To test the hypothesis that early exercise training after myocardial infarction (MI)
could preserve cardiac function, alleviate left ventricular (LV) remodeling and induce
a protective effect on morphology, male Sprague-Dawley rats underwent coronary ligation
or sham operation, and were assigned to 3 groups: Sham, sedentary MI (SedMI), and
exercise MI (ExMI). We measured the changes in collagen volume fraction, matrix metalloproteinase
(MMP) 1, tissue inhibitor matrix metalloproteinase 1 (TIMP-1), angiotensin II receptor
type 1 (AT1), and angiotensin converting enzyme (ACE) at gene and protein levels after
8 weeks of exercise training. Cardiac functions were determined by echocardiographic
and hemodynamic measurements. Early exercise training after MI had no effect on LV
wall thinning. Cardiac function was significantly preserved in the ExMI group in comparison
to the SedMI group. The collagen volume fraction in the ExMI group was significantly
lower than in the SedMI group. Compared to the SedMI group, the ExMI group showed
a markedly decrease at both the gene and protein levels in TIMP-1 (P<0.05). No significant
differences were found in MMP-1 among the three groups. MMP-1/TIMP-1 ratio in the
ExMI group was significantly higher than in the SedMI group. In addition, the expression
of AT1 protein in the ExMI group was significantly lower than in the SedMI group.
Furthermore, both ACE mRNA expression and ACE binding in the ExMI group are significantly
decreased compared to the SedMI group. Our results suggest that early exercise training
after MI reduces TIMP-1 expression, improves the balance between MMPs and TIMPs, and
mitigates the expressions of ACE and AT1 receptor. These improvements, in turn, attenuate
myocardial fibrosis and preserve post-MI cardiac function.