During the last year we have performed quantitative studies of ventricular performance in the modified working rat heart apparatus that demonstrate an increase in the intrinsic contractility and reserve of hearts of conditioned rats. Studies in the open-chest physically trained rat demonstrated increased reserve capacity can also be demonstrated in the blood perfused heart in vivo. We demonstrated that the exercise induced changes in cardiac performance and in actomyosin ATPase, that reach their maximum at about eight weeks of exercise, can be completely reversed by cessation of exercise for two weeks. We have demonstrated that the response of myofibrillar ATPase in heart of conditioned rats is qualitatively similar to that from sedentary animals, but that the quantitative is greater in the hearts of conditioned rats. We have studied the effects of physical training on cardiac mitochondria and have demonstrated normal oxidative phosphorylation indices, but some measurements of calcium binding and uptake are reduced in the hearts of the physically trained animals. However, we have found evidence of higher content of mitochondrial substance in the hearts of physically trained rats and therefore total calcium binding appeared to be normal. In the coming year we plan to evaluate the effect of ischemia on hearts of physically trained rats and also to determine if the effect of training on heart rate is related in any way to mechanics and biochemistry changes. We will examine the responses of hearts to cyclic AMP and continue studies on the control of contractile protein ATPase activity.