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.

Partial and Complete Fluid Replacement Maintains Exercise Performance in a Warm Environment Following Prolonged Cold-Water Immersion.

ABSTRACT: Wheelock, CE, Stooks, J, Schwob, J, Hess, HW, Pryor, RR, and Hostler, D. Partial and complete fluid replacement maintains exercise performance in a warm environment following prolonged cold-water immersion. J Strength Cond Res 38(2): 290-296, 2024-Special warfare operators may be exposed to prolonged immersion before beginning a land-based mission. This immersion will result in substantial hypohydration because of diuresis. This study tested the hypothesis that both partial and full postimmersion rehydration would maintain performance during exercise in the heat. Seven men (23 ± 2 years; V̇o2max: 50.8 ± 5.3 ml·kg-1·min-1) completed a control trial (CON) without prior immersion and 3 immersion (18.0°C) trials without rehydration (NO) or with partial (HALF) or full (FULL) rehydration. After immersion, subjects completed a 60-minute weighted ruck march (20.4 kg; 5.6 kph) and a 15-minute intermittent exercise protocol (iEPT) in a warm environment (30.0°C and 50.0% relative humidity). The primary outcome was distance (km) covered during the iEPT. A priori statistical significance was set to p ≤ 0.05. Immersion resulted in 2.3 ± 0.4% loss of body mass in all immersion trials (p < 0.01). Distance covered during the first 13-minute interval run portion of iEPT was reduced in the NO rehydration trial (1.59 ± 0.18 km) compared with all other conditions (CON: 1.88 ± 0.18 km, p = 0.03; HALF: 1.80 ± 0.18 km, p < 0.01; FULL: 1.86 ± 0.28 km, p = 0.01). During the final 2 minutes of the iEPT, distance in the NO rehydration trial (0.31 ± 0.07 km) was reduced compared with the FULL rehydration trial (0.37 ± 0.07 km; p < 0.01) but not compared with CON (0.35 ± 0.07 km; p = 0.09) or HALF (0.35 ± 0.07 km; p = 0.08). Both partial and full postimmersion fluid replacement maintained intermittent exercise performance and should be applied as rehydration strategies.

Resistance Training in the Heat: Mechanisms of Hypertrophy and Performance Enhancement.

ABSTRACT: Pryor, JL, Sweet, D, Rosbrook, P, Qiao, J, Hess, HW, and Looney, DP. Resistance training in the heat: Mechanisms of hypertrophy and performance enhancement. J Strength Cond Res 38(7): 1350-1357, 2024-The addition of heat stress to resistance exercise or heated resistance exercise (HRE) is growing in popularity as emerging evidence indicates altered neuromuscular function and an amplification of several mechanistic targets of protein synthesis. Studies demonstrating increased protein synthesis activity have shown temperature-dependent mammalian target of rapamycin phosphorylation, supplemental calcium release, augmented heat shock protein expression, and altered immune and hormone activity. These intriguing observations have largely stemmed from myotube, isolated muscle fiber, or rodent models using passive heating alone or in combination with immobilization or injury models. A growing number of translational studies in humans show comparable results employing local tissue or whole-body heat with and without resistance exercise. While few, these translational studies are immensely valuable as they are most applicable to sport and exercise. As such, this brief narrative review aims to discuss evidence primarily from human HRE studies detailing the neuromuscular, hormonal, and molecular responses to HRE and subsequent strength and hypertrophy adaptations. Much remains unknown in this exciting new area of inquiry from both a mechanistic and functional perspective warranting continued research.

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.

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.

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.

Carotid body chemosensitivity is not attenuated during cold water diving.

Tonic carotid body (CB) activity is reduced during exposure to cold and hyperoxia. We tested the hypotheses that cold water diving lowers CB chemosensitivity and augments CO2 retention more than thermoneutral diving. Thirteen subjects [age: 26 ± 4 yr; body mass index (BMI): 26 ± 2 kg/m2) completed two 4-h head-out water immersion protocols in a hyperbaric chamber (1.6 ATA) in cold (15°C) and thermoneutral (25°C) water. CB chemosensitivity was assessed with brief hypercapnic ventilatory response ([Formula: see text]) and hypoxic ventilatory response ([Formula: see text]) tests before dive, 80 and 160 min into the dive (D80 and D160, respectively), and immediately after and 60 min after dive. Data are reported as an absolute mean (SD) change from predive. End-tidal CO2 pressure increased during both the thermoneutral water dive [D160: +2 (3) mmHg; P = 0.02] and the cold water dive [D160: +1 (2) mmHg; P = 0.03]. Ventilation increased during the cold water dive [D80: 4.13 (4.38) and D160: 7.75 (5.23) L·min-1; both P < 0.01] and was greater than the thermoneutral water dive at both time points (both P < 0.01). [Formula: see text] was unchanged during the dive (P = 0.24) and was not different between conditions (P = 0.23). [Formula: see text] decreased during the thermoneutral water dive [D80: -3.45 (3.61) and D160: -2.76 (4.04) L·min·mmHg-1; P < 0.01 and P = 0.03, respectively] but not the cold water dive. However, [Formula: see text] was not different between conditions (P = 0.17). In conclusion, CB chemosensitivity was not attenuated during the cold stress diving condition and does not appear to contribute to changes in ventilation or CO2 retention.

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.

Variability in venous gas emboli following the same dive at 3,658 meters.

Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the Cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver presented with symptoms of DCS following the dive or two hours post-dive at altitude. Despite inter- and intra-diver variability of VGE grade following the dives, the majority (11/20 dives) presented a peak VGE Grade 0, three VGE Grade 1, one VGE Grade 2, four VGE Grade 3, and one VGE Grade 4. Using the Cross correction method for a 66-fsw dive at 12,000 feet of altitude resulted in a relatively low decompression stress and no cases of DCS.

Variability in venous gas emboli following the same dive at 3,658 meters.

Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the Cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver presented with symptoms of DCS following the dive or two hours post-dive at altitude. Despite inter- and intra-diver variability of VGE grade following the dives, the majority (11/20 dives) presented a peak VGE Grade 0, three VGE Grade 1, one VGE Grade 2, four VGE Grade 3, and one VGE Grade 4. Using the Cross correction method for a 66-fsw dive at 12,000 feet of altitude resulted in a relatively low decompression stress and no cases of DCS.

Respiratory muscle training and exercise ventilation while diving at altitude.

Introduction: Pre-dive altitude exposure may increase respiratory fatigue and subsequently augment exercise ventilation at depth. This study examined pre-dive altitude exposure and the efficacy of resistance respiratory muscle training (RMT) on respiratory fatigue while diving at altitude. Methods: Ten men (26±5 years; VO2peak: 39.8±3.3 mL• kg-1•min-1) performed three dives; one control (ground level) and two simulated altitude dives (3,658 m) to 17 msw, relative to ground level, before and after four weeks of resistance RMT. Subjects performed pulmonary function testing (e.g., inspiratory [PI] and expiratory [PE] pressure testing) pre- and post-RMT and during dive visits. During each dive, subjects exercised for 18 minutes at 55% VO2peak, and ventilation (VE), breathing frequency (ƒb,), tidal volume (VT) and rating of perceived exertion (RPE) were measured. Results: Pre-dive altitude exposure reduced PI before diving (p=0.03), but had no effect on exercise VE, ƒb, or VT at depth. At the end of the dive in the pre-RMT condition, RPE was lower (p=0.01) compared to control. RMT increased PI and PE (p<0.01). PE was reduced from baseline after diving at altitude (p<0.03) and this was abated after RMT. RMT did not improve VE or VT at depth, but decreased ƒb (p=0.01) and RPE (p=0.048) during the final minutes of exercise. Conclusion: Acute altitude exposure pre- and post-dive induces decrements in PI and PE before and after diving, but does not seem to influence ventilation at depth. RMT reduced ƒb and RPE during exercise at depth, and may be useful to reduce work of breathing and respiratory fatigue during dives at altitude.

Whole-body active heating does not preserve finger temperature or manual dexterity during cold-water immersion.

Background: Cold-water immersion impairs manual dexterity when finger temperature is below 15°C. This exposes divers to increased risk of error. We hypothesized that whole-body active heating would maintain finger temperatures and dexterity during cold-water immersion. Methods: Twelve subjects (six males) (22 ± 2 years old; BMI 23.9 ± 2.5; body fat 16 ± 6%) completed 60-minute head-out water immersion (HOWI) wearing a 7mm wetsuit and 3mm gloves in thermoneutral water (TN 25°C) and cold water (CW 10°C) while wearing a water-perfused suit (WP) with 37°C water circulated over the torso, arms, and legs. Gross (Minnesota Manual Dexterity Test [MMDT]) and fine (modified Purdue Pegboard [PPT]) dexterity were assessed before, during and after immersion. Core body and skin temperatures were recorded every 10 minutes. Results: MMDT (TN -25 ± 14%; CW -72 ± 23%; WP -67 ± 29%; p<0.05) and PPT (TN -16 ± 9%; CW: -45 ± 10%; WP: -38 ± 13%; p<0.05) performance decreased during immersion. MMDT and PPT did not differ between CW and WP. Immediately following immersion gross dexterity was recovered in all conditions. Post-immersion fine dexterity was still impaired in CW (p<0.01), but not WP or TN. Core and skin temperatures decreased during immersion in CW and WP (p<0.05) but did not differ between CW and WP. Conclusion: Manual dexterity decreased during immersion. Dexterity was further impaired during cold-water immersion and was not maintained by water perfusion active heating. Warm water perfusion did not maintain finger temperature above 15°C but hand temperature remained above these limits, suggesting a need to reassess thermal thresholds for working divers in cold-water conditions.

Cold water submersion attenuates post-submersion aerobic performance and orthostatic tolerance irrespective of partial rehydration with water.

Purpose: This study examined the independent effects of cold-water submersion and a rehydration strategy on an aerobic endurance performance and orthostatic tolerance following a four-hour dive in cold water (10°C). Methods: Nine male subjects completed a control (CON) performance and lower-body negative pressure test (LBNP) and two water immersion visits with either no rehydration (NR) or a post-immersion rehydration (RH) with 1 L of water. Following submersion, subjects ran to exhaustion and submitted to LBNP. Results: Core body temperature declined during submersion and remained reduced from baseline until the run (P ⟨ 0.001) and was not different between NR and RH (P = 0.13). Total urine output during submersion was not different between groups (1.69 ± 0.49 (NR), 1.75 ± 0.52 (RH) L; P = 0.74) eliciting a body mass reduction of -2.2 ± 0.3 and -0.8 ±; 0.3% (P ⟨ 0.01), respectively. Run duration was not different (547 ± 141 (NR), 566 ± 152 (RH) s; P = 0.79); however, both NR and RH run duration was shorter compared to CON (722 ± 170 s; P = 0.04). Cumulative stress index was suppressed in NR (534 ± 163 mmHg*min) and RH (591 ± 129 mmHg*min) compared to CON (707 ± 170 mmHg*min, P V#8804; 0.03), with no differences between submersion trials (P = 0.23). Conclusion: Compared to a non-submersed state, run duration and orthostatic tolerance was reduced following a four-hour cold-water submersion. Rehydration with 1 L of water following submersion did not offer a performance advantage over no rehydration.

Effect of rehydration schedule after four-hour head-out water immersion on running performance and recovery.

Introduction: Head-out water immersion (HOWI) results in diuresis, which could potentially limit performance after egress to land. We examined the effect of rehydration on endurance, cardiovascular stability, and overnight recovery following a four-hour thermoneutral HOWI on 12 subjects. Methods: Twelve males completed a crossover design consisting of no hydration, replacement of fluid loss during immersion (RD), and replacement of fluid after the immersion period (RA). Sixty minutes following immersion, subjects ran to exhaustion at ~80% maximum heart rate. After completing the run, each subject submitted to a head-up tilt test (HUTT). Vital signs and ECG were monitored overnight. Results: HOWI resulted in a transient diuresis in NH and RA, while it was sustained throughout immersion in the RD protocol, resulting in greater urine [l] output (1.27 ± 0.48 (NH), 1.18 ± 0.43 (RA), 2.32 ± 0.77 (RD) (p ⟨ 0.001). Body mass change (%) was greater in NH than RD, but not RA (-1.58 ± 0.56 (NH), -0.66 ± 0.47 (RD), and -0.92 ± 0.76 (RA)). Run times were 17% versus 20% in NH compared to RD and RA, respectively, but were not statistically different. Time to orthostasis during the HUTT did not differ by condition. Overnight heart rate variability and blood pressures were not different. Conclusion: Rehydration during water immersion resulted in a large, sustained diuresis without improving performance or recovery after exiting the water. Loss of body water during thermoneutral HOWI was modest, and both rehydration strategies minimally affected aerobic performance and overnight recovery in young, healthy males.

Elevations in sweat sodium concentration following ischemia-reperfusion injury during passive heat stress.

Renal ischemia-reperfusion (I/R) injury results in damage to the renal tubules and causes impairments in sodium [Na+] reabsorption. Given the inability to conduct mechanistic renal I/R injury studies in vivo in humans, eccrine sweat glands have been proposed as a surrogate model given the anatomical and physiological similarities. We tested the hypothesis that sweat Na+ concentration is elevated following I/R injury during passive heat stress. We also tested the hypothesis that I/R injury during heat stress will impair cutaneous microvascular function. Fifteen young healthy adults completed ∼160 min of passive heat stress using a water-perfused suit (50°C). At 60 min of whole body heating, one upper arm was occluded for 20 min followed by a 20-min reperfusion. Sweat was collected from each forearm via an absorbent patch pre- and post-I/R. Following the 20-min reperfusion, cutaneous microvascular function was measured via local heating protocol. Cutaneous vascular conductance (CVC) was calculated as red blood cell flux/mean arterial pressure and normalized to CVC during local heating to 44°C. Na+ concentration was log-transformed and data were reported as a mean change from pre-I/R (95% confidence interval). Changes in sweat sodium concentration from pre-I/R differed between arms post-I/R (experimental arm: +0.97 [+0.67 - 1.27] [LOG] Na+; control arm: +0.68 [+0.38 - 0.99] [LOG] Na+; P < 0.01). However, CVC during the local heating was not different between the experimental (80 ± 10%max) and control arms (78 ± 10%max; P = 0.59). In support of our hypothesis, Na+ concentration was elevated following I/R injury, but likely not accompanied by alterations in cutaneous microvascular function.NEW & NOTEWORTHY In the present study, we have demonstrated that sweat sodium concentration is elevated following ischemia-reperfusion injury during passive heat stress. This does not appear to be mediated by reductions in cutaneous microvascular function or active sweat glands, but may be related to alterations in local sweating responses during heat stress. This study demonstrates a potential use of eccrine sweat glands to understand sodium handling following ischemia-reperfusion injury, particularly given the challenges of in vivo studies of renal ischemia-reperfusion injury in humans.

Carbohydrate or Electrolyte Rehydration Recovers Plasma Volume but Not Post-immersion Performance Compared to Water After Immersion Diuresis.

INTRODUCTION: We tested the hypothesis that a carbohydrate (CHO: 6.5%) or carbohydrate-electrolyte (CHO + E: 6.5% + 50 mmol/L NaCl) drink would better recover plasma volume (PV) and exercise performance compared to water (H2O) after immersion diuresis. METHODS: Twelve men (24 ± 2 years; 82.4 ± 15.5 kg; and V̇O2max: 49.8 ± 5.1 mL · kg-1 · min-1) completed four experimental visits: a no-immersion control (CON) and three 4-h cold-water (18.0 °C) immersion trials (H2O, CHO, and CHO + E) followed by exercise in a warm environment (30 °C, 50% relative humidity). The exercise was a 60-minute loaded march (20.4 kg; 55% VO2max) followed by a 10-minute intermittent running protocol. After immersion, subjects were rehydrated with 100% of body mass loss from immersion diuresis during the ruck march. PV is reported as a percent change after immersion, after the ruck march, and after the intermittent running protocol. The intermittent running protocol distance provided an index of exercise performance. Data are reported as mean ± SD. RESULTS: After immersion, body mass loss was 2.3 ± 0.7%, 2.3 ± 0.5%, and 2.3 ± 0.6% for H2O, CHO, and CHO + E. PV loss after immersion was 19.8 ± 8.5% in H2O, 18.2 ± 7.0% in CHO, and 13.9 ± 9.3% in CHO + E, which was reduced after the ruck march to 14.7 ± 4.7% (P = .13) in H2O, 8.8 ± 8.3% (P < .01) in CHO, and 4.4 ± 10.9% (P = .02) in CHO + E. The intermittent running protocol distance was 1.4 ± 0.1 km in CON, 1.4 ± 0.2 km in H2O, 1.4 ± 0.1 km in CHO, and 1.4 ± 0.2 km in CHO + E (P = .28). CONCLUSIONS: Although CHO and CHO + E better restored PV after immersion, post-immersion exercise performance was not augmented compared to H2O, highlighting that fluid replacement following immersion diuresis should focus on restoring volume lost rather than fluid constituents.

Ad libitum drinking prevents dehydration during physical work in the heat when adhering to occupational heat stress recommendations.

Government entities issue recommendations that aim to maintain core temperature below 38.0°C and prevent dehydration [>2% body mass loss] in unacclimated workers exposed to heat. Hydration recommendations suggest drinking 237 mL of a cool sport drink every 15-20 min. This is based on the premise that ad libitum drinking results in dehydration due to inadequate fluid replacement, but this has never been examined in the background of recommendation compliant work in the heat. Therefore, we tested the hypothesis that ad libitum drinking results in >2% body mass loss during heat stress recommendation compliant work. Ten subjects completed four trials consisting of 4 hours of exposure to wet bulb globe temperatures (WBGT) of 24.1 ± 0.3°C (A), 26.6 ± 0.2°C (B), 28.5 ± 0.2°C (C), 29.3 ± 0.6°C (D). Subjects walked on a treadmill and work-rest ratios were prescribed as a function of WBGT [work:rest per hour - A: 60:0, B: 45:15, C: 30:30, D: 15:45] and were provided 237 mL of a cool sport drink every 15 min to drink ad libitum. Mean core temperature was higher in Trial A (37.8 ± 0.4°C; p = 0.03) and Trial B (37.6 ± 0.3°C; p = 0.01) versus Trial D (37.3 ± 0.3°C) but did not differ between the other trials (p ≥ 0.20). Body mass loss (A: -0.9 ± 0.7%, B: -0.7 ± 0.5%, C: -0.3 ± 0.5%, D: -0.4 ± 0.6%) was greater in Trial A compared to Trial D (p = 0.04) and was different from 2% body mass loss in all trials (p ≤ 0.01). Ad libitum drinking during recommendation compliant work in the heat rarely resulted in dehydration. Registered Clinical Trial (NCT04767347).