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Testosterone Thresholds

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I remember reading that decrease in effectiveness was not so much due to homeostasis in the reduction of AR' date=' but rather an increase in circulating Cortisol. The increase in Cort (as I take it) was an attempt to slow the accretion of muscle mass in order to maintain homeostasis. The more hormones, the more the anabolic signal overides the catabolic, and the more cort is produced.[/quote']

 

Can you share some of this literature?

 

FWIW I think the limiting factor comes from higher-up stuff like myostatin. GH and Test will inhibit the hell out of it, for about 10 weeks I believe. I will have to dig some stuff up before I start rambling though and you turn around and ask me for the literature, lol....

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Honestly the hardest part is not the gym stuff.

 

Its the libido. And the confidence.

 

I mean, I was a walking hard on.

 

How much of which ester were you using for how long?

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How much of which ester were you using for how long?

 

 

 

500mg to 1 gram...per 500mg mix was....200 cyp, 150 enth, 150 undec.

 

Really gets additive with those half lives.

 

I would throw in some t-gel or suspension before a "special event".

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500mg to 1 gram...per 500mg mix was....200 cyp, 150 enth, 150 undec.

 

Really gets additive with those half lives.

 

I would throw in some t-gel or suspension before a "special event".

 

Having a fair amount of longer esters as well as the short ones, has really sneaked up on me in the past on longer cycles, Tren build up from that was responsible for me getting quite sick.

J

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Can you share some of this literature?

 

FWIW I think the limiting factor comes from higher-up stuff like myostatin. GH and Test will inhibit the hell out of it, for about 10 weeks I believe. I will have to dig some stuff up before I start rambling though and you turn around and ask me for the literature, lol....

 

Maybe, but look at the size and musculature of follistatin knockout mice. They look very similar to myostatin knockout.

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Can you share some of this literature?

 

FWIW I think the limiting factor comes from higher-up stuff like myostatin. GH and Test will inhibit the hell out of it, for about 10 weeks I believe. I will have to dig some stuff up before I start rambling though and you turn around and ask me for the literature, lol....

 

I'm going to have to dig through the literature. I don't even remember if I quote an actual study, or if it was all just speculation.

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Maybe' date=' but look at the size and musculature of follistatin knockout mice. They look very similar to myostatin knockout.[/quote']

Follistatin inhibition + myostatin inhibition > myostatin inhibition IIRC

J

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I'm going to take some issue with that. In my favoritest study of all time they dosed a group of normal men with 600mg/week test enthanate and told them to sit on their hands. They compared these guys to a matched group who got placebo but lifted three days a week. At the end of three months, the couch+test group had gained 3.2kg of LBM and the group who had been lifting gained 1.9kg and the 1RM squat and 1RM bench of both groups increased about the same amount.

 

Of course, the guys who got test AND worked out did phenomenally better than either of the other groups.

 

Test didnt make me bigger, just allowed me to stay big and lean with doing almost nothing basically.

YMMV.

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Maybe' date=' but look at the size and musculature of follistatin knockout mice. They look very similar to myostatin knockout.[/quote']

 

independent, complementary and addtive mechanisms.

 

http://www.ncbi.nlm.nih.gov/m/pubmed/22711699/

 

Follistatin-mediated skeletal muscle hypertrophy is regulated by Smad3 and mTOR independently of myostatin.

 

Follistatin is essential for skeletal muscle development and growth, but the intracellular signaling networks that regulate follistatin-mediated effects are not well defined. We show here that the administration of an adeno-associated viral vector expressing follistatin-288aa (rAAV6:Fst-288) markedly increased muscle mass and force-producing capacity concomitant with increased protein synthesis and mammalian target of rapamycin (mTOR) activation. These effects were attenuated by inhibition of mTOR or deletion of S6K1/2. Furthermore, we identify Smad3 as the critical intracellular link that mediates the effects of follistatin on mTOR signaling. Expression of constitutively active Smad3 not only markedly prevented skeletal muscle growth induced by follistatin but also potently suppressed follistatin-induced Akt/mTOR/S6K signaling. Importantly, the regulation of Smad3- and mTOR-dependent events by follistatin occurred independently of overexpression or knockout of myostatin, a key repressor of muscle development that can regulate Smad3 and mTOR signaling and that is itself inhibited by follistatin. These findings identify a critical role of Smad3/Akt/mTOR/S6K/S6RP signaling in follistatin-mediated muscle growth that operates independently of myostatin-driven mechanisms.

 

 

http://www.ncbi.nlm.nih.gov/m/pubmed/19435857/

 

Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin.

.

 

Follistatin (FS) inhibits several members of the TGF-beta superfamily, including myostatin (Mstn), a negative regulator of muscle growth. Mstn inhibition by FS represents a potential therapeutic approach of muscle atrophy. The aim of our study was to investigate the mechanisms of the FS-induced muscle hypertrophy. To test the role of satellite cells in the FS effect, we used irradiation to destroy their proliferative capacity. FS overexpression increased the muscle weight by about 37% in control animals, but the increase reached only 20% in irradiated muscle, supporting the role of cell proliferation in the FS-induced hypertrophy. Surprisingly, the muscle hypertrophy caused by FS reached the same magnitude in Mstn-KO as in WT mice, suggesting that Mstn might not be the only ligand of FS involved in the regulation of muscle mass. To assess the role of activin (Act), another FS ligand, in the FS-induced hypertrophy, we electroporated FSI-I, a FS mutant that does not bind Act with high affinity. Whereas FS electroporation increased muscle weight by 32%, the muscle weight gain induced by FSI-I reached only 14%. Furthermore, in Mstn-KO mice, FSI-I overexpression failed to induce hypertrophy, in contrast to FS. Therefore, these results suggest that Act inhibition may contribute to FS-induced hypertrophy. Finally, the role of Act as a regulator of muscle mass was supported by the observation that ActA overexpression induced muscle weight loss (-15%). In conclusion, our results show that satellite cell proliferation and both Mstn and Act inhibition are involved in the FS-induced muscle hypertrophy.

 

 

-------

by the way dont know if Grb10 induces more skeletal muscle than follistatin overexpression

 

http://www.fasebj.org/content/26/9/3658

 

Grb10 regulates the development of fiber number in skeletal muscle.

 

Grb10 is an intracellular adaptor protein that acts as a negative regulator of insulin and insulin-like growth factor 1 (IGF1) receptors. Since global deletion of Grb10 in mice causes hypermuscularity, we have characterized the skeletal muscle physiology underlying this phenotype. Compared to wild-type (WT) controls, adult mice deficient in Grb10 have elevated body mass and muscle mass throughout adulthood, up to 12 mo of age. The muscle enlargement is not due to increased myofiber size, but rather an increase in myofiber number (142% of WT, P<0.01). There is no change in myofiber type proportions between WT and Grb10-deficient muscles, nor are the metabolic properties of the muscles altered on Grb10 deletion. Notably, the weight and cross-sectional area of hindlimbs from neonatal mice are increased in Grb10-deficient animals (198 and 137% of WT, respectively, both P<0.001). Functional gene signatures for myogenic signaling and proliferation are up-regulated in Grb10-deficient neonatal muscle. Our findings indicate that Grb10 plays a previously unrecognized role in regulating the development of fiber number during murine embryonic growth. In addition, Grb10-ablated muscle from adult mice shows coordinate gene changes that oppose those of muscle wasting pathologies, highlighting Grb10 as a potential therapeutic target for these conditions.

 

in any case

 

http://www.ncbi.nlm.nih.gov/m/pubmed/22087027/?i=2&from=/22711699/

 

The type 1 insulin-like growth factor receptor (IGF-IR) pathway is mandatory for the follistatin-induced skeletal muscle hypertrophy.

 

Myostatin inhibition by follistatin (FS) offers a new approach for muscle mass enhancement. The aim of the present study was to characterize the mediators responsible for the FS hypertrophic action on skeletal muscle in male mice. Because IGF-I and IGF-II, two crucial skeletal muscle growth factors, are induced by myostatin inhibition, we assessed their role in FS action. First, we tested whether type 1 IGF receptor (IGF-IR) is required for FS-induced hypertrophy. By using mice expressing a dominant-negative IGF-IR in skeletal muscle, we showed that IGF-IR inhibition blunted by 63% fiber hypertrophy caused by FS. Second, we showed that FS caused the same degree of fiber hypertrophy in wild-type and IGF-II knockout mice. We then tested the role of the signaling molecules stimulated by IGF-IR, in particular the Akt/mammalian target of rapamycin (mTOR)/70-kDa ribosomal protein S6 kinase (S6K) pathway. We investigated whether Akt phosphorylation is required for the FS action. By cotransfecting a dominant-negative form of Akt together with FS, we showed that Akt inhibition reduced by 65% fiber hypertrophy caused by FS. Second, we evaluated the role of mTOR in FS action. Fiber hypertrophy induced by FS was reduced by 36% in rapamycin-treated mice. Finally, because the activity of S6K is increased by FS, we tested its role in FS action. FS caused the same degree of fiber hypertrophy in wild-type and S6K1/2 knockout mice. In conclusion, the IGF-IR/Akt/mTOR pathway plays a critical role in FS-induced muscle hypertrophy. In contrast, induction of IGF-II expression and S6K activity by FS are not required for the hypertrophic action of FS.

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independent, complementary and addtive mechanisms.

 

http://www.ncbi.nlm.nih.gov/m/pubmed/22711699/

 

Follistatin-mediated skeletal muscle hypertrophy is regulated by Smad3 and mTOR independently of myostatin.

 

Follistatin is essential for skeletal muscle development and growth, but the intracellular signaling networks that regulate follistatin-mediated effects are not well defined. We show here that the administration of an adeno-associated viral vector expressing follistatin-288aa (rAAV6:Fst-288) markedly increased muscle mass and force-producing capacity concomitant with increased protein synthesis and mammalian target of rapamycin (mTOR) activation. These effects were attenuated by inhibition of mTOR or deletion of S6K1/2. Furthermore, we identify Smad3 as the critical intracellular link that mediates the effects of follistatin on mTOR signaling. Expression of constitutively active Smad3 not only markedly prevented skeletal muscle growth induced by follistatin but also potently suppressed follistatin-induced Akt/mTOR/S6K signaling. Importantly, the regulation of Smad3- and mTOR-dependent events by follistatin occurred independently of overexpression or knockout of myostatin, a key repressor of muscle development that can regulate Smad3 and mTOR signaling and that is itself inhibited by follistatin. These findings identify a critical role of Smad3/Akt/mTOR/S6K/S6RP signaling in follistatin-mediated muscle growth that operates independently of myostatin-driven mechanisms.

 

 

http://www.ncbi.nlm.nih.gov/m/pubmed/19435857/

 

Follistatin induces muscle hypertrophy through satellite cell proliferation and inhibition of both myostatin and activin.

.

 

Follistatin (FS) inhibits several members of the TGF-beta superfamily, including myostatin (Mstn), a negative regulator of muscle growth. Mstn inhibition by FS represents a potential therapeutic approach of muscle atrophy. The aim of our study was to investigate the mechanisms of the FS-induced muscle hypertrophy. To test the role of satellite cells in the FS effect, we used irradiation to destroy their proliferative capacity. FS overexpression increased the muscle weight by about 37% in control animals, but the increase reached only 20% in irradiated muscle, supporting the role of cell proliferation in the FS-induced hypertrophy. Surprisingly, the muscle hypertrophy caused by FS reached the same magnitude in Mstn-KO as in WT mice, suggesting that Mstn might not be the only ligand of FS involved in the regulation of muscle mass. To assess the role of activin (Act), another FS ligand, in the FS-induced hypertrophy, we electroporated FSI-I, a FS mutant that does not bind Act with high affinity. Whereas FS electroporation increased muscle weight by 32%, the muscle weight gain induced by FSI-I reached only 14%. Furthermore, in Mstn-KO mice, FSI-I overexpression failed to induce hypertrophy, in contrast to FS. Therefore, these results suggest that Act inhibition may contribute to FS-induced hypertrophy. Finally, the role of Act as a regulator of muscle mass was supported by the observation that ActA overexpression induced muscle weight loss (-15%). In conclusion, our results show that satellite cell proliferation and both Mstn and Act inhibition are involved in the FS-induced muscle hypertrophy.

 

 

-------

by the way dont know if Grb10 induces more skeletal muscle than follistatin overexpression

 

http://www.fasebj.org/content/26/9/3658

 

Grb10 regulates the development of fiber number in skeletal muscle.

 

Grb10 is an intracellular adaptor protein that acts as a negative regulator of insulin and insulin-like growth factor 1 (IGF1) receptors. Since global deletion of Grb10 in mice causes hypermuscularity, we have characterized the skeletal muscle physiology underlying this phenotype. Compared to wild-type (WT) controls, adult mice deficient in Grb10 have elevated body mass and muscle mass throughout adulthood, up to 12 mo of age. The muscle enlargement is not due to increased myofiber size, but rather an increase in myofiber number (142% of WT, P<0.01). There is no change in myofiber type proportions between WT and Grb10-deficient muscles, nor are the metabolic properties of the muscles altered on Grb10 deletion. Notably, the weight and cross-sectional area of hindlimbs from neonatal mice are increased in Grb10-deficient animals (198 and 137% of WT, respectively, both P<0.001). Functional gene signatures for myogenic signaling and proliferation are up-regulated in Grb10-deficient neonatal muscle. Our findings indicate that Grb10 plays a previously unrecognized role in regulating the development of fiber number during murine embryonic growth. In addition, Grb10-ablated muscle from adult mice shows coordinate gene changes that oppose those of muscle wasting pathologies, highlighting Grb10 as a potential therapeutic target for these conditions.

 

in any case

 

http://www.ncbi.nlm.nih.gov/m/pubmed/22087027/?i=2&from=/22711699/

 

The type 1 insulin-like growth factor receptor (IGF-IR) pathway is mandatory for the follistatin-induced skeletal muscle hypertrophy.

 

Myostatin inhibition by follistatin (FS) offers a new approach for muscle mass enhancement. The aim of the present study was to characterize the mediators responsible for the FS hypertrophic action on skeletal muscle in male mice. Because IGF-I and IGF-II, two crucial skeletal muscle growth factors, are induced by myostatin inhibition, we assessed their role in FS action. First, we tested whether type 1 IGF receptor (IGF-IR) is required for FS-induced hypertrophy. By using mice expressing a dominant-negative IGF-IR in skeletal muscle, we showed that IGF-IR inhibition blunted by 63% fiber hypertrophy caused by FS. Second, we showed that FS caused the same degree of fiber hypertrophy in wild-type and IGF-II knockout mice. We then tested the role of the signaling molecules stimulated by IGF-IR, in particular the Akt/mammalian target of rapamycin (mTOR)/70-kDa ribosomal protein S6 kinase (S6K) pathway. We investigated whether Akt phosphorylation is required for the FS action. By cotransfecting a dominant-negative form of Akt together with FS, we showed that Akt inhibition reduced by 65% fiber hypertrophy caused by FS. Second, we evaluated the role of mTOR in FS action. Fiber hypertrophy induced by FS was reduced by 36% in rapamycin-treated mice. Finally, because the activity of S6K is increased by FS, we tested its role in FS action. FS caused the same degree of fiber hypertrophy in wild-type and S6K1/2 knockout mice. In conclusion, the IGF-IR/Akt/mTOR pathway plays a critical role in FS-induced muscle hypertrophy. In contrast, induction of IGF-II expression and S6K activity by FS are not required for the hypertrophic action of FS.

 

 

 again on Grb10 and other villains

 

 

Molecular brakes regulating mTORC1 activation in skeletal muscle following synergist ablation

 

http://ajpendo.physiology.org/content/early/2014/06/23/ajpendo.00674.2013

 

"SA (synergist ablation) resulted in significant increases in muscle mass of ~4% per day throughout the 21 days of the experiment" 

 

 

the molecular brakes, at least; decreased IRS1/2 protein (Grb10 phosphorilation, effector), UPR activation (CHOP/BiP elevated,  IRE1α levels decreased. effectors),  Ampk activation  (TSC2 phosphorylation, effector)

 

.

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On 3/5/2013 at 10:44 PM, STENDEC said:

Ever wonder how high your T levels need to be to make anabolic changes?

 

According to this, you need to have levels at +1200ng/dl to make a difference...somewhat less if you are also supplementing with growth hormone...

 

 

J Gerontol A Biol Sci Med Sci. 2011 Jan;66(1):122-9. doi: 10.1093/gerona/glq183. Epub 2010 Nov 8.

Testosterone threshold levels and lean tissue mass targets needed to enhance skeletal muscle strength and function: the HORMA trial.

Sattler F, Bhasin S, He J, Chou CP, Castaneda-Sceppa C, Yarasheski K, Binder E, Schroeder ET, Kawakubo M, Zhang A, Roubenoff R, Azen S.

Source

 

Department of Medicine, University of Southern California, 2020 Zonal Avenue, Los Angeles, CA 90033, USA. fsattler@usc.edu

Abstract

BACKGROUND:

 

In the HORMA (Hormonal Regulators of Muscle and Metabolism in Aging) Trial, supplemental testosterone and recombinant human growth hormone (rhGH) enhanced lean body mass, appendicular skeletal muscle mass, muscle performance, and physical function, but there was substantial interindividual variability in outcomes.

METHODS:

 

One hundred and twelve men aged 65-90 years received testosterone gel (5 g/d vs 10 g/d via Leydig cell clamp) and rhGH (0 vs 3 vs 5 μg/kg/d) in a double-masked 2 × 3 factorial design for 16 weeks. Outcomes included lean tissue mass by dual energy x-ray absorptiometry, one-repetition maximum strength, Margaria stair power, and activity questionnaires. We used pathway analysis to determine the relationship between changes in hormone levels, muscle mass, strength, and function.

RESULTS:

 

Increases in total testosterone of 1046 ng/dL (95% confidence interval = 1040-1051) and 898 ng/dL (95% confidence interval = 892-904) were necessary to achieve median increases in lean body mass of 1.5 kg and appendicular skeletal muscle mass of 0.8 kg, respectively, which were required to significantly enhance one-repetition maximum strength (≥ 30%). Co-treatment with rhGH lowered the testosterone levels (quantified using liquid chromatography-tandem mass spectrometry) necessary to reach these lean mass thresholds. Changes in one-repetition maximum strength were associated with increases in stair climbing power (r = .26, p = .01). Pathway analysis supported the model that changes in testosterone and insulin-like growth factor 1 levels are related to changes in lean body mass needed to enhance muscle performance and physical function. Testosterone's effects on physical activity were mediated through a different pathway because testosterone directly affected Physical Activity Score of the Elderly.

CONCLUSIONS:

 

To enhance muscle strength and physical function, threshold improvements in lean body mass and appendicular skeletal muscle mass are necessary and these can be achieved by targeting changes in testosterone levels. rhGH augments the effects of testosterone. To maximize functional improvements, the doses of anabolic hormones should be titrated to achieve target blood levels.

 

PMID: 21059836

 

FFT

This is an old post, but I was reviewing some of the data we have on test doses => test levels, with the ultimate goal of comparing subq and IM. 

 

I reviewed this study and found it interesting that at 5g/day of 1% test (50mg/day) men had levels of about 600-700ng/dl test. So at 350mg/week of test base, that was translating to that level of hormone. That seems so ultra low. The 10g group went up to around 1000-1200, which still seems low for 700mg/week of test base. To be fair, the ranges were very high (+143±379 in 5g group and +510±503 in the 10g group (baseline @ 363-493, depending on assay method)). Also, while the changes in total test seem really low given the doses, the change in free test in the 10g was quite dramatic (+201±231 pg/ml), which in my eyes is pretty god damn anabolic. 

 

I thought that was interesting.

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On 3/27/2013 at 2:54 PM, Trapman said:

http://www.ncbi.nlm.nih.gov/pubmed/12067856

 

the above is a nice simple guideline summarizing what I was saying with my reply to Benson...

In case anyone is looking for it, this is one of the studies of interest that actually tell us how much total test to expect given a fixed dose of test/week. idk if there are others, but many of the ones posted here don't actually give this information and you have to back calculate it from other data they give you (and it's hard since they dont give you the raw numbers; you have to interpolate from the bargraphs and markers)

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5 hours ago, Growth Factor said:

I reviewed this study and found it interesting that at 5g/day of 1% test (50mg/day) men had levels of about 600-700ng/dl test.

 

I don't think this is atypical.

 

For no good reason, the typical recommendation for TRT is to shoot for mid range and so the dosing schemes of most replacement products is designed to get most guys there.

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On 5/3/2013 at 11:14 PM, STENDEC said:

Ever wonder how high your T levels need to be to make anabolic changes?

 

According to this, you need to have levels at +1200ng/dl to make a difference...somewhat less if you are also supplementing with growth hormone...

 

 

J Gerontol A Biol Sci Med Sci. 2011 Jan;66(1):122-9. doi: 10.1093/gerona/glq183. Epub 2010 Nov 8.

Testosterone threshold levels and lean tissue mass targets needed to enhance skeletal muscle strength and function: the HORMA trial.

Sattler F, Bhasin S, He J, Chou CP, Castaneda-Sceppa C, Yarasheski K, Binder E, Schroeder ET, Kawakubo M, Zhang A, Roubenoff R, Azen S.

Source

 

Department of Medicine, University of Southern California, 2020 Zonal Avenue, Los Angeles, CA 90033, USA. fsattler@usc.edu

Abstract

BACKGROUND:

 

In the HORMA (Hormonal Regulators of Muscle and Metabolism in Aging) Trial, supplemental testosterone and recombinant human growth hormone (rhGH) enhanced lean body mass, appendicular skeletal muscle mass, muscle performance, and physical function, but there was substantial interindividual variability in outcomes.

METHODS:

 

One hundred and twelve men aged 65-90 years received testosterone gel (5 g/d vs 10 g/d via Leydig cell clamp) and rhGH (0 vs 3 vs 5 μg/kg/d) in a double-masked 2 × 3 factorial design for 16 weeks. Outcomes included lean tissue mass by dual energy x-ray absorptiometry, one-repetition maximum strength, Margaria stair power, and activity questionnaires. We used pathway analysis to determine the relationship between changes in hormone levels, muscle mass, strength, and function.

RESULTS:

 

Increases in total testosterone of 1046 ng/dL (95% confidence interval = 1040-1051) and 898 ng/dL (95% confidence interval = 892-904) were necessary to achieve median increases in lean body mass of 1.5 kg and appendicular skeletal muscle mass of 0.8 kg, respectively, which were required to significantly enhance one-repetition maximum strength (≥ 30%). Co-treatment with rhGH lowered the testosterone levels (quantified using liquid chromatography-tandem mass spectrometry) necessary to reach these lean mass thresholds. Changes in one-repetition maximum strength were associated with increases in stair climbing power (r = .26, p = .01). Pathway analysis supported the model that changes in testosterone and insulin-like growth factor 1 levels are related to changes in lean body mass needed to enhance muscle performance and physical function. Testosterone's effects on physical activity were mediated through a different pathway because testosterone directly affected Physical Activity Score of the Elderly.

CONCLUSIONS:

 

To enhance muscle strength and physical function, threshold improvements in lean body mass and appendicular skeletal muscle mass are necessary and these can be achieved by targeting changes in testosterone levels. rhGH augments the effects of testosterone. To maximize functional improvements, the doses of anabolic hormones should be titrated to achieve target blood levels.

 

PMID: 21059836

 

FFT

 

 

me, now on 1000+

 

 

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On 3/7/2018 at 7:56 AM, Growth Factor said:

This is an old post, but I was reviewing some of the data we have on test doses => test levels, with the ultimate goal of comparing subq and IM. 

 

I reviewed this study and found it interesting that at 5g/day of 1% test (50mg/day) men had levels of about 600-700ng/dl test. So at 350mg/week of test base, that was translating to that level of hormone. That seems so ultra low. The 10g group went up to around 1000-1200, which still seems low for 700mg/week of test base. To be fair, the ranges were very high (+143±379 in 5g group and +510±503 in the 10g group (baseline @ 363-493, depending on assay method)). Also, while the changes in total test seem really low given the doses, the change in free test in the 10g was quite dramatic (+201±231 pg/ml), which in my eyes is pretty god damn anabolic. 

 

I thought that was interesting.

 

So I combed through this thread, saw my younger self in 2013, shuddered, moved on.

 

Question, I'm trying to decide if ~250mg/10 days of test e would get me into supraphysiological ranges of test? That is what I was running the last few months of my last cycle, one where up to a gram of androgens a week was not abnormal. I found that at a threshold level of one 250mg test e shot every couple weeks I was super lean, not holding tons of water, and able to make gains I was quite happy with. 

 

Now my question is, was I even at a level higher than my own natty t production potential? I'm planning a TD run now, so I guess I'll find out soon enough. Just hoping maybe someone has some n=1 experience to shuttle my way. Thanks all. 

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.

 

 

Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline

https://academic.oup.com/jcem/article/103/5/1715/4939465

 

T enanthate or cypionate  150–200 mg IM every 2 wk or 75–100 mg/wk  After a single IM injection, serum T concentrations rise into the supraphysiological range, then decline gradually into the hypogonadal range by the end of the dosing interval 

 

 

 

.

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17 minutes ago, dr. frankenstein said:

.

 

 

Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline

https://academic.oup.com/jcem/article/103/5/1715/4939465

 

T enanthate or cypionate  150–200 mg IM every 2 wk or 75–100 mg/wk  After a single IM injection, serum T concentrations rise into the supraphysiological range, then decline gradually into the hypogonadal range by the end of the dosing interval 

 

 

 

.

 

I did quite a bit of digging around on this subject recently and I came to the conclusion that for most men, a weekly IM injection of  100-125mg would put them in high normal T range for most of the week.

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