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.

Tarp-Assisted Cooling for Exertional Heat Stroke Treatment in Wildland Firefighting.

INTRODUCTION: Exertional heat stroke is a life-threatening emergency necessitating immediate treatment with rapid body cooling. A field-expedient alternative may be tarp-assisted cooling, requiring only water and a tarp. The objective of this study was to compare core temperature (Tc) cooling rates of tarp-assisted cooling using the limited resources available to a wildland firefighter and the current standard care provided in wilderness settings. METHODS: This cross-over, randomized control trial of 17 healthy individuals consisted of exercise in a 42±1°C, 32±4% relative humidity environment while wearing wildland firefighter attire, followed by cooling. Body cooling consisted of either pouring 11 L of 25±1°C water over the torso while lying supine on a tarp configured to hold water close to the individual (Tarp) or dousing the water on the participant followed by lying supine with a light breeze, current standard care in the wilderness (Current Care). Cooling occurred until Tc reached 38°C. RESULTS: Participants walked until a similar Tc was achieved in Tarp (39.59±0.04°C) and Current Care (39.55±0.22°C; P=0.36). Core temperature cooling rate was not different between Tarp (0.076±0.042°C·min-1) and Current Care (0.088±0.046°C·min-1; P=0.41). CONCLUSIONS: In hyperthermic individuals, Tarp did not provide a faster cooling rate compared to the current exertional heat stroke care provided in the wilderness, and both provided a slower cooling rate than that provided by the traditional method of cold water immersion (>0.20°C·min-1) to treat exertional heat stroke patients.

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.

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.

Human thermoregulation during prolonged exposure to warm and extremely humid environments expected to occur in disabled submarine scenarios.

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.

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.

Kidney injury risk during prolonged exposure to current and projected wet bulb temperatures occurring during extreme heat events in healthy young men.

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 [+26.9 (27.1) (ng/mL)2/1,000) compared with the 31°C [+6.2 (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 [+77.6 (47.5) ng/min] compared with the 31°C [+16.2 (25.1) ng/min] trial (P < 0.01). Plasma IL-17a, an inflammatory marker, was elevated at 8 h in the 34°C [+199.3 (90.0) fg/dL; P < 0.01] compared with the 31°C [+9.0 (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.NEW AND NOTEWORTHY We have demonstrated that kidney injury risk is increased when men are exposed over an 8-h period to a wet bulb temperature of 31°C and exacerbated at a wet bulb temperature of 34°C. Importantly, these heat stress conditions parallel those that are encountered during current (31°C) and future (34°C) extreme heat events. The kidney injury biomarker analyses indicate both the proximal and distal tubules as the locations of potential renal injury and that the injury is likely due to oxidative stress and inflammation.