Clearly, the near-immediate response seen in such situations and replicated by injecting a rapidly available form of testosterone in mice, requires a much faster mechanism than the genomic effects of testosterone provide.16 Genomic changes take hours to days to manifest, while non-genomic take seconds to minutes.

            A third avenue by which AAS appear to promote muscle growth is by inhibiting the catabolism (muscle wasting) caused by cortisol and other glucocorticoids. The balance between anabolism (muscle building) and catabolism (muscle wasting) is generally attributed to the testosterone-cortisol ratio; of course, there are many other factors involved.17 Testosterone is generally considered to promote anabolism, while cortisol promotes catabolism. However, there is some research supporting the idea that testosterone may also reduce catabolism, either by attaching to the glucocorticoid (cortisol) receptor and blocking the catabolic effect or reducing the concentration of glucocorticoid receptors by turning down the “manufacturing” signal from the nucleus (DNA).5

Chemical Structure Of AAS
AAS differ from testosterone by minor changes in the chemical structure that can dramatically affect the absorption, androgenicity, metabolism, receptor affinity, conformation of the AAS-AR complex and potency of each specific AAS. Testosterone is not a drug that can be taken orally because it is rapidly degraded and eliminated by enzymes in the intestines and liver.18 However, when the 17-carbon is bound to a small carbon chain (17a-alkylation), the AAS is protected from these enzymes. Unfortunately, 17a-alkylated AAS are associated with liver damage and potentially life-threatening tumors, as well as negative changes in (good) HDL cholesterol.19 Certain AAS will place a double-bond at the 1-carbon which provides some, but less, protection from degradation. The prototypical oral AAS, Dianabol, combined with the use of 17a-alkylation and a 1-carbon double bond; oral-turinabol, the AAS most commonly used by East Germany during their era of Olympic dominance, adds a chlorine to the 5-carbon, conferring further protection. Certainly, there are many other possible modifications but these represent the more commonly encountered oral AAS. The effects of oral AAS are short-lived, as they are cleared in a matter of hours.

            Common injectable AAS are naturally produced androgens (testosterone, nortestosterone, boldenone) that are bound to a fatty acid by an ester bond at the 17-carbon. Rather than protecting against enzymes, as the 17a-alkylated AAS are, the 17b-esters merely increase the time that the bound AAS remains in an oil globule, after injection, before it circulates through the body. Once an AAS-ester hits the bloodstream, the fatty acid is rapidly split off by enzymes called esterases. A long fatty acid makes the AAS more lipid-soluble and it will disperse from the injected oil depot more slowly (days to weeks). Without the addition of an ester, injected testosterone will clear the system in a matter of hours.

            AAS can also be placed into gels or patches containing permeation-enhancers that allow the AAS to be absorbed across the skin or the gum/cheeks of the mouth.20 Intranasal testosterone is also being developed, as the lining of the nose and airways is also an effective site for absorption.21 AAS absorbed across skin or mucosa does not need to be modified. Transdermal and mucosal testosterone do not maintain elevated concentrations for long after the application (patch, gel or spray) has been removed. Thus, they are applied daily.