Title

Muscular mechanical hyperalgesia after lengthening contractions in rats depends on stretch velocity and range of motion

Document Type

Journal Article

Publisher

John Wiley and Sons

School

Centre for Exercise and Sports Science Research / School of Medical and Health Sciences

RAS ID

22752

Comments

Originally published as: Hayashi,K. ,Katanosaka,K. ,Abe,M. ,Yamanaka,A. ,Nosaka,K. ,Mizumura,K. ,Taguchi,T. (2016). Muscular mechanical hyperalgesia after lengthening contractions in rats depends on stretch velocity and range of motion. European Journal of Pain. 21(1),125 - 139. Original article available here

Abstract

Background

The current study investigated stretch variables and mechanical factors of lengthening contractions (LC) in the processes leading to muscular mechanical hyperalgesia in rats to understand mechanisms underpinning delayed onset muscle soreness (DOMS).

Methods

Under isoflurane anaesthesia, ankle extensor muscles were loaded with repetitive LC with angular stretch velocities (50°, 100°, 200° and 400°/s) at a fixed range of motion (ROM) of 90°, and with ROMs (30°, 60°, 90° and 120°) at a fixed velocity of 200°/s.

Results

Mechanical hyperalgesia was observed in a velocity- and ROM-dependent manner. Under the fixed ROM, integrated torque generated during LC (iTq[max]) was inversely correlated with the velocity, but the rate of torque increase during LC (rTq[max]) was positively and significantly correlated with the velocity, and the magnitude of hyperalgesia was correlated with rTq[max] (p < 0.001). When the velocity was fixed, iTq[max] was significantly correlated with ROM, and the magnitude of hyperalgesia was correlated with iTq[max] (p < 0.01). Necrotic myofibres were observed only sparsely (<0.8%) after any of the LC protocols tested. Up-regulation of nerve growth factor and glial cell line-derived neurotrophic factor mRNA in the muscle was positively correlated with the increases in the LC velocity and ROM (p < 0.05~0.001).

Conclusions

Both velocity and ROM are pivotal variables determining the initiation of mechanical hyperalgesia. Neurotrophic factor-mediated peripheral mechanisms, but apparently not inflammatory changes caused by myofibre damage, are responsible for the mechanical hyperalgesia.

Significance

Mechanical hyperalgesia appears after LC in a stretch velocity- and range of motion-dependent manner. The rate of torque increase and integrated torque are the crucial factors. Neurotrophic factor-mediated peripheral pain mechanisms without robust inflammatory changes caused by myofibre damage were required for this mechanical hyperalgesia.

DOI

10.1002/ejp.909

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