MECHANISMS CAUSING SYMPATHETIC DISCHARGE DURING EXERCISE

描述（申请人摘要）：收缩引起的反射 骨骼肌和“中央指挥”被广泛认为是两个 在运动中控制交感神经系统的机制。 对每种机制的贡献存在相当大的争议 运动引起的交感神经输出增加， 灌注后肢骨骼肌、后肢皮肤和肾脏的床。 例如，在人类中，中央指挥被认为显著增加， 交感神经流出到皮肤，但只有很小的影响， 骨骼肌相反，反射被认为会显著增加 交感神经流出到后肢骨骼肌，但几乎没有 对皮肤的影响。在人类中没有关于 两种机制在肾交感神经调控中的作用 在运动过程中放电。同时记录下 单纤维节后纤维，我们建议比较， 未麻醉的去脑猫，反射的贡献， 运动时交感神经放电。我们 将验证我们正在记录交感神经放电：1）通过 证明了纤维是被电脉冲激活的 适用于胸部或腰部链; 2）通过证明这一点， 通过神经节阻滞防止激活;和3）通过证明 刺激动脉压力感受器会抑制基线放电。 中央指挥部会被电子或化学物质 刺激丘脑底和中脑运动区的部位。 该反射将由低强度电刺激引起， 供应小腿三头肌的周围神经。拟议 实验将检验以下假设。第一，反射， 而不是中枢指令激活交感神经流出到肾脏。 第二，中央指令，而不是反射，激活了交感神经， 流出到皮肤。第三，反射，而不是中央指令， 激活交感神经流出到非运动后肢骨骼肌。 此外，我们将能够确定使用单纤维记录 技术是否中央命令和反射冲击相同 节后纤维这些实验将首先提供 时间，关于中央指挥部所扮演角色的明确信息 运动时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.