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J Appl Physiol 92: 1524-1530, 2002. First published December 21, 2001; doi:10.1152/japplphysiol.00405.2001
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Vol. 92, Issue 4, 1524-1530, April 2002

Exercise training normalizes altered calcium-handling proteins during development of heart failure

Lu Lu1, Dan Feng Mei2, An-Guo Gu1, Su Wang1, Benjamin Lentzner1, David E. Gutstein3, Donna Zwas4, Shunichi Homma5, Geng-Hua Yi1, and Jie Wang1

Divisions of 1 Circulatory Physiology and 5 Cardiology, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York City 10032; 2 Bronx Sciences High School, Bronx; 3 Division of Cardiology, Mt. Sinai Medical Center, New York, New York 10021; and 4 Division of Cardiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania 19107

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 chronic heart failure (CHF). Ten dogs were chronically instrumented to permit hemodynamic measurements. Five dogs underwent 4 wk of cardiac pacing (210 beats/min for 3 wk and 240 beats/min for the 4th wk), whereas five dogs underwent the same pacing regimen plus daily ET (5.1 ± 0.3 km/h, 2 h/day). Paced animals developed CHF characterized by hemodynamic abnormalities and reduced ejection fraction. ET preserved resting hemodynamics and ejection fraction. Left ventricular samples were obtained from all dogs and another five normal dogs for mRNA (Northern analysis, band intensities normalized to glyceraldehyde-3-phosphate dehydrogenase) 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 with 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 with 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. In conclusion, long-term ET may ameliorate cardiac deterioration during development of CHF, in part via normalization of myocardial calcium-handling proteins.

ryanodine receptor; sodium/calcium exchanger; cardiac sarcoplasmic reticulum calcium-adenosinetriphosphatase


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