Abstract
Plasma HSP72 (eHSP72) is suggested to play a role in exercise and heat stress by activating the innate immune system and signaling the release of proinflammatory cytokines. Impairment in the release of eHSP72, possibly after a severe heat injury, could alter the stress response signaling cascade and potentially lead to serious physiological consequences. What remains unknown is whether eHSP72 release is impaired in individuals with prior heat stroke. PURPOSE: To determine eHSP72 response between military personnel with and without a prior heat stroke during 150 minutes of exercise in the heat. METHODS: Sixty-one military personnel completed continuous treadmill walking (3.3 mph, 4.0% grade) for 150 minutes in 40°C and 40% RH. Twenty-eight (24.7 ± 3.8 yrs, 178.7 ± 6.9 cm, 86.2 ± 8.8 kg) had a prior documented heat stroke (rectal temperature (Trec) ≥ 40°C with varying grades of CNS dysfunction at the onset of injury) and 33 (25.0 ± 5.5 yrs, 176.8 ± 7.6 cm, 82.8 ± 12.0 kg) had never experienced a heat injury. Heat-injured individuals were tested a minimum of 6 weeks after their injury. Trec and heart rate (HR) were measured continuously throughout the 150-min trial. Plasma obtained from pre and post venipuncture samples was stored at -80°C and then analyzed using high-sensitivity ELISA kits for determination of eHSP72. RESULTS: Mean ending values for Trec and HR for the 28 heat-injured and 33 non-injured participants were 38.1 ± 0.3°C and 124 ± 15 bpm, and 38.3 ± 0.4°C and 132 ± 17 bpm, respectively. Pre eHSP72 values between each group were not statistically different from each other (Heat-Injured: 2.12 ±0.51, Non-Injured: 2.05 ± 0.51 ng/ml, p = 0.57). Likewise, post eHSP72 values between each group were not statistically different from each other (Heat-Injured: 2.19 ±0.49, Non-Injured: 2.12 ± 0.48 ng/ml, p = 0.61). CONCLUSIONS: Findings suggest that after 6 weeks of recovery, responses of eHSP72 in heat-injured military personnel are similar to those in military personnel that have never experienced a heat injury; demonstrating that under these stressors there is no impairment in eHSP72 response in individuals with prior heat stroke. Future research should focus on examining serial eHSP72 levels closer to the time of injury onset and increasing exercise intensity or heat stress to elicit a more pronounced response of eHSP72.
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