Document Detail

Anti-apoptotic and pro-survival effects of exercise training on hypertensive hearts.
MedLine Citation:
PMID:  22207725     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Activated cardiac apoptosis was found in hearts from hypertensive animals, but little information regarding the effects of exercise training on cardiac apoptosis in hypertension is available. The purpose of this study was to evaluate the anti-apoptotic and pro-survival effects of exercise training on hypertensive hearts.
METHODS: 28 spontaneously hypertensive rats were divided into sedentary group (SHR) or underwent running exercise on treadmill for 1 h/day, 5 sessions/wk, for 12 wk (SHR-EX). Fourteen age-matched Wistar Kyoto rats served as a sedentary normotensive group (WKY). After exercise training or sedentary status, the excised hearts were measured by hemotoxylin and eosin staining, terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling (TUNEL) assay, and Western blotting.
RESULTS: Fewer TUNEL-positive apoptotic cells were in SHR-EX groups than those in SHR. Protein levels of Fas ligand, Fas death receptor, tumor necrosis factor (TNF)-α, TNF receptor 1, Fas-associated death domain (FADD), activated caspase-8, and activated caspase-3 (Fas-dependent apoptotic pathways), as well as Bid, t-Bid, Bad, p-Bad, Bak, cytochrome c, activated caspase 9, and activated caspase-3 (mitochondria-dependent apoptotic pathways) were decreased in the SHR-EX group compared with the SHR group. Protein levels of IGF-1, IGF-1R, p-PI3K, p-Akt, p-Bad, and Bcl2 (cardiac pro-survival pathway) become more activated in SHR-EX groups than SHR and WKY.
CONCLUSIONS: Exercise training prevented hypertension-enhanced cardiac Fas-dependent and mitochondria-dependent apoptotic pathways and enhanced cardiac pro-survival pathway in rat models. Our findings demonstrate new therapeutic effects of exercise training on hypertensive hearts for preventing apoptosis and enhancing survival.
Chih-Yang Huang; Ai-Lun Yang; Yueh-Min Lin; Fan-Ni Wu; James A Lin; Yi-Sheng Chan; Fuu-Jen Tsai; Chang-Hai Tsai; Chia-Hua Kuo; Shin-Da Lee
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-12-29
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  112     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-03-02     Completed Date:  2012-09-11     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  883-91     Citation Subset:  IM    
Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
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MeSH Terms
Antigens, CD95 / genetics,  metabolism
Apoptosis / genetics,  physiology*
Body Weight / physiology
Fas Ligand Protein / metabolism
Heart / physiopathology*
Hypertension / genetics,  metabolism,  pathology,  therapy*
In Situ Nick-End Labeling / methods
Mitochondria, Heart / genetics,  metabolism,  pathology
Myocardium / metabolism,  pathology*
Physical Conditioning, Animal / physiology*
Rats, Inbred SHR
Rats, Inbred WKY
Signal Transduction / physiology
Teaching / methods
Reg. No./Substance:
0/Antigens, CD95; 0/Fas Ligand Protein

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