MECHANISMS CAUSING SYMPATHETIC DISCHARGE DURING EXERCISE

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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.