Lifelong Physical Activity Modulation of the Skeletal Muscle Mitochondrial Proteome in Mice

The aim of this study was to investigate the influence of lifestyle on the aging alterations in skeletal muscle mitochondrial proteins. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young, Y; old sedentary, S; and old active, A). The S and A mice were individually pl...

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Bibliographic Details
Published in:The journals of gerontology. Series A, Biological sciences and medical sciences Biological sciences and medical sciences, 2010-08, Vol.65A (8), p.832-842
Main Authors: Alves, Renato M. P., Vitorino, Rui, Figueiredo, Pedro, Duarte, José Alberto, Ferreira, Rita, Amado, Francisco
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - biosynthesis
Aging
Aging - metabolism
Animals
BN-PAGE
Electron Transport
Electrophoresis, Gel, Two-Dimensional
Exercise
Gerontology
Lifestyles
Male
Mice
Mice, Inbred C57BL
Mitochondria
Mitochondria, Muscle - chemistry
Mitochondrial aging
Mitochondrial Proteins - analysis
Mitochondrial Proteins - metabolism
Muscle, Skeletal - metabolism
Musculoskeletal system
Oxidative Stress
Physical Conditioning, Animal
Protein Carbonylation
Proteins
Proteome
Proteomics
Respiratory chain functionality
Rodents
Two-dimensional electrophoresis
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Summary:The aim of this study was to investigate the influence of lifestyle on the aging alterations in skeletal muscle mitochondrial proteins. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young, Y; old sedentary, S; and old active, A). The S and A mice were individually placed into standard cages and in cages with running wheels for 25 months. Upon killing, mitochondria from the hind limb skeletal muscles were isolated for the evaluation of general proteome alterations, carbonylation, and electron transport chain (ETC) activity. We identified 77 different proteins mostly from the oxidative phosphorylation and mitochondrial metabolism. Sedentary mice presented a significant loss of ETC functionality in opposition to active mice. Although some proteins were found damaged in both A and S mice, damage to ETC proteins was more evident in S. Moreover, it is also possible to conclude that lifestyle is a key modulator for preventing the aging-induced protein expression and functionality in mitochondria.
ISSN:1079-5006
1758-535X
DOI:10.1093/gerona/glq081