Twet) during extreme heat events are commonly 31°C. Recent predictions indicate that Twet will approach or exceed 34°C. Epidemiological data indicate that exposure to extreme heat events increases kidney injury risk. We tested the hypothesis that kidney injury risk is elevated to a greater extent during prolonged exposure to Twet = 34°C compared with Twet = 31°C. Fifteen healthy men rested for 8 h in Twet = 31 (0)°C and Twet = 34 (0)°C. Insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP-2), and thioredoxin 1 (TRX-1) were measured from urine samples. The primary outcome was the product of IGFBP7 and TIMP-2 ([IGFBP7·TIMP-2]), which provided an index of kidney injury risk. Plasma interleukin-17a (IL-17a) was also measured. Data are presented at preexposure and after 8 h of exposure and as mean (SD) change from preexposure. The increase in [IGFBP7·TIMP-2] was markedly greater at 8 h in the 34°C [þ26.9 (27.1) (ng/mL)²/ 1,000) compared with the 31°C [þ6.2 (6.5) (ng/mL)²/1,000] trial (P < 0.01). Urine TRX-1, a marker of renal oxidative stress, was higher at 8 h in the 34°C [þ77.6 (47.5) ng/min] compared with the 31°C [þ16.2 (25.1) ng/min] trial (P < 0.01). Plasma IL-17a, an inflammatory marker, was elevated at 8 h in the 34°C [þ199.3 (90.0) fg/dL; P < 0.01] compared with the 31°C [þ9.0 (95.7) fg/dL] trial. Kidney injury risk is exacerbated during prolonged resting exposures to Twet experienced during future extreme heat events (34°C) compared with that experienced currently (31°C), likely because of oxidative stress and inflammatory processes. [ABSTRACT FROM AUTHOR]

Objective: Movement efficiency can be quantified during physical tasks by measuring the rate of change of acceleration (jerk). Jerk captures the smoothness of a motion and has been used to quantify movement for upper extremity and torso-based tasks. We collected triaxial accelerometer data during four physical tasks commonly performed in the work place to determine if jerk increases with physiologic strain. Methods: Participants completed a circuit of activities that mimicked the demands of manual labor in hot (40°C) and temperate (18°C) conditions. The circuit included walking on a treadmill carrying a load on the shoulder, lifting objects from the floor to the table, using a dead blow to strike the end of a heavy steel beam, and a kneeling rope pull. After the 9 min circuit, the participant had a standing rest for 1 min before repeating the circuit 3 additional times. Participants were instrumented with four 3-axis accelerometers (Actigraph wGT3X) secured to the torso, wrist, and upper arm. Results: There were 20 trials in the hot condition and 12 trials in the temperate condition. Heart rate and core body temperature increased during both protocols (p < 0.001). Measures of jerk varied by accelerometer location and activity. During treadmill walking, the wrist, torso, arm accelerometers measured higher jerk during the fourth circuit in the hot condition. During the lifting task, mean jerk increased in the hot condition in all accelerometers. Max jerk increased in the temperate condition in the arm accelerometer and jerk cost increased in the hot condition in the torso and arm accelerometers. Conclusions: Forty minutes of paced work performed in the heat resulted in increased acceleration and jerk in accelerometers placed on the torso, arm, and wrist. The accelerometers most consistently reporting these changes were task specific and suggest that a limited number of worn sensors could identify the onset of fatigue and increased injury risk. [ABSTRACT FROM AUTHOR]

Occupational heat exposure is linked to the development of kidney injury and disease in individuals who frequently perform physically demanding work in the heat. For instance, in Central America, an epidemic of chronic kidney disease of nontraditional origin (CKDnt) is occurring among manual laborers, whereas potentially related epidemics have emerged in India and Sri Lanka. There is growing concern that workers in the United States suffer with CKDnt, but reports are limited. One of the leading hypotheses is that repetitive kidney injury caused by physical work in the heat can progress to CKDnt. Whether heat stress is the primary causal agent or accelerates existing underlying pathology remains contested. However, the current evidence supports that heat stress induces tubular kidney injury, which is worsened by higher core temperatures, dehydration, longer work durations, muscle damaging exercise, and consumption of beverages containing high levels of fructose. The purpose of this narrative review is to identify occupations that may place US workers at greater risk of kidney injury and CKDnt. Specifically, we reviewed the scientific literature to characterize the demographics, environmental conditions, physiological strain (i.e., core temperature increase, dehydration, heart rate), and work durations in sectors typically experiencing occupational heat exposure, including farming, wildland firefighting, landscaping, and utilities. Overall, the surprisingly limited available evidence characterizing occupational heat exposure in US workers supports the need for future investigations to understand this risk of CKDnt. [ABSTRACT FROM AUTHOR]

Military and civilian emergency situations often involve prolonged exposures to warm and very humid environments. We tested the hypothesis that increases in core temperature and body fluid losses during prolonged exposure to warm and very humid environments are dependent on dry bulb temperature. On three occasions, 15 healthy males (23 ± 3 yr) sat in 32.1 ± 0.1°C, 33.1 ± 0.2°C, or 35.0 ± 0.1°C and 95 ± 2% relative humidity normobaric environments for 8 h. Core temperature (telemetry pill) and percent change in body weight, an index of changes in total body water occurring secondary to sweat loss, were measured every hour. Linear regression models were fit to core temperature (over the final 4 h) and percent changes in body weight (over the entire 8 h) for each subject. These equations were used to predict core temperature and percent changes in body weight for up to 24 h. At the end of the 8-h exposure, core temperature was higher in 35°C (38.2 ± 0.4°C, P < 0.01) compared with 32°C (37.2 ± 0.2°C) and 33°C (37.5 ± 0.2°C). At this time, percent changes in body weight were greater in 35°C (-1.9 ± 0.5%) compared with 32°C (-1.4 ± 0.3%, P < 0.01) but not 33°C (-1.6 ± 0.6%, P = 0.17). At 24 h, predicted core temperature was higher in 35°C (39.2 ± 1.4°C, P < 0.01) compared with 32°C (37.6 ± 0.9°C) and 33°C (37.5 ± 0.9°C), and predicted percent changes in body weight were greater in 35°C (-6.1 ± 2.4%) compared with 32°C (-4.6 ± 1.5%, P = 0.04) but not 33°C (-5.3 ± 2.0%, P = 0.43). Prolonged exposure to 35°C, but not 32°C or 33°C, dry bulb temperatures and high humidity is uncompensable heat stress, which exacerbates body fluid losses. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

The purpose of this study was to test the hypothesis that consuming a soft drink (i.e., a highfructose, caffeinated beverage) during and following exercise in the heat elevates biomarkers of acute kidney injury (AKI) in humans. Twelve healthy adults drank 2 liters of an assigned beverage during 4 h of exercise in the heat [35.1 (0.1)°C, 61 (5)% relative humidity] in counterbalanced soft drink and water trials, and ≥1 liter of the same beverage after leaving the laboratory. Stage 1 AKI (i.e., increased serum creatinine [0.30 mg/dl) was detected at postexercise in 75% of participants in the Soft Drink trial compared with 8% in Water trial (P = 0.02). Furthermore, urinary neutrophil gelatinase-associated lipocalin (NGAL), a biomarker of AKI, was higher during an overnight collection period after the Soft Drink trial compared with Water in both absolute concentration [6 (4) ng/dl vs. 5 (4) ng/dl, P < 0.04] and after correcting for urine flow rate [6 (7) (ng/dl)/(ml/min) vs. 4 (4) (ng/dl)/(ml/min), P = 0.03]. Changes in serum uric acid from preexercise were greater in the Soft Drink trial than the Water trial at postexercise (P < 0.01) and 24 h (P = 0.05). There were greater increases from preexercise in serum copeptin, a stable marker of vasopressin, at postexercise in the Soft Drink trial (P < 0.02) than the Water trial. These findings indicate that consuming a soft drink during and following exercise in the heat induces AKI, likely via vasopressin- mediated mechanisms. [ABSTRACT FROM AUTHOR]

Purpose: We tested the hypothesis that elevations in biomarkers of acute kidney injury are influenced by the magnitude of hyperthermia and dehydration elicited by two common firefighter work durations. Methods: Twenty-nine healthy adults (10 females) wearing firefighter protective clothing completed two randomized trials where they walked at 4.8 km⋅h-1, 5% grade in a 38°C, 50% RH environment. In the short trial, subjects completed two 20-min exercise bouts. In the long trial (LONG), subjects completed three 20-min exercise bouts. Each exercise bout was separated by 10 min of standing rest in an ~20°C environment. Venous blood samples were obtained before and immediately after exercise, and after 1 h recovery. Dependent variables included changes in core temperature, body weight, plasma volume, serum creatinine, and plasma neutrophil gelatinase-associated lipocalin, a marker of renal tubule injury. Results: Changes in core temperature (+2.0°C ± 0.7°C vs +1.1 °C ± 0.4°C, P < 0.01), body weight (-0.9% ± 0.6% vs -0.5% ± 0.5%, P < 0.01), and plasma volume (-11% ± 5% vs -8% ± 6%, P < 0.01) during exercise were greater in LONG. Increases in creatinine were higher in LONG postexercise (0.18 ± 0.15 vs 0.08 ± 0.07 mg⋅dL-1, P < 0.01) and after recovery (0.21 ± 0.16 vs 0.14 ± 0.10 mg⋅dL-1, P < 0.01). Increases in neutrophil gelatinase-associated lipocalin were greater in LONG postexercise (27.0 ± 20.5 vs 12.7 ± 18.0 ng⋅mL-1, P = 0.01) and after recovery (16.9 ± 15.6 vs 1.5 ± 15.1 ng⋅mL-1, P = 0.02). Conclusions: Biomarkers of acute kidney injury are influenced by the magnitude of hyperthermia and hypovolemia elicited by exercise in the heat. [ABSTRACT FROM AUTHOR]

Purpose: We tested the hypothesis that physiological and perceptual heat strain is exacerbated on the second of back-to-back days of fire suppression work despite evidence of full recovery. Methods: Twenty-six career and volunteer firefighters (age = 31 ± 8 yr) completed 20 min of near maximal fire suppression work on consecutive days. Dependent variables were core temperature, heart rate, perceived exertion, and thermal sensation, which were measured before and after fire suppression. Urine specific gravity and body mass were also measured upon arrival at the fire academy as an index of hydration and recovery between days. Results: Urine specific gravity (1.007 ± 0.006 vs 1.005 ± 0.006), body mass (87.7 ± 16.1 vs 87.8 ± 16.0 kg), heart rate (77 ± 14 vs 76 ± 14 bpm), and core temperature (37.2°C ± 0.4°C vs 37.1°C ± 0.7°C) were not different upon arrival on day 1 compared with day 2 (P ≥ 0.26). The increase in core temperature during fire suppression was higher on day 2 (0.7°C ± 0.3°C vs 1.1°C ± 0.5°C, P < 0.01). Heart rate did not differ (after fire suppression: day 1 = 174 ± 19, day 2 = 169 ± 30 bpm, P = 0.60). The magnitude of increase in perceived exertion during fire suppression was greater on day 2 (6.7 ± 1.6 vs 7.4 ± 1.6 a.u., P < 0.01). Absolute thermal sensation at the end of fire suppression was greater on day 2 (3.8 ± 0.8 vs 4.3 ± 0.6 a.u., P < 0.01). Conclusions: Physiological and perceptual heat strain is higher on the second of back-to-back days of fire suppression work. [ABSTRACT FROM AUTHOR]

During normothermia, a reduction in near-infrared spectroscopy (NIRS)-derived tissue oxygen saturation (SO2) is an indicator of central hypovolemia. Hyperthermia increases skin blood flow and reduces tolerance to central hypovolemia, both of which may alter the interpretation of tissue SO2 during central hypovolemia. This study tested the hypothesis that maximal reductions in tissue SO2 would be similar throughout normothermic and hyperthermic central hypovolemia to presyncope. Ten healthy males (means ± SD; 32 ± 5 yr) underwent central hypovolemia via progressive lower-body negative pressure (LBNP) to presyncope during normothermia (skin temperature ≈34°C) and hyperthermia (+1.2 ± 0.1°C increase in internal temperature via a water-perfused suit, skin temperature ≈39°C). NIRS-derived forearm (flexor digitorum profundus) tissue SO2 was measured throughout and analyzed as the absolute change from pre-LBNP. Hyperthermia reduced (P < 0.001) LBNP tolerance by 49 ± 33% (from 16.7 ± 7.9 to 7.2 ± 3.9 min). Pre-LBNP, tissue SO2 was similar (P = 0.654) between normothermia (74 ± 5%) and hyperthermia (73 ± 7%). Tissue SO2 decreased (P < 0.001) throughout LBNP, but the reduction from pre-LBNP to presyncope was greater during normothermia (-10 ± 6%) than during hyperthermia (-6 ± 5%; P = 0.041). Contrary to our hypothesis, these findings indicate that hyperthermia is associated with a smaller maximal reduction in tissue SO2 during central hypovolemia to presyncope. [ABSTRACT FROM AUTHOR]

Heat-related decreases in cerebral perfusion are partly the result of ventilatory-related reductions in arterial CO2 tension. Cerebral perfusion likely contributes to an individual's tolerance to a challenge like lower body negative pressure (LBNP). Thus increasing cerebral perfusion may prolong LBNP tolerance. This study tested the hypothesis that a hypercapniainduced increase in cerebral perfusion improves LBNP tolerance in hyperthermic individuals. Eleven individuals (31 ± 7 yr; 75 ± 12 kg) underwent passive heat stress (increased intestinal temperature ~1.3°C) followed by a progressive LBNP challenge to tolerance on two separate days (randomized). From 30 mmHg LBNP, subjects inhaled either (blinded) a hypercapnic gas mixture (5% CO2, 21% oxygen, balanced nitrogen) or room air (SHAM). LBNP tolerance was quantified via the cumulative stress index (CSI). Mean middle cerebral artery blood velocity (MCAvmean,) and end-tidal CO2 (PETCO2) were also measured. CO2 inhalation of 5% increased PETCO2 at ~40 mmHg LBNP (by 16 ± 4 mmHg) and at LBNP tolerance (by 18 ± 5 mmHg) compared with SHAM (P 0.01). Subsequently, MCAvmean was higher in the 5% CO2 trial during ~40 mmHg LBNP (by 21 ± 12 cm/s, ~31%) and at LBNP tolerance (by 18 ± 10 cm/s, ~25%) relative to the SHAM (P 0.01). However, hypercapnia-induced increases in MCAvmean did not alter LBNP tolerance (5% CO2 CSI: 339 ± 155 mmHg X min; SHAM CSI: 273 ± 158 mmHg X min; P = 0.26). These data indicate that inhaling a hypercapnic gas mixture increases cerebral perfusion during LBNP but does not improve LBNP tolerance when hyperthermic. [ABSTRACT FROM AUTHOR]

Hyperthermia reduces the capacity to withstand a simulated hemorrhagic challenge, but volume loading preserves this capacity. This study tested the hypotheses that acute volume expansion during hyperthermia increases cerebral perfusion and attenuates reductions in cerebral perfusion during a simulated hemorrhagic challenge induced by lower- body negative pressure (LBNP). Eight healthy young male subjects underwent a supine baseline period (pre-LBNP), followed by 15- and 30-mmHg LBNP while normothermic, hyperthermic (increased pulmonary artery blood temperature ~1.1°C), and following acute volume infusion while hyperthermic. Primary dependent variables were mean middle cerebral artery blood velocity (MCAvmean), serving as an index of cerebral perfusion; mean arterial pressure (MAP); and cardiac output (thermodilution). During baseline, hyperthermia reduced MCAvmean (P = 0.001) by 12 ± 9% relative to normothermia. Volume infusion while hyperthermic increased cardiac output by 2.8 ± 1.4 l/min (P < 0.001), but did not alter MCAvmean (P = 0.99) or MAP (P = 0.39) compared with hyperthermia alone. Relative to hyperthermia, at 30-mmHg LBNP acute volume infusion attenuated reductions (P < 0.001) in cardiac output (by 2.5 ± 0.9 l/min; P < 0.001), MAP (by 5 ± 6 mmHg; P = 0.004), and MCAvmean (by 12 ± 13%; P = 0.002). These data indicate that acute volume expansion does not reverse hyperthermia-induced reductions in cerebral perfusion pre-LBNP, but that it does attenuate reductions in cerebral perfusion during simulated hemorrhage in hyperthermic humans. [ABSTRACT FROM AUTHOR]

This study aimed to identify whether reductions in peak oxygen uptake (VO2peak) dictate performance outcomes during 30 min of self-paced exercise in the heat, which is expected to induce minimal hyperthermia. On 4 occasions, 11 male subjects completed peak and self-paced exercise in both hot (HOT, 40.2 ± 0.3 °C) and moderate (MOD; 20.4 ± 0.7 °C) conditions. During peak exercise, submaximal oxygen uptake (VO2) was ∼8% higher in HOT, but VO2peak (MOD, 4.64 ± 0.83 L·min–1; HOT, 4.54 ± 0.77 L·min-1) and peak cardiac output (Qpeak) were similar. Self-paced exercise performance was reduced by ∼21% in HOT. VO2 was similar through 15 min, but lower in HOT thereafter. Relative to MOD, this represented a higher and lower %VO2peak during the initial and latter stages. Cardiac output was similar in both trials (MOD, 31.6 ± 6.6 L·min–1; HOT, 30.1 ± 6.0 L·min–1), representing a similar percentage of Qpeak throughout. Rectal temperature was similar in both conditions until 30 min (MOD, 38.5 ± 0.3 °C; HOT, 38.7 ± 0.3 °C), while skin temperature was higher throughout in HOT (mean: MOD, 32.4 ± 1.1 °C; HOT, 37.3 ± 0.4 °C). Perceived exertion rose similarly in both conditions, while thermal discomfort was higher in HOT. These data indicate that when only skin temperature is elevated, reductions in exercise performance during moderate-duration self-paced exercise are not associated with changes in VO2peak. Rather, increases in VO2 at a given submaximal external workload and (or) thermal discomfort appear to play a larger role. [ABSTRACT FROM AUTHOR]

An epidemic of chronic kidney disease (CKD) is occurring in laborers who undertake physical work in hot conditions. Rodent data indicate that heat exposure causes kidney injury, and when this injury is regularly repeated it can elicit CKD. Studies in humans demonstrate that a single bout of exercise in the heat increases biomarkers of acute kidney injury (AKI). Elevations in AKI biomarkers in this context likely reflect an increased susceptibility of the kidneys to AKI. Data largely derived from animal models indicate that the mechanism(s) by which exercise in the heat may increase the risk of AKI is multifactorial. For instance, heat-related reductions in renal blood flow may provoke heterogenous intrarenal blood flow. This can promote localized ischemia, hypoxemia and ATP depletion in renal tubular cells, which could be exacerbated by increased sodium reabsorption. Heightened fructokinase pathway activity likely exacerbates ATP depletion occurring secondary to intrarenal fructose production and hyperuricemia. Collectively, these responses can promote inflammation and oxidative stress, thereby increasing the risk of AKI. Equivalent mechanistic evidence in humans is lacking. Such an understanding could inform the development of countermeasures to safeguard the renal health of laborers who regularly engage in physical work in hot environments. [ABSTRACT FROM AUTHOR]

• Motivational conflict decreases warm-seeking behavior during cold exposure. • The effect of motivational conflict on cooling during heat exposure was unknown. • It was found that voluntary cooling is lower when physical effort is required. • These findings elucidate the control of cool-seeking behavior during heat events. 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. [ABSTRACT FROM AUTHOR]