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AAS anti-catabolic?

Andy13

Elite Mentor
Platinum
I guess you have to define what anti-catabolic means.

If you look at the big picture and see that you gain more muscle mass than you lose and call this "anti-catabolic" then I guess AAS are indeed anti-catabolic.

But on a molecular level, anti-catabolic means, by some mechanism, protein degredation is detoured.. An example would be blocking of corticoid receptors or delaying the proteolysis of some cellular protein. Insulin is a good example of a hormone that is both anabolic as well as anti-catabolic since it stimulates the synthesis of fatty acids and glycogen (anabolic) and causes phosphorilation (turning off) of degredary proteins which leads to the turning off of other catabolic enzymes like lipase and enzymes involved with the hydrolosis of glycogen polymers as well as glycolytic enzymes and amino acid transaminases (anti-catabolic).

So are AAS anti-catabolic in this sence or, rather, are they simply anabolic?
 
Actually, I heard Dharkham go so far as to say that steroids are technically catabolic.
However, they are not as catabolic as cortisol. They offset cortisol which is a nasty
bitch sent here to destroy us all. No actually cortisol is just a chemical signal which
opens the door to the process of burning certain things to fuel your body. Steroids
mostly offset that evolutionary blueprint your body follows to keep you from starving
to death in your cave. They probably do that by blocking your cortisol receptors.
 
There is some research showing the interaction between AS and the glucocorticoid receptor. This is one theory as to why AS are anti-catabolic.
 
Binding of glucocorticoid antagonists to androgen and glucocorticoid hormone receptors in rat skeletal muscle.

J Steroid Biochem 1986 Feb;24(2):481-7 (ISSN: 0022-4731)

Danhaive PA; Rousseau GG [Find other articles with these Authors]

The binding of ten steroids possessing antiglucocorticoid activity has been studied in rat skeletal muscle cytosol. The affinity of these steroids for both the androgen and the glucocorticoid receptors was determined by competition with radioactive R1881 (methyltrienolone, metribolone) and dexamethasone, respectively. The antiglucocorticoid activity of these compounds was assessed in rat hepatoma (HTC) cells by measuring their inhibitory effect on the glucocorticoid-induced tyrosine aminotransferase activity. This led to identification of five novel in vitro glucocorticoid antagonists. All the steroids tested bound to both the glucocorticoid and the androgen receptors in muscle. Four steroids had an affinity for the glucocorticoid receptor higher than for the androgen receptor. The assumption is made that the steroids tested also behave as antagonists when binding to the glucocorticoid receptor in muscle and behave as agonists when binding to the androgen receptor. On this basis, the data allow one to compute a potential anticatabolic (PAG) and a potential anabolic (PAA) index for each compound. These indices might be of predictive value to determine whether these steroids exert their anabolic action in muscle through the glucocorticoid receptor or through the androgen receptor. The data also make it unlikely that satellite cells are a preferential target for anabolic steroids in muscle.
 
Evidence for sex-dependent anabolic response to androgenic steroids mediated by muscle glucocorticoid receptors in the rat.

J Steroid Biochem 1988 Jun;29(6):575-81 (ISSN: 0022-4731)

Danhaive PA; Rousseau GG [Find other articles with these Authors]
Faculte de Medecine Veterinaire, Universite de Liege, Belgium.

The muscle anabolic/anti-catabolic activity of the androgenic steroids testosterone and trenbolone was studied in rats to investigate whether such steroids act as agonists via muscle androgen receptors, or as antagonists that oppose the catabolic effects of endogenous glucocorticoids via their interaction with muscle glucocorticoid receptors. For comparison, the effects of the potent glucocorticoid antagonist RU486 were also examined. The parameters measured included growth rate, muscle weight, serum growth hormone and corticosterone levels, and receptor binding parameters in muscle cytosol. Females responded better than males to anabolic treatment with the androgenic steroids. Ovariectomy or adrenalectomy abolished this response. Neither the sex difference nor the requirement for ovaries or adrenals could be explained in terms of muscle receptor parameters or serum growth hormone levels. The muscle anabolic activity of androgenic steroids was restored when castrated males were treated with oestradiol and when adrenalectomized females were treated with corticosterone. RU486 also prevented the catabolic/anti-anabolic activity of exogenous corticosterone in adrenalectomized rats. Testosterone and RU486 behaved as anti-glucocorticoids in vivo since they inhibited glucocorticoid-induced liver tyrosine aminotransferase activity. The results suggest that anabolic steroids can act via muscle glucocorticoid receptors, thereby antagonizing the catabolic activity of endogenous glucocorticoids, rather than via muscle androgen receptors.
 
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