Type-IIx
Well-known Member
Yes bro, it's a common misconception. Predictive modeling of chemical design to target some desired biological effect is something that we cannot yet do with accuracy (loads of false positives), and was certainly not even fathomable in the 1960s & 70s. Really, the research from that era is just a testament to the process of old-fashioned tinkering and post hoc explanations of chemical modifications to testosterone. The explanations were prescient and remarkable in their accuracy. Vida's 3-dimensional model of steroid binding and structure-activity relationship was shockingly accurate, as we have since modeled and visualized as crystalline structures common AR-ligand interactions with modern sophisticated equipment and techniques, and they are just as he drew freehand 50-odd years ago.Good to know lol
Decreased estrogen activity in synovial cells due to reduced estrogen uptake (tissue-/cell- level antiestrogenic effects).I’m not sure what “dries out your joints” really means? I hear people using the phrase but what is the actual mechanism?
Estrogens are antinociceptive & are naturally increased for childbirth in women. Decreased aromatase activity in synovial cells is associated with reduced IL-6 expression in the joint, which acts as both a pro- and anti- inflammatory cytokine & as a mediator of bone loss. Further, estrogen might indirectly augment IGF-I activity & thereby increase collagen content of tendon.
Winstrol raises another mechanism for joint pain:My understanding is that Winstrol enhances collagen synthesis but at the expense of connective tissue laxity; tendons become more brittle and prone to injury due to upregulated cross-linking. I’m sure I’ve seen a paper on this but a 10 minute search right now didn’t bring up what I was looking for. Maybe someone can chime in.
enhanced hepatic C1-INH production, via direct hepatic action rather than AR action per se ⇒ ↑C1-INH & C4.
C1/C1-INH complexes are formed when C1-INH combines with and removes C1r & C1s from activated C1, and these complexes - representative of classical complement pathway activation - are associated with arthritic & rheumatological conditions.
Anyway, what you reported were increased soft tissue injuries. These could be a result simply of increased load or strain (your training intensity) because of increased strength by AAS without sufficient adaptations in soft tissues. While AAS generally do increase collagenous activity and probably net deposition, certainly in the extracellular matrix; and the tendons (bone-muscle attachment]) & ligament (bone-bone attachment), this tends to increase tendon stiffness at the muscle-tendon junction.
Repetition efforts (i.e., performing sets of exercises for > 5 repetitions) decreases tendon stiffness at the muscle-tendon junction, reducing the likelihood of catastrophic strain-induced injury.