First Cycle and PCT
- Thread starter heavyiron
- Start date
heavyiron
Community Veteran
Thank you brother.
It has been interesting to note the reactions of various boards members over the years to proposed cycles. There's an apparent "board philosophy" on many websites. Some are conservative, others seem more liberal. Early on I used to have some set philosophies that I have had to re evaluate over the years. However I think it would be a good discussion to ask why we have these philosophies. Why is 1 gram too much? Why is 600mg OK? Why 8 weeks? Why 14 weeks? Why 22 years old? Why 20 years old?
There are some good reasons for the answers but some are a bit murky and feel grey area to me. Lets look at the above study and evaluate it against a conservative mindset.
1. 18 year olds participated in the study
2. The Testosterone was administered for 20 weeks
3. The participants did not undergo any strength training.
So the scientists felt it was ethical for an 18 year old to use Testosterone for 20 weeks and NOT work out. LOL! The experts (not some guy on the net) have a VERY different philosophy then most of us. Why?
Now, I'm not arguing for an 18 year old to run 600mg of T for 20 weeks and not train so please don't misunderstand me. The experts however thought is was perfectly fine. Lets look at the flip side. These subjects were monitored by doctors the entire 20 weeks so there was precautionary measures. I have no illusions your typical 18 year old will seek medical supervision though. It just isn't likely especially since steroid use is often illegal in various Countries.
Anyway, we all have our ideas on what is the threshold for use and I try not to judge those that use more or less than I think but we all have our pre-concieved ideas, myself included. At the end of the day I want guys to be safe and educated so that is probably one of the strongest motivators we all use to make our judgments.
PCT can be accomplished many ways but a SERM is one component I always like to see in post cycle therapy (pct). Interestingly, no PCT often times results in full recovery if the subject is young, healthy and ran a shorter cycle but it will be prolonged without a SERM.
E2 may be high post PCT so getting labs to determine Aromatase inhibitor (AI) use is probably the best course of action.
Creatine has been shown to increase IGF-1 levels at higher doses and may even be slightly anabolic. The use of Creatine has shown to increase ATP metabolism and cellular water storage among many other things. This is beneficial because it provides for heightened nutrient storage and a slight increase in anabolism as well as workout stamina.
Lapple
Eternal Student
Great post man! Very informative, us "old newbs" love this kind of data!
A good friend of mine back east suggested an Aromatase inhibitor (AI) (liquidex) for my first cycle, he said it helped with the water gain and he said he felt he had less water loss and kept more size after his cycle. Thoughts?
A good friend of mine back east suggested an Aromatase inhibitor (AI) (liquidex) for my first cycle, he said it helped with the water gain and he said he felt he had less water loss and kept more size after his cycle. Thoughts?
heavyiron
Community Veteran
Thank you!
I'm very pro Aromatase inhibitor (AI) use. Estrogen at high levels is not our friend so I always run an Aromatase inhibitor (AI) with aromatizing compounds.
heavyiron
Community Veteran
In this study, 600mg per week of Testosterone Enanthate was shown to increase the number of Androgen Receptors in healthy men. This science shows that down-regulation of the AR is untenable in the presence of Testosterone.
Androgen Receptor in Human Skeletal Muscle and Cultured Muscle Satellite Cells: Up-Regulation by Androgen Treatment
Indrani Sinha-Hikim, Wayne E. Taylor, Nestor F. Gonzalez-Cadavid, Wei Zheng and Shalender Bhasin
Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California 90059
Address all correspondence and requests for reprints to: Shalender Bhasin, M.D., Charles R. Drew University of Medicine and Science, 1731 East 120th Street, Los Angeles, California 90059. E-mail: sbhasin@ucla.edu.
Abstract
Androgens stimulate myogenesis, but we do not know what cell types within human skeletal muscle express the androgen receptor (AR) protein and are the target of androgen action. Because testosterone promotes the commitment of pluripotent, mesenchymal cells into myogenic lineage, we hypothesized that AR would be expressed in mesenchymal precursor cells in the skeletal muscle. AR expression was evaluated by immunohistochemical staining, confocal immunofluorescence, and immunoelectron microscopy in sections of vastus lateralis from healthy men before and after treatment with a supraphysiological dose of testosterone enanthate. Satellite cell cultures from human skeletal muscle were also tested for AR expression. AR protein was expressed predominantly in satellite cells, identified by their location outside sarcolemma and inside basal lamina, and by CD34 and C-met staining. Many myonuclei in muscle fibers also demonstrated AR immunostaining. Additionally, CD34+ stem cells in the interstitium, fibroblasts, and mast cells expressed AR immunoreactivity. AR expression was also observed in vascular endothelial and smooth muscle cells. Immunoelectron microscopy revealed aggregation of immunogold particles in nucleoli of satellite cells and myonuclei; testosterone treatment increased nucleolar AR density. In enriched cultures of human satellite cells, more than 95% of cells stained for CD34 and C-met, confirming their identity as satellite cells, and expressed AR protein. AR mRNA and protein expression in satellite cell cultures was confirmed by RT-PCR, reverse transcription and real-time PCR, sequencing of RT-PCR product, and Western blot analysis. Incubation of satellite cell cultures with supraphysiological testosterone and dihydrotestosterone concentrations (100 nM testosterone and 30 nM dihydrotestosterone) modestly increased AR protein levels. We conclude that AR is expressed in several cell types in human skeletal muscle, including satellite cells, fibroblasts, CD34+ precursor cells, vascular endothelial, smooth muscle cells, and mast cells. Satellite cells are the predominant site of AR expression. These observations support the hypothesis that androgens increase muscle mass in part by acting on several cell types to regulate the differentiation of mesenchymal precursor cells in the skeletal muscle.
Androgen Receptor in Human Skeletal Muscle and Cultured Muscle Satellite Cells: Up-Regulation by Androgen Treatment
Indrani Sinha-Hikim, Wayne E. Taylor, Nestor F. Gonzalez-Cadavid, Wei Zheng and Shalender Bhasin
Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California 90059
Address all correspondence and requests for reprints to: Shalender Bhasin, M.D., Charles R. Drew University of Medicine and Science, 1731 East 120th Street, Los Angeles, California 90059. E-mail: sbhasin@ucla.edu.
Abstract
Androgens stimulate myogenesis, but we do not know what cell types within human skeletal muscle express the androgen receptor (AR) protein and are the target of androgen action. Because testosterone promotes the commitment of pluripotent, mesenchymal cells into myogenic lineage, we hypothesized that AR would be expressed in mesenchymal precursor cells in the skeletal muscle. AR expression was evaluated by immunohistochemical staining, confocal immunofluorescence, and immunoelectron microscopy in sections of vastus lateralis from healthy men before and after treatment with a supraphysiological dose of testosterone enanthate. Satellite cell cultures from human skeletal muscle were also tested for AR expression. AR protein was expressed predominantly in satellite cells, identified by their location outside sarcolemma and inside basal lamina, and by CD34 and C-met staining. Many myonuclei in muscle fibers also demonstrated AR immunostaining. Additionally, CD34+ stem cells in the interstitium, fibroblasts, and mast cells expressed AR immunoreactivity. AR expression was also observed in vascular endothelial and smooth muscle cells. Immunoelectron microscopy revealed aggregation of immunogold particles in nucleoli of satellite cells and myonuclei; testosterone treatment increased nucleolar AR density. In enriched cultures of human satellite cells, more than 95% of cells stained for CD34 and C-met, confirming their identity as satellite cells, and expressed AR protein. AR mRNA and protein expression in satellite cell cultures was confirmed by RT-PCR, reverse transcription and real-time PCR, sequencing of RT-PCR product, and Western blot analysis. Incubation of satellite cell cultures with supraphysiological testosterone and dihydrotestosterone concentrations (100 nM testosterone and 30 nM dihydrotestosterone) modestly increased AR protein levels. We conclude that AR is expressed in several cell types in human skeletal muscle, including satellite cells, fibroblasts, CD34+ precursor cells, vascular endothelial, smooth muscle cells, and mast cells. Satellite cells are the predominant site of AR expression. These observations support the hypothesis that androgens increase muscle mass in part by acting on several cell types to regulate the differentiation of mesenchymal precursor cells in the skeletal muscle.
THE-DET-OAK
IncreasedMyT @ ULV
Ok so no down reg, but how about saturation? how do you know that has happened?
heavyiron
Community Veteran
The above science is basically saying when we use Testosterone our bodies make more androgen receptors so it's very possible that at some point that effect diminishes. I have seen rough calculations on AR saturation but the doses are quite high and the data used to determine the dose was preliminary. I hate to speculate but 3.5 grams weekly may be the point of saturation for an average male. Again, this is just a guess.
THE-DET-OAK
IncreasedMyT @ ULV
ok would that be just for testosterone or would the number change depending on compounds? or DHT?
heavyiron
Community Veteran
The rough calculation was with Testosterone.
heavyiron
Community Veteran
Not only does Testosterone make your muscles bigger but it also is associated with more satellite cells.
Testosterone-induced muscle hypertrophy is associated with an increase in satellite cell number in healthy, young men
Indrani Sinha-Hikim,1 Stephen M. Roth,2 Martin I. Lee,1 and Shalender Bhasin1
1Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California 90059; and 2Department of Human Genetics, University of Pittsburgh, Pittsburgh, Pennsylvamia 15261
Submitted 22 August 2002 ; accepted in final form 26 March 2003
ABSTRACT
Testosterone (T) supplementation in men induces muscle fiber hypertrophy. We hypothesized that T-induced increase in muscle fiber size is associated with a dose-dependent increase in satellite cell number. We quantitated satellite cell and myonuclear number by using direct counting and spatial orientation methods in biopsies of vastus lateralis obtained at baseline and after 20 wk of treatment with a gonadotropin-releasing hormone agonist and a 125-, 300-, or 600-mg weekly dose of T enanthate. T administration was associated with a significant increase in myonuclear number in men receiving 300- and 600-mg doses. The posttreatment percent satellite cell number, obtained by direct counting, differed significantly among the three groups (ANCOVA P < 0.000001); the mean posttreatment values (5.0 and 15.0%) in men treated with 300- and 600-mg doses were greater than baseline (2.5 and 2.5%, respectively, P < 0.05 vs. baseline). The absolute satellite cell number measured by spatial orientation at 20 wk (1.5 and 4.0/mm) was significantly greater than baseline (0.3 and 0.6/mm) in men receiving the 300- and 600-mg doses (P < 0.05). The change in percent satellite cell number correlated with changes in total (r = 0.548) and free T concentrations (r = 0.468). Satellite cell and mitochondrial areas were significantly higher and the nuclear-to-cytoplasmic ratio lower after treatment with 300- and 600-mg doses. We conclude that T-induced muscle fiber hypertrophy is associated with an increase in satellite cell number, a proportionate increase in myonuclear number, and changes in satellite cell ultrastructure.
J Clin Endocrinol Metab. 2006 Aug;91(8):3024-33. Epub 2006 May 16.
Effects of testosterone supplementation on skeletal muscle fiber hypertrophy and satellite cells in community-dwelling older men.
Sinha-Hikim I, Cornford M, Gaytan H, Lee ML, Bhasin S.
Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University, Los Angeles, CA 90059, USA.
Abstract
OBJECTIVE: In this study, we determined the effects of graded doses of testosterone on muscle fiber cross-sectional area (CSA) and satellite cell number and replication in older men.
PARTICIPANTS: Healthy men, 60-75 yr old, received a long-acting GnRH agonist to suppress endogenous testosterone production and 25, 50, 125, 300, or 600 mg testosterone enanthate im weekly for 20 wk.
METHODS: Immunohistochemistry, light and confocal microscopy, and electron microscopy were used to perform fiber typing and quantitate myonuclear and satellite cell number in vastus lateralis biopsies, obtained before and after 20 wk of treatment.
RESULTS: Testosterone administration in older men was associated with dose-dependent increases in CSA of both types I and II fibers. Satellite cell number increased dose dependently at the three highest doses (3% at baseline vs. 6.2, 9.2, and 13.0% at 125, 300, and 600 mg doses, P < 0.05). Testosterone administration was associated with an increase in the number of proliferating cell nuclear antigen+ satellite cells (1.8% at baseline vs. 3.9, 7.5, and 13% at 125, 300, and 600 mg doses, P < 0.005). The expression of activated Notch, examined only in the 300-mg group (baseline, 2.3 vs. 9.0% after treatment, P < 0.005), increased in satellite cells after testosterone treatment. The expression of myogenin (baseline, 6.2 vs. 20.7% after treatment, P < 0.005), examined only in the 300-mg group, increased significantly in muscle fiber nuclei after testosterone treatment, but Numb expression did not change.
CONCLUSIONS: Older men respond to graded doses of testosterone with a dose-dependent increase in muscle fiber CSA and satellite cell number. Testosterone-induced skeletal muscle hypertrophy in older men is associated with increased satellite cell replication and activation.
PMID: 16705073 [PubMed - indexed for MEDLINE]
Testosterone-induced muscle hypertrophy is associated with an increase in satellite cell number in healthy, young men
Indrani Sinha-Hikim,1 Stephen M. Roth,2 Martin I. Lee,1 and Shalender Bhasin1
1Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California 90059; and 2Department of Human Genetics, University of Pittsburgh, Pittsburgh, Pennsylvamia 15261
Submitted 22 August 2002 ; accepted in final form 26 March 2003
ABSTRACT
Testosterone (T) supplementation in men induces muscle fiber hypertrophy. We hypothesized that T-induced increase in muscle fiber size is associated with a dose-dependent increase in satellite cell number. We quantitated satellite cell and myonuclear number by using direct counting and spatial orientation methods in biopsies of vastus lateralis obtained at baseline and after 20 wk of treatment with a gonadotropin-releasing hormone agonist and a 125-, 300-, or 600-mg weekly dose of T enanthate. T administration was associated with a significant increase in myonuclear number in men receiving 300- and 600-mg doses. The posttreatment percent satellite cell number, obtained by direct counting, differed significantly among the three groups (ANCOVA P < 0.000001); the mean posttreatment values (5.0 and 15.0%) in men treated with 300- and 600-mg doses were greater than baseline (2.5 and 2.5%, respectively, P < 0.05 vs. baseline). The absolute satellite cell number measured by spatial orientation at 20 wk (1.5 and 4.0/mm) was significantly greater than baseline (0.3 and 0.6/mm) in men receiving the 300- and 600-mg doses (P < 0.05). The change in percent satellite cell number correlated with changes in total (r = 0.548) and free T concentrations (r = 0.468). Satellite cell and mitochondrial areas were significantly higher and the nuclear-to-cytoplasmic ratio lower after treatment with 300- and 600-mg doses. We conclude that T-induced muscle fiber hypertrophy is associated with an increase in satellite cell number, a proportionate increase in myonuclear number, and changes in satellite cell ultrastructure.
J Clin Endocrinol Metab. 2006 Aug;91(8):3024-33. Epub 2006 May 16.
Effects of testosterone supplementation on skeletal muscle fiber hypertrophy and satellite cells in community-dwelling older men.
Sinha-Hikim I, Cornford M, Gaytan H, Lee ML, Bhasin S.
Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University, Los Angeles, CA 90059, USA.
Abstract
OBJECTIVE: In this study, we determined the effects of graded doses of testosterone on muscle fiber cross-sectional area (CSA) and satellite cell number and replication in older men.
PARTICIPANTS: Healthy men, 60-75 yr old, received a long-acting GnRH agonist to suppress endogenous testosterone production and 25, 50, 125, 300, or 600 mg testosterone enanthate im weekly for 20 wk.
METHODS: Immunohistochemistry, light and confocal microscopy, and electron microscopy were used to perform fiber typing and quantitate myonuclear and satellite cell number in vastus lateralis biopsies, obtained before and after 20 wk of treatment.
RESULTS: Testosterone administration in older men was associated with dose-dependent increases in CSA of both types I and II fibers. Satellite cell number increased dose dependently at the three highest doses (3% at baseline vs. 6.2, 9.2, and 13.0% at 125, 300, and 600 mg doses, P < 0.05). Testosterone administration was associated with an increase in the number of proliferating cell nuclear antigen+ satellite cells (1.8% at baseline vs. 3.9, 7.5, and 13% at 125, 300, and 600 mg doses, P < 0.005). The expression of activated Notch, examined only in the 300-mg group (baseline, 2.3 vs. 9.0% after treatment, P < 0.005), increased in satellite cells after testosterone treatment. The expression of myogenin (baseline, 6.2 vs. 20.7% after treatment, P < 0.005), examined only in the 300-mg group, increased significantly in muscle fiber nuclei after testosterone treatment, but Numb expression did not change.
CONCLUSIONS: Older men respond to graded doses of testosterone with a dose-dependent increase in muscle fiber CSA and satellite cell number. Testosterone-induced skeletal muscle hypertrophy in older men is associated with increased satellite cell replication and activation.
PMID: 16705073 [PubMed - indexed for MEDLINE]
THE-DET-OAK
IncreasedMyT @ ULV
Yea I just meant would the number change, if you were talking about tren, or anything that has a higher affinity to the AR, my question is would the total amount to saturate the receptors be less because of that higher affinity?
heavyiron
Community Veteran
Well, I think the practical application of using Tren at those doses kind of makes the question moot but I don't think anyone has the answer to your question. This is already a highly speculative topic brother. We are making assumptions based on preliminary data so I just don't feel comfortable speculating this much. But it is fun to dream...
heavyiron
Community Veteran
By the way, for anyone following here is the science that supports Tren's heightened binding affinity to the AR.
Steroids. 2010 Jun;75(6):377-89. Epub 2010 Feb 4.
Tissue selectivity and potential clinical applications of trenbolone (17beta-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity.
Yarrow JF, McCoy SC, Borst SE.
Geriatric Research, Education & Clinical Center, VA Medical Center, Gainesville, FL 32608, United States. jfyarrow@ufl.edu
Abstract
Recently, the development of selective androgen receptor modulators (SARMs) has been suggested as a means of combating the deleterious catabolic effects of hypogonadism, especially in skeletal muscle and bone, without inducing the undesirable androgenic effects (e.g., prostate enlargement and polycythemia) associated with testosterone administration. 17beta-Hydroxyestra-4,9,11-trien-3-one (trenbolone; 17beta-TBOH), a synthetic analog of testosterone, may be capable of inducing SARM-like effects as it binds to androgen receptors (ARs) with approximately three times the affinity of testosterone and has been shown to augment skeletal muscle mass and bone growth and reduce adiposity in a variety of mammalian species. In addition to its direct actions through ARs, 17beta-TBOH may also exert anabolic effects by altering the action of endogenous growth factors or inhibiting the action of glucocorticoids. Compared to testosterone, 17beta-TBOH appears to induce less growth in androgen-sensitive organs which highly express the 5alpha reductase enzyme (e.g., prostate tissue and accessory sex organs). The reduced androgenic effects result from the fact that 17beta-TBOH is metabolized to less potent androgens in vivo; while testosterone undergoes tissue-specific biotransformation to more potent steroids, dihydrotestosterone and 17beta-estradiol, via the 5alpha-reductase and aromatase enzymes, respectively. Thus the metabolism of 17beta-TBOH provides a basis for future research evaluating its safety and efficacy as a means of combating muscle and bone wasting conditions, obesity, and/or androgen insensitivity syndromes in humans, similar to that of other SARMs which are currently in development.
Published by Elsevier Inc.
PMID: 20138077 [PubMed - indexed for MEDLINE]
Steroids. 2010 Jun;75(6):377-89. Epub 2010 Feb 4.
Tissue selectivity and potential clinical applications of trenbolone (17beta-hydroxyestra-4,9,11-trien-3-one): A potent anabolic steroid with reduced androgenic and estrogenic activity.
Yarrow JF, McCoy SC, Borst SE.
Geriatric Research, Education & Clinical Center, VA Medical Center, Gainesville, FL 32608, United States. jfyarrow@ufl.edu
Abstract
Recently, the development of selective androgen receptor modulators (SARMs) has been suggested as a means of combating the deleterious catabolic effects of hypogonadism, especially in skeletal muscle and bone, without inducing the undesirable androgenic effects (e.g., prostate enlargement and polycythemia) associated with testosterone administration. 17beta-Hydroxyestra-4,9,11-trien-3-one (trenbolone; 17beta-TBOH), a synthetic analog of testosterone, may be capable of inducing SARM-like effects as it binds to androgen receptors (ARs) with approximately three times the affinity of testosterone and has been shown to augment skeletal muscle mass and bone growth and reduce adiposity in a variety of mammalian species. In addition to its direct actions through ARs, 17beta-TBOH may also exert anabolic effects by altering the action of endogenous growth factors or inhibiting the action of glucocorticoids. Compared to testosterone, 17beta-TBOH appears to induce less growth in androgen-sensitive organs which highly express the 5alpha reductase enzyme (e.g., prostate tissue and accessory sex organs). The reduced androgenic effects result from the fact that 17beta-TBOH is metabolized to less potent androgens in vivo; while testosterone undergoes tissue-specific biotransformation to more potent steroids, dihydrotestosterone and 17beta-estradiol, via the 5alpha-reductase and aromatase enzymes, respectively. Thus the metabolism of 17beta-TBOH provides a basis for future research evaluating its safety and efficacy as a means of combating muscle and bone wasting conditions, obesity, and/or androgen insensitivity syndromes in humans, similar to that of other SARMs which are currently in development.
Published by Elsevier Inc.
PMID: 20138077 [PubMed - indexed for MEDLINE]
simpllyhuge
New member
What Test level do you think 250 would get most people if you had to guess?
heavyiron
Community Veteran
It depends on several factors such as ester, time injected in relation to time blood drawn and duration the Testosterone has been used, etc.
However we know after 16 weeks of use that levels measured on average 1,345ng/dl ± 139ng/dl when blood was drawn 7 days after administering 300mg of enanthate.
Testosterone dose-response relationships in healthy young men
littlemaster
http://anabolicsteroidssa
I am confused that mostly people said that steroids is not good for health. But lot of companies and educated people use it. What is reason?
