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However, SARMs like Ligandrol are more tissue-selective, which means that they are able to target specific muscle and bone tissuesin order to induce significant bone accretion, rather than inducing an increase in muscle mass. This has not, to our knowledge, been previously tested in vivo. How did a single administration of 20 IU/kg/day of Ligandrol help increase myostatin mRNA in the skeletal muscle of mice? This was not because Ligandrol was having any particularly beneficial effect, but rather because there are a number of different myostatin isoforms, each with specific tissue localization of their effects. The myostatin I isoform (myostatin II) binds to myostatin proteins through cytoplasmic interactions. When given alone, myostatin I has a stimulatory effect to enhance muscle mass (25, 26) and is thus well-suited to stimulate muscle mass in rodents with a high myostatin level (>20 µM). Ligandrol is different from most other interventions in inducing weight gain or muscle size. Unlike Ligandrol, we found that Ligandrol had the opposite effect (i.e., increasing muscle size), whereas the effects of other myostatin isoforms, most notably Ligandrol-delta, could not be predicted. Our data suggest that muscle growth in Ligandrol-treated mice involves the stimulation of mitochondrial biogenesis and muscle remodeling, thereby promoting muscle mass. It is possible that a combination of myostatin I and II and the stimulation of mitochondrial biogenesis may have synergistic effects on stimulating muscle growth, and further investigations on the mechanisms of this potential phenomenon are warranted. Whether the effects we report in our study could also be achieved in humans is unknown. Ligandrol was well-tolerated, and no contraindications were noted. Based on these considerations, this study can be considered a potential treatment for skeletal muscle-associated cancer. Similar articles: