Neuromotor deficits and altered physiological responses to repeated exertional heat stroke exposures in mice

Exertional heat stroke (EHS) is a life-threatening illness that can lead to negative health outcomes. Using a 'severe' preclinical mouse model of EHS, we tested the hypotheses that one EHS exposure results in altered susceptibility to a subsequent EHS and reduced neuromotor performance. Female, C57BL/6 mice underwent two protocols, two weeks apart, either an EHS trial (EHS) or a sham exercise control trial (EXC). For EHS, mice ran in a forced running wheel at 37.5°C/40% relative humidity until loss of consciousness, followed by a slow cooling protocol (2 h recovery in 37.5°C). EXC mice exercised equally but in ~22°C. Mice were randomized into 3 groups: 1) EXC-EXC (two consecutive EXC, n=6, 2) EHS-EXC (EHS followed by EXC, n=5) and 3) EHS-EHS (repeated EHS, n=9). Mice underwent noninvasive neuromotor and behavioral tests during recovery, and isolated soleus force measurements at the end of recovery. At the first EHS, mice reached average peak core temperatures (Tc,max) of 42.4°C, (46% mortality). On the second EHS, average Tc,max was reduced by ~0.7°C (P<0.05; mortality 18%). After the first EHS, both EHS-EX and EHS-EHS showed significant reductions in maximum strength (24 h and 1 wk post). Following the second EHS, strength, horizontal rotation, hind limb tone, suspended hindlimb splay, trunk curl and provoked biting continued to decline in the EHS-EHS group. In conclusion, exposure to a second EHS after two weeks, leads to increased exercise times in the heat, symptom limitation at a lower Tc,max, and greater deficits in neuromotor and behavioral function during recovery.

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