## 4 Implication of Satellite Cells and Myonuclear Accretion  
One remarkable property of muscle tissue is to continuously renew itself thanks to the presence of muscle stem cells, also referred as satellite cells (SCs) discovered in 1961 by [PERSON] [186]. SCs are mononucleated cells located between the basal lamina and the plasmalemma of myofibers. Upon stimulation, SCs have the ability to drive out of their quiescent state to modulate their gene expression profile, and to start proliferating. These activated SCs termed myoblasts can stop their proliferation and differentiate into muscle progenitors (myocytes), which fuse with existing myofibers. Fusion of myoblasts with preexistent myofibers can lead to enhance myonuclear number (referred to \"myonuclear accretion\") [187; 188]. Adult SCs are in a quiescent state, expressing both paired box protein 7 (Pax7) and cluster of differentiation 56 (CD56) myogenic factors, and get activated under muscle stimulation or injury [189; 190]. SCs myogenic lineage progression requires myogenic regulatory factors (MRFs), such as myogenic factor 5 (Myf-5), myoblast determination protein D (MyoD), myogenin, and myogenic regulatory factor 4 (MRF4). Activation of quiescent SCs occurs with the simultaneous increased expression of Myf-5 and MyoD. A subset of activated SCs downregulates MyoD expression to self-renew the quiescent SCs pool. Another subset undergoes myogenic commitment by subsequent expression of MRF4 and myogenin whereas Pax7, CD56, and Myf5 factors are no longer expressed. Differentiation then occurs and myoblasts fuse with preexisting myofibers while MyoD expression decreases [191] (Figure 4). Whereas the role of SCs in fiber damage repair and remodeling is well described, SCs implication in muscle growth and hypertrophy has been debated for a long time in adult skeletal muscle. The addition of new myonucleik takes place during myofiber hypertrophy thanks to SCs, providing additional cytoplasmic volume in fiber syncytium [192; 193; 194]. On the contrary, muscle inactivity decreases SCs proliferation [195] and muscle atrophy is associated with a loss of myonuclei [196; 197]. Activation of SCs occurs within skeletal muscle following a single bout of exercise [198] and, conversely, abrogation of muscle progenitors seems to impede exercise-induced hypertrophy [199; 200; 201]. Exercise is known to be an essential anabolic stimulus for muscle tissue, and it was shown that, according to the type of intervention, exercise modulates SCs activation for fiber repair or hypertrophy. Studies on endurance training reported conflicting results on the involvement of SCs, probably due to differences in exercise intensity, volume and duration, as well as the muscle type analyzed [191; 202]. An increase in SCs activation was reported after exhaustive eccentric endurance exercises in mice [203]. Accordingly, it was suggested that new myonuclear accretion induced by continued muscle loading may be associated with fiber repair and regeneration after exercise-induced injury [204]. In humans, SCs activation seems to be more related to exercise intensity and eccentric actions rather than duration of endurance exercises, these training modalities promoting higher mechanical strains and muscle damages [198; 205; 206; 207]. Sustained and intense endurance exercise can induce the activation of SCs to ensure muscle damage repair and it remains difficult to attribute SCs activation to the hypertrophic response rather than to a regeneration process [208; 209]. Long-term endurance or resistance training was found to increase the pool of SCs in both rodents and humans, as well as combination of endurance and resistance training (i.e., \"concurrent training\") [207; 210; 211]. Of note, resistance exercise is more prone to induce muscle hypertrophy than endurance exercise, and results are less conflicting concerning SCs response. [PERSON] et al.