Found this on another site and it has some interesting points. Androgen receptors are in satellite cells (muscle stem cells) and smooth muscle cells as well (intestines etc), probably a partial reason for "hgh gut". Androgen receptors are also on vascular endothelial cells (increasing vascularity). There's also a picture of muscle cells with the AR stained (and 1 nucleus with an androgen receptor stained, and 1 nucleus in a neighbor cell shown without an androgen receptor).
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http://jcem.endojournals.org/content/89/10/5245.long
Androgens stimulate myogenesis, but we do not know what cell types within human skeletal muscle express the androgen receptor (AR) protein and are the target of androgen action.
Satellite cell cultures from human skeletal muscle were also tested for AR expression. AR protein was expressed predominantly in satellite cells, identified by their location outside sarcolemma and inside basal lamina, and by CD34 and C-met staining. Many myonuclei in muscle fibers also demonstrated AR immunostaining. Additionally, CD34+ stem cells in the interstitium, fibroblasts, and mast cells expressed AR immunoreactivity. AR expression was also observed in vascular endothelial and smooth muscle cells. Immunoelectron microscopy revealed aggregation of immunogold particles in nucleoli of satellite cells and myonuclei; testosterone treatment increased nucleolar AR density. Incubation of satellite cell cultures with supraphysiological testosterone and dihydrotestosterone concentrations (100 nm testosterone and 30 nm dihydrotestosterone) modestly increased AR protein levels. Satellite cells are the predominant site of AR expression.
image.jpg
Satellite cells at the top of the section are shown by black arrows, and a myonucleus at the lower right side is shown by an arrowhead. A myonucleus without AR staining is shown by a green arrow.
On average, only 50% of the myonuclei showed AR immunostaining; in contrast, almost all satellite cells expressed AR. Studies report significant differences in the intensity of AR expression in different muscle groups. In general, more androgen-responsive muscle groups, such as levator ani, express higher levels of AR than less responsive muscle groups, such as gastrocnemius (29, 30). AR expression in the skeletal muscle decreases after castration and is up-regulated by androgen administration
In summary, although multiple cell types within the human skeletal muscle express AR protein, satellite cells, and myonuclei are the predominant sites of AR expression. ARs aggregate within the nucleoli of satellite cells and myonuclei. Testosterone and DHT up-regulate AR expression in vivo and in vitro. These data are consistent with the proposal that androgens induce skeletal muscle hypertrophy by acting at multiple sites within the muscle through multiple mechanisms
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Another study shows a link between IGF-1 and androgen receptors
http://jcem.endojournals.org/content/84/8/2705.full
More recent evidence lends support to the complementary roles of androgens, ARs, and IGF-I. Urban et al. (5) found increased mRNA concentrations of IGF-I in skeletal muscle of elderly men given 4 weeks of replacement doses of TE. Further, by inducing severe androgen deficiency in young men for 10 weeks, Mauras et al. (27) showed marked decreases in mRNA concentrations of IGF-I and suggested that within skeletal muscle tissue, androgens are necessary for local IGF-I production, independent of GH production and systemic IGF-I concentrations
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