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Is eq good for endurance just because it increases hemoblobin and only for that reason?
or are there other things that make eq good for endurance? more than other steroids.?
The reason I ask is because I already have quite high hemoblobin 16.5 and hemocrit 53. I want better strength and endurance, but if it only increases the hemoglobin it is not good and must then avoid it.
EQ is a terrible steroid in general which supposedly helps increase endurance by raising RBC but it’s simply not worthwhile and personally I never experienced an increase in endurance but rather a decrease and feeling like crap. Worst steroid of all I have tried and I’ve tried a lot.
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.
Could we stop parroting this now? One of its downstream metabolites exhibits an EXTREMELY low anti-aromatase potentiation, but it is so low as to be a complete non-factor. What most guys see is a reduced E2 value in comparison to test, herpa derp on the fact that it’s a 50% substrate, and assume it has an anti-estrogenic property. Just no. You will never take a preexisting stack, add boldenone to it, and see a lower E2 value as a result (it will go up), so the metabolite isn’t even enough to notably offset the 50% aspect, so not even worth considering.Quote:
Originally Posted by Lethal Hamburger
This could be the case if only looking at the singular metabolite hypothesis.Quote:
Originally Posted by Gallowmere
However.. Note the term i used was "anti estrogenic propensities" and not "aromatase inhibition properties".
Alluding to the point that it would appear that boldenone infact acts like aromatase antagonist via binding affinity over that of testosterone. The resultant cascade of synthetic metabolites as a product of aromatisation of boldenone, exhibit an interaction with estrogen alpha and beta receptors that would appear to make them biologically inactive.
I tend not to "parrot" anything that I have witnessed first hand in veterinary clinical trials and now with the mountainous pile of anecdotal evidence observed in humans, indicating boldenones ability to compete with aromatising compounds for the aromatising enzyme, thus lowering e2. (Edit, removed "since" as was part of a draft sentence). Boldenone does infact aromatise at half the rate of testosterone.
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. Or if we want to compare like to like, you could say that Dianabol is just as anti-estrogenic, as it’s a roughly 35-50% substrate. Though obviously that doesn’t play out well, when you consider the methylestradiol aspect.Quote:
Originally Posted by Lethal Hamburger
Bear in mind, I’m not saying you’re wrong, I’m saying it’s irrelevant in any useful context.
Quote:
Originally Posted by Lethal Hamburger
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.Quote:
Originally Posted by Gallowmere
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.
Absolutely. I think what we had was just a misunderstanding based upon the usage of the phrase “anti-estrogenic”. My concern is more a practical one that a technical one.Quote:
Originally Posted by Lethal Hamburger
Random example: guy is taking 600mg/week of test, starts growing titties. Guy has read that Boldenone is anti-estrogenic, and figures if he adds it onto his existing dosage, the estrogen should start to come under control.
We both know that’s not going to happen, but someone reading “X AAS is anti-estrogenic” can lead to these leaps. A better way of putting is just as what we put across: it aromatizes at a roughly 50% rate, so replace a certain amount of testosterone with it, NOT add to, and things will start to improve. The only AAS that could be directly added at that point that wouldn’t make the problem worse, are the various DHTs (other than Anadrol, because that weird beast does some strange activations on its own) and possibly Trenbolone, assuming that the problem is truly estrogenic in nature.
I’m talking from my own experience, I do tons of cardio. EQ didn’t ever help me but that may be due to the fact my cardio endurance was already very high. Many anabolic steroids increase rbc and are less dangerous. I tried being open minded but I’m never using EQ again even though I have some. It’s crap period.
As most top athletes find, their training will plateau around the same time as drug use. They ur one and the same thing.Quote:
Originally Posted by redz
I have seen excessive use of eq and limited use of eq as part of a well arranged cycle. Eq should not be mistook for a compound used as the main anabolic/ driving force of a cycle. There are better drugs for this purpose.
Eq isn't for everyone, I agree with you there.
As for eq's agonism of EpoR, and it's effect on rbcs? Well that is dose and duration dependant yes? It does have it's use for this reason but must be utilised as one part of the complete package.
I see it simply run too high all too often by those who don't fully understand its utility. Some do understand but its like tren, just not for them.
It will slaughter estradiol when run too high period.