Impact of lifelong sedentary behavior on mitochondrial function of mice skeletal muscle

• Published in: The journals of gerontology. Series A, Biological sciences and medical sciences Vol. 64; no. 9; p. 927
• Main Authors: Figueiredo, Pedro A, Powers, Scott K, Ferreira, Rita M, Amado, Francisco, Appell, Hans J, Duarte, José A
• Format: Journal Article
• Language: English
• Published: United States 01.09.2009
• Subjects: Aconitate Hydratase - metabolism; Adenosine Diphosphate - pharmacology; Aging - physiology; Animals; Citrate (si)-Synthase - metabolism; Mice; Mice, Inbred C57BL; Mitochondria, Muscle - physiology; Muscle, Skeletal - physiology; Oxidative Stress; Oxygen Consumption; Phosphorylation; Physical Conditioning, Animal
• ISSN: 1758-535X
• DOI: 10.1093/gerona/glp066

This study investigated the impact of lifelong sedentariness on skeletal muscle mass and mitochondrial function. Thirty C57BL/6 strain mice (2 months) were randomly divided into three groups (young-Y; old sedentary-OS; old active-OA). Young animals were sacrificed after 1 week of quarantine, and OS and OA groups were individually placed into standard cages and in cages with running wheels, respectively, until sacrifice (25 months). Body weights and hind-limb skeletal muscle wet weights were obtained from all groups. Mitochondrial respiratory functional measures (i.e., state 3 and 4 respiration, respiratory control ratio, and ratio of nanomoles of ADP phosphorylated by nanomoles of O2 consumed [ADP/O]) and biochemical markers of oxidative damage (aconitase activity, protein carbonyl derivatives, sulfhydryl groups) were measured in isolated mitochondrial suspensions. Our results reveal that lifelong sedentary behavior has a negative impact on the age-related loss of skeletal muscle mass and on the isolated mitochondrial function of mixed skeletal muscle of mice, which is associated with an increased oxidative damage to mitochondrial biomolecules.