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Updated: Jul 10, 2026
08:12
Measurement of Mitochondrial Respiration in Human and Mouse Skeletal Muscle Fibers by High-Resolution Respirometry
Published on: October 4, 2024
Mitochondrial function and apoptotic susceptibility in aging skeletal muscle.
Béatrice Chabi1, Vladimir Ljubicic, Keir J Menzies
1Department of Biology, York University, Toronto, Ontario, Canada.
Aging Cell
|November 22, 2007
Summary
Aging muscle loses mass and function due to sarcopenia, linked to mitochondrial dysfunction. This study found older rats had less muscle, greater fatigue, increased mitochondrial reactive oxygen species (ROS), and higher apoptotic susceptibility, suggesting impaired mitochondrial health.
Area of Science:
- Gerontology
- Skeletal Muscle Physiology
- Mitochondrial Biology
Background:
- Aging is associated with sarcopenia, characterized by muscle mass loss and functional decline.
- Mitochondrial dysfunction is a suspected contributor to age-related muscle impairments.
- Understanding age-related changes in mitochondrial function is crucial for addressing sarcopenia.
Purpose of the Study:
- To investigate skeletal muscle contractile properties, mitochondrial biogenesis, function, and apoptotic susceptibility in young versus senescent rats.
- To identify the specific mitochondrial mechanisms contributing to age-related sarcopenia and muscle fatigability.
Main Methods:
- Comparison of muscle mass, maximal force production, and in situ contractile properties between young (6-month) and senescent (36-month) Fischer 344 Brown Norway rats.
- Assessment of subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondrial content, biogenesis (PGC-1alpha levels), enzyme activities, and oxygen consumption.
- Measurement of mitochondrial reactive oxygen species (ROS) production, DNA repair enzyme (8-oxoguanine glycosylase 1) levels, and apoptotic markers (cytochrome c, endonuclease G release).
Main Results:
- Senescent rats exhibited lower muscle mass, reduced maximal force, and increased fatigability, consistent with sarcopenia.
- Mitochondrial content and PGC-1alpha levels were reduced in fast-twitch muscle of senescent rats.
- Despite similar enzyme activities and respiration rates, senescent rat mitochondria showed increased ROS production and higher susceptibility to apoptosis.
Conclusions:
- Age-related sarcopenia and muscle fatigability are linked to reduced mitochondrial biogenesis signaling.
- Increased mitochondrial ROS production and enhanced apoptotic susceptibility in senescent muscle contribute to functional decline.
- Mitochondrial dysfunction plays a significant role in the pathogenesis of age-related skeletal muscle impairments.
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