Acetyl-L-Carnitine Supplementation to Old Rats Partially Reverts the Age-Related Mitochondrial Decay of Soleus Muscle by Activating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α-Dependent Mitochondrial Biogenesis

The age-related decay of mitochondrial function is a major contributor to the aging process. We tested the effects of 2-month-daily acetyl-L-carnitine (ALCAR) supplementation on mitochondrial biogenesis in the soleus muscle of aged rats. This muscle is heavily dependent on oxidative metabolism. Mitochondrial (mt) DNA content, citrate synthase activity, transcript levels of some nuclear-and mitochondrial-coded genes (cytochrome c oxidase subunit IV [COX-IV], 16S rRNA, COX-I) and of some factors involved in the mitochondrial biogenesis signaling pathway (peroxisome proliferator-activated receptor gamma [PPAR gamma] coactivator-1 alpha [PGC-1 alpha], mitochondrial transcription factor A mitochondrial [TFAM], mitochondrial transcription factor 2B [TFB2]), as well as the protein content of PGC-1 alpha were determined. The results suggest that the ALCAR treatment in old rats activates PGC-1 alpha-dependent mitochondrial biogenesis, thus partially reverting the age-related mitochondrial decay.