The impact of exertional-heat stress on gastrointestinal integrity, gastrointestinal symptoms, systemic endotoxin and cytokine profile

Rhiannon M. J. Snipe, Anthony Khoo, Cecilia M. Kitic, Peter R. Gibson, Ricardo J. S. Costa

Research output: Contribution to journalArticleResearchpeer-review

13 Citations (Scopus)

Abstract

Purpose: The study aimed to determine the effects of exertional-heat stress on gastrointestinal integrity, symptoms, systemic endotoxin and inflammatory responses; and assess the relationship between changes in body temperature and gastrointestinal perturbations. Methods: Ten endurance runners completed 2 h running at 60% V˙ O2max in hot (HOT: 35 °C) and temperate (TEMP: 22 °C)-ambient conditions. Rectal temperature (Tre) and gastrointestinal symptoms were recorded every 10 min during exercise. Blood samples were collected pre- and post-exercise, and during recovery to determine plasma intestinal fatty acid binding protein (I-FABP), cortisol, bacterial endotoxin and cytokine profile. Calprotectin was determined from pre- and post-exercise faecal samples. Urinary lactulose:l-rhamnose ratio was used to measure intestinal permeability. Results: Compared with TEMP, HOT significantly increased Tre (1.4 ± 0.5 vs 2.4 ± 0.8 °C, p < 0.001), cortisol (26 vs 82%, p < 0.001), I-FABP (127 vs 432%, p < 0.001), incidence (70 vs 90%) and severity (58 counts vs 720 counts, p = 0.008) of total gastrointestinal symptoms. Faecal calprotectin and circulating endotoxin increased post-exercise in both trials (mean increase 1.5 ± 2.5 µg/g, p = 0.032, and 6.9 ± 10.3 pg/ml, p = 0.047, respectively), while anti-endotoxin antibodies increased 28% post-exercise in TEMP and decreased 21% in HOT (p = 0.027). However, intestinal permeability did not differ between trials (p = 0.185). Inflammatory cytokines were greater on HOT compared to TEMP (p < 0.05). Increases in Tre were positively associated with I-FABP, IL-10, cortisol, nausea and urge to regurgitate (p < 0.05). Conclusions: Exertional-heat stress induces a thermoregulatory strain that subsequently injures the intestinal epithelium, reduces endotoxin clearance capacity, promotes greater cytokinaemia, and development of gastrointestinal symptoms.

Original languageEnglish
Pages (from-to)389-400
Number of pages12
JournalEuropean Journal of Applied Physiology
Volume118
Issue number2
DOIs
Publication statusPublished - 1 Feb 2018

Keywords

  • Calprotectin
  • Euhydration
  • I-FABP
  • Inflammation
  • Permeability
  • Running

Cite this

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title = "The impact of exertional-heat stress on gastrointestinal integrity, gastrointestinal symptoms, systemic endotoxin and cytokine profile",
abstract = "Purpose: The study aimed to determine the effects of exertional-heat stress on gastrointestinal integrity, symptoms, systemic endotoxin and inflammatory responses; and assess the relationship between changes in body temperature and gastrointestinal perturbations. Methods: Ten endurance runners completed 2 h running at 60{\%} V˙ O2max in hot (HOT: 35 °C) and temperate (TEMP: 22 °C)-ambient conditions. Rectal temperature (Tre) and gastrointestinal symptoms were recorded every 10 min during exercise. Blood samples were collected pre- and post-exercise, and during recovery to determine plasma intestinal fatty acid binding protein (I-FABP), cortisol, bacterial endotoxin and cytokine profile. Calprotectin was determined from pre- and post-exercise faecal samples. Urinary lactulose:l-rhamnose ratio was used to measure intestinal permeability. Results: Compared with TEMP, HOT significantly increased Tre (1.4 ± 0.5 vs 2.4 ± 0.8 °C, p < 0.001), cortisol (26 vs 82{\%}, p < 0.001), I-FABP (127 vs 432{\%}, p < 0.001), incidence (70 vs 90{\%}) and severity (58 counts vs 720 counts, p = 0.008) of total gastrointestinal symptoms. Faecal calprotectin and circulating endotoxin increased post-exercise in both trials (mean increase 1.5 ± 2.5 µg/g, p = 0.032, and 6.9 ± 10.3 pg/ml, p = 0.047, respectively), while anti-endotoxin antibodies increased 28{\%} post-exercise in TEMP and decreased 21{\%} in HOT (p = 0.027). However, intestinal permeability did not differ between trials (p = 0.185). Inflammatory cytokines were greater on HOT compared to TEMP (p < 0.05). Increases in Tre were positively associated with I-FABP, IL-10, cortisol, nausea and urge to regurgitate (p < 0.05). Conclusions: Exertional-heat stress induces a thermoregulatory strain that subsequently injures the intestinal epithelium, reduces endotoxin clearance capacity, promotes greater cytokinaemia, and development of gastrointestinal symptoms.",
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The impact of exertional-heat stress on gastrointestinal integrity, gastrointestinal symptoms, systemic endotoxin and cytokine profile. / Snipe, Rhiannon M. J.; Khoo, Anthony ; Kitic, Cecilia M.; Gibson, Peter R.; Costa, Ricardo J. S.

In: European Journal of Applied Physiology, Vol. 118, No. 2, 01.02.2018, p. 389-400.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - The impact of exertional-heat stress on gastrointestinal integrity, gastrointestinal symptoms, systemic endotoxin and cytokine profile

AU - Snipe, Rhiannon M. J.

AU - Khoo, Anthony

AU - Kitic, Cecilia M.

AU - Gibson, Peter R.

AU - Costa, Ricardo J. S.

PY - 2018/2/1

Y1 - 2018/2/1

N2 - Purpose: The study aimed to determine the effects of exertional-heat stress on gastrointestinal integrity, symptoms, systemic endotoxin and inflammatory responses; and assess the relationship between changes in body temperature and gastrointestinal perturbations. Methods: Ten endurance runners completed 2 h running at 60% V˙ O2max in hot (HOT: 35 °C) and temperate (TEMP: 22 °C)-ambient conditions. Rectal temperature (Tre) and gastrointestinal symptoms were recorded every 10 min during exercise. Blood samples were collected pre- and post-exercise, and during recovery to determine plasma intestinal fatty acid binding protein (I-FABP), cortisol, bacterial endotoxin and cytokine profile. Calprotectin was determined from pre- and post-exercise faecal samples. Urinary lactulose:l-rhamnose ratio was used to measure intestinal permeability. Results: Compared with TEMP, HOT significantly increased Tre (1.4 ± 0.5 vs 2.4 ± 0.8 °C, p < 0.001), cortisol (26 vs 82%, p < 0.001), I-FABP (127 vs 432%, p < 0.001), incidence (70 vs 90%) and severity (58 counts vs 720 counts, p = 0.008) of total gastrointestinal symptoms. Faecal calprotectin and circulating endotoxin increased post-exercise in both trials (mean increase 1.5 ± 2.5 µg/g, p = 0.032, and 6.9 ± 10.3 pg/ml, p = 0.047, respectively), while anti-endotoxin antibodies increased 28% post-exercise in TEMP and decreased 21% in HOT (p = 0.027). However, intestinal permeability did not differ between trials (p = 0.185). Inflammatory cytokines were greater on HOT compared to TEMP (p < 0.05). Increases in Tre were positively associated with I-FABP, IL-10, cortisol, nausea and urge to regurgitate (p < 0.05). Conclusions: Exertional-heat stress induces a thermoregulatory strain that subsequently injures the intestinal epithelium, reduces endotoxin clearance capacity, promotes greater cytokinaemia, and development of gastrointestinal symptoms.

AB - Purpose: The study aimed to determine the effects of exertional-heat stress on gastrointestinal integrity, symptoms, systemic endotoxin and inflammatory responses; and assess the relationship between changes in body temperature and gastrointestinal perturbations. Methods: Ten endurance runners completed 2 h running at 60% V˙ O2max in hot (HOT: 35 °C) and temperate (TEMP: 22 °C)-ambient conditions. Rectal temperature (Tre) and gastrointestinal symptoms were recorded every 10 min during exercise. Blood samples were collected pre- and post-exercise, and during recovery to determine plasma intestinal fatty acid binding protein (I-FABP), cortisol, bacterial endotoxin and cytokine profile. Calprotectin was determined from pre- and post-exercise faecal samples. Urinary lactulose:l-rhamnose ratio was used to measure intestinal permeability. Results: Compared with TEMP, HOT significantly increased Tre (1.4 ± 0.5 vs 2.4 ± 0.8 °C, p < 0.001), cortisol (26 vs 82%, p < 0.001), I-FABP (127 vs 432%, p < 0.001), incidence (70 vs 90%) and severity (58 counts vs 720 counts, p = 0.008) of total gastrointestinal symptoms. Faecal calprotectin and circulating endotoxin increased post-exercise in both trials (mean increase 1.5 ± 2.5 µg/g, p = 0.032, and 6.9 ± 10.3 pg/ml, p = 0.047, respectively), while anti-endotoxin antibodies increased 28% post-exercise in TEMP and decreased 21% in HOT (p = 0.027). However, intestinal permeability did not differ between trials (p = 0.185). Inflammatory cytokines were greater on HOT compared to TEMP (p < 0.05). Increases in Tre were positively associated with I-FABP, IL-10, cortisol, nausea and urge to regurgitate (p < 0.05). Conclusions: Exertional-heat stress induces a thermoregulatory strain that subsequently injures the intestinal epithelium, reduces endotoxin clearance capacity, promotes greater cytokinaemia, and development of gastrointestinal symptoms.

KW - Calprotectin

KW - Euhydration

KW - I-FABP

KW - Inflammation

KW - Permeability

KW - Running

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U2 - 10.1007/s00421-017-3781-z

DO - 10.1007/s00421-017-3781-z

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VL - 118

SP - 389

EP - 400

JO - European Journal of Applied Physiology

JF - European Journal of Applied Physiology

SN - 1439-6319

IS - 2

ER -