Abstract
The physiological consequences of environment-induced heat stress (EIHS), caused by prolonged exposure to excess heat and humidity, are largely unknown. The purpose of this investigation was to determine the extent to which EIHS alters cardiac health. We hypothesized that 24 h of EIHS would cause cardiac injury and cellular dysfunction in a murine EIHS model. To test this hypothesis, 7-wk-old female mice were housed under thermoneutral (TN) conditions (n = 12; 31.2 ± 1.01°C, 35 ± 0.7% humidity) or EIHS conditions (n = 14; 37.6 ± 0.01°C, 42.0 ± 0.06% humidity) for 24 h. Environment-induced heat stress increased rectal temperature by 2.1°C (P < 0.01) and increased subcutaneous temperature by 1.8°C (P < 0.01). Body weight was decreased by 10% (P = 0.03), heart weight/body weight was increased by 26% (P < 0.01), and tissue water content was increased by 11% (P < 0.05) in EIHS compared with TN. In comparison with TN, EIHS increased protein abundance of heat shock protein (HSP) 27 by 84% (P = 0.01); however, HSPs 90, 60, 70, and phosphorylated HSP 27 were similar between groups. Histological inspection of the heart revealed that EIHS animals had increased myocyte vacuolation in the left ventricle (P = 0.01), right ventricle (P < 0.01), and septum (P = 0.01) compared with TN animals. Biochemical indices are suggestive of mitochondrial remodeling, increased autophagic flux, and robust activation of endoplasmic reticulum stress in hearts from EIHS mice compared with TN mice. These data demonstrate that 1 day of EIHS is sufficient to induce myocardial injury and biochemical dysregulation.NEW & NOTEWORTHY The consequences of prolonged environment-induced heat stress (EIHS) on heart health are largely unknown. We discovered that a 24-h exposure to environmental conditions sufficient to cause EIHS resulted in cardiac edema and histopathologic changes in the right and left ventricles. Furthermore, among other biochemical changes, EIHS increased autophagic flux and caused endoplasmic reticulum stress. These data raise the possibility that thermic injury, even when insufficient to cause heat stroke, can damage the myocardium.