EAA and/or RET stimulate muscle protein synthesis rate and suppression of autophagy activation in muscle of DEX-treated mice. Integrated myofibrillar protein synthesis rate in (A) gastrocnemius muscle (mixed muscle), (B) soleus muscle (slow oxidative muscle), and (C) tibialis anterior muscle (fast glycolytic muscle) for 14 days (n = 5–6 per muscle type). (D) Representative image and relative protein expression of mTOR and rps6 in gastrocnemius (n = 5–6). Representative image and relative protein expression of (E) MyoD and (F) myogenin in gastrocnemius (n = 5–6). (G) Representative image and relative protein expression of ubiquitinated-protein in gastrocnemius (n = 5–6). (H) Representative image and relative protein expression of the ratio of LC3B II/I and (I) ATG7 in gastrocnemius (n = 5–6). Data are presented as mean ± S.E. # Significant difference from control group (p < 0.05). * Significant difference between labeled groups (p < 0.05). CON, sedentary control; DEX, dexamethasone; EAA, essential amino acids; RET, resistance exercise training; MPS, myofibrillar protein synthesis; mTORC1, mammalian target of rapamycin complex 1; rps6, ribosomal protein s6; MyoD, myoblast determination protein 1; LC3, microtubule-association protein 1A/1B-light chain 3; ATG7, autophagy-related 7; GAS, gastrocnemius muscle; SOL, soleus muscle; TA, tibialis anterior muscle.