Article Impact Level: HIGH Data Quality: STRONG Summary of Communications Biology, 8(1), 1–12. https://doi.org/10.1038/s42003-025-07484-3 Dr. Jamal M. Alzahrani et al.
Points
- A single exertional heat stroke (EHS) exposure in mice led to lasting metabolic and cardiovascular health issues over three months.
- EHS-exposed mice showed accelerated diet-induced obesity, liver steatosis, and cardiac hypertrophy, particularly when placed on a high-fat Western diet post-recovery.
- The mice exhibited reduced metabolic flexibility in the heart, favoring glucose metabolism and glycolysis, which could impair normal myocardial function.
- EHS exposure made mice more susceptible to additional metabolic stress, evidenced by severe hypoproteinemia and increased weight gain.
- The study highlights the need for better prevention and treatment strategies for heat stroke, given its potential to cause chronic multi-organ damage, particularly in the face of climate change.
Summary
A recent study used a preclinical mouse model to examine the long-term effects of a single exposure to exertional heat stroke (EHS). The study found that, following recovery from EHS, mice exhibited significant and lasting health consequences. Over a three-month follow-up period, the mice were observed for changes in their metabolic and cardiovascular health. Compared to sham-exercise controls, the EHS-exposed mice showed accelerated diet-induced obesity, low-level cardiac hypertrophy, and increased liver steatosis. These mice also exhibited severe hypoproteinemia and a loss of metabolic flexibility in the myocardium, evidenced by a shift toward glucose metabolism and glycolysis. Notably, these changes were observed after the mice were placed on a high-fat Western diet two weeks post-recovery, suggesting that EHS exposure increases vulnerability to secondary metabolic stressors.
The study’s findings emphasize the long-lasting impact of heat stroke on multiple organ systems. After exposure to EHS, mice were found to have significantly compromised metabolic flexibility, particularly in the heart. The heart’s metabolic shift towards glucose metabolism and glycolysis indicate potential disruptions in normal myocardial function. Furthermore, the mice demonstrated a more pronounced response to subsequent stress, as evidenced by accelerated weight gain and obesity in those on a high-fat diet. These results highlight the possibility that a single instance of heat stroke could lead to chronic, progressive damage to vital organs.
This research underscores the importance of preventing heat-related injuries, particularly in the context of global warming. With the number of heat-related injuries on the rise, especially heat stroke, the study calls for further investigation into the long-term consequences of such injuries. The findings are significant for public health, as they suggest that heat stroke may lead to multi-organ damage and chronic metabolic dysfunction, which could worsen with secondary stressors. The research sets the stage for future studies to identify potential treatments to mitigate these long-term effects.
Link to the article: https://www.nature.com/articles/s42003-025-07484-3
References Alzahrani, J. M., Smuder, A. J., Gambino, B. J., Delgado, C., Rua, M. T., Montalvo, R. N., Fitton, F. P., Morse, D. A., & Clanton, T. L. (2025). Mice develop obesity and lose myocardial metabolic flexibility months after exertional heat stroke. Communications Biology, 8(1), 1–12. https://doi.org/10.1038/s42003-025-07484-3
