YOu think I can't get near you with it?Great sex between whom? I'm out if you think you're getting anywhere near me with that thing.
Look next to your left foot....
YOu think I can't get near you with it?Great sex between whom? I'm out if you think you're getting anywhere near me with that thing.
Ahhh...what the...damn that thing is about as thick as a pencil.YOu think I can't get near you with it?
Look next to your left foot....
Yeah, yeah.....but it sure is long isn't it? *smooch*Ahhh...what the...damn that thing is about as thick as a pencil.
okay, I guess this one IS getting away from us.Yeah, yeah.....but it sure is long isn't it? *smooch*
Humor and good advice. You can't beat that.okay, I guess this one IS getting away from us.
On topic, however, aside from having amusing dialogue, I appreciate CED's call for advice and the people who have advised. Really brings home the great advantage of having this forum and such conversations. Props to all...
Don't know where you got that from but research suggests otherwise. Testosterone administration actually upregulates the AR for a very long time. Doses given to men showed upregulation of up to 6 months before any type opf down regulation ocurred and even then it never went below baseline.
You have to look at other genetic factors on why people stop responding (probably diet anyway).
I don't understand the point of cruising in a normal healthy man. You are only going to increase the chances of lower test production in the long run.
In long term studies in humans we get yet a different picture. In work conducted by Sheffield-Moore et. al., (16) older men were supplemented with testosterone so as to bring their testosterone levels into the mid to high physiological range. Androgen receptor expression had more than doubled after one month of treatment, yet by 6 months had returned to baseline. If this downregulation occurs when supraphysiological doses of testosterone are used, it could very well explain why gains tend to slow during a long cycle.
Testosterone administration to older men improves muscle function: molecular and physiological mechanisms.
Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Department of Surgery, The University of Texas Medical Branch, Galveston, Texas 77550, USA. [email protected]
We investigated the effects of 6 mo of near-physiological testosterone administration to older men on skeletal muscle function and muscle protein metabolism. Twelve older men (> or =60 yr) with serum total testosterone concentrations <17 nmol/l (480 ng/dl) were randomly assigned in double-blind manner to receive either placebo (n = 5) or testosterone enanthate (TE; n = 7) injections. Weekly intramuscular injections were given for the 1st mo to establish increased blood testosterone concentrations at 1 mo and then changed to biweekly injections until the 6-mo time point. TE doses were adjusted to maintain nadir serum testosterone concentrations between 17 and 28 nmol/l. Lean body mass (LBM), muscle volume, prostate size, and urinary flow were measured at baseline and at 6 mo. Protein expression of androgen receptor (AR) and insulin-like growth factor I, along with muscle strength and muscle protein metabolism, were measured at baseline and at 1 and 6 mo of treatment. Hematological parameters were followed monthly throughout the study. Older men receiving testosterone increased total and leg LBM, muscle volume, and leg and arm muscle strength after 6 mo. LBM accretion resulted from an increase in muscle protein net balance, due to a decrease in muscle protein breakdown. TE treatment increased expression of AR protein at 1 mo, but expression returned to pre-TE treatment levels by 6 mo. IGF-I protein expression increased at 1 mo and remained increased throughout TE administration. We conclude that physiological and near-physiological increases of testosterone in older men will increase muscle protein anabolism and muscle strength.
Publication Types:
Clinical Trial
Randomized Controlled Trial
PMID: 11832363 [PubMed - indexed for MEDLINE]
I don't remember where I read it. Someone had theorized this and I read it as convincing.
It would seem logical that the human body would adapt in some manner to establish a homeostasis at some point.
A quick search pulls up something Nandi claims:
http://www.wannabebig.com/printarticle.php?articleid=225
Here is the study he cited:
Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ. Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7
I couldn't find anything like this that may say whether or not exercise has an influence on the AR.
Bobo - Comments?
Helps to actually read the article KwyckeDose / Before / After / Change / p-value
25 mg / 593 ± 48 / 253 ± 66 / 340 ± 85 / 0.0029
50 mg / 566 ± 78 / 306 ± 58 / 260 ± 64 / 0.0037
125 mg / 553 ± 53 / 570 ± 75 / 57 ± 75 / 0.7425
300 mg / 653 ± 50 / 1,345 ± 139 / 691 ± 143 / 0.0005
600 mg / 632 ± 63 / 2,370 ± 150 / 1,737 ± 156 / 0.0001
Taken From:
Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1172-81.
Testosterone dose-response relationships in healthy young men.
Bhasin S, Woodhouse L, Casaburi R, Singh AB, Bhasin D, Berman N, Chen X, Yarasheski KE, Magliano L, Dzekov C, Dzekov J, Bross R, Phillips J, Sinha-Hikim I, Shen R, Storer TW.
Maybe shutdown is not so dose dependent? Hmmm...........well...........I dunno......ALR told me otherwise, now I"m confused again........... *bah* i hate learning ****.
Wow...I didin't have access to the entire article.Helps to actually read the article Kwycke ....
Effects of chronic testosterone administration in normal men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production.Wow...I didin't have access to the entire article.
So, ALR was probably right on when he said that shutdown is dose-dependent. Makes sense since some ppl don't shut down easily--based on that info, I asked him if that's b/c of higher natty T levels, he said yes (one of a few possible factors).
Thx for the article....now, if only I could find a study where endogenous test was not supressed :twisted:
I've noticed that orals can shut me down, but when I'm on the test solo, at 500mg/wk, i hardly feel it and my nutz dont' shrink for jack, even if I lay off the hcg.
thx exnihilo
You are very right, if you have the patience to do it, but an AI could sub for the SERM on such a long cruise I bet....I am thoroughly convinced at this point that a cruising period lasting 8-10 weeks at the end of a cycle with tapering doses from 100-25mg or so in conjunction with low dose SERM usage is the right way to go. Now I just need test subjects to validate my hypothesis
No, not really.Wow...I didin't have access to the entire article.
So, ALR was probably right on when he said that shutdown is dose-dependent. Makes sense since some ppl don't shut down easily--based on that info, I asked him if that's b/c of higher natty T levels, he said yes (one of a few possible factors).
thx exnihilo
No children. However, I truly do try to help individuals from making short term mistakes that could effect one's long term well being. BBing/training/fitness should be about health, well being, and looking/feeling good, and not only aobut getting big.Hey size, do you have any children because you would make a great father. If only you could get your alcoholism under control. Just kidding.
Atrophy is caused by a lack of sperm production (since the bulk is made up of sertoli cells, not leydig cells) than testosterone production. IOW you could be shut down and have no atrophy but the longer time goes on more chance sperm production is hindered causing more atrophy.I've noticed that orals can shut me down, but when I'm on the test solo, at 500mg/wk, i hardly feel it and my nutz dont' shrink for jack, even if I lay off the hcg.
thx exnihilo
Keep time on short and they stay "plump"Atrophy is caused by a lack of sperm production (since the bulk is made up of sertoli cells, not leydig cells) than testosterone production. IOW you could be shut down and have no atrophy but the longer time goes on more chance sperm production is hindered causing more atrophy.
Has nothing to do with orals. Deca and Tren will do the same.So yeah, it appears that oral steroids can shut you down really hard
I never said you did x2.I have never disputed the idea of using HCG to maintain testicular sensitivity to LH.
I never said that 65% LH levels = 65% of natural testosterone production, though if the testes are functioning properly and there are no other negative feedback mechanisms in play that is what I would expect.
I never argued against androgenic supression.
I never stated that orals were they only things that were extremely supressive.
SWALE stated that in his experience, the androgenic supression effects of testosterone were sufficient to obviate any effect SERMs would have @ 200+ mg/week.
Of course swale has seen some people shut down completely at 100mg of testosterone a week. Everyone is different, ask him if that is the predominant norm in his experience (the way he mentions it, it doesn't sound like it is). Also, if you look at the study I posted they mention that 100mg of testosterone is sufficient to raise plasta T concentrations to 1.5 times above baseline. The study that showed 100mg of testosterone a week was only sufficient to maintain baseline testosterone levels also utilized a GnRH agonist to completely supress endogenous T production, so the fact that 100mg of testosterone is enough to supress some people isn't THAT suprising is it? I'm advocating a protocol that does seem to have some scientific grounding (though of course I'm missing the full texts of a couple articles and thus there may be some nuances that have escaped me - I'm sure you can relate). I have stated repeatedly that the final determinant of the efficacy of the protocol would be determined by direct experimentation, and I'm willing to put my time and money where my mouth is on that score.
Also, could you please reference books or articles written by Dr. Crisler that you are constantly paraphrasing?
Some of you guys are making this issue more black and white than it really is. I will agree that desensitization to HP stimulation over long periods of exogenous hormone use seems to be the biggest factor, but dose and the specific steroid do play a role too. It is shown that hCG response is greater when FSH levels are high. FSH levels are higher when estradiol is low. Estradiol is low when an AI is administered in conjunction with hCG or test (as I suggested before on the cruising). Estrogen suppresses Leydig function at doses so low that LH is not even affected first! Even Sertoli cells are capable of estrogen secretion. Also when prolactin levels are higher, there is synergism with LH in stimulating Leydig cells to produce test. There is a latency period with prolactin spikes and test production, as seen with dopamine antagonists like haloperidol. LH/hCG spikes don't directly correspond to increased test production really. When GNRH is administered with LH, plasma test concentrations are more reliably increased without this latency phenomenon. I have advocated use of halotestin as a "bridge" option during PCT based on this research. In real life, I have found it to be effective in that recovery proceeds without delay and spermatogenesis is augmented. LH spikes are reduced in number, but not their magnitude. In this case, LH spikes do seem to correlate more closely with test secretion! So it is a complicated issue and everyone must experiment to find their own limitations. Some will find "tricks" that work, while other will not be able to break the rules.
Bridging with Halo...that's a new one...lol.
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