Copyright © 2002 by the European Society of Cardiology.
Peak oxygen uptake is not determined by cardiac noradrenaline spillover in heart failure
Division of Cardiology, Department of Medicine, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada
revised July 24, 2001; accepted July 25, 2001
Abstract
Aims We recently found that resting muscle sympathetic nerve activity is inversely related to peak oxygen uptake (VO2 peak) in patients with heart failure, suggesting a peripheral neurogenic limit to exercise in heart failure. No such relationship was observed in healthy controls. To determine whether this observation is specific to sympathetic discharge to skeletal muscle, we tested the null hypothesis that VO2 peak would not relate to resting cardiac noradrenaline spillover, which is also elevated in heart failure.
Methods and Results We measured cardiac noradrenaline spillover at rest by a radiotracer technique and VO2 peak, during cycle ergometry, by open circuit spirometry in 49 heart failure patients (mean age 54·4±1·4 (SE)). There was a significant relationship between age and peak VO2 (P=0·022). There was no significant relationship between cardiac noradrenaline spillover and either absolute or relative VO2 peak (P=0·136), with age included in a multiple linear regression model, and none between cardiac noradrenaline spillover and the percent predicted VO2 peak achieved (P=0·34).
Conclusions Reduced exercise capacity in heart failure relates more closely to sympathetic traffic to skeletal muscle than to cardiac sympathetic outflow, as assessed by noradrenaline spillover. This finding lends further support to the concept of a predominately peripheral neurogenic limit to exercise.
Key Words: Cardiac noradrenaline spillover, heart failure, exercise capacity, oxygen uptake
f1 Correspondence: Dr J. S. Floras, Suite 1614, 600 University Avenue, Toronto, Ontario, Canada, M5G 1X5.
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