The integrated response to severe exercise involves fourfold to fivefold increases in cardiac output, which are due primarily to increases in cardiac rate and to a lesser extent to augmentation of stroke volume. The increase in stroke volume is partly due to an increase in end-diastolic cardiac size (Frank-Starling mechanism) and secondarily due to a reduction in end-systolic cardiac size. The full role of the Frank-Starling mechanism is masked by the concomitant tachycardia. The reduction in end-systolic dimensions can be related to increased contractility, mediated by beta adrenergic stimulation. Beta adrenergic blockade prevents the inotropic response, the decrease in end-systolic dimensions, and approximately 50% of the tachycardia of exercise. The enhanced cardiac output is distributed preferentially to the exercising muscles including the heart. Blood flow to the heart increases fourfold to fivefold as well, mainly reflecting the augmented metabolic requirements of the myocardium due to near maximal increases in cardiac rate and contractility. Blood flow to the inactive viscera (e.g., kidney and gastrointestinal tract) is maintained during severe exercise in the normal dog. It is suggested that local autoregulatory mechanisms are responsible for maintained visceral flow in the face of neural and hormonal autonomic drive, which acts to constrict renal and mesenteric vessels and to reduce blood flow. However, in the presence of circulatory impairment, where oxygen delivery to the exercising muscles is impaired as occurs to complete heart block where normal heart rate increases during exercise are prevented, or in congestive right heart failure, where normal stroke volume increases during exercise are impaired, or in the presence of severe anemia, where oxygen-carrying capacity of the blood is limited, visceral blood flows are reduced drastically and blood is diverted to the exercising musculature. Thus,, visceral flow is normally maintained during severe exercise as long as all other compensatory mechanisms remain intact. However, when any other compensatory mechanism is disrupted (even the elimination of splenic reserve in the dog), reduction and diversion of visceral flow occur.