Summary Background “Exercise‐induced gastrointestinal syndrome” refers to disturbances of gastrointestinal integrity and function that are common features of strenuous exercise. Aim To systematically review the literature to establish the impact of acute exercise on markers of gastrointestinal integrity and function in healthy populations and those with chronic gastrointestinal conditions. Methods Search literature using five databases (PubMed, EBSCO, Web of Science, SPORTSdiscus, and Ovid Medline) to review publications that focused on the impact of acute exercise on markers of gastrointestinal injury, permeability, endotoxaemia, motility and malabsorption in healthy populations and populations with gastrointestinal diseases/disorders. Results As exercise intensity and duration increases, there is considerable evidence for increases in indices of intestinal injury, permeability and endotoxaemia, together with impairment of gastric emptying, slowing of small intestinal transit and malabsorption. The addition of heat stress and running mode appears to exacerbate these markers of gastrointestinal disturbance. Exercise stress of ≥2 hours at 60% VO2max appears to be the threshold whereby significant gastrointestinal perturbations manifest, irrespective of fitness status. Gastrointestinal symptoms, referable to upper‐ and lower‐gastrointestinal tract, are common and a limiting factor in prolonged strenuous exercise. While there is evidence for health benefits of moderate exercise in patients with inflammatory bowel disease or functional gastrointestinal disorders, the safety of more strenuous exercise has not been established. Conclusions Strenuous exercise has a major reversible impact on gastrointestinal integrity and function of healthy populations. The safety and health implications of prolonged strenuous exercise in patients with chronic gastrointestinal diseases/disorders, while hypothetically worrying, has not been elucidated and requires further investigation.

Exertional heat stress (EHS) disturbs the integrity of the gastrointestinal tract leading to endotoxaemia and cytokinaemia, which have symptomatic and health implications. This study aimed to determine the effects of carbohydrate and protein intake during EHS on gastrointestinal integrity, symptoms, and systemic responses. Eleven (male, n = 6; female, n = 5) endurance runners completed 2 h of running at 60% maximal oxygen uptake in 35 °C ambient temperature on 3 occasions in randomised order, consuming water (WATER), 15 g glucose (GLUC), or energy-matched whey protein hydrolysate (WPH) before and every 20 min during EHS. Rectal temperature and gastrointestinal symptoms were recorded every 10 min during EHS. Blood was collected pre- and post-EHS, and during recovery to determine plasma concentrations of intestinal fatty-acid binding protein (I-FABP) as a marker of intestinal epithelial injury, cortisol, endotoxin, and inflammatory cytokines. Urinary lactulose/l-rhamnose ratio was used to measure small intestine permeability. Compared with WATER, GLUC, and WPH ameliorated EHS associated intestinal epithelial injury (I-FABP: 897 ± 478 pg·mL vs. 123 ± 197 pg·mL and 82 ± 156 pg·mL, respectively, p < 0.001) and small intestine permeability (lactulose/l-rhamnose ratio: 0.034 ± 0.014 vs. 0.017 ± 0.005 and 0.008 ± 0.002, respectively, p = 0.001). Endotoxaemia was observed post-EHS in all trials (10.2 pg·mL, p = 0.001). Post-EHS anti-endotoxin antibodies were higher (p < 0.01) and cortisol and interleukin-6 lower (p < 0.05) on GLUC than WATER only. Total and upper gastrointestinal symptoms were greater on WPH, compared with GLUC and WATER (p < 0.05), in response to EHS. In conclusion, carbohydrate and protein intake during EHS ameliorates intestinal injury and permeability. Carbohydrate also supports endotoxin clearance and reduces stress markers, while protein appears to increase gastrointestinal symptoms, suggesting that carbohydrate is a more appropriate option.

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.

The study aimed to determine the effects of mild exertional heat stress on intestinal injury, permeability, gastrointestinal symptoms, and systemic endotoxin and cytokine responses. Ten endurance runners completed 2 h of running at 60% V̇O in warm (WARM: 30°C) and temperate (TEMP: 22°C) ambient conditions. Rectal temperature (T) 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) and cortisol concentrations, and systemic endotoxin and inflammatory cytokine profiles. Urinary lactulose:L-rhamnose ratio (L/R) was used to measure small intestine permeability. Compared with TEMP, WARM significantly increased T from 50 min onwards (38.1±0.3°C vs. 38.4±0.5°C, respectively; p<0.01), gastrointestinal symptoms (p=0.017), post-exercise plasma cortisol (26% vs. 59%, respectively; p<0.001) and I-FABP (127% vs. 184%, respectively; p<0.001) concentrations. Circulatory anti-endotoxin antibodies increased post-exercise (p<0.001) on WARM (20%) and TEMP (28%). No differences were observed for plasma endotoxin concentration (6% vs. 5% increase, respectively) or small intestine permeability (L/R 0.026±0.010 and 0.025±0.015, respectively). Both pro- and anti-inflammatory cytokines increased post-exercise, with inflammatory response cytokines TNF-α (p=0.015) and IL-8 (p=0.044), and compensatory anti-inflammatory cytokines IL-10 (p=0.065), and IL-1ra higher on WARM than TEMP. Findings suggest that exposure to warm ambient conditions during prolonged submaximal running induces transient intestinal epithelial injury, increases gastrointestinal symptoms, and promotes greater perturbations to the systemic cytokine profile compared to running in temperate conditions.

A short-term GFD had no overall effect on performance, GI symptoms, well-being, and a select indicator of intestinal injury or inflammatory markers in nonceliac endurance athletes.