Abstract
Acclimation to heat or hypoxic stress activates the heat shock response and accumulation of cytoprotective heat shock proteins (HSPs). By inhibiting the NF-κB pathway HSP72 can preserve epithelial function and reduce systemic inflammation. The aim of this study was to determine the time course of mHSP72 accumulation during acclimation, and to assess intestinal barrier damage and systemic inflammation following hypoxic exercise. Three groups completed 10 × 60-min acclimation sessions (50% normoxic VO2peak) in control (n = 7; 18°C, 35% RH), hypoxic (n = 7; FiO2 = 0.14, 18°C, 35% RH), or hot (n = 7; 40°C, 25% RH) conditions. Tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), interleukin 10 (IL-10), and intestinal fatty acid binding protein (I-FABP) were determined at rest and following a cycling normoxic stress test (NST; ~2 weeks before acclimation), pre-acclimation hypoxic stress test (HST1; FiO2 = 0.14, both at 50% normoxic VO2peak; ~1 week before acclimation) and post-acclimation HST (48 h; HST2). Monocyte HSP72 (mHSP72) was determined before and after exercise on day 1, 3, 5, 6, and 10 of acclimation. Accumulation of basal mHSP72 was evident from day 5 (p < 0.05) of heat acclimation and increased further on day 6 (p < 0.01), and day 10 (p < 0.01). In contrast, basal mHSP72 was elevated on the final day of hypoxic acclimation (p < 0.05). Following the NST, plasma TNF-α (–0.11 ± 0.27 ng.mL−1), IL-6 (+0.62 ± 0.67 ng.mL−1) IL-10 (+1.09 ± 9.06 ng.mL−1) and I-FABP (+37.6 ± 112.8 pg.mL−1) exhibited minimal change. After HST1, IL-6 (+3.87 ± 2.56 ng.mL−1), IL-10 (+26.15 ± 26.06 ng.mL−1) and I-FABP (+183.7 ± 182.1 pg.mL−1) were elevated (p < 0.01), whereas TNF-α was unaltered (+0.08 ± 1.27; p > 0.05). A similar trend was observed after HST2, with IL-6 (+3.09 ± 1.30 ng.mL−1), IL-10 (+23.22 ± 21.67 ng.mL−1) and I-FABP (+145.9 ±123.2 pg.mL−1) increased from rest. Heat acclimation induces mHSP72 accumulation earlier and at a greater magnitude compared to matched work hypoxic acclimation, however neither acclimation regime attenuated the systemic cytokine response or intestinal damage following acute exercise in hypoxia.
Highlights
Cells obtained after red cell lysis were fixed and permeabilised (AbD Serotec, Kidlington, UK) and a negative control (FITC, AbD Serotec, Kidlington, UK) or anti-heat shock protein 72 (HSP72) antibody (SPA-810, Enzo lifesciences, Exeter, UK) was added to a final concentration of 100 μg·ml−1, this was used to label 1 × 106 cells according to the manufacturer’s instructions and incubated for 30 min in the dark
We show that heat acclimation produces a gradual and progressive increase in resting Monocyte HSP72 (mHSP72) throughout the 10-day period, whereas the accumulation of resting mHSP72 was only evident on the final day of hypoxic acclimation
This study presents data which show that heat acclimation per-se is a more time efficient means of increasing constitutive stores of monocyte HSP72 when compared to the same period of hypoxic acclimation
Summary
Acclimation to heat or hypoxic stress activates the heat shock response and accumulation of cytoprotective heat shock proteins (HSPs). The aim of this study was to determine the time course of mHSP72 accumulation during acclimation, and to assess intestinal barrier damage and systemic inflammation following hypoxic exercise. Heat acclimation induces mHSP72 accumulation earlier and at a greater magnitude compared to matched work hypoxic acclimation, neither acclimation regime attenuated the systemic cytokine response or intestinal damage following acute exercise in hypoxia. Stress a loss of epithelial integrity, increased GI permeability, and bacterial translocation induce a strong inflammatory response, which is characterized by activation, production, and release of cytokines, which are linked to exertional heat stroke (Bouchama and Knochel, 2002; Leon and Helwig, 2010). 2 h at 4,800 m) has been shown to reduce splanchnic perfusion via a reduction in blood flow to the superior mesenteric artery (Loshbaugh et al, 2006), this finding is not consistent across studies (Mekjavic et al, 2016), with perfusion increasing during prolonged (3 day) exposure (Kalson et al, 2010)
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