Here’s what I know. One group of enzymes - 17β-HSD. Many isotypes affecting estrogens and androgens: HSD17B1, B2, B4, B6, B7 and so on. Some of them are widely distributed (general expression: liver, brain, heart, adipose tissue, etc.), some are located in specific tissues and abundant (so they act only specifically for a tissue, like for retina). It’s very hard to predict the exact effect of it’s group final activity (conversion to one compound or another), because of massive isoform distinction within a group and their unpredictable distribution.
That’s what they do: estrone <-> estradiol (a reversible redox reaction depended on NADPH/NAD+).
That’s the answer for a question - “and what about endogenous estradiol reservoir?”. I mean, the reaction above, partly. A given isoform density and activity decides in which direction it runs. An excess of one of the two reagents will be metabolised in matter of hours, at most, and this is not the only reaction affecting those reagents, obviously (most importantly the excess must be removed from the body, mainly with urine).
What I mean… It’s so complicated that I can’t tell you WHY EXACTLY AND WHEN something happens with those two and no one will tell you for sure.
What’s also known for sure is, Le Chatelier’s principle affects your body constantly. You give a woman an oral E2 - her estrone levels increases in matter of minutes. After E2 is removed - her estrone level decreases proportionately fast and is back on it’s level. The equilibrium of the reaction depends on the substrate concentration, so the effect - the issue of an enzyme activity is a secondary matter here in short-term. Yes, the same about your E2 peak and related side effects from supraphysiological TEST level. That’s a reaction of aromatization, same principle - more substrate, more product, equilibrium maintained.
There’s the thing. An AI helps you to inhibit the reaction of aromatization if you need it, so less product is made and more substrate in your blood. You can’t inhibit your 17β-HSD, because you have no drug to do that. More E2 leads to more estrone, and vice versa, that’s it. Nothing about magical customization of your tissues to move an excess of estradiol to estrone in SHORT-TERM. The magic happens in LONG-TERM (matter of weeks, at least) - your body restructures it’s enzyme machinery and do it’s best to let your hormones be in correct proportions. What’s worse - the fact comes from anecdotal evidence, mainly.
That’s why using an AI is an option and works great AD HOC. You cycle often - you definitely want an AI to react as fast as possible and enjoy the benefits of AAS.
Not using an AI would work great too, but much later - so long, that you will be depressed (and how long exactly - nobody knows!), but not necessarily. Good for TRT (not for everybody), definitely bad for frequent AAS rotation.