Dopaminergic properties of masteron probably induce the libido positive effect noted from the compound. DHT metabolites furthermore elict positive effects in relation to neurotransmission (many DHT metabolites act as neurosteroids)
1G test is a loooooot, for some this is past the point of diminishing returns in which more doesn’t equate to better but merely induces more side effects. Give it time before you mess with other variables, otherwise you won’t know what induces dysfunction and what exerts a positive effect… unless you wish to lower the dosages, then I’m all for it
you’re aware of the potential cardiovascular, neurological effects etc right? No judgement, I use gear too, it’s just important that we as a community remain educated in relation to the risks involved (and the mechanisms behind these risks so we can perhaps mitigate them)
What’s you’re resting heart rate on these dosages? I find supra dosages elevate my resting heart rate from 45-49 to 60-70. Increased catecholamine uptake and sensitivity to catecholamine release will exert pro-arrythmiac effects, combine this with other substances that further sensitise this reaction and it can be far more detrimental in nature. Combine AAS and alcohol (or even AAS sometimes in itself) and you may notice (if you’re highly in tune with you’re body) premature ectopic beats during exercise or at rest, while most people (40-75% of the populace) have these regardless during the day, the increased sensitivity to catecholamines may induce more to occur. Furthermore pro arrhythmic effects can predispose one to potentially lethal arrhythmia if the right conditions are presented (VF, A-FIB etc)
The potential for adverse cardiac adaptations furthermore exists, though the relationship between AAS and development of dangerous/adverse structural changes in the myocardium is hotly debated. Whether the dysfunction is subclinical, serious or whether it happens at all over time depends on a myriad of factors (genetic, lifestyle, dose, duration etc). Animal models give us somewhat of a picture given rodents have a four chambered heart similar to humans, however various differences in relation to cardiac morphology, antioxidant, elimination profiles etc exist within rodents making such models highly flawed. In-vitro eliminates environmental and intervening variables (antioxidants etc), thus at this moment we simply don’t have quite enough science for me to come to a conclusion rather than say the string of deaths in the bodybuilding community is concerning (though genetic factors, and the fact many are dropping the day before/the day after a show hints at potentially other variables in conjunction with AAS being at play such as lethal dieuretic induced electrolyte imbalance)
That being said, using AAS with genetics harboured for severe onset early CVD, congenital cardiomyopathy (saying you have this), cardiac defects will DRASTICALLY heighten death risk. Getting cardiac screening prior to use is pivotal, if you can continually have screening done (not practical for most given the stigma) it’d be optimal. I know for a fact my heart is/was healthy and free of any defect. Autonomic dysfunction however is a variable I have to live with which makes me very cautious about my dosages, that and fear for risk.
