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Myocardial tolerance to ischemia-reperfusion injury, training intensity and cessation
Authors:Esposito Fabio  Ronchi Raffaella  Milano Giuseppina  Margonato Vittoria  Di Tullio Simona  Marini Marina  Veicsteinas Arsenio  Samaja Michele
Institution:(1) Department of Sport, Nutrition and Health Sciences, University of Milan, Via G. Colombo 71, 20133 Milan, Italy;(2) Department of Medicine, Surgery and Dentistry, San Paolo Hospital, University of Milan, Milan, Italy;(3) Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland;(4) Department of Histology, Embryology, and Applied Biology, University of Bologna, Bologna, Italy;(5) Center of Sport Medicine, Don Gnocchi Foundation, Milan, Italy
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% (V)\dot]\textO2max {\dot{{V}}\text{O}}_{2\max } ) or high (80% (V)\dot]\textO2max {\dot{{V}}\text{O}}_{2\max } ) 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.
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