| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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
This article has been cited by other articles:
|
|
 |
|
  G. E. Billman Cardiac autonomic neural remodeling and susceptibility to sudden cardiac death: effect of endurance exercise training Am J Physiol Heart Circ Physiol, October 1, 2009; 297(4): H1171 - H1193. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Q. Jiao, Y. Bai, T. Akaike, H. Takeshima, Y. Ishikawa, and S. Minamisawa Sarcalumenin is essential for maintaining cardiac function during endurance exercise training Am J Physiol Heart Circ Physiol, August 1, 2009; 297(2): H576 - H582. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. S. F. Oliveira, J. C. B. Ferreira, E. R. M. Gomes, N. A. Paixão, N. P. L. Rolim, A. Medeiros, S. Guatimosim, and P. C. Brum Cardiac anti-remodelling effect of aerobic training is associated with a reduction in the calcineurin/NFAT signalling pathway in heart failure mice J. Physiol., August 1, 2009; 587(15): 3899 - 3910. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C.-H. Shao, X. H. T. Wehrens, T. A. Wyatt, S. Parbhu, G. J. Rozanski, K. P. Patel, and K. R. Bidasee Exercise training during diabetes attenuates cardiac ryanodine receptor dysregulation J Appl Physiol, April 1, 2009; 106(4): 1280 - 1292. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. D. Garciarena, O. A. Pinilla, M. B. Nolly, R. P. Laguens, E. M. Escudero, H. E. Cingolani, and I. L. Ennis Endurance Training in the Spontaneously Hypertensive Rat: Conversion of Pathological into Physiological Cardiac Hypertrophy Hypertension, April 1, 2009; 53(4): 708 - 714. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. J. Chicco, S. A. McCune, C. A. Emter, G. C. Sparagna, M. L. Rees, D. A. Bolden, K. D. Marshall, R. C. Murphy, and R. L. Moore Low-Intensity Exercise Training Delays Heart Failure and Improves Survival in Female Hypertensive Heart Failure Rats Hypertension, April 1, 2008; 51(4): 1096 - 1102. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Medeiros, N. P. L. Rolim, R. S. F. Oliveira, K. T. Rosa, K. C. Mattos, D. E. Casarini, M. C. Irigoyen, E. M. Krieger, J. E. Krieger, C. E. Negrao, et al. Exercise training delays cardiac dysfunction and prevents calcium handling abnormalities in sympathetic hyperactivity-induced heart failure mice J Appl Physiol, January 1, 2008; 104(1): 103 - 109. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. P. L. Rolim, A. Medeiros, K. T. Rosa, K. C. Mattos, M. C. Irigoyen, E. M. Krieger, J. E. Krieger, C. E. Negrao, and P. C. Brum Exercise training improves the net balance of cardiac Ca2+ handling protein expression in heart failure Physiol Genomics, May 11, 2007; 29(3): 246 - 252. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. M. Minhas, R. M. Saraiva, K. H. Schuleri, S. Lehrke, M. Zheng, A. P. Saliaris, C. E. Berry, K. M. Vandegaer, D. Li, and J. M. Hare Xanthine Oxidoreductase Inhibition Causes Reverse Remodeling in Rats With Dilated Cardiomyopathy Circ. Res., February 3, 2006; 98(2): 271 - 279. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. A. Emter, S. A. McCune, G. C. Sparagna, M. J. Radin, and R. L. Moore Low-intensity exercise training delays onset of decompensated heart failure in spontaneously hypertensive heart failure rats Am J Physiol Heart Circ Physiol, November 1, 2005; 289(5): H2030 - H2038. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-K. Kim, R. A. Augustyniak, J. A. Sala-Mercado, R. L. Hammond, E. J. Ansorge, N. F. Rossi, and D. S. O'Leary Heart failure alters the strength and mechanisms of arterial baroreflex pressor responses during dynamic exercise Am J Physiol Heart Circ Physiol, October 1, 2004; 287(4): H1682 - H1688. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
