Patients with heart failure (HF) often have limited exercise capacity because of dyspnea and fatigue . It was previously thought that this exercise limitation was due entirely to cardiac dysfunction, and that treatment with inotropes and vasodilators, such as angiotensin converting enzyme inhibitors and the combination of hydralazine and nitrates, would improve exercise capacity. (See "Inotropic agents in heart failure due to systolic dysfunction" and "ACE inhibitors in heart failure due to systolic dysfunction: Therapeutic use".)
Although these drugs can improve the cardiac output and, with certain vasodilators, patient survival, they may not acutely improve exercise tolerance [2-5]. Thus, factors in addition to the low cardiac output and reduced skeletal muscle blood flow must contribute to poor exercise tolerance and fatigue.
In the 1970s, exercise training of HF patients was discouraged due to concerns of worsening symptoms and detriment to the disease process itself. Early observations in the 1980s documented improvements in exercise function for patients with HF with a low rate of complications.
These observations were followed by a series of studies that demonstrated that significant biochemical and functional abnormalities in skeletal muscle are present in patients with HF and play a large role in the exercise intolerance . Inactivity is in part responsible, leading to muscle atrophy. In addition, skeletal muscle utilizes high-energy phosphates in an inefficient manner; as a result, lactic acid accumulates at a more rapid rate than in normal controls, contributing to muscle fatigue and limited exercise capacity. Skeletal muscle dysfunction can also involve the respiratory muscles, which may contribute to fatigue and dyspnea on exertion . These biochemical and functional abnormalities, when added to deconditioning, can result in even greater impact on physical function. (See "Skeletal muscle dysfunction and exercise intolerance in heart failure".)
The importance of skeletal muscle dysfunction provides part of the rationale for the use of cardiac rehabilitation in patients with HF. This topic will review the evidence demonstrating the benefit of cardiac rehabilitation in patients with mild to moderate (NYHA class II to III) heart failure (table 1) and make recommendations about an exercise prescription. Measurement of peak oxygen uptake (peak VO2) to assess exercise capacity and prognosis is discussed separately. (See "Exercise capacity and VO2 in heart failure".)