Adrenergic Regulation During Exercise in Patients with Heart Failure
Sympathetic nervous activity in chronic heart failure is augmented when compared with normal subjects at identical exercise workloads. There are two possible mechanisms for this alteration, relating to the somatic reflex evoked by chemosensitive muscle afferents; one is an exaggerated somatic exercise reflex resulting from decreased inhibitory influences of arterial and cardiopulmonary baroreceptors, and the other is an increase in hypoxic or related metabolic stimuli to muscle afferents caused by an inadequate perfusion of exercising muscle.
To clarify which mechanism is more important, we analyzed the somatic reflex from the response of plasma norepinephrine (NE) levels to graded muscle hypoxia induced by 3-stage bicycle exercise in 5 patients without organic heart disease and 27 patients with heart failure. Muscle hypoxia was assessed by mixed venous oxygen tension (PVO2). Plasma NE levels increased exponentially with a decrease in PVO2. The relationship between plasma NE levels and PVO2 was not affected by the presence or the severity of heart failure, indicating that the somatic reflex is not exaggerated in heart failure. To simulate a low perfusion of exercising muscle, restudy was performed after an administration of 40 mg metoprolol in 6 of the patients. After the administration, PVO2 decreased and plasma NE levels increased at each exercise level, and their relationship was exactly similar to that before administration. Thus, we conclude that the augmented sympathetic response to exercise in heart failure is attributed to an increase in hypoxic stimulus to muscle afferents caused by an inadequate perfusion of active muscle, but not to an exaggerated somatic exercise reflex.
KeywordsHeart Failure Chronic Heart Failure Sympathetic Nervous Activity Plasma Norepinephrine Bicycle Exercise
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