Document Type

Journal Article

Publisher

Elsevier

School

Medical and Health Sciences

RAS ID

24971

Comments

Originally published as: Perrin, C., Nosaka, K., & Steele, J. (2017). Could titin have a role in strain-induced injuries?. Journal of Sport and Health Science. 6(2). 143-144. Original article available here

Abstract

It has been known for some time that strain injuries occur through the excessive lengthening of a muscle. However, the precise mechanism for strain injury remains elusive and has been the subject of recent debate in the Journal of Sport and Health Science, but it seems sensible to consider mechanisms at the level of the muscle fiber. It was previously believed that damage was the result of non-uniform stretching of sarcomeres on the descending limb of the length–tension curve, with the weakest sarcomeres undergoing the greatest deformation and ultimately damaging the myofibril. This non-uniform lengthening was also believed to explain the residual force enhancement observed during lengthening contractions, as the rapid lengthening of some sarcomeres gives rise to passive tension whilst allowing the remaining sarcomeres to operate closer to their optimal length. While it has been shown sarcomeres do lengthen non-uniformly, it does not appear to be dependent on the strength of the sarcomere. Furthermore, the increase in sarcomere length non-uniformity after active stretching is not correlated to the residual increase in force (r = −0.309). Although this does not disprove the notion that sarcomere lengthening is responsible for muscle damage and injury, it does contradict the idea that the weakest sarcomeres lengthen first as suggested by the sarcomere popping theory.

DOI

10.1016/j.jshs.2017.03.003

Creative Commons License

Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

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