| Abstract | Repeated exposure to hot environments is accompanied by a number of physiological adaptations, including improved thermoregulatory mechanisms which reduce physiological strain within the body and improve heat tolerance during subsequent exertional heat stress (EHS) exposures. To our knowledge, minimal data exists examining the relationship between circulating immuno-inflammatory mediators and the improvements in physiological heat tolerance accompanying repeated EHS exposures. PURPOSE: To examine the immune-inflammatory responses in untrained males following repeated EHS exposures and their relationship to classical physiological adaptations.
METHODS: Nine sedentary males (Age = 27 ± 2 years, = 52 ± 2 mL·kgLBM-1·min-1, 17 ± 2% body fat) walked to exhaustion (Exh) at 4.5 km·h-1 with 2% elevation in a climatic chamber (40°C; 30% R.H.) while wearing encapsulating protective clothing for 9-days. Whole blood venous samples were collected at baseline (B) and Exh on Days 1 and 9 and analyzed by ELISA for circulating concentrations of IL-6, IL-1ra, nitric oxide (NO), soluble (s)CD14 and c-reactive protein (CRP).
RESULTS: Repeated exertional heat stress exposure produced significant reductions in HR (142 ± 4 vs. 154 ± 4 b·min-1) and an increased time to Exh (145 ± 13 vs. 95± 8 min) on Day 9 compared to Day 1, respectively. No changes were observed in core temperature at B (36.7 ± 0.1 vs 36.6 ± 0.1 °C, p = 0.63), while a tendency for an increased core temperature tolerated at Exh (38.8 ± 0.1 vs 39.1 ± 0.1°C, p = 0.06) was observed between Days 1 and 9. Significantly elevated basal levels of sCD14, as well as tendencies for increased CRP (p = 0.06) and IL-1ra (p = 0.17), were observed on Day 9 compared to Day 1. During EHS, a significant increase in IL-6 (p = 0.01) and a tendency for enhanced NO production (p = 0.10) accompanied improved thermoregulation on Day 9.
CONCLUSIONS: These findings suggest that classical thermoregulatory adaptations may be linked to immuno-inflammatory modulation following repeated EHS exposures, contributing to thermoregulatory adaptations and conferring enhanced cytoprotection for a given level of thermal strain. |
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