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A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
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Exercise training does not improve cardiac function in compensated or decompensated left ventricular hypertrophy
Elza D van Deel1, Martine de Boer, Diederik W Kuster
1Experimental Cardiology, Thoraxcenter, Cardiovascular Research School COEUR, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands.
Journal of Molecular and Cellular Cardiology
|February 5, 2011
Summary
Exercise did not improve cardiac function in mice with left ventricular (LV) hypertrophy caused by aortic constriction. The benefits of exercise on pathological LV hypertrophy depend on the underlying condition.
Area of Science:
- Cardiovascular Physiology
- Exercise Science
- Cardiac Pathophysiology
Background:
- Regular exercise benefits left ventricular (LV) function in ischemic heart disease and hypertension.
- Effects of exercise on LV hypertrophy and dysfunction from outflow obstruction remain unstudied.
Purpose of the Study:
- To investigate exercise effects on LV hypertrophy and dysfunction induced by transverse aortic constriction (TAC).
- To determine if exercise mitigates cardiac remodeling and dysfunction in response to pressure overload.
Main Methods:
- Mice underwent mild (mTAC) or severe (sTAC) transverse aortic constriction.
- Mice were subjected to 8 weeks of voluntary wheel running.
- Cardiac function, hypertrophy markers, apoptosis, and fibrosis were assessed.
Main Results:
- mTAC caused hypertrophy without functional decline; exercise did not alter LV function but increased collagen.
- sTAC induced severe hypertrophy, dysfunction, apoptosis, and fibrosis; exercise failed to improve function or hypertrophy.
- Exercise attenuated increased passive force but worsened fibrosis in sTAC.
Conclusions:
- Exercise offers no benefit for cardiac function in LV hypertrophy due to outflow obstruction.
- Exercise's impact on pathological cardiac hypertrophy is critically dependent on the underlying cause.
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