Skip to main content
Fig. 3 | Skeletal Muscle

Fig. 3

From: The beneficial role of proteolysis in skeletal muscle growth and stress adaptation

Fig. 3

Exercise- and starvation-induced autophagy pathways and their beneficial role in muscle stress adaptation. Nutrient deprivation decreases signaling through insulin/growth factor receptors, which decreases Akt activation and allows for the AMPK-dependent phosphorylation of FoxO3. FoxO3 is then able to translocate into the nucleus and initiate the transcription of autophagy-related genes. Activated AMPK also phosphorylates mTORC1 (preventing its action on ULK1, a key autophagy-related kinase) and ULK1 to allow for efficient autophagosome formation and clearance of encapsulated material. Moreover, the lack of intake of essential amino acids further prevents mTORC1 activation and promotes autophagy induction. Taken together, these processes recycle nutrients for muscle cells and the body as a whole during lean periods. While starvation-induced autophagy is undoubtedly a part of muscle biochemistry during exercise, physical activity also activates beclin-1 through its phosphorylation-dependent release from the BCL2-beclin-1 complex. Beclin-1 is critical to autophagosome formation and the efficient clearance of damaged organelles and proteins that arise from physical stress

Back to article page