That’s an interesting question.
Lets look at enzyme kinetics first.
That’s the Michaelis Menten kinetic which applies to many enzymes including the aromatase. You can see there’s an upper limit which is the maximum capacity the enzyme molecules have to produce the product of the reaction. It’s measured in product molecules per time unit which is Vmax. Then there’s the x-axis which shows [S] which is the substrate concentration and is measured in molecules per volume. So you can see: the higher the substrate concentration the higher the velocity until the enzyme capacity is reached (Vmax).
This answers one point of your question: With higher testosterone (the substrate) there will be a higher conversion rate to estrogen (v comes closer to VMax) and estrogen rises.
One important point to remember for later: Vmax depends on how many enzymes you have,more enzymes means higher Vmax. If you got more enzymes then more substrate can be bound and can react simultaneously.
Now it gets more complicated. Km is the Michaelis Menten constant which is a constant value for a specific enzyme, it’s defined as the substrate concentration at which the enzyme velocity is at half Vmax. So the enzyme is at half the speed it could go. You can see if Km is higher then the enzyme is less efficient (the binding of the substrate is loose) because you need more substrate to get to half the maximal speed. If Km is lower the enzyme is more efficient which means the enzyme is faster relative to its maximum capacity. This is important to know because inhibitors get described through their action on Km.
Now let’s look at the inhibitors:
First there’s competitive and noncompetitive AIs.
Noncompetitive inhibitors bind the enzyme irreversibly (not necessarily always but in this case, sometimes they just bind to another part of the enzyme), this means the enzyme is dead (suicide inhibitors). In our example this is exemestane. Exemestane’s effect on the kinetics is a reduction in the number of enzymes since bound enzymes are not active anymore and can’t be reactivated. This means exemestane lowers Vmax but Km stays the same, so the curve’s upper limit decreases. Hereby in our example E2 gets lowered by lowering the conversion rate through lowering the number of the enzymes.
Competitive inhibitors like letrozol/anastrozole compete with the substrate at the active center of the enzyme and are often more efficient at binding to the enzyme which leads to the ousting of the substrate testosterone. The enzyme stays active though. Now if you increase the concentration of testosterone, it can displace the inhibitor again since more molecules T compete with the AI. From a kinetics standpoint this results in no effect on the number of enzymes (Vmax stays the same) but in a need for a higher concentration of T ([S]) to reach the same conversion rate (v). In other words: the concentration needed for reaching half maximal speed is higher (= Km increases)
or put simply, the concentration needed to get the same amount of E2 increases. So competitive AIs decrease E2 by decreasing the binding efficiency to the set number of enzymes.
This is illustrated here:
To answer your question now:
If you are using a constant dose of a competitive inhibitor like anastrozol (slower curve in the picture) and you are giving the enzyme more substrate (test) then you are going closer to vmax which means there will be more estrogen in the same time span. This is good! Since you want to increase E2 proportionally which should roughly happen since you are still on the same curve with the AI (curve is partially nearly linear). It could be a bit off because the rate increase is not really linear which means you could need a tiny bit more or less AI. The probability for a competitive AI to be in the linear part of the curve is higher.
If you are taking Exemestane the game changes since you lowered the upper limit which means if you tripple your T dose and that should triple your plasma levels (it won’t triple it but for the sake of the argument we round up), this nearly always puts you at a 100% capacity (except if you had a very low starting point). Which kills the practical near linearity of the curve. So in my opinion you could need less Exemestane on cycle to feel optimal.
Disclaimer: This is a purely theoretical perspective. 1. It’s not clear if the relationship between E2 and T should be proportional to feel optimal.
2. It’s not clear where you fall on the curve completely depends on your body and could change the outlaid scenario completely (for example if you have so much aromatase that you are under 30% capacity on TRT)
3. The kinetics of E2 or other estrogens play a role here. Since the elimination is of equal importance to the plasma level.
4. It left out the upward adjustment of the T levels during the first weeks and I went straight from what happens at steady state.
To feel and perform optimally you need to experiment and let your body adjust to the changes and that’s what could make all of this here irrelevant. Cause if you are not long enough on to dial all variables in, there’s no need to overthink this.
If I was you I’d keep the AI dose the same until you reached steady state with your blast then when you’re there, see how you feel and get bloods. Then adjust a slight bit up or down. My guess is you won’t have to adjust the AI dose severely in one direction so be careful (except for you being an outlier).
Good night fellas