A prospective study was undertaken to determine the frequency of detectable gastrointestinal bleeding in participants of a 100-mile running race. Pre- and postrace questionnaires were utilized to determine training data, gastrointestinal symptoms, diet, and the use of medications during training and during the race, prior known gastrointestinal disease, and 100-mile race experience. Three prerace and the first three postrace stools were sampled for blood using the standard Hemoccult method in 35 runners: 85% of the participants who were Hemoccult negative before the race converted to positive in their postrace samples. Runners with the postrace Hemoccult-positive stools had more frequent and intense nausea, diarrhea, abdominal cramping, and bloating (P less than 0.05) during the race. Lower gastrointestinal symptoms correlated with Hemoccult positivity (P less than 0.05), whereas upper gastrointestinal symptoms did not. The majority of participants showed evidence of gastrointestinal bleeding after the race. Digestive symptoms are common and lower gastrointestinal symptoms correlate with gastrointestinal bleeding.

Occult gastrointestinal bleeding occurs in 8-30% of marathon runners. We hypothesized that cimetidine would decrease bleeding by reducing acid-mediated injury and conducted a blinded, placebo-controlled prospective trial to determine the impact of cimetidine on gastrointestinal symptoms and bleeding during a marathon. Thirty participants in the 1989 Marine Corps or New York City marathons completed pre- and postrace: (1) a questionnaire evaluating demographic, medication usage, training history, and gastrointestinal symptoms; (2) three consecutive stool Hemoccult (HO) cards; and (3) a stool Hemoquant (HQ). Fourteen runners (CR) took 800 mg of cimetidine by mouth 2 hr before the start and 16 runners (PR) took placebo. Three subjects were HO+ prerace and were not analyzed. Three subjects failed to take drug as directed and were analyzed as PR. Five of 14 PR and two of 13 CR were HO+ postrace (P greater than 0.05). Prerace HQ values (PR: 1.49 +/- 0.6 and CR: 0.60 +/- 0.1 mg hemoglobin/g stool) were not significantly different from postrace HQ values (PR: 0.73 +/- 0.2 and CR: 0.86 +/- 0.2 mg Hgb/g stool). Despite postrace HO+ conversion, no individual postrace HQ became abnormal. The frequency of gastrointestinal symptoms was similar for CR and PR, as well as HO- and HO+ individuals. Cimetidine did not significantly affect occult gastrointestinal bleeding as measured by HO or HQ results. This suggests that marathon-associated gastrointestinal symptoms and bleeding may be due to lesions other than acid-mediated disease or hemorrhagic gastritis.

A prospective observational study was undertaken to compare the effect of cimetidine usage immediately before and during a 100-mile running race on the frequency of detectable gastrointestinal bleeding and to relate these data to the frequency and intensity of gastrointestinal symptoms and to training data collected from pre- and postrace questionnaires. Nine of 25 runners in the 1989 Old Dominion 100-mile Endurance Race took 800 mg of cimetidine 1 hr before the start and at 50 miles. Sixteen other runners acted as controls and were not different in age, gender, or training data. All runners also submitted three stool specimens from the week before the race and from the first three bowel movements after the race on standard Hemoccult cards. All runners were Hemoccult negative before the race. One of the 9 (11%) cimetidine runners and 14 of the 16 (87.5%) control runners were Hemoccult positive afterwards (P less than or equal to 0.05). Nausea and vomiting were less in those runners taking cimetidine (P less than or equal to 0.05). There was no difference in the race performance as related to the ability to finish or in the number of miles run during the race. This study may help to define the etiology of this common gastrointestinal bleeding in these ultradistance runners and may be useful in preventing some of the symptoms associated with long-distance running.

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