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BLOOD FLOW RESTRICTED RESISTANCE TRAINING ATTENUATES MYOSTATIN GENE EXPRESSION IN A PATIENT WITH INCLUSION BODY MYOSITIS
Inclusion body myositis is a rare idiopathic inflammatory myopathy that produces extreme muscle weakness. Blood flow restricted resistance training has been shown to improve muscle strength and muscle hypertrophy in inclusion body myositis. Objective: The aim of this study was to evaluate the effect...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Institute of Sport in Warsaw
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4042658/ https://www.ncbi.nlm.nih.gov/pubmed/24899776 http://dx.doi.org/10.5604/20831862.1097479 |
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author | Santos, A.R. Neves, M.T. Gualano, B. Laurentino, G.C. Lancha, A.H. Ugrinowitsch, C. Lima, F.R. Aoki, M.S. |
author_facet | Santos, A.R. Neves, M.T. Gualano, B. Laurentino, G.C. Lancha, A.H. Ugrinowitsch, C. Lima, F.R. Aoki, M.S. |
author_sort | Santos, A.R. |
collection | PubMed |
description | Inclusion body myositis is a rare idiopathic inflammatory myopathy that produces extreme muscle weakness. Blood flow restricted resistance training has been shown to improve muscle strength and muscle hypertrophy in inclusion body myositis. Objective: The aim of this study was to evaluate the effects of a resistance training programme on the expression of genes related to myostatin (MSTN) signalling in one inclusion body myositis patient. Methods: A 65-year-old man with inclusion body myositis underwent blood flow restricted resistance training for 12 weeks. The gene expression of MSTN, follistatin, follistatin-like 3, activin II B receptor, SMAD-7, MyoD, FOXO-3, and MURF-2 was quantified. Results: After 12 weeks of training, a decrease (25%) in MSTN mRNA level was observed, whereas follistatin and follistatin-like 3 gene expression increased by 40% and 70%, respectively. SMAD-7 mRNA level was augmented (20%). FOXO-3 and MURF-2 gene expression increased by 40% and 20%, respectively. No change was observed in activin II B receptor or MyoD gene expression. Conclusions: Blood flow restricted resistance training attenuated MSTN gene expression and also increased expression of myostatin endogenous inhibitors. Blood flow restricted resistance training evoked changes in the expression of genes related to MSTN signalling pathway that could in part explain the muscle hypertrophy previously observed in a patient with inclusion body myositis. |
format | Online Article Text |
id | pubmed-4042658 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Institute of Sport in Warsaw |
record_format | MEDLINE/PubMed |
spelling | pubmed-40426582014-06-04 BLOOD FLOW RESTRICTED RESISTANCE TRAINING ATTENUATES MYOSTATIN GENE EXPRESSION IN A PATIENT WITH INCLUSION BODY MYOSITIS Santos, A.R. Neves, M.T. Gualano, B. Laurentino, G.C. Lancha, A.H. Ugrinowitsch, C. Lima, F.R. Aoki, M.S. Biol Sport Case Report Inclusion body myositis is a rare idiopathic inflammatory myopathy that produces extreme muscle weakness. Blood flow restricted resistance training has been shown to improve muscle strength and muscle hypertrophy in inclusion body myositis. Objective: The aim of this study was to evaluate the effects of a resistance training programme on the expression of genes related to myostatin (MSTN) signalling in one inclusion body myositis patient. Methods: A 65-year-old man with inclusion body myositis underwent blood flow restricted resistance training for 12 weeks. The gene expression of MSTN, follistatin, follistatin-like 3, activin II B receptor, SMAD-7, MyoD, FOXO-3, and MURF-2 was quantified. Results: After 12 weeks of training, a decrease (25%) in MSTN mRNA level was observed, whereas follistatin and follistatin-like 3 gene expression increased by 40% and 70%, respectively. SMAD-7 mRNA level was augmented (20%). FOXO-3 and MURF-2 gene expression increased by 40% and 20%, respectively. No change was observed in activin II B receptor or MyoD gene expression. Conclusions: Blood flow restricted resistance training attenuated MSTN gene expression and also increased expression of myostatin endogenous inhibitors. Blood flow restricted resistance training evoked changes in the expression of genes related to MSTN signalling pathway that could in part explain the muscle hypertrophy previously observed in a patient with inclusion body myositis. Institute of Sport in Warsaw 2014-04-05 2014-06 /pmc/articles/PMC4042658/ /pubmed/24899776 http://dx.doi.org/10.5604/20831862.1097479 Text en Copyright © Biology of Sport 2014 http://creativecommons.org/licenses/by-nc-nd/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Case Report Santos, A.R. Neves, M.T. Gualano, B. Laurentino, G.C. Lancha, A.H. Ugrinowitsch, C. Lima, F.R. Aoki, M.S. BLOOD FLOW RESTRICTED RESISTANCE TRAINING ATTENUATES MYOSTATIN GENE EXPRESSION IN A PATIENT WITH INCLUSION BODY MYOSITIS |
title | BLOOD FLOW RESTRICTED RESISTANCE TRAINING ATTENUATES MYOSTATIN GENE EXPRESSION IN A PATIENT WITH INCLUSION BODY MYOSITIS |
title_full | BLOOD FLOW RESTRICTED RESISTANCE TRAINING ATTENUATES MYOSTATIN GENE EXPRESSION IN A PATIENT WITH INCLUSION BODY MYOSITIS |
title_fullStr | BLOOD FLOW RESTRICTED RESISTANCE TRAINING ATTENUATES MYOSTATIN GENE EXPRESSION IN A PATIENT WITH INCLUSION BODY MYOSITIS |
title_full_unstemmed | BLOOD FLOW RESTRICTED RESISTANCE TRAINING ATTENUATES MYOSTATIN GENE EXPRESSION IN A PATIENT WITH INCLUSION BODY MYOSITIS |
title_short | BLOOD FLOW RESTRICTED RESISTANCE TRAINING ATTENUATES MYOSTATIN GENE EXPRESSION IN A PATIENT WITH INCLUSION BODY MYOSITIS |
title_sort | blood flow restricted resistance training attenuates myostatin gene expression in a patient with inclusion body myositis |
topic | Case Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4042658/ https://www.ncbi.nlm.nih.gov/pubmed/24899776 http://dx.doi.org/10.5604/20831862.1097479 |
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