The diminished cardiac output response to exercise with advancing age may be attributable to intrinsic inability of the old ventricle to respond appropriately and/or to an additional loading imposed upon the ventricle by the aged vascular system. The steady (resistance) and pulsatile (characteristic impedance) load components together comprise the vascular load faced by the ejecting ventricle. To study the effect of exercise on both vascular components of load, the aortic input impedance was measured in chronically instrumented young and old beagle dogs during graded treadmill exercise before and after beta blockade. Ascending aortic flow was measured by a cuff electromagnetic flow probe, and pressure was measured by a high-fidelity semiconductor transducer. At low levels of exercise the old animals demonstrated a striking 20% increase in characteristic impedance and a 28% decrease in peripheral resistance with no increase in stroke volume. This vascular loading and limitation in stroke volume persisted across the higher exercise levels. In contrast, the young group demonstrated no increase in characteristic impedence, a progressive decrease in peripheral resistance, and a progressive increase in stroke volume across the same exercise levels. These age differences in vascular response and ventricular output were abolished by beta blockade. The groups did not demonstrate a difference in heart rate response, but the young had a greater increase in external left ventricular power than the old across exercise. These data demonstrated a profound difference in the response of young and old vasculature to exercise. At low and intermediate exercise levels the pulsatile vascular load appeared to be a major factor in the limitation of stroke volume in old dogs. At high levels of exercise, the limited exercise response in the old dog may be caused in part by a diminished inotropic responsiveness as well as by the vascular loading.