The underlying pathophysiology in most patients with congestive heart failure is depressed systolic functron of the left ventricle, resulting from either loss of muscle (e.g., myocardial infarction) or diminished contractility. This causes several central hemodynamic changes: (1) decreased cardiac output during exercise or, in more severe congestive heart failure, at rest; (2) elevated left ventricular filling pressures, again with exercise or activity, if not at rest; (3) elevated pulmonary artery and central venous pressures, when congestive heart failure is severe and chronic. These hemodynamic changes lead to signs and symptoms, including dyspnea, fluid retention, exercise intolerance, and peripheral organ dysfunction. This concept of the pathophysiology of congestive heart failure in which the heart and circulation are viewed as a pump and conduit system is, however, an oversimplification. In reality, much of the clinical presehtation of patients with tiongestive heart failure reflects compensatory responses to the underlying myocardial dysfunction, and much of the treatment is devoted to ameliorating excessive manifestations of these adaptive mechanisms. Many of the compensatory responses in congestive heart failure are mediated by neuroendocrine responses and result in changes in the peripheral circulation and organ function, which may themselves negatively influence cardiac function clinical status, and prognosis. Thus, the heart and the periphery are tightly linked, although not always in a simple manner. This article examines one aspect of the periphery, namely, skeletal muscle, and relates changes in muscle blood flow and metaboiism to one of the cardinal manifestations of congestive heart failure-exercise intolerance.