In our study, it was found that the protein of Akt and mTOR was significantly down regulated after hindlimb unloading, and LIPUS with different intensities significantly promoted the expression of Akt, and 80 mW/cm2 LIPUS significantly promoted the expression of mTOR, indicating that MSTN/Akt/mTOR signal pathway may be the key molecular mechanisms of LIPUS preventing muscular atrophy caused by hindlimb suspension. The gene discussed is AKT1; the disease is muscular atrophy.