Rhaponticum Carthamoides and ecdysterones in general have been incorrectly positioned as steroid alternatives. While several attributes have been found to be similar (glycogen storage, protein synthesis, etc) its mechanism of action is completely different and requires a catalyst in order to obtain the desired effects.
Anabolic steroids work by increasing the entire protein turnover cycle. They do this via steroid receptor binding and DNA transcription, a message to the cell nucleus to “turn on” your cellular protein machinery. That is, they accelerate both protein breakdown and protein synthesis, obviously in favor of the latter.
It’s something rarely discussed or pointed out, but very significant.
Further, it is well established that steroids do not work well (or certainly as well) in a caloric deficit. Why? Less insulin. In a caloric deficit less insulin is generated by reduced food intake. Insulin slows protein breakdown. With less of it being generated, you end up with less net muscle gained. The point is, anabolics will artificially accelerate both protein breakdown and synthesis, with gains being largely amplified by insulin.
By contrast, a catabolic environment is necessary for adaptogens to excel, subsequently accelerating assembly of new muscle proteins via increased ribosomal translation. Yet gains are hampered in this state by the fact less insulin is present to slow muscle breakdown. Amino acid pools normally used for growth are diverted to support energy needs due to insufficient calories from other sources (carbs/fats). The athlete then runs adaptogens in a calorie maintenance or surplus state, skipping the critical step of introducing the biological stressors needed for valid adaptogens to exert their full effect.
So what’s the solution?
I believe being in a caloric surplus is a mistake when preparing your body for the use of adaptogens. Rather, a caloric deficit should be used to create protein breakdown and thus, the catalyst needed to activate the protein turnover cycle.