Delayed onset muscle soreness: Involvement of neurotrophic factors

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.

Characterisation of Delayed Onset of Muscle Soreness (DOMS) in the hand, wrist and forearm using a finger dynamometer: A pilot study

“…The characteristics and time course of DOMS was similar to that previously reported for other body parts including arms and legs [1]. The aching nature of the pain is likely to re lect musculoskeletal trauma [2,3], although the location of pain differed substantially between participants and included ingers, palm of hand, wrist, lower and upper arm and shoulder. This might re lect variations in strategies used to pull the inger trigger that lead to recruitment of different muscle groups.…”

“…Delayed onset of muscle soreness is related to microtrauma in sarcomeres and an associated inflammatory response with the involvement of neurotrophic factors manifesting as pain, stiffness, muscle tenderness, decreased strength and swelling [2,3]. Symptoms are delayed in onset with severity reaching a peak between 24 to 72 hours and disappearing by seven days after exercise.…”

Thin‐fibre receptors expressing acid‐sensing ion channel 3 contribute to muscular mechanical hypersensitivity after exercise

“…Delayed onset muscle soreness (DOMS) is a type of muscle pain or mechanical hyperalgesia commonly experienced for a few days after lengthening contractions (LC), in which the contracting muscle is simultaneously stretched (Mizumura & Taguchi, ). In our previous study, intramuscular injection of amiloride, a non‐selective blocker of acid‐sensing ion channels (ASICs), was found to reverse mechanical hypersensitivity in a rat model of DOMS (Fujii et al, ).…”

Eccentric contraction–induced muscle damage in human flexor pollicis brevis is accompanied by impairment of motor nerve

“…Second, we measured nerve conduction velocity only in muscle nerves. However, ECC‐induced muscle soreness is assumed to be the result of inflammatory response, so we speculate that sensory nerves may also be affected by ECCs. To resolve this issue, future studies are needed to examine the conduction velocities of sensory nerves.…”