Myofascial trigger points (MTrPs) are hyperirritable sites within skeletal muscle that cause local and referred pain. Their biochemical basis remains unclear. Classical models emphasize ischemia and energy depletion, while newer findings point to motor endplate hyperactivity, calcium imbalance, and local inflammation as key drivers.
A narrative review of literature from 2015–2025 (PubMed, Scopus, Web of Science) was conducted, including seminal earlier studies. Empirical and theoretical works on biochemical and molecular mechanisms of MTrPs were analyzed across five domains: endplate dysfunction, ion regulation, metabolism, inflammation, and structure.
Evidence supports excessive acetylcholine release and sustained calcium influx at the motor endplate, leading to local contraction and hypoxia. Ion channel impairment (RyR, K-ATP) perpetuates calcium overload, while metabolic stress produces acidosis and accumulation of nociceptive substances such as bradykinin, CGRP, and substance P. Elevated cytokines (IL-1β, TNF-α) and fibrosis further increase tissue stiffness and sensitivity.
MTrPs represent a biochemical–mechanical feedback loop in which motor, metabolic, and inflammatory factors interact to sustain pain and contracture. Integrating classical and modern models provides a coherent explanation and supports multimodal physiotherapeutic approaches targeting both muscle function and its biochemical environment.
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- Tobias Giesen (Autor), 2025, Biochemical Mechanisms in the Formation of Myofascial Trigger Points. An Integrative Review of Recent Theoretical and Molecular Evidence, Múnich, GRIN Verlag, https://www.grin.com/document/1670893
