REFLEX REGULATION OF MUSCLE PERFUSION DURING EXERCISE

骨骼肌在运动过程中需要大量的血流量， 动态运动可能会造成最严重的， 对循环的神经控制的挑战。 如果血液流向 肌肉的新陈代谢能力太低，代谢物积累并激活 肌肉中的感觉神经 这些神经的激活激发了反射 动脉压升高--称为肌肉化学反射。肌肉 化学反射可能是循环的有力调节剂， 这可能是导致动脉压过度升高的原因 运动时周围血管疾病患者的经验 跛行。 肌肉化学反射何时以及如何调节肌肉血液 流动？ 研究将在运动犬（跑步机）中进行， 确保运动单位募集的正常模式，同时避免 麻醉和急性手术创伤的有害影响。 第一个目标 是确定肌肉化学反射何时处于紧张性活动状态 在动态运动中。 方法是制造一种超正常的血液 在自由灌注的肢体中流动，以观察肌肉代谢物的减少是否 减少了这条肢体的化学反射驱动（关闭反射）。 的 第二个目标是确定肌肉化学反射如何调节肌肉血液 当所有活跃肌肉的化学反射被激活时， 同时进行高强度的动态锻炼。 这里的方法是 通过降低心率来减少心输出量（流向所有肌肉的血液） 手术诱导房室（AV）犬的心室起搏 块 关键问题是：肌肉化学反射是否具有血管收缩活性 肌肉？ 第三个目的是确定是否只有心动过速， 神经指令信号的下降导致心输出量的正常增加 和轻度动态运动开始时的动脉压。 的方法 这是通过增加心室起搏来模拟命令信号， 房室传导阻滞犬运动开始是通过神经节的 封锁 第四个目标是确定肌肉化学反射是否 直接影响动脉压力反射。 这里的方法是比较 房室阻滞犬的压力反射曲线（心房率与动脉压） 当1）没有化学反射激活（轻度运动）和2）有 恒定水平的肌肉化学反射激活（恒定的低肌肉 通过髂动脉压迫的血流）。第五个目标是确定 交感血管收缩神经活动是否正常地指向 活跃的肌肉 这里的方法是比较肌肉血管 阻断前后相同血流量和功率下的电导 交感神经 最终目标是量化对 肌肉灌注的一种无反射机制，即肌肉泵。 的方法 这是为了观察是否由二硝基酚输注（低 血液流动和无肌肉泵）结合肌肉泵送作用， 温和的动态运动可以提高肌肉血流量， 在相似的耗氧量下进行适度运动。

The enormous levels of blood flow demanded by skeletal muscle during dynamic exercise probably creates the most severe, routinely imposed challenge to the neural control of the circulation. If blood flow to muscle is too low for its metabolism, metabolites accumulate and activate sensory nerves in the muscle. Activation of these nerves elicits a reflex rise in arterial pressure--called a muscle chemoreflex. Muscle chemoreflexes are potentially a powerful regulator of the circulation and probably account for the exaggerated rise in arterial pressure during exercise when patients with peripheral vascular disease experience claudication. When and how do muscle chemoreflexes regulate muscle blood flow? Studies are to be carried out in exercising dogs (treadmill) thereby ensuring normal patterns of motor unit recruitment while avoiding detrimental effects of anesthesia and acute surgical trauma. The first aim is to determine when, if ever, muscle chemoreflexes are tonically active during dynamic exercise. The approach is to produce a supranormal blood flow in a freely perfused limb to see if a reduction in muscle metabolites reduces the chemoreflex drive from this limb (shuts the reflex off). The second aim is to determine how muscle chemoreflexes regulate muscle blood flow when chemoreflexes from all active muscles are activated simultaneously during heavy dynamic exercise. The approach here is to reduce cardiac output (blood flow to all muscles) by reducing the rate of ventricular pacing in dogs with surgically induced atrioventricular (AV) block. The key question is: do muscle chemoreflexes vasoconstrict active muscle? The third aim is to determine if tachycardia alone, generated by descending neural command signals produces a normal rise in cardiac output and arterial pressure at the onset of mild dynamic exercise. The approach here is to mimic the command signals by increasing ventricular pacing at the onset of exercise in dogs with AV-block made are flexic by ganglionic blockade. The fourth aim is to determine whether muscle chemoreflexes directly influence arterial baroreflexes. The approach here is to compare baroreflex curves (atrial rate vs. arterial pressure) in AV-blocked dogs when 1) there is no chemoreflex activation (mild exercise) and 2) there is a constant level of muscle chemoreflex activation (constant low muscle blood flow by iliac artery compression). The fifth aim is to determine whether sympathetic vasoconstrictor nerve activity is normally directed to active muscle. The approach here is to compare muscle vascular conductance at the same blood flow and work rate before and after blockade of sympathetic nerves. The final aim is to quantify the contribution to muscle perfusion of a non-reflex mechanism, the muscle pump. The approach here is to see if hypermetabolism induced by dinitrophenol infusion (low blood flow and no muscle pump) combined with the muscle-pumping action of mild dynamic exercise raises muscle blood flow to the level achieved during moderate exercise at a similar oxygen consumption.