Hindlimb unloading (HU) is commonly used to simulate weightless condition which induces severe muscle atrophy. Dietary leucine enhances muscle growth by stimulating mammalian target of rapamycin ( mTOR) signaling and protein synthesis. We hypothesize that dietary supplementation of leucine enhances mTOR signaling and mitigates the atrophy of non-weight-bearing muscle. Thirty Spraque-Dawley rats were separated into 5 treatments: control rats without treatment; rats with HU by tail suspension; rats with HU plus 5% leucine supplement; rat with HU plus 5% casein supplement; rats with HU plus 5% starch supplement based on dry feed weight. Trial was lasted for 2 weeks. HU induced severe loss of soleus muscle mass (P<0.01) but only had mild effect on extensor digitorum longus muscle mass, showing that unloading mainly induced atrophy of red muscle fibers. Rats treated with 5% of leucine mitigated muscle atrophy in soleus muscle (P<0.05). Leucine treatment reduced (P<0.05) the phosphorylation of AMP- activated protein kinase (AMPK). No difference in total AMPK, Akt and acetyl CoA carboxylase (ACC) was observed among treatment groups. Currently, we are measuring the phosphorylation of mTOR, ACC and ribosomal protein S6 kinase to further examine signaling pathways leading to the mitigation of muscle atrophy due to leucine supplementation.