Selenium (Se) is an essential trace element for fish, and deficient or excess dietary Se influence their growth. The body growth of fish is mainly influenced by muscle growth, which is mainly determined by the deposition rate of protein in muscle tissue. There is evidence that the autophagic degradation of fish muscle protein is significantly influenced by the level of dietary Se. The autophagy lysosomal pathway is one of the main pathways for muscle protein degradation. Studies have shown that adequate dietary Se (4.0 mg Se/kg diet) inhibited autophagic degradation in rainbow trout (Oncorhynchus mykiss) muscle. However, the effects of deficient or excess dietary Se on the autophagic degradation of rainbow trout muscle requires further exploration. This study aimed to explore the effects and possible mechanisms of dietary Se level on the growth of rainbow trout. Different amounts of Se yeast (as source of Se) were added to the basal diet to reach deficient (DSe, 0 mg Se/kg diet), adequate (ASe, 4.0 mg Se/kg diet), and excessive (ESe, mg Se/kg diet) Se levels. Results showed that DSe and ESe diets were not conducive to the growth performance of rainbow trout. The final body weight and weight gain rate in the rainbow trout fed DSe and ESe diets were significantly lower than those fed ASe diets (P＜0.05). The feed conversion ratio of fish in the ASe group was significantly higher than those in DSe and ESe groups. There was no significant difference in condition factor or feed intake. Furthermore, the diameter of rainbow trout muscle fibers in the DSe and ESe groups was significantly lower than those in the ASe group (P＜0.05). Additionally, dietary Se significantly affected the protein and total Se content of rainbow trout muscle. The autophagy-related gene (Atg) expression and autophagy markers (microtubule-associated protein light chain 3 (LC3) and P62 level are important biomarkers for assessing the level of autophagy. Results showed that mRNA levels of Atg4b, Atg12l, LC3B, Atg13, Atg7, and Atg5 in the muscle of rainbow trout in DSe and ESe groups were significantly higher than those in the ASe group (P＜0.05). The LC3-II level of rainbow trout in DSe and ESe groups was significantly induced, while the content of P62 was significantly reduced (P＜0.05). These results indicate that deficient or excess dietary Se led to increased levels of autophagy in the muscle of rainbow trout. The protein kinase B-target of rapamycin (Akt-TOR) and amp-activated protein kinase (AMPK) pathways are important pathways for autophagy regulation. Both deficient and excessive Se levels significantly inhibited the phosphorylation of Akt and TOR and inhibited the activity of the Akt-TOR pathway. The AMPK activity of rainbow trout muscle was induced in DSe and ESe groups. The malondialdehyde and lipid peroxide contents of rainbow trout muscle were significantly higher in the DSe and ESe groups than that in the ASe group, as revealed through analysis of the oxidation status of rainbow trout muscle. The muscle oxidative stress was intensified, which may have allowed dietary Se to affect the Akt-TOR and AMPK pathways. In summary, this study explored the comprehensive effects of dietary Se on somatic and muscle growth in rainbow trout. The effects and possible mechanisms of dietary Se level on autophagic degradation of rainbow trout muscle protein were also preliminarily revealed. The results can enrich our understanding of the nutritional function of Se and provide a foundation for further research on the mechanism by which Se regulates fish growth.