Sweat loss during heat stress contributes to subsequent reductions in lower‐body negative pressure tolerance

Abstract

New findings: What is the central question of this study? Heat stress compromises blood pressure control, reducing an individual's tolerance to a simulated hemorrhagic challenge. The contribution of sweating, and the resulting loss of total body water, during heat stress on heat‐induced reductions in haemorrhagic tolerance is unknown. What is the main finding and its importance? Unreplaced sweat loss and the associated reduction in blood volume contribute to reductions in haemorrhagic tolerance in heat‐stressed individuals; however, this impairment is secondary to the negative impact of heat stress itself. These findings highlight the importance of adequate hydration in individuals who are exposed to heat stress and are at a higher risk for a haemorrhagic injury, such as soldiers, firefighters and construction workers. The contribution of sweating to heat stress‐induced reductions in haemorrhagic tolerance is not known. This study tested the hypothesis that fluid loss due to sweating contributes to reductions in simulated haemorrhagic tolerance in conditions of heat stress. Eight subjects (35 ± 8 years old; 77 ± 5 kg) underwent a normothermic time control and two heat stress trials (randomized). The two heat stress trials were as follows: (i) with slow intravenous infusion of lactated Ringer solution sufficient to offset sweat loss (IV trial); or (ii) without intravenous infusion (dehydration; DEH trial). Haemorrhage was simulated via progressive lower‐body negative pressure (LBNP) to presyncope after core body (intestinal) temperature was raised by ∼1.5°C using a water‐perfused suit or a normothermic time control period. The LBNP tolerance was quantified via a cumulative stress index. Middle cerebral artery blood velocity (transcranial Doppler) and mean blood pressure (Finometer®) were measured continuously. Relative changes in plasma volume were calculated from haematocrit and haemoglobin. Increases in core body temperature and sweat loss (∼1.6% body mass deficit) were similar ( P > 0.05) between heat stress trials. Slow intravenous infusion (1.2 ± 0.3 litres) prevented heat‐induced reductions in plasma volume (IV trial, −0.6 ± 6.1%; and DEH trial, −6.6 ± 5.1%; P = 0.01). Intravenous infusion improved LBNP tolerance (632 ± 64 mmHg min) by ∼20% when compared with the DEH trial (407 ± 117 mmHg min; P = 0.01), yet tolerance remained 44% lower in the IV trial relative to the time control normothermic trial (1138 ± 183 mmHg min; P < 0.01). These data indicate that although sweat‐induced dehydration impairs simulated haemorrhagic tolerance, this impairment is secondary to the negative impact of heat stress itself.