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Biochem Biophys Res Commun. 2015 May 29;461(2):354-60. doi: 10.1016/j.bbrc.2015.04.038. Epub 2015 Apr 15.

Strenuous exercise induces mitochondrial damage in skeletal muscle of old mice.

Author information

1
Department of Physical Education, Hankuk Univrsity of Foreign Studies, Seoul 130-791, South Korea.
2
Department of Sports Medicine, College of Health Science, Cheongju University, Cheongju 363-764, South Korea.
3
Department of Physical Education, Hankuk Univrsity of Foreign Studies, Seoul 130-791, South Korea; Laboratory of Physiological Hygiene and Exercise Science, School of Kinesiology, University of Minnesota at Twin Cities, Minneapolis, MN 55455, USA. Electronic address: kangx119@umn.edu.

Abstract

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.

KEYWORDS:

Exercise; Inflammation; Mitochondria; Redox signals; Skeletal muscle

PMID:
25887799
DOI:
10.1016/j.bbrc.2015.04.038
[Indexed for MEDLINE]

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