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Preventive effects of intense continuous endurance training on isoproterenol-induced cardiac apoptosis and protein synthesis gene expression in wistar rats | ||
| Cardiovascular Biomedicine | ||
| Volume 2, Issue 1, September 2022, Pages 42-50 PDF (483.6 K) | ||
| Document Type: original articles | ||
| DOI: 10.18502/cbj.v1i2.10592 | ||
| Authors | ||
| Majid Gholipour* 1; Meharn Ghahremani2; Mohammad Reza Asad2; Arezoo Tabrizi1 | ||
| 1Department of Physical Education, Sharif University of Technology, Tehran, Iran | ||
| 2Department of Physical Education and Sports Sciences, Payam-e Noor University, Alborz, Iran | ||
| Abstract | ||
| Objectives: Heart failure contributes to cellular lesions and left ventricular dysfunction. The present study aimed to determine the effects of intense continuous endurance training on protein synthesis gene expression and prevention of isoproterenol-induced cardiac apoptosis. Methods: In this experimental study, 16 male Wistar rats were assigned to exercise and control groups. After eight-week treadmill running, with 15° inclination, at 65-75% of VO2max for 30-60 minutes, Isoproterenol (3 mg/kg) was injected into the rats subcutaneously for 7 days. And 24 hours after the last injection, the left ventricular tissue was stored at -80°C for qRT-PCR and TUNEL assay. Between-group differences were determined by parametric and non-parametric tests, using SPSS software version 24. Results: There was a significant increase in mTORC1 gene expression in the training group (P = 0.026) but AMPK alterations failed to be significant. eEF2K gene expression was suppressed in the training group (P = 0.001) which resulted in a significant increase in eEF2 expression (P = 0.005). Left ventricular weight and heart weight/body weight increased compared to the control group (P = 0.028, P = 0.010, respectively). And the training protocol effectively prevented the formation of isoproterenol-induced apoptotic cells (P <0.001). Conclusions: The exercise training protocol increased protein synthesis gene expression, and improved cardiac protection by reducing apoptosis. This protocol can be considered a promising modality in preventing and reducing apoptosis induced by heart disease such as myocardial infarction. | ||
| Keywords | ||
| Treadmill endurance training; Cardio protection; mRNA translation; Apoptosis; Wistar rat | ||
| References | ||
|
1. Nakamura M, Sadoshima J. Mechanisms of physiological and pathological cardiac hypertrophy. Nat Rev Cardiol. 2018; 15(7): 387-407.
2. Tao L, Bei Y, Lin S, et al. Exercise training protects against acute myocardial infarction via improving myocardial energy metabolism and mitochondrial biogenesis. Cell Physiol Biochem. 2015; 37(1): 162-175.
3. Mishra PK, Adameova A, Hill JA, et al. Guidelines for evaluating myocardial cell death. Am J Physiol Heart Circ Physiol. 2019;317(5):H891-H922.
4. Teringova E, Tousek P. Apoptosis in ischemic heart disease. J Transl Med. 2017;15(1):87.
5. Mossmann D, Park S, Hall MN. mTOR signalling and cellular metabolism are mutual determinants in cancer. Nat Rev Cancer 2018; 18(12): 744-757.
6. Wang X, Xie J, Proud CG. Eukaryotic elongation factor 2 kinase (eEF2K) in cancer. Cancers 2017; 9(12): 162.
7. Herzig S, Shaw RJ. AMPK: guardian of metabolism and mitochondrial homeostasis. Nat Rev Mol Cell Bio. 2018; 19(2): 121-135.
8. Chan AY, Soltys CL, Young ME, et al. Activation of AMP-activated protein kinase inhibits protein synthesis associated with hypertrophy in the cardiac myocyte. J Biol Chem. 2004; 279(31): 32771- 32779.
9. Schoenfeld BJ, Grgic J, Van Every DW, et al. Loading recommendations for muscle strength, hypertrophy, and local endurance: A re-examination of the repetition continuum. Sports. 2021; 9(2): 32.
10. Konopka AR, Harber MP. Skeletal muscle hypertrophy after aerobic exercise training. Exerc Sport Sci Rev. 2014; 42(2): 53-61.
11. Donniacuo M, Urbanek K, Nebbioso A, et al. Cardioprotective effect of a moderate and prolonged exercise training involves sirtuin pathway. Life Sci. 2019; 222: 140-147.
12. Ko IG, Kim SE, Kim CJ, et al. Treadmill exercise alleviates aging-induced apoptosis in rat cardiac myocytes. Int J Gerontol. 2013; 7(3): 152-157.
13. Pei Z, Yang C, Guo Y, et al. Effect of different exercise training intensities on age-related cardiac damage in male mice. Aging. 2021; 13(17): 21700-21711.
14. Krüger K, Mooren FC. Exercise-induced leukocyte apoptosis. Exerc Immunol Rev 2014; 20: 117-134.
15. Lu K, Wang L, Wang C, et al. Effects of high-intensity interval versus continuous moderate-intensity aerobic exercise on apoptosis, oxidative stress and metabolism of the infarcted myocardium in a rat model. Mol Med Rep. 2015; 12(2): 2374-2382.
16. Wisløff U, Helgerud J, Kemi OJ, et al. Intensity-controlled treadmill running in rats: V̇ o 2 max and cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2001;280(3):H1301-10.
17. Kemi OJ, Haram PM, Loennechen JP, et al. Moderate vs. high exercise intensity: differential effects on aerobic fitness, cardiomyocyte contractility, and endothelial function. Cardiovasc Res. 2005; 67(1): 161-172.
18. Gyongyosi A, Zilinyi R, Czegledi A, et al. The role of autophagy and death pathways in dose-dependent isoproterenol-induced cardiotoxicity. Curr Pharm Design. 2019; 25(19): 2192-2198.
19. Dreyer HC, Fujita S, Cadenas JG, et al. Resistance exercise increases AMPK activity and reduces 4E‐BP1 phosphorylation and protein synthesis in human skeletal muscle. J Physiol. 2006; 576(2): 613-624.
20. Leprivier G, Remke M, Rotblat B, et al. The eEF2 kinase confers resistance to nutrient deprivation by blocking translation elongation. Cell. 2013; 153(5): 1064-1079.
21. Kumar EA, Giles D, Dalby K. AMPK can stimulate EEF2 phosphorylation without regulating its cognate kinase EEF2K. FASEB J. 2020; 34(S1): 1-1.
22. Hodson N, West DW, Philp A, et al. Molecular regulation of human skeletal muscle protein synthesis in response to exercise and nutrients: A compass for overcoming age-related anabolic resistance. Am J Physiol Cell Physiol. 2019; 317(6):C1061-C1078.
23. Yamada S, Kamata T, Nawa H, et al. AMPK activation, eEF2 inactivation, and reduced protein synthesis in the cerebral cortex of hibernating chipmunks. Sci Rep. 2019; 9(1):11904.
24. Coffey VG, Hawley JA. The molecular bases of training adaptation. Sports Med. 2007; 37(9): 737-763.
25. Zhuo XZ, Wu Y, Ni YJ, et al. Isoproterenol instigates cardiomyocyte apoptosis and heart failure via AMPK inactivation-mediated endoplasmic reticulum stress. Apoptosis. 2013; 18(7): 800-810.
26. Marino G, Niso-Santano M, Baehrecke EH, et al. Self-consumption: the interplay of autophagy and apoptosis. Nat Rev Mol Cell Biol. 2014; 15(2): 81-94.
27. Parzych KR, Klionsky DJ. An overview of autophagy: morphology, mechanism, and regulation. Antioxid Redox Signal. 2014; 20(3):460-473.
28. Sudhakar SR, Varghese J. Insulin signalling activates multiple feedback loops to elicit hunger-induced feeding in Drosophila. Dev Biol. 2020;459(2):87-99.
29. Xie J, Wang Y, Ai D, et al. The role of the Hippo pathway in heart disease. FEBS J 2021.
30. Gan W, Dai X, Dai X, et al. LATS suppresses mTORC1 activity to directly coordinate Hippo and mTORC1 pathways in growth control. Nat Cell Biol. 2020; 22(2): 246-56.
31. Gholipour M, Tabrizi A. The role of Hippo signaling pathway in physiological cardiac hypertrophy. BioImpacts. 2020; 10(4): 251-257. | ||
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