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Title: Strenuous exercise induces mitochondrial damage in skeletal muscle of old mice

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. - Highlights: • Effect of exercise on mitochondrial function of aged skeletal muscles was studied. • Strenuous exercise triggered excessive ROS production and inflammatory cytokines. • Strenuous exercise suppressed mitochondrial function in senescent muscle.

Authors:
;  [1];  [2];  [1];  [1];  [3]
  1. Department of Physical Education, Hankuk Univrsity of Foreign Studies, Seoul 130-791 (Korea, Republic of)
  2. Department of Sports Medicine, College of Health Science, Cheongju University, Cheongju 363-764 (Korea, Republic of)
  3. (United States)
Publication Date:
OSTI Identifier:
22462063
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 461; Journal Issue: 2; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; DAMAGE; ELDERLY PEOPLE; EXERCISE; FISSION; INFLAMMATION; LYMPHOKINES; MICE; MITOCHONDRIA; MORPHOLOGY; MUSCLES

Citation Formats

Lee, Sangho, Kim, Minjung, Lim, Wonchung, Kim, Taeyoung, Kang, Chounghun, E-mail: kangx119@umn.edu, and Laboratory of Physiological Hygiene and Exercise Science, School of Kinesiology, University of Minnesota at Twin Cities, Minneapolis, MN 55455. Strenuous exercise induces mitochondrial damage in skeletal muscle of old mice. United States: N. p., 2015. Web. doi:10.1016/J.BBRC.2015.04.038.
Lee, Sangho, Kim, Minjung, Lim, Wonchung, Kim, Taeyoung, Kang, Chounghun, E-mail: kangx119@umn.edu, & Laboratory of Physiological Hygiene and Exercise Science, School of Kinesiology, University of Minnesota at Twin Cities, Minneapolis, MN 55455. Strenuous exercise induces mitochondrial damage in skeletal muscle of old mice. United States. doi:10.1016/J.BBRC.2015.04.038.
Lee, Sangho, Kim, Minjung, Lim, Wonchung, Kim, Taeyoung, Kang, Chounghun, E-mail: kangx119@umn.edu, and Laboratory of Physiological Hygiene and Exercise Science, School of Kinesiology, University of Minnesota at Twin Cities, Minneapolis, MN 55455. Fri . "Strenuous exercise induces mitochondrial damage in skeletal muscle of old mice". United States. doi:10.1016/J.BBRC.2015.04.038.
@article{osti_22462063,
title = {Strenuous exercise induces mitochondrial damage in skeletal muscle of old mice},
author = {Lee, Sangho and Kim, Minjung and Lim, Wonchung and Kim, Taeyoung and Kang, Chounghun, E-mail: kangx119@umn.edu and Laboratory of Physiological Hygiene and Exercise Science, School of Kinesiology, University of Minnesota at Twin Cities, Minneapolis, MN 55455},
abstractNote = {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. - Highlights: • Effect of exercise on mitochondrial function of aged skeletal muscles was studied. • Strenuous exercise triggered excessive ROS production and inflammatory cytokines. • Strenuous exercise suppressed mitochondrial function in senescent muscle.},
doi = {10.1016/J.BBRC.2015.04.038},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 461,
place = {United States},
year = {2015},
month = {5}
}