Chronic heart failure (CHF) is a common condition with a poor prognosis. It is associated with debilitating limiting symptoms, even with optimal modern medical management. Foremost among these symptoms is severe exercise intolerance with pronounced fatigue and dyspnoea at low exercise workloads. The UK National Health Service has highlighted it as a key target for improved treatment with the aim of symptom relief and restoration of optimal functional capacity.1 The severity of symptomatic exercise limitation varies between patients, and this appears to bear little relation to the extent of the left ventricular systolic dysfunction measured at rest, or to markers of central haemodynamic disturbance (fig 1).2 There may be several reasons for this. It may be that measurements of ventricular function at rest bear only a poor relation to changes in central haemodynamic function that occur on exercise,3 and therefore predict only poorly exercise capacity. It may be that on the background of left ventricular impairment, variability in preservation of right ventricular function and the adequacy of the pulmonary vasculature to dilate and accept a blood flow and to match this flow with ventilation is impaired. Thirdly, it may be that changes, which occur in the periphery as a consequence of the systemic effects of heart failure, may have become the factors limiting exercise more than the heart dysfunction that initiated the syndrome.4 There is evidence in the literature for all three of these hypotheses.