Exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis. - GreenMedInfo Summary

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 VO2max, reversed or attenuated significant age-associated (detrimental) declines in mitochondrial mass (SDH, citrate synthase, COX4, mtDNA), SIRT1 activity, AMPK, pAMPK and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), UCP3 and the Lon protease. Exercise training also decreased the gap between young and old animals in other measured parameters including NRF1, TFAM, Fis1, Mfn1 and polynucleotide phosphorylase (PNPase) levels. We conclude that exercise training can help minimize detrimental skeletal muscle aging deficits by improving mitochondrial protein quality control and biogenesis.