American journal of physiology. Regulatory, integrative and comparative physiologyJun 10, 2026

How common chronic diseases affect cell cleanup and stress in immune cells during heat stress in older men

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jun 11, 2026

Abstract

Mean body temperature increased by 0.84°C in hot conditions during high-intensity exercise among older males.

Autophagic function showed greater indices, such as LC3-II, in healthy older males compared to those with chronic diseases like hypertension and type 2 diabetes.
The differences in autophagic responses were less pronounced after heated exercise, indicating potential effects of ambient conditions on autophagy.
Lower levels of p62 were observed in older males with hypertension and type 2 diabetes, suggesting an impact of chronic diseases on cellular stress responses.
Apoptotic responses were similar across all groups, indicating that cell death mechanisms were not significantly affected by chronic diseases in this context.
Disease-related alterations in IL-6 responses may contribute to the differences in autophagy regulation observed in older males during exertional heat stress.

Simplified

Autophagy plays a key role in maintaining cellular function during acute physiological stress, including exercise and heat stress. While autophagic function declines with increasing age, the extent to which age-related chronic disease (e.g., hypertension, type 2 diabetes) influences autophagic responses during exertional heat stress remains unknown. Older males (mean [SD]: aged 70 [5] years) without (n=10) and with hypertension (n=10) or type 2 diabetes (n=10) performed high-intensity semi-recumbent cycling (70% of maximal oxygen consumption) in temperate (25°C, 15% relative humidity) or hot (40°C, 15% relative humidity) ambient conditions. Mean body temperature (rectal and skin) was measured throughout, while proteins associated with autophagy and cellular stress were assessed in peripheral blood mononuclear cells before and after exercise and following 6h of seated recovery via Western blot. Mean body temperature increased similarly across all groups at end-exercise in temperate (+0.40°C) and hot conditions (+0.84°C). Indices of autophagy, including LC3-II, were greater in the healthy compared to both chronic disease groups at end-exercise and throughout the 6h recovery in temperate conditions. However, between-group differences in LC3-II levels were less pronounced following heated exercise (p=0.03), and p62 content was lower in individuals with hypertension and type 2 diabetes. While apoptotic responses were similar across groups, disease-associated blunting of IL-6 responses may contribute to the observed differential levels in autophagic regulation in older males. Therefore, our findings reveal altered autophagic responses to exertional heat stress in older males with chronic health conditions, which may have implications for altered cellular vulnerability during exertional heat stress.

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How common chronic diseases affect cell cleanup and stress in immune cells during heat stress in older men

Abstract

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