Strenuous exercise induces mitochondrial damage in skeletal muscle of old mice

Sangho Lee, Minjung Kim, Wonchung Lim, Taeyoung Kim, Chounghun Kang

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Strenuous exercise is known to cause excessive ROS generation and inflammation. However, the mechanisms responsible for the regulation of mitochondrial integrity in the senescent muscle during high-intensity exercise (HE) are not well studied. Here, we show that HE suppresses up-regulation of mitochondrial function despite increase in mitochondrial copy number, following excessive ROS production, proinflammatory cytokines and NFκB activation. Moreover, HE in the old group resulted in the decreasing of both fusion (Mfn2) and fission (Drp1) proteins that may contribute to alteration of mitochondrial morphology. This study suggests that strenuous exercise does not reverse age-related mitochondrial damage and dysfunction by the increased ROS and inflammation.

Original languageEnglish (US)
Pages (from-to)354-360
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - May 8 2015

Bibliographical note

Funding Information:
This work was supported by Hankuk University of Foreign Studies Research Fund of 2015.

Publisher Copyright:
© 2015 Elsevier Inc. All rights reserved.


  • Exercise
  • Inflammation
  • Mitochondria
  • Redox signals
  • Skeletal muscle


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