increase capillary permeability (Granger et al., 1981) and have been reported to produce mucosal lesions in the small intestine of humans (Klemperer et al., 1940), dogs (Chiu et al., 1970), rats (Bacalzo et al., 1971), and cats (Haglurid and Lundgren, 1973). The pathogenesis of the rise in capillary permeability has been attributed to the production of superoxide radicals (Granger et al., 1981), and the pathogenesis of the mucosal lesions has been attributed to hypoxia (Ahren and Haglund, 1973). Thus, it has been hypothesized that severe hyperthermia (a) produces mucosal lesions in the small intestine from tissue hypoxia, (b) increases capillary permeability, and (c) results in endotoxemia (see Figure 4-1). Systemic endotoxemia has been shown in human heat stroke victims (Coridis et al., 1972; Graber et al., 1971), in ultramarathon runners who collapsed during competition in the heat (Brock-Utne et al., 1988), and following strenuous exercise (Bosenberg et al., 1988).

The diarrhea that occurs in marathon runners, if coincident with bleeding, may be a clinical manifestation of ischemic enteropathy (Bounous and McArdle, 1980). The effects of exercise-heat stress on GI function and performance can range from mild discomfort to serious impairment. For example, GI bleeding, which is often coincident with diarrhea, may be trivial (Eichner, 1989) or lethal (Thompson et al., 1982).

Gaudin et al. (1990) performed a standard endoscopy examination on seven runners 15 minutes before and 12 hours after they performed a maximal distance training run (18 to 50 km). Because the race was not competitive, stress was not considered to be a factor. Mucosal biopsy specimens of the upper digestive track revealed histologically pathological features in all runners (Table 4–2). These features included vascular lesions, ranging from congestion to hemorrhage, and evidence of reduced mucosal secretion (estimated from PAS [para -aminosalicylic acid] staining). The intensity of the lesions was independent of running distance, and a measure of running intensity was not provided. The prevalence of the lesions was independent of clinical symptoms.

Schwartz et al. (1990) studied 41 runners who completed the 1988 Chicago Marathon. Nine of the runners experienced GI bleeding, and three of these consented to esophagogastroduodenoscopy and colonoscopy within 48 hours after the race. Four other runners consented to these procedures 4 to 30 days after the race. Of the three runners examined within 48 hours, two had oozing gastric antral erosions, and the third had patchy areas of hyperemic and eroded mucosa limited to the splenic flexure. The latter portion of the colon is a circulatory watershed area, which suggests that a condition of reduced blood flow may contribute to necrosis of the colonic mucosa. Thus, injury can occur in both upper and lower segments of the GI track. There were no endoscopic findings in the four runners examined three or more days after the race, which suggests that restoration of the