To determine whether prolonged, intense exercise training can improve left ventricular function in patients with coronary artery disease, we studied 25 patients, 52 ± 2 years old (mean + SE), who completed a 12 month program of endurance exercise training and 14 additional patients with comparable maximal exercise capacities and ejection fractions who did not exercise. The training program consisted of endurance exercise of progressively increasing intensity, frequency, and duration. During the last 3 months the patients were running an average of 18 miles/week, or doing an equivalent amount of exercise on a cycle ergometer. Maximal attainable V02 increased 37% (p < .001). Of the 10 patients with effort angina, five became asymptomatic, three experienced less angina, and two were unchanged after training. Ejection fraction was determined by equilibrium radionuclide ventriculography. At rest, ejection fraction was 53 + 3% before and 54 ± 3% after training (p = NS). Ejection fraction did not change during maximal supine exercise before training (52 ± 3%), but after training it increased to 58 + 3% (p < .01). During maximal exercise, systolic blood pressure and the rate-pressure product were higher after training. The systolic blood pressure-end-systolic volume relationship was shifted upward and to the left, with an increase in maximal systolic blood pressure (p < .001) and a smaller end-systolic volume (p < .05), providing evidence for an improvement in contractile state after training. In patients who did not participate in training neither this relationship nor the ejection fraction response to exercise was changed after 12 months. Exercise-induced regional wall motion disorders worsened in the training group. Our finding that prolonged, intense exercise training can bring about an improvement in left ventricular contractile function essentially independent of cardiac loading conditions in some patients with coronary artery disease provides evidence for a reduction in the severity of myocardial ischemia despite an increase in the myocardial 02 requirement.