The current working hypothesis of exercise intolerance in patients with CHF indicates that an initial reduction in cardiac output, secondary to either systolic or diastolic dysfunction, results in a variety of complex and inter-related pathophysiologic alterations in the skeletal muscle, the vasculature, the pulmonary system, and several neurohumoral systems. These numerous compensatory mechanisms, although they work to preserve vital body functions, they ultimately result in exercise intolerance. Thus, the syndrome of CHF provides a unique opportunity to evaluate the role of several fundamental principles of exercise physiology.