you told me how long each of the two drugs lasted in the body... i didnt ask that, i can read the war too...

HOW LONG TILL THE DRUG BECOMES ACTIVE???

I found this out off a web site, hope it helps.

Injectable Steroids

The injectable AAS are very effectively degraded in just a single pass through the liver. If this is so, then how can the injectables be effective? The answer is called a "depot" (or reservoir), which allows a regular release of steroid into the bloodstream. As steroid is removed from the bloodstream by the liver, more steroid is being released into the bloodstream from the depot. There are several ways to provide such a reservoir of the steroid. Esters
The other way to provide a depot of steroid is to use a water-insoluble form of the steroid that can be converted in the body to the parent steroid, which has some solubility in water (bloodstream). Most commonly, the parent molecule is esterified with an organic acid, and the resulting ester is soluble in oil, but only very slightly soluble in water. Commonly used organic acid groups are acetate (C2), propionate (C3), enanthate (C7), decanoate (C10), and undecylenate (C11). The longer the carbon chain of the acid, the more oil-soluble the ester, and the longer it takes for the ester to turn into the parent steroid (de-esterification). A type of enzyme that is found throughout the body facilitates the de-esterification reaction to form the parent steroid from the ester. The enzyme actually catalyzes the reaction in both directions, so it can also attach an organic acid back onto the parent steroid. So, for example, testosterone enanthate can actually be turned into testosterone palmitate. There is some good evidence that steroid esters are, to some extent, stored in fat cells.

It is commonly believed that esters form a depot of oil/ester that stays at the injection site. This is not true. While the depot concept holds true for esters (because they slowly release the parent steroid over time), the esters actually disperse throughout the body after injection, prior to (and during) the de-esterification reaction to form the parent steroid. They do not stay at the injection site. For example, the ester testosterone enanthate has been found in tissues throughout the body, including hair samples of subjects who have injected T200. If a bio-contaminant is introduced at the time of injection (non-sterile conditions), the body will attempt to encapsulate the contaminated material, and an abscess will form. In this case it appears as if the ester has remained at the injection site. But under normal sterile conditions, the oily solution will disperse. Injecting too much at one site or injecting too frequently at one site will not cause an abscess.

Transport of Steroids in the Bloodstream
Once the steroid has been released from the depot (or the oral steroid has been absorbed from the intestine), it is transported throughout the body in the bloodstream. Carrier proteins (Albumin and Sex Hormone binding Globulin) bind about 98% of testosterone under natural conditions. Thus, only 2% of the hormone is free to carry out its actions. When exogenous steroid is present, the level of free steroid is much higher than 2%. Bear in mind that the hormone is not permanently bound to the some of the proteins, but is constantly binding and un-binding from the protein. At any given time, about 2% of the hormone is un-bound in the natural state. So, if the 2% unbound hormone were to magically disappear, then the proteins would release more hormone such that 2% (of the remaining total) would come unbound. The bloodstream is the mechanism by which the hormones reach their target tissues (muscle).

Action of Steroids

Androgen Receptor Activation
Once a free molecule of steroid reaches the muscle cell, it diffuses into the cell. The diffusion can be with or without transport-protein assistance. Once in the cell, the AAS is makes its way to the cell nucleus where it can bind with an androgen receptor (AR), and activate the receptor. Two of these activated receptor complexes join together to form the androgen response element (ARE). The ARE interacts with DNA in the nucleus, and increases the transcription of certain genes (such as muscle protein genes). As long as the ARE is intact, it accelerates gene transcription. Remember, though, that the AAS and the receptor are in a state of flux (binding and un-binding), just like with the Carrier proteins. So the ARE can be deactivated just by losing one of the two AAS that are bound to the AR's. This equilibrium situation explains why 1 gram per week testosterone is more effective than 1/2 gram per week, even though 1/2 gram appears to be more than enough to saturate all the AR's in the body. The higher concentration makes it more likely that the receptors will be occupied by an AAS, and the ARE will be intact for a longer period of time, on average.

Other Actions
Activation of the androgen receptor is a key mechanism in the action of AAS. However, this mechanism by itself does not explain the differences between steroids (i.e., nandrolone activates the AR better than testosterone, but is not as good of a mass-building product). Other actions involve primarily the central nervous system, and involve actions such as motor activation (muscle coordination) and mood (i.e., aggressiveness). The mechanism by which AAS effect these actions is not well understood at this time. Another effect occurs in the liver, where some steroids cause the release of certain Growth Factors. The different actions of the different AAS explains why a stack of two different types of AAS is often better than one by itself.

Elimination of Steroids
The liver is a primary route to deactivation of steroids, the chemical structure is changed here to make the steroid more soluble in water for excretion through the kidneys. A good portion of many steroids also are excreted as-is, without any alteration by the liver, or by formation of the sulphate, which is more water soluble. Many in the medical community have believed that AAS cause liver damage because levels of certain enzymes (AST and ALT) are elevated when steroids are used. Elevated levels of these enzymes are seen in patients with liver damage from other causes, so the conclusion is that AAS must cause liver damage because these enzymes are elevated. Recent work, however, has shown that a true marker of liver damage, GGT, remains unchanged when some AAS are used, and now it is questioned whether AAS are really damaging to the liver (the 17 alpha-alkylated AAS do cause damage in some rare cases, and this damage is reversible upon cessation of steroid use). The same thought processes were used to claim kidney damage, but that is unlikely as well.