Document Detail

Exercise training alters left ventricular geometry and attenuates heart failure in dahl salt-sensitive hypertensive rats.
MedLine Citation:
PMID:  19255362     Owner:  NLM     Status:  MEDLINE    
The clinical efficacy of exercise training in individuals with heart failure is well established, but the mechanism underlying such efficacy has remained unclear. An imbalance between cardiac hypertrophy and angiogenesis is implicated in the transition to heart failure. We investigated the effects of exercise training on cardiac pathophysiology in hypertensive rats. Dahl salt-sensitive rats fed a high-salt diet from 6 weeks of age were assigned to sedentary or exercise (swimming)-trained groups at 9 weeks. Exercise training attenuated the development of heart failure and increased survival, without affecting blood pressure, at 18 weeks. It also attenuated left ventricular concentricity without a reduction in left ventricular mass or impairment of cardiac function. Interstitial fibrosis was increased and myocardial capillary density was decreased in the heart of sedentary rats, and these effects were attenuated by exercise. Exercise potentiated increases in the phosphorylation of Akt and mammalian target of rapamycin observed in the heart of sedentary rats, whereas it inhibited the downregulation of proangiogenic gene expression apparent in these animals. The abundance of the p110alpha isoform of phosphatidylinositol 3-kinase was decreased, whereas those of the p110gamma isoform of phosphatidylinositol 3-kinase and the phosphorylation of extracellular signal-regulated kinase and p38 mitogen-activated protein kinase were increased, in the heart of sedentary rats, and all of these effects were prevented by exercise. Thus, exercise training had a beneficial effect on cardiac remodeling and attenuated heart failure in hypertensive rats, with these effects likely being attributable to the attenuation of left ventricular concentricity and restoration of coronary angiogenesis through activation of phosphatidylinositol 3-kinase(p110alpha)-Akt-mammalian target of rapamycin signaling.
Masaaki Miyachi; Hiroki Yazawa; Mayuko Furukawa; Koji Tsuboi; Masafumi Ohtake; Takao Nishizawa; Katsunori Hashimoto; Toyoharu Yokoi; Tetsuhito Kojima; Takashi Murate; Mitsuhiro Yokota; Toyoaki Murohara; Yasuo Koike; Kohzo Nagata
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-03-02
Journal Detail:
Title:  Hypertension     Volume:  53     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-03-20     Completed Date:  2009-04-22     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  701-7     Citation Subset:  IM    
Department of Medical Technology, Nagoya University School of Health Sciences, 1-1-20 Daikominami, Higashi-ku, Nagoya 461-8673, Japan.
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MeSH Terms
1-Phosphatidylinositol 3-Kinase / metabolism
Coronary Circulation / physiology
Heart Failure / physiopathology*,  therapy*,  ultrasonography
Hypertension / physiopathology*
Hypertrophy, Left Ventricular / physiopathology*,  therapy*,  ultrasonography
Kaplan-Meiers Estimate
Myocardial Contraction / physiology
Myocardium / pathology
Neovascularization, Physiologic / physiology
Physical Conditioning, Animal*
Proto-Oncogene Proteins c-akt / metabolism
Rats, Inbred Dahl
Signal Transduction / physiology
Reg. No./Substance:
EC 3-Kinase; EC Proteins c-akt
Comment In:
Hypertension. 2009 Aug;54(2):e14; author reply e15-6   [PMID:  19564540 ]
Hypertension. 2009 Apr;53(4):600-1   [PMID:  19255360 ]

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