Sarcopenia affects not only physical performance, but also increases the risk for cardiovascular diseases. Aminolevulinic acid (ALA) is a raw material for the mitochondrial electron carriers, heme and cytochrome C. In the present study, physical performance of ALA-treated mice (0.03%-ALA/ chow weight) was examined as to elucidate the usefulness of ALA for the treatment of sarcopenia.Design and Method:
Alteration in physical performance and muscle mass were examined in ALA-treated mice. Harvested skeletal muscle was examined for expression of genes related to mitochondrial amount and function.Results:
Muscle mass and mitochondrial amount were increased in the skeletal muscle of ALA-treated mice. Expressions of the mitochondrial activation genes, PGC1a and UCP3 were up-regulated. Decreased muscle strength, exercise endurance and glucose tolerance of aging mice and 5/6 nephrectomized mice, which were sarcopenic with reduced amount of muscle mitochondria, were improved by the ALA-feeding for 8weeks. In the experiments using cultured myocytes treated with ALA, expressions of PGC1a and UCP3, and mitochondrial amount were increased, associated with augmented oxygen utilization. Suppression of electron transport by antimycin A attenuated the increases in oxygen utilization, PGC1a expression and mitochondrial amount in ALA-treated myocytes.Conclusions:
ALA improved exercise endurance and glucose intolerance of sarcopenic mice through increases in muscle mass, muscle PGC1a expression and mitochondrial amount. These results indicated the usefulness of ALA for improvement of physical performance and glucose tolerance in sarcopenic patients through both muscle enhancement and activation of muscle mitochondria.