Sports Dietitians Australia and Ultra Sports Science Foundation Joint Position Statement: A Practitioner Guide to the Prevention and Management of Exercise-Associated Gastrointestinal Perturbations and Symptoms

Abstract

It is now well-established that exercise can disturb various aspects of gastrointestinal integrity and function. The pathophysiology of these perturbations, termed "exercise-induced gastrointestinal syndrome (EIGS)," can lead to exercise-associated gastrointestinal symptom (Ex-GIS) inconveniences. EIGS outcomes can impact physical performance and may lead to clinical manifestation warranting medical intervention, as well as systemic responses leading to fatality. Athlete support practitioners seek prevention and management strategies for EIGS and Ex-GIS. This current position statement aimed to critically appraise the role of EIGS and Ex-GIS prevention and management strategies to inform effective evidence-based practice and establish translational application. Intervention strategies with mostly consistent beneficial outcomes include macronutrient (i.e., carbohydrate and protein) intake and euhydration before and during exercise, dietary manipulation of fermentable oligo-, di-, and mono-saccharides and polyols (FODMAP), and gut training or feeding tolerance adjustments for the specific management of Ex-GIS from gastrointestinal functional issues. Strategies that may provide benefit and/or promising outcomes, but warrant further explorations include heat mitigating strategies and certain nutritional supplementation (i.e., prebiotics and phenols). Interventions that have reported negative outcomes included low-carbohydrate high-fat diets, probiotic supplementation, pharmaceutical administration, and feeding intolerances. Owing to individual variability in EIGS and Ex-GIS outcomes, athletes suffering from EIGS and/or support practitioners that guide athletes through managing EIGS, are encouraged to undertake gastrointestinal assessment during exercise to identify underlying causal and exacerbation factor/s, and adopt evidence-based strategies that provide individualized beneficial outcomes. In addition, abstaining from prevention and management strategies that present unclear and/or adverse outcomes is recommended.

Fig. 1

Updated schematic description of exercise-induced gastrointestinal syndrome (EIGS) and links to exercise-associated gastrointestinal symptoms (Ex-GIS). Text boxes: Darkest grey, instigation and final outcome; dark grey, primary causal mechanisms; medium grey, secondary outcomes to the causal mechanisms; light grey, subsequent follow-on outcomes in response to the secondary outcomes. Beige arrows indicate EIGS pathway flow and direction, and black arrows indicate intra-EIGS linkage. ^aSpecialized antimicrobial protein-secreting (i.e., Paneth cells) and mucus-producing (goblet cells) cells aid in preventing intestinal-originating pathogenic microorganisms entering systemic circulation. ^bIncrease in neuroendocrine activation and suppressed submucosal and myenteric plexuses may result in epithelial cell loss and subsequent perturbed epithelial tight junctions [49, 54]. ^cSplanchnic hypoperfusion and subsequent intestinal ischemia and injury (including mucosal erosion) may result in direct (e.g., enteric nervous system and/or enteroendocrine cell) or indirect (e.g., braking mechanisms) alterations to gastrointestinal motility [–29, 37, 55]. ^dGastrointestinal brake mechanisms: nutritive and non-nutritive residue along the small intestine, including the terminal ileum, results in neural and enteroendocrine negative feedback to gastric activity [, –58]. ^eAggressive acute or low-grade, prolonged mechanical strain is proposed to contribute to disturbances to epithelial integrity (i.e., epithelial cell injury and tight junction dysregulation) and subsequent “knock-on” effects for gastrointestinal functional responses [50]. ^fMetabolic acidosis associated with high intensity exercise and hypoglycemia associated with prolonged endurance exercise may prompt Ex-GIS [–53]. ^gLumen originating to circulatory translocation of pathogenic agents may include, but is not limited to: whole bacteria, bacterial endotoxins (e.g., lipopolysaccharide, lipid A, flagella, and/or peptidoglycan), exocrine originated digestive enzymes, and/or food protein allergens [38]. ^hBacteria and bacterial endotoxin MAMPs and stress induced DAMPs are proposed to contribute toward the magnitude of systemic immune responses (e.g., systemic inflammatory profile) [59]. *Primary role in EIGS pathophysiology still warrants substantial exploration and investigation. EIGS, exercise-induced gastrointestinal syndrome; GIS, gastrointestinal symptoms; MAMPs, microorganism molecular patterns; DAMPs, danger-associated molecular patterns. Adapted with permission from “Systematic review: exercise-induced gastrointestinal syndrome- implication for health and disease,” by R.J.S. Costa, R.M.J. Snipe, C. Kitic, and P. Gibson, 2017, Alimentary Pharmacology and Therapeutics, 46(3), pp. 246–265. Copyright 2017 by John Wiley & Sons Ltd. [3]

Fig. 2

Schematic flow illustration of the professional practice guidance for the prevention or management of exercise-induced gastrointestinal syndrome (EIGS) and aligned exercise-associated gastrointestinal symptoms (Ex-GIS) [12, 67, 75]