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  • Age-associated declines in mitochondrial biogenesis and protein quality control factors are minimized by exercise training.

Age-associated declines in mitochondrial biogenesis and protein quality control factors are minimized by exercise training.

American journal of physiology. Regulatory, integrative and comparative physiology (2012-05-11)
Erika Koltai, Nikolett Hart, Albert W Taylor, Sataro Goto, Jenny K Ngo, Kelvin J A Davies, Zsolt Radak
ABSTRACT

A decline in mitochondrial biogenesis and mitochondrial protein quality control in skeletal muscle is a common finding in aging, but exercise training has been suggested as a possible cure. In this report, we tested the hypothesis that moderate-intensity exercise training could prevent the age-associated deterioration in mitochondrial biogenesis in the gastrocnemius muscle of Wistar rats. Exercise training, consisting of treadmill running at 60% of the initial Vo(2max), reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (succinate dehydrogenase, citrate synthase, cytochrome-c oxidase-4, mtDNA), SIRT1 activity, AMPK, pAMPK, and peroxisome proliferator-activated receptor gamma coactivator 1-α, UCP3, and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters, including nuclear respiratory factor 1, mitochondrial transcription factor A, fission-1, mitofusin-1, and polynucleotide phosphorylase levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.

MATERIALS
Product Number
Brand
Product Description

Sigma-Aldrich
Anti-UCP-3 antibody produced in rabbit, affinity isolated antibody, buffered aqueous solution
Sigma-Aldrich
Anti-α-Tubulin antibody, Mouse monoclonal, clone DM1A, purified from hybridoma cell culture