AAS Research Mega Thread (not pro hormones)

I apologize in advance if I repost any studies already posted in this thread…theres a lot of information out there hahah


Effects of maturity on histopathological alteration after a growth promoter boldenone injection in rabbits

Boldenone is a derivative of the testosterone and it has dual effects on humans, directly and indirectly; directly as injection to build muscles and indirectly as through consuming meat of animals that where treated with boldenone. However, the action of these steroids on the liver, kidney and testes structure in immature animals still unclear, therefore, the aim of the present study was to investigate the effect of maturity on the intramuscular injection of boldenone undecylenate on the hepatic, renal and testicular structures. Thirty two New Zealand rabbits were divided into main groups (16 immature and 16 mature rabbits) and each main group is divided into four groups (4 animals each). Control group (G1) includes animals that injected intramuscularly with olive oil. Groups 2, 3 and 4 (G2; G3 and G4) include animals that receive one, two and three intramuscular injections of 5 mg/Kg body weight boldenone undecylenate dissected after 3, 6 and 9 weeks respectively. The present results showed that intramuscular injection of rabbits with boldenone has a marked adverse effects on the liver, kidney and testes tissues and this effects were more observed in immature than in mature rabbits and this histopathological alternations were increased with the increase the boldenone dose injection. Our results showed that; immature rabbits that receive boldenone showed disturbances of the hepatocytes radially arranged cords with multifocal hepatocellular vacuolations in the liver, glomerulus mass reduction with multifocal glomerular injury in the kidney and disturbances of the cycle of spermatogenesis in the testes. These findings suggested that misuse of growth promoter boldenone undecylenate may contribute to a continuously damage of the hepatic, renal and testicular function and structure that may lead to a hepatic, renal and genital progressive diseases so young people especially should be careful if they want to use such steroids to enhance their strength and endurance.

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Deterioration of glomerular endothelial surface layer and the alteration in the renal function after a growth promoter boldenone injection in rabbits.

Boldenone is an anabolic steroid developed for veterinary use. Recently, it is used by bodybuilders in both off-season and precontest, where it is well known for increasing vascularity while preparing for a bodybuilding contest. However, the side effect of this steroid on the human health is still unclear. Therefore, the present study was designed to investigate the possible effect of the growth promoter, boldenone undecylenate, on the function and structure of the rabbit's kidneys. A total of 36 adult New Zealand rabbits were divided into 4 groups. Control group includes animals that were injected intramuscularly with olive oil and dissected after 3 weeks. Three experimental groups include animals that receive one, two and three intramuscular injections of 5 mg/kg body weight boldenone, and dissected after 3, 6, and 9 weeks, respectively, and the interval of each dose of boldenone was 3 weeks. The biochemical analysis of the blood serum of treated rabbit showed a significant increase in the total protein, urea and creatinine concentrations, with a significant decrease in albumin/globulin (A/G) ratio. At the same time, a significant glomerulus mass reduction that accompanied with the expression of CD34, a marker for endothelial cells deterioration, was also determined. The incidence of the glomerulosclerosis was significantly increased compared with the control group (0.46 ± 0.05, p < 0.05). The glomerulosclerosis scores were 1.32 ± 0.10, 2.14 ± 0.11 and 3.02 ± 0.09 in groups 2, 3 and 4, respectively. These findings suggest that misuse of the boldenone undecylenate may contribute to the occurrence of a chronic renal injury that may lead to a progressive renal failure.



I thought this was worth posting as well. Its a bodybuilder research case study which includes eq. Please click the link below to see the full chart:
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The subject consumed an estimated daily average of 5699-7281 kcalories throughout all periods. Throughout all periods the percentage of calories from foodstuffs consisted of; protein: 19%-28%, carbohydrates: 51%-58%, fats: 19%-30%. Meals were usually spaced approximately 2.5 to 3 hours apart.

Period 1
The greatest lean body weight gain was seen the first ten days. The lean body mass gain of 8.9 lbs (0.988 lb / day) was undoubtedly due to the introduction of drugs. Oxymetholone (Anadrol) was used this period with an average administration of 55.6 mg / Daily for approximately 9 days.

Period 2
A substantially smaller gain in lean body weight was seen the second period consisting of approximately 14 days. The gain in lean body mass was only 2.9 lbs (0.207 lb / day). Beginning two days preceding the period, an average of 62.5 mg of Oxymetholone (Anadrol) was taken for four days. Also beginning the same time, 300 mg of Boldenone undecylenate (Equipoise) was administered every week. An average daily dosage of 60.7 mg / day was taken with both drugs combined.

Period 3
The third period reflected an acceptable gain in lean body mass when both Boldenone undecylenate (Equipoise) and Oxymetholone (Anadrol) were administered at an average dosage of 78.6 mg / daily. Beginning two days preceding the period, 300 mgs of Boldenone undecylenate (Equipoise) was administered every week and an average of 35.7 mgs of Oxymetholone (Anadrol) was taken daily in descending fashion ranging from 50 mg - 7.5 mg . In 14 days, 4.5 lbs (.321 lbs / day) in lean body mass was seen.

Period 4
A gain of only 1 lb (.066 lb / day) in lean body mass was seen the fourth period of 15 days. Three days preceding this period, suspected counterfeit Testosterone cypionate (Depo-Testosterone) and Nandrolone decanoate (Deca Durabolin) were administered. According to the concentrations indicated on their labels, 600 mgs. of Testosterone cypionate (Depo-Testosterone) and 175 mg of Nandrolone decanoate (Deca Durabolin) was administered. The subject felt and saw no effect after the first week then proceeded to administer 50 mgs of Stanozolol (Winstrol-V) every other day until the end of the period. Despite the greater than average dosage of Testosterone cypionate (Depo-Testosterone), the average daily dosage of all drugs in that period was only 65 mg / day.

Period 5
The fifth period lasted only 6 days. Three days preceding the period, 650 mgs of Boldenone undecylenate (Equipoise) were administered over three days, since one syringe could only hold 3 cc, or 150 mgs, only .4 lbs (.06 lbs / day) of lean body weight was seen with 108.33 mg / day of Equipoise.

Period 6
The sixth period, lasting 8 days, yielded a larger gain of 3.2 lbs (.4 lbs / day) in lean body mass. One day preceding the period, 100 mgs of Oxymetholone (Anadrol) was taken all but one day in which 50 mgs of Fluoxymesterone (Halotestin) was replaced out of lack of a reliable supply. So, an average of 87.5 mgs / day of Oxymetholone (Anadrol) and an average of 6.25 mgs / day of Fluoxymesterone (Halotestin) were taken during this period for a total of 93.75 mgs daily for both drugs.

Period 7
A greater dosage of Oxymetholone (Anadrol) was taken in the seventh period that lasted 7 days. Beginning three days preceding the period, 150 mg of Oxymetholone (Anadrol) was taken daily for the first 2 days proceeded by 200 mg of Oxymetholone (Anadrol) daily thereafter. A gain of 3.5 lbs ( .5 lbs / day) of lean body mass was made from an average daily dosage of 178.6 mgs of (Oxymetholone) Anadrol.

Period 8
The eighth period lasted 8 days. Two days preceding the period an daily average of 162.5 mgs of Oxymetholone (Anadrol) was administered daily in descending fashion for the full duration of the period. A loss of 1.5 lbs (-.188 lbs / day) of lean body weight became the result.

Period 9
A loss of lean body mass was also characteristic of the ninth period lasting 6 days. The day of the period, an average of 54.2 mg of Stanozolol (Winstrol-V) was administered daily throughout the period. Fluoxymesterone (Halotestin) was also taken the first three days in descending fashion, averaging only 15 mg for these few days. The average daily dosage for both drugs was only 61.6 mgs. A total of 2.6 lbs (-.433 lbs / day) of lean body mass was lost during this period. The dosage difference from the previous week did not seem to be significantly reduced. Suspicion may be placed on the characteristics of the descending drug program.

Period 10
The tenth period lasted 7 days. Beginning the day of the cycle day, an average of 57.1 mg of Oxymetholone (Anadrol) and 57.1 mg of (Stanozolol) Winstrol-V were taken daily throughout the period. Also beginning the same time, 50 mg of Primobolan Depot was administered for 5 days. Methenolone enanthate (Primobolan Depot) was taken daily in this manner out of convenience despite its longer acting quality. An average daily dosage of 157.1 mg of drugs were taken during this period. As a result, 4.8 lbs (.686 lbs / day) of lean body mass was obtained.

Period 11
The eleventh period lasted 7 days. Beginning the day of the period, an average of 114.3 mg of Oxymetholone (Anadrol) was taken daily. Also beginning the same time, 50 mg of Stanozolol (Winstrol-V) was taken daily except for the second and third days of the period. A daily average dosage of 150 mg was taken from both drugs. A loss of 1.6 lbs (-.229 lbs) of lean body weight was the result.

No Drugs were taken after one day before the physique competition. This was done because Anadrol taken preceding the show was thought to contribute to subcutaneous water retention. No other drug was taken due to convenience and the relatively small contribution an administration was thought to have the day preceding the show.

Final Week
Since fat reduction was not as a great of a concern the last week, the total caloric intake was increased slightly in attempt to allow adequate calories for recovery and increased glycogen stores. Resistive training was stopped four days before the show in effort to restore glycogen in the muscle. Walking and posing practice were continued. Posing with the aid of a mirror was greatly reduced. Walking was used more as a means of stress management than fat burning activity in the final days before the show. Three days before the show, an effort was made to reduce food volume and maintain an elevated caloric intake by eating less more often in order to reduce abdominal circumference caused by intestinal volume. In addition, foods suspected of causing gas and minor food allergies were eliminated. Foods containing added salt were discontinued two days before the show in effort to deplete subcutaneous water. Timing was crucial at this point since it was feared that a premature sodium depletion would trigger negative feedback from the body's receptors resulting in a retention of sodium by the body. Tap water was also replaced by distilled water two days before the show to insure a reduced sodium intake. Posing was increased two days before the show in effort to expel subcutaneous water. Water intake was increased the day before the show in attempt to inhibit Anti-diuretic Hormone produced in the body. Approximately six ounces of beer were consumed the evening before the show as to further inhibit Anti-diuretic hormone in effort to deplete subcutaneous water.

Competition Day A
Water was consumed sparingly upon arising the morning of the show to maintain the diuretic effects noted after slumber. A suppository laxative was used the morning of the show in effort to further reduce inter-intestinal volume. Water was consumed as desired approximately an hour or so before the morning prejudging. On the morning of the contest, a total body weight of 226 lbs was recorded from a scale used for competition weigh in. Minor cramping was experienced with virtually no effect upon posing performance. Moderate sweating was noted on stage with little hindrance on appearance. The subject won his weight class and the overall competition, therefore qualifying for national competition.

Period 12
The twelfth period lasted seven days. The day of the period, 150 mg of Winstrol-V was administered. No other administrations of Winstrol-V or any other drug was taken during this period in anticipation of possible drug testing. The physique contest discussed above was on the second day of this period. A loss of 1.4 lbs (-.2 lbs / day) of lean body mass was noted at the end of this period.

Period 13
Little data was recorded the thirteenth period which lasted five days. Approximately the same dietary and exercise modifications used before the last competition were practiced before the national competition. Abstinence from anabolic-androgenic steroids was continued throughout this period lasting up until four days prior to national competition. Defend (Power Distributors, Marina Del Rey, CA) was taken before drug testing as directed by the manufacturer. A "weigh-in" and a "random drug test" was scheduled three days prior to the event. The subject was not selected for testing, but was measured at 230 lbs on the scale used for official weigh in. On the same day, immediately after "weigh-in", 300 mg of Oxymetholone (Anadrol) was consumed throughout the remainder of the day. The following day, 200 mg of Oxymetholone (Anadrol) was consumed, followed by 150 mg the next day.

Competition Day B
Finally, 50 mg of Oxymetholone (Anadrol) was taken on the day of the show. No body weight was taken on the actual day of the show. Excessive sweating was experienced during prejudging which negatively affected appearance.

Period 14
The subject broke his contest diet soon after the conclusion of the final competition. A few days after the nationals, a body weight of 238 lbs was reported.
 
Identification of drostanolone and 17-methyldrostanolone metabolites produced by cryopreserved human hepatocytes

Methyldrostanolone (2alpha,17alpha-dimethyl-17beta-hydroxy-5alpha-androstan-3-one) was synthesized from drostanolone (17beta-hydroxy-2alpha-methyl-5alpha-androstan-3-one) and identified in commercial products. Cultures of cryopreserved human hepatocytes were used to study the biotransformation of drostanolone and its 17-methylated derivative. For both steroids, the common 3alpha- (major) and 3beta-reduced metabolites were identified by GC-MS analysis of the extracted culture medium and the stereochemistry confirmed by incubation with 3alpha-hydroxysteroid dehydrogenase. Structures corresponding to hydroxylated metabolites in C-12 (minor) and C-16 were proposed for other metabolites based upon the evaluation of the mass spectra of the pertrimethylsilyl (TMS-d(0) and TMS-d(9)) derivatives. Finally, on the basis of the GC-MS and (1)H NMR data and through chemical synthesis of the 17-methylated model compounds, structures could be proposed for metabolites hydroxylated in C-2. All the metabolites extracted from hepatocyte culture medium were present although in different relative amounts in urines collected following the administration to a human volunteer, therefore confirming the suitability of the cryopreserved hepatocytes to generate characteristic metabolites and study biotransformation of new steroids.

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Androgen Receptor CAG Repeats and Body Composition Among Ariaal Men

To determine population variation in the androgen receptor (AR) and its association with body composition in a subsistence population we sampled 87 settled and 65 nomadic males ages 20+ among the Ariaal of northern Kenya. Anthropometric measures included height, body mass index (BMI), fat free mass (FFM), upper arm muscle plus bone area (AMPBA), % body fat (%BF), suprailliac skinfold (SISF), and waist to hip ratio (WHR). Salivary testosterone (T) was determined from both morning (Am T) and afternoon (Pm T) samples. Hair roots were obtained for genotyping AR CAG repeat length. AR CAG repeat length did not vary between the two sub-groups (overall value = 22.6 ± 3.1). Multiple regression models, controlling for age and residence, indicate that Pm T was positively associated with all measures of body composition. AR CAG repeat length was a significant positive predictor of height, FFM % BF, SISF and waist circumference There was a significant negative Pm T by AR CAG repeat length interaction in predicting all measures but AMPBA. These findings provide evidence for population variation in AR CAG repeat length and suggest that both T and androgen receptor CAG length play a role in body composition in this extremely lean population.

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Here is a very nice FULL PDF for people looking to get a better viewpoint of the pharmacokinetic activities associated with AAS usage that want more than just an abstract.

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As I have included a decent amount of research into this video and have gotten great feedback on it, I wanted to post it up in here to simply help teach people how these anabolics work within our body.

[video=youtube;mzrMzp8636k]https://www.youtube.com/watch?v=mzrMzp8636k[/video]

I plan on doing multiple videos of this nature on the pharmacokinetics of PEDs.
 
Metabolism of Testosterone, Dihydrotestosterone, Estrone and Estradiol
Aede de Groot, Willem Koert

Testosterone is the most important androgenic-anabolic steroid. It is biosynthesized in the testes and per day about 4-10 mg of testosterone is produced by a grown up man. About 0.5 mg per day is produced in the adrenaline cortex of men and women.
Testosterone is converted to two other important hormones. It is reduced to dihydrotestosterone in specific tissues like the skin and the prostate and it is oxidized to estradiol. In men this oxidation mainly takes place in adipose tissue and in the testes. In women the biosynthesis of estradiol takes place in the ovaria.

Testosterone and dihydrotestosterone together are responsible for the typically male sex characteristics, but their function is different. In the adolescence testosterone induces the sex drive in men, enlargement of the penis, the production of sperm, increase of muscle mass and lowering of the voice, the so called anabolic effects.
Dihydrotestosterone is responsible for an increase of body hair, beard grow, acne, and at a later age for baldness and enlargement of the prostate. These are the androgenic effects.

Much research has been devoted to unravel the biosynthesis of steroid hormones, because promising medical applications were expected. Many reviews have appeared in the literature about the biosynthetis of the male and female sex hormones [1][2]. The main features of the biosynthetic pathways of testosterone, dihydrotestosterone, estrone and estradiol are know today as they are depicted in Schemes 1 and 2.
The biosynthesis of the sex hormones starts with the oxidation of the side chain of cholesterol, which is catalyzed by the enzyme cytochrome P450scc. This cytochrome P450 oxidizes the side chain on C20 and C22 by the introduction of two hydroxyl groups. After that the chain is broken in between these two atoms by the same enzyme, under formation of pregnenolone.
The next steps in the biosynthesis of testosterone can proceed via two different routes. Pregnenolone can be oxidised first by cytochrome P45017a to 17a-hydroxypregnenolone. This route is known as the 5-ene route because all biosynthetic intermediates in this route possess a D5-double bond.
The enzyme 3b-HSD also can convert pregnenolone first into progesterone by oxidation of the 3b-hydroxy group followed by a shift of the double bond from the C5-C6 to the C4-C5 position. This route is known as the 4-ene route because here all biosynthetic intermediates possess a D4-double bond.

Both pregnenolone and progesterone are accepted as substrate by the enzyme cytochrome P45017a. In both compounds a hydroxyl group is introduced in the 17a-position, as is indicated in the name of the enzyme. The rupture of the C17-C20 bond is catalyzed by the same enzyme. This results in the complete removal of the side chain under formation of a carbonyl group at C17. In this way 4-androstene-3,17-dione (A-dione) is obtained via the 4-ene route, and 3b-hydroxy-5-androstene-17-one (DHEA) via de 5-ene route. The acronyme DHEA originates from the old-fashioned name dehydroepiandrosterone for this compound. DHEA has a weak anabolic activity from itself.


The oxidation of the 3b-hydroxyl group and the shift of the D5-double bond to the D4-position, are also catalyzed by one enzyme, called 3b-hydroxy-steroid dehydrogenase/D5-D4-isomerase, or 3b-HSD.

The enzyme 3b-HSD first oxidizes the hydroxyl group at C3 to a carbonyl group and after that the same enzyme catalyzes the isomerisation of the double bond to the D4-position. This oxidation-isomerisation reaction proceeds in only one direction. In principle this enzyme accepts all compounds in the left column of Scheme 1 as a substrate but pregnenolone and DHEA are the main substrates. This is indicated in Scheme 1 with bold arrows.
The transformation of A-dione into testosterone now only needs the reduction of the C17 carbonyl group to a 17b-hydroxyl group. This reaction is catalysed again by a dehydrogenase enzyme, called 17b-hydroxy-steroid dehydrogenase or 17b-hydroxysteroid oxidoreductase or simply 17b-HSD. This enzyme adds two H-atoms to the carbonyl group, one to the O-atom and the other one to the bottom of C17, which results in the b-position of the hydroxyl group.
In several tissues testosterone is converted into 5a-dihydrotestosterone (DHT) by the enzyme 3-oxo-a-steroid-D4-dehydrogenase, or 5AR. The indication “5a-steroid-D4 ” in the name of this enzyme shows that the H-atom is delivered to the bottom, the a-side, of the molecule of the D4-double bond, as is indicated in the structural formula of dihydrotestosterone by a hatched bond. Also this reaction proceeds in only one direction.
The estrogens estrone and estradiol are, together with progesterone, the most important female sex hormones. The estrogens are responsible for the typical female sex features, such as the growth and development of the vagina, the uterus, the Fallopian tubes, the development of breasts and the increase of fat tissue. Together with progesterone they regulate the menstruation cycle. The activity of estradiol is much larger than that of estrone. Both compounds can be interconverted by the enzyme 17b-HSD.


The biosynthesis of the female sex hormones starts from A-dione and can proceed by two different routes (see Scheme 2). The C17 carbonyl group in A-dione can be reduced first to a 17b-hydroxyl group under formation of testosterone, followed by oxidation and removal of the C19 methyl group and aromatisation of ring A.
The oxidation and removal of the C19 methyl group and the aromatisation of ring A can take place also first, under formation of estrone. Reduction of the carbonyl group at C17 then gives estradiol.
The oxidation of the C19 methyl group is catalyzed by a complex of cytochrome P450 enzymes, indicated with the code P450aromatase or simply as aromatase. The methyl group is first oxidized to a hydroxyl group and than to a carbonyl group (an aldehyde). The removal of this group together with a H-atom from C1 than leads to aromatisation of ring A. An important step in this aromatisation process is the fission of the C10-C19 bond. Also this reaction proceeds in only one direction. In chapter 15 more will be explained about aromatisation of anabolic steroids.


In schemes 1 and 2 we have seen that testosterone can be metabolized in two ways. In Scheme 1 the reductive metabolism leading to dihydrotestosterone and in Scheme 2 the oxidative metabolism to estradiol is shown. The reduction of testosterone takes place in target tissues like the prostate and the skin and of course metabolism takes place in the liver. In male a very small part (0.2%) of the testosterone is converted into estradiol. This process mainly takes place in adipose tissue and for about 20% in the testes.
The metabolisme of testosterone and dihydrotestosterone takes place for 90% in the liver. There reductases and dehydrogenases catalyse the reactions of the D4-double bond, the C3-carbonyl group and the C17-hydroxyl group. Finally the hydroxyl groups are connected to glucuronic acid or sulphate, followed by excretion with the urine [3] [4].
The reduction of the D4-double bond is not an equilibrium reaction and goes only in one direction to give a 5a and/or a 5b-steroid skeleton (see Scheme 3). The ezyme 5a-reductase is especially active in the prostate giving 5a-dihydrotestosterone. In the liver 5a- and 5b-reductases both are active and convert testosterone and other steroids into 5a- and 5bsteroid skeletons in ratios that depend on the structure of the steroid.
An example is the different ratio of 5a- and 5b-reduction products in testosterone and A-dione. The difference in their structures is that testosterone has a C17b-hydroxyl group and A-dione has a C17-carbonyl group. In testosterone the ratio between 5b : 5a-reduction products is 87 : 13. In A-dione this ratio is 53 : 47 (see Scheme 3) [3]. In other steroids this ratio can be completely different. There is mostly a preference for 5b-reduction.


After reduction of the D4-double bond often a quick reduction of the C3-carbonyl group is observed. In the 5a-steroids there is a preference for reduction to the 3b-hydroxyl compounds. In the 5b-steroids mostly reduction to the 5a-hydroxyl compounds takes place.
The C3-and C17-dehydrogenases catalyse reversible reactions, thus reactions that can proceed in two directions. The C3-dehydrogenases can reduce the C3-carbonyl group to 3a- or 3b-hydroxyl groups, which both can be oxidized again to a carbonyl group. The C17-dehydrogenases oxidise the 17b-hydroxyl group to a carbonyl group, which can be reduced again to a 17b- or a 17a-hydroxyl group.
Finally a molecule of glucuronic acid is connected to the hydroxyl groups at C3, C17 or both by an enzyme called glucuronosyl transferase (UGT) [5]. About 10% of the hydroxyl groups are converted into sulfates by sulfatases. Both groups enhance the polarity of the whole molecule considerably and in this way the apolar steroids become soluble in water and can be excreted with the urine.
In Scemes 4 and 5 a number of the possible metabolic reactions of testosterone and dihydrotestosterone are depicted. The most important excretion products are 3a-hydroxy-5b-andronstane-17-one (also called etiocholanolone) and 3a-hydroxy-5a-androstane-17-one (also called androsterone). They are mostly excreted as glucuronides. These compounds are enclosed in a frame in schemes 4 and 5.


The other possible metabolites have been found in the urine in only minor concentrations. These are 5a- or 5b-reduced steroids with 3a- or 3b-hydroxylgroups, 17 carbonyl groups and 17a- or 17b-hydroxyl groups. These compounds are depicted only partly in schemes 4 and 5.
The metabolisme of orally taken testosterone is fast. About 90% of the hormone is already metabolized before it reaches the bloodstream. After that the half-life of testosterone is less then 30 minutes, which means that the concentration halves within every half hour. It is therefore not a surprise that many researchers have investigated other ways of administration.


In the case of testosterone solutions for this problem have been found in the use of esters. These derivatives are converted slowly into free testosterone by esterases. Other solutions are the application of plasters or crèmes which slowly release testosterone directly in the bloodstream. As soon as the synthetic testosterone reaches the blood, it is metabolised quickly again, which necessitates a constant supply.
Chemists also can change the structure of the steroid a bit so that metabolism is slowed down or prevented. These possibilities have been investigated extensively and have been directed toward the development of orally active anabolic steroids. Also enhanced activity and a better separation between anabolic and androgenic effects are still under investigation.

[1] Brown, G.D. Natural Product Reports (1998) 661-665.
[2] Brueggemeier R.W. Encyclopedia of Molecular Cell Biology and Molecular Medicine Vol 13, 1-69.
[3] Schanzer W. Clinical Chemistry (1996) 42, 1101-1020.
[4] Van Eenoo P., Delbeeke F.T. J. of Steroid Biochem. and Mol. Biochem. (2006) 101, 161-178.
[5] Belanger A., Pelletier G., Labrie F., Barbier O. and Chouinard S. Trends in Endocrin. and Metab. (2003) 14, 473-479
 
Clomiphene Citrate Effects on Testosterone/Estrogen Ratio in Male Hypogonadism

Ahmad Shabsigh, MD 1 , Young Kang, MD 1 , Ridwan Shabsign, MD 1 , Mark Gonzalez, MD 1 , Gary Liberson, MD 1 , Harry Fisch, MD 1 , and Erik Goluboff, MD 1
1 Department of Urology, NY Presbyterian Medical Center, New York, NY, USA
Correspondence to Harry Fisch, MD, 944 Park Ave, New York, NY 10020, USA. Tel: 212-879-0800; Fax: 212-988-1634; E-mail: [email protected]
Copyright Blackwell Publishing Ltd 2005

ABSTRACT

Aim. Symptomatic late-onset hypogonadism is associated not only with a decline in serum testosterone, but also with a rise in serum estradiol. These endocrine changes negatively affect libido, sexual function, mood, behavior, lean body mass, and bone density. Currently, the most common treatment is exogenous testostosterone therapy. This treatment can be associated with skin irritation, gynecomastia, nipple tenderness, testicular atrophy, and decline in sperm counts. In this study we investigated the efficacy of clomiphene citrate in the treatment of hypogonadism with the objectives of raising endogenous serum testosterone (T) and improving the testosterone/estrogen (T/E) ratio.

Methods. Our cohort consisted of 36 Caucasian men with hypogonadism defined as serum testosterone level less than 300 ng/dL. Each patient was treated with a daily dose of 25 mg clomiphene citrate and followed prospectively. Analysis of baseline and follow-up serum levels of testosterone and estradiol levels were performed.

Results. The mean age was 39 years, and the mean pretreatment testosterone and estrogen levels were 247.6 ± 39.8 ng/dL and 32.3 ± 10.9, respectively. By the first follow-up visit (4–6 weeks), the mean testosterone level rose to 610.0 ± 178.6 ng/dL (P < 0.00001). Moreover, the T/E ratio improved from 8.7 to 14.2 (P < 0.001). There were no side effects reported by the patients.

Conclusions. Low dose clomiphene citrate is effective in elevating serum testosterone levels and improving the testosterone/estadiol ratio in men with hypogonadism. This therapy represents an alternative to testosterone therapy by stimulating the endogenous androgen production pathway. Shabsigh A, Kang Y, Shabsign R, Gonzalez M, Liberson G, Fisch H, and Goluboff E. Clomiphene citrate effects on testosterone/estrogen ratio in male hypogonadism. J Sex Med 2005;2:716–721.
 
I love this thread. In case you were wondering, it is still very much appreciated!

Glad you do brother!

I appreciate the kind words! I just got so overrun with client programming the past week I didnt have much time to update but I'll make sure to keep it coming!
 
The effects of catabolic and anabolic steroids on amino acid incorporation by skeletal-muscle ribosomes

A method is described for the routine isolation of ribosomes from small quantities of skeletal muscle that have been homogenized with the Ultra-Turrax tissue disintegrator. 2. Ribosomes prepared by this method from rats receiving triamcinolone acetonide or rabbits receiving cortisone acetate show a marked fall in their ability to incorporate amino acids when compared with ribosomes from control animals. 3. This fall in activity can be partially prevented in rats by pretreating the animals with an anabolic steroid, steroid 36644-Ba. 4. Testosterone (5mg./kg.) administered to rabbits in conjunction with cortisone acetate is not effective in maintaining ribosomal activity. However, steroid 36644-Ba at one-tenth of an equiandrogenic dose (0·05mg./kg.) is extremely effective. 5. The results with ribosomes isolated from rabbits support the concept that steroid 36644-Ba and possibly all anabolic steroids have an ability to counteract the catabolic action of corticosteroids that is greater than their androgenic activity would suggest.

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Comparison of the effects of high dose testosterone and 19-nortestosterone to a replacement dose of testosterone on strength and body composition in normal men.

We examined the extent to which supraphysiological doses of androgen can modify body composition and strength in normally virilized men. In doubly blind tests, 30 healthy young men received testosterone enanthate (TE) or 19-nortestosterone decanoate (ND), at 100 mg/wk or 300 mg/wk for 6 weeks. The TE-100 mg/wk group served as replacement dose comparison, maintaining pretreatment serum testosterone levels, while keeping all subjects blinded to treatment, particularly through reduction in testicular volumes. Isokinetic strength measurements were made for the biceps brachii and quadriceps femoris muscle groups before treatment and 2-3 days after the 6th injection. Small improvements were noted in all groups but the changes were highly variable; a trend to greater and more consistent strength gain occurred in the TE-300 mg/wk group. There was no change in weight for TE-100 mg/wk but an average gain of 3 kg in each of the other groups. No changes in 4 skinfold thicknesses or in estimated percent body fat were observed. Of 15 circumferences, significant increases were observed only for men receiving TE-300 mg/wk (shoulders) and ND-300 mg/wk (shoulders and chest). The data suggest that high dose androgens increase body mass and may increase strength in normal men but, except for a consistent weight gain with greater than replacement doses, the detectable changes were highly variable and relatively small, especially in comparison to the significant alterations which were observed for other markers of androgen action.
 
Anabolic-androgenic steroid interaction with rat androgen receptor in vivo and in vitro: a comparative study.

Anabolic steroids are synthetic derivatives of testosterone and are characterized by their ability to cause nitrogen retention and positive protein metabolism, thereby leading to increased protein synthesis and muscle mass. There are disagreements in the literature in regards to the interaction of anabolic steroids with the androgen receptor (AR) as revealed by competitive ligand binding assays in vitro using cytosolic preparations from prostate and skeletal muscle. By use of tissue extracts, it has been shown that some anabolic steroids have binding affinities for the AR that are higher than that of the natural androgen testosterone, while others such as stanozolol and methanedienone have significantly lower affinities as compared with testosterone. In this study we show that stanozolol and methanedienone are low affinity ligands of the rat recombinant AR as revealed by a ligand binding assay in vitro, however, based on a cell-based AR-dependent transactivation assay, they are potent activators of the AR. We also show that a single injection of stanozolol and methanedienone causes a rapid cytosolic depletion of AR in rat skeletal muscle. Based on these results, we conclude that anabolic steroids with low affinity to AR in vitro, can in fact in vivo act on the AR to cause biological responses
 
Pharmacokinetics and Pharmacodynamics of Nandrolone Esters in Oil Vehicle: Effects of Ester, Injection Site and Injection Volume

We studied healthy men who underwent blood sampling for plasma nandrolone, testosterone and inhibin measurements before and for 32 days after a single i.m. injection of 100 mg of nandrolone ester in arachis oil. Twenty-three men were randomized into groups receiving nandrolone phenylpropionate (group 1, n = 7) or nandrolone decanoate (group 2, n = 6) injected into the gluteal muscle in 4 ml of arachis oil vehicle or nandrolone decanoate in 1 ml of arachis oil vehicle injected into either the gluteal (group 3, n = 5) or deltoid (group 4,n = 5) muscles. Plasma nandrolone, testosterone and inhibin concentrations were analyzed by a mixed-effects indirect response model. Plasma nandrolone concentrations were influenced (P < .001) by different esters and injection sites, with higher and earlier peaks with the phenylpropionate ester, compared with the decanoate ester. After nandrolone decanoate injection, the highest bioavailability and peak nandrolone levels were observed with the 1-ml gluteal injection. Plasma testosterone concentrations were also influenced (P < .001) by the ester and injection site, with the most rapid, but briefest, suppression being due to the phenylpropionate ester, whereas the most sustained suppression was achieved with the 1-ml gluteal injection. Plasma inhibin concentrations were also significantly influenced by injection volume and site, with the lowest nadir occurring after the nandrolone decanoate 1-ml gluteal injection. Thus, the bioavailability and physiological effects of a nandrolone ester in an oil vehicle are greatest when the ester is injected in a small (1 ml vs. 4 ml) volume and into the glutealvs. deltoid muscle. We conclude that the side-chain ester and the injection site and volume influence the pharmacokinetics and pharmacodynamics of nandrolone esters in an oil vehicle in men.
 
^very interesting...
Thanks for keeping this thread kicking so well man
 
^very interesting...
Thanks for keeping this thread kicking so well man

I'm glad people are enjoying it!

And just a quick note…I have implemented the specific injection sites for a couple of my clients utilizing nandrolone and the specific sites proved to be more beneficial for them than their previous usage of nandrolone while only utilizing quadricep injections….obviously not every variable was 100% the exact same between both cycles but the difference makes it promising
 
Clomiphene Citrate Effects on Testosterone/Estrogen Ratio in Male Hypogonadism

Ahmad Shabsigh, MD 1 , Young Kang, MD 1 , Ridwan Shabsign, MD 1 , Mark Gonzalez, MD 1 , Gary Liberson, MD 1 , Harry Fisch, MD 1 , and Erik Goluboff, MD 1
1 Department of Urology, NY Presbyterian Medical Center, New York, NY, USA
Correspondence to Harry Fisch, MD, 944 Park Ave, New York, NY 10020, USA. Tel: 212-879-0800; Fax: 212-988-1634; E-mail: [email protected]
Copyright Blackwell Publishing Ltd 2005

ABSTRACT

Aim. Symptomatic late-onset hypogonadism is associated not only with a decline in serum testosterone, but also with a rise in serum estradiol. These endocrine changes negatively affect libido, sexual function, mood, behavior, lean body mass, and bone density. Currently, the most common treatment is exogenous testostosterone therapy. This treatment can be associated with skin irritation, gynecomastia, nipple tenderness, testicular atrophy, and decline in sperm counts. In this study we investigated the efficacy of clomiphene citrate in the treatment of hypogonadism with the objectives of raising endogenous serum testosterone (T) and improving the testosterone/estrogen (T/E) ratio.

Methods. Our cohort consisted of 36 Caucasian men with hypogonadism defined as serum testosterone level less than 300 ng/dL. Each patient was treated with a daily dose of 25 mg clomiphene citrate and followed prospectively. Analysis of baseline and follow-up serum levels of testosterone and estradiol levels were performed.

Results. The mean age was 39 years, and the mean pretreatment testosterone and estrogen levels were 247.6 ± 39.8 ng/dL and 32.3 ± 10.9, respectively. By the first follow-up visit (4–6 weeks), the mean testosterone level rose to 610.0 ± 178.6 ng/dL (P < 0.00001). Moreover, the T/E ratio improved from 8.7 to 14.2 (P < 0.001). There were no side effects reported by the patients.

Conclusions. Low dose clomiphene citrate is effective in elevating serum testosterone levels and improving the testosterone/estadiol ratio in men with hypogonadism. This therapy represents an alternative to testosterone therapy by stimulating the endogenous androgen production pathway. Shabsigh A, Kang Y, Shabsign R, Gonzalez M, Liberson G, Fisch H, and Goluboff E. Clomiphene citrate effects on testosterone/estrogen ratio in male hypogonadism. J Sex Med 2005;2:716–721.
alexb13
 
Nitrogen metabolism in cockerels treated with 17-α-methyl-17-β-hydroxyandrosta-Δ1, 4-3-one (methandrostenolone)

Intramuscular administrations of a saline suspension of 17-α-methyl-17-β-hydroxyandrosta-Δ1, 4-3-one (methandrostenolone) ranging from 0.25 to 10 mg per kilogram body weight per day were given to noncastrated White Rock cockerels from the fifth to the seventh week of age. It was found that the anabolic response to this steroid in chicks was similar to that of other androgens. Excessive dosages (1.25 mg per kilogram per day) resulted in slower gains in body weight, while moderate dosages (0.50 mg per kilogram per day) produced small but significant increases in weight over saline-injected controls. Although not as clearly defined, a similar pattern was observed in retention of nitrogen. Pectoralis muscle weights were depressed with 2.50 mg per kilogram per day while 5.00 mg per kilogram per day was required to reduce semi-membranosus weights. In general these reductions in muscle mass by excessive administration of the steroid could be accounted for by the lower body weights; however, the reductions in pectoralis weight at the 10 mg per kilogram per day dose level were greater than could be accounted for by correction for the lower body weight. Concentration of nitrogen in muscle or the percentage of water were not significantly changed at the dosages employed. Levels of the hormone sufficient to induce significant gains in weight and nitrogen retention also caused noticeable changes in sexual characteristics, including increased comb weight and maturation of the germinal epithelium within the seminiferous tubules.
 
BeastFitness
with clomid study just to Clarify would 25mg work as pct for potent ds/ph ?
Sorry I know this strict injectable aas.
also what's the reason or why 50/50/25/25 is protocol is the most recommended .
 
BeastFitness
with clomid study just to Clarify would 25mg work as pct for potent ds/ph ?
Sorry I know this strict injectable aas.
also what's the reason or why 50/50/25/25 is protocol is the most recommended .

I understand your desire for answers but please don't derail threads when a simple private message would have sufficed! Just board courtesy.

PM'd
 
Isn't there a thread specifically for PH/DS info?
 
BeastFitness
with clomid study just to Clarify would 25mg work as pct for potent ds/ph ?
Sorry I know this strict injectable aas.
also what's the reason or why 50/50/25/25 is protocol is the most recommended .

I understand your desire for answers but please don't derail threads when a simple private message would have sufficed! Just board courtesy.

PM'd

Isn't there a thread specifically for PH/DS info?

My apologies I goofed.

No worries! I'll shoot you a PM brother!
 
EFFECT OF AN ANABOLIC STEROID (METHANDIENONE) ON THE METABOLISM OF CORTISOL IN THE HUMAN

Possible mechanisms whereby the anabolic steroid methandienone lowers the urinary excretion of 17-KS and 17-OHCS have been studied in eight patients. Administration of the drug was associated with a delayed catabolism of infused cortisol and of endogenous cortisol, and a fall in cortisol production rate. In several patients, treatment was accompanied by a rise in certain serum enzyme levels and abnormal bromsulpthalein retention, but in others, these liver function tests were unaffected. Methandienone may thus inhibit the hepatic detoxification of cortisol without necessarily inducing changes in conventional liver function tests. The suppression of adrenocortical secretion was considered to be in part secondary to the effect of delayed cortisol catabolism, but evidence is also given suggesting a direct effect of the drug on the hypothalamus or pituitary, inhibiting the production or release of ACTH.

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Question in here for any UK guys/ people who've travelled to UK on cycle -
Starting a cycle 2moro -
Have to travel to UK next Wednesday -
Just wondering what it's like bringing orals in??
I'll be bringing basics -
Oral - enough for 2 days - which will equate to 2 pills
Plus cycle support:
Ar1macare Pro.
MK-677
Melatonin
Hopefully won't need to be bringing any nolva or exem at that stage.
Any thoughts/experiences??
Can PM me :)
Thanks!!!
 
Question in here for any UK guys/ people who've travelled to UK on cycle -
Starting a cycle 2moro -
Have to travel to UK next Wednesday -
Just wondering what it's like bringing orals in??
I'll be bringing basics -
Oral - enough for 2 days - which will equate to 2 pills
Plus cycle support:
Ar1macare Pro.
MK-677
Melatonin
Hopefully won't need to be bringing any nolva or exem at that stage.
Any thoughts/experiences??
Can PM me :)
Thanks!!!

Sorry brother! Research only thread ;)
 
Effects of growth promoter Boldenone undecylenate on weaned male lambs

This study aimed to observe the effects of an anabolic androgenic synthetic commercial steroid (Boldenone, BOL) on the growth performance of prepubertal male lambs. Lambs were divided into three equal groups (n=4), the first group injected 5mg boldenone, the second group injected 2.5 mg and the third one injected olive oil served as control. All treated groups received 5 injections at three week interval. Blood samples and body weight were taken until the seventh week after last injection. Blood serum total proteins, albumin, urea, total cholesterol and high density lipoproteins (HDL), ALT and AST and creatinine were recorded in addition to some whole blood haemogram parameters. Testosterone, T3 and T4 were assayed. The results indicated a significant increase in body gain in treated groups, total proteins and haemoglonbin with a decrease in urea. An insignificant increase in testosterone was recorded in both treated groups. The study proved that boldenone improved the performance of male lambs and treated lambs reached puberty earlier than control.

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I think people should be brave and drop requests for educational & study based AAS questions too

We can do our best to dig up answers.

Hard to remember what hasn't been covered yet though...

Have we done comparative studies on androgenic/anabolic effects?
Would be nice to find comparative lean mass growth between a group on a more anabolic vs. More androgenic compound.

1RM changes too, as one may think the androgenic compounds offer more strength

I'd also love to see study on protein turnover rates, and an approximation of how much additional protein one should add in while "on"
 
Any specific studies pertaining to trestolone (other than for its clinical purpose as male birth control).

Any specific studies regarding EQ and its effects on collagen synthesis? Most people claim its effects on joints/tendons to be purely myth, slim to none. No real world / obvious effects.
 
Any info on women using any compounds; changes in health markers, observed virilization (temporary and permanent), anything really.

Feel like I have a grasp on both typical anavar and anadrol protocols for ladies but would be very interesting to see human studies on testosterone (all esters) and primobolan depot in women.
 
Any specific studies pertaining to trestolone (other than for its clinical purpose as male birth control).

Any specific studies regarding EQ and its effects on collagen synthesis? Most people claim its effects on joints/tendons to be purely myth, slim to none. No real world / obvious effects.

It doesn't cross the junction/bridge making the collagen synthesis aspects irrelevant.
 
I think people should be brave and drop requests for educational & study based AAS questions too

We can do our best to dig up answers.

Hard to remember what hasn't been covered yet though...

Have we done comparative studies on androgenic/anabolic effects?
Would be nice to find comparative lean mass growth between a group on a more anabolic vs. More androgenic compound.

1RM changes too, as one may think the androgenic compounds offer more strength

I'd also love to see study on protein turnover rates, and an approximation of how much additional protein one should add in while "on"

Any specific studies pertaining to trestolone (other than for its clinical purpose as male birth control).

Any specific studies regarding EQ and its effects on collagen synthesis? Most people claim its effects on joints/tendons to be purely myth, slim to none. No real world / obvious effects.

Any info on women using any compounds; changes in health markers, observed virilization (temporary and permanent), anything really.

Feel like I have a grasp on both typical anavar and anadrol protocols for ladies but would be very interesting to see human studies on testosterone (all esters) and primobolan depot in women.

It doesn't cross the junction/bridge making the collagen synthesis aspects irrelevant.


I LOVE THE REQUESTS!!!

Perfect! I'll keep an on going list! I'll try and get some today/tomorrow. Many clients in prep right now AND grad school is coming to a close so time is pretty limited lately haha
 
We appreciate whatever you can contribute, on your own time! Thank you sir

As long as people appreciate it I'll keep doing it! :)
 
A COMPARATIVE STUDY OF THE ANABOLIC AND ANDROGENIC EFFECTS OF VARIOUS STEROIDS

A series of 14 anabolic-androgenic agents was compared for androgenic and anabolic activities; they included: testosterone propionate; testosterone; 17α-methyltestosterone; Δ1-testosterone; Δ1-methyltestosterone; 4,5α-dihydrotestosterone; 2-hydroxymethylene-17α-methyl-4,5α-dihydrotestosterone; 17β-hydroxy-17α-methylandrostano (3,2-c) pyrazole; 1-methyl-Δ1-4,5α-dihydrotestosterone, as the acetate and the enanthate; 19-nortestosterone; 17α-ethyl-19-nortestosterone; 19-nortestosterone, β-phenylpropionate, and 13β,17α-diethyl-17β-hydroxy-4-gonen-3-one. Myotrophic and androgenic potencies were based upon levator ani muscle and ventral prostate responses of young, castrated, male rats (Hershberger test). Anabolic evaluations were supplemented by studies of body growth acceleration in young, intact, male rats. 13β,17α-Diethyl-17β-hydroxy-4-gonen-3-one (Wy 3475) was the most potent myotrophic agent of the series; in addition, it produced acceleration of body growth at a dose of 300 μg, a lower dose than that required for any of the other compounds examined. Androgenicity of this compound was low; therefore, it showed a marked separation of androgenic and anabolic effects.

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Effects of Long Term Supplementation of Anabolic Androgen Steroids on Human Skeletal Muscle

The effects of long-term (over several years) anabolic androgen steroids (AAS) administration on human skeletal muscle are still unclear. In this study, seventeen strength training athletes were recruited and individually interviewed regarding self-administration of banned substances. Ten subjects admitted having taken AAS or AAS derivatives for the past 5 to 15 years (Doped) and the dosage and type of banned substances were recorded. The remaining seven subjects testified to having never used any banned substances (Clean). For all subjects, maximal muscle strength and body composition were tested, and biopsies from the vastus lateralis muscle were obtained. Using histochemistry and immunohistochemistry (IHC), muscle biopsies were evaluated for morphology including fiber type composition, fiber size, capillary variables and myonuclei. Compared with the Clean athletes, the Doped athletes had significantly higher lean leg mass, capillary per fibre and myonuclei per fiber. In contrast, the Doped athletes had significantly lower absolute value in maximal squat force and relative values in maximal squat force (relative to lean body mass, to lean leg mass and to muscle fiber area). Using multivariate statistics, an orthogonal projection of latent structure discriminant analysis (OPLS-DA) model was established, in which the maximal squat force relative to muscle mass and the maximal squat force relative to fiber area, together with capillary density and nuclei density were the most important variables for separating Doped from the Clean athletes (regression  =  0.93 and prediction  =  0.92, p<0.0001). In Doped athletes, AAS dose-dependent increases were observed in lean body mass, muscle fiber area, capillary density and myonuclei density. In conclusion, long term AAS supplementation led to increases in lean leg mass, muscle fiber size and a parallel improvement in muscle strength, and all were dose-dependent. Administration of AAS may induce sustained morphological changes in human skeletal muscle, leading to physical performance enhancement.

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The space between the joint itself.

Oh I see. So the compound doesn't cross this junction, is this what you're saying? I always thought that it's effects are receptor mediated, which would signal the body in general to produce collagen (not site specific). But you're saying that the compound needs to be reaching the joint itself for it to work?
 
Oh I see. So the compound doesn't cross this junction, is this what you're saying? I always thought that it's effects are receptor mediated, which would signal the body in general to produce collagen (not site specific). But you're saying that the compound needs to be reaching the joint itself for it to work?

In a nutshell, yes. Application is far more important than raw (mainly inapplicable) data.
 
I'm not sure what you mean by junction/bridge?

The space between the joint itself.

Oh I see. So the compound doesn't cross this junction, is this what you're saying? I always thought that it's effects are receptor mediated, which would signal the body in general to produce collagen (not site specific). But you're saying that the compound needs to be reaching the joint itself for it to work?

In a nutshell, yes. Application is far more important than raw (mainly inapplicable) data.

^^^THIS x10000!!!!

I love my research. I post it up because I still feel its beneficial to try and learn the most about everything within our lifestyle as there can always be takeaways from them. But ACTUAL application cannot be replicated in a study to have it match our physique lifestyle.

Gutter, do you have joint issues?
 
^^^THIS x10000!!!!

I love my research. I post it up because I still feel its beneficial to try and learn the most about everything within our lifestyle as there can always be takeaways from them. But ACTUAL application cannot be replicated in a study to have it match our physique lifestyle.

Gutter, do you have joint issues?

I'm know they aren't steroids but could we see some research on tb-500 and bcp-157?
 
Cellular and molecular mechanisms responsible for the action of testosterone on human skeletal muscle. A basis for illegal performance enhancement.


Kadi F. Br J Pharmacol. 2008.


Abstract
The popularity of testosterone among drug users is due to its powerful effects on muscle strength and mass. Important mechanisms behind the myotrophic effects of testosterone were uncovered both in athletes using steroids for several years and in short-term controlled studies. Both long-term and short-term steroid usage accentuates the degree of fibre hypertrophy in human skeletal muscle by enhancing protein synthesis. A mechanism by which testosterone facilitates the hypertrophy of muscle fibres is the activation of satellite cells and the promotion of myonuclear accretion when existing myonuclei become unable to sustain further enhancement of protein synthesis. Interestingly, long-term steroid usage also enhances the frequency of fibres with centrally located myonuclei, which implies the occurrence of a high regenerative activity. Under the action of testosterone, some daughter cells generated by satellite cell proliferation may escape differentiation and return to quiescence, which help to replenish the satellite cell reserve pool. However, whether long-term steroid usage induces adverse effects of satellite cells remains unknown. Testosterone might also favour the commitment of pluripotent precursor cells into myotubes and inhibit adipogenic differentiation. The effects of testosterone on skeletal muscle are thought to be mediated via androgen receptors expressed in myonuclei and satellite cells. Some evidence also suggests the existence of an androgen-receptor-independent pathway. Clearly, testosterone abuse is associated with an intense recruitment of multiple myogenic pathways. This provides an unfair advantage over non-drug users. The long-term consequences on the regenerative capacity of skeletal muscle are unknown.

PMID 18414389 [PubMed - indexed for MEDLINE] PMCID PMC2439525
 
I'm know they aren't steroids but could we see some research on tb-500 and bcp-157?

I'll post up in a different thread

Cellular and molecular mechanisms responsible for the action of testosterone on human skeletal muscle. A basis for illegal performance enhancement.


Kadi F. Br J Pharmacol. 2008.


Abstract
The popularity of testosterone among drug users is due to its powerful effects on muscle strength and mass. Important mechanisms behind the myotrophic effects of testosterone were uncovered both in athletes using steroids for several years and in short-term controlled studies. Both long-term and short-term steroid usage accentuates the degree of fibre hypertrophy in human skeletal muscle by enhancing protein synthesis. A mechanism by which testosterone facilitates the hypertrophy of muscle fibres is the activation of satellite cells and the promotion of myonuclear accretion when existing myonuclei become unable to sustain further enhancement of protein synthesis. Interestingly, long-term steroid usage also enhances the frequency of fibres with centrally located myonuclei, which implies the occurrence of a high regenerative activity. Under the action of testosterone, some daughter cells generated by satellite cell proliferation may escape differentiation and return to quiescence, which help to replenish the satellite cell reserve pool. However, whether long-term steroid usage induces adverse effects of satellite cells remains unknown. Testosterone might also favour the commitment of pluripotent precursor cells into myotubes and inhibit adipogenic differentiation. The effects of testosterone on skeletal muscle are thought to be mediated via androgen receptors expressed in myonuclei and satellite cells. Some evidence also suggests the existence of an androgen-receptor-independent pathway. Clearly, testosterone abuse is associated with an intense recruitment of multiple myogenic pathways. This provides an unfair advantage over non-drug users. The long-term consequences on the regenerative capacity of skeletal muscle are unknown.

PMID 18414389 [PubMed - indexed for MEDLINE] PMCID PMC2439525


Thanks for posting dude!
 
The biological activity of 7 alpha-methyl-19-nortestosterone is not amplified in male reproductive tract as is that of testosterone.

Based on the premise that testosterone, but not 7 alpha-methyl-androgens, is reduced at the 5 alpha-position in the prostate and seminal vesicles, the differential bioactivities of these androgens were investigated in castrated rats. The ability of 7 alpha-methyl-19-nortestosterone acetate (MENT) to increase the weights of ventral prostate and seminal vesicles of castrated rats was four times higher than that of testosterone, while its effect on the weights of bulbocavernosus plus levator ani muscles (muscle), was 10 times that of testosterone. MENT was also approximately 12 times more potent than testosterone in the suppression of serum gonadotropin levels. A dose of testosterone that maintains serum gonadotropin levels and muscle mass also maintains prostate and seminal vesicle weights in castrated rats. By contrast, a dose of MENT that maintains muscle and gonadotropins does not maintain prostate and seminal vesicles. The action of other 7 alpha-methylated androgens were similar to that of MENT. The importance of 5 alpha reductase in the differential action of testosterone and MENT on prostate was confirmed by using a 5 alpha-reductase inhibitor. The activity of testosterone was significantly suppressed in the ventral prostate and seminal vesicles but not on muscle by the 5 alpha-reductase inhibitor (N,N-diethyl-3-oxo-4-aza-5 alpha-androst-1-ene-17 beta-carboxamide). The enzyme inhibitor, however, had no influence on the activity of MENT on either tissue. In contrast, cyproterone acetate, an antiandrogen that competitively binds to the androgen receptors, inhibited the action of MENT and of testosterone on the prostate as well as on the muscle. In conclusion, these observations show that 7 alpha-methylated androgens can maintain muscle mass and normal gonadotropin levels in androgen deficient rats without hyperstimulating the prostate. These findings suggest that 7 alpha-methylated androgens may offer some health benefits to men who require androgen treatment.

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Effects of sex steroids on indices of protein turnover in rainbow trout (Oncorhynchus mykiss) white muscle

Effects of 17b-estradiol (E2), testosterone, and 5a-dihydrotestosterone (DHT) on protein turnover and proteolytic gene expression were determined in rainbow trout (Oncorhynchus mykiss) primary myocytes and white muscle tissue. E2 reduced rates of protein synthesis and increased rates of protein degradation in primary myocytes by 45% and 27%, respectively. DHT reduced rates of protein synthesis by 27%. Tes- tosterone did not affect protein synthesis and neither testosterone nor DHT affected rates of protein deg- radation. Single injections of E2 increased expression of ubiquitin ligase genes fbxo32, fbxo25, and murf1, and the proteasome subunit psmd6 by 24 h after injection. Within the cathepsin-lysosome pathway, E2 increased expression of cathepsins ctsd and ctsl, as well as autophagy-related genes atg4b and lc3b. Addi- tionally, E2 injection up-regulated the expression of casp3 and casp9 caspase genes. Incubation of primary myocytes with E2 also increased expression of ubiquitin ligase genes. Therefore, catabolic effects of E2 on protein turnover result in part from E2-induced increases in proteolytic gene expression directly in mus- cle. Injection of testosterone increased milli-calpain (capn2) and casp3 expression, and DHT increased ctsd expression in vivo, whereas both androgens up-regulated fbxo32 expression in primary myocytes. These results suggest that effects of androgens on protein turnover in muscle are not driven primarily by direct effects of these hormones in this tissue.

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Claims for the anabolic effects of growth hormone: a case of the Emperor’s new clothes?

This review examines the evidence that growth hormone has metabolic effects in adult human beings. The conclusion is that growth hormone does indeed have powerful effects on fat and carbohydrate metabolism, and in particular promotes the metabolic use of adipose tissue triacylglycerol. However, there is no proof that net protein retention is promoted in adults, except possibly of connective tissue. The overexaggeration of the effects of growth hormone in muscle building is effectively promoting its abuse and thereby encouraging athletes and elderly men to expose themselves to increased risk of disease for little benefit.

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Pharmacokinetics and degree of aromatization rather than total dose of different preparations determine the effects of testosterone: a nonhuman primate study in Macaca fascicularis.

Currently available testosterone (T) preparations differ substantially in their pharmacokinetic profile that might influence their androgenic properties in terms of suppression of the gonadal axis, effects on anabolic parameters, lipid metabolism, and erythropoiesis. The present work was undertaken to determine the physiological effects of three T preparations with different serum kinetics. Twenty adult male cynomolgus monkeys (Macaca fascicularis) were randomly assigned to receive treatment for 28 weeks with either T enanthate (TE) every 4 weeks, T buciclate (TB) every 7 weeks, or T undecanoate (TU) every 10 weeks or remaining untreated (controls). Each injection delivered 20 mg pure T per kilogram body weight. Pharmacokinetic profiles demonstrated higher peak levels of T for TE-treated animals; serum half-lives were longer for TU or TB. Estradiol levels (area under the curve) were significantly higher in TB vs TU or TE. All T regimens suppressed serum luteinizing hormone bioactivity and testicular volumes declined (all P <.001 vs controls). Sperm counts were markedly lowered in all animals but least in TE (P <.01 vs TB or TU). During recovery phase, return to normal for all three parameters occurred significantly earlier in TE-treated animals, followed by those given TU, compared with TB (all P <.001 between groups). Body weight increased significantly during T exposure. This effect was stronger and more sustained in TB vs TU or TE (both P <.001). Serum creatinine and hemoglobin increased with high significance in all T-treated animals (all P <.001 vs controls). The lowering impact of T on serum lipids was markedly stronger in the longer-acting T preparations in comparison with TE, as were effects on purine metabolism (all P <.001). The pattern of exposure and degree of aromatization rather than overall exposure to T determine its effects in the preclinical primate model. Both fluctuations of androgen concentrations and the conversion rate to estradiol influence gonadal suppression as well as metabolism. These results have to be considered in men receiving treatment for hypogonadism or regimens for hormonal contraception.


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Injectable testosterone undecanoate has more favourable pharmacokinetics and pharmacodynamics than testosterone enanthate.

Testosterone preparations producing constant physiological testosterone serum levels are desirable for long-term treatment of androgen deficiency. However, all injectable testosterone esters used clinically for substitution of male hypogonadism are characterized by unfavourable pharmacokinetics. We therefore tested two groups of five long-term orchidectomized cynomolgus monkeys (Macaca fascicularis), which received a single intramuscular injection of 10 mg/kg body weight of an injectable testosterone undecanoate (TU) preparation or testosterone enanthate (TE) in a preclinical study to assess the pharmacokinetic and pharmacodynamic characteristics of TU in comparison to TE. The dose was equivalent to 6.3 and 7.2 mg of pure testosterone per kilogram body weight in the TU and TE group, respectively. Following injection of TU, mean serum testosterone rose to 58 +/- 18 nmol/l on day 1 and remained at moderately supraphysiological levels of 40-68 nmol/l for 45 days. Thereafter, testosterone levels were maintained in the normal range of intact monkeys for another 56 days. The TE injection resulted in highly supraphysiological levels of 100-177 nmol/l from immediately after the injection to day 5. A rapid decline followed and testosterone levels reached the lower limit of normal after 31 days. Serum testosterone levels were significantly higher in the TE-than in the TU-treated animals on days 0.5-7 (p < 0.05). Significantly lower testosterone levels were seen in the TE than in the TU group on days 16, 22, 25 and 31 (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)


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Growth hormone, insulin, prolactin and total thyroxine in the plasma of sheep implanted with the anabolic steroid trenbolone acetate alone or with oestradiol

The mode of action of the anabolic steroid trenbolone acetate (19-norandrost-4,9,11-trien-3-one-17-acetate) was studied through the endogenous hormonal response of castrated male sheep to subcutaneous implantation of 140 mg of trenbolone acetate and 20 mg of oestradiol both separately and in combination. Radioimmunoassay of delta-4,9,11-trienic steroids and oestradiol-17 beta in plasma confirmed that simultaneous administration of trenbolone acetate with oestradiol led to a significantly greater persistence of oestradiol-17 beta residues in plasma (P less than 0.05) than with implantation of oestradiol alone. Oestradiol treatment increased concentrations of growth hormone and insulin (P less than 0.05; P less than 0.001 respectively) in plasma samples collected weekly. Trenbolone acetate by itself had no significant effect and the oestrogenic response was blocked on the simultaneous implantation of trenbolone acetate and oestradiol (despite higher plasma levels of oestradiol-17 beta with this treatment). Plasma total thyroxine was markedly depressed to 45 per cent of its basal level by trenbolone acetate, alone or with oestradiol (P less than 0.001) and depressed to 80 per cent of basal by oestradiol treatment alone (P less than 0.001). Plasma prolactin was unaltered by the above treatments.


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In conclusion, these observations show that 7 alpha-methylated androgens can maintain muscle mass and normal gonadotropin levels in androgen deficient rats without hyperstimulating the prostate. These findings suggest that 7 alpha-methylated androgens may offer some health benefits to men who require androgen treatment.

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Great news for MENT! I've read that before but it's definitely great for people to know this about it.
 
Great news for MENT! I've read that before but it's definitely great for people to know this about it.

Remember though, nothing in these studies hold 100% TRUE in all cases
 
Release of prolactin is independent of the secretion of thyrotrophin-releasing hormone into hypophysial portal blood of sheep.

In order to determine whether pituitary prolactin release was directly related to the secretion of TRH into hypophysial portal blood, serial portal and jugular venous blood samples were collected from seven lactating and three non-lactating ewes. In another experiment, samples were collected from five ovariectomized ewes while being exposed to an audio-visual stress and then later administered with chlorpromazine. Secretion of TRH was pulsatile in all ewes and independent of prolactin secretion; TRH pulses coincided with significant increases in prolactin secretion in only 15% of cases and only 29% of prolactin pulses were associated with TRH pulses. Sixty-seven per cent of suckling bouts were associated with increases in prolactin secretion, but only 22% of these were associated with significant increases in TRH secretion. Chlorpromazine increased prolactin levels fourfold but did not affect portal concentrations of TRH. Audio-visual stress was not a reliable method of causing prolactin release in this model. Mean portal concentrations of TRH and jugular concentrations of prolactin were not significantly correlated. These results show that hypothalamic TRH and pituitary prolactin are secreted independently in the sheep, implying that increases in prolactin release caused by suckling or chlorpromazine are not the direct result of increased TRH secretion.


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