SARMs while on cycle.

[Turbo3000]

^^ there is no receptor competition Turbo, none at all. In the presence of excess androgens the life span of androgen receptors nearly doubles as does the rate of production of new androgen receptors.
There is no static number of androgen receptors. The number is always changing and you are always using new receptors. Hell the lifespan of an androgen receptor is only like 3 hrs an it doubles to 6 when excess androgens are present.
Receptor competition is a myth.

Receptor down regulation is not a myth. The receptors don't multiply when dealing with excess in the body. The human body wants nothing more than homeostasis. Receptors, ratelimiting steps, feedback loops, all designed to keeps things in balance.

[Turbo3000]

The amount of AR mRNA increased 2- to 10-fold with androgen withdrawal and decreased below control levels after androgen stimulation in rat ventral prostate, coagulating gland, epididymis, seminal vesicle, kidney, and brain, and in a human prostate cancer cell line, LNCaP. - See more at: http://press.endocrine.org/doi/abs/1....RhJ7UhUy.dpuf

[Turbo3000]

Here is your info on excess androgen increasing AR half life. It was shown to occur in cancerous environments. Not really a good repression of healthy bodybuilder. Cancer cells=No rules followed.

The half-life of AR protein varies depending on the context of the cell environment. Androgens have been reported to stabilize AR protein in various cell contexts (91). The half-life of AR in LNCaP cells is approximately 3 h in the absence of androgens and is longer than 10 h in the presence of 10 nm DHT. Interestingly, the half-life of AR from the androgen-independent subline of LNCaP that was grown without androgen treatment, LNCaP-C4–2, is 7 h in the absence of androgens (108). A prolonged half-life of AR protein in the absence of androgens was also observed in recurrent CWR22 tumors ( - See more at: http://press.endocrine.org/doi/full/....S3NaczIX.dpuf

[Bouncer]

Check pm turbo. Question for you

[Mr I]

Great work turbo. Respect even if it's an alternative view

[Turbo3000]

Great work turbo. Respect even if it's an alternative view

AR research is way behind the times.

[StanG]

Here is your info on excess androgen increasing AR half life. It was shown to occur in cancerous environments. Not really a good repression of healthy bodybuilder. Cancer cells=No rules followed.

The half-life of AR protein varies depending on the context of the cell environment. Androgens have been reported to stabilize AR protein in various cell contexts (91). The half-life of AR in LNCaP cells is approximately 3 h in the absence of androgens and is longer than 10 h in the presence of 10 nm DHT. Interestingly, the half-life of AR from the androgen-independent subline of LNCaP that was grown without androgen treatment, LNCaP-C4–2, is 7 h in the absence of androgens (108). A prolonged half-life of AR protein in the absence of androgens was also observed in recurrent CWR22 tumors ( - See more at: http://press.endocrine.org/doi/full/....S3NaczIX.dpuf

No thats certainly not what I would use to support that contention. I would be more inclined to use something along the lines of this:

J Biol Chem. 1985 Jan 10;260(1):455-61.
Mechanism of androgen-receptor augmentation. Analysis of receptor synthesis and degradation by the density-shift technique.
Syms AJ, Norris JS, Panko WB, Smith RG.
The ductus deferens smooth muscle tumor cell line (DDT1MF-2) contains receptors for, and is stimulated by, androgens. Cells cultured in the absence of androgens maintain a basal level of androgen receptors. Following incubation with various concentrations of the synthetic androgen methyltrienolone (R1881) for 1-6 h, the concentration of these receptors increased from 6.0 to 12.2 fmol/micrograms of DNA, while the equilibrium dissociation constant (Kd) of 0.5 nM for this steroid remained unchanged. The steroid-induced increase in androgen receptor levels was specific for androgens and dependent upon protein synthesis. The mechanism of receptor augmentation was examined by utilization of isotopically dense amino acids to determine rates of receptor appearance and degradation in the presence or absence of [3H]R1881. In the absence of androgens, the half-life of the androgen receptor was 3.1 h, with a rate constant (kD) of 0.22/h. In the presence of 1 nM [3H]R1881, however, the half-life was 6.6 h, with kD = 0.11/h. The rate constant for receptor synthesis (ks) in the absence or presence of [3H]R1881 was calculated to be 1.35 and 2.23 fmol/micrograms of DNA/h, respectively. Thus, androgen-induced androgen-receptor augmentation is explained by an increase both in receptor half-life and in rates of receptor synthesis.

[StanG]

Receptor down regulation is not a myth. The receptors don't multiply when dealing with excess in the body. The human body wants nothing more than homeostasis. Receptors, ratelimiting steps, feedback loops, all designed to keeps things in balance.

The body DOES try to achieve homeostasis and in an effort to utilize the excess androgens present the ar half life and rate of production does in fact almost double. Ar downreg is a myth and has been dispelled by the likes of Bill Roberts and Karl Hoffman (Nandi) as well. (The example i cited above was not the one I was looking for, I will find it, it was posted by nandi and it id not deal with cancerous cells. Also you have posted nothing that proves that downreg does occur your argument is simply that the rate of production and half life only occurs in cancerous cells, which is not correct When I find the original post by Nandi I am referring to the study he cites will prove that.
The belief that dowregulation does occur is the belief that is outdated and behind the times. It has also been proven in those that are on trt. There is a demonstrated increase in their AR due to thee excess androgens they are introducing.

[StanG]

TRT Example:
Sinha-Hikim I, Taylor WE, Gonzalez-Cadavid NF, Zheng W, Bhasin S. Androgen Receptor in Human Skeletal Muscle and Cultured Muscle Satellite Cells: Up-Regulation by Androgen Treatment. Journal of Clinical Endocrinology & Metabolism 2004;89(10):5245-55. Androgen Receptor in Human Skeletal Muscle and Cultured Muscle Satellite Cells: Up-Regulation by Androgen Treatment

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. Because testosterone promotes the commitment of pluripotent, mesenchymal cells into myogenic lineage, we hypothesized that AR would be expressed in mesenchymal precursor cells in the skeletal muscle. AR expression was evaluated by immunohistochemical staining, confocal immunofluorescence, and immunoelectron microscopy in sections of vastus lateralis from healthy men before and after treatment with a supraphysiological dose of testosterone enanthate. Satellite cell cultures from human skeletal muscle were also tested for AR expression."