Maje the time if it’s important to you. That’s the number one “reason “ people tell themselves. “ I dont have time”. I know I’ve used it to myself many times until I realized I was lying to myself. Get up an hour earlier. You won’t be interrupted and you will have time.I am 29 and wanna get huge hard and lean.
So i also havd to do roids why training until "reaching some limit".?
That sounds like a fucking waste of time.
So i have to train like for 5 years then im ready?.
I bet in 5 years I dont have time to train because then im busy with other stuff.
It is a VERY accomplished design. That a team of Turkish medicinal chemists came up with something almost identical suggests that it's just about the most potent steroid known.
...led me to the theory that there is no such thing as anabolic hormones, only anticatabolic ones, and the "anabolic" effects from T and anabolic steroids are actually the result of their antagonism to cortisol (and potentially estrogen).
An old study I found makes the same claim, and highlights the well-known fact that muscle contains almost exclusively glucocorticoid receptors (GR), while androgen receptors (AR) are mostly expressed in tissues like prostate, gonads, brain and skin. Thus, if a steroid is found to have an "anabolic" effect in muscle that is due almost exclusively to antagonism of GR.
Steroids with strong androgenic effects would also have anabolic effects but those would be secondary to GR antagonism and reserved mostly for tissues with high expression of AR - i.e. prostate, gonads, sex organs, brain, etc.
Although the anabolic activity of androgenic steroids has been recognized for a long time, the way in which these steroids act in muscle is ill-understood. It is also known that glucocorticoids exert a catabolic and anti-anabolic effect on protein metabolism in skeletal muscle. Androgen and glucocorticoid receptors have been demonstrated in this tissue. Since several steroids, including androgens, behave as glucocorticoid antagonists when binding to the glucocorticoid receptor in other tissues such steroids could antagonise the catabolic action of endogenous glucocorticoids by preventing binding of the latter to their cytosolic receptors in muscle. Thus, muscle anabolism could result either from agonist steroid binding to the androgen receptor, or from antagonist binding to the glucocorticoid receptor, or both.
Interestingly, the potent anabolic steroid trenbolone bound to the glucocorticoid receptor with an affinity almost as high as that of corticosterone, the endogenous glucocorticoid in the rat
Indeed, antiglucocorticoid activity is expected to counteract protein catabolism, while androgenic activity would stimulate anabolism."
The latter possibility is supported by the observation that the anabolic action of androgens results from inhibition of protein catabolism rather than from stimulation of anabolism. Indeed, antiglucocorticoid activity is expected to counteract protein catabolism, while androgenic activity would stimulate anabolism.
Thus, if one would like to combine the best of both worlds, one would need a steroid which is a strong antagonist at GR and a strong agonist at AR. This present a possible issue as the binding requirements for both receptors differ. Strong GR antagonists are usually pregnane derivatives, which also have at least one unsaturated (double) bond in the A-ring of the steroid core. Such steroids do not have great affinity for the AR.
On the other hand, strong AR agonists are usually fully saturated androstane steroids like DHT, and androsterone as well as synthetic derivatives like mesterolone and oxandrolone (among many others). However, fully reduced androstane steroids do not bind well to the GR even though they are antagonist to it. Thus, DHT is expected to be a relatively weak anabolic steroid in muscle and highly anabolic in AR-rich tissues, which has been confirmed in practice countless times.
...
As can be immediately seen, progesterone is one of the most potent antagonists of GR as it satisfies all the requirements. Known "anabolic" steroids like testosterone and other AAS are also GR antagonists, but as the study above noted, relatively weak ones
Estrogens are generated mainly by the action of aromatase (enzyme), which converts testosterone to estradiol
