https://orcid.org/0000-0003-3069-486X
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ABSTRACT
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.
Acknowledgments
AM and RC contributed to the introduction. RC and RS contributed to the description of EIGS. AM, RC, and RS contributed to the impact of exertional-heat stress on EIGS. RC, AM, SG, and RS contributed to various parts of the prevention and management strategies. RC, AM, and SG contributed to various parts of the practical recommendations. RC was responsible to compiling the manuscript sections. All authors reviewed the full manuscript and approved the final version. The material within is the result of work supported with resources and the use of facilities at BASE Facility, Monash University, Department of Nutrition Dietetics & Food. Funding support from BASE Facility, Monash University, Department of Nutrition Dietetics & Food; Monash University, Faculty of Medicine Nursing & Health Sciences, Strategic Grant Scheme; and Sports Medicine Australia Research Foundation Grant.
Abbreviations
| BM | = | Body mass |
| BML | = | Exercise-induced body mass loss |
| CFU | = | Colony-forming units |
| CH4 | = | Methane |
| CO2 | = | Carbon dioxide |
| CARS | = | Compensatory anti-inflammatory response syndrome |
| EAH | = | Exercise-associate hyponatremia |
| EIGS | = | Exercise-induced gastrointestinal syndrome |
| FFM | = | Fat free mass |
| FODMAP | = | Fermentable oligo-di-mono-saccharides and polyols |
| GIS | = | Gastrointestinal symptoms |
| H2 | = | Hydrogen |
| H2S | = | Hydrogen sulfide |
| I-FABP | = | Intestinal fatty acid binding protein |
| IL | = | Interleukin |
| LBP | = | Lipopolysaccharide binding protein |
| LPS | = | Lipopolysaccharide |
| L/R | = | Lactulose to rhamnose ratio |
| NFκβ | = | Nuclear factor kappa beta |
| OCTT | = | Orocecal transit time |
| POsmol | = | Plasma osmolality |
| Pv | = | Plasma volume |
| RH | = | Relative humidity |
| RPE | = | Rating of perceived exertion |
| sCD14 | = | Soluble CD14 |
| SIRS | = | Systemic inflammatory response syndrome |
| Tamb | = | Ambient temperature |
| Tmax | = | Maximal temperature |
| TNF | = | Tumor necrosis factor |
| Tre | = | Rectal temperature |
| Ttymp | = | Tympanic temperature |
| V̇O2max | = | Maximal oxygen uptake |
| Wmax | = | Maximal power (wattage) output |
Disclosure statement
No potential conflict of interest was reported by the authors.