FAVORABLE LEFT-VENTRICULAR REMODELING FOLLOWING LARGE MYOCARDIAL-INFARCTION BY EXERCISE TRAINING - EFFECT ON VENTRICULAR MORPHOLOGY AND GENE-EXPRESSION
Tl. Orenstein et al., FAVORABLE LEFT-VENTRICULAR REMODELING FOLLOWING LARGE MYOCARDIAL-INFARCTION BY EXERCISE TRAINING - EFFECT ON VENTRICULAR MORPHOLOGY AND GENE-EXPRESSION, The Journal of clinical investigation, 96(2), 1995, pp. 858-866
Continued adverse remodeling of myocardium after infarction may lead t
o progressive ventricular dilation and heart failure, We tested the hy
pothesis that exercise training in a healed myocardial infarction-dysf
unction rat model can favorably modify the adverse effects of ventricu
lar remodeling including attenuation of abnormal myosin gene expressio
n. Sprague-Dawley rats were subjected to either proximal LAD ligation
or sham operation, At 5 wk after the operation, animals were randomly
assigned to sedentary conditions or 6 wk of graduated swim training, c
reating four experimental groups: infarct sedentary (IS), infarct exer
cise (IE), sham sedentary (SS), and sham exercise (SE), At 11 wk all r
ats were sacrificed and analyzed. Compared to sedentary infarct contro
ls, exercise training attenuated left ventricular (LV) dilation and al
lowed more hypertrophy of the non infarct wall, The exercise trained h
earts also showed a reduction in the estimated peak wall tension, Nort
hern blot analysis showed an increase in beta-myosin heavy chain expre
ssion in the hearts of the sedentary infarction group soon after infar
ction when compared to sham controls, However, with exercise training,
there was a significant attenuation of the beta-myosin heavy chain ex
pression in the myocardium. Exercise training in a model of left ventr
icular dysfunction after healed myocardial infarction can improve the
adverse remodeling process by attenuating ventricular dilation and red
ucing wall tension. The abnormal beta-myosin expression was also atten
uated in the exercise trained group, This is evidence that abnormal ge
ne expression following severe myocardial infarction dysfunction can b
e favorably modified by an intervention.