An illustration of a rational approach to an androgen (AAS) course
Author: Type-IIx
The individual is a healthy young man that derives an income from his physique (modeling, acting). His principal objective is recomp (↑FFM & ↓FM) for an upcoming photo shoot.
Considerations:
i. Absolute unwillingness to "blast & cruise," therefore
ii. Maximal maintenance of FFM (particularly, skeletal muscle) after the course has been completed
iii. Inaccessibility to or no availability for hCG & hMG (that serve the task of maintenance of HPG axis functioning [spermatogenesis & steroidogenesis, etc.])
Then,
Planning considerations include:
a. theoretical minimal suppression coupled with maximal anabolism (favorable risk/reward tradeoff with respect to HPG axis functioning) to preserve muscle size increases post-cessation
b. temporal placement (i.e., first) of potent & moderately suppressive androgens that are synergistic in combination (such that we can lower dose & attenuate HPG axis suppressive effects) & subsequent temporal placement (i.e., last) of less suppressive androgens that serve to taper net suppressive effects
c. durations of activity & time-course (pharmacokinetic and pharmacodynamic considerations) of HPG axis suppression (decrement to/withdrawal from LH, etc.) of the individual androgens (e.g., ester chain lengths; biological PK/PD data)
Compound selection is oriented around the overarching objective (recomp) & the task, here, attenuation of HPG axis suppression (to preserve muscle mass after cessation):
The optimal compounds here, then are:
Testosterone Propionate (TP)
Trenbolone Acetate (TBA; Tren)
Drostanolone Propionate (Mast P; Masteron)
Oxandrolone (Anavar)
Practical (Design & Implementation) Considerations:
I. A 6+2 design. The initial 6 weeks will be oriented towards maximal muscle anabolism, seeking to use doses & compounds that are synergistic (greater than additive; 1 + 1 > 2) and potent, with some suppressive effects certainly, but that can be ameliorated by temporal placement (i.e., first) and modest dosing considering durations of activity, PK/PD, clearance/elimination half-life, etc., and a subsequent temporal placement (i.e., last) of less suppressive compounds that serve as a sort of taper in net suppressive effects
Weeks 1 - 6: initial temporal placement (i.e., first) of potent short ester compounds that are synergistic in combination x 6 weeks (i.e., TBA & TP) but suppressive of HPG axis functioning
Weeks 7 - 8: subsequent temporal placement (i.e., last) of milder & less suppressive androgens x 2 weeks (drostanolone propionate & oxandrolone)
- a.m./waking oral ingestion (i.e., Anavar) preferred & with consideration of durations of activity/suppressive effects on LH, etc.
II. Chemistry:
Weeks 1 - 6:
- Testosterone Propionate (TP): androst-4-ene-3-one [e.g., 450 mg weekly, moderate (150 mg T, R, Su)]
- Trenbolone Acetate (Tren; TBA): triene (Δ4,9,11) [e.g., 150 mg weekly, moderate (50 mg T, R, Su)]
Weeks 7 - 8:
- Drostanolone Propionate (Mast P; Masteron): 5α-androstan-3-one [e.g., 150 mg weekly, low (75 mg R, Su)]
- Oxandrolone (Anavar): 5α-androstan-3-one [e.g., 25 mg T - Su, low-moderate (e.g., 150 mg weekly)], a.m./waking ingestion
Assumptions:
1. total exogenous androgen/AAS washout is not necessary to remove the stressors to HPG axis functioning and to exert a permissible effect on restoration of spermatogenesis & steroidogenesis
2. modest concentrations arising from such from doses & metabolism/excretion of short-chained esters (e.g., acetate, propionate), given the illustrative examples, are less than maximally suppressive
3. The reader understands the unique features of these compounds (i.e., TMT) and anti-adipogenic & lipolytic mechanisms, interactions between aromatizable & non-aromatizable androgens, contribution of estrogens/progestagenic androgens to HPG axis suppression, etc.
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