**5. Conclusions**

In summary, autophagy represents a crucial mechanism for cell homeostasis and cell survival. Autophagy constitutes a recycling process that degrades used or flawed internal structures into amino acid, enabling cells to survive in difficult circumstances. The identification of Ulk1 as a direct target of AMPK represents a significant step toward understanding how cellular energy stress regulates autophagy machinery in muscle cells. Based on the data presented here, it is clearly conceivable that the autophagy pathway must be considered in muscle pathologies such as sarcopenia and myopathies. Fine molecular studies on AMPK/FoxO3a and AMPK/ Ulk1 axes will offer new and promising strategies in the treatment of muscular loss associated not only to several pathologies like cancer, AIDS, and neuromuscular diseases but also to agerelated disorders. Further investigations must be conducted in order to better understand whether exercise-induced autophagy can also prevent skeletal muscle diseases. In addition, autophagy is involved in skeletal muscle adaptation to endurance exercise in a healthy population. While autophagy is important to prevent mitochondria alteration and exacerbated oxidative stress in response to severe acute exercise, its role in the improvement of endurance capacity has also been demonstrated in response to endurance training. In addition, the feeding pattern and the environment, especially altitude exposure, have to be considered since they represent additional modulators of protein turnover and autophagy pathway. Regular exercise is associated with an enhanced quality of life and represents the most profitable way to limit metabolic disorders and the loss of muscle mass. As a result, these research directions are of major interest in the battle against a wide range of diseases and have to be sustained.
