Exercise intolerance is a major cause of morbidity in chronic heart failure (CHF) and has traditionally been attributed to skeletal muscle hypoperfusion during exercise. However, intrinsic abnormalities in skeletal muscle biochemistry and histology may also play an important role in the pathophysiology of exertional fatigue in CHF. Studies using 31P nuclear magnetic resonance (NMR) spectroscopy have demonstrated early skeletal muscle metabolic changes during exercise including excessive acidification and phosphocreatine depletion. Patients with CHF show muscle fibre atrophy with transformation of type I to II fibres accompanied by a decrease in oxidative enzyme capacity. Most of the drugs currently used to treat patients with CHF do not improve oxygen availability within exercising muscle or exercise capacity although some of them increase blood flow to skeletal muscle or alter the pattern of blood flow distribution. Physical training programmes improve exercise performance, ventilation, autonomic function and symptomatic status in CHF. Training can also increase cardiac output and reduce peripheral vascular resistance with concomitant increases in blood flow to exercising muscle and reduced arterial and venous lactate. 31P-NMR studies in patients with CHF have demonstrated significantly less acidification and phosphocreatine depletion during exercise after physical training. Animal studies suggest that the NMR changes in skeletal muscle of CHF depend on both the severity of heart failure and physical deconditioning, whereas training may reverse or prevent these alterations.