Effects Of Age And Exercise Training On The Expression Of Mitochondrial Genes In Skeletal Muscle

Mechanisms underlying sarcopenia in skeletal muscle have not been fully elucidated, but mitochondrial dysfunction appears to play a role. The PGC-1α mediated pathway plays an important role in promoting skeletal muscle mitochondrial biogenesis, but it is unclear how the expression of genes involved in this signaling pathway change in aging muscle. We studied the effects of exercise training on age-related alterations in the PGC-1α pathway in gastrocnemius muscle from FBN rats divided into 3 groups: Young Sedentary (Y, 6 months), Old Sedentary (O, 36 months), and Old Trained (OT, 36 months). PGC-1α mRNA levels were increased in O vs. Y rats (fold change > 2), while OT rats showed no significant difference in PGC-1α mRNA levels compared to Y. Nrf1, Nrf2, and CaMK mRNA levels were all increased in O vs. Y, but there was no difference seen in OT vs. Y in these genes. Uncoupling Protein 2 (UCP2) and 3 (UCP3) gene expression was increased in O vs. Y rats, but there was no difference between OT and Y. Citrate Synthase (CS) activity was examined as a marker for mitochondrial function and was significantly increased in OT vs. O and Y rats, while there was no difference between CS activity in O vs. Y. Our data suggests that aging is associated with increased mitochondrial gene expression, but that this increased expression does not result in improved function. Exercise training apparently increases mitochondrial function during aging and thus may attenuate the need for elevated gene expression. Supported by NIH AG 030423