CARDIAC ADAPTATIONS TO CHRONIC EXERCISE IN MICE

Transgenic mice can be created to serve as models of human cardiac dis ease. Despite the technology available to manipulate the cardiovascula r system of the mouse, there is relatively little information availabl e concerning the normal physiology of the mouse heart. Therefore, we h ave characterized the response of the adult mouse to chronic physical conditioning by swimming. Adult female C57/Bl6 mice were conditioned b y swimming up to 90 min twice daily for 4 wk, resulting in a 10% incre ase in heart weight and a 16% increase in heart weight-to-body weight ratios compared with sedentary controls. The heart rate response to a submaximal work load decreased > 20% with this conditioning program. S uccinate dehydrogenase activity increased markedly in the soleus muscl es of the conditioned animals, from 28 +/- 3 to 44 +/- 3 nmol . mg(-1) . min(-1). In contrast to these changes, which also characterize the exercise model in the rat, no increase in cardiac tissue norepinephrin e content or in cardiac myosin or myofibrillar adenosinetriphosphatase (ATPase) activities was observed, and no change in the V-1 predominan t myosin isoform or cy-myosin heavy chain mRNA profiles was seen in th e hearts of the swimmers. This study establishes that mice are able to develop cardiac hypertrophy in response to chronic conditioning which is not associated with changes in the ATPase activities of cardiac mu scle. These data should be of use to investigators using murine models to define the molecular basis of adaptive cardiac hypertrophy in vivo .