The effects of exercise on central hemodynamic mechanisms and the changes induced by treatment have been studied invasively in approximately 500 men with essential hypertension. In patients with mild hypertension, the increase in blood pressure (BP) during dynamic exercise is similar to that seen in normal subjects, but in patients with severe hypertension it is steeper. During dynamic exercise total peripheral resistance is increased in all categories of hypertensive patients, including young subjects with apparently "normal" resistance at rest. The increase in stroke volume in transition from rest to exercise is subnormal, probably reflecting increased stiffness in the left ventricle. Static exercise causes dramatic increase in systolic as well as diastolic BP. Most antihypertensive agents control BP similarly during exercise and at rest. The hemodynamic mechanisms, however, differ greatly. The beta blockers induce a long-term reduction in cardiac output, muscle blood flow and, frequently, endurance capacity. In contrast, alpha-receptor blockers, calcium antagonists and angiotensin converting enzyme inhibitors all reduce total peripheral resistance and do not decrease blood flow. Increase in endurance time has been reported with long-term calcium antagonist treatment. It would seem logical to select an antihypertensive drug that does not reduce exercise capacity when treating physically active patients with mild and moderate hypertension.