Document Type : Research Paper I Open Access I Released under CC BY-NC 4.0 license
Authors
1 PhD of Exercise Physiology, neuromuscular Branch, University of Tehran, Tehran, IranTehran university
2 Associate Professor, Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, University of Tehran, Tehran, Iran
3 . Assistant professor, Department of Sport Science, Faculty of Humanities, Tarbiat Modares University, Tehran, IRAN
Abstract
The aim of this study was to investigate the expression of PGC-1 alpha isoforms in response to eccentric and concentric resistance exercise in healthy subjects.
Materials and Methods: Ten healthy men were randomly divided into two groups (5 men concentric and 5 men eccentric). Isokinetic contraction protocols included eccentric and concentric knee extension with maximum power and angular velocity of 60 degrees per second. The torques for each subject were 60 degrees per second to match the workload in both identical protocols and the rotational speed. Contractions consisted of a maximum of 12 sets of 10 repetitions for the right leg, a rest time of 30 seconds between each set. At the beginning and end of the study, lateralis muscle tissue was biopsied. Biopsies were performed in both distal and proximal directions of the lateral flank. Real time PCR was used to evaluate PGC1α-1 and PGC1α-4 gene expression in each tissue group. Data were analyzed using dependent t-test and covariance test.
Results: The intra-group changes of PGC1α-1 were not significant in eccentric (p = 0.168) and concentric (p = 0.959) groups. There was also a significant difference between PGC1α-4, eccentric group (p = 0.012) and concentric group (p = 0.02).
Conclusion: It seems that lack of significant changes in the desired variables due to the lack of exercise pressure is sufficient to stimulate the increase of PGC1α-1 and PGC1α-4. with regard to reviewing the answer, it seems that the compatibility debate has different results that need to be addressed.
Keywords
2. Puigserver P, Spiegelman BM. Peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α): transcriptional coactivator and metabolic regulator. Endocrine reviews. 2003;24(1):78-90.
3. Olesen J, Kiilerich K, Pilegaard H. PGC-1alpha-mediated adaptations in skeletal muscle. Pflugers Archiv : European journal of physiology. 2010;460(1):153-62.
4. Ruas JL, White JP, Rao RR, Kleiner S, Brannan KT, Harrison BC, et al. A PGC-1α isoform induced by resistance training regulates skeletal muscle hypertrophy. Cell. 2012;151(6):1319-31.
5. Dieli-Conwright CM, Kiwata JL, Tuzon CT, Spektor TM, Sattler FR, Rice JC, et al. Acute Response of PGC-1alpha and IGF-1 Isoforms to Maximal Eccentric Exercise in Skeletal Muscle of Postmenopausal Women. Journal of strength and conditioning research. 2016;30(4):1161-70.
6. Adams G, Haddad F. The relationships among IGF-1, DNA content, and protein accumulation during skeletal muscle hypertrophy. Journal of applied physiology. 1996;81(6):2509-16.
7. Ma K, Mallidis C, Bhasin S, Mahabadi V, Artaza J, Gonzalez-Cadavid N, et al. Glucocorticoid-induced skeletal muscle atrophy is associated with upregulation of myostatin gene expression. American Journal of Physiology-Endocrinology and Metabolism. 2003;285(2):E363-E71.
8. Sandri M, Lin J, Handschin C, Yang W, Arany ZP, Lecker SH, et al. PGC-1α protects skeletal muscle from atrophy by suppressing FoxO3 action and atrophy-specific gene transcription. Proceedings of the National Academy of Sciences. 2006;103(44):16260-5.
9. Phillips SM. Resistance exercise: good for more than just Grandma and Grandpa’s muscles. Applied Physiology, Nutrition, and Metabolism. 2007;32(6):1198-205.
10. Wang L, Mascher H, Psilander N, Blomstrand E, Sahlin K. Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle. Journal of applied physiology. 2011;111(5):1335-44.
11. Franchi MV, Reeves ND, Narici MV. Skeletal muscle remodeling in response to eccentric vs. concentric loading: morphological, molecular, and metabolic adaptations. Frontiers in physiology. 2017;8:447.
12. Koskinen SO, Lehti M. Molecular and Cellular Markers in Skeletal Muscle Damage after Acute Voluntary Exercise Containing Eccentric Muscle Contractions. Muscle Cell and Tissue: Current Status of Research Field. 2018:19.
13. Hortobagyi T, Barrier J, Beard D, Braspennincx J, Koens P, Devita P, et al. Greater initial adaptations to submaximal muscle lengthening than maximal shortening. Journal of applied physiology. 1996;81(4):1677-82.
462 علوم زیستی ورزشی، دورة 11 ، شمارة 4، زمستان 1398
14. Kay D, St Clair Gibson A, Mitchell MJ, Lambert MI, Noakes TD. Different neuromuscular recruitment patterns during eccentric, concentric and isometric contractions. Journal of electromyography and kinesiology : official journal of the International Society of Electrophysiological Kinesiology. 2000;10(6):425-31.
15. Millay DP, Olson EN. Making muscle or mitochondria by selective splicing of PGC-1α. Cell metabolism. 2013;17(1):3-4.
16. Ruas JL, White JP, Rao RR, Kleiner S, Brannan KT, Harrison BC, et al. A PGC-1alpha isoform induced by resistance training regulates skeletal muscle hypertrophy. Cell. 2012;151(6):1319-31.
17. Cannon B, Houstek J, Nedergaard J. Brown Adipose Tissue: More Than an Effector of Thermogenesis? a. Annals of the New York Academy of Sciences. 1998;856(1):171-87.
18. Lira VA, Benton CR, Yan Z, Bonen A. PGC-1α regulation by exercise training and its influences on muscle function and insulin sensitivity. American Journal of Physiology-Endocrinology and Metabolism. 2010;299(2):E145-E61.
19. Ogborn DI, McKay BR, Crane JD, Safdar A, Akhtar M, Parise G, et al. Effects of age and unaccustomed resistance exercise on mitochondrial transcript and protein abundance in skeletal muscle of men. American journal of physiology Regulatory, integrative and comparative physiology. 2015;308(8):R734-41.
20. Wang L, Mascher H, Psilander N, Blomstrand E, Sahlin K. Resistance exercise enhances the molecular signaling of mitochondrial biogenesis induced by endurance exercise in human skeletal muscle. Journal of applied physiology. 2011;111(5):1335-44.
21. Pugh JK, Faulkner SH, Jackson AP, King JA, Nimmo MA. Acute molecular responses to concurrent resistance and high-intensity interval exercise in untrained skeletal muscle. Physiological reports. 2015;3(4).
22. Tadaishi M, Miura S, Kai Y, Kawasaki E, Koshinaka K, Kawanaka K, et al. Effect of exercise intensity and AICAR on isoform-specific expressions of murine skeletal muscle PGC-1alpha mRNA: a role of beta(2)-adrenergic receptor activation. American journal of physiology Endocrinology and metabolism. 2011;300(2):E341-9.
23. Jäger S, Handschin C, Pierre JS-, Spiegelman BM. AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1α. Proceedings of the National Academy of Sciences. 2007;104(29):12017-22.
24. Schwarz NA, McKinley-Barnard SK, Spillane MB, Andre TL, Gann JJ, Willoughby DS. Effect of resistance exercise intensity on the expression of PGC-1α isoforms and the anabolic and catabolic signaling mediators, IGF-1 and myostatin, in human skeletal muscle. Appl Physiol Nutr Metab. 2016 Aug;41(8):856-63.
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