Duration-dependent myocardial strain and altered antioxidant dynamics in male Sprague-Dawley rats subjected to repeated heat stress

Abstract

Heat stress imposes a multisystem physiological burden, with the heart bearing a disproportionate share of the haemodynamic and metabolic consequences. Cardiac troponin I (cTnI) is a highly organ-specific biomarker whose elevation in the circulation signals disruption of cardiomyocyte membrane integrity. This study evaluated serum cTnI concentrations in male Sprague-Dawley rats subjected to repeated heat exposure, while superoxide dismutase activity and malondialdehyde levels were assessed as indices of antioxidant defence and lipid peroxidation, respectively. Twenty healthy male rats weighing 100–150 g were randomized into four groups of five rats each. Group I served as control and was maintained at ambient room temperature, while Groups II, III, and IV were exposed to 38–40°C for exactly 2 hours daily for 14, 28, and 42 days, respectively. At the end of exposure, serum was harvested following cardiac puncture. Cardiac troponin I was quantified using enzyme-linked immunosorbent assay (ELISA), malondialdehyde by the thiobarbituric acid reactive substances (TBARS) method, and superoxide dismutase by the pyrogallol autoxidation inhibition method. Data were analysed using one-way analysis of variance followed by Tukey’s Honestly Significant Difference post-hoc test. Serum cardiac troponin I increased progressively across the groups, with values of 25.57 ± 3.83, 34.46 ± 1.21, 55.52 ± 9.12, and 87.28 ± 1.50 pg/mL in the control, 14-day, 28-day, and 42-day groups, respectively. Significant elevations were observed at 28 and 42 days. Interestingly, both malondialdehyde and superoxide dismutase decreased significantly at 14 and 28 days before partial recovery at 42 days. This early parallel decline suggests a complex metabolic adaptation rather than a simple linear pattern of oxidative damage. The findings indicate that repeated passive heat exposure induces duration-dependent myocardial strain and alters antioxidant dynamics in male Sprague-Dawley rats.