| Abstract | Recent evidence in humans has shown a greater endotoxin leakage in sedentary untrained
(UT) compared with endurance trained (TR) males at core temperatures below those
normally assumed to be essential for the progression of heat illness or heat stroke during
acute exertional heat stress (EHS) exposure [1]. Minimal data exists examining the role of
gastrointestinal (GI) barrier function, circulating immuno-inflammatory mediators and
physiological heat tolerance that accompanies repeated EHS exposures and whether the
same cytoprotective responses observed in TR individuals [2] may be induced during
repeated EHS in UT. The purpose of this work was to examine the immuno-inflammatory
cascades accompanying classical physiological adaptations in untrained males following
repeated EHS exposures.
Nine UT males (Age = 27 ± 2 years, VO₂peak= 52 ± 2 mL·kgLBM⁻¹·min⁻¹, 17 ± 2% body
fatness) 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 on 9 separate days.
Venous whole blood samples were collected at baseline (PRE), 38.0C, 38.5C, 39.0C and
EXH on Days 1 and 9, while PRE/EXH samples were drawn on Days 5 and 6. Samples
were analyzed for endogenous endotoxin, endotoxin neutralizing capacity (ENC) and for
circulating immuno-inflammatory mediators macrophage inflammatory protein (MIP)-1β, IL-6,
IL-10, lipopolysaccharide binding protein (LBP), soluble (s) CD14 and extracellular (e)
HSP72 by ELISA. In addition, intracellular (i) HSP72 was examined in circulating leukocyte
subsets by flow cytometry.
Classical physiological adaptations, including reduced HR and increased tolerance time,
delta core temperature tolerated, plasma volume and sweat rates were observed during
repeated EHS exposure. Mild endotoxemia (21.3 ± 5 pg/mL) was observed at EXH on Days
1, 5, 6, 9 as well as a 14% reduction in ENC (12014 ± 717 vs. 10292 ± 929 ENU/mL) from
PRE to EXH on Day 1. Accompanying the changes in endogenous endotoxin and
thermoregulatory adaptations were enhanced circulating levels of IL-6, IL-10, LBP, sCD14
as well as cytoprotective increases in both eHSP72 and iHSP72.
These findings suggest that GI barrier dysfunction may be an important mechanism of
immuno-inflammatory modulation and cytoprotective adaptations observed following
repeated EHS exposures. |
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