Abstract

In isolated cell and animal studies, a single exposure to sublethal heat stress protects them from a subsequent lethal heat shock. This increase in thermotolerance is associated with intracellular accumulation of heat shock protein 72 (Hsp72). In humans, whole body heat acclimation (HA), which involves exercise in hot environments for several days, increases intracellular Hsp72. However, it is not known if whole body HA is able to increase thermotolerance in isolated human peripheral blood mononuclear cells (PBMC). PURPOSE: To determine if HA alters in vitro PBMC thermotolerance. We hypothesized that HA would increase PBMC tolerance to heat. METHODS: 7 male and 2 female subjects (mean ± SD, age 24 ± 3 yrs, 75 ± 5 kg, 53 ± 8 mL.kg-1.min−1) were heat acclimated by walking or running on a treadmill (56% VO2max) for 100 minutes (two 50 min exercise bouts separated by 15 min of rest) in a hot environment (42°C and 30% rh) for 10 days. Blood was drawn, and PBMC were separated and cultured on days 1 and 10 of HA pre-and post-exercise. 24 hours later, pre-exercise PBMC were incubated in a hot water bath (42.5°C for 2 hours). Intracellular Hsp72 was assayed by ELISA. Lactate dehydrogenase (LDH) was measured as a marker of cell damage. RESULTS: HA was confirmed by the classic signs of attenuated (p<0.05) peak heart rate, skin and core temperatures on day 1 vs. day 10 of HA. LDH release increased (p<0.05) after 42.5°C for 2 hours but it was not different between days 1 and 10 of HA (1.11 ± 0.08 and 1.10 ± 0.10 relative LDH release, respectively). Pre-exercise Hsp72 was higher (p<0.05) on day 10 compared to day 1 of HA (13 ± 5 and 8 ± 5 ng.mL−1, respectively). Post-exercise Hsp72 was not different (p>0.05) on day 1 compared to day 10 of HA (13 ± 5 and 17 ± 8 ng.mL−1, respectively). Heat stressing the pre-exercise PBMC to 42.5°C for 2 hours induced a greater increase in Hsp72 than post-exercise (p<0.05), and it was greater on day 1 than day 10 of HA (129 ± 46 and 80 ± 32 ng.mL−1, respectively). CONCLUSION: Whole body HA increases intracellular Hsp72 but it does not reduce cell damage to heat, as measured by LDH. We suggest that the heat stress applied during HA is not sufficient to induce enough Hsp72 to improve cell thermotolerance. Supported by GSSI student award and NIH grant AR40771.

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