I know there is. But for the most part its research from the Research companies, thus using a Human version.
At the bottom I have something on Mamals, just the way you like it 
You take a little of this:
Hepatocyte growth factor. Hepatocyte growth factor (HGF) is a multifunctional cytokine initially described as a mitogen in mature hepatocytes (122). Recently, HGF and its receptor c-Met have been localized to satellite cells and adjacent myofibers but are absent in the adjacent fibroblasts. In addition, HGF expression is proportional to the degree of muscle injury (33, 174, 182). Multiple roles for HGF have been proposed for the regulation of the satellite cell, including a role as a potent chemotactic factor, an activator of the satellite cell, and an inhibitor of myoblast differentiation (Table 3). HGF is capable of activating and selectively promoting satellite cell proliferation (4). Furthermore, HGF administration attenuates satellite cell differentiation through the transcriptional inhibition of the myogenic regulatory factors (i.e., MyoD and myogenin)
Mix in some:
Fibroblast growth factors. Fibroblast growth factor (FGF) has nine different isoforms (FGF-1 to FGF-9). Although many of the FGF isoforms are broadly expressed, FGF-6 is restricted to skeletal muscle (59). Sheehan and Allen (173) investigated in detail the role of the FGF family on satellite cell proliferation in culture. In these studies, it was demonstrated that FGF-1, -2, -4, -6, and -9 stimulated cellular proliferation, whereas FGF-5, -7, and -8 had no mitogenic activity. The investigators further observed that addition of HGF to either FGF-2, -4, -6, or -9 resulted in a synergistic increase in satellite cell proliferation. In addition to an increase in satellite cell proliferation, the FGF family has also been observed to attenuate satellite cell differentiation to myofibers (30, 91, 173, 178).
The release of FGF-2 from the damaged myofibers, like HGF, is proportional to the degree of injury (29). FGF levels are coordinated with FGF receptor expression. When receptor expression is increased, satellite cells propagated in culture demonstrate an increased proliferation and decreased differentiation (160). Conversely, when receptor expression is diminished, proliferation is decreased and there is a concomitant increase in satellite cell differentiation. Interestingly, during the period of satellite cell activation and proliferation (0-48 h after injury), FGF receptor (FGF-R1) mRNA is increased fivefold, and this increase is further enhanced in the presence of HGF (173).
Interleukin-6 cytokines. Leukemia inhibitory factor (LIF) and interleukin-6 (IL-6) are members of the IL-6 family of cytokines produced by many different cells, including myoblasts and macrophages. These cytokines share a common receptor component, and their actions are mediated through the same signaling pathways (81, 144). Skeletal muscle regeneration after injury in LIF mutant mice is attenuated, whereas exogenous administration of LIF increased the regenerative process and produced enlarged myofibers (101). The permissive effect of LIF was associated only with the muscle lineage and had no effect on nonmuscle cells in skeletal muscle (101). IL-6 promotes the degradation of necrotic tissue, synchronizes the cell cycle of satellite cells, and induces apoptosis of macrophages following muscle injury (22). Unlike LIF, however, IL-6 expression in injured muscle does not increase satellite cell proliferation (96). Collectively, this family of growth factors appears to play an integral role in skeletal muscle regeneration.
Few animal studies have examined the effect of growth factors in vivo. Chakravarthy et al. (26) observed that local IGF-I administration to atrophied muscle increased satellite cell proliferation and muscle mass within 2 wk. Unlike the observations with IGF-I, the intramuscular injection of HGF, at specified intervals following skeletal muscle injury, increased satellite cell proliferation and either had no effect or impaired the rate of regeneration (124). Similarly, administration of FGF at timed intervals and selected dosages did not appreciably affect muscle regeneration (125). Future studies that combine cell culture methodologies and overexpression or loss of function models using molecular technologies will be helpful in the definition of the role of growth factors in satellite cell biology.
Few animal studies have examined the effect of growth factors in vivo. Chakravarthy et al. (26) observed that local IGF-I administration to atrophied muscle increased satellite cell proliferation and muscle mass within 2 wk. Unlike the observations with IGF-I, the intramuscular injection of HGF, at specified intervals following skeletal muscle injury, increased satellite cell proliferation and either had no effect or impaired the rate of regeneration (124). Similarly, administration of FGF at timed intervals and selected dosages did not appreciably affect muscle regeneration (125). Future studies that combine cell culture methodologies and overexpression or loss of function models using molecular technologies will be helpful in the definition of the role of growth factors in satellite cell biology.
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Resistance training induces muscle hypertrophy through a process of satellite cell activation, proliferation, chemotaxis, and fusion to existing myofibers to contribute to muscle growth (Fig. 4; Ref. 167). The migratory capacity (chemotaxis) of satellite cells is dependent on the integrity of the basal lamina. After the rupture or interruption of the basal lamina in response to myotrauma, satellite cells may migrate to adjacent myofibers utilizing tissue bridges (164, 191). In response to limited myotrauma, where no rupture of the basal lamina occurs, satellite cells migrate from the proximal intact portion of the myofiber, under the basal lamina, to the site of injury to participate in the repair process
Macrophages are essential in the orchestration of the repair process as they secrete a collection of cytokine factors that regulate the satellite cell pool (133). Importantly, in the absence of a macrophage response, muscle regeneration is absent; in the presence of an enhanced macrophage response, there is an increase in satellite cell proliferation and differentiation (110).
Sorry for seemingly posting random crap- but this came from a few days looking for "Something New". ITs a collection of things I cut and pasted in a word doc dealing with sattalite cells and GH's and such. The last part is the begining of of my research into creating the best enviroment for hyperplasia as opposed to hyperplasia.
Im thinking I should camoe up with a better way of peicing it together, but theres a methoed to the madness- to the order I put these things in.
