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 language | English |
|---|---|
| Pages (from-to) | 859-868 |
| Number of pages | 10 |
| Journal | European Journal of Applied Physiology |
| Volume | 111 |
| Issue number | 5 |
| DOIs | |
| Publication status | Published - May 2011 |
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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 journal › Article
}
TY - JOUR
T1 - Myocardial tolerance to ischemia-reperfusion injury, training intensity and cessation
AU - Esposito, Fabio
AU - Ronchi, Raffaella
AU - Milano, Giuseppina
AU - Margonato, Vittoria
AU - Di Tullio, Simona
AU - Marini, Marina
AU - Veicsteinas, Arsenio
AU - Samaja, Michele
PY - 2011/5
Y1 - 2011/5
N2 - 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.
AB - 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.
KW - Cardioprotection
KW - Exercise
KW - HSP70
KW - Mn-SOD
KW - VEGF
UR - http://www.scopus.com/inward/record.url?scp=79958768583&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79958768583&partnerID=8YFLogxK
U2 - 10.1007/s00421-010-1707-0
DO - 10.1007/s00421-010-1707-0
M3 - Article
C2 - 21063725
AN - SCOPUS:79958768583
VL - 111
SP - 859
EP - 868
JO - European Journal of Applied Physiology
JF - European Journal of Applied Physiology
SN - 1439-6319
IS - 5
ER -