Journal article
Long-term aerobic exercise protects the heart against ischemia/reperfusion injury via PI3 kinase-dependent and Akt-mediated mechanism
Apoptosis (London), Vol.12(9), pp.1579-1588
09/01/2007
DOI: 10.1007/s10495-007-0090-8
PMID: 17505785
Abstract
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. 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. 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-3β 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. 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.[PUBLICATION ABSTRACT]
Details
- Title: Subtitle
- Long-term aerobic exercise protects the heart against ischemia/reperfusion injury via PI3 kinase-dependent and Akt-mediated mechanism
- Creators
- Kun-ru Zhang - Air Force Medical UniversityHai-tao Liu - Air Force Medical UniversityHai-feng ZhangQuan-jiang Zhang - Air Force Medical UniversityQiu-xia Li - Air Force Medical UniversityQiu-jun YuWen-yi GuoHai-chang Wang - Air Force Medical UniversityFeng Gao - Air Force Medical University
- Resource Type
- Journal article
- Publication Details
- Apoptosis (London), Vol.12(9), pp.1579-1588
- Publisher
- Springer Nature B.V
- DOI
- 10.1007/s10495-007-0090-8
- PMID
- 17505785
- ISSN
- 1360-8185
- eISSN
- 1573-675X
- Language
- English
- Date published
- 09/01/2007
- Academic Unit
- Cardiovascular Medicine; Internal Medicine
- Record Identifier
- 9984359835002771
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