The Effects of Heat Acclimation on Heat Shock Protein-72 mRNA and Apoptosis in Lymphocytes

Abstract

Heat shock proteins (HSP) improve cellular thermotolerance and protect against stress-induced cell death by reducing molecular damage and mediating apoptotic pathways. HSP72 levels increase due to nonlethal heat stress in vitro, and increase due to physiologically stressful conditions in vivo. Multiple bouts of exercise in the heat lead to improved whole-body thermotolerance, which may be related to an accumulation of cellular HSP72. Increased HSP72 has been shown to decrease apoptosis in vitro; however, the relationship between physiological adaptations to heat acclimation and subsequent adaptations at the cellular level are less understood. PURPOSE: The purpose of this study was to determine if heat acclimation (HA) increases HSP72 mRNA and if its protective mechanisms decrease apoptosis in lymphocytes. METHODS: Twelve recreationally active males completed 8 consecutive days of cycling in 38°C for ∼90 min at ∼45%VO2max. Lymphocytes were collected pre- and post-exercise on days 1 and 8 of HA. Pre-exercise lymphocytes were heat shocked in vitro for 20, 40, or 60 min at 37, 41, 43, or 45°C to analyze apoptotic responses to heat, and post-exercise samples were analyzed to determine apoptotic responses to exercise. RESULTS: After HA, participants exhibited improved thermotolerance. They experienced a resting plasma volume expansion of 6.29±6.18%, increased sweat loss (p=0.001), and decreased heart rate, core temperature, and skin temperature at all time points on day 8 of HA (p=0.046; p=0.023; and p=0.002, respectively). HSP72 mRNA increased during exercise on days 1 and 8 (4.08±3.76 and 3.80±1.72 fold, respectively), and resting HSP72 mRNA levels increased 2.11±1.21 fold from days 1 to 8 (nonsignif.). There was no change in in vitro apoptosis due to HA (p=0.385); however, there was an interaction of the time × temperature design used to treat cells (p=0.000), with 45°C being most lethal at all time points. There was no change in apoptosis due to exercise or HA (p=0.870 and p=0.683, respectively). CONCLUSIONS: Whole body HA did not reduce lymphocyte apoptosis and apoptotic responses were not related to the HSP72 mRNA levels. Under the conditions tested, improved thermotolerance at the organism level was not associated with improved thermotolerance at the cellular level.