Significant controversy surrounds the etiology of exercise-related GI motility disorders. Some have speculated that compression of the colon by psoas muscle hypertrophy alters GI motility (3). Others have proposed that increased sympathetic nerve tone during exercise disrupts GI transit by preferentially shunting blood away from the gut to skin and skeletal muscles (3,6). Investigators have also postulated that running alters bowel transit time by jostling the abdomen, although the bouncing of abdominal contents during exercise has not been clearly shown to alter GI motility significantly (16,17). Hormonal fluctuations of catecholamines, secretin, glucagon, motilin, gastrin, beta-endorphin, and vasoactive intestinal peptide (VIP) have all been observed during exercise and may play an additional role in affecting GI motility (4,5,6,14,18,19,20,21).

The impact of physical activity on whole gut transit has not been clearly determined. Most researchers have concluded that mild to moderate physical activity does not lead to significantly altered mouth-to-cecum transit time (7,12,13,14,15,16,18,22,23), but some have suggested that exercise does accelerate this process (3,4,19). It is clear that each organ, from the esophagus to the colon, plays a unique role in gut transit time during exercise. Esophageal peristaltic contractions undergo altered durations, amplitudes, and frequencies as exercise intensity
increases (7,20,22,24,25,26). However, there is no clear consensus that the functional esophageal changes that occur with physical activity significantly modify esophageal motility (9,27). Light to moderate exercise (<70% VO_{2 max}) minimally impacts gastric emptying, whereas more intense exercise significantly delays emptying of the stomach (3,6,7,9,12,14,18,22,23,28). Small bowel data is conflicting, but transit time and propulsion speed typically decline as physical activity levels increase (6,12,14,15,29). Exercise negligibly alters large intestine motility, the single greatest contributing factor to whole gut transit (3,6,12,13,29). Thus, the overall impact of exercise on the speed with which food passes from the mouth to the anus during physical activity is likely clinically insignificant (21,28,29).

Although GI motility disorders that occur in association with exercise most likely have a multifactorial etiology, relative ischemia of the GI tract contributes significantly (3,4,5,6,10,18). Visceral blood has been noted to decrease by 30% during mild to moderate activity (11) and by up to 80% during maximal exertion (5,19,22,30). Hyperthermia during exercise may also exacerbate relative ischemia (10). In addition, intense physical exertion may disrupt the intestinal barrier, increase permeability, enhance the uptake of toxic substances, and augment ischemic-related GI distress (5,14,31). Hydration status is also significant, and a greater percentage of body weight lost during a marathon is a strong predictor of increased GI motility complaints (3,6). Of note, routine ingestion of sports drinks containing carbohydrates during exercise leads to more GI complaints than water consumption (8).

Owing to the mild symptoms of most GI motility disorders, athletes often do not seek medical attention (10). Among those athletes who present for evaluation, consideration should be given to other causes including inflammatory bowel disease, irritable bowel syndrome, travel-related illnesses, infectious diarrhea, and colon cancer. Clinical suspicion of these conditions merits testing for fecal leukocytes, erythrocytes, ova, parasites, fat, and bacterial pathogens (5). Upper and lower endoscopy may also be necessary in certain cases. Initial therapy should focus on hydrating the athlete with cold, low-osmolarity solutions (3). Severely dehydrated athletes may need intravenous (IV) hydration or hospitalization. After symptoms subside, training intensity and duration should be reduced for 1 to 2 weeks. Cross training in temperate conditions may help minimize symptoms when resuming exercise (5).

Awareness and prevention of GI motility disorders among athletes is essential to minimize the frequency and severity of symptoms. Exacerbating substances such as high fiber or high fat foods, milk, and fruits should be avoided for several hours before exercise (5,13). Moderate consumption of caffeinated beverages is acceptable, as there do not appear to be any significant negative GI motility effects of consuming limited amounts of caffeine before exercise (8). The routine use of cathartics or laxatives should be avoided (3,12). Supplemental protein and herb extracts may induce GI upset, so their use before activity should be minimized (6). Urination or bowel movements before exercise may also help attenuate symptoms (12). If symptoms regularly occur despite the interventions mentioned in the previous text, then a trial of anti-peristalsis agents such as loperamide may be considered, although their use may negatively affect performance (3,5). In general, most GI motility disorders are relatively benign and can be conservatively managed with limited medical intervention.

Identifying an upper GI or lower GI source of an athlete’s bleeding is usually challenging. Hemorrhagic gastritis is the most commonly identified cause of exercise-related GI bleeding (3,12,14). The colon is the second most frequently implicated site, but no confirmed cases of esophageal bleeding have been reported in association with physical activity (12,14,30). Although small bowel bleeding is rare, exercise-related anemia due to ileal ulcers diagnosed by capsule endoscopy has been reported (35). Exercise-induced GI bleeding may also be related to irritated hemorrhoids or anal fissures. Nonetheless, the causes of athletic GI bleeding often remain obscure, and most cases have no identified sources (12,30,32).

Some have suggested that the use of NSAIDs may increase the risk of GI bleeding among active individuals (6,32,33,34), but others have found no significant associations between athletic NSAID use and GI bleeding (3,5,12,30,36). One study of 34 healthy runners who completed the Chicago marathon found that runners who ingested ibuprofen had significantly increased intestinal
permeability, but the reported GI symptoms did not correlate with the observed alterations in permeability (31). Moreover, the use of NSAIDs was not associated with the frequency or severity of subjective GI symptoms. Nonetheless, NSAID-induced toxicity results in over 100,000 hospitalizations and 16,500 deaths yearly in the United States for serious GI complications, often without any prior symptoms of GI distress (2). As such, NSAID use should be limited by athletes, especially because there is no conclusive evidence supporting the routine use of NSAIDs in treating most soft tissue injuries (37).

Several etiologies have been proposed to explain exercise-related GI bleeding. Most researchers believe that relative bowel ischemia produces regional blood flow attenuation (3,11,12,13,30,32,36). As noted previously, intestinal blood flow may decrease by 30% to 80%, depending on the intensity and duration of activity, and this diminished bowel perfusion may subsequently increase the risk of bleeding (5,11,14,17,19,28). However, the amount or intensity of exercise has not been consistently correlated with GI bleeding, so other factors likely also play a role (12). The proximal colon appears to be particularly susceptible to ischemia and may be traumatized by high-impact mechanical jarring during exercise, the “cecal-slap syndrome”(5,30,32). Decreased lower esophageal sphincter pressures that occur during exercise increase the risk of bleeding due to irritation of the gastroesophageal junction by the stomach contents (33). Arachidonic acid is the precursor of the mucosal-protecting prostaglandins through the cyclooxygenase enzymes (COX-1, COX-2), and decreased levels of arachidonic acid in the membranes of GI mucosa have been postulated to be another risk factor for GI bleeding in active older adults (38). Finally, athletic GI bleeding may occur as a result of inflammatory bowel disease, coagulation disorders, systemic connective tissue disorders, or GI cancer (3,5,39).

Small amounts of GI bleeding have not been shown to produce detrimental health effects, and most sports-related cases are self-limited and spontaneously resolve. Nonetheless, significant or life-threatening blood loss may occur among athletes (12,30). Athletes with brisk GI bleeding need prompt stabilization and treatment. The athlete should be placed supine with the legs elevated to assist blood return to the heart (Trendelenburg position). Intravenous access should be obtained with two large-bore (16-gauge) catheters. Fluid resuscitation may be accomplished with normal saline or Ringer’s lactate solution. Athletes with substantial blood loss should be transferred to an appropriate facility for endoscopic evaluation and further treatment. Blood transfusions may rarely be necessary. Physical activity should be discontinued until symptoms have fully resolved and a comprehensive evaluation completed (5). Athletes who have successfully recovered from significant exercise-related GI bleeding will need to advance activities slowly under careful supervision.

Prevention of GI bleeding may be effective in some instances. Dehydration and hypovolemia should be avoided, as they both can augment intestinal ischemia (33). In addition, the routine use of an H₂-receptor antagonists (H₂RAs) before exercise may help prevent GI bleeding due to hemorrhagic gastritis (3,5,30). If NSAIDs are regularly used by athletes with a history of GI bleeding, concomitant treatment with a proton pump inhibitor (PPI) should be considered, but H₂RAs do not appear to have the same protective effect (1,2). Routine, moderate intensity exercise among older adults has been associated with a decreased risk of severe GI bleeding and may have preventive effects in certain populations (36). Appropriate training with gradual activity progression may minimize episodes of GI bleeding by enhancing GI blood flow, although the gut generally adapts poorly to the increased physiological stress of high-intensity exercise (6).