The purpose of this investigation was to determine whether cardiovascular adaptations characteristic of long-term endurance exercise compensate more effectively during cardioselective ₁-adrenergic receptor (BAR) blockade-induced reductions in sympathoadrenergic stimulated contractility. Endurance trained athletes (ET, n=8) and average trained (AT, n=8) subjects performed submaximal cycling exercise at moderate (45% VO_2max) and heavy (70% VO_2max) workloads with and without metoprolol. Cardiac output (Qc), heart rate (HR), and systolic blood pressure (SBP) were recorded at rest and during exercise. Cardiac work was calculated from the triple product of HR, SV, and SBP and myocardial efficiency is represented as cardiac work for a given total body oxygen consumption (VO₂). Metoprolol reduced Qc at 45% VO_2max (p=0.004) and 70% VO_2max (p=0.022) in ET subjects but did not alter Qc in the AT subjects. In ET subjects at 45% VO_2max, metoprolol-induced reductions in Qc were a result of decreases in HR (P < 0.05) and the absence of a compensatory increase in stroke volume (SV, P > 0.05). The cardiac work and calculated cardiac efficiency were reduced with metoprolol in ET subjects at both exercise intensities and in the AT subjects during the high intensity workload, p<0.01. The cardiac work and the calculated cardiac efficiency were not affected by metoprolol in the AT subjects during the 45% VO_2max exercise. Therefore, beta-blockade reduced the amount of pressure generation necessary to produce the same amount of work during moderate intensity exercise which would prove beneficial to patients with heart disease.