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Updated: Jul 18, 2025

The Use of Thermal Infra-Red Imaging to Detect Delayed Onset Muscle Soreness
08:51

The Use of Thermal Infra-Red Imaging to Detect Delayed Onset Muscle Soreness

Published on: January 22, 2012

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A link between mitochondrial damage and the immune microenvironment of delayed onset muscle soreness

Zheng Li1, Lina Peng1, Lili Sun2

  • 1College of Sport Human Sciences, Harbin Sport University, No. 1, Dacheng Road, Nangang District, 150008, Harbin, China.

BMC Medical Genomics
|August 23, 2023
PubMed
Abstract

Insights

Skeletal muscle mitochondrial damage contributes to inflammatory pain in delayed onset muscle soreness (DOMS). This study identifies key genes involved in DOMS pathogenesis and mitochondrial dysfunction, offering insights for future clinical applications.

Area of Science:

  • Muscle physiology
  • Mitochondrial biology
  • Immunology

Background:

  • Delayed onset muscle soreness (DOMS) is characterized by inflammatory pain.
  • Mitochondrial morphology changes are increasingly linked to pain, but their role in DOMS pathogenesis and immune microenvironment remains unclear.

Purpose of the Study:

  • To investigate the role of mitochondria in DOMS pathogenesis.
  • To explore the relationship between mitochondrial function and the immune microenvironment in DOMS.
  • To identify key genes associated with mitochondrial damage in DOMS.

Main Methods:

  • Utilized bioinformatics analysis of mitochondrial gene expression data from public databases.
  • Constructed a network of mitochondrial function and immune microenvironment in DOMS.
  • Validated bioinformatics findings using qPCR, histology, and transmission electron microscopy in a rat model.

Main Results:

  • Identified altered expression of mitochondria-related genes in DOMS.
  • Discovered four hub genes (AMPK, PGC1-α, SLC25A25, ARMCX1) differentially expressed in DOMS, linked to immune cell infiltration and mitochondrial metabolism.
  • Bayesian inference suggested IL-6 and PGC1-α as key regulators of mitochondrial damage; electron microscopy showed mitochondrial swelling and myofilament disorganization.

Conclusions:

  • Skeletal muscle mitochondrial damage is a significant contributor to inflammatory factor accumulation in DOMS.
  • The identified hub genes provide a reference for potential clinical applications in managing DOMS.
Keywords:
Immune cells5Inflammatory factors1Inflammatory pain3Mitochondrial4Sports injury2

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