Eq and endurance

[Lethal Hamburger]

Yes, eq does increase endurance if you are an athlete training outside of the PCr energy bracket or in simpler terms it does very little for short term energy production as seen in muscle hyperthrophy training.
This is where the lines get crossed with what I have found to be a very useful compound. With low doses of 1.7 to 1.8mg per pound of body weight, you will see some impressive results in running distances supra 3 miles after 5 weeks once the dosage reaches peak plasma concentration.

If you listen to bro science it just doesnt make sense what has been parroted, as the energy system used in weights training is anaerobic meaning it is supplied without the need for O2, so therefor the red blood cell and subsequent oxyhaemoglobin increase seen with boldenone use would not be of usefulness in this training zone.

It certainly will increase rbc. It is a decent anabolic compound, that is frequently dosed excessively instead of being stacked with complimentary coumponds such as Tren, mast, npp and nandrolone decanoate. It exhibits anti estrogenic propensities and will not add to progesterone load.
Rbc inflation becomes apparent with high dosages conjointly with duration. This compounds duration would be best kept under 16 weeks as after the last dosing will have a lingering cer.

I hope this helps.

Yes, it has a slightly higher affinity, yes it converts at 50% the rate of test, but that only actually matters when you put it up against testosterone itself, by replacing test with Boldenone. Adding it to a stack, especially one above any therapeutic levels (though there are no real ‘therapeutic’ levels of Boldenone when you consider that it was never approved for human use in any context) in and of itself, will result in higher e2 levels. By using the metrics you’re outlining here, we could say that Primobolan is even more anti-estrogenic, because it is a 0% substrate.
Bear in mind, I’m not saying you’re wrong, I’m saying it’s irrelevant in any useful context.

Yes and no for the points you make. Thank you fir your time reading through my off the top of my head and struggle for diction spiller et spill.
Speaking three languages can cause issues as you may understand it can become difficult to accurately convey an article of observation.

Most users of aas would indicate the use of testosterone as a base compound in a cycle, for the clear benefits of its metabolites seen from the aromatase and 5 alpha reductase pathways (to name just two) . So therefore when testosterone is dosed along with other non aromatising aas AND boldenone you will see competition for aromatase enzyme by boldenone and the resultant metabolites (of which being biologically inactive), in effect, blocking the binding of biologically active estrogens (derived from testosterone) to the the alpha and beta ER. Estrogenic activity is reduced via this observed physiological mechanism.
I have observed this in monogastric model studies using porcine subjects, investgating fcrs (feed conversation ratios) in conjunction with selected (common to foreign meat industry) aas, with PGh (Porcine growth hormone) and with PGh an insulin.
A key observation made was that the affinity at which boldenone competed for the aromatase enzyme (pCYP19A1) in the catalyzing estrogen synthesis process, was on an individual to individual basis. Genetics being a likely source for this divergence in data trends.