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 to Twet=31°C. Fifteen healthy men rested for eight hours 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 pre and after eight hours of exposure, and as mean (SD) change from preexposure. The increase in [IGFBP7·TIMP-2] was markedly greater at eight hours in the 34°C (+26.9 (27.1) [ng/mL]2/1000) compared to the 31°C (+6.2 (6.5) [ng/mL]2/1000) trial (p<0.01). Urine TRX-1, a marker of renal oxidative stress, was higher at eight hours in the 34°C (+77.6 (47.5) ng/min) compared to the 31°C (+16.2 (25.1) ng/min) trial (p<0.01). Plasma IL-17a, an inflammatory marker, was elevated at eight hours in the 34°C (+199.3 (90.0) fg/dL; p<0.01) compared to 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 to that experienced currently (31°C), likely due to oxidative stress and inflammatory processes.
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.
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; V̇O2peak: 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% V̇O2peak, and ventilation (V̇ E), 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 V̇E, 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 V̇E 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.
In the event of a disabled submarine a pressurized rescue module (PRM) may be deployed. Safe deployment of the PRM depends on understanding the challenges should failures occur. If a PRM were to become disabled, temperature and humidity are predicted to rise quickly, and submariners may need to endure environments approaching 35°C, 95% relative humidity (RH) until rescued. Models predicting increases in core temperature (i.e., hyperthermia) and the magnitude of hypohydration incurred over 24 h in 95% RH environments yield physiologically impossible outcomes at ambient temperatures ≥32°C. Thus, it is not possible to accurately predict the magnitudes of hyperthermia and hypohydration during prolonged exposures to warm and very humid environments. By extension, the fluid prescription required to prevent unsafe levels of hypohydration, defined as a loss of body weight >4%, in a disabled PRM is also unknown.PurposeTest the hypothesis that the predicted magnitudes of hyperthermia and hypohydration during a 24 h exposure to a 95% RH environment are dependent on ambient temperature.Methods10 healthy males (23 ± 3 y) sat in a 95 ± 2% RH normobaric environment for 8 h on three occasions separated by ≥7 days. Trials differed by temperature (32 ± 0°C, 33 ± 0°C, 35 ± 0°C). The order of the trials was randomly assigned. Subjects were not allowed to eat or drink throughout. Core temperature (telemetry pill) and percent changes in body weight (%ΔBW), an index of changes in total body water, were measured every hour. Sweat rate was calculated from %ΔBW. Linear regression models were fit to core temperature (over the final 3 h of exposure), and %ΔBW and sweat rate (over the entire 8 h exposure) over time for each subject. The resulting equations were used to predict the magnitudes of hyperthermia, %ΔBW, and sweat losses for up to 24 h. The volume of fluid required to prevent >4% loss of body weight was calculated accordingly. Data are presented as mean ± SD.ResultsAt the end of the 8 h exposure, core temperature was higher in 35°C (38.0 ± 0.3°C, P<0.01) compared to 32°C (37.6 ± 0.2°C) and 33°C (37.5 ± 0.2°C). At this time, %ΔBW was greater in 35°C (−2.0 ± 0.5%, P<0.01) compared to 32°C (−1.5 ± 0.5%) and 33°C (−1.7 ± 0.4%). At 24 h, predicted core temperature was higher in 35°C (39.0 ± 1.1°C, P<0.01) compared to 32°C (37.7 ± 1.0°C) and 33°C (37.8 ± 0.9°C), and the predicted %ΔBW was greater in 35°C (−6.1 ± 1.2%, P<0.01) compared to 32°C (−4.5 ± 1.2%) and 33°C (−5.3 ± 1.3%). Predicted sweat loss at 24 h was greater in 35°C (−5.2 ± 1.4 L, P<0.01) compared to 32°C (−3.8 ± 1.6 L) and 33°C (−4.4 ± 1.1 L). The predicted fluid prescription required to prevent >4% loss of body weight was greater in 35°C (1.8 ± 0.9 L) compared to 32°C (0.7 ± 0.8 L, P<0.02), and 33°C (1.0 ± 0.8 L, P=0.06).ConclusionIn a 95% RH environment, the magnitudes of hyperthermia and hypohydration predicted to occur during a 24 h exposure are dependent on ambient temperature. Moreover, the volume of fluid required to prevent >4% loss in body weight during a 24 h exposure in ambient temperatures ≤35°C is ~1.8 L.Support or Funding InformationNaval Sea Systems Command Award N00024‐18‐C‐4316.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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