Dude, this is a terrific idea… But let’s turn it up a notch and add in some beta-2 agonists. Beta adrenergic receptors desensitise fairly quickly, add in something that can slightly offset this.
Perhaps, we don’t have enough literature to go on relating to potential pain-blunting mechanisms. Furthermore, the majority of the data we have at had pertains to rodent models. Rats have different metabolic/elimination pathways/enzymes and as a result results garnered within rodent models can differ when the same stimulus/exposure is give to a human.
I can link some data relating to the impact of nandrolone on healing rates regarding tendon rupture/injury. I don’t spend all that much time on the Pharma section nowadays. Talking about anabolic steroids online just seems like a bad idea.
Not really, the concept of HED is important. A human equivalent dose for 8mg/kg for a 100kg male would be around 130mg/wk. Interestingly testosterone dosages of around 5mg/kg induce cardiac pathology within rodent models.
There’s an in-vitro study of which indicates nandrolone is likely more destructive when regarding vascular health. The study design is rather poor, but it grants further evidence to state nandrolone should probably be left out if longevity is at hand. The researchers expose endothelial cells (in vitro) to nandrolone, nandrolone metabolites, testosterone etc. Androgen concentrations were increased until 50% of the cells present had undergone apoptosis. Nandrolone did so at a concentration 11x lower than testosterone (the concentration was still massive as the effect had to be garnered within an acute timeframe)
15*100 (lets say you’re 100kg) * 7
/6.2 = 1693.5
My left ventricle would explode…
All AAS seem to have an effect regarding catecholamine up-regulation. Some are more sensitive to the autonomic destabilisation induced via AAS, hence arrhythmias, resting tachycardia/increased pulse rate etc. Nandrolone/19-nors and testosterone appear to be particularly potent, haven’t seen much data on other synthetics.