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Delayed onset muscle soreness: Involvement of neurotrophic factors

updated

Tags: DOMS, neat, exercise, self-treatment, treatment, inflammation, pain problems, muscle

Four articles on PainSci cite Mizumura 2016: (1) Post-Exercise, Delayed-Onset Muscle Soreness(2) Eccentric Contraction(3) Your Back Is Not Out of Alignment(4) Massage Does Not Reduce Inflammation

PainSci notes on Mizumura 2016:

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 Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

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.

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