What your worried about is atrophy of the leydig cells. Leydig cells produce testosterone in the presence of LH. After doing research I am going to run HCG at low doses during cycle. I think the phrase "use it or lose it" comes to mind. Basically whats happening with steroids is your body does not need to produce testosterone so it tries to save resources by downregulating its testosterone producing capabilities.(= bad
) I don't see why there is any reason not to use physiological doses of HCG during cycle. Desensitisation should not occur if your running physiological doses of HCG.
I cannot find the other study I was looking for but basically it said HCG densensitizies the Leydig cells on an HCG-LH recepetor per cell basis, but because of the hyperplasia, the total number of HCG receptors actually upregulates(just like testosterone, upregulation in the presence of its receptor activator) because of the increase in cells.
Luteinizing hormone on Leydig cell structure and function.
Mendis-Handagama SM.
Department of Animal Science, College of Veterinary Medicine, University of Tennessee 37996, USA.
The effects of luteinizing hormone (LH) and human chorionic gonadotrophic hormone (hCG) on Leydig cell structure and function are reviewed in this paper under two main headings; responses to LH and hCG stimulation and responses to LH deprivation. With acute LH stimulation, up to 2 hours following the LH injection, there was no change in the volume of a Leydig cell. However, Leydig cell peroxisomal volume and intraperoxisomal SCP2 content showed a rapid and transient change. These changes can be considered to be specific because: i) no other Leydig cell organelle including smooth endoplasmic reticulum (SER) showed such a change, and ii) only the intraperoxisomal SCP2 but not catalase (a marker enzyme for peroxisomes) showed such a change within 30 minutes of LH stimulation. As these changes occurred prior to the peak testosterone levels following this treatment, it is suggested that SCP2 and peroxisomes may have an association with testosterone biosynthesis prior to cholesterol transport into mitochondria. With LH or hCG stimulation for longer periods, i.e. one day or more, the same morphological changes are produced in Leydig cells irrespective of the age of the species, dosage of LH or hCG, and with single or multiple doses. These changes include, Leydig cells hypertrophy and/or hyperplasia, increase in the cellular organelle content (mostly SER and mitochondria) and depletion of lipid droplets. In addition, a recent study showed that Leydig cell peroxisomal volume, SCP2 content, the amount of intraperoxisomal SCP2 and testosterone secretory capacity were also significantly increased in response to chronic LH treatment. The effects of LH deprivation by whatever means (e.g. hypophysectomy, with testosterone and 17 beta-estradiol silastic implants, LH antisera) on Leydig cell structure and function is generally described as opposite to those observed following LH or hCG stimulation. These include Leydig cell hypotrophy and hypoplasia, reductions in the cytoplasmic organelle content in general and specific reductions in SER and peroxisomal volumes, reductions in total catalase and SCP2 in Leydig cells together with reductions in the intraperoxisomal SCP2 content in Leydig cells and their testosterone secretory capacity.
Morphological and functional responses of rat Leydig cells to a prolonged treatment with human chorionic gonadotropins.
Andreis PG, Cavallini L, Malendowicz LK, Belloni AS, Rebuffat P, Mazzocchi G, Nussdorfer GG.
Department of Anatomy, University of Padua, Italy.
The morphological and functional responses of rat Leydig cells to a 3- and 6-day treatment with human chorionic gonadotropins (hCG) (10 IU/kg/day) were investigated by morphometric and radioimmunological techniques. hCG-administration induced a notable time-dependent enhancement in the steroidogenic capacity and growth of Leydig cells; this last was almost exclusively due to hypertrophy (and not to hyperplasia). The volume of mitochondrial and peroxisome compartments, as well as the surface area per cell of mitochondrial cristae and smooth endoplasmic reticulum (SER) were significantly increased after hCG treatment, and showed a highly significant positive linear correlation with both basal and stimulated testosterone production by isolated Leydig cells of the contralateral testis. Also the volume of nuclei and lipid-droplet compartment and the surface area per cell of Golgi apparatus displayed a notable hCG-induced rise, but they did not correlate with testosterone secretion. These findings suggest that, in addition to mitochondria and SER, in which the enzymes of steroid synthesis are located, peroxisomes are also specifically involved in the secretory activity of rat Leydig cells.
Leydig cell hypertrophy and hyperplasia in adult rats treated with an excess of human chorionic gonadotrophin (hCG).
Lamano-Carvalho TL, Favaretto AL, Silva AA, Antunes-Rodrigues J.
A morphometric study was undertaken to determine to what extent the increase in LEYDIG cell activity is related to an increase in their number and/or size. An attempt was also made to consider the morphological characteristics of the cells in terms of their probable functional capacity. Following 8 h to 3 d of excess hCG treatment, LEYDIG cells nuclear volume exhibited an increase of 16 to 18% while no significant increase in cells number was observed. By 7 d of hCG treatment, the nuclear hypertrophy (42%) coexisted with hyperplasia (33%). After 14 d of stimulation, a 41% augment in cells number and 31% increase in nuclear volumes were found. Such morphometric parameters were correlated with plasma levels of testosterone. The results suggest that hypertrophy plays a more important role in the enhancement of LEYDIG cells secretory activity in the initial phase of hCG stimulation. A subsequent hyperplasia seems to become relatively more important in longer periods of treatment. Our findings support the statement that both hCG dose and time of treatment, and consequently the plasma level of testosterone, are important parameters to be considered when the functional activity of LEYDIG cells is been evaluated by morphometric techniques.
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