While it is recognized that the etiology of exercise-induced gastrointestinal distress is multifactorial, gastrointestinal ischemia is often acknowledged as the main pathophysiological mechanism for the emergence of the symptoms [5, 17, 18]. The other factors are mechanical and nutritional in nature.
Effects of Exercise on Gut Function
The effects of exercise on gastrointestinal function have been studied in different ways. Traditionally, the research focused on gut perfusion, but more recently the effects of exercise on motility, gut barrier function, and absorption have been studied. Having an understanding of the physiology of the gut during exercise is essential to elucidating the factors that may contribute to the development of gastrointestinal symptoms.
Large heterogeneity exists in the response of the gastrointestinal system to exercise. Splanchnic hypoperfusion during exercise ranges from mild circulatory changes to profound gastrointestinal ischemia . In line with this, the consequences of hypoperfusion within the gastrointestinal tract (i.e., epithelial injury and changes in gastrointestinal permeability and epithelial barrier function) differ greatly between individuals. During strenuous physical activity or exercise, norepinephrine is released from nerve endings and on binding to α-adrenoreceptors of the sympathetic nervous system, induces splanchnic vasoconstriction. This will result in an increase in the total splanchnic vascular resistance [20, 21], while, at the same time, vascular resistance with increased activity during exercise in other tissues, such as the heart, lungs, active muscle, and skin, is decreased [22, 23]. During maximal exercise, splanchnic blood flow may be reduced by up to 80 % to provide sufficient blood flow to working muscle and skin. As blood is shunted from viscera to the active tissues , gut mucosal ischemia may result, as well as increases in mucosal permeability [19, 24]. This in turn may be linked to nausea, vomiting, abdominal pain, and diarrhea [17, 25], although convincing evidence for this is lacking .
Changes in Motility
Changes in motility might be observed at different levels of the intestinal tract: the esophagus, the stomach, and the intestine. Decreases in esophageal peristaltic activity, a decrease in lower esophageal sphincter tone, and increased transient lower sphincter relaxation have been observed and could be linked to gastro-esophageal reflux during exercise . The effects on gastric emptying are less clear, but several studies, including a very early study , reported no effect of moderate exercise on gastric emptying. However, during exercise at very high intensity or during intermittent activity, gastric emptying may be affected .
When gastric emptying was studied using the Loughborough intermittent shuttle test, gastric emptying of fluids was reduced approximately by half. Exercising in the heat per se did not appear to affect gastric emptying very much, except at extreme temperatures (49 °C) . However, exercising in a hypohydrated state does seem to significantly affect gastric emptying [30, 31].
Studies performed so far suggest that the effects of exercise on the small bowel as well as on the colon are limited. In one study, motility was investigated in symptomatic and asymptomatic runners using a telemetric pH sensor . It was observed that small bowel and colonic transit times were similar in the two groups at rest. Interestingly, although diarrhea was reported in that study, there was no link with colonic transit time and therefore there must be another cause for the observed gastrointestinal symptoms.
Overall, it seems that moderate exercise has little effect on gastrointestinal tract motility, but when exercise becomes more severe, there may be some inhibiting effects, especially at the level of gastric emptying.
Absorption and Gut Permeability
Studies also suggest that exercise has little effect on intestinal absorption of both water and carbohydrate [33, 34]. However, it must be noted that most studies used exercise intensities that were moderate and durations of exercise that were no longer than 2 h. It is feasible that, during higher intensities of exercise when intestinal blood flow is more compromised, and also after more prolonged exercise, that absorption could be reduced. It has also been reported that with fluid restriction intestinal permeability may be increased , possibly because dehydration ultimately influences gut perfusion.
Oktedalen et al.  reported increased intestinal permeability after a marathon, indicating damage to the gut and impaired gut function. There are numerous techniques available to study gut permeability but to date there is limited information. The information that is available suggests that gut permeability can be compromised in athletes . Although this has not been conclusively linked to gastrointestinal symptoms, one study showed that gut permeability in symptomatic runners was greater than in asymptomatic runners . On the other hand, in one long-distance triathlon in extreme conditions in which gastrointestinal symptoms were highly prevalent, no compromised gut barrier function was observed as measured by bacterial translocation (lipopolysaccharide stimulation). This technique is a marker of mucosal damage and the invasion of Gram-negative intestinal bacteria and/or their toxic constituents (endotoxins) into the blood circulation . More research needs to be conducted before there is a clear understanding of the causes of gastrointestinal distress.
Summary of the Effects of Exercise on Gut Function
In summary, exercise results in numerous changes in the intestinal tract, and most of these effects are intensity dependent. Many of the functions are not affected at low-intensity exercise but become progressively affected at higher intensities. The changes include a reduction in mesenteric blood flow, decreases in esophageal peristaltic activity, decreases in lower esophageal sphincter tone, and increased transient lower sphincter time and a reduction of gastric emptying. As a result of reduced gastrointestinal tract perfusion, absorption might be affected and gut barrier function might be compromised.
The mechanical causes of gastrointestinal problems are related to either impact or posture. For example, symptoms are more common in runners than in cyclists . This is thought to be a result of the repetitive high-impact mechanics of running and subsequent damage to the intestinal lining . This repetitive gastric jostling is also thought to contribute to lower gastrointestinal symptoms such as flatulence, diarrhea, and urgency. The mechanical trauma suffered by the gut from the repetitive impact of running in combination with gut ischemia is probably the cause of the bleeding [3, 25].
Posture can also have an effect on gastrointestinal symptoms. For example, on a bicycle, upper gastrointestinal symptoms are more prevalent possibly due to increased pressure on the abdomen as a result of the cycling position, particularly when in the ‘aero’ position. ‘Swallowing’ air as a result of increased respiration and drinking from water bottles can result in mild to moderate stomach distress. In general, the only way to reduce the effects of these mechanical causes is by training [3, 39].
It is known that nutrition can have a strong influence on gastrointestinal distress, although many of the problems can occur in the absence of any food intake before or during exercise. Fiber, fat, protein, and fructose have all been associated with a greater risk of developing gastrointestinal symptoms. Dehydration, possibly as a result of inadequate fluid intake, may also exacerbate the symptoms. A study by Rehrer et al.  demonstrated a link between nutritional practices and gastrointestinal complaints during a half-Ironman triathlon. Gastrointestinal problems were more likely to occur with the ingestion of fiber, fat, protein, and concentrated carbohydrate solutions during the triathlon. Beverages with high osmolalities (>500 mOsm/L) seemed to be associated with an increased incidence of symptoms.
It appears that foods that delay gastric emptying and might cause a shift of fluids into the intestinal lumen are more likely to cause gastrointestinal symptoms. Highly concentrated carbohydrate solutions with high osmolalities could have this effect. Although subject numbers were too small to perform meaningful statistical analysis, a study by Wallis et al.  reported more severe gastrointestinal symptoms in women with a high carbohydrate intake (1.0 or 1.5 g/min) than in those with a low intake (0 or 0.5 g/min). However, the data are equivocal. For example, in a field study in which runners ran two 16-mile races while consuming carbohydrate at a high rate (1.4 g/min) in the form of gels, very few gastrointestinal symptoms were observed (~10 % of runners reported symptoms) . Perhaps the duration of the exercise was not long enough to cause significant gastrointestinal distress, or, alternatively, carbohydrate content per se is not as important a factor as has often been assumed. In a larger study, with 221 endurance athletes competing in various events including marathons and Ironman races, carbohydrate intake was positively correlated to nausea and flatulence . However, nausea was relatively mild and a higher carbohydrate intake was also correlated with faster finish times, suggesting that nausea did not have any negative effects on performance. Of course, no causal relationships can be obtained from these correlations so the data must be interpreted with caution.
It may be speculated that it is not simply carbohydrate intake that causes gastrointestinal symptoms, but it may be a complex interplay of a number of factors such as carbohydrate concentration, the type of carbohydrate, osmolality and acidity of a beverage that might be linked with gastrointestinal problems. More research is definitely needed to find carbohydrate solutions that reduce the risk of developing gastrointestinal symptoms.