MECHANISMS CAUSING SYMPATHETIC DISCHARGE DURING EXERCISE

Project: Research project

Project Details

Description

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.
StatusFinished
Effective start/end date9/1/957/31/96

Funding

  • National Heart, Lung, and Blood Institute

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