Oh sorry. My fault.
Increased skeletal muscle strength
and/or endurance
and/or hypertrophy
and/or decreased fatty tissue
resulting from any mechanism of the compound's action or inaction.
So right out of the gate we can throw the below list out as largely irrelevant as none pertain to the above.
Endocrine effects:
- suppression of LH/FSH
- suppression of T
- suppression of SHBG
Growth of male sex organs:
- seminal vesicles
- prostate
Masculinizing effects:
- hirsutism (excessive growth of body hair)
- dysphonia (voice deepening, hoarseness)
- clitomegaly (in women)
What remains are what you describe as 'features' of androgenicity:
Anti-adipogenic mechanisms
Neural mechanisms [of] [increased] aggression
To that I'll add
- increased blood volume and/or improved or increased vascularity
- increased oxygen delivery
- increased uptake of proteins, sugars, and any other macro or micronutrients
by and in skeletal muscle tissue or adipose tissue which would be features of what I would describe as directly anabolic in nature.
All that remains then is MY originally badly worded question which put better might be, "Of the 4 compounds I originally mentioned, which is doing the majority or minority of each function respectively?"
Thanks!
These are good questions, and frankly a lot of them are still outstanding (not yet answered) by my research. There is a study I am still seeking:
Molinari PF, Rosenkrantz H. Erythropoietic activity and androgenic implications of 29 testosterone derivatives in orchiectomized rats. J Lab Clin Med. 1971 Sep;78(3):399-410. PMID: 5092861.
Since your question is just broadly aimed at teasing out what we know about the features of these androgens I'll just give you a brain dump on them and try to mention as much about these features as at least I have learned about them.
When it comes to these compounds: EQ, Deca, Tren, Adrol: there's only good human data on 2 of them, Deca and Adrol. The Parenabol study (EQ) in humans is poor for a number of reasons, very low doses, silly outcomes measured, and very sick subjects (many were late-stage amphetamine addicts and alcoholics).
Deca is the most potent compound for skeletal muscle hypertrophy of all. Deca alters dopamine metabolism unlike T, so the psychological effects attributed to it might be at least partly explained by reduced dopamine receptor number and (in humans) increased dopamine metabolism. It is a very potent stimulator of erythropoiesis, likely stronger than Adrol at therapeutic doses and higher.
Adrol is a decent anabolic and very potent strength-increasing steroid. What's interesting about Adrol is that (Schanzer view) it may act predominantly as a prohormone to more active metabolites. C-2 attachment seems highly relevant for altering activity, e.g., with Adrol it seems to yield a potently strength-increasing androgen, likely via neural mechanisms (though frankly the connexion between androgens and neural drive is not well researched). Adrol seems to cause fluid retention and pseudo-aromatization sides, yet is not aromatizable nor 5alpha-reducible, which leaves open the question whether this feature is due primarily to a tendency to increase 17-OHP, a weak progestin (note that Adrol has no direct PR binding)... open questions include its potential for MR agonism or potential activation of RAAS. It IS a relatively potent hematinic agent as well, and used clinically for this feature (it's easy to administer/adhere to because it's orally active and works well).
EQ is a very interesting compound, primarily because so little real data exists on it that is extrapolable to man. Its metabolism causes widely divergent effects that vary substantially between individuals. My own hypothesis about EQ is that its acting for some as an anti-estrogen, for some being principally aromatized to E1 (estrone [a weak estrogen]), largely resistant to (abating rather than abolishing) aromatization is perhaps because of its secondary 17β-hydroxy group plus the C-1,2 double bond (again supporting the importance of C-2 in altering steroid behavior); given interindividual differences in 17β-HSD, I believe this is an isozyme that substantially alters its behavior between individuals. It's not particularly nephrotoxic/kidney toxic in man according to any good science. I can only speculate about its relative erythropoietic activity: it may be more potent than nandrolone at this, or it may not. It may have been primarily marketed to combat and endurance athlete for this feature because demand was low (to stimulate demand). There are anecdotes from both camps, that it is not particularly potent in augmenting HCT/Hb; and that it is particularly potent. Perhaps this is another feature deriving from wide interindividual variation.
Tren, I've already mentioned its unique features in this very thread. As for stimulating erythropoiesis or acting otherwise as a hematinic agent, big unknown. No clue honestly. It is an outstanding insulin sensitizing agent and improves (lowers) HOMA-IR as a proxy for insulin resistance. I've seen evidence in man of its lowering blood glucose concentrations (bloodwork), and evidence in animals of its lowering blood insulin concentrations... this is in addition to the very good evidence that it lowers serum IGF-I concentrations in man and animals alike. As a Δ4,9,11 steroid it slides into the AR like a knife but also has good affinity for PR, ERa/ERb. I believe it boosts strength via neural drive as well as via some GPCR/membrane bound receptor (nongenomic effects), as a potent androgen it acts like an even more potent DHT as we see it in rat/animal models, i.e., where it's not rapidly metabolized but actually relatively resistant to metabolism.
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