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.
McCormick et al. (Wed,) studied this question.