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Cyclosporin A does not block exercise-induced cardiac hypertrophy
Tess Hainsey1, Anna Csiszar, Shuangdan Sun
1Department of Physiology, New York Medical College, Valhalla, NY 10595, USA.
Medicine and Science in Sports and Exercise
|August 8, 2002
Summary
Cyclosporin A (CsA) did not prevent exercise-induced cardiac hypertrophy in rats. However, CsA alone altered myocardial gene expression, suggesting a shift towards a pathological phenotype.
Area of Science:
- Cardiology
- Exercise Physiology
- Molecular Biology
Background:
- Cyclosporin A (CsA) inhibits pathological cardiac hypertrophy, implicating calcium-dependent pathways.
- The effect of CsA on exercise-induced cardiac hypertrophy, a physiological overload model, is not well understood.
Purpose of the Study:
- To investigate whether CsA alters exercise-induced cardiac hypertrophy in a rodent model.
Main Methods:
- Male rats received CsA or vehicle, followed by sedentary or swim training for one week.
- Cardiac hypertrophy markers, including ventricular weight and myosin heavy chain (MHC) expression, were analyzed.
Main Results:
- Swim training increased left ventricular weight and atrial natriuretic factor (ANF)-mRNA, but not alpha-myosin heavy chain (MHC).
- CsA treatment significantly increased beta-myosin heavy chain (MHC) expression at both mRNA and protein levels.
- CsA did not block exercise-induced cardiac hypertrophy but influenced myocardial phenotype.
Conclusions:
- Calcium-dependent pathways are not essential for early exercise-induced cardiac adaptations.
- CsA alone may induce a shift in MHC isoform expression towards a pathological phenotype.
- The impact of CsA-induced phenotype shifts on exercise capacity in transplant patients requires further investigation.