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Departments of Medicine and Pathology, The University of Chicago, Chicago, Illinois 60637
Dilated cardiomyopathy
(DC) is a leading cause of cardiovascular morbidity, and
nonpharmacological therapies, such as exercise training, have been
suggested. The effects of exercise on left ventricular (LV) function
and mortality remain controversial. Using a recently described
murine model of DC, which involves a dominant-negative form of the cAMP
response element binding protein (CREB) transcription factor
(CREBA133) under the control of the cardiac
myocyte-specific
-myosin heavy chain promoter, we sought to assess
the effects of moderate-intensity exercise training on LV
performance and mortality. Thirty-two transgenic mice were subjected to
exercise training and compared with sedentary controls. There was
progressive enlargement in LV dimensions in both the sedentary and
exercise-trained mice. LV performance was progressively impaired, and
exercise training did not prevent this decline. The sedentary
CREBA133 mice displayed a significantly increased rate of
death, and exercise training did not prevent or delay this excess
mortality. The CREBA133 murine model of inherited DC
demonstrated progressive ventricular dilatation and dysfunction with
increased mortality, which was not altered with 12 wk of moderate-intensity exercise training.
echocardiography; congestive heart failure; treadmill; left ventricular
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