On test when do they start to shrink?
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On test when do they start to shrink?
When the body starts to realise your pumping more in than its making!
I am at week 11 of Test Cyp cycle and my nuts have not shrank. I am running 600mg a week shot 300mg x2
im on week 7 on test ent 500mg/week... still got my nuts
i thought i had low dosed juice... what do u think it is?Quote:
Originally Posted by RANE2001
nuts do not always shrink different for everyone
some people nuts dont shrink as much to were you would notice..... others they disappear.. your stuff could be weak and underdosed too.... or it was so gradual that they are and you dont notice
Nothing like the whole "kick in the testes" feeling to tell you your nuts are shrinking.
I was at a bar a couple weeks ago and out of no where I got this aching pain in my nuts like someone hit it with a baseball bat, and the funny thing is I at the end of my cycle, so I assumed my testes were bouncing back and not shut dowing.
Some do atrophy, others dont. I'm one of the lucky ones.
HCG and Naltrexone will prevent good ol' shrinkage.
Testicular atrophy is not a sign of HPTA shutdown.
Intresting, can't it be a factor though? Because if the testicules are shutting down it means the body is trying to achieve homeostatsis which could me the HPTA is being hindered.Quote:
Originally Posted by Swifto
test cyp right now i shrank up around 5 weeks
It meerly means ITT (Intra-Testicular testosterone) has been shutdown. As thats a primary hormone that regulates size.Quote:
Originally Posted by Immortal Soldier
1: Endocrinology. 1992 Dec;131(6):2839-45.
Links
Leydig cell peroxisomes and sterol carrier protein-2 in luteinizing hormone-deprived rats.Mendis-Handagama SM, Watkins PA, Gelber SJ, Scallen TJ.
Department of Population Dynamics, Johns Hopkins School of Hygiene and Public Health, Kennedy Institute, Baltimore, Maryland 21205.
We investigated the effects of 8 days of LH withdrawal on rat Leydig cell peroxisomal volume, total and intraperoxisomal catalase and sterol carrier protein-2 (SCP2) contents, and LH-stimulated testosterone secretion in vitro. Three groups of adult male Sprague-Dawley rats, i.e. control, TE-implanted (testosterone-17 beta-estradiol-filled Silastic implants to suppress LH), and TELH-implanted (TE-implanted and LH replacement via Alzet mini osmotic pumps), were used. After 8 days, Leydig cell organelle volumes (stereology), intraperoxisomal catalase and SCP2 contents (immunocytochemistry), LH-stimulated testosterone secretion by isolated Leydig cells in vitro (determined by RIA), and total catalase and SCP2 contents in equal numbers of Leydig cells (immunoblot analyses) were determined. Results showed that the TELH-implanted rats were identical to controls in every parameter tested. Testis volume and Leydig cell number per testis in control and TE-implanted rats were not significantly different; however, reductions (P < 0.05) were observed in the average volume of a Leydig cell (one third of controls) and the volume of Leydig cells per testis. All Leydig cell organelle volumes tested were significantly lower in TE-implanted rats than in the controls; however, the volumes of smooth endoplasmic reticulum (SER) and peroxisomes were the most reduced (lowered to one sixth of control values). LH-stimulated testosterone secretion per Leydig cell in vitro correlated well with these changes in the volumes of Leydig cell SER and peroxisomes. Intraperoxisomal catalase in Leydig cells was unchanged in TE-implanted rats, although immunoblotting demonstrated a loss of total catalase content (which reflected the reduction in the volume of peroxisomes). SCP2 in Leydig cells of TE-implanted rats was undetectable with immunoblot analysis (explained by the reductions in Leydig cell peroxisome volume and intraperoxisomal SCP2). These results demonstrate that the organelles SER and peroxisomes and the protein SCP2 in Leydig cells are more LH dependent than the other organelles (e.g. mitochondria, lysosomes) and protein catalase, respectively. Moreover, the findings of this study are consistent with the hypothesis that Leydig cell peroxisomes play a significant role in testosterone production.
PMID: 1446622 [PubMed - indexed for MEDLINE]
You can maintain ITT when "shutdown" from anabolic steroids, this should (never seen a case where it hasnt) maintain testicluar size and funtion. This is why HCG is essential IMHO when cycling. It doesnt just maintain size and ITT, it also maintains the leydig cells to remain responsive and continueing to produce endogenous testosterone.
1: J Clin Endocrinol Metab. 2005 May;90(5):2595-602. Epub 2005 Feb 15.
Links
Low-dose human chorionic gonadotropin maintains intratesticular testosterone in normal men with testosterone-induced gonadotropin suppression.
Coviello AD, Matsumoto AM, Bremner WJ, Herbst KL, Amory JK, Anawalt BD, Sutton PR, Wright WW, Brown TR, Yan X, Zirkin BR, Jarow JP.
Department of Medicine, University of Washington School of Medicine, Seattle, Washington 98195, USA. [email protected]
In previous studies of testicular biopsy tissue from healthy men, intratesticular testosterone (ITT) has been shown to be much higher than serum testosterone (T), suggesting that high ITT is needed relative to serum T for normal spermatogenesis in men. However, the quantitative relationship between ITT and spermatogenesis is not known. To begin to address this issue experimentally, we determined the dose-response relationship between human chorionic gonadotropin (hCG) and ITT to ascertain the minimum dose needed to maintain ITT in the normal range. Twenty-nine men with normal reproductive physiology were randomized to receive 200 mg T enanthate weekly in combination with either saline placebo or 125, 250, or 500 IU hCG every other day for 3 wk. ITT was assessed in testicular fluid obtained by percutaneous fine needle aspiration at baseline and at the end of treatment. Baseline serum T (14.1 nmol/liter) was 1.2% of ITT (1174 nmol/liter). LH and FSH were profoundly suppressed to 5% and 3% of baseline, respectively, and ITT was suppressed by 94% (1234 to 72 nmol/liter) in the T enanthate/placebo group. ITT increased linearly with increasing hCG dose (P < 0.001). Posttreatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group, and 26% greater than baseline in the 500 IU hCG group. These results demonstrate that relatively low dose hCG maintains ITT within the normal range in healthy men with gonadotropin suppression. Extensions of this study will allow determination of the ITT concentration threshold required to maintain spermatogenesis in man.
PMID: 15713727 [PubMed - indexed for MEDLINE]
When you have to pay for the divorce settlement usually.
God that is so true.......................:nutkick:Quote:
Originally Posted by marcus300
running test e. over a month in a mine are good to go still... and its pharmacy shit. so not bullshit
then what are the reasons for testicular atrophy, just that some get it some don't?Quote:
Originally Posted by Swifto
The ones who claim they dont, just have small nuts to begin with, so they cant tell the difference when on or off:wg:Quote:
Originally Posted by Jumbo18
I'd guess its whether your leydig cells lose volume when not stimulated. Some do, some dont.Quote:
Originally Posted by Jumbo18
ITT being shut off too.
New lesson of the day...
Your testes are also a producer of GH.
Growth Hormone: Roles in Male Reproduction.
Endocrine. 13(3):243-250, December 2000.
Hull, Kerry L. 1; Harvey, Steve 2
Growth hormone (GH), as its name suggests, is obligatory for growth and development. It is, however, also required for sexual differentiation and pubertal maturation and participates in gonadal steroidogenesis and gametogenesis. These roles are likely to reflect the endocrine actions of pituitary GH, directly at gonadal sites and indirectly via hepatic insulin-like growth factor-1. However, because GH is also produced in gonadal tissues, it may act in paracrine or autocrine ways to regulate local processes that are strategically regulated by pituitary GH. The concept that GH is a major regulator of male reproduction is the focus of this review.
(C) 2000 Humana Press