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. |
| |
Keywords: | |
本文献已被 PubMed SpringerLink 等数据库收录! |
|