We tested the hypothesis that the pericardium, by restricting heart size, limits maximal cardiac output and oxygen consumption. We studied 15 pigs. Five underwent maximal treadmill running before and 14-21 days after thoracotomy and pericardiectomy; these pigs also received sequential volume infusions to determine end-diastolic pressure-dimension relationships. Five underwent maximal treadmill running before and 14-21 days after thoracotomy (pericardium undisturbed) to determine the effect of thoracotomy on exercise performance. Finally, five underwent thoracotomy, instrumentation, loose closure of the pericardium, and sequential volume infusions to determine the effect of thoracotomy without pericardiectomy on end-diastolic pressure-dimension relationships. Pericardiectomy caused similar increases in maximal cardiac output (29% increase; P = 0.007) and maximal oxygen consumption (31% increase; P = 0.02). These results were associated with increased left ventricular end-diastolic dimension (10% increase; P = 0.01) and an estimated 33% increase in end-diastolic volume. In addition, left ventricular mass was increased by pericardiectomy (18% increase; P < 0.04). Thus the pericardium, by limiting utilization of the Starling mechanism, limits maximal cardiac output, and the limit to cardiorespiratory performance lies not in oxygen utilization, but in oxygen delivery. Furthermore, removal of pericardium is associated with myocardial hypertrophy.