## 1 Introduction  
Skeletal muscle degeneration causes physical disability and reduces quality of life as described in muscular dystrophies, neuromuscular diseases, and cancer cachexia. Additionally, muscle injuries resulting from prolonged exercise and trauma are well documented [1, 2]. Recently, skeletal muscle-derived stem cells (MDSCs) have been introduced as a powerful tool to improve muscle regeneration. Following muscle injury, MDSCs undergo cyclic division to restore cell numbers and express specific myogenic regulatory factors (MRFs), including MyoD and myogenin [3]. Simultaneously, cells are committed to a myogenic differentiation fate, and a small population returns to quiescence to maintain the stem cell pool [4]. The combined expression of these myogenic factors leads to the activation of myogenic regulatory factor 4 (MRF4) and the expression of muscle fiber-specific contractile proteins [5]. MRF4 plays a role in the maturation of myotubes into adult muscle fibers [6]. Physical activity induces mechanical stress, which can alter gene expression and lead to adaptations in muscle protein synthesis, as well as affecting the performance of MDSCs [7; 8]. Studies have shown that cells change their physiological parameters, such as proliferation and differentiation, in response to mechanical stimulation, and the observed changes were influenced by various factors including cell-matrix interaction, substrate properties, and external forces such as expansion, compression, and shear stress [8; 9; 10]. The adaptation of cells is characterized by alterations in cell focal adhesion and the remodeling of cytoskeletal proteins, which activate mechanosensitive ion channels, leading to changes in gene expression and cell fate [7; 8]. The application of stretch stress modulates cell differentiation based on the direction, magnitude, frequency, and duration of the force applied [8]. Research has shown that while stretch stress promotes the osteogenic differentiation of mesenchymal stem cells (MSCs) in humans [11], it inhibits adipogenic differentiation [12]. Similarly, stretching stress increases the size of myotubes in vitro by promoting protein synthesis and hypertrophy [13]. In this context, stretching muscle fibers not only activates MDSCs in their niche but also enhances their proliferative capacity in vitro [7; 14]. Additionally, mechanical stress has been shown to trigger Ca\({}^{2+}\) flow into quiescent cells, inducing cyclic division [15]. Previous studies have shown that pressure stress can enhance the osteogenic and chondrogenic differentiation of MSCs [16; 17]. Additionally, cyclic compression has been found to increase the regenerative capacity of MSCs in the tibialis anterior muscle following injury in mice [18]. The effect of fluid shear stress on the differentiation fate of MSCs is dependent on various parameters, such as strength, frequency, direction, and duration [19]. Meanwhile, the application of FSS has different effects on cell differentiation depending on the intensity. Although intensive FSS promoted cardiovascular cell differentiation [20], a less intensive FSS was required to drive the osteogenic differentiation of MSCs [21]. In skeletal muscle, the interstitial fluid generates physiological local pressure during muscle contraction [7; 22]. Applying approximately 0.4-1.4 Pa of pulsed FSS on C2C12 myotubes activates the signaling pathways involved in muscle fiber size alteration [23]. A study demonstrated that an FSS of 0.016 Pa enhanced myogenic differentiation by upregulating myogenic differentiation markers and promoting extensive myotube formation [24]. Furthermore, FSS increased nitric oxide (NO) production, cell adhesion, and cell proliferation in mouse MDSCs [25]. The oxygen concentration in tissues is typically around 3%. However, in skeletal muscles, it is approximately 5% [26]. Modulating the oxygen concentration can affect the regenerative capacity of MDSCs.