Gastrointestinal physiology has traditionally been studied at rest and the methodology is typically vali dated for resting conditions. Experimental stress on the GI tract is more typically generated by drugs or disease. Evaluation of GI physiology under the stress of exercise often requires extensive modifications in experimental techniques and most GI physiologists are untrained in these methods. Intestinal motility, for example, is extremely sensitive to motion artifact. This has limited the published literature.
The most dramatic change associated with exercise is that cardiac output is diverted to exercising muscles and visceral blood flow falls by 50-80% of baseline values [1,2]. During prolonged events there is increased demand for absorption of water, electrolytes and nutrients. This relative hypovolemia may be compounded by hyperthermia, dehydration and, potentially, the use of non-steroidal anti-inflammatory drugs (NSAIDs). The stomach and colon seem particularly sensitive to ischemia induced by exercise.
The autonomic nervous system (ANS) is altered by acute and chronic exercise. During acute stress, the sympathetic nervous system predominates. However, with habitual exercise, the ANS adapts and parasym-pathetic effects predominate. These effects alter intestinal transit, blood flow and permeability. GI hormones are variably changed by exercise and these changes can also alter a variety of GI functions.
The mechanical effects of exercise on the GI tract are uncertain but could alter GI function by changing intra-abdominal pressure or facilitating trauma to more mobile sections of the GI tract.
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