quote:

---

Bill Roberts:
Anabolic steroids work by more than one mechanism: activating the androgen receptor is only one of them. Some steroids are effective in some ways but not in others. It is best to use a combination that covers both androgen receptor-mediated activity, and non-AR-mediated activity. Dianabol, Anadrol, and Winstrol are examples of drugs that work principally by a non-AR-mediated mechanism, or more than one such mechanism. Deca and Primo are examples of drugs that presumably work mostly or only via the AR-mediated mechanism. Testosterone works both ways.

---

quote:

---

Bill Roberts:
Unfortunately we cannot yet identify how many non-AR-mediated activities there may be. There are I think at least two: activity in microsomes and activities in nerves. There may be more. For example, differentiation of satellite cells of muscle into mature muscle cells might be a non-AR mediated activity.

---

quote:

---

Originally posted by liftingnjuicing:
I'll post the source. THe idea is not that low cortisol makes you big but that low cortisol plus high AAS makes you big.

I think that testosterone, unlike dbol, can actually make your cortisol go up alot.

---

Hey no source posting!!

quote:

---

Originally posted by HUCKLEBERRY FINNaplex:
Steroid molecules interacting with neurons,interaction at the microsomal level,satellite cell differentiation into full blown muscle cells,genetic expression independent of A/R transport

---

Hey huck, do you have a good understanding
of what these mechanisms are in layman's
terms. More importantly, which of these
mechanisms are permanent?

GCR is glucocorticoid receptors.

quote:

---

Originally posted by liftingnjuicing:
some aas make you strong because they strengthen the nerve connections to the muscle tissue you have.

---

Exactly! This effect is VERY temporary
I think. Even if it were permanent, it
don't make you bigger.

quote:

---

Originally posted by liftingnjuicing:
I got the info about the dbol and cortisol from someone else besides BIll ROberts. YOu won't find that at his mesomorph site.

---

quote:

---

Originally posted by JuanDeLaCruz:
Huckleberry's explanation of non AR mediated growth mechanisms sounds like the right answer to me. For some reason I don't think lowered cortisol levels is what allows you to build muscle above and beyond your genetic limit.

---

J Appl Physiol 1991 Mar;70(3):1038-43

Effect of anabolic steroids on mitochondria and sarcotubular system of skeletal muscle.

Saborido A, Vila J, Molano F, Megias A.

Department of Biochemistry and Molecular Biology I, Faculty of Chemistry, Complutense University, Madrid, Spain.

Soleus and extensor digitorum longus (EDL) mitochondria and sarcotubular system were examined in sedentary and trained (treadmill for 12 wk) male rats that were treated with fluoxymesterone or methandrostanolone (2 mg/kg, 5 days/wk, for 8 wk). Neither physical exercise nor anabolic/androgenic steroid administration resulted in a significant change in muscle wet weight. Treatment with the anabolizing androgens increased succinate dehydrogenase activity in fast-twitch muscle mitochondria; this effect was not enhanced by training and was not observed in soleus mitochondria. On the other hand, the content of the slow-twitch muscle in sarcotubular fraction was increased in sedentary rats by fluoxymesterone or methandrostanolone treatment, whereas no significant changes were found in EDL. The training program affected adenosinetriphosphatase (ATPase) activities in the sarcotubular fraction; Mg2(+)-ATPase was increased in both soleus and EDL, but Ca2(+)-ATPase was decreased only in soleus. However, in sedentary animals only the Mg2(+)-dependent activity of EDL was increased by anabolizing androgen treatment, and this change was not potentiated by additional training. The present data indicate that anabolic/androgenic steroids can affect mitochondrial and sarcotubular enzymes in skeletal muscle. The effects are muscle-type specific.