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Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions
Inexperienced vigorous exercise, including eccentric contraction (ECC), causes muscle pain and damage. Similar prior light exercise suppresses the development of muscle pain (repeated-bout effect), but the molecular mechanisms behind this are not sufficiently understood. In this study, the influence...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6204166/ https://www.ncbi.nlm.nih.gov/pubmed/30405861 http://dx.doi.org/10.1155/2018/3080715 |
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author | Nagahisa, Hiroshi Ikezaki, Kazumi Yamada, Ryotaro Yamada, Takashi Miyata, Hirofumi |
author_facet | Nagahisa, Hiroshi Ikezaki, Kazumi Yamada, Ryotaro Yamada, Takashi Miyata, Hirofumi |
author_sort | Nagahisa, Hiroshi |
collection | PubMed |
description | Inexperienced vigorous exercise, including eccentric contraction (ECC), causes muscle pain and damage. Similar prior light exercise suppresses the development of muscle pain (repeated-bout effect), but the molecular mechanisms behind this are not sufficiently understood. In this study, the influence of a nondamaging preconditioning ECC load (Precon) on muscle pain-related molecules and satellite cell-activating factors was investigated at the mRNA expression level. Nine-week-old male Wistar rats (n=36) were divided into 2 groups: a group receiving only a damaging ECC (100 contractions) load (non-Precon) and a group receiving a nondamaging ECC (10 contractions) load 2 days before receiving the damaging ECC load (Precon). ECC was loaded on the left leg, and the right leg was regarded as the intact control (CTL). The medial head of the gastrocnemius muscle from all rats was excised 2 or 4 days after the damaging ECC loading, and the relative mRNA expression levels of muscle pain- and satellite cell-related molecules were quantitated using real-time RT PCR. Precon suppressed increases in MHC-embryonic and MHC-neonatal mRNA expressions. Enhancement of HGF, Pax7, MyoD, and myogenin mRNA expression was also suppressed, suggesting that Precon decreased the degree of muscle damage and no muscle regeneration or satellite cell activation occurred. Similarly, increases in mRNA expression of muscle pain-related molecules (BKB(2) receptor, COX-2, and mPGEC-1) were also suppressed. This study clearly demonstrated that at the mRNA level, prior light ECC suppressed muscle damage induced by later damaging ECC and promoted recovery from muscle pain. |
format | Online Article Text |
id | pubmed-6204166 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-62041662018-11-07 Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions Nagahisa, Hiroshi Ikezaki, Kazumi Yamada, Ryotaro Yamada, Takashi Miyata, Hirofumi Pain Res Manag Research Article Inexperienced vigorous exercise, including eccentric contraction (ECC), causes muscle pain and damage. Similar prior light exercise suppresses the development of muscle pain (repeated-bout effect), but the molecular mechanisms behind this are not sufficiently understood. In this study, the influence of a nondamaging preconditioning ECC load (Precon) on muscle pain-related molecules and satellite cell-activating factors was investigated at the mRNA expression level. Nine-week-old male Wistar rats (n=36) were divided into 2 groups: a group receiving only a damaging ECC (100 contractions) load (non-Precon) and a group receiving a nondamaging ECC (10 contractions) load 2 days before receiving the damaging ECC load (Precon). ECC was loaded on the left leg, and the right leg was regarded as the intact control (CTL). The medial head of the gastrocnemius muscle from all rats was excised 2 or 4 days after the damaging ECC loading, and the relative mRNA expression levels of muscle pain- and satellite cell-related molecules were quantitated using real-time RT PCR. Precon suppressed increases in MHC-embryonic and MHC-neonatal mRNA expressions. Enhancement of HGF, Pax7, MyoD, and myogenin mRNA expression was also suppressed, suggesting that Precon decreased the degree of muscle damage and no muscle regeneration or satellite cell activation occurred. Similarly, increases in mRNA expression of muscle pain-related molecules (BKB(2) receptor, COX-2, and mPGEC-1) were also suppressed. This study clearly demonstrated that at the mRNA level, prior light ECC suppressed muscle damage induced by later damaging ECC and promoted recovery from muscle pain. Hindawi 2018-10-14 /pmc/articles/PMC6204166/ /pubmed/30405861 http://dx.doi.org/10.1155/2018/3080715 Text en Copyright © 2018 Hiroshi Nagahisa et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Nagahisa, Hiroshi Ikezaki, Kazumi Yamada, Ryotaro Yamada, Takashi Miyata, Hirofumi Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions |
title | Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions |
title_full | Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions |
title_fullStr | Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions |
title_full_unstemmed | Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions |
title_short | Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions |
title_sort | preconditioning contractions suppress muscle pain markers after damaging eccentric contractions |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6204166/ https://www.ncbi.nlm.nih.gov/pubmed/30405861 http://dx.doi.org/10.1155/2018/3080715 |
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