Chronic heart failure is a well-recognized syndrome in which left ventricular impairment produces a constellation of secondary changes in other organ symptoms leading to symptoms such as muscular fatigue and dyspnoea and objective limitation to exercise tolerance. With modern drug therapy of diuretics and ACE inhibitors, the majority of patients have minimal if any signs of congestion, and yet severe symptomatic limitation remains. This limitation bears little relationship to conventional measures of either left ventricular function or the haemodynamic profile of the patient. The symptoms limiting exercise are predominantly fatigue or dyspnoea, and yet the classical pathophysiological explanations for their genesis now seem inadequate. Recent investigations, as demonstrated, in part, by the research presented in this symposium, attest to the importance of abnormalities in peripheral blood flow and in skeletal muscle in producing both objective limitation to exercise and in explaining the generation of the exercise-limiting symptoms of the syndrome of stable optimally treated chronic heart failure. In addition it is now evident that these muscle changes may in addition have pathophysiological significance for the maintenance of sympatho-excitation during exercise and potentially therefore in the progression of left ventricular remodelling and in the susceptibility to ventricular arrhythmias. This paper presents some of the background evidence which leads to the hypothesis that a feedback loop links changes in skeletal muscle to abnormal reflex cardiopulmonary control which may both limit exercise and be harmful in the progression of the syndrome.