Delayed onset muscle soreness: Involvement of neurotrophic factors
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†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.
related content
- “Bradykinin and nerve growth factor play pivotal roles in muscular mechanical hyperalgesia after exercise (delayed-onset muscle soreness),” an article in J Neurosci, 2010.
- “Decreased nerve growth factor upregulation is a mechanism for reduced mechanical hyperalgesia after the second bout of exercise in rats,” an article in Scandinavian Journal of Medicine & Science in Sports, 2013.
- “Upregulated glial cell line-derived neurotrophic factor through cyclooxygenase-2 activation in the muscle is required for mechanical hyperalgesia after exercise in rats,” an article in Journal of Physiology, 2013.
These three articles on PainScience.com cite Mizumura 2016 as a source:
- PS Post-Exercise, Delayed-Onset Muscle Soreness — The biology & treatment of “muscle fever,” the deep muscle soreness that surges 24-48 hours after an unfamiliar workout intensity
- PS Eccentric Contraction — A weird bit of muscle physiology
- PS Your Back Is Not Out of Alignment — Debunking the obsession with alignment, posture, and other biomechanical bogeymen as major causes of pain
