Dyspnea is almost a universal complaint of patients with heart failure, particularly during work or exercise. The increase in perception of the work of breathing results from a combination of factors, including excessive ventilation during exercise due to increased dead space from ventilationperfusion mismatching, as well as possibly due to stimulation of receptors in weakened atrophic respiratory muscles that remain underperfused. Because there is little or no correlation between maximal exercise capacity and the extent of left ventricular dysfunction, one cannot assume that patients are markedly disabled simply because their left ventricular ejection fraction is quite low. In nearly all cases of congestive heart failure, a maximal exercise test is useful in terms of quantitatmg the extent of disability and in determining prognosis and suitability for possible heart transplantation. Maximal exercise testing has not proven to be useful with regard to measuring efficacy of drug therapy. Unfortunately, it is not possible to measure VU2 max in all patients with heart failure, and the search is on for a simple and quantitative submaximal exercise end point. The 6 min walk test has been validated to be useful in this regard and is gaining in popularity. Exercise testing is also helpful when attempting to separate pulmonary from cardiac dyspnea. Patients with heart failure are characterized as having an early anaerobic threshold but preserved maximal ventilatory capacity. Patients with pulmonary dyspnea stop exercising because of shortness of breath shortly after or even before achieving an AT. It seems astonishing that the precise mechanism whereby dyspnea occurs in patients with heart failure is still poorly understood. However, it is clear that it is not simply a product of heightened pulmonary capillary wedge pressure. Undoubtedly, abnormal skeletal muscle composition also plays an important role, and simple deconditioning is likely responsible for much of the exercise tolerance in patients with chronic heart failure. Despite our uncertainties regarding the mechanism of exercise intolerance in the syndrome of heart failure, exercise testing remains a useful and sometimes even therapeutic modality in this large patient population. The exalted role of exercise testing in the development and approval of new drugs for the treatment of heart failure, however, can be challenged.