Become Slim [ A Must See ]

    Become Slim [ A Must See ]
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    Natural bodybuilding is the practice or participation in the form of body modification, known as bodybuilding; and to do this without the use of banned substances (most commonly referring to the use of illegal performance-enhancing drugs, such as anabolic steroids and human growth hormone).



     In the sport of natural bodybuilding, the classification of “natural” is based on the division in which the bodybuilders compete. While natural bodybuilders do not use drugs or illegal substances, they do use nutritional supplements and other legal products.


    Drug testing
    In the sport of Natural Bodybuilding, the classification of natural is based on the organization you are competing in. For example, The I.N.B.A. (International Natural Bodybuilding Association) is the largest and most strict drug-free bodybuilding and fitness organization in the world. The INBA follows the I.O.C. (International Olympics Committee) and W.A.D.A. (World Anti-Doping Association) Banned Substance Lists.



    All Athletes are fully tested by urinalysis, even amateur level. On the other end of the spectrum, you have the N.P.C. (National Physique Committee) which only tests for Anabolic steroids, Pro- hormone and prescripted Diuretics, and testing is different depending on the competition you are competing in. There are many organization for Natural Bodybuilding including the INBA, INBF (International Natural Bodybuilding Federation) , NGA (National Gym Association), NANBF (North American Natural Bodybuilding Federation),NPC, NPA (Natural physique association), and OCB (Organization of Competitive Bodybuilders). All of which has their own “Banned Substances” and testing methods. These methods range from polygraph, to Urinalysis, in some cases like the Olympics, there is even blood testing.



     Drug testing bodies
    Drug testing is generally organized at a national level. Often the body engaged by the sanctioning Federation/Promoter is the national drug/anti-doping body of the jurisdiction.


    The national drug/anti-doping bodies are organized under the auspices of the World Anti-Doping Agency(WADA). They include:
    * Australian Sports Anti-Doping Authority (ASADA) formally Australian Sports Drug Agency (ASDA)
    * New Zealand Sports Drug Agency (NZSDA)


     Professional class

    Like the IFBB, which is not a natural competition, Natural Bodybuilding has many organizations with competitions where one can earn the rank of a natural professional bodybuilder. Such organizations routinely test for controlled and banned substances including Anabolic steroids, Prohormone and Diuretics.


    Professional natural bodybuilding organizations include the IFPA (International Fitness and Physique Association), professional affiliate to the OCB and NANBF, PNBA (Professional Natural Bodybuilding Association), professional affiliate of the INBA, WNBF (World Natural Bodybuilding Federation), professional affiliate to the INBF, and Musclemania and NGA, professional affiliates to their counterpart amateur organizations of the same name.


    Anabolic steroid
    Crystal structure of human sex hormone-binding globulin, transporting 5α-dihydrotestosterone
    Anabolic steroids, officially known as anabolic-androgen steroids (AAS) or colloquially simply as “steroids”, are drugs which mimic the effects of the male sex hormones testosterone and dihydrotestosterone. They increase protein synthesis within cells, which results in the buildup of cellular tissue (anabolism), especially in muscles.


     Anabolic steroids also have androgenic and virilizing properties, including the development and maintenance of masculine characteristics such as the growth of the vocal cords and body hair. The word anabolic comes from the Greek ἀναβολή anabole, “that which is thrown up, mound”, and the word androgenic from the Greek ἀνδρός andros, “of a man” + -γενής -genes, “born”.


    Anabolic steroids were first isolated, identified and synthesized in the 1930s, and are now used therapeutically in medicine to stimulate bone growth and appetite, induce male puberty, and treat chronic wasting conditions, such as cancer and AIDS.
    The American College of Sports Medicine acknowledges that AAS, in the presence of adequate diet, can contribute to increases in body weight, often as lean mass increases, and that the gains in muscular strength achieved through high-intensity exercise and proper diet can be additionally increased by the use of AAS in some individuals.


     Some health risks can be produced by long-term use or excessive doses of anabolic steroids. These effects include harmful changes in cholesterol levels (increased low-density lipoprotein and decreased high-density lipoprotein), acne, high blood pressure, liver damage (mainly with oral steroids), and dangerous changes in the structure of the left ventricle of the heart.


    Ergogenic uses for anabolic steroids in sports and bodybuilding are controversial because of their adverse effects and the potential to gain an advantage conventionally considered “cheating.” Their use is referred to as doping and banned by all major sporting bodies. For many years AAS have been by far the most detected doping substances in IOC-accredited laboratories. In countries where AAS are controlled substances, there is often a black market in which smuggled or even counterfeit drugs are sold to users.


    Isolation of gonadal AAS
    Chemical structure of the natural anabolic hormone testosterone
    The use of gonadal steroids pre-dates their identification and isolation. Medical use of testicle extract began in the late 19th century while its effects on strength were still being studied.The isolation of gonadal steroids can be traced back to 1931 when Adolf Butenandt, a chemist in Marburg, purified 15 milligrams of the male hormone androstenone from tens of thousands of litres of urine. This steroid was subsequently synthesized in 1934 by Leopold Ruzicka, a chemist in Zurich.


    In the 1930s it was already known that the testes contained a more powerful androgen than androstenone, and three groups of scientists, funded by competing pharmaceutical companies in the Netherlands, Nazi Germany and Switzerland, raced to isolate it. This hormone was first identified by Karoly Gyula David, E. Dingemanse, J. Freud and Ernst Laqueur in a May 1935 paper “On Crystalline Male Hormone from Testicles (Testosterone).”

     They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The chemical synthesis of testosterone was achieved in August that year, when Butenandt and G. Hanisch published a paper describing “A Method for Preparing Testosterone from Cholesterol.” Only a week later, the third group, Ruzicka and A. Wettstein, announced a patent application in a paper “On the Artificial Preparation of the Testicular Hormone Testosterone (Androsten-3-one-17-ol).”


    Ruzicka and Butenandt were offered the 1939 Nobel Prize in Chemistry for their work, but the Nazi government forced Butenandt to decline the honor, although he accepted the prize after the end of World War II.


    Clinical trials on humans, involving either oral doses of methyltestosterone or injections of testosterone propionate, began as early as 1937.Testosterone propionate is mentioned in a letter to the editor of Strength and Health magazine in 1938; this is the earliest known reference to an anabolic steroid in a U.S. weightlifting or bodybuilding magazine.


    There are often reported rumors that German soldiers were administered anabolic steroids during the Second World War, the aim being to increase their aggression and stamina, but these are, as yet, unproven. Adolf Hitler himself, according to his physician, was injected with testosterone derivatives to treat various ailments. AAS were used in experiments conducted by the Nazis on concentration camp inmates, and later by the allies attempting to treat the malnourished victims that survived Nazi camps.


    Development of synthetic AAS
    Chemical structure of the synthetic steroid Methandrostenolone (Dianabol). 17α-methylation (upper right corner) enhances oral bioavailability.
    The development of muscle-building properties of testosterone was pursued in the 1940s, in the Soviet Union and in Eastern Bloc countries such as East Germany, where steroid programs were used to enhance the performance of Olympic and other amateur weight lifters. In response to the success of Russian weightlifters, the U.S. Olympic Team physician Dr. John Ziegler worked with synthetic chemists to develop an anabolic steroid with reduced androgenic effects.


    Ziegler’s work resulted in the production of methandrostenolone, which Ciba Pharmaceuticals marketed as Dianabol. The new steroid was approved for use in the U.S. by the Food and Drug Administration (FDA) in 1958. It was most commonly administered to burn victims and the elderly. The drug’s off-label users were mostly bodybuilders and weight lifters. Although Ziegler prescribed only small doses to athletes, he soon discovered that those who abused Dianabol suffered from enlarged prostates and atrophied testes.


    AAS were placed on the list of banned substances of the IOC in 1976, and a decade later the committee introduced ‘out-of-competition’ doping tests because many athletes used AAS in their training period rather than during competition.


    Three major ideas governed modifications of testosterone into a multitude of AAS: alkylation at 17-alpha position with methyl or ethyl group created orally active compounds because it slows the degradation of the drug by the liver, esterification of testosterone and nortestosterone at the 17-beta position allows the substance to be administered parenterally and increases the duration of effectiveness because agents soluble in oily liquids may be present in the body for several months, and finally alterations of the ring structure were applied for both oral and parenteral agents to seeking to obtain different anabolic to androgenic effect ratios.


     Pharmacology
    Routes of administration
    A vial of injectable testosterone cypionate
    There are three common forms in which anabolic steroids are administered: oral pills, injectable steroids, and skin patches. Oral administration is the most convenient. Testosterone administered by mouth is rapidly absorbed, but it is largely converted to inactive metabolites, and only about 1/6 is available in active form. In order to be sufficiently active when given by mouth, testosterone derivatives are alkylated at the 17 position, e.g. methyltestosterone and fluoxymesterone. This modification reduces the liver’s ability to break down these compounds before they reach the systemic circulation.


    Testosterone can be administered parenterally, but it has more irregular prolonged absorption time and greater activity in propionate, enanthate, undecanoate or cypionate ester form. These derivatives are hydrolyzed to release free testosterone at the site of injection. Injectable steroids are typically administered into the muscle, not into the vein, to avoid sudden changes in the amount of the drug in the bloodstream. Transdermal patches (adhesive patches placed on the skin) may also be used to deliver a steady dose through the skin and into the bloodstream.


    Injection is the most common method used by individuals administering anabolic steroids for non-medical purposes.The traditional routes of administration do not have differential effects on the efficacy of the drug. Studies indicate that the anabolic properties of anabolic steroids are relatively similar despite the differences in pharmacokinetic principles such as first-pass metabolism. However, the orally available forms of AAS may cause liver damage in high doses.


    The pharmacodynamics of anabolic steroids are unlike peptide hormones. Water-soluble peptide hormones cannot penetrate the fatty cell membrane and only indirectly affect the nucleus of target cells through their interaction with the cell’s surface receptors. Conversely, as fat-soluble hormones, anabolic steroids are membrane permeable and influence the nucleus of cells by direct action.


    The pharmacodynamic action of anabolic steroids begin when the exogenous hormone penetrates the membrane of the target cell and binds to an androgen receptor located in the cytoplasm of that cell. From there, the compound hormone-receptor diffuses into the nucleus, where it either alters the expression of genes or activates processes that send signals to other parts of the cell. Different types of anabolic steroids bind to the androgen receptor with different affinities, depending on their chemical structure.


    Some anabolic steroids such as methandrostenolone bind weakly to this receptor in vitro, but still exhibit androgenic effects in vivo. The reason for this discrepancy is not known.


     The effect of anabolic steroids on muscle mass is caused in at least two ways: first, they increase the production of proteins; second, they reduce recovery time by blocking the effects of stress hormone cortisol on muscle tissue, so that catabolism of muscle is greatly reduced. It has been hypothesized that this reduction in muscle breakdown may occur through anabolic steroids inhibiting the action of other steroid hormones called glucocorticoids that promote the breakdown of muscles.


    Anabolic steroids also affect the number of cells that develop into fat-storage cells, by favouring cellular differentiation into muscle cells instead. Anabolic steroids can also decrease fat by increasing basal metabolic rate (BMR), since an increase in muscle mass increases BMR.


     Anabolic and androgenic effects
    As the name suggests, anabolic-androgenic steroids have two different, but overlapping, types of effects: anabolic, meaning that they promote anabolism (cell growth), and androgenic (or virilising), meaning that they affect the development and maintenance of masculine characteristics.


    Some examples of the anabolic effects of these hormones are increased protein synthesis from amino acids, increased appetite, increased bone remodeling and growth, and stimulation of bone marrow, which increases the production of red blood cells. Through a number of mechanisms anabolic steroids stimulate the formation of muscle cells and hence cause an increase in the size of skeletal muscles, leading to increased strength.


    The androgenic effects of AAS are numerous. Processes affected include pubertal growth, sebaceous gland oil production, and sexuality (especially in fetal development). Some examples of virilizing effects are growth of the clitoris in females and the penis in male children (the adult penis does not grow even when exposed to high doses of androgens), increased growth of androgen-sensitive hair (pubic, beard, chest, and limb hair), increased vocal cord size, deepening the voice, increased libido, suppression of natural sex hormones, and impaired production of sperm.


    The androgenic:anabolic ratio of an AAS is an important factor when determining the clinical application of these compounds. Compounds with a high ratio of androgenic to a anabolic effects are the drug of choice in androgen-replacement therapy, whereas compounds with a reduced androgenic:anabolic ratio are preferred for anemia, osteoporosis, and to reverse protein loss following trauma, surgery or prolonged immobilization.


    Determination of androgenic:anabolic ratio is typically performed in animal studies, which has led to the marketing of some compounds claimed to have anabolic activity with weak androgenic effects. This disassociation is less marked in humans, where all anabolic steroids have significant androgenic effects.


    A commonly used protocol for determining the androgenic:anabolic ratio, dating back to the 1950s, uses the relative weights of ventral prostate (VP) and levator ani muscle (LA) of male rats. The VP weight is an indicator of the androgenic effect, while the LA weight is an indicator of the anabolic effect. Two or more batches of rats are castrated and given no treatment and respectively some AAS of interest. The LA/VP ratio for an AAS is calculated as the ratio of LA/VP weight gains produced by the treatment with that compound using castrated but untreated rats as baseline.


    The LA/VP weight gain ratio from rat experiments is not unitary for testosterone , but it’s normalized for presentation purposes, and used as basis of comparison for other AAS, which have their androgenic:anabolic ratios scaled accordingly. In the early 2000s this procedure was standardized and generalized throughout OECD in what is now known as the Hershberger assay.


     Body composition and strength improvements
    A review spanning more than three decades of experimental studies in men found that body weight may increase by 2–5 kg as a result of short term (<10 weeks) AAS use, which may be attributed mainly to an increase of lean mass. Animal studies also found that fat mass was reduced, but most studies in humans failed to elucidate significant fat mass decrements.


    The effects on lean body mass have been shown to be dose dependent. Both muscle hypertrophy and the formation of new muscle fibers have been observed. The hydration of lean mass remains unaffected by AAS use, although small increments of blood volume cannot be ruled out.


    The upper region of the body (thorax, neck, shoulders and upper arm) seems to be more susceptible for AAS than other body regions because of predominance of androgen receptors in the upper body. The largest difference in muscle fibre size between AAS users and non-users was observed in type I muscle fibres of the vastus lateralis and the trapezius muscle as a result of long-term AAS self-administration. After drug withdrawal the effects fade away slowly, but may persist for more than 6–12 weeks after cessation of AAS use.


    The same review observed strength improvements in the range of 5-20% of baseline strength, largely depending on the drugs and dose used as well as the administration period. Overall, the exercise where the most significant improvements were observed was the bench press. For almost two decades it was assumed that AAS only exerted significant effects in experienced strength athletes, particularly based on the studies of Hervey and coworkers.


    In 1996 a randomized controlled trial published in the New England Journal of Medicine demonstrated however that even in novice athletes a 10-week strength training program accompanied by testosterone enanthate at 600 mg/week may improve strength more than training alone does.


    The same study found that dose was sufficient to significantly improve lean muscle mass relative to placebo even in subjects that did not exercise at all. A 2001 study by the same first author, showed that the anabolic effects of testosterone enanthate were highly dose dependent.


     Adverse effects
    Anabolic steroids can cause many adverse effects. Most of these side effects are dose-dependent, the most common being elevated blood pressure, especially in those with pre-existing hypertension,and harmful changes in cholesterol levels: some steroids cause an increase in LDL cholesterol and a decrease in HDL cholesterol.


    Anabolic steroids have been shown to alter fasting blood sugar and glucose tolerance tests. Anabolic steroids such as testosterone also increase the risk of cardiovascular disease[40] or coronary artery disease. Acne is fairly common among anabolic steroid users, mostly due to stimulation of the sebaceous glands by increased testosterone levels.


    Conversion of testosterone to dihydrotestosterone can accelerate the rate of premature baldness for males who are genetically predisposed, but testosterone itself can produce baldness in females.


    High doses of oral anabolic steroid compounds can cause liver damage, as the steroids are metabolized in the digestive system to increase their bioavailability and stability.


    There are also sex-specific side effects of anabolic steroids. Development of breast tissue in males, a condition called gynecomastia (which is usually caused by high levels of circulating estradiol), may arise because of increased conversion of testosterone to estradiol by the enzyme aromatase.


    Reduced sexual function and temporary infertility can also occur in males. Another male-specific side effect which can occur is testicular atrophy, caused by the suppression of natural testosterone levels, which inhibits production of sperm (most of the mass of the testes is developing sperm).


    This side effect is temporary: the size of the testicles usually returns to normal within a few weeks of discontinuing anabolic steroid use as normal production of sperm resumes. Female-specific side effects include increases in body hair, deepening of the voice, enlarged clitoris, and temporary decreases in menstrual cycles.
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