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The mechanisms which determine the response of stroke volume to mild, moderate, and severe exercise were compared in nine dogs running on a level treadmill. The dogs ran for 3-minute periods at 3-^ mph (mild exercise), 6-8 mph (moderate exercise), and 10-14 mph (severe exercise). Heart rate increased from a standing control value of 107 ± 6 beats/min to 191 ± 10 beats/min in mild, 221 ± 8 beats/min in moderate, and 263 ± 9 beats/min in severe exercise. Stroke volume increased 14%, 19%, and 15* for mild, moderate, and severe exercise, respectively. During mild exercise, left ventricular internal diameter decreased at end-systole but was unchanged at end-diastole. During moderate and severe exercise, end-diastolic diameter increased consistently as did left ventricular end-diastolic pressure. It was concluded that, despite extremely high heart rates, stroke volume increased during exercise. The augmentation in stroke volume was due to the combined effects of an increase in contractility, caused by increased sympathetic nervous system activity, and the operation of the Frank-Starling mechanism. MethodsNine mongrel dogs, weighing 17-27 kg, were trained to run on a level treadmill. Subsequently, each dog underwent a sterile thoracotomy under sodium pentobarbital anesthesia. As described previously (4), during a brief inflow occlusion of the superior and inferior vena cava, two discoid sonocardiometer transducers were implanted within the left ventricle through a stab incision in the anterior wall. The transducers were positioned across the greatest internal transverse diameter of the left ventricle, one on the anterior and the other on the posterior endocardia! wall. Through

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