Hard to know. The two together could indeed be a bit much.
Have you ever used Arimistane before? 75mg looks like the daily dose in AlphaMax. I have seen some sensitive to it notice joint aches above 50mg but others run as high as 175mg. As for exotherm I don't think you'll notice too much joint pain associated with exotherm alone, but on top of 75mg arim it may aggravate joints.
I'm almost thinking it would be better to run AlphaMax + DermaStr3ngth as a cycle, then run exotherm at the end to dry up a bit more and burn off that last bit of fat.
Default Aromatase Inhibitors & Joint Pain
Some people always report joint pain when using Arimidex/Letro/Aromasin.
Common belief: AI's make your joints too "dry" because E2 is overly low.
Too many people perpetuating this urban bro legend without any E2 data to support it. Often E2 is just fine.
Well, you should find this interesting:
Steroidal and non-steroidal third-generation aromatase inhibitors induce pain-like symptoms via TRPA1.
Fusi C1, Materazzi S1, Benemei S1, Coppi E1, Trevisan G2, Marone IM1, Minocci D1, De Logu F1, Tuccinardi T3, Di Tommaso MR4, Susini T4, Moneti G5, Pieraccini G5, Geppetti P1, Nassini R1.
Author information
Abstract
Use of aromatase inhibitors (AIs), exemestane, letrozole and anastrozole, for breast cancer therapy is associated with severe pain symptoms, the underlying mechanism of which is unknown. The electrophilic nature of AIs suggests that they may target the transient receptor potential ankyrin 1 (TRPA1) channel, a major pathway in pain transmission and neurogenic inflammation. AIs evoke TRPA1-mediated calcium response and current in rodent nociceptors and human cells expressing the recombinant channel. In mice, AIs produce acute nociception, which is exaggerated by pre-exposure to proalgesic stimuli, and, by releasing sensory neuropeptides, neurogenic inflammation in peripheral tissues. AIs also evoke mechanical allodynia and decreased grip strength, which do not undergo desensitization on prolonged AI administration. These effects are markedly attenuated by TRPA1 pharmacological blockade or in TRPA1-deficient mice. TRPA1 is a major mediator of the proalgesic actions of AIs, thus suggesting TRPA1 antagonists for the treatment of pain symptoms associated with AI use.