Delayed onset muscle soreness: Involvement of neurotrophic factors
Four articles on PainSci cite Mizumura 2016: 1. A Deep Dive into 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.
related content
- “Bradykinin and nerve growth factor play pivotal roles in muscular mechanical hyperalgesia after exercise (delayed-onset muscle soreness),” Shiori Murase, Etsuji Terazawa, Fernando Queme, Hiroki Ota, Teru Matsuda, Kenji Hirate, Yasuko Kozaki, Kimiaki Katanosaka, Toru Taguchi, Hisako Urai, and Kazue Mizumura, J Neurosci, 2010.
- “Decreased nerve growth factor upregulation is a mechanism for reduced mechanical hyperalgesia after the second bout of exercise in rats,” H Urai, S Murase, and K Mizumura, 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,” Shiori Murase, Etsuji Terazawa, Kenji Hirate, Hiroki Yamanaka, Hirosato Kanda, Koichi Noguchi, Hiroki Ota, Fernando Queme, Toru Taguchi, and Kazue Mizumura, Journal of Physiology, 2013.
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:
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- A double-blinded randomised controlled study of the value of sequential intravenous and oral magnesium therapy in patients with chronic low back pain with a neuropathic component. Yousef 2013 Anaesthesia.
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