Resistance exercise exacerbates muscle atrophy of skeletal muscle-specific Beclin1 conditioned knockout (cKO) mice

• Published in: Advanced Exercise and Health Science Vol. 1; no. 2; pp. 108 - 118
• Main Authors: Zeng, Zhengzhong, Zhang, Hu, Liang, Jiling, Lv, Jun, Wu, Liangwen, Chen, Ning
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.06.2024
• Subjects: Autophagy; Beclin1 conditioned knockout; Protein degradation; Resistance exercise; Skeletal muscle atrophy; Skeletal muscle atrophy; Protein degradation; Autophagy; Beclin1 conditioned knockout; Resistance exercise
• ISSN: 2950-273X
• DOI: 10.1016/j.aehs.2024.03.001

The autophagy-lysosome pathway is the major route for protein and organelle clearance, and the functional status of autophagy plays an important role in the performance of skeletal muscle. The functional impairment of autophagy can cause atrophy and contractile dysfunction of skeletal muscle. Exercise can induce autophagy or regulate the functional status of autophagy to promote an increase in muscle mass for the prevention and treatment of muscular atrophy. However, the role and factors of autophagy in this process remain unclear. Meanwhile, the skeletal muscle-specific autophagy-related gene 6 (Atg6/Beclin1) conditioned knockout (BECN1cKO) mice revealed the accumulation of swollen and vacuolated mitochondria, disorganization of sarcomeres with irregular shapes, and the aggregation of centralized nuclei in the skeletal muscle, as well as the atrophy of skeletal muscle. In contrast, compared with the mice with normal functional status of autophagy, resistance exercise further exacerbated skeletal muscle atrophy in the BECN1cKO mice, suggesting a determinant role of autophagy in combating muscle atrophy as a result of exercise intervention.