Acetyl-L-carnitine rejuvenates old muscles
Older muscles function and perform less well than young muscles, and that is partly because older muscles convert nutrients into energy less effectively. In older muscle cells the mitochondria, the power plants of the cell, work less well. According to an animal study, that Italian molecular biologists from the University of Bari published in Rejuvenation Research in 2010, acetyl-L-carnitine supplementation can partially eliminate that aging effect.
During 2 months the researchers administered a little acetyl-L-carnitine to a group of aged 28-month-old lab rats through their drinking water. The human equivalent of the dose used was about 1000-1500 milligrams per day. Another group of equally old lab rats did not receive supplements.
When the supplementation period was over, the researchers studied cells from the soleus muscle of the rats. They compared those with muscle cells from young adult rats of 6 months.
Supplementation with acetyl-L-carnitine increased the amount of new mitochondria in the cells of the old rats, and partially compensated for the reduction in the number of well-functioning mitochondria due to aging. As the activity of the citrate synthase gene also increased, the researchers assume that acetyl-L-carnitine really makes the muscle cells generates more energy.
Acetyl-L-carnitine increased the amount of the enzyme PGC-1-alpha and TFAM. TFAM is a molecular switch that enables the mitochondria to read their DNA.
"Our analysis reveals that 2 months of acetyl-L-carnitine administration to aged rats is able to activate the PGC-1alpha-dependent mitochondrial biogenesis in soleus muscle through the increase of mitochondrila DNA content, citrate synthase activity, as well as the levels of some mitochondrial and nuclear transcripts, and the expression of factors for the mitochondrial biogenesis, in particular PGC-1alpha [and] TFAM [...]", the researchers wrote.
"These data confirm a role for acetyl-L-carnitine in the maintenance of the oxidative fiber character of skeletal muscle during aging through stimulation of organelle biogenesis. The activation of the PGC-1a–dependent mitochondrial biogenesis pathway should partially compensate the age-dependent increase in the number of malfunctioning mitochondria and preserve a still sufﬁcient bioenergetic capability."
"This may provide useful insights for the application of dietary interventions in counteracting the age-related mammalian skeletal muscle mitochondrial decay."
Rejuvenation Res. 2010 Apr-Jun;13(2-3):148-51.
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