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Exercise training normalizes altered calcium-handling proteins during development of heart failure
Lu Lu1, Dan Feng Mei, An-Guo Gu
1Division of Circulatory Physiology, Department of Medicine, College of Physicians and Surgeons, Columbia University, New York City, NY 10032, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|March 16, 2002
Summary
Exercise training (ET) helps preserve heart function during chronic heart failure (CHF) by normalizing key calcium-handling proteins like SERCA2a and NCX1, unlike in untrained failing hearts.
Area of Science:
- Cardiology
- Molecular Biology
- Exercise Physiology
Background:
- Myocyte calcium regulation is crucial for cardiac function.
- Proteins like SERCA2a, NCX1, and RyR2 are key in calcium handling.
- Chronic heart failure (CHF) often involves altered calcium handling.
Purpose of the Study:
- To investigate the impact of exercise training (ET) on cardiac calcium-handling proteins during CHF development.
- To compare protein and mRNA levels of SERCA2a, NCX1, and RyR2 in paced-induced CHF with and without ET.
Main Methods:
- Utilized a canine model of pacing-induced CHF.
- Compared groups with pacing alone versus pacing plus daily ET.
- Measured cardiac sarcoplasmic reticulum calcium-ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX1), and ryanodine receptor (RyR2) mRNA and protein levels via Northern and Western analyses.
Main Results:
- In CHF, SERCA2a mRNA and protein significantly decreased, an effect attenuated by ET.
- NCX1 mRNA and protein levels increased in CHF, with ET partially normalizing these changes.
- RyR2 levels remained unaltered in all experimental groups.
Conclusions:
- Long-term exercise training may mitigate cardiac deterioration in CHF.
- ET appears to normalize myocardial calcium-handling proteins, including SERCA2a and NCX1, contributing to preserved cardiac function.
- RyR2 is not significantly affected by pacing-induced CHF or exercise training in this model.