Peak oxygen uptake is not determined by cardiac noradrenaline spillover in heart failure

Aims We recently found that resting muscle sympathetic nerve activity is inversely related to peak oxygen uptake (W, 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 mill hypothesis that 10, 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 10, 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 1 0, (P=0.022). There was no significant relationship between cardiac noradrenaline spillover and either absolute or relative Vover dotO(2) peak (P=0.136), with age included in a multiple linear regression model, and none between cardiac noradrenaline spillover and the percent predicted Vover dotO(2) 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. (C) 2001 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.