Control of Heart Rate by the Autonomic Nervous System
Studies in Man on the Interrelation Between Baroreceptor Mechanisms and Exercise
The control of heart rate by the autonomic nervous system was investigated in conscious human subjects by observing the effects of β-adrenergic blockade with propranolol, of parasympathetic blockade with atropine, and of combined sympathetic and parasympathetic blockade. The increase in heart rate with mild exercise in supine men was mediated predominantly by a decrease in parasympathetic activity; at higher levels of work, however, sympathetic stimulation also contributed to cardiac acceleration. When the response to 80° head-up tilt was compared with the response to exercise in the same subject supine, it appeared that the attainment of an equivalent heart rate was associated with a significantly greater degree of sympathetic activity during tilting than during exercise. Although heart rate was always higher at any given pressure during exercise than it had been at rest, the changes in heart rate that followed alterations in arterial pressure were found to be of similar magnitudes at rest and during exercise; it was therefore concluded that the sensitivity of the baroreceptor system was not altered during exercise. Investigation of the efferent pathways concerned in mediating the baroreceptor-induced changes in heart rate suggested that the relative roles of the sympathetic and parasympathetic systems were nearly equal in the resting state. During exercise, on the other hand, changes in sympathetic activity appeared to be the predominant mechanism by which speeding and slowing of the heart was achieved. It thus appears that baroreceptor-induced alterations in heart rate may be mediated by increased or decreased activity of either efferent system; the ultimate balance, however, is critically dependent on the preexisting level of background autonomic activity.
- atropine sympathetic nervous system
- beta-adrenergic receptors
- heart rate control
- baroreceptor reflex
- Accepted April 4, 1966.
- © 1966 American Heart Association, Inc.