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Fever, exercise, and exposure to a hot environment can all cause symptoms of gastrointestinal dysfunction as they elevate body temperature. Nonetheless, the link between hyperthermia per se and these symptoms is unknown. To test the functional significance of increased body temperature, we investigated the influence of substantial passive hyperthermia on orocecal transit in 12 young, healthy men. Transit time was determined by a consistent rise in H2 concentration in a rebreathing apparatus after oral ingestion of 0.7 g lactulose/kg body weight. Lactulose was given in combination with a 350-ml liquid meal (360 kcal). After raising core temperature in warm water to 38.3 degrees C, orocecal transit time was identical to control (90 +/- 13 min at 38.3 degrees C, 92 +/- 13 min at 37.1 degrees C). While hyperthermia did elevate heart rate and minute ventilation, serum motilin, gastrin, and cortisol were similar in the two conditions. The failure of a passive core temperature rise to alter mouth-to-cecum transit suggests that this aspect of alimentary function is independent of body temperature.

Anecdotes and animal experiments alike suggest that physiological and psychological stress can profoundly alter gastrointestinal function. However, few studies have examined, in humans, real-world stress to see if free-living persons exhibit gut alterations similar to those produced in the laboratory. To investigate this possibility, we studied 16 medical and premedical students during final written examinations. As compared to a control day, the examination created a classic stress response: elevated serum cortisol (16 +/- 1 to 21 +/- 3 micrograms/dl; P < 0.05), ACTH (31 +/- 1 to 33 +/- 1 pg/ml; P < 0.05), heart rate (72 +/- 3 to 79 +/- 3 beats/min; P < 0.05), arterial blood pressure (systolic pressure 106 +/- 2 to 120 +/- 2 torr; P < 0.05; diastolic pressure 72 +/- 2 to 77 +/- 1 torr; P < 0.05), and subjective anxiety (raw score 28 +/- 2 to 47 +/- 3; P < 0.0001). In contrast, subjects displayed identical orocecal liquid transit time (of 0.36 g/kg lactulose in a 240-ml, 250-kcal liquid meal) under control (103 +/- 8 min) and examination conditions (106 +/- 8 min; P = NS). Mean subjective reports of gas, diarrhea, and borborygmi were unchanged on the day of the experiment, although the examination did increase reported abdominal pain (from 0.5 +/- 0.4 to 2.1 +/- 0.5 on a 0-5 analog scale; P < 0.05). We conclude that examination stress in humans can increase gastrointestinal symptoms without altering orocecal transit.

Previous work in our laboratory has found that mild physical activity accelerates mouth-to-large intestinal transit of lactulose in a mixed liquid meal. Because loperamide is commonly used as an antidiarrheal agent, we wondered if it would blunt the orocecal transit acceleration provoked by mild exercise. We investigated this equation in 12 healthy persons by comparing orocolonic liquid transit at rest and in mild exercise. Each subject ingested 8 mg loperamide 1 hr prior to study under both resting and exercise conditions. With loperamide treatment, exercise (walking at 5.6 km/hr) failed to hasten increased H2 excretion (mean transit time 72 +/- 12 min at rest, 90 +/- 15 min in exercise; P = NS). This result contrasts sharply with previously reported controls: loperamide completely abolished exercise-induced orocecal transit acceleration (-23 +/- 5 min in controls; +18 +/- 13 min with loperamide; P0.05). Compared with these same controls, resting transit was not significantly slowed by the drug, while transit in exercise was retarded (64 +/- 5 min in controls, 90 +/- 15 min with loperamide; P = 0.06). Loperamide left unchanged the heart rate and oxygen uptake rises associated with exercise. In summary, by showing that loperamide blocks an exercise effect on the upper gut, these results suggest that the drug might prove effective in treating some gut symptoms induced by physical activity.