From the intro of the reference that @highpull provided:
Testosterone is produced by Leydig cells in the interstitial space of the testis. As a result of the local production, testosterone levels in the testis in men are 25 to 125-fold greater in the testis (340 to 2,000 nM) as compared to serum (8.7–35 nM). Testosterone levels are similarly elevated in rodent testes.6–10 Thus far, the specific physiologic requirements for high levels of testosterone in the testis are not known. However, it has been established that spermatogenesis does not proceed in the absence of relatively high levels of testosterone (>70 nM in the rat).11
Using “high level” of exogenous T as a means to reach the Sertoli cells would not be a very efficient method and also doesn’t address the intra-testicular ratio of estradiol to testosterone which is also quite critical. You are cutting off LH/FSH and then through diffusion from serum to testis trying to overcome this with exogenous T (1 step forward and 10 steps backward). This is more of a hand-waving approach to justify stepping back on the gas pedal :-).
More info can be found here:
Stick with hCG/hMG or a SERM (if needed) if concerned with fertility.
Here’s the reason PED-using bodybuilders father children without fertility drugs:
Testosterone/AAS induced infertility is time dependent, dose dependent and absolutely positively not foolproof. It’s also largely reversible dependent on the individual and duration of use.
