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bibliography * The PainScience Bibliography contains plain language summaries of thousands of scientific papers and others sources, like a specialized blog. This page is about a single scientific paper in the bibliography, Mizumura 2016.

Delayed onset muscle soreness: Involvement of neurotrophic factors

updated
Mizumura K, Taguchi T. Delayed onset muscle soreness: Involvement of neurotrophic factors. J Physiol Sci. 2016 Jan;66(1):43–52. PubMed #26467448.
Tags: DOMS, neat, exercise, self-treatment, treatment, inflammation, pain problems, muscle

PainSci summary of Mizumura 2016?This page is one of thousands in the PainScience.com bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided at the bottom of the page, as often as possible. ★★★★☆?4-star ratings are for bigger/better studies and reviews published in more prestigious journals, with only quibbles. Ratings are a highly subjective opinion, and subject to revision at any time. If you think this paper has been incorrectly rated, please let me know.

This paper summarizes the results a series of Japanese studies (Murase, Urai, Murase) since 2010 showing that the pain of delayed onset muscle soreness is related to neurotrophic factors (substances secreted by muscles cells that goose nerve growth. In other words, DOMS is “nerve growing pains” — exercise develops our nerves, and that’s uncomfortable.

original abstract

Delayed-onset muscle soreness (DOMS) is quite a common consequence of unaccustomed strenuous exercise, especially exercise containing eccentric contraction (lengthening contraction, LC). Its typical sign is mechanical hyperalgesia (tenderness and movement related pain). Its cause has been commonly believed to be micro-damage of the muscle and subsequent inflammation. Here we present a brief historical overview of the damage-inflammation theory followed by a discussion of our new findings. Different from previous observations, we have observed mechanical hyperalgesia in rats 1-3 days after LC without any apparent microscopic damage of the muscle or signs of inflammation. With our model we have found that two pathways are involved in inducing mechanical hyperalgesia after LC: activation of the B2 bradykinin receptor-nerve growth factor (NGF) pathway and activation of the COX-2-glial cell line-derived neurotrophic factor (GDNF) pathway. These neurotrophic factors were produced by muscle fibers and/or satellite cells. This means that muscle fiber damage is not essential, although it is sufficient, for induction of DOMS, instead, NGF and GDNF produced by muscle fibers/satellite cells play crucial roles in DOMS.

related content

These two articles on PainScience.com cite Mizumura 2016 as a source:


This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights: