Medical Hypotheses Medicof ffypofheres(19%) 33, 261- 264
Runners: The Intestinal
G. BOUNOUS and A. H. MCARDLE The Montreal General Hospital/McGill (Reprint requests to GB, The Montreal Quebec, Canada H3G IA41
University, Department of Surgery, Montreal, Quebec, Canada. General Hospital, 1650 Cedar Avenue, Room 966, USC, Montreal,
Abstract - Intestinal complications following strenuous, protracted physical activity have been increasingly recognized. Diarrhea, sometimes associated with blood loss, described in marathon runners does not appear to be a common diarrhea but rather the clinical expression of ischemic enteropathy. On the basis of experimental evidence and some clinical data, it is suggested that prefeeding an elemental semi-hydrolyzed diet might reduce the incidence and severity of this intestinal handicap in marathon runners. Perhaps, more importantly, the potentially adverse effects of acute ischemic enteropathy on the cardiovascular system might be accordingly reduced.
Long-distance running has become increasingly popular during the past two decades. The literature concerning gastrointestinal complications of such strenuous and protracted activity has also grown rapidly. During recent years, reports on intestinal blood loss in marathon runners have appeared (7,19,20,31,32) and the possible contribution of such bleeding to runner’s anemia has been discussed (19). Stool specimens converted from hemoccult negative to positive in 22% (32), 13% (19), or 23% (31) of marathon runners. Sometimes frank hemorrhagic diarrhea with visible mucosal lesions are reported (7, 20). The most intriguing finding was that the younger the age and the faster the running times, the more positive was guaiac-test in runners. It was suggested that this sub-group exerted themselves more than the older group did (32). If occult intestinal blood loss Date received Date accepted
is secondary to intestinal ischemia, these lesions could be initiated by increased exertion. Sympathetic vasoconstriction of abdominal viscera occurs during exercise, lending physiologic evidence to this hypothesis (8). It was recently demonstrated that long term fast walking actually prolongs the mouth-to-cecum transit-time of human volunteers. Hence, shortened transit-time could not be construed to be a factor in runner diarrhea (30). Indeed, a more attractive hypothesis is that intestinal blood loss is secondary to intestinal ischemia. Fordtran and Saltin (14) cited evidence that exercise reduces active intestinal absorption in humans. Williams et al (37) observed increased blood levels of catecholamines and corticosteroids in dogs during exercise. Activation of splanchnic nerves or infusion of norepinephrine produces a characteristic vasoconstriction with a
17 October 1989 20 February 1990
262 decrease in intestinal blood flow in proportion to the frequency of stimulation (12). Moreover, the intestinal mucosa is specifically susceptible to low flow states as evidenced by the occurrence of ante-mortem necrosis of the epithelium and the tips of the intestinal villi, along with gastroduodenal erosions, described for some time in dogs as the first recognizable anatomical lesion when systemic blood pressure is lowered to 35 - 40 mmHg for 3 - 4 h (4 - 6,10,29). Similarly, ischemic necrosis of the intestinal mucosa with gastroduodenal erosions has been recognized at autopsy in patients who died after congestive heart failure, burn, hemorrhage and sepsis (3). Endoscopic examination has allowed the observation that gastroduodenal erosions occur within 5 h of injury in more than 80% of the patients with severe burn (11). Experimental evidence has shown in early responses in ischemia that pancreatic elastase interferes with the brush-border protective glycoproteins, and enterocyte membrane disruption exposes the underlying intracellular structures to the digestive action of trypsin (3,4). The first experimental evidence of an ‘intestinal factor’ in the pathogenesis of cardiovascular collapse was produced in 1957 when Lillehei (26) perfused selectively at normal blood pressure, the superior mesenteric artery of dogs in severe hypovolemic hypotension and noted prolonged survival with absence of ischemic enteropathy. Extended survival of dogs was also reported by partial enterectomy before hemorrhagic hypotension (15). Experimental and clinical data strongly suggest that the ischemic intestinal mucosa releases substances, including enteric bacteria toxins and histamine, to which numerous investigators have attributed an important role in the pathogenesis of myocardial failure and death (1,2,17,18,22-24,34,38). Auto-infection with common enteric microorganisms, some of which are antibiotic-resistant, is now recognized to be a leading cause of late morbidity and mortality following trauma, hypotension and shock (27). Indeed, bacterial translocation from the gut, a process whereby indigenous intestinal microflora relocate extraluminally may be responsible for the multiple organ failure syndrome (35). Intravenous injection of E. coli endotoxin is a commonly used experimental method to induce cardiovascular failure and shock (13) in animals. The use of an elemental diet, in the prophylaxis of experimental ischemic enteropathy and shock (6) was conceived with the object to re-
duce, by dietary means, the concentration of potentially noxious physiologic constituents of the intestinal thyme including pancreatic proteases (16,21), prior to shock. Indeed, the pre-feeding during three days of an elemental diet, containing most nutrients in their simple molecular form, has been found to minimize the gastrointestinal lesions in laboratory animals subjected to severe hypovolemia or burn and, in accordance with the role of the ‘intestinal factor’ in the pathogenesis of shock, survival was improved (6,10,25,29,36). This type of protection is mostly prophylactic since a majority of the control animals die in shock within a few hours. In humans, the degree of ischemia-anoxia, and hence the time-sequence and severity of morbid events in the gastrointestinal mucosa, may vary over a wide range. Recent reports in the medical literature indicate that the prophylactic effect of elemental diet on acute ischemic enteropathy may apply to man. Immediate post-operative enteral feeding of an elemental diet was shown to reduce complications of sepsis after major abdominal trauma (33). Significant prevention of hemorrhagic necrosis of the gastrointestinal mucosa and improved survival were obtained in severely burned patients by enteral feeding of an elemental diet (9,28) from the time of admission. If strenuous exercise indeed induces selective gut ischemia, then the administration of an elemental diet for 2- 3 days prior to the athletic event might conceivably minimize the development of ischemic enteropathy. Perhaps, more importantly, the systemic adverse effects of acute ischemic enteropathy on the cardiovascular system might be accordingly reduced. With regard to the above, the following anecdote may be of interest. Rev. Bryan Pearce, Chaplain of The Montreal General Hospital as well as a sled dog racer, consulted us about a problem he was having with one of his dogs. The dog was a good runner, but had limited endurance; the dog would have diarrhea, and when put to the stress of racing, would produce bloody diarrhea. An intestinal biopsy taken by the dog’s veterinarian showed atrophied villous structure. We recommended placing the dog on an elemental diet, giving it 800- 1000 KcaVday. The diarrhea disappeared, the dog gained weight, and after two weeks, a second intestinal biopsy showed normal villous structure. It is of course difficult to extrapolate data from dogs to man. However, it should be noted that
RUNNERS: THE INTESTINAL
even the initial non-hemorrhagic types of ischemic enteropathy, in which only the superficial intestinal epithelium is affected, can produce myocardial depressant effect (25). It is interesting to note that wolves and big cats in the wild instinctively stop their high speed chase of their prey after a relatively short run. It is doubtful that hemorrhagic diarrhea even occurs in these animals. If man persists in his determination to do what wild animals in their natural wisdom will not attempt to do, he should use his intellect in order to better understand the pathophysiology of protracted strenuous exercise. The diarrhea described in marathon runners does not appear to be a common diarrhea but rather the clinical expression of an ischemic enteropathy. The ischemic intestine may release toxins which could adversely affect the cardiovascular function of the athlete and perhaps produce long lasting effects.
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