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Certain strains of coxsackievirus A-9 induce minimal necrosis and interstitial inflammation of the murine heart (1, 2). Although affected mice appear well, cardiac size is increased. During the first 2 wk of infection, virus is present in the heart. When examined later, these myocardia are normal in size and are free of histologic change (3-5). Swimming increases myocardial replication of virus but does not alter the benignity of the process (6).On the other hand, when weanling mice are inoctflated with coxsackievirus B-3 (Nancy), a necrotic carditis involving 25-50% of the entire myocardiUm results. As with coxsackievirus A-9, coxsackievirus B-3 may be isolated only very early. Here, too, the infected baby mice continue to appear well. However, in the case of coxsackievirus B-3, healing is accompanied by myocardial fibrosis, deposition of calcium, and continuing inflammation. Since the continuing carditis is not associated with virus multiplication, we have called the entire process a myocardiopathy (7-9).Human cardiac disease occurs, similar to that caused by the benign coxsackievirus A-9 and having lesions similar to the murine lesions caused by the virulent coxsackievirus B-3. The present experiments bring striking data to bear upon the role of the exercise induced by swimming upon routine coxsackievirus B-3 myocardiopathy. Materials and MethodsMice.--Pregnant albino Swiss ICR mice were obtained at term. After delivery, each mother with its brood was housed in a separate cage. Nurslings were weaned at about 3 wk and, thereafter, were fed standard Rockland rat chow.

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