Rhiannon M J Snipe1, Anthony Khoo1, Cecilia M Kitic2, Peter R Gibson3, Ricardo J S Costa4. 1. Department of Nutrition Dietetics and Food, Monash University, Level 1, 264 Ferntree Gully Road, Notting Hill, VIC, 3168, Australia. 2. Sport Performance Optimisation Research Team, School of Health Sciences, University of Tasmania, Locked Bag 1322, Launceston, TAS, 7250, Australia. 3. Department of Gastroenterology, The Alfred Hospital, Monash University, 55 Commercial Road, Melbourne, VIC, 3004, Australia. 4. Department of Nutrition Dietetics and Food, Monash University, Level 1, 264 Ferntree Gully Road, Notting Hill, VIC, 3168, Australia. ricardo.costa@monash.edu.
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% [Formula: see text]O2max in hot (HOT: 35 °C) and temperate (TEMP: 22 °C)-ambient conditions. Rectal temperature (T re) 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 T re (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 T re 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.
RCT Entities:
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% [Formula: see text]O2max in hot (HOT: 35 °C) and temperate (TEMP: 22 °C)-ambient conditions. Rectal temperature (T re) 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 T re (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 T re 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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