Brief ambient cooling preserves autophagy in peripheral blood mononuclear cells from older adults during 9 hours of heat exposure.

Abstract

Heat waves can cause dangerous elevations in body temperature that can compromise cellular function and increase the risk of heat stroke and major cardiovascular events. Visiting a cooling center or other air-conditioned location is commonly recommended by health agencies to protect heat-vulnerable older persons but the associated cellular effects remain underexplored. We evaluated cellular stress responses in peripheral blood mononuclear cells (PBMC) from 19 older adults (71 [SD 2] years; 9 females) before and after a 9-hour heat exposure (40.3°C and 9.3% relative humidity [RH]), with exposure to a cool room (~23°C) for hours 5 and 6 (cooling group). Responses were compared to 17 older adults (72 [4] years; 7 females) who remained in the heat for the entire 9 hours (control group). Changes in proteins associated with autophagy, apoptotic signaling, acute inflammation, and the heat shock response (HSR) were assessed via Western blot. While both groups experienced similar elevations in physiological strain prior to the cooling center intervention, brief cooling resulted in stark albeit transient reductions in core temperature and heart rate. At the end-exposure, autophagy proteins LC3-II and p62 were elevated 1.9-fold [95% CI: 1.2, 2.8] and 2.3-fold [1.4, 3.8], respectively, in the control group relative to cooling group. This was paired with a 2.8-fold [1.6, 4.7] greater rise in apoptotic protein cleaved-caspase-3 in the control group compared to the cooling group. Our findings indicate that 2-hours of ambient cooling midway through a 9-hour simulated heat wave may preserve autophagy and mitigate heat-induced cellular stress in older adults.