Strategies to mitigate acute kidney injury risk during physical work in hot environments.

Prolonged physical work in the heat can reduce renal function and increase the risk of acute kidney injury (AKI). This is concerning given that the latest climate change projections forecast a rise in global temperature as well as the frequency, intensity, and duration of heatwaves. This means that outdoor and indoor workers in the agriculture or construction industries will be exposed to higher heat stress in the years ahead. Several studies indicate a higher incidence of chronic kidney disease from nontraditional origins (CKDnt) in individuals exposed to high temperatures, intense physical work, and/or recurrent dehydration. It has been proposed that prolonged physical work in the heat accompanied by dehydration results in recurrent episodes of AKI that ultimately lead to permanent kidney damage and the development of CKDnt. Thus, there is a need to identify and test strategies that can alleviate AKI risk during physical work in the heat. The purpose of this review is to present strategies that might prevent and mitigate the risk of AKI induced by physical work in the heat.

Creatinine clearance is maintained in a range of wet-bulb globe temperatures and work-rest ratios during simulated occupational heat stress.

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 non-compliance would result in a reduction in GFR compared to a work-rest matched compliant trial. Twelve healthy adults completed five trials (four NIOSH compliant, one non-compliant) that consisted of four hours of exposure to a range of WBGTs. Subjects walked on a treadmill (Hprod: ~430 W) and work-rest ratios (work per hour: 60, 45, 30, 15 min) were prescribed as a function of WBGT (24°C, 26.5°C, 28.5°C, 30°C, 36°C), and subjects drank a sport drink ad libitum. Peak core temperature (TC) and percentage change in body weight (%DBW) 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 vs. non-compliant trials (p<0.001). %DBW did not differ among NIOSH compliant trials (p=0.131) or between compliant vs. non-compliant trials (p=0.185). Creatinine clearance did not change or differ among compliant trials (p³0.079). Creatinine clearance did not change or differ between compliant vs. non-compliant trials (p³0.661). Compliance with the NIOSH recommendations maintained GFR. Surprisingly, despite a greater heat strain in a non-compliant trial, GFR was maintained highlighting the potential relative importance of hydration.

Renal vascular control during normothermia and passive heat stress does not differ between healthy younger men and women.

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.NEW & NOTEWORTHY The mechanisms underlying greater heat-induced acute kidney injury risk in men versus women remain unknown. This study examined renal vascular control, including both vasodilatory (oral protein load) and vasoconstrictor (cold presser test) responses, during normothermia and heat stress and compared these responses between men and women. The results indicated that in both conditions neither renal vasodilatory nor vasoconstrictor responses differ between younger men and younger women.

Activation of cardiac parasympathetic and sympathetic activity occurs at different skin temperatures during face cooling.

Sufficiently cold-water temperatures (<7°C) are needed to elicit the sympathetic response to the cold pressor test using the hand. However, it is not known if stimulating the trigeminal nerve via face cooling, which increases both sympathetic and cardiac parasympathetic activity, also has a threshold temperature. We tested the hypothesis that peak autonomic activation during a progressive face cooling challenge would be achieved when the stimulus temperature is ≤7°C. Twelve healthy participants (age: 25 ± 3 yr, four women) completed our study. Six pliable bags, each containing water or an ice slurry (34°C, 28°C, 21°C, 14°C, 7°C, and 0°C) were applied sequentially to participants' forehead, eyes, and cheeks for 5 min each. Mean arterial pressure (photoplethysmography; index of sympathetic activity) and heart rhythm (3-lead ECG) were averaged in 1-min increments at the end of baseline and throughout each temperature condition. Heart rate variability in the time [(root mean square of successive differences (RMSSD)] and frequency [high-frequency (HF) power] domains was used to estimate cardiac parasympathetic activity. Data are presented as the increase from baseline ± SD. Mean arterial pressure only increased from baseline in the 7°C (13.1 ± 10.3 mmHg; P = 0.018) and 0°C (25.2 ± 7.8 mmHg; P < 0.001) conditions. Only the 0°C condition increased RMSSD (160.6 ± 208.9 ms; P = 0.009) and HF power (11,450 ± 14,555 ms2; P = 0.014) from baseline. Our data indicate that peak increases in sympathetic activity during face cooling are initiated at a higher forehead skin temperature than peak increases in cardiac parasympathetic activity.

Interactive effects of exercise intensity and recovery posture on postexercise hypotension.

Postexercise reduction in blood pressure, termed postexercise hypotension (PEH), is relevant for both acute and chronic health reasons and potentially for peripheral cardiovascular adaptations. We investigated the interactive effects of exercise intensity and recovery postures (seated, supine, and standing) on PEH. Thirteen normotensive men underwent a V̇o2max test on a cycle ergometer and five exhaustive constant load trials to determine critical power (CP) and the gas exchange threshold (GET). Subsequently, work-matched exercise trials were performed at two discrete exercise intensities (10% > CP and 10% < GET), with 1 h of recovery in each of the three postures. For both exercise intensities, standing posture resulted in a more substantial PEH (all P < 0.01). For both standing and seated recovery postures, the higher exercise intensity led to larger reductions in systolic [standing: -33 (11) vs. -21 (8) mmHg; seated: -34 (32) vs. -17 (37) mmHg, P < 0.01], diastolic [standing: -18 (7) vs. -8 (5) mmHg; seated: -10 (10) vs. -1 (4) mmHg, P < 0.01], and mean arterial pressures [-13 (8) vs. -2 (4) mmHg, P < 0.01], whereas in the supine recovery posture, the reduction in diastolic [-9 (9) vs. -4 (3) mmHg, P = 0.08) and mean arterial pressures [-7 (5) vs. -3 (4) mmHg, P = 0.06] was not consistently affected by prior exercise intensity. PEH is more pronounced during recovery from exercise performed above CP versus below GET. However, the effect of exercise intensity on PEH is largely abolished when recovery is performed in the supine posture.NEW & NOTEWORTHY The magnitude of postexercise hypotension is greater following the intensity above the critical power in a standing position.

Relation between resting spleen volume and apnea-induced increases in hemoglobin mass.

Introduction: Indigenous populations renowned for apneic diving have comparatively large spleen volumes. It has been proposed that a larger spleen translates to heightened apnea-induced splenic contraction and elevations in circulating hemoglobin mass (Hbmass), which, in theory, improves O2 carrying and/or CO2/pH buffering capacities. However, the relation between resting spleen volume and apnea- induced increases in Hbmass is unknown. Therefore, we tested the hypothesis that resting spleen volume is positively related to apnea-induced increases in total Hbmass. Methods: Fourteen healthy adults (six women; 29 ± 5 years) completed a two-minute carbon monoxide rebreathe procedure to measure pre-apneas Hbmass and blood volume. Spleen length, width, and thickness were measured pre-and post-five maximal apneas via ultrasound. Spleen volume was calculated via the Pilström equation (test-retest CV:2 ± 2%). Hemoglobin concentration ([Hb]; g/dl) and hematocrit (%) were measured pre- and post-apneas via capillary blood samples. Post-apneas Hbmass was estimated as post-apnea [Hb] x pre-apnea blood volume. Data are presented as mean ± SD. Results: Spleen volume decreased from pre- (247 ± 95 mL) to post- (200 ± 82 mL, p<0.01) apneas. [Hb] (14.6 ± 1.2 vs. 14.9 ± 1.2 g/dL, p<0.01), hematocrit (44 ± 3 vs. 45 ± 3%, p=0.04), and Hbmass (1025 ± 322 vs. 1046 ± 339 g, p=0.03) increased from pre- to post-apneas. Pre-apneas spleen volume was unrelated to post-apneas increases in Hbmass (r=-0.02, p=0.47). O2 (+28 ± 31 mL, p<0.01) and CO2 (+31 ± 35 mL, p<0.01) carrying capacities increased post-apneas. Conclusion: Larger spleen volume is not associated with a greater rise in apneas-induced increases in Hbmass in non-apnea-trained healthy adults.

Diagnostic accuracy of thermal, hydration, and heart rate assessments in discriminating positive acute kidney injury risk following physical work in the heat.

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.

Aerobic exercise performance is reduced following prolonged cold-water immersion.

Background: We tested the hypotheses that self-paced aerobic exercise performance is reduced following four hours of cold-water immersion when breathing air and further reduced when breathing 100% oxygen (O2). Nine healthy adults (four women; age 24 ± 3 years; body fat 17.9 ± 6.4%; VO2max 48±9 mL • kg • minute⁻¹) completed three visits: a no-immersion control trial and two experimental trials consisting of a four-hour cold-water immersion (20.1±0.3°C) either breathing air (FIO2 = 0.21) or O2 (FIO2 = 1.0). During the no-immersion control trial and following immersion in the experimental trials, subjects first completed a 60-minute ruck-march carrying 20% of body mass in a rucksack, immediately followed by an unweighted, self-paced 5-km time trial on a motorized treadmill. Core temperature, heart rate, and rating of perceived exertion were recorded every 1,000 meters during the 5-km time trial. Data are presented mean± SD. Time trial performance was reduced following immersion in both the 100% O2 trial (32±6 minutes; p=0.01) and air trial (32±5 minutes; p=0.01) compared to the control trial (28± 4 minutes). However, there was no difference between the 100% O2 and air trials (p=0.86). Heart rate, core temperature, and rating of perceived exertion increased during the time trial (time effect: p≺0.01), but were not different between trials (trial effect: p≥0.33). These findings suggest that prolonged cold-water immersion attenuates self-paced aerobic exercise performance, but does not appear to be further affected by breathing gas type.

Water consumption patterns impact hydration markers in males working in accordance with the National Institute for Occupational Safety and Health recommendations.

The impact of water consumption bolus volume and frequency on hydration biomarkers during work in the heat is unknown. In a randomized, crossover fashion, eight males consumed either 500 mL of water every 40 min or 237 mL of water every 20 min during 2 hr of continuous walking at 6.4 kph, 1.0% grade in a 34 °C/30% relative humidity environment, followed by 2 hr of rest. Hydration biomarkers and variables were assessed pre-work, post-work, and after the 2 hr recovery. There were no differences in body mass between trials at any time point (all p > 0.05). Percent change in plasma volume during work was not different when 237 mL of water was repeatedly consumed (-1.6 ± 8.2%) compared to 500 mL of water (-1.3 ± 3.0%, p = 0.92). Plasma osmolality was maintained over time (p = 0.55) with no difference between treatments (p = 0.21). When consuming 500 mL of water repeatedly, urine osmolality was lower at recovery (205 ± 108 mOsmo/L) compared to pre-work (589 ± 95 mOsmo/L, p < 0.01), different from repeatedly consuming 237 mL of water which maintained urine osmolality from pre-work (548 ± 144 mOsmo/L) through recovery (364 ± 261 mOsmo/L, p = 0.14). Free water clearance at recovery was greater with repeated consumption of 500 mL of water (1.2 ± 1.0 mL/min) compared to 237 mL of water (0.4 ± 0.8 mL/min, p = 0.02). Urine volume was not different between treatments post-work (p = 0.62), but greater after 2 hr of recovery when repeatedly consuming 500 mL of water compared to 237 mL (p = 0.01), leading to greater hydration efficiency upon recovery with repeated consumption of 237 mL of water (68 ± 12%) compared to 500 mL (63 ± 14%, p = 0.01). Thirst and total gastrointestinal symptom scores were not different between treatments at any time point (all p > 0.05). Body temperatures and heart rate were not different between treatments at any time point (all p > 0.05). Drinking larger, less frequent water boluses or drinking smaller, more frequent water boluses are both reasonable strategies to promote adequate hydration and limit changes in body mass in males completing heavy-intensity work in the heat.

Glomerular filtration rate reserve is reduced during mild passive heat stress in healthy young adults.

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.

Increased spleen volume provoked by temperate head-out-of-water immersion.

This study tested the hypotheses that 1) spleen volume increases during head-out-of-water immersion (HOWI) and returns to pre-HOWI values postdiuresis, and 2) the magnitude of apnea-induced spleen contraction increases when preapnea spleen volume is elevated. Spleen volume was measured before and after a set of five apneas in 12 healthy adults (28 ± 5 yr, 3 females) before, during (at 30 and 150 min), and 20 min after temperate temperature (36 ± 1°C) HOWI. At each time point, spleen length, width, and thickness were measured via ultrasound, and spleen volume was calculated using the Pilström equation. Compared with pre-HOWI (276 ± 88 mL), spleen volume was elevated at 30 (353 ± 94 mL, P < 0.01) and 150 (322 ± 87 mL, P < 0.01) min of HOWI but returned to pre-HOWI volume at post-HOWI (281 ± 90 mL, P = 0.58). Spleen volume decreased from pre- to postapnea bouts at each time point (P < 0.01). The magnitude of reduction in spleen volume from pre- to postapneas was elevated at 30 min of HOWI (-69 ± 24 mL) compared with pre-HOWI (-52 ± 20 mL, P = 0.04) but did not differ from pre-HOWI at 150 min of HOWI (-54 ± 16 mL, P = 0.99) and post-HOWI (-50 ± 18 mL, P = 0.87). Thus, spleen volume is increased throughout 180 min of HOWI, and whereas apnea-induced spleen contraction is augmented after 30 min of HOWI, the magnitude of spleen contraction is unaffected by HOWI thereafter.

Biomarkers of heatstroke-induced organ injury and repair.

NEW FINDINGS: What is the topic of this review? The status and potential role of novel biological markers (biomarkers) that can help identify the patients at risk of organ injury or long-term complications following heatstroke. What advances does it highlight? Numerous biomarkers were identified related to many aspects of generalized heatstroke-induced cellular injury and tissue damage, and heatstroke-provoked cardiovascular, renal, cerebral, intestinal and skeletal muscle injury. No novel biomarkers were identified for liver or lung injury. ABSTRACT: Classic and exertional heatstroke cause acute injury and damage across numerous organ systems. Moreover, heatstroke survivors may sustain long-term neurological, cardiovascular and renal complications with a persistent risk of death. In this context, biomarkers, defined as biological samples obtained from heatstroke patients, are needed to detect early organ injury, and predict outcomes to develop novel organ preservation therapeutic strategies. This narrative review provides preliminary insights that will guide the development and future utilization of these biomarkers. To this end, we have identified numerous biomarkers of widespread heatstroke-associated cellular injury, tissue damage and repair (extracellular heat shock proteins 72 and 60, high mobility group box protein 1, histone H3, and interleukin-1α), and other organ-specific biomarkers including those related to the cardiovascular system (cardiac troponin I, endothelium-derived factors, circulation endothelial cells, adhesion molecules, thrombomodulin and von Willebrand factor antigen), the kidneys (plasma and urinary neutrophil gelatinase-associated lipocalin), the intestines (intestinal fatty acid-binding protein 2), the brain (serum S100ß and neuron-specific enolase) and skeletal muscle (creatine kinase, myoglobin). No specific biomarkers have been identified so far for liver or lung injury in heatstroke. Before translating the identified biomarkers into clinical practice, additional preclinical and clinical prospective studies are required to further understand their clinical utility, particularly for the biomarkers related to long-term post-heatstroke health outcomes.

Markers of kidney tubular and interstitial injury and function among sugarcane workers with cross-harvest serum creatinine elevation.

OBJECTIVES: Serum creatinine (SCr) is a routine marker of kidney injury but also increases with dehydration and muscular work. This study was to elucidate whether increase in SCr is associated with more specific markers of kidney tubular and interstitial injury and function, during prolonged heat stress among workers at high risk of chronic kidney disease of non-traditional origin (CKDnt). METHODS: Urine monocyte chemoattractant protein-1 (MCP-1), kidney injury molecule-1 (KIM-1), calbindin, glutathione S-transferase-π (GST-π), clusterin, interleukin 18 and albumin, fractional excretion of potassium (FEK), blood haemoglobin, serum potassium, ferritin and erythropoietin were measured before and after harvest in a sample of 30 workers with a ≥0.3 mg/dL SCr increase across harvest (cases), and 53 workers with stable SCr (controls). RESULTS: Urine MCP-1 (p for differential cross-harvest trend <0.001), KIM-1 (p=0.002), calbindin (p=0.02), GST-π (p=0.04), albumin (p=0.001) and FEK (p<0.001) increased in cases, whereas blood haemoglobin (p<0.001) and serum erythropoietin (p<0.001) decreased. CONCLUSION: Several markers of tubular and interstitial injury and function changed as SCr increased across a harvest season, supporting the use of SCr as an indicator of kidney injury in physically active workers regularly exposed to heat stress. Repeated injury similar to that described here, and continued work under strenuous and hot conditions with similarly elevated injury markers is likely to worsen and possibly initiate CKDnt.

Ultrasonographic Inferior Vena Cava Measurement is More Sensitive Than Vital Sign Abnormalities for Identifying Moderate and Severe Hemorrhage.

BACKGROUND: Ultrasound inferior vena cava (IVC) diameter has been shown to decrease in response to hemorrhage. IVC diameter cut points to identify moderate and severe blood loss have not been established. OBJECTIVES: This study sought to find ultrasound IVC diameter cut points to identify moderate and severe hemorrhage and assess the performance of these cut points vs. vital sign abnormalities. METHODS: This is a secondary analysis of data from a study that described changes in vital signs and sonographic measurements of the IVC during a lower body negative pressure model of hemorrhage. Using receiver operator curve analyses, optimal cut points for identifying moderate and severe hemorrhage were identified. The ability of these cut points to identify hemorrhage in patients with no vital sign abnormalities was then assessed. RESULTS: In both long- and short-axis views, maximum and minimum IVC diameters (IVCmax and IVCmin) were significantly lower than baseline in severe blood loss. The optimal cut point for IVCmax in both axes was found to be ≤ 0.8 cm. This cut point is able to distinguish between no blood loss vs. moderate blood loss, and no blood loss vs. severe blood loss. The optimal cut point for IVCmin was variable between axes and blood loss severity. IVC diameter cut points obtained were able to identify hemorrhage in patients with no vital sign abnormalities. CONCLUSION: An ultrasound IVCmax of ≤ 0.8 cm may be useful in identifying moderate and severe hemorrhage before vital sign abnormalities are evident.

Physical symptoms provoked by normobaric hot and humid disabled pressurized rescue module scenarios.

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.

Thermoregulation during a six-hour exposure to warm, humid hyperbaric conditions.

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. Conclusions: 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.

Do the National Institute for Occupational Safety and Health recommendations for working in the heat prevent excessive hyperthermia and body mass loss in unacclimatized males?

The National Institute for Occupational Safety and Health recommendations for work in the heat suggest workers consume 237 mL of water every 15-20 min and allow for continuous work at heavy intensities in hot environments up to 34 °C and 30% relative humidity. The goal was to determine whether the National Institute for Occupational Safety and Health recommendations prevented core temperature from exceeding 38.0 °C and greater than 2% body mass loss during heavy-intensity work in the heat. Eight males consumed 237 mL of water every 20 min during 2 hr of continuous heavy-intensity walking (6.4 kph, 1% grade) in a 34 °C/30% relative humidity environment, in accordance with the National Institute for Occupational Safety and Health recommendations. Projected core temperature and percent body mass loss were calculated for 4 and 8 hr of continuous work. Core temperature rose from baseline (36.8 ± 0.3 °C) to completion of 2 hr of work (38.1 ± 0.6 °C, p < 0.01), with two participants reaching the 38.0 °C threshold. Projected core temperatures remained elevated from baseline (p < 0.01), did not change from 2 to 4 hr (38.1 ± 0.7 °C, p > 0.99) and 4 to 8 hr (38.1 ± 0.8 °C, p > 0.99), respectively, and one participant exceeded 38.0 °C at 4 to 8 hr. There was no change in body mass loss over time (p > 0.99). During 2 hr of continuous heavy-intensity work in the heat, 75% of participants did not reach 38 °C core temperature and 88% did not reach 2% body mass loss when working to National Institute for Occupational Safety and Health recommendations.

Sugar-sweetened soft drink consumption acutely decreases spontaneous baroreflex sensitivity and heart rate variability.

In healthy humans, fructose-sweetened water consumption increases blood pressure variability (BPV) and decreases spontaneous cardiovagal baroreflex sensitivity (cBRS) and heart rate variability (HRV). However, whether consuming commercially available soft drinks containing high levels of fructose elicits similar responses is unknown. We hypothesized that high-fructose corn syrup (HFCS)-sweetened soft drink consumption increases BPV and decreases cBRS and HRV to a greater extent compared with artificially sweetened (diet) and sucrose-sweetened (sucrose) soft drinks and water. Twelve subjects completed four randomized, double-blinded trials in which they drank 500 mL of water or commercially available soft drinks matched for taste and caffeine content. We continuously measured beat-to-beat blood pressure (photoplethysmography) and R-R interval (ECG) before and 30 min after drink consumption during supine rest for 5 min during spontaneous and paced breathing. BPV was evaluated using standard deviation (SD), average real variability (ARV), and successive variation (SV) methods for systolic and diastolic blood pressure. cBRS was assessed using the sequence method. HRV was evaluated using the root mean square of successive differences (RMSSD) in R-R interval. There were no differences between conditions in the magnitude of change from baseline in SD, ARV, and SV (P ≥ 0.07). There were greater reductions in cBRS during spontaneous breathing in the HFCS (-3 ± 5 ms/mmHg) and sucrose (-3 ± 5 ms/mmHg) trials compared with the water trial (+1 ± 5 ms/mmHg, P < 0.03). During paced breathing, HFCS evoked greater reductions in RMSSD compared with water (-26 ± 34 vs. +2 ± 26 ms, P < 0.01). These findings suggest that sugar-sweetened soft drink consumption alters cBRS and HRV but not BPV.

Occupational heat exposure and the risk of chronic kidney disease of nontraditional origin in the United States.

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.

Impact of passive heat acclimation on markers of kidney function during heat stress.

NEW FINDINGS: What is the central question of this study? Does passive heat acclimation alter glomerular filtration rate and urine-concentrating ability in response to passive heat stress? What is the main finding and its importance? Glomerular filtration rate remained unchanged after passive heat stress, and heat acclimation did not alter this response. However, heat acclimation mitigated the reduction in urine-concentrating ability and reduced the incidence of albuminuria in young healthy adults after passive heat stress. Collectively, these results suggest that passive heat acclimation might improve structural integrity and reduce glomerular permeability during passive heat stress. ABSTRACT: Little is known about the effect of heat acclimation on kidney function during heat stress. The purpose of this study was to determine the impact of passive heat stress and subsequent passive heat acclimation on markers of kidney function. Twelve healthy adults (seven men and five women; 26 ± 5 years of age; 72.7 ± 8.6 kg; 172.4 ± 7.5 cm) underwent passive heat stress before and after a 7 day controlled hyperthermia heat acclimation protocol. The impact of passive heat exposure on urine and serum markers of kidney function was evaluated before and after heat acclimation. Glomerular filtration rate, determined from creatinine clearance, was unchanged with passive heat stress before (pre, 133 ± 41 ml min-1 ; post, 127 ± 51 ml min-1 ; P = 0.99) and after (pre, 129 ± 46 ml min-1 ; post, 130 ± 36 ml min-1 ; P = 0.99) heat acclimation. The urine-to-serum osmolality ratio was reduced after passive heating (P < 0.01), but heat acclimation did not alter this response. In comparison to baseline, free water clearance was greater after passive heating before (pre, -0.86 ± 0.67 ml min-1 ; post, 0.40 ± 1.01 ml min-1 ; P < 0.01) but not after (pre, -0.16 ± 0.57 ml min-1 ; post, 0.76 ± 1.2 ml min-1 ; P = 0.11) heat acclimation. Furthermore, passive heating increased the fractional excretion rate of potassium (P < 0.03) but not sodium (P = 0.13) or chloride (P = 0.20). Lastly, heat acclimation reduced the fractional incidence of albuminuria after passive heating (before, 58 ± 51%; after, 8 ± 29%; P = 0.03). Collectively, these results demonstrate that passive heat stress does not alter the glomerular filtration rate. However, heat acclimation might improve urine-concentrating ability and filtration within the glomerulus.