Here's one:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1573883/
Excerpt from:
Growth hormone secretagogues modulate the electrical and contractile properties of rat skeletal muscle through a ghrelin-specific receptor
Sabata Pierno, et. al.
Br J Pharmacol. 2003 June; 139(3): 575–584. Published online 2003 June 9.
"
Discussion:
This study shows for the first time that GHS directly affect skeletal muscle function. We demonstrate that peptidic and nonpeptidic GHS, as well as ghrelin, the endogenous ligand of GHS receptor, applied in vitro to rat skeletal muscle produce a concentration-dependent reduction of gCl and gK. This reduction is totally suppressed by [D-Lys-3]-GHRP-6 (Kojima et al., 1999), indicating the presence of a specific GHS receptor in skeletal muscle. At the moment, we cannot say whether the GHS receptor of rat skeletal muscle is the same as that found in the pituitary (GHS-R Ia) (Howard et al., 1996), or whether it is a receptor subtype like that described in the heart (Bodart et al., 1999), or perhaps one still to be identified (Muccioli et al., 2002). Some authors have supposed that the GHS binding sites found in human skeletal muscle are different from the first one cloned in the pituitary because they showed lower affinity for ghrelin and for some nonpeptidic GHS (Papotti et al., 2000). Recent studies have shown expression of the mRNA for ghrelin but not that of GHS-R Ia in human skeletal muscle, suggesting a role for ghrelin in this tissue and its possible interaction with a still unknown GHS-R subtype (Gnanapavan et al., 2002)."
And another:
http://www.molbiolcell.org/cgi/content/full/18/3/986
Exerpt from:
Ghrelin and Des-Acyl Ghrelin Promote Differentiation and Fusion of C2C12 Skeletal Muscle Cells
Nicoletta Filigheddu et. al.
Molecular Biology of the Cell Vol. 18, 986–994, March 200
"
Results:
Ghrelin and Des-Acyl Ghrelin Promote Differentiation and Fusion of C2C12 Myoblasts in Growth Medium
C2C12 myoblasts, a skeletal muscle satellite-derived cell line, is a common model to investigate cellular and molecular mechanisms of muscle differentiation.
Upon culture in 2% horse serum, C2C12 cells exit the cell cycle, differentiate, and fuse into multinucleated skeletal myotubes expressing contractile proteins (Blau et al., 1985). The extracellular signals triggering growth arrest and the molecular mechanisms involved in the induction of myoblasts differentiation and fusion still remain to be elucidated."
(lolz, horse serum...)
"
Discussion:
Upon muscular injury, skeletal myoblasts are activated to terminally differentiate through an autocrine/paracrine loop.
We may speculate that GHR would contribute to skeletal muscle plasticity, promoting the differentiation and fusion of myoblasts in the damaged muscles. If this hypothesis would be proved, the activation of the receptor mediating GHR and D-GHR differentiative activity as well as the overexpression of the hormone may provide novel therapeutic strategies for the reduction or retardation of several skeletal muscle pathologies, including dystrophies, atrophies, and cachexia. "
