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

We recently found that resting muscle sympathetic nerve activity is inversely related to peak oxygen uptake (VO(2) 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 VO(2) peak would not relate to resting cardiac noradrenaline spillover, which is also elevated in heart failure.

We measured cardiac noradrenaline spillover at rest by a radiotracer technique and VO(2) 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 VO(2) (P=0.022). There was no significant relationship between cardiac noradrenaline spillover and either absolute or relative VO(2) 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).

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 predominantly peripheral neurogenic limit to exercise.