## 1 Introduction  
Skeletal muscles are essential for the maintenance of body's integrity and health. Failure in muscle homeostasis leads to physiological integrity impairment, which contributes to chronic pathologies such as cachexia, metabolic and respiratory diseases, chronic inflammation, liver cirrhosis, and sarcopenia [1, 2, 3, 4, 5, 6]. Muscle deficiency involves detrimental changes including deteriorations of cell metabolism and loss of muscle volume and strength, resulting in poor physical performance and quality of life [7, 8, 9, 10]. Alteration of skeletal muscle mass and strength is in part attributable to dysregulation of the balance between synthesis and breakdown of proteins and other cellular components, such as organelles [11, 12, 13, 14]. Several signal transduction pathways promote muscle atrophy and hypertrophy. Atrophy is the result of increased degradation of cellular proteins and sometimes decreased protein synthesis flux. This state of muscle weakness can be observed in the terminal phase of diseases, such as AIDS, cancer, renal insufficiency, nerve degeneration or metabolic diseases (e.g., diabetes), and even during muscle trauma, immobilization, and aging. Conversely, skeletal muscle hypertrophy is related to enhanced protein synthesis leading to enlargement of pre-existing fibers without variation of myofiber number (i.e., hyperplasia) in humans [11; 12; 13; 14]. The mechanistic/mammalian target of rapamycin complex 1 (mTORC1) was identified as a major regulator of skeletal muscle hypertrophy in response to an increased workload, such as resistance exercise [15; 16; 17; 18; 19; 20; 21; 22]. In past decades, mTORC1 was found to regulate a myriad of fundamental muscle physiological processes, including autophagy [23; 24; 25; 26; 27; 28], cell growth and survival [29; 30; 31], satellite cells activation associated with muscle regeneration [32; 33; 34], and ribosome biogenesis [35; 36]. Moreover, the mTOR pathway appears important for survival of telomerase-deficient mice displaying short telomeres in the liver, heart, and skeletal muscle [37]. Emerging evidence also suggests that mTORC1 plays a dual role in the development of cancer cachexia [38]. On one hand, reduction of anabolic mTORC1 signaling contributes to loss of muscle mass during cachexia. On the other hand, its inhibition upregulates the autophagy pathway and prevents the production of pro-cachetic factors, protecting from tumor cachexia [38]. Recently, the role of the eukaryotic initiation factor 3f (eIF3f) in mTORC1 activity was highlighted in skeletal muscle [39; 40], as well as other regulators, such as diacylglycerol (DAG) and DAG kinases (DGKs) during mechanical stimulation [16; 41; 42; 43; 44; 45; 46; 47]. Importantly, the involvement of satellite cells in skeletal muscle mass regulation has been recently questioned but new data highlighted their importance in myonuclear accretion and muscle remodeling during exercise training [48; 49; 50]. Finally, recent data underlined the importance of an epigenetic regulation (e.g., DNA and histone modifications, expression of specific microRNAs) of skeletal muscle mass, especially during resistance exercise [51; 52]. Physical exercise is a common strategy to improve muscle function by enhancing cell size and metabolism [14; 53]. Through its remarkable effects on various organs, exercise training has a direct impact on the whole organism by improving global homeostasis (e.g., glucose homeostasis) with a major impact on morbidity [54; 55; 56]. Chronic exercise affects muscle mass and metabolism through the modulation of fiber composition and size, the improvement of organelle functioning and cell components recycling [14]. Among the multiple mechanisms involved in adaptations to training, increase of muscle mass and strength is associated with enhancement of myofiber cross-sectional area, as well as myofibrillar adjustments, such as transition of myosin heavy chains (MHC) to MHC2A and MHC2X.