The Journal of Physiological Sciences

, Volume 66, Issue 1, pp 43–52 | Cite as

Delayed onset muscle soreness: Involvement of neurotrophic factors

  • Kazue MizumuraEmail author
  • Toru Taguchi


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.


Delayed-onset muscle soreness Exercise Mechanical hyperalgesia Nerve growth factor Glial cell line-derived neurotrophic factor 


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© The Physiological Society of Japan and Springer Japan 2015

Authors and Affiliations

  1. 1.Department of Physical Therapy, College of Life and Health SciencesChubu UniversityKasugaiJapan
  2. 2.Department of Neuroscience II, Research Institute of Environmental MedicineNagoya UniversityNagoyaJapan

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