Myocardial tolerance to ischemia-reperfusion injury, training intensity and cessation.

Details

Serval ID
serval:BIB_F269D167A1D6
Type
Article: article from journal or magazin.
Collection
Publications
Title
Myocardial tolerance to ischemia-reperfusion injury, training intensity and cessation.
Journal
European Journal of Applied Physiology
Author(s)
Esposito F., Ronchi R., Milano G., Margonato V., Di Tullio S., Marini M., Veicsteinas A., Samaja M.
ISSN
1439-6327 (Electronic)
ISSN-L
1439-6319
Publication state
Published
Issued date
2011
Volume
111
Number
5
Pages
859-868
Language
english
Abstract
Training has been shown to induce cardioprotection. The mechanisms involved remain still poorly understood. Aims of the study were to examine the relevance of training intensity on myocardial protection against ischemia/reperfusion (I/R) injury, and to which extent the beneficial effects persist after training cessation in rats. Sprague-Dawley rats trained at either low (60% [Formula: see text]) or high (80% [Formula: see text]) intensity for 10 weeks. An additional group of highly trained rats was detrained for 4 weeks. Untrained rats served as controls. At the end of treatment, rats of all groups were split into two subgroups. In the former, rats underwent left anterior descending artery (LAD) ligature for 30 min, followed by 90-min reperfusion, with subsequent measurement of the infarct size. In the latter, biopsies were taken to measure heat-shock proteins (HSP) 70/72, vascular endothelial growth factor (VEGF) protein levels, and superoxide dismutase (SOD) activity. Training reduced infarct size proportionally to training intensity. With detraining, infarct size increased compared to highly trained rats, maintaining some cardioprotection with respect to controls. Cardioprotection was proportional to training intensity and related to HSP70/72 upregulation and Mn-SOD activity. The relationship with Mn-SOD was lost with detraining. VEGF protein expression was not affected by either training or detraining. Stress proteins and antioxidant defenses might be involved in the beneficial effects of long-term training as a function of training intensity, while HSP70 may be one of the factors accounting for the partial persistence of myocardial protection against I/R injury in detrained rats.
Pubmed
Web of science
Create date
13/05/2011 9:27
Last modification date
20/08/2019 16:19
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