Work by a number of laboratories over the last decade has revealed that skeletal muscle in patients with congestive heart failure (CHF) exhibits altered metabolism, biochemistry, and histology. These alterations appear to be at least in part independent of systemic hemodynamic abnormalities and they lead to abnormal muscle function. Furthermore, muscle dysfunction may play a role in limiting exercise capacity. While blood flow to exercising muscle may be impaired in CHF, both the functional and metabolic changes are, to some degree, independent of the changes in blood flow. Deconditioning and muscle atrophy may be responsible for some of these functional metabolic alterations in muscle, but other factors appear to be operating as well. Finally, the finding that many of the changes in skeletal muscle associated with CHF can be reversed by exercise training suggests that activity should be encouraged in patients with CHF.