Calorie restriction limits the generation but not the progression of mitochondrial abnormalities in aging skeletal muscle

@article{Bua2004CalorieRL,
  title={Calorie restriction limits the generation but not the progression of mitochondrial abnormalities in aging skeletal muscle},
  author={Entela Bua and Susan H. McKiernan and Judd M. Aiken},
  journal={The FASEB Journal},
  year={2004},
  volume={18}
}
The effect of early‐onset calorie restriction and aging on the accumulation of electron transport system (ETS) abnormalities was studied in rat skeletal muscle. Rectus femoris and vastus lateralis muscle fibers were analyzed for cytochrome c oxidase (COX) and succinate dehydrogenase (SDH) enzyme activities. Fibers displaying COX negative and SDH hyper reactive (COX–/SDH++) phenotype were followed through 1000–2000 micrometers to determine the frequency and length of these abnormalities as well… 
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Caloric restriction delays aging-induced cellular phenotypes in rhesus monkey skeletal muscle
Adult-onset calorie restriction delays the accumulation of mitochondrial enzyme abnormalities in aging rat kidney tubular epithelial cells.
TLDR
It is demonstrated that COX-deficient renal tubular epithelial cells with mitochondrial abnormalities presented cellular characteristics indicative of physiological dysfunction, and that these cells contained unique, clonally expanded mtDNA deletion mutations.
Synergistic effects of caloric restriction with maintained protein intake on skeletal muscle performance in 21‐month‐old rats: a mitochondria‐mediated pathway
TLDR
The synergistic effects of CR with maintained protein intake may help to limit the progression of sarcopenia by optimizing the turnover rates and functions of major proteins in skeletal muscle.
Absence of uncoupling protein-3 leads to greater activation of an adenine nucleotide translocase-mediated proton conductance in skeletal muscle mitochondria from calorie restricted mice.
Sarcopenia of aging: Underlying cellular mechanisms and protection by calorie restriction
TLDR
Preliminary evidence indicates that moderate CR may promote muscle mitochondrial biogenesis in middle‐aged human subjects, and further research is warranted to investigate whether CR may represent a safe and efficient strategy to delay the onset and mitigate the progression of sarcopenia in older adults.
Calorie restriction in mice overexpressing UCP3: Evidence that prior mitochondrial uncoupling alters response
Apoptosis and necrosis mediate skeletal muscle fiber loss in age‐induced mitochondrial enzymatic abnormalities
TLDR
The link between ETC abnormalities, apoptosis, fiber atrophy, and necrosis supports the hypothesis that mitochondrial DNA deletion mutations are causal in myofiber loss.
Age- and calorie restriction-related changes in rat brain mitochondrial DNA and TFAM binding
TLDR
The decreased TFAM binding is a novel finding that may explain the mtDNA loss in spite of the compensatory TFAM increased amount, and in aged CR rats, TFAM amount increased and mtDNA content decreased with respect to young rats’ values, but the extent of the changes was smaller than in aged AL rats.
Tumor necrosis factor α signaling in skeletal muscle: effects of age and caloric restriction
Aging and Calorie Restriction Oppositely Affect Mitochondrial Biogenesis through TFAM Binding at Both Origins of Mitochondrial DNA Replication in Rat Liver
TLDR
An age-related decrease in mitochondrial DNA content and mitochondrial transcription factor A amount was found and a marked increase in the TFAM-bound amounts of mtDNA at both origins of replication with aging, fully prevented by CR.
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References

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