Exercise-induced gastrointestinal syndrome (EIGS) is a common characteristic of exercise. The causes appear to be multifactorial in origin, but stem primarily from splanchnic hypoperfusion and increased sympathetic drive. These primary causes can lead to secondary outcomes that include increased intestinal epithelial injury and gastrointestinal hyperpermeability, systemic endotoxemia, and responsive cytokinemia, and impaired gastrointestinal function (i.e. transit, digestion, and absorption). Impaired gastrointestinal integrity and functional responses may predispose individuals, engaged in strenuous exercise, to gastrointestinal symptoms (GIS), and health complications of clinical significance, both of which may have exercise performance implications. There is a growing body of evidence indicating heat exposure during exercise (i.e. exertional-heat stress) can substantially exacerbate these gastrointestinal perturbations, proportionally to the magnitude of exertional-heat stress, which is of major concern for athletes preparing for and competing in the upcoming 2020 Tokyo Olympic Games. To date, various hydration and nutritional strategies have been explored to prevent or ameliorate exertional-heat stress associated gastrointestinal perturbations. The aims of the current review are to comprehensively explore the impact of exertional-heat stress on markers of EIGS, examine the evidence for the prevention and (or) management of EIGS in relation to exertional-heat stress, and establish best-practice nutritional recommendations for counteracting EIGS and associated GIS in athletes preparing for and competing in Tokyo 2020.

The study aimed to determine the effects of 24-h high (HFOD) and low (LFOD) fermentable oligo-, di-, monosaccharide, and polyol (FODMAP) diets before exertional heat stress on gastrointestinal integrity, function, and symptoms. Eighteen endurance runners consumed a HFOD and a LFOD (double-blind crossover design) before completing 2 h of running at 60% maximal oxygen uptake in 35 °C ambient temperature. Blood samples were collected before and after exercise to determine plasma cortisol and intestinal fatty acid binding protein (I-FABP) concentrations, and bacterial endotoxin and cytokine profiles. Breath hydrogen (H2) and gastrointestinal symptoms (GIS) were determined pre-exercise, every 15 min during, and in recovery. No differences were observed for plasma cortisol concentration between diets. Plasma I-FABP concentration was lower on HFOD compared with LFOD (p = 0.033). A trend for lower lipopolysaccharide binding protein (p = 0.088), but not plasma soluble CD14 (p = 0.478) and cytokine profile (p > 0.05), responses on HFOD was observed. A greater area under the curve breath H2 concentration (p = 0.031) was observed throughout HFOD (mean and 95% confidence interval: HFOD 2525 (1452–3597) ppm·4 h−1) compared with LFOD (1505 (1031–1978) ppm·4 h−1). HFOD resulted in greater severity of GIS compared with LFOD (pre-exercise, p = 0.017; during, p = 0.035; and total, p = 0.014). A 24-h HFOD before exertional heat stress ameliorates disturbances to epithelial integrity but exacerbates carbohydrate malabsorption and GIS severity in comparison with a LFOD. Novelty Twenty-four-hour high FODMAP diet ameliorated disturbances to gastrointestinal integrity. Twenty-four-hour high FODMAP diet results in greater carbohydrate malabsorption compared with low FODMAP diet. Incidence of GIS during exertional heat stress were pronounced on both low and high FODMAP diets, but greater GIS severity was observed with high FODMAP diet.

Strenuous exercise is synonymous with disturbing gastrointestinal integrity and function, subsequently prompting systemic immune responses and exercise-associated gastrointestinal symptoms, a condition established as “exercise-induced gastrointestinal syndrome.” When exercise stress and aligned exacerbation factors (i.e., extrinsic and intrinsic) are of substantial magnitude, these exercise-associated gastrointestinal perturbations can cause performance decrements and health implications of clinical significance. This potentially explains the exponential growth in exploratory, mechanistic, and interventional research in exercise gastroenterology to understand, accurately measure and interpret, and prevent or attenuate the performance debilitating and health consequences of exercise-induced gastrointestinal syndrome. Considering the recent advancement in exercise gastroenterology research, it has been highlighted that published literature in the area is consistently affected by substantial experimental limitations that may affect the accuracy of translating study outcomes into practical application/s and/or design of future research. This perspective methodological review attempts to highlight these concerns and provides guidance to improve the validity, reliability, and robustness of the next generation of exercise gastroenterology research. These methodological concerns include participant screening and description, exertional and exertional heat stress load, dietary control, hydration status, food and fluid provisions, circadian variation, biological sex differences, comprehensive assessment of established markers of exercise-induced gastrointestinal syndrome, validity of gastrointestinal symptoms assessment tool, and data reporting and presentation. Standardized experimental procedures are needed for the accurate interpretation of research findings, avoiding misinterpreted (e.g., pathological relevance of response magnitude) and overstated conclusions (e.g., clinical and practical relevance of intervention research outcomes), which will support more accurate translation into safe practice guidelines.

Considering the recent growth of exercise gastroenterology research focusing on exercise-induced gastrointestinal syndrome mechanisms, response magnitude, prevention and management strategies, the standardized assessment of gastrointestinal symptoms (GIS) is warranted. The current methodological study aimed to test the reliability of a modified visual analog scale for assessing GIS during exercise, in response to a variety of exertional-stress scenarios, with and without dietary intervention. Recreational endurance runners (n = 31) performed one of the three exercise protocols, which included: 2-hr running at 70% in temperate (24.7 °C) ambient conditions, with fluid restriction; 2-hr running at 60% in hot (35.1 °C) ambient conditions, while consuming chilled water immediately before and every 15 min during exercise; and 2-hr running at 60% in temperate (23.0 °C) ambient conditions, while consuming 30 g/20 min carbohydrate (2∶1 glucose∶fructose, 10% temperate w/v), followed by a 1-hr distance test. GIS was monitored pre-exercise, periodically during exercise, and immediately postexercise. After wash out, participants were retested in mirrored conditions. No significant differences (p > .05) were identified between test–retest using Wilcoxon signed-rank test for all GIS (specific and categorized), within each exercise protocol and the combined protocols. Strong correlations were observed for gut discomfort, total GIS, upper GIS, and nausea (rs = .566 to rs = .686; p < .001), but not for lower GIS (rs = .204; p = .232). Cohen’s magnitude of difference was minimal for all GIS (specific δ < 0.14 and categorized δ < 0.08). The modified visual analog scale for assessing GIS during exercise appears to be a reliable tool for identifying incidence and severity of GIS in cohort populations and is sensitive enough to detect exertional and intervention differences.

Purpose: The study aimed to determine the effect of diurnal versus nocturnal exercise on gastrointestinal integrity and functional responses, plasma lipopolysaccharide binding protein (LBP) and soluble CD14 (sCD14) concentrations (as indirect indicators of endotoxin responses), systemic inflammatory cytokine profile, gastrointestinal symptoms, and feeding tolerance. Methods: Endurance runners (n = 16) completed 3 h of 60% V ˙O2max (22.7°C, 45% relative humidity) running, on one occasion performed at 0900 h (400 lx; DAY) and on another occasion at 2100 h (2 lx; NIGHT). Blood samples were collected pre-and postexercise and during recovery to determine plasma concentrations of cortisol, catecholamines, claudin-3, I-FABP, LBP, and sCD14 and inflammatory cytokine profiles by ELISA. Orocecal transit time (OCTT) was determined by lactulose challenge test given at 150 min, with concomitant breath hydrogen (H 2 ) and gastrointestinal symptom determination. Results: Cortisol increased substantially pre-to postexercise on NIGHT (+182%) versus DAY (+4%) (trial-time, P = 0.046), with no epinephrine (+41%) and norepinephrine (+102%) trial differences. I-FABP, but not claudin-3, increased pre-to postexercise on both trials (mean = 2269 pg•mL −1 , 95% confidence interval = 1351-3187, +143%) (main effect of time [MEOT], P < 0.001). sCD14 increased pre-to postexercise (trial-time, P = 0.045, +5.6%) and was greater on DAY, but LBP decreased (MEOT, P = 0.019, −11.2%) on both trials. No trial difference was observed for systemic cytokine profile (MEOT, P = 0.004). Breath H 2 responses (P = 0.019) showed that OCTT was significantly delayed on NIGHT (>84 min, with n = 3 showing no breath H 2 turning point by 180 min postexercise) compared with DAY (mean = 54 min, 95% confidence interval = 29-79). NIGHT resulted in greater total gastrointestinal symptoms (P = 0.009) compared with DAY. No difference in feeding tolerance markers was observed between trials. Conclusion: Nocturnal exercise instigates greater gastrointestinal functional perturbations and symptoms compared with diurnal exercise. However, there are no circadian differences to gastrointestinal integrity and systemic perturbations in response to the same exertional stress and controlled procedures.