Mechanisms of exercise intolerance in cardiac failure: abnormalities of skeletal muscle and pulmonary function

The syndrome of chronic heart failure is characterized by exercise intolerance. Exercise is limited by shortness of breath and fatigue, and either symptom occurs in the same patient depending on the type of exercise performed. Exercise capacity correlates poorly with indices of central hemodynamic function, but the increased ventilatory response in chronic heart failure correlates well with exercise capacity. Possible pulmonary causes have been explored, including increased dead space ventilation, abnormal airway function, and abnormal diffusion capacity. However, the finding of hypocapnia and hyperoxemia in arterial blood during exercise in patients with heart failure suggests that blood gas values reflect hyperventilation, and that any abnormality of pulmonary function is secondary to changes elsewhere. Skeletal muscle is abnormal in chronic heart failure, and shows changes in structure, bulk, exercise capacity, blood flow, and intrinsic metabolic activity. The relative importance of these abnormalities is not clearly determined, but the possible presence of an ergo- or metaboloreceptor connection between abnormal exercising muscle and the ventilatory response to exercise suggest a mechanism linking the two cardinal symptoms of chronic heart failure.