MECHANISMS CAUSING SYMPATHETIC DISCHARGE DURING EXERCISE

描述(申请人的摘要)：因合同而产生的反射 骨骼肌和“中枢指挥”被广泛认为是两个 运动中控制交感神经系统的机制。 对于每一种机制的贡献都存在相当大的争议 运动引起的血管交感神经输出的增加 充满后肢骨骼肌、后肢皮肤和肾脏的床。 例如，在人类中，中央指挥权被认为显著增加 交感神经流出到皮肤，但对皮肤只有很小的影响 骨骼肌。相比之下，这种反射被认为明显增加。 交感神经流出到后肢骨骼肌，但几乎没有 对皮肤的影响。在人类身上没有关于 这两种机制在控制肾交感神经中的作用 在运动过程中出院。在记录大脑的冲动活动时 单纤维节后纤维，我们建议在 未麻醉去大脑的猫，反射的贡献与 运动时由中枢指挥到交感神经放电。我们 将验证我们是否记录到交感神经放电：1)通过 证明纤维是由电脉冲激活的 应用于胸链或腰链；2)通过证明这一点 通过神经节阻滞来阻止激活；以及3)通过展示 刺激动脉压力感受器会抑制基线放电。 中央司令部将由电气或化学物质引发 刺激丘脑下部和中脑运动区。 这种反射将由低强度电刺激引起 供应小腿三头肌的周围神经。建议数 实验将检验以下假设。首先，这种反射， 但不是中枢指令，而是激活交感神经流出到肾脏。 其次，激活交感神经的是中枢指令，而不是反射 流出到皮肤。第三，条件反射，而不是中央命令， 激活交感神经流出到非锻炼的后肢骨骼肌。 此外，我们将能够使用单光纤记录来确定 无论是中枢性指令还是反射技术都冲击在一起 神经节后纤维。这些实验将为第一次 时间，关于中央司令部所扮演角色的明确信息 运动中控制交感神经放电的反射。

DESCRIPTION (Applicant's abstract): A reflex arising from contracting skeletal muscle and "central command" are widely believed to be the two mechanisms that control the sympathetic nervous system during exercise. Considerable controversy exists over the contribution of each mechanism to the exercise-induced increase in sympathetic outputs to the vascular beds perfusing hindlimb skeletal muscle, hindlimb skin, and the kidney. In humans, for example, central command is thought to increase markedly sympathetic outflow to skin, but to have only a small effect on that to skeletal muscle. The reflex in contrast is thought to increase markedly the sympathetic outflow to hindlimb skeletal muscle, but to have little effect on that to the skin. There is no information in humans on the roles played by the two mechanisms in controlling renal sympathetic discharge during exercise. While recording the impulse activity of single fiber post-ganglionic fibers, we propose to compare in unanesthetized decerebrate cats, the contributions of the reflex with those of central command to sympathetic discharge during exercise. We will verify that we are recording sympathetic discharge: 1) by demonstrating that the fibers are activated by an electrical pulse applied to the thoracic or lumbar chain; 2) by demonstrating that this activation is prevented by ganglionic blockade; and 3) by demonstrating that stimulation of arterial baroreceptors inhibits baseline discharge. Central command will be elicited by either electrical or chemical stimulation of sites in the subthalamic and midbrain locomotor regions. The reflex will be elicited by low intensity electrical stimulation of peripheral nerves supplying the triceps surae muscles. The proposed experiments will test the following hypotheses. First, that the reflex, but not central command, activates sympathetic outflow to the kidney. Second, that central command, but not the reflex, activates sympathetic outflow to the skin. Third, that the reflex, but not central command, activates sympathetic outflow to non-exercising hindlimb skeletal muscle. In addition, we will be able to determine using single fiber recording techniques whether central command and the reflex impinge on the same post-ganglionic fibers. These experiments will provide, for the first time, definitive information about the roles played by central command the reflex in controlling sympathetic discharge during exercise.