Figure 3

General hypothesis for exercise-induced backward adaptation: mitochondrial biogenesis versus autophagy. As an upstream kinase, AMP-activated kinase (AMPK) and mammalian target of rapamycin (mTOR) concurrently control autophagy and protein synthesis in cell, and thus balance mitochondrial biogenesis and mitophagy, muscle growth and autophagy. Both endurance and resistance exercise activate AMPK and mTOR signaling. Autophagic responses to acute and chronic exercise will be so important for exercise-induced phenotype as mitochondrial biogenesis and protein synthesis, this hypothesis is expected to clearly explain: why does AMPK activation during resistance exercise not induce the increase in mitochondrial content? why does mTOR activation during endurance exercise not induce the increase in muscle mass? Upon the activation of AMPK and mTOR, skeletal muscle autophagy is surely involved in the development of exercise-induced phenotype. Ulk1, unc-51-like kinase 1.