
Originally Posted by
Sgt. Hartman
^^Bro science at its finest. I'm no expert on HCG but it took less than 30 seconds to find this:
Testicular responsiveness to chronic human chorionic gonadotropin administration in hypogonadotropic hypogonadism.
D'Agata R, Vicari E, Aliffi A, Maugeri G, MongioƬ A, Gulizia S.
Abstract
Steroidogenic responsiveness to long term hCG administration (1500 U three times a week for 23 months) was characterized in 8 males with hypogonadotropic hypogonadism (HH). During hCG treatment, testosterone (T), which was in the prepuberal range under basal conditions, rose considerably to the upper end of the normal range and remained at that level during the 23 months of observation. A 2.5-fold increase was observed in serum levels of 17 beta-estradiol (E2) an increment less than seen with T. The increment in 17 alpha-hydroxyprogesterone was also lower than that in T throughout the study; thus, the 17 alpha-hydroxyprogesterone to T ratio, despite continuous hCG administration, remained low. Serum androstenedione was slightly increased during hCG therapy. No significant changes were observed in serum levels of dehydroepiandrosterone. These data indicate that continuous long term hCG administration stimulated T levels in HH, with a relatively small change in E2. The kinetics of the T and E2 responses to 2000 U hCG, evaluated after 23 months of therapy, indicated that the testicular response was markedly reduced. No increment in T levels was observed at 24 h; the maximal response occurred at 48 h. This pattern of T response supports the idea that partial testicular desensitization occurs in HH patients receiving chronic treatment with hCG.
I don't understand why it would be more beneficial to run larger doses at the end of cycle in order to get the desired effect of restarting the testes or shocking them when the same can be achieved with moderate/small doses throughout cycle.