Does oral ingestion of nutrients during exercise interfere with the blood flow to exercising skeletal muscles?

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Nutrient ingestion induces a profound increase in the splanchnic blood flow because the gastrointestinal organs lemand energy supply for digesting and absorbing the nutrients ingested. On the contrary, exercise stimulus causes a decrease in the splanchnic blood flow to drive a lager portion of cardiac output to the exercising skeletal muscles. It has not yet been known which signal between nutrition and exercise has a priority when these opposite signals occurred simultaneously It is also unclear how the cardiovascular system compromises these conflicting demands during exercise. The pin-pose in the present study is to investigate these questions. In the first experiments : We determined whether oral ingestion of glucose and fructose increased the blood flow in superior mesenteric artery (SMA), one of major arteries supplied to the gastrointestinal tract, during rest and sustained static exercise. Ten healthy female volunteers orally ingested 100-140 ml of 5 % of glucose or fructose so … More lution during rest. The blood flow in SMA (SMBF) was measured by Doppler ultrasound technique, and heart rate and arterial blood pressure measured by ECG and Finapres methods. It was found that the glucose ingestion produced a significant increase in SMBF approximately 15 mm after the ingestion, whereas the fructose ingestion had no effects on SMBF despite the identical volume and concentration in both drinks. In the second experiments : These subjects also joined the experiments to perform sustained static handgrip exercise at 30 % of maximum voluntary contraction for 2 mm before and after ingestion of 5 % glucose solution. The results showed that the exercise did not change SMBF from the resting level and rather increased slightly at the end of sustained exercise. The slight increase in SMBF was significantly greater during exercise after glucose ingestion than that during the exercise before glucose ingestion. These results indicated that drinking glucose solution was probably more powerful stimulus than the exercise stimulus. The SMA might be to some degree exempt from flow-reducing participation during exercise. In the third experiments : The results in the first experiments raise a question whether SMA was not a target vessel for the muscle metaboreflex arising from exercising skeletal although the muscle metaboreflex has been believed to induce a reduction in the splanchnic vascular beds. To verify this question, we examined the effects of postexercise muscle ischemia on SMBF. The subjects performed the same static exercise as mentioned in the first experiments and followed by a 3-min arterial occlusion. The arterial occlusion was done by pressure cuff inflation above 22OmmHg applied to the upper arm of exercised forearm. The postexercise ischemia showed a significant increase in SMBF in both exercise performed before and after glucose ingestion. The increase in SMBF observed during postexercise muscle ischemia was in parallel with the significant increase in arterial blood pressure. From these results, it appeared that SMA was not sensitive to the muscle metaboreflexes and that the profound increase in SMBF during postexercise ischemia was related to the elevation of arterial blood pressure. Less