This review summarizes the recent studies to understand the mechanisms of sarcopenia of aging. A decrease in mitochondrial and nuclear gene transcriptions in skeletal muscle is likely to be responsible for reduced synthesis rates of muscle mitochondrial protein, myosin heavy chain (MHC) and actin. A decrease in muscle mitochondrial protein synthesis could contribute to reduced mitochondrial function. A decrease in synthesis rate of MHC and actin, the key contractile proteins could be responsible for reduced muscle strength. The MHC synthesis rate seems to result from a selective decrease in transcription of MHC isoforms (MHCIIa and IIx) responsible for fast-twitch fibers. Resistance training increases MHC-I isoform mRNA levels with an overall increase in MHC synthesis rate. Aerobic training increases muscle oxidative enzymes equally in young and old but its impact on overall mitochondrial function remains to be clearly defined. Long-term studies are needed to determine the potential benefits and undesirable effects of replacements of various hormones that decline with aging. An individualized exercise prescription involving both aerobic and resistance training is definitely helpful to overcome many aging-related muscle dysfunctions.