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Aqui tienen una informacion de como funcionan los esteroides, por supuesto esta en ingles, asi que los que tengan dudas le preguntan a su madre ejejeej.
No broma, con mucho gusto le ayudaremos.
TYPES OF STEROIDS
Anabolic/Androgenic Steroids can be roughly classified into two types, oral and injectable. When you eat food or consume anything orally, the great majority of the ingested substances pass through the liver prior to entering the bloodstream. For this reason, "injectable" AAS cannot be taken orally because the liver will deactivate the steroids in this "first pass". Deactivation in the liver usually involves the addition of one or more hydroxyl (OH) groups to increase the solubility of the molecule in water, making excretion in the urine more easily accomplished.
Oral Steroids
Oral steroids involve modification of the parent steroid to make it harder for the liver to degrade the steroid molecules. This modification is almost always the addition of an alkyl (methyl) group at the 17 position of the steroid ring. The liver can still degrade the steroid, but not as effectively as the un-modified steroid. Therefore, oral steroids make several cycles through the bloodstream before being excreted. Most oral steroids are, to various degrees, excreted from the body unchanged.
Injectable Steroids
The injectable AAS are very effectively degraded in just a single pass through the liver. If this is so, then how can the injectables be effective? The answer is called a "depot" (or reservoir), which allows a regular release of steroid into the bloodstream. As steroid is removed from the bloodstream by the liver, more steroid is being released into the bloodstream from the depot. There are several ways to provide such a reservoir of the steroid.
Suspension
The first way is to use pure testosterone (a crystalline solid) suspended in water. Testosterone has a low solubility in water, and the crystals slowly dissolve in the watery environment of the tissue in which it is injected. The dissolved testosterone is carried throughout the body by the bloodstream. For Testosterone suspension, the "depot" is the actual physical site where the injection is made. The crystals do not migrate to other parts of the body, and the presence of the crystalline testosterone can cause some pain at the injection site. The testosterone dissolves at a (relatively) constant rate, and lasts for a few days in the body. Winstrol suspension is similar.
Esters
The other way to provide a depot of steroid is to use a water-insoluble form of the steroid that can be converted in the body to the parent steroid, which has some solubility in water (bloodstream). Most commonly, the parent molecule is esterified with an organic acid, and the resulting ester is soluble in oil, but only very slightly soluble in water. Commonly used organic acid groups are acetate (C2), propionate (C3), enanthate (C7), decanoate (C10), and undecylenate (C11). The longer the carbon chain of the acid, the more oil-soluble the ester, and the longer it takes for the ester to turn into the parent steroid (de-esterification). A type of enzyme that is found throughout the body facilitates the de-esterification reaction to form the parent steroid from the ester. The enzyme actually catalyzes the reaction in both directions, so it can also attach an organic acid back onto the parent steroid. So, for example, testosterone enanthate can actually be turned into testosterone palmitate. There is some good evidence that steroid esters are, to some extent, stored in fat cells.
It is commonly believed that esters form a depot of oil/ester that stays at the injection site. This is not true. While the depot concept holds true for esters (because they slowly release the parent steroid over time), the esters actually disperse throughout the body after injection, prior to (and during) the de-esterification reaction to form the parent steroid. They do not stay at the injection site. For example, the ester testosterone enanthate has been found in tissues throughout the body, including hair samples of subjects who have injected T200. If a bio-contaminant is introduced at the time of injection (non-sterile conditions), the body will attempt to encapsulate the contaminated material, and an abscess will form. In this case it appears as if the ester has remained at the injection site. But under normal sterile conditions, the oily solution will disperse. Injecting too much at one site or injecting too frequently at one site will not cause an abscess.
Transport of Steroids in the Bloodstream
Once the steroid has been released from the depot (or the oral steroid has been absorbed from the intestine), it is transported throughout the body in the bloodstream. Carrier proteins (Albumin and Sex Hormone binding Globulin) bind about 98% of testosterone under natural conditions. Thus, only 2% of the hormone is free to carry out its actions. When exogenous steroid is present, the level of free steroid is much higher than 2%. Bear in mind that the hormone is not permanently bound to the some of the proteins, but is constantly binding and un-binding from the protein. At any given time, about 2% of the hormone is un-bound in the natural state. So, if the 2% unbound hormone were to magically disappear, then the proteins would release more hormone such that 2% (of the remaining total) would come unbound. The bloodstream is the mechanism by which the hormones reach their target tissues (muscle).
Action of Steroids
Androgen Receptor Activation
Once a free molecule of steroid reaches the muscle cell, it diffuses into the cell. The diffusion can be with or without transport-protein assistance. Once in the cell, the AAS is makes its way to the cell nucleus where it can bind with an androgen receptor (AR), and activate the receptor. Two of these activated receptor complexes join together to form the androgen response element (ARE). The ARE interacts with DNA in the nucleus, and increases the transcription of certain genes (such as muscle protein genes). As long as the ARE is intact, it accelerates gene transcription. Remember, though, that the AAS and the receptor are in a state of flux (binding and un-binding), just like with the Carrier proteins. So the ARE can be deactivated just by losing one of the two AAS that are bound to the AR's. This equilibrium situation explains why 1 gram per week testosterone is more effective than 1/2 gram per week, even though 1/2 gram appears to be more than enough to saturate all the AR's in the body. The higher concentration makes it more likely that the receptors will be occupied by an AAS, and the ARE will be intact for a longer period of time, on average.
Other Actions
Activation of the androgen receptor is a key mechanism in the action of AAS. However, this mechanism by itself does not explain the differences between steroids (i.e., nandrolone activates the AR better than testosterone, but is not as good of a mass-building product). Other actions involve primarily the central nervous system, and involve actions such as motor activation (muscle coordination) and mood (i.e., aggressiveness). The mechanism by which AAS effect these actions is not well understood at this time. Another effect occurs in the liver, where some steroids cause the release of certain Growth Factors. The different actions of the different AAS explains why a stack of two different types of AAS is often better than one by itself.
Elimination of Steroids
The liver is a primary route to deactivation of steroids, the chemical structure is changed here to make the steroid more soluble in water for excretion through the kidneys. A good portion of many steroids also are excreted as-is, without any alteration by the liver, or by formation of the sulphate, which is more water soluble. Many in the medical community have believed that AAS cause liver damage because levels of certain enzymes (AST and ALT) are elevated when steroids are used. Elevated levels of these enzymes are seen in patients with liver damage from other causes, so the conclusion is that AAS must cause liver damage because these enzymes are elevated. Recent work, however, has shown that a true marker of liver damage, GGT, remains unchanged when some AAS are used, and now it is questioned whether AAS are really damaging to the liver (the 17 alpha-alkylated AAS do cause damage in some rare cases, and this damage is reversible upon cessation of steroid use). The same thought processes were used to claim kidney damage, but that is unlikely as well.
The Causes of Inhibition
Elevated hormone levels, in general, will cause inhibition of natural testosterone production. What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim�s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.
Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.
The Hypothalamic/Pituitary/Testicular Axis (HPTA)
To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn�t respond only to current hormone levels, but also to the past history of hormone levels.
The hypothalamus itself cannot produce any sex hormones � instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.
The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary�s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.
LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.
Inhibition From AAS Cycles
Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:
� Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
� Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and Deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
� In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.
Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise (not an exclusive list of aromatizable AAS, but the main ones) to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition. The best dosing pattern, in my opinion, is to take ˝ tab (125 mg) on arising, and then Ľ tab at six and 12 hours later. Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug. Some individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness) from Cytadren, but that is uncommon at this dose.
Arimidex: This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.
Clomid: After a cycle is over, Clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle Clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.
Nolvadex: This works in the same manner as Clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If Clomid is used, there is no need for Nolvadex.
HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.
Ephedrine/clenbuterol: It is possible that the beta agonist activities of these drugs may assist in recovery. Personally, I do recommend the use of ephedrine post-cycle to those who can use it. Clenbuterol has the same effect but acts around the clock, having a longer half life, and allowing a higher effective dose (amount times potency) due to having less relative effect on beta receptors in the heart. I am not sure that clenbuterol has any better effect with regard to recovery though.
Oral AAS: These do not assist recovery of natural testosterone production, but if used only in the morning, can help sustain muscle mass while in the recovery phase, with little or no adverse effect on recovery.
No broma, con mucho gusto le ayudaremos.
TYPES OF STEROIDS
Anabolic/Androgenic Steroids can be roughly classified into two types, oral and injectable. When you eat food or consume anything orally, the great majority of the ingested substances pass through the liver prior to entering the bloodstream. For this reason, "injectable" AAS cannot be taken orally because the liver will deactivate the steroids in this "first pass". Deactivation in the liver usually involves the addition of one or more hydroxyl (OH) groups to increase the solubility of the molecule in water, making excretion in the urine more easily accomplished.
Oral Steroids
Oral steroids involve modification of the parent steroid to make it harder for the liver to degrade the steroid molecules. This modification is almost always the addition of an alkyl (methyl) group at the 17 position of the steroid ring. The liver can still degrade the steroid, but not as effectively as the un-modified steroid. Therefore, oral steroids make several cycles through the bloodstream before being excreted. Most oral steroids are, to various degrees, excreted from the body unchanged.
Injectable Steroids
The injectable AAS are very effectively degraded in just a single pass through the liver. If this is so, then how can the injectables be effective? The answer is called a "depot" (or reservoir), which allows a regular release of steroid into the bloodstream. As steroid is removed from the bloodstream by the liver, more steroid is being released into the bloodstream from the depot. There are several ways to provide such a reservoir of the steroid.
Suspension
The first way is to use pure testosterone (a crystalline solid) suspended in water. Testosterone has a low solubility in water, and the crystals slowly dissolve in the watery environment of the tissue in which it is injected. The dissolved testosterone is carried throughout the body by the bloodstream. For Testosterone suspension, the "depot" is the actual physical site where the injection is made. The crystals do not migrate to other parts of the body, and the presence of the crystalline testosterone can cause some pain at the injection site. The testosterone dissolves at a (relatively) constant rate, and lasts for a few days in the body. Winstrol suspension is similar.
Esters
The other way to provide a depot of steroid is to use a water-insoluble form of the steroid that can be converted in the body to the parent steroid, which has some solubility in water (bloodstream). Most commonly, the parent molecule is esterified with an organic acid, and the resulting ester is soluble in oil, but only very slightly soluble in water. Commonly used organic acid groups are acetate (C2), propionate (C3), enanthate (C7), decanoate (C10), and undecylenate (C11). The longer the carbon chain of the acid, the more oil-soluble the ester, and the longer it takes for the ester to turn into the parent steroid (de-esterification). A type of enzyme that is found throughout the body facilitates the de-esterification reaction to form the parent steroid from the ester. The enzyme actually catalyzes the reaction in both directions, so it can also attach an organic acid back onto the parent steroid. So, for example, testosterone enanthate can actually be turned into testosterone palmitate. There is some good evidence that steroid esters are, to some extent, stored in fat cells.
It is commonly believed that esters form a depot of oil/ester that stays at the injection site. This is not true. While the depot concept holds true for esters (because they slowly release the parent steroid over time), the esters actually disperse throughout the body after injection, prior to (and during) the de-esterification reaction to form the parent steroid. They do not stay at the injection site. For example, the ester testosterone enanthate has been found in tissues throughout the body, including hair samples of subjects who have injected T200. If a bio-contaminant is introduced at the time of injection (non-sterile conditions), the body will attempt to encapsulate the contaminated material, and an abscess will form. In this case it appears as if the ester has remained at the injection site. But under normal sterile conditions, the oily solution will disperse. Injecting too much at one site or injecting too frequently at one site will not cause an abscess.
Transport of Steroids in the Bloodstream
Once the steroid has been released from the depot (or the oral steroid has been absorbed from the intestine), it is transported throughout the body in the bloodstream. Carrier proteins (Albumin and Sex Hormone binding Globulin) bind about 98% of testosterone under natural conditions. Thus, only 2% of the hormone is free to carry out its actions. When exogenous steroid is present, the level of free steroid is much higher than 2%. Bear in mind that the hormone is not permanently bound to the some of the proteins, but is constantly binding and un-binding from the protein. At any given time, about 2% of the hormone is un-bound in the natural state. So, if the 2% unbound hormone were to magically disappear, then the proteins would release more hormone such that 2% (of the remaining total) would come unbound. The bloodstream is the mechanism by which the hormones reach their target tissues (muscle).
Action of Steroids
Androgen Receptor Activation
Once a free molecule of steroid reaches the muscle cell, it diffuses into the cell. The diffusion can be with or without transport-protein assistance. Once in the cell, the AAS is makes its way to the cell nucleus where it can bind with an androgen receptor (AR), and activate the receptor. Two of these activated receptor complexes join together to form the androgen response element (ARE). The ARE interacts with DNA in the nucleus, and increases the transcription of certain genes (such as muscle protein genes). As long as the ARE is intact, it accelerates gene transcription. Remember, though, that the AAS and the receptor are in a state of flux (binding and un-binding), just like with the Carrier proteins. So the ARE can be deactivated just by losing one of the two AAS that are bound to the AR's. This equilibrium situation explains why 1 gram per week testosterone is more effective than 1/2 gram per week, even though 1/2 gram appears to be more than enough to saturate all the AR's in the body. The higher concentration makes it more likely that the receptors will be occupied by an AAS, and the ARE will be intact for a longer period of time, on average.
Other Actions
Activation of the androgen receptor is a key mechanism in the action of AAS. However, this mechanism by itself does not explain the differences between steroids (i.e., nandrolone activates the AR better than testosterone, but is not as good of a mass-building product). Other actions involve primarily the central nervous system, and involve actions such as motor activation (muscle coordination) and mood (i.e., aggressiveness). The mechanism by which AAS effect these actions is not well understood at this time. Another effect occurs in the liver, where some steroids cause the release of certain Growth Factors. The different actions of the different AAS explains why a stack of two different types of AAS is often better than one by itself.
Elimination of Steroids
The liver is a primary route to deactivation of steroids, the chemical structure is changed here to make the steroid more soluble in water for excretion through the kidneys. A good portion of many steroids also are excreted as-is, without any alteration by the liver, or by formation of the sulphate, which is more water soluble. Many in the medical community have believed that AAS cause liver damage because levels of certain enzymes (AST and ALT) are elevated when steroids are used. Elevated levels of these enzymes are seen in patients with liver damage from other causes, so the conclusion is that AAS must cause liver damage because these enzymes are elevated. Recent work, however, has shown that a true marker of liver damage, GGT, remains unchanged when some AAS are used, and now it is questioned whether AAS are really damaging to the liver (the 17 alpha-alkylated AAS do cause damage in some rare cases, and this damage is reversible upon cessation of steroid use). The same thought processes were used to claim kidney damage, but that is unlikely as well.
The Causes of Inhibition
Elevated hormone levels, in general, will cause inhibition of natural testosterone production. What then besides estrogen can cause inhibition? DHT, which does not aromatize, has been extensively shown to cause inhibition of testosterone production. Androgen alone, then, is sufficient to cause inhibition. In Jim�s case, androgen use was moderately heavy, and androgen alone would seem the cause of the inhibition.
Progesterone is another hormone that can cause inhibition, when used long-term. Paradoxically, in the short term it can be stimulatory. Other relevant factors include beta agonists, opiates, melatonin, prolactin, and probably other compounds. With the exception of beta agonists (e.g. ephedrine and Clenbuterol) and opiates (natural endorphins on the one hand being inhibitory, and Nubain blocking such inhibition) manipulation of these would not seem useful in bodybuilding.
The Hypothalamic/Pituitary/Testicular Axis (HPTA)
To understand inhibition of testosterone production, we need to know first how it is produced and how production is controlled. The broad general picture is that the hypothalamus receives a variety of inputs, for example, levels of various hormones, and decides whether or not more sex hormones should be produced. If the inputs are high, for example, high estrogen or high androgen or both, then it decides that little or no sex hormones should now be produced, but if all inputs are low, then it may decide that more sex hormones should be produced. It seems that the hypothalamus doesn�t respond only to current hormone levels, but also to the past history of hormone levels.
The hypothalamus itself cannot produce any sex hormones � instead it produces LHRH, or luteinizing hormone (LH) releasing hormone, also called GnRH (gonadotropin releasing hormone.) This then stimulates the pituitary gland.
The pituitary uses the amount of LHRH as one of its signals in deciding how much LH it should produce. Proper response depends on having sufficient receptors for LHRH. These receptors must be activated for LH to be produced. The pituitary also uses sex hormone levels, both current and the past history, in deciding how much LH to produce. Some aspects of the pituitary�s behavior are peculiar. For example, too much LHRH results in the pituitary downregulating LHRH receptors, with the result that very high LHRH production, which one would think should result in high testosterone production, actually lowers testosterone production. Another oddity is that while high estrogen levels inhibit the pituitary, still some estrogen is required to maintain a high number of LHRH receptors. So both very low and high levels of estrogen can inhibit LH production.
LH produced by the pituitary then stimulates the testicles to produce testosterone. Here, the amount of LH is the main factor, and high levels of sex hormones do not seem to cause inhibition at this level.
Inhibition From AAS Cycles
Because high androgen levels sustained around the clock will cause inhibition, traditional cycles simply cannot avoid inhibition of LH production while on cycle. There are three ways to avoid it:
� Avoid having high androgen levels around the clock. This can be done, for example, by using oral AAS only in the morning, with the last dose being approximately at noontime. Even 100 mg/day Dianabol can be used in this fashion with little inhibition. The problem with this approach is that gains are not very good compared to what is seen when high androgen levels are sustained around the clock.
� Use an amount and kind of AAS that is low enough to avoid much inhibition. Primobolan at 200-400 mg/week may achieve this effect. Again, gains will be compromised compared to a more substantial cycle. Testosterone esters and Deca are substantially inhibitory even at 100 mg/week so using a low dose of these drugs will simply result in both inhibition and poor gains.
� In principle, one could use an antiandrogen, but this would totally defeat the purpose of the cycle.
Where AAS doses are sufficient for good gains, an interesting pattern is seen. For the first two weeks of the cycle, only the hypothalamus is inhibited, and it produces much less LHRH as a result of the high levels of sex hormones it senses. The pituitary is not inhibited at all: in fact, it is actually sensitized, and will respond to LHRH (if any is provided) even moreso than normally. After two weeks however, the pituitary also becomes inhibited, and even if LHRH is provided, the pituitary will produce little or no LH. This then is a deeper type of inhibition. After this point, there seems to be no definite further "switching point" where inhibition again becomes deeper and harder to reverse. As a general rule, I would say that there seems to be little difference between using AAS for 3 weeks vs. 8 weeks: recovery is about the same either way. Between 8 and 12 weeks, it becomes more and more likely that recovery will be difficult and slow, though even at 12 weeks it is common for recovery to not be too problematic, taking only a few weeks. Cycles past 12 weeks seem much more likely to cause substantial problems with recovery. In the hundreds of consultations I have done for people with recovery problems, very few (I can recall two) were for very short cycles such as 6 weeks, while most were for usages of 12 weeks straight or more.
Cytadren: This drug can be used to reduce conversion of testosterone, Dianabol, and Equipoise (not an exclusive list of aromatizable AAS, but the main ones) to estrogen. Some feel that when estrogen levels are kept under control during the cycle, recovery is faster after the cycle is over, though that is not proven. It is a good idea though. And if testosterone esters were used prior to ending the cycle, some levels of these will remain for weeks, and continued use of Cytadren will help prevent conversion to estrogen, and thereby reduce inhibition. The best dosing pattern, in my opinion, is to take ˝ tab (125 mg) on arising, and then Ľ tab at six and 12 hours later. Use of more Cytadren than this, or a different pattern, may lead to an adverse effect on cortisol production, with subsequent cortisol rebound after discontinuing the drug. Some individuals suffer some lethargy (feeling of tiredness and laziness, or sleepiness) from Cytadren, but that is uncommon at this dose.
Arimidex: This accomplishes the same purposes as Cytadren but without the possible side effects mentioned above. It is however far more expensive. A typical dose is 1 mg./day. The timing of the dosage does not matter, since the drug has a long half-life.
Clomid: After a cycle is over, Clomid at 50 mg/day is usually very effective in restoring natural testosterone production. It acts by blocking estrogen receptors at the hypothalamus and pituitary. If androgen levels are not elevated, this is enough to cause production of at least normal amounts of LH, or often more LH than normal. During the cycle Clomid cannot prevent inhibition, though some think using it during the cycle will allow a faster recovery afterwards. That is not proven though. If nothing else, though, it is useful as an antigyno/antibloating agent during the cycle.
Nolvadex: This works in the same manner as Clomid, but not nearly so well with regard to reversing inhibition. It is better to use this only as an anti-gyno/antibloating agent, if at all. If Clomid is used, there is no need for Nolvadex.
HCG: This does nothing with regard to inhibition of the hypothalamus and pituitary. Rather it acts like LH, and causes the testicles to produce testosterone just as if LH were present. It is useful then for avoiding testicular atrophy during the cycle. The best dosing method is to use small amounts frequently: 500 IU per day is sufficient, and 1000 IU may optionally be used. The amount may be given as a single daily dose or divided into two doses. Administration may be intramuscular or subcutaneous. More is not better: too much HCG can result in downregulation of the LH receptors in the testes, and is therefore counterproductive. Overdosing of HCG can also result in gynecomastia.
Ephedrine/clenbuterol: It is possible that the beta agonist activities of these drugs may assist in recovery. Personally, I do recommend the use of ephedrine post-cycle to those who can use it. Clenbuterol has the same effect but acts around the clock, having a longer half life, and allowing a higher effective dose (amount times potency) due to having less relative effect on beta receptors in the heart. I am not sure that clenbuterol has any better effect with regard to recovery though.
Oral AAS: These do not assist recovery of natural testosterone production, but if used only in the morning, can help sustain muscle mass while in the recovery phase, with little or no adverse effect on recovery.
