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

Fabio Esposito, Raffaella Ronchi, Giuseppina Milano, Vittoria Margonato, Simona Di Tullio, Marina Marini, Arsenio Veicsteinas, Michele Samaja

Research output: Contribution to journalArticle

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% V̇O 2max) or high (80% V̇O 2max) 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.

Original languageEnglish
Pages (from-to)859-868
Number of pages10
JournalEuropean Journal of Applied Physiology
Volume111
Issue number5
DOIs
Publication statusPublished - May 2011

Fingerprint

Reperfusion Injury
Superoxide Dismutase
Vascular Endothelial Growth Factor A
HSP72 Heat-Shock Proteins
HSP70 Heat-Shock Proteins
Heat-Shock Proteins
Reperfusion
Ligation
Sprague Dawley Rats
Proteins
Up-Regulation
Arteries
Antioxidants
Biopsy

Keywords

  • Cardioprotection
  • Exercise
  • HSP70
  • Mn-SOD
  • VEGF

ASJC Scopus subject areas

  • Public Health, Environmental and Occupational Health
  • Orthopedics and Sports Medicine
  • Physiology (medical)

Cite this

Myocardial tolerance to ischemia-reperfusion injury, training intensity and cessation. / Esposito, Fabio; Ronchi, Raffaella; Milano, Giuseppina; Margonato, Vittoria; Di Tullio, Simona; Marini, Marina; Veicsteinas, Arsenio; Samaja, Michele.

In: European Journal of Applied Physiology, Vol. 111, No. 5, 05.2011, p. 859-868.

Research output: Contribution to journalArticle

Esposito, F, Ronchi, R, Milano, G, Margonato, V, Di Tullio, S, Marini, M, Veicsteinas, A & Samaja, M 2011, 'Myocardial tolerance to ischemia-reperfusion injury, training intensity and cessation', European Journal of Applied Physiology, vol. 111, no. 5, pp. 859-868. https://doi.org/10.1007/s00421-010-1707-0
Esposito, Fabio ; Ronchi, Raffaella ; Milano, Giuseppina ; Margonato, Vittoria ; Di Tullio, Simona ; Marini, Marina ; Veicsteinas, Arsenio ; Samaja, Michele. / Myocardial tolerance to ischemia-reperfusion injury, training intensity and cessation. In: European Journal of Applied Physiology. 2011 ; Vol. 111, No. 5. pp. 859-868.
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