Document Detail

Long-term aerobic exercise protects the heart against ischemia/reperfusion injury via PI3 kinase-dependent and Akt-mediated mechanism.
MedLine Citation:
PMID:  17505785     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Physical activity has been shown to improve cardiovascular function and to be beneficial to type 2 diabetic patients. However, the effects of aerobic exercise (AE) on myocardial ischemia/reperfusion (MI/R) are largely unclear. Therefore, the aims of the present study were to determine whether long-term AE can protect the heart against I/R injury, and if so, to investigate the underlying mechanism. METHODS: Adult male Sprague-Dawley rats were randomly subjected to 8 weeks of either sedentary or free-loading swimming exercise (3 h/day, 5 d/week). Then the animals were subjected to 30 min MI followed by 4 h R. Arterial blood pressure and left ventricular pressure (LVP) were monitored throughout the whole MI/R procedure. Plasma creatine kinase (CK) and lactate dehydrogenase (LDH) activities were measured spectrophotometrically. Myocardial infarction and myocardial apoptosis (TUNEL analysis) were determined in a blinded manner. RESULTS: MI/R caused significant cardiac dysfunction and myocardial apoptosis (strong TUNEL-positive staining). Compared with sedentary group, rats subjected to 8 weeks of AE showed protection against MI/R as evidenced by reduced myocardial infarction (26.8 +/- 1.5% vs. 35.3 +/- 2.4%, n = 8, P < 0.05), inhibited cardiomyocyte apoptosis (decreased apoptotic index (12.4 +/- 1.1% vs. 21.0 +/- 1.7%, n = 8, P < 0.01) and decreased myocardial caspase-3 activity), decreased plasma CK and LDH activities and improved recovery of cardiac systolic/diastolic function (including LVSP and +/-LVdP/dt) at the end of R. Moreover, exercise resulted in 1.7-fold, 2.5-fold and 2.5-fold increases in Akt expression, Akt phosphorylation and glycogen synthase kinase-3beta phosphorylation in I/R myocardium, respectively (n = 3, all P < 0.05). More importantly, treatment with wortmannin, a PI3 kinase inhibitor, 15 min before R not only significantly blocked Akt phosphorylation (P < 0.05) in exercise rats, but also abolished long-term AE-induced cardioprotection for the I/R heart as manifested by increased apoptosis and myocardial infarction, and reduced cardiac function. CONCLUSION: Long-term AE exerts cardioprotective effect against MI/R injury, including anti-cardiomyocyte apoptosis, which is at least partly via PI3 kinase-dependent and Akt-mediated mechanism.
Kun-Ru Zhang; Hai-Tao Liu; Hai-Feng Zhang; Quan-Jiang Zhang; Qiu-Xia Li; Qiu-Jun Yu; Wen-Yi Guo; Hai-Chang Wang; Feng Gao
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Apoptosis : an international journal on programmed cell death     Volume:  12     ISSN:  1360-8185     ISO Abbreviation:  Apoptosis     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-07-26     Completed Date:  2007-10-26     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9712129     Medline TA:  Apoptosis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1579-88     Citation Subset:  IM    
Department of Physiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
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MeSH Terms
1-Phosphatidylinositol 3-Kinase / physiology*
Androstadienes / pharmacology
Apoptosis / physiology*
Caspase 3 / metabolism
Creatine Kinase / blood
Heart / physiology
Hydro-Lyases / blood
In Situ Nick-End Labeling
Myocardial Infarction / pathology
Myocardial Reperfusion Injury / prevention & control*
Myocardium / metabolism*
Myocytes, Cardiac / pathology
Physical Conditioning, Animal / physiology*
Proto-Oncogene Proteins c-akt / physiology*
Rats, Sprague-Dawley
Reg. No./Substance:
0/Androstadienes; 19545-26-7/wortmannin; EC 3-Kinase; EC Proteins c-akt; EC Kinase; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 4.2.1.-/Hydro-Lyases; EC dehydratase

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