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Cardiopulmonary exercise testing (CPET) has been used for the assessment of severity of heart failure (HF), secondary to left ventricular systolic dysfunction. Initial studies determined that oxygen consumption (VO2) during exercise, as a measure of functional capacity, correlated well with the hemodynamic responses related to chronic HF. These studies led to the use of peak VO2 as a prognostic indicator in chronic HF. In addition, the use of several ventilatory parameters, eg, minute ventilation/carbon dioxide production during submaximal and peak exercise, were shown to have additive and (in some studies) superior prognostic value in patients with chronic HF. However, most of these studies were performed before beta-adrenergic blockade became the main focus of therapy in chronic HF. Unlike other drugs used in the treatment of HF, these drugs do not consistently improve exercise capacity as measured by peak VO2. Several retrospective studies and one prospective study have examined the effect of long-term beta-blocker therapy on the prognostic value of CPET in patients with chronic HF. These studies indicate that patients on beta-blockers have improved overall cardiovascular outcomes compared with patients not on these drugs. In addition, peak exercise VO2 still has prognostic value in beta-blocked patients; however, the thresholds for increased risk and need for transplantation have to be lower than in patients not on these drugs. There appears to be a real demand for a comprehensive survival score tool that includes the use of beta-blockade, along with CPET performance.

Patients with chronic heart failure have diminished exercise capacity as a major aspect of their clinical syndrome, regardless of the cause of their left ventricular contractile dysfunction. The mechanisms for the reduction in exercise capacity are multifactorial and include central cardiac, peripheral vascular, respiratory, and skeletal muscle maladaptations that accompany the pathophysiology of heart failure. Increased sympathetic nervous system activity and elevations in circulating neurohormones and cytokines also influence the cardiovascular and metabolic responses to exercise in these patients. Despite the improvements in clinical outcomes with beta-blockers and resynchronization therapy in heart failure patients, their exercise capacity remains substantially reduced when compared with normal age-matched patients. Exercise training has the potential to reverse or improve most of the abnormal physiologic responses to exercise in these patients, and it may serve as adjunctive therapy to standard medical care of these patients. In addition, a body of evidence is being accumulated that suggests that exercise training itself has important secondary prevention benefit in these patients. This review identifies the potential mechanisms whereby exercise training may improve exercise capacity in patients with chronic heart failure and presents the current information regarding clinical outcomes of this therapy.