objective: To explore the molecular mechanism of autophagy mediated by protein kinase B(AKT)/ mammalian target protein of rapamycin (mTOR) pathway in the rehabilitation of muscle atrophy associated with rotator cuff tears (RCTs). Methods: Forty male C57 mice were randomly assigned to the following four groups: sham group, RCTs group, RCTs+ exercise group and RCTs+ exercise+rapamycin group, with 10 mice in each group. At the eighth week after grouping, the healing of bone-tendon interface and muscle cell atrophy were analyzed by histology. The mRNA expression levels of muscle atrophy related genes (Atrogin-1, Bnip 3, MuRF-1) in supraspinatus muscle tissue were measured by real-time quantitative reverse transcription polymerase chain reaction. The expression of LC3 and AKT/mTOR signal pathway in supraspinatus muscle tissue of different groups was detected by western blot, and the production of autophagy in each group was analyzed by transmission electron microscope. Results: Compared with sham operation group, the maturity score of bone-tendon interface at supraspinatus tendon anchorage and the cross-sectional area of supraspinatus muscle fibers in RCTs group decreased significantly (P<0.001), and the muscle loss and the expression of Atrogin-1, Bnip 3 and MuRF-1 genes increased significantly (P<0.001). Compared with RCTs group, RCTs+ exercise group significantly increased the bone-tendon interface maturity score and the cross-sectional area of supraspinatus muscle fibers (P<0.01), and decreased the muscle loss and the expression of Atrogin-1, Bnip 3 and MuRF-1 genes (P<0.01). Compared with the sham group, the LC3Ⅰ/LC3Ⅱ and number of autophagy in supraspinatus muscle of RCTs group increased significantly (P<0.001), while the p-Akt/Akt, p-mTOR/mTOR decreased significantly (P<0.01). Compared with RCTs group, the LC3Ⅰ/LC3Ⅱ and number of autophagy in RCTs+ exercise group decreased significantly (P<0.01), and the number of p-Akt/Akt and p-mTOR/mTOR increased significantly (P<0.001). The addition of rapamycin significantly inhibited the improvement of exercise on bone-tendon interface healing, muscle atrophy and loss, AKT/mTOR signaling pathway and autophagy number induced by RCTs. Conclusion: This study confirme the anti-atrophy effect of exercise rehabilitation in RCTs diseases, and its mechanism is related to activating AKT/mTOR signal to inhibit autophagy.