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

营养素的摄入引起内脏血流量的显著增加，因为胃肠器官为消化和吸收所摄入的营养素提供能量。相反，运动刺激导致内脏血流量减少，从而将更大部分的心输出量驱动到运动的骨骼肌。目前尚不清楚当营养和运动之间的信号同时发生时，这些相反的信号具有优先权，也不清楚心血管系统如何在运动期间协调这些相互冲突的需求。本研究的pin-pose就是对这些问题的探讨。在第一个实验中：我们确定口服葡萄糖和果糖是否增加了上级肠系膜动脉（SMA）的血流量，供应到胃肠道的主要动脉之一，在休息和持续的静态运动。10名健康女性志愿者口服5%的葡萄糖或果糖100-140 ml， ...更多信息 休息时的清洁。应用多普勒超声技术测量SMA（SMBF）血流，用心电图法和Finapres法测量心率和动脉血压。结果发现，葡萄糖摄入产生了显着增加SMBF摄入后约15毫米，而果糖摄入SMBF没有影响，尽管相同的体积和浓度在两种饮料。在第二个实验中：这些受试者还加入实验，在摄入5%葡萄糖溶液之前和之后以30%的最大自主收缩进行持续的静态握力锻炼2 mm。结果表明，运动并没有改变SMBF从休息水平，而是略有增加，在持续运动结束。运动后SMBF的轻微增加显著大于运动前。这些结果表明，饮用葡萄糖溶液可能是比运动刺激更强大的刺激。SMA可能在某种程度上免于在运动期间减少流量的参与。在第三个实验中：第一个实验的结果提出了一个问题，即SMA是否不是运动骨骼肌引起的肌肉代谢反射的靶血管，尽管肌肉代谢反射被认为会诱导内脏血管床的减少。为了验证这个问题，我们研究了运动后肌肉缺血对SMBF的影响。受试者进行与第一次实验中提到的相同的静态运动，然后进行3分钟的动脉闭塞。动脉闭塞是通过将高于22 OmmHg的压力袖带充气施加到运动前臂的上臂来完成的。运动后缺血显示，在摄入葡萄糖之前和之后进行的运动中SMBF显著增加。运动后肌肉缺血期间观察到的SMBF增加与动脉血压显著增加平行。从这些结果看来，SMA对肌肉代谢反射不敏感，运动后缺血时SMBF的显著增加与动脉血压升高有关。少

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