Does chronic physical conditioning by swimming induce cardiac hypertrophy and alter cardiac muscle ATPase activities in adult female C57/B16 mice?
Chronic swimming in mice induces adaptive cardiac hypertrophy without altering cardiac muscle ATPase activities, providing a useful in vivo model for studying molecular mechanisms of hypertrophy.
Transgenic mice can be created to serve as models of human cardiac disease. Despite the technology available to manipulate the cardiovascular system of the mouse, there is relatively little information available concerning the normal physiology of the mouse heart. Therefore, we have characterized the response of the adult mouse to chronic physical conditioning by swimming. Adult female C57/B16 mice were conditioned by swimming up to 90 min twice daily for 4 wk, resulting in a 10% increase 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. Succinate dehydrogenase activity increased markedly in the soleus muscles 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 norepinephrine content or in cardiac myosin or myofibrillar adenosinetriphosphatase (ATPase) activities was observed, and no change in the V1 predominant myosin isoform or alpha-myosin heavy chain mRNA profiles was seen in the 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 muscle. These data should be of use to investigators using murine models to define the molecular basis of adaptive cardiac hypertrophy in vivo.
Kaplan et al. (1994) studied this question.