I've never heard of this, can you give me a source so I can read about it. Thanks.
It's a fairly complex topic, but normal function of the seminiferous tubule is dependent on the pituitary gland and on the adjacent Leydig cells, with both FSH (follicle stimulating hormone) and androgens being necessary for initiating and maintaining normal sperm production. The major site of FSH action is the Sertoli (sperm-producing) cell in the seminiferous tubules. These tubules also contain androgen receptors. Androgen is indeed essential for the initial phases of sperm production, whereas FSH is required for the terminal (end) stages of spermatid development.
The Sertoli cell can not synthesize steroid hormones de novo and is dependent on testosterone that diffuses in from the adjacent Leydig (testosterone-producing) cells. Sertoli cells then convert testosterone to estradiol and dihydrotestosterone. The tubules also produce "inhibin," a polypeptide hormone that regulates FSH secretion by the hypothalamic-pituitary axis. Inhibin is the primary physiologic regulator of FSH, but testosterone (and estradiol) also can inhibit FSH secretion.
This is a very sensitive and precise dual-control mechanism by which both the Leydig cells and the spermatogenic tubules produce factors that feed back upon the hypothalamic-pituitary-testicular axis (HPTA) to regulate their own function. This feed back loop is disrupted when exogenous androgens are introduced into the system.
High levels of intratesticular testosterone, secreted by the leydig cells,
are necessary for spermatogenesis. Intratesticular testosterone is mainly bound to androgen binding protein and secreted into the seminiferous tubules. Inside the sertoli cells, testosterone is selectively bound to the androgen receptor and activation of the receptor will result in initiation and maintenance of the spermatogenic process and inhibition of germ cell apoptosis. The androgen receptor is found in all male reproductive organs and can be stimulated by either testosterone or its more potential metabolite dihydrotestosterone. However, the
exogenous administration of testosterone and its metabolite estrogen will suppress both GnRH production by the hypothalamus and LH production by the pituitary gland and subsequently
suppress testicular testosterone production. High levels of testosterone are needed inside the testis and this can
never be accomplished by oral or parenteral administration of androgens. Through its effects on the HPTA, AAS-induced suppression of testosterone production by the leydig cells will result in a deficient spermatogenesis, and lead to an irreversible death of testicular cells.
Why utilize hcg, then? It acts as an LH analog. Also available is the use of a LH-releasing hormone (LHRH). It is used by some physicians for chronic therapy of infertility due to hypogonadotrophic hypogonadism. The problem, though, is that it is necessary in frequent boluses (25 to 200 ng/kg of body weight every 2 hours), requiring either an infusion pump or nasal application to make it practical to use. In the clinical setting, however, it does not appear to be more efficacious than gonadotropin in returning sperm counts to normal, so stick with hcg.
