Preconditioning Contractions Suppress Muscle Pain Markers after Damaging Eccentric Contractions

Author:

Nagahisa Hiroshi1,Ikezaki Kazumi1,Yamada Ryotaro2,Yamada Takashi2,Miyata Hirofumi1ORCID

Affiliation:

1. Biological Sciences, Graduate School of Sciences and Technology for Innovation, Yamaguchi University, Yoshida 1677-1, Yamaguchi 753-8515, Japan

2. Graduate School of Health Sciences, Sapporo Medical University, Sapporo 060-8556, Japan

Abstract

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 (BKB2 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.

Funder

Japanese Ministry of Education, Science and Culture

Publisher

Hindawi Limited

Subject

Anesthesiology and Pain Medicine,Neurology

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