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Articles in PresS, published online ahead of print December 21, 2001
J Appl Physiol, 10.1152/jap.00405.2001
Submitted on April 27, 2001
Accepted on December 19, 2001
1 Medicine/Circulatory Physiology, College of P&S Columbia University, NY, NY, USA
2 Bronx Sciences High School, Bronx, NY, USA
3 Medicine, Mt. Sinai Medical Center, NY, NY, USA
4 Medicine, Thomas Jefferson University Hospital, Philadelphia, PA, USA
5 Medicine/Cardiology, College of P&S Columbia University, NY, NY, USA
* To whom correspondence should be addressed. E-mail: jw147{at}columbia.edu.
Background. The cardiac sarcoplasmic reticulum calcium ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX1) and ryanodine receptor (RyR2) are proteins involved in the regulation of myocyte calcium. We tested whether exercise training (ET) alters those proteins during development of heart failure (CHF). Methods and Results. Ten dogs were chronically instrumented to permit hemodynamic measurements. Five dogs underwent four weeks of cardiac pacing (210 b/min for 3 weeks and 240 b/min for the 4th week) whereas five dogs underwent the same pacing regimen plus daily ET (5.1±0.3 km/hr, 2 hours per day). Paced animals developed CHF characterized by hemodynamic abnormalities and reduced ejection fraction (EF). ET preserved resting hemodynamics and EF. Left ventricular samples were obtained from all dogs and another 5 normal dogs for mRNA (Northern analysis, band intensities normalized to GAPDH) and protein level (Western analysis, band intensities normalized to tubulin) measurements. In failing hearts, SERCA2a was decreased by 33% (p<0.05) and 65% (p<0.05) in mRNA and protein level, respectively, compared to normal hearts; there was only an 8.6% reduction in mRNA and a 32% reduction in protein in exercised animals (p<0.05 from CHF). mRNA expression of NCX1 increased by 44% in paced-only dogs compared to normal (p<0.05), but only by 22% in trained dogs (p<0.05 vs CHF); protein level of NCX1 was elevated in paced-only dogs (71%, p<0.05) but partially normalized by ET (33%, p<0.05 from CHF). RyR2 was not altered in any of the dogs. Conclusion. Long-term ET may ameliorate cardiac deterioration during development of CHF, in part via normalization of myocardial calcium handling proteins.
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