Heat and Hypoxic Acclimation Increase Monocyte Heat Shock Protein 72 but Do Not Attenuate Inflammation following Hypoxic Exercise

Ben J Lee, Charles D Thake

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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.

Original languageEnglish
Pages (from-to)811
JournalFrontiers in Physiology
Volume8
DOIs
Publication statusPublished - 16 Oct 2017

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HSP72 Heat-Shock Proteins
Acclimatization
Monocytes
Hot Temperature
Inflammation
Fatty Acid-Binding Proteins
Exercise Test
Interleukin-10
Interleukin-6
Heat-Shock Response
Heat-Shock Proteins

Keywords

  • Journal Article

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Heat and Hypoxic Acclimation Increase Monocyte Heat Shock Protein 72 but Do Not Attenuate Inflammation following Hypoxic Exercise. / Lee, Ben J; Thake, Charles D.

In: Frontiers in Physiology, Vol. 8, 16.10.2017, p. 811.

Research output: Contribution to journalArticle

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title = "Heat and Hypoxic Acclimation Increase Monocyte Heat Shock Protein 72 but Do Not Attenuate Inflammation following Hypoxic Exercise",
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.",
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N2 - 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.

AB - 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.

KW - Journal Article

U2 - 10.3389/fphys.2017.00811

DO - 10.3389/fphys.2017.00811

M3 - Article

VL - 8

SP - 811

JO - Frontiers in Physiology

JF - Frontiers in Physiology

SN - 1664-042X

ER -