| Thermotolerance (cellular adaptations that allow survival after an acute, severe heat exposure) and heat acclimation (systemic adaptations that improve heat dissipation following chronic heat exposure) have traditionally been considered separate phenomena. However, recent studies in animals suggest these adaptations may be related through the heat shock response. Methods. We evaluated the effects of a standard laboratory heat shock response-inhibitor (QUERCETIN) on established markers of thermotolerance [gastrointestinal barrier permeability, plasma TNF-a, Il-6, and Il-10 concentrations; leukocyte HSP70 content(HSP70)] and heat acclimation [reduced body temperatures, heart rate, and physiologic strain in response to exercise/heat stress] in male subjects (n=8) completing a 7-day heat acclimation protocol. Thermotolerance markers were assessed in blood drawn before (pre), after (post), 2hr after (2-post) and 4hr after (4-post) exercise on day 1 and day 7 of heat acclimation. Heat acclimation markers were assessed by a standard heat tolerance test, performed at baseline, and on day 6 of heat acclimation. Subjects completed an identical protocol under placebo supplementation (PLACEBO), in counter-balanced order, under double-blind conditions, with sufficient washout. Results. QUERCETIN increased gastrointestinal barrier permeability and TNF-a on the 1st day of exercise/heat stress, no differences in these variables were reported in PLACEBO. 7 days of exercise/heat stress in PLACEBO decreased subjects' exercise Il-6 and Il-10 and increased HSP70; it also reduced exercise body temperatures, heart rate, and physiologic strain. Striking differences were noted in these same subjects under QUERCETIN. Here gastrointestinal barrier permeability remained elevated, Il-6 and Il-10 were not reduced, HSP70 was not increased, and exercise body temperatures were not reduced. While exercise heart rate and physiologic strain were reduced, this occurred much later in exercise. Conclusions. Consistent with the concept of whole-organism adaptation, repeated exercise/heat stress reduces circulating cytokine concentrations and increases cytoprotective HSP70, contributing to reductions in systemic markers of heat strain. Exercising under the influence of a heat shock response inhibitor may prevent these responses, contributing to loss of benefits normally incurred by a standard heat acclimation protocol in humans. |
