Ciekawe arty w jêzyku angielskim, które s± warte t³umaczenia

[Tomi!]

^ taken, jutro do 9 am powinno ujrzec czytelnie

edit: jak sie do 30 min wyrobie na tym smiesznym 8/kb sec to bedzie do 9

[gl]

Estrogen on Cycle: The Good, The Bad, and The Proper Management of Both.
The relevance of Estrogen management is more important than ever now in my opinion. This is due to several factors. First of all the knowledge of Estrogen and its effects in males has grown substantially in the last few years. Also a more basic but very real reason is the trend we have seen in cycles over the last several years. It used to be cycles were 6 - 8 weeks in length. In the past it was common that short ester cycles were run 6 weeks and long estered ones 8 weeks. Now cycle lengths of 12-16 weeks+ have become the norm. This added time and exposure to the deleterious effects of unmanaged or improperly managed estrogen makes the topic more important than ever.

So lets take a look at the effects of Estrogen in Males both positive and negative.
On the positive side:
* Estrogen plays a key role in immune system function and inflammatory response.
* It has a positive impact on cholesterol.
* Estrogen is essential for GH and IGF synthesis.
*It plays a role in maintaining proper '"fluid balance" within the body.
*Essential for bone density
*Assists in glucose uptake

The Negatives:
*Increased Risk of Heart Disease
*Increased risk of Prostate cancer
*Increased blood clotting
*Increased risk of Hypertension (high blood pressure)
* Increased risk of cardiovascular event or stroke.
*Gynecomastia
* Improper Fluid Balance (or water retention)
*Estrogens relationship with other hormones. For example, Estrogen has a proportional
relationship with the hormone Prolactin. An increase in Estrogen results in an increase
in Prolactin.

As you can see there are numerous serious positives and negatives when it comes to the effect''s of Estrogen in males. Some of these effects are dependent upon the levels of Estrogen present. For example proper estrogen levels result in improved lipid profiles and cardiovascular health. However elevated estrogen levels result in adverse effects on cardiovascular health and increased risk of heart attack or stroke. Based on this it becomes very clear the optimal situation when it comes to Estrogen while on cycle is to MANAGE it properly. Not eliminate it, not ignore it, but manage it.

To further clarify and specify what I would consider proper Estrogen Management, especially in light of the fact that many positive effects of Estrogen become negative when it is elevated too much, I would define estrogen management as maintaining Estrogen levels in the clinically normal range even while on cycle. In other words keep our E2 levels the same on or off cycle. To take it a step further if Estrogen levels can be kept between 25-30 while on cycle, we can reap the positive effects of Estrogen while virtually eliminating the negative ones.

Lets take a look at Estrogen management while on AAS cycle and how it has evolved over the years, what compounds are available to assist us, and the effects and interactions of these compounds.

Years ago the first attempts at managing Estrogen really didn''t manage it at all;they just eliminated some undesirable side effects while having no impact on Estrogen levels at all. These early attempts were made using serms such as clomid or tamoxifen while on cycle. The specific side effect of elevated estrogen that the use of serms would address is the one of gynecomastia. Serms bind to the Estrogen receptor in breast tissue, blocking estrogen from exerting its effect there and preventing undesired breast tissue growth. As you can see this was an improvement over using nothing at all, however serm use does nothing to address the other negative effects of elevated Estrogen. Some of these negative effects are very serious, much more serious than Gyno from a medical (as well as common sense) not aesthetic perspective. While serms do not address the majority of negative issues of elevated Estrogen it does not mean they do not have a place in this discussion or in treating of addressing this issue. I will get into that more later.

The next progression in Estrogen management is the use of Aromatase Inhibitors to control overall Estrogen levels. This has been a huge advancement in the management of estrogen. Aromatase Inhibitors act upon the Aromatase enzyme. This is the enzyme responsible for the conversion of testosterone to estrogen within the body. Aromatase Inhibitors prevent the binding of Aromatase to testosterone so the process of Aromatozation of test to Estrogen cannot take place. This sounds like the ultimate solution to the problem of Estrogen Management on cycle and too a large degree it is. However there are different Aromatase Inhibitors that may make one a more prudent choice than the other for certain situations or individuals. Also the value of Serms and their role in estrogen management cannot be dismissed just yet.

So we see we have 2 categories of compounds that can be of use to us in properly managing Estrogen or its side effects, Serms and AIs. Let''s take a look at our options in categories, their differences and potential interactions with one another, and how they might be used together to accomplish our goal.

First we will look at AIs as in my opinion they are the core of our Estrogen Management program. We essentially have 2 types of AI''s to choose from. Type 1 AIs like Exemestane and Type 2 AI''s such as letrozole or Anastrozole (arimidex). The difference in these types is as follows. A Type 1 AI like Exemestane binds permanently to the site on the Aromatase Enzyme where it binds to testosterone allowing its conversion to Estrogen. This permanent binding renders the Aromatase totally and permanently inactive. In contrast Type 2 AIs temporarily bind to this site on the Aromatase Enzyme rendering it inactive as long as the AI is being used. Onçe use of type 2 AI stops the aromatase will reactivate. So whats the difference in these Ai types for our purposes? Well Due to the '"reactivation" if you will of existing Aromatase with a Type 2 AI, when you stop using it a spike in Estrogen (often referred to as rebound) will occur due to the sudden increase availability of Aromatase Enzyme. Another important distinction when it comes to Type 1 and Type 2 AI''s. A Type 1 AI like Exemestane remains unaffected by the introduction of a serm into your Estrogen management program. Type 2 AIs like letrozole and Arimidex suffer a reduced in blood levels and effectiveness with the introduction of some serms. I will touch more on why we may need to introduce a serm a little farther on in this article.

When it comes to the strength of these AI''s letrozole would be the strongest followed by Arimidex and then by Exemestane. Now people might be up in arms saying Exemestane is stronger than Arimidex however when one looks and compare data from studies done on MALES the order of strength is exactly as I stated it, quite often much confusion comes in to play when people recite data on AI's taken from studies on women. The fact is AI's behave differently in males, they are less effective in males, and for our purposes it is only prudent to compare data gathered from studies on males to portray an accurate picture.

The next aspect to be considered when looking at AIs are the effects they indirectly illicit in other areas. We stated the positive effects of Estrogen, we must realize by lowering Estrogen via Ai use some of these positive effects may be compromised. It is important to look at the various AI options available and possibly use the data to help pick which AI we use. letrozole is an extremely potent AI and its effects demonstrate this as would be expected. letrozole has an adverse effect on lipid profile and somewhat on IGF levels. On the other hand Arimdex has a small impact in the area of IGF and depending upon which studies you cite a small adverse impact on lipids to no adverse impact on lipids. Exemestane seems to have no clinical impact on either IGF or lipids.

It is important to realize that it may seem like Exemestane shines as a clear cut winner when it comes to choice of AI, however I do not necessarily believe this to be the case for everyone. In some cases or maybe better said in some people, an extremely powerful AI like letrozole must be used to manage Estrogen properly. Some may respond better to Arimidex than Exemestane. I believe there is a place for all 3 of these. That being said, if possible my personal first choice of AI is Exemestane due to its lack of interaction with other compounds we may need to introduce such as certain serms, its positive effects on IGF and Lipids over other options, and also its lack of potential "rebound"(although I think that is an overstated issue quite often).

Regardless of which AI you choose for the vast majority of us our goal can be accomplished of maintaining Estrogen levels in the normal range while on cycle. It might seem like the discussion is over. Why do we even need to look at Serms? Read on:

So we have our Estrogen levels managed, all should be good. Well yes in most cases it will be but what if it isn't? What if you start to get sensitive, itchy or painful nipples? What if you get a lump around your nipple area? What if you are so predisposed to gyno you still get symptoms using an AI? It shouldnt happen but if it does your immediate solution should be a serm.

So we know what serms do. As stated above they bind to the Estrogen receptor in breast tissue, preventing Estrogen from eliciting its effects, which in this case is undesired breast development and tissue growth. However all serms are not created equal for this purpose. I am of the opinion that Raloxifene and Tamoxifen are the 2 best suited serms for this purpose.

Raloxifene is the serm with the highest binding affinity to the Estrogen receptor in breast tissue. Tamoxifen would be second. This means Raloxifene is the most effective serm available for gyno treatment and or prevention. Another point that bears mentioning, when using a Type 2 AI like Arimidex or letrozole, Tamoxifen reduces blood levels of both of these AI's. Raloxifene on the other hand has no effect on blood levels of these AI's, allowing them to be run in conjunction with Raloxifene with no decrease in AI effectiveness. As was mentioned above any serm can be run with Exemestane (a Type 1 AI) with no impact on Exemestane's effectiveness.

Tamoxifen is the serm with probably the most clinical data supporting its use for gyno prevention and treatment, in all likelihood due to the age of the drug. It is very effective for this purpose and very versatile as it is equally if not more effective in the area of PCT as well, meaning often it is likely on hand so it is readily available for most to use in the case of gyno symptoms.

So let's begin to put this all together. An AI should be the core of your Estrogen management program; the goal should be Estrogen levels in the clinically normal range even while on cycle. Id say between 25-30. I cannot emphasize enough the importance of blood work as a management tool. It really is the only effective means of proper Estrogen management (hormone profile management for that matter).

All AI''s can effectively manage Estrogen. My preference in order for this purpose would be Exemestane , then Arimidex , then letrozole however as stated earlier they all have their place. If Exemestane works well for you you have the luxury of the least amount of undesirable side effects and the most versatility as far as combining with a serm should the need arise for gyno prevention and treatment.

The logical question is why do even need to worry about a serm if I mange Estrogen with an Ai? Well hopefully you don't however in some cases it may become necessary due to predisposition, preexisting gyno , very high dosages of aromatizing steroids and so on. For this purpose Raloxifene is in my opinion the top choice offering no reduction in effectiveness of any AI you are running and the most powerful protection against gyno due to its binding affinity to the E receptor in brest tissue. Tamoxifen is also a very solid option especially if running Exemestane as your Ai. If you are running letrozole or arimidex a corresponding increase in the dosage of Ai may be required due to tamoxifen reducing blood levels and effectiveness of these 2 AIs.

Bringng it to theReal World:

1- Manage Estrogen levels with an AI: Exemestane offers the most versatility with fewest adverse effects.
2- Have a Serm on hand in case of Gyno flare up. Raloxifene is most effective and has no adverse interactions with any AIs.

Run a low dose AI with your cycle to try to keep estrogen in the clinically normal range so you can reap the benefits and reduce the deleterious effects. Have a serm on hand just in case gyno rears its head. If it does start a serm immediately. At this point you NEED blood work so you can properly assess your situation and possibly adjust AI dosage up which may allow discontinuation of serm. It may not. You may need to run a serm and AI in conjunction on cycle but it is very unlikely. An Ai should be able to manage Estrogen properly for the vast majority of us. If you do need to run a serm and AI together I cannot emphasize enough that you need to reevaluate your situation. Elevated estrogen has some serious effects as I mentioned above. You should consider this option as I would encourage many too do anyway. Reduce the amount of aromatizing steroids in your cycle and replace them with non-aromatizing compounds. I cannot emphasize this enough. For example a lower test dose will allow for easier estrogen management. This is probably the single biggest thing any of us can do to help ensure proper estrogen management (besides blood work', which again is essential).

One more topic I want to touch on is Gyno. Gyno is considered the worst side effect of elevated estrogen but the fact is it is far from it. There are many much more serious issues going on inside of you if you start growing breasts. That being said when it does occur or start to occur we want to stop it. So often I see people recommend letrozole to treat gyno. This is a horrible idea in my opinion. letrozole works to treat gyno by lowering overall Estrogen levels so much there is no circulating Estrogen to bind to the Estrogen receptor in breast tissue. If you paid attention above you saw the beneficial effects of Estrogen. Some aren''t even beneficial, they are essential. I think to eliminate estrogen to this point throughout your entire body is foolish. Introduce a serm such as raloxifene, block the Estrogen receptor in the breast. The gyno then cannot grow. Then again using blood work adjust your AI dose to MANAGE estrogen levels while taking the serm to prevent the continuation of the gyno.

The above is an interesting topic. I hope this info proved useful to some and I would love to discuss it further.

JimiThing

[gl]

written by BASK8KACE If you've read some of my posts on other boards, you probably already have seen that I advocate suggesting low doses for beginners. Why jump into 600mg per week of test as a first or second cycle when it is highly likely you will get great gains using 200-300mg (in initial cycles)? I keep seeing people write that 200mg of testosterone per week does nothing more than shut down a man's natural test production and bring him near "normal levels"--this is not quite correct (part of the statement is correct part of it is not). This incorrect statement has endured probably because someone wrote down thier idea/theory of what happens in the body, it sounded good, and other people repeated it. But, it is not correct. Yes, 200mg of a long lasting ester of testosterone will shut down natural test production, BUT the amount of 200mg of a long lasting ester of testosterone is more than twice the "normal levels" of test in the body of a healthy non-steroid using male. Therefore, 200mg of a long lasting ester of testosterone per week is far more than enough to grow on. (I explain more below) I was paranoid about side effects of testosterone on a normally functioning body, so I had my blood levels checked while on 200-250mg per week. The results of the tests indicated that the amount of testosterone in my blood was more than twice the high end of the normal range (The normal free testosterone range is 50.0-210.0 pg/ml*. My levels were found to be near 550 pg/ml). I also talked to my doctor and UPJOHN nurses a lot about using testosterone at these doses. Here's a brief bit of what I've learned from my doctor, the UPJOHN nursing staff (UPJOHN was the original manufacturer of Depo-testosterone a.k.a Testosterone Cypionate.  The rights of Depo-testosterone was sold to PFIZER which now produces it under the name PHARMACIA), and professional medical documents: *--NOTE: pg/ml is the correct unit notation. Using a long acting ester testosterone (CYP and ENAN) does not mimic the normally functioning male body's circadian rhythm (daily rise and fall of testosterone). Testosterone, in a normally functioning body, does not explode up to high levels then gradually fall over a 1-2 week period as it does when injecting a testosterone such as CYP or ENAN. On the contrary, the body produces a small amount each day which is far below 200mg (It's around 10mg). That small amount is concentrated at the beginning of the day and then falls low by the end of the day. This process repeats itself every day and by the end of two weeks, a normally functioning body produces approximately 140mg of testosterone (appx. 70mg per week). The use of long acting esters are in theory supposed to slowly release the testosterone over a two week period, but this is not quite what happens. To keep it simple, the delay of the esters actually allows large amounts of testosterone to build up--especially if you are taking 200mg every week as opposed to once every two weeks (biweekly) which is what the dose is supposed to be. (I'm simplifying here). Remember the "normally functioning" male produces only (appx.) 70mg per week (=140mg per two weeks). The dose doctors are recommended to perscribe is 200mg every 2 weeks (biweekly), but they tend to give 200mg every week. So, it is fallacious reasoning to compare the TOTAL amount of testosterone produced in daily spurts in a normally functioning body over a 2 week period to the same amount of testosterone injected in one shot at the beginning of a week and reshot every week (before the previous week's dose is used up). The latter case (injections once per week) results in an overlap and build up of dose which causes the levels of testosterone to be HIGHER than normal. (Remember the shots should actually be 200mg every TWO weeks--not every week). These excess levels of testosterone are sufficient to build lean body mass faster than the "normally functioning" male. In other words: addding up what the average male body produces per week then comparing that to the amount that is shot every week is like comparing apples to oranges. There is a whole diferent set of advantageous reactions happening in the body when it is given a full 2-week load (200mg) at the beginning of a week as opposed to getting naturally occuring, small, daily spurts of appx 10mg over the same period of time (2 weeks). This is why a low dose cycle can yeild REASONABLE gains. Understand, I'm not talking mega-huge-fast gains. I'm talking noticably-faster-than-normal gains, which when coupled with a strict diet, sufficient rest and an excellent bodybuilding work ethic, can yeild large, solid gains (especially early in a person's cycle experience).

[gl]

GENE EXPRESSION IN TENDS/COLLAGEN AFTER HEAVY AAS USE

Researchers in the European Journal of Applied Physiology examined how heavy use of the anabolic steroid Deca-Durabolin affected collagen strength in rats. The rats were separated into two groups: natural training and training with heavy anabolic steroid use. The dose the researchers administered to the rats was considered supra-physiological – Deca-Durabolin (nandrolone decanoate) 5mg/kg of bodyweight.

The rats were cleverly forced to perform resistance exercise, but you can’t just tell a rat to start benching – so the researchers attached weights to the rats’ backs. They dropped the rats into a tank of water and the rats immediately jumped out of the water as soon as they were dunked. Every week, the researchers gradually made the weight on the rats’ backs heavier and heavier until at the end of seven weeks the weight was 80 percent of their bodyweight. The researchers dropped the rats in the tank so that they performed this for 4 sets x 10 repetitions of “jumps” with 30-second rest periods. After that, they rats were sacrificed and the rats’ tendons and collagen were examined for gene expression.

There were some very interesting findings after seven weeks of training with anabolic steroids, compared with the natty (natural) group of rats. The natty group did not have any biochemical changes in the rat tendon/collagen properties, while the anabolic steroid group had major changes.(6) The Deca-Durabolin group had reduced biochemical properties of genes involving tendon and collagen strength.

It is interesting to note that AAS administration reduced the accumulation of IGF-1 mRNA levels in some tendon regions, compared to the non-treated, trained group. This decrease of IGF-1 mRNA levels induced by AAS administration may be related to the observed decreases collagen expression when considering the possible connection between IGF-1 and collagen synthesis.(8) The AAS treatment also decreased the MMP-2 mRNA expression (this gene encodes an enzyme for collagen).

The above study is similar to another recently published study, which showed that nandrolone impaired the healing of rotator cuffs of rabbits. In the latter study, male rabbits underwent an incision in the rotator cuff and were divided into groups with anabolic steroids (nandrolone decanoate, 10mg/kg) and natural recovery. Groups that did not receive anabolic steroids showed better healing and more tendon strength compared to groups that received anabolic steroids. Microscopic examination of specimens from the groups with anabolic steroid use showed focal fibroblastic reaction and inflammation, suggesting an impaired healing response.(7)

The key point is that many of these studies were using supraphysiological dosages of steroids that could be like the typical Olympia stack – but the new research suggests that a high-volume approach to training with less weight may be a better approach to use for a bodybuilder than a high-intensity, heavy weight program that puts more stress on the tendons and makes them more susceptible to injury.

By Robbie Durand, M.A., Senior Science Editor of Muscular Development


References:

1. Evans NA, Bowrey DJ, Newman GR (1998) Ultrastructural analysis of ruptured tendon from anabolic steroid users. Injury, 29:769-773.
2: Marqueti RC, Prestes J, Paschoal M, Ramos OH, Perez SE, Carvalho HF, Selistre-de-Araujo HS (2008) Matrix metallopeptidase 2 activity in tendon regions: effects of mechanical loading exercise associated to anabolic-androgenic steroids, Eur J Appl Physiol, 104:1087-1093.
3: Marqueti RC, Prestes J, Wang CC, Ramos OH, Perez SE, Nakagaki WR, Carvalho HF, Selistre-de-Araujo HS (2010). Biomechanical responses of different rat tendons to nandrolone decanoate and load exercise. Scand J Med Sci Sports, 29.
4: Marqueti RC, Parizotto NA, Chriguer RS, Perez SEA, Selistre-de-Araujo HS (2006) Androgenic-anabolic steroids associated with mechanical loading inhibit matrix metallopeptidase activity and affect the remodeling of the Achilles tendon in rats. Am J Sport Med, 34:1274-1280.
5: Oikarinen A, Autio P, Vuori J, Va¨a¨na¨nen K, Risteli L, Kiistala U, Risteli J (1992) Systemic glucocorticoid treatment decreases serum concentrations of carboxyterminal propeptide of type I procollagen and aminoterminal propeptide of type III procollagen. Br J Dermatol, 126:172-178.
6: Marqueti RC, Heinemeier KM, Durigan JL, de Andrade Perez SE, Schjerling P, Kjaer M, Carvalho HF, Selistre-de-Araujo HS. Erratum to: Gene expression in distinct regions of rat tendons in response to jump training combined with anabolic androgenic steroid administration. Eur J Appl Physiol, 2011 Sep 8.
7: Papaspiliopoulos A, Papaparaskeva K, Papadopoulou E, Feroussis J, Papalois A, Zoubos A. The effect of local use of nandrolone decanoate on rotator cuff repair in rabbits. J Invest Surg, 2010 Aug;23(4):204-7.
8: Heinemeier KM, Olesen JL, Schjerling P, Hassad F, Langberg H, Baldwin KM, Kjaer M (2007b) Short-term strength training and the expression of myostatin and IGF-1 isoforms in rat muscle and tendon: differential effects of specific contraction types. J Appl Physiol, 102:573-581.

[gl]

By Swale

I advise my AAS patients to use small amounts of HCG (250IU to 500IU) two days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.

Any more than 500IU of HCG per day causes too much aromatase activity. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).

If 250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn’t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.

The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM’s at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.

I want my patients to stop taking HCG within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a “bridge”. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can’t “fool” the body—it is smarter than you are.

I like arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).

All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other protocols.

[gl]

Short-term oxandrolone administration stimulates net muscle protein synthesis in young men.Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR, Ferrando AA.
Department of Surgery, University of Texas Medical Branch, and Shriners Burn Hospital for Children, Galveston 77550, USA. [link widoczny dla zalogowanych U¿ytkowników]

Short term administration of testosterone stimulates net protein synthesis in healthy men. We investigated whether oxandrolone [Oxandrin (OX)], a synthetic analog of testosterone, would improve net muscle protein synthesis and transport of amino acids across the leg. Six healthy men [22+/-1 (+/-SE) yr] were studied in the postabsorptive state before and after 5 days of oral OX (15 mg/day). Muscle protein synthesis and breakdown were determined by a three-compartment model using stable isotopic data obtained from femoral arterio-venous sampling and muscle biopsy. The precursor-product method was used to determine muscle protein fractional synthetic rates. Fractional breakdown rates were also directly calculated. Total messenger ribonucleic acid (mRNA) concentrations of skeletal muscle insulin-like growth factor I and androgen receptor (AR) were determined using RT-PCR. Model-derived muscle protein synthesis increased from 53.5+/-3 to 68.3+/-5 (mean+/-SE) nmol/min.100 mL/leg (P < 0.05), whereas protein breakdown was unchanged. Inward transport of amino acids remained unchanged with OX, whereas outward transport decreased (P < 0.05). The fractional synthetic rate increased 44% (P < 0.05) after OX administration, with no change in fractional breakdown rate. Therefore, the net balance between synthesis and breakdown became more positive with both methodologies (P < 0.05) and was not different from zero. Further, RT-PCR showed that OX administration significantly increased mRNA concentrations of skeletal muscle AR without changing insulin-like growth factor I mRNA concentrations. We conclude that short term OX administration stimulated an increase in skeletal muscle protein synthesis and improved intracellular reutilization of amino acids. The mechanism for this stimulation may be related to an OX-induced increase in AR expression in skeletal muscle.

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testosterone injection stimulates net protein synthesis but not tissue amino acid transport.Ferrando AA, Tipton KD, Doyle D, Phillips SM, Cortiella J, Wolfe RR.
Department of Surgery, University of Texas Medical Branch, Galveston, Texas 77550, USA.

testosterone administration (T) increases lean body mass and muscle protein synthesis. We investigated the effects of short-term T on leg muscle protein kinetics and transport of selected amino acids by use of a model based on arteriovenous sampling and muscle biopsy. Fractional synthesis (FSR) and breakdown (FBR) rates of skeletal muscle protein were also directly calculated. Seven healthy men were studied before and 5 days after intramuscular injection of 200 mg of testosterone enanthate. protein synthesis increased twofold after injection (P < 0.05), whereas protein breakdown was unchanged. FSR and FBR calculations were in accordance, because FSR increased twofold (P < 0.05) without a concomitant change in FBR. Net balance between synthesis and breakdown became more positive with both methodologies (P < 0.05) and was not different from zero. T injection increased arteriovenous essential and nonessential nitrogen balance across the leg (P < 0.05) in the fasted state, without increasing amino acid transport. Thus T administration leads to an increased net protein synthesis and reutilization of intracellular amino acids in skeletal muscle

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Insulin action on muscle protein kinetics and amino acid transport during recovery after resistance exercise.Biolo G, Williams BD, Fleming RY, Wolfe RR.
Department of Internal Medicine, University of Texas Medical Branch, and the Shriners Burns Hospital, Galveston, USA.

We have determined the individual and combined effects of insulin and prior exercise on leg muscle protein synthesis and degradation, amino acid transport, glucose uptake, and alanine metabolism. Normal volunteers were studied in the postabsorptive state at rest and about 3 h after a heavy leg resistance exercise routine. The leg arteriovenous balance technique was used in combination with stable isotopic tracers of amino acids and biopsies of the vastus lateralis muscle. Insulin was infused into a femoral artery to increase the leg insulin concentrations to high physiologic levels without substantively affecting the whole-body level. protein synthesis and degradation were determined as rates of intramuscular phenylalanine utilization and appearance, and muscle fractional synthetic rate (FSR) was also determined. Leg blood flow was greater after exercise than at rest (P<0.05). Insulin accelerated blood flow at rest but not after exercise (P<0.05). The rates of protein synthesis and degradation were greater during the postexercise recovery (65+/-10 and 74+/-10 nmol x min(-1) x 100 ml(-1) leg volume, respectively) than at rest (30+/-7 and 46+/-8 nmol x min(-1) x 100 ml(-1) leg volume, respectively; P<0.05). Insulin infusion increased protein synthesis at rest (51+/-4 nmol x min(-1) x 100 ml(-1) leg volume) but not during the postexercise recovery (64+/-9 nmol x min(-1) x 100 ml(-1) leg volume; P<0.05). Insulin infusion at rest did not change the rate of protein degradation (48+/-3 nmol x min(-1) 100 ml(-1) leg volume). In contrast, insulin infusion after exercise significantly decreased the rate of protein degradation (52+/-9 nmol x min(-1) x 100 ml(-1) leg volume). The insulin stimulatory effects on inward alanine transport and glucose uptake were three times greater during the postexercise recovery than at rest (P<0.05). In contrast, the insulin effects on phenylalanine, leucine, and lysine transport were similar at rest and after exercise. In conclusion, the ability of insulin to stimulate glucose uptake and alanine transport and to suppress protein degradation in skeletal muscle is increased after resistance exercise. Decreased amino acid availability may limit the stimulatory effect of insulin on muscle protein synthesis after exercise.

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Nutritional and pharmacological support of the metabolic response to injury.Herndon DN.
Shriners Hospitals for Children-Galveston Burns Hospital, SHC-G, Professor of Pediatrics &amp; Surgery, University of Texas Medical Branch, UTMB, USA. [link widoczny dla zalogowanych U¿ytkowników]

Severe burn incites metabolic disturbances which last up to one year post injury. Persistent profound catabolism after severe burn hampers rehabilitative efforts delaying meaningful return of individuals to society. The simplest effective anabolic strategies for severe burn injuries are early excision and grafting of the burn wound, prompt treament of sepsis, maintenance of environmental temperature at 30-32 inverted exclamation mark C, continuous enteral feeding of a high carbohydrate, high protein diet, early institution of vigorous resistive and aerobic resistive exercise programs. To further minimize erosion of lean body mass administration of recombinant human growth hormone, insulin, oxandrolone or propranolol are all reasonable approaches. Exogenous continuous low dose insulin infusion, beta blockade with propranolol and the use of the synthetic testosterone analog, oxandrolone are the most cost effective and least toxic pharmaco therapies to date.

Quote:
The effect of oxandrolone treatment on human osteoblastic cells.Bi LX, Wiren KM, Zhang XW, Oliveira GV, Klein GL, Mainous EG, Herndon DN.
Department of Oral and Maxillofacial Surgery, University of Texas Medical Branch, Galveston, TX, USA. [link widoczny dla zalogowanych U¿ytkowników]

OBJECTIVE: Oxandrolone, administered to severely burned children over the first year postburn, produces increased lean body mass by 6 months; however, an increase in total body bone mineral requires 12 months. Consequently, this bone mineral response may be due to increased muscle mass. Alternatively, oxandrolone may act directly on bone. The current study seeks to determine whether oxandrolone can transactivate the androgen receptor in osteoblasts. METHODS: Collagen, alkaline phosphatase, osteocalcin, osteoprotegerin, and androgen receptor abundance were determined by qRT-PCR, confocal laser scanning microscopy, or immunoquantitative assay. To determine the effect of oxandrolone on gene expression in differentiated cells, osteocytic cultures were grown to confluence in differentiation medium and then treated 24 hours or 5 days with 15 microg/mL oxandrolone. RESULTS: Increased nuclear fluorescence of the androgen receptor and increased cellular type I collagen were observed with oxandrolone at 15 and 30 microg/mL but not at lower doses. Alkaline phosphatase (7%-20%) and osteocalcin (13%-18%) increases were modest but significant. Short-term treatment produced no significant effects, but at 5 days androgen receptor levels were increased while collagen levels were significantly decreased, with little effect on alkaline phosphatase, osteocalcin, or osteoprotegerin. CONCLUSIONS: These data suggest oxandrolone can stimulate production of osteoblast differentiation markers in proliferating osteoblastic cells, most likely through the androgen receptor; however, with longer treatment in mature cells, oxandrolone decreases collagen expression. Thus it is possible that oxandrolone given to burned children acts directly on immature osteoblasts to stimulate collagen production, but also may have positive effects to increase bone mineral through other mechanisms

Oxandrolone enhances skeletal muscle myosin synthesis and alters global gene expression profile in Duchenne muscular dystrophy.Balagopal P, Olney R, Darmaun D, Mougey E, Dokler M, Sieck G, Hammond D.
Nemours Children's Clinic, Jacksonville, FL 32207, USA. [link widoczny dla zalogowanych U¿ytkowników]

Earlier studies have shown that the progressive, unrelenting muscle loss associated with Duchenne muscular dystrophy (DMD) involves an imbalance between the rates of synthesis and degradation of muscle proteins. Although previous studies have suggested that oxandrolone may be beneficial in DMD, the mechanism of action of oxandrolone on muscle in DMD remains unclear. To address these issues, we combined stable isotope studies and gene expression analysis to measure the fractional synthesis rate of myosin heavy chain (MHC), the key muscle contractile protein, the transcript levels of the isoforms of MHC, and global gene expression profiles in four children with DMD before and after 3 mo of treatment with oxandrolone. Gastrocnemius muscle biopsies and blood samples were collected during the course of a primed 6-h continuous infusion of l-[U-(13)C]leucine on two separate occasions, before and after the 3-mo treatment with oxandrolone (0.1 mg.kg(-1).day(-1)). Gene expression analysis was done with microarrays and RT-qPCR. In response to the treatment, MHC synthesis rate increased 42%, and this rise was accounted for, at least in part, by an upregulation of the transcript for MHC8 (perinatal MHC). Gene expression data suggested a decrease in muscle regeneration as a consequence of oxandrolone therapy, presumably because of a decrease in muscle degeneration. These findings suggest that 1) oxandrolone has a powerful protein anabolic effect on a key contractile protein and 2) larger and longer-term studies are warranted to determine whether these changes translate into meaningful therapy for these patients.

Comparing Oxandrin and Anadrol-50.Vazquez E.
AIDS: Oxandrin and Anadrol-50 are both oral anabolic steroids approved by the Food and Drug Administration (FDA), and they are competing for market share in the world of HIV treatments. Both are described as "open label" drugs and as such, are prescribed to reverse wasting and metabolic complications associated with HIV. Anadrol-50 is among the most potent steroids ever developed for building muscle, and study participants gained an average of 14.5 pounds for each 100 pounds of weight. Early studies indicate minimal side effects with liver toxicity, but that is not a certainty since oral anabolics are known for liver toxicity. Many studies have documented Oxandrin's safety and effectiveness in treating HIV wasting. It is metabolized in the kidney and acts without the masculinizing side effects associated with other steroids, such as Anadrol-50. One study showed an average weight gain of 24 pounds following 8 months of treatment. Oxandrin is the best choice for those at the earliest stages of AIDS wasting syndrome. However, when a more aggressive treatment is necessary, Anadrol-50 is stronger, less expensive, and more effective, but liver function must be monitored closely.

Oxandrolone for weight gain.[No authors listed]
AIDS: Oxandrolone, an oral drug that promotes weight gain in people experiencing weight loss, has been approved by the Food and Drug Administration (FDA) for patients with HIV. Oxandrolone's effectiveness in HIV-related weight loss is unknown. The drug is a man-made anabolic steroid. Several small studies have shown encouraging results for HIV-related weight loss when doses two to eight times the recommended dosage were used. Daily doses ranging from 20 to 80 mg appear to be needed for treating HIV-associated wasting syndrome. A host of side effects usually associated with anabolic steroids are not seen as frequently with oxandrolone, including liver toxicity. More information can be obtained by contacting the Project Inform Hotline.

[fallenursus]

Jesus.
Cliffs?
:p

[gl]

I was like, should I post it or no and then aaaa what the Hell, why not;)

mam wiecej jak cos ale nie wiem czy chcesz??

[fallenursus]

Jasne skoñczy mi siê Adhd jak siê obudze to przeczytam wiêcej jak 3 wersy :)

[gl]

hehehe nie ma to tamto 3a czytac;)
To Badanie jest niezle, sami sobie zaprzeczaja ale w sumie to dobrze robimy ze jesmy duzo bialeczka mniam mnia
trzeba tylko pamietac o Calcium i vit D i bedzie git

High Protein Diets
Increased protein intakes and supplementation have generally been focused on athletic populations. However, over the past few years high protein diets have become a method used by the general population to enhance weight reduction. The low-carbohydrate, high protein, high fat diet promoted by Atkins may be the most popular diet used today for weight loss in the United States (Johnston et al., 2004). The basis behind this diet is that protein is associated with feelings of satiety and voluntary reductions in caloric consumption (Araya et al., 2000; Eisenstein et al., 2002). A recent study has shown that the Atkins diet can produce greater weight reduction at 3 and 6 months than a low-fat, high carbohydrate diet based upon U.S. dietary guidelines (Foster et al., 2003). However, potential health concerns have arisen concerning the safety of high protein diets. In 2001, the American Heart Association published a statement on dietary protein and weight reduction and suggested that individuals following such a diet may be at potential risk for metabolic, cardiac, renal, bone and liver diseases (St. Jeor et al., 2001).

Protein Intake and Metabolic Disease Risk
One of the major concerns for individuals on high protein, low carbohydrate diets is the potential for the development of metabolic ketosis. As carbohydrate stores are reduced the body relies more upon fat as its primary energy source. The greater amount of free fatty acids that are utilized by the liver for energy will result in a greater production and release of ketone bodies in the circulation. This will increase the risk for metabolic acidosis and can potentially lead to a coma and death. A recent multi-site clinical study (Foster et al., 2003) examined the effects of low-carbohydrate, high protein diets and reported significant elevation in ketone bodies during the first three months of the study. However, as the study duration continued the percentage of subjects with positive urinary ketone concentrations became reduced, and by six months urinary ketones were not present in any of the subjects.

Dietary Protein and Cardiovascular Disease Risk
High protein diets have also been suggested to have negative effects on blood lipid profiles and blood pressure, causing an increase risk for cardiovascular disease. This is primarily due to the higher fat intakes associated with these diets. However, this has not been proven in any scientifically controlled studies. Hu et al., (1999) have reported an inverse relationship between dietary protein (animal and vegetable) and risk of cardiovascular disease in women, and Jenkins and colleagues (2001) reported a decrease in lipid profiles in individuals consuming a high protein diet. Furthermore, protein intake has been shown to often have a negative relationship with blood pressure (Obarzanek et al., 1996). Thus, the concern for elevated risk for cardiovascular disease from high protein diets appears to be without merit. Likely, the reduced body weight associated with this type of diet is facilitating these changes.

In strength/power athletes who consume high protein diets, a major concern was the amount of food being consumed that was high in saturated fats. However, through better awareness and nutritional education many of these athletes are able to obtain their protein from sources that minimizes the amount of fat consumed. For instance, removing the skin from chicken breast, consuming fish and lean beef, and egg whites. In addition, many protein supplements are available that contain little to no fat. It should be acknowledged though that if elevated protein does come primarily from meats, dairy products and eggs, without regard to fat intake, there likely would be an increase in the consumption of saturated fat and cholesterol.

Dietary Protein and Renal FunctionThe major concern associated with renal function was the role that the kidneys have in nitrogen excretion and the potential for a high protein diet to over-stress the kidneys. In healthy individuals there does not appear to be any adverse effects of a high protein diet. In a study on bodybuilders consuming a high protein (2.8 g&middot;kg-1) diet no negative changes were seen in any kidney function tests (Poortsman and Dellalieux, 2000). However, in individuals with existing kidney disease it is recommended that they limit their protein intake to approximately half of the normal RDA level for daily protein intake (0.8 g&middot;kg-1&middot;day-1). Lowering protein intake is thought to reduce the progression of renal disease by decreasing hyperfiltration (Brenner et al., 1996).

Dietary Protein and Bone
High protein diets are associated with an increase in calcium excretion. This is apparently due to a consumption of animal protein, which is higher in sulfur-based amino acids than vegetable proteins (Remer and Manz, 1994; Barzel and Massey, 1998). Sulfur-based amino acids are thought to be the primary cause of calciuria (calcium loss). The mechanism behind this is likely related to the increase in acid secretion due to the elevated protein consumption. If the kidneys are unable to buffer the high endogenous acid levels, other physiological systems will need to compensate, such as bone. Bone acts as a reservoir of alkali, and as a result calcium is liberated from bone to buffer high acidic levels and restore acid-base balance. The calcium released by bone is accomplished through osteoclast-mediated bone resorption (Arnett and Spowage, 1996). Bone resorption (loss or removal of bone) will cause a decline in bone mineral content and bone mass (Barzel, 1976), increasing the risk for bone fracture and osteoporosis.

The effect of the type of protein consumed on bone resorption has been examined in a number of studies. Sellmeyer and colleagues (2001) examined the effects of various animal-to- vegetable protein ratio intakes in elderly women (> 65 y). They showed that the women consuming the highest animal to vegetable protein ratio had nearly a 4-fold greater risk of hip fractures compared with women consuming a lower animal to vegetable protein ratio. Interestingly, they did not report any significant association between the animal to vegetable protein ratio and bone mineral density. Similar results were shown by Feskanich et al (1996), but in a younger female population (age range = 35 - 59 mean 46). In contrast, other studies examining older female populations have shown that elevated animal protein will increase bone mineral density, while increases in vegetable protein will have a lowering effect on bone mineral density (Munger et al., 1999; Promislow et al., 2002). Munger and colleagues (1999) also reported a 69% lower risk of hip fracture as animal protein intake increased in a large (32,000) postmenopausal population. Other large epidemiological studies have also confirmed elevated bone density following high protein diets in both elderly men and women (Dawson-Hughes et al., 2002; Hannan et al., 2000). Hannon and colleagues (2000) demonstrated that animal protein intake in an older population, several times greater than the RDA requirement, results in a bone density accruement and significant decrease in fracture risk. Dawson-Hughes et al (2002), not only showed that animal protein will not increase urinary calcium excretion, but was also associated with higher levels of IGF-I and lower concentrations of the bone resorption marker N-telopeptide.

These conflicting results have contributed to the confusion regarding protein intake and bone. It is likely that other factors play an important role in further understanding the influence that dietary proteins have on bone loss or gain. For instance, the intake of calcium may have an essential function in maintaining bone. A higher calcium intake results in more absorbed calcium and may offset the losses induced by dietary protein and reduce the adverse effect of the endogenous acidosis on bone resorption (Dawson-Hughes, 2003). Furthermore, it is commonly assumed that animal proteins have a higher content of sulfur-containing amino acids per g of protein. However, examination of Table 4 shows that this may not entirely correct. If protein came from wheat sources it would have a mEq of 0.69 per g of protein, while protein from milk contains 0.55 mEq per g of protein. Thus, some plant proteins may have a greater potential to produce more mEq of sulfuric acid per g of protein than some animal proteins (Massey, 2003). Finally, bone resorption may be related to the presence or absence of a vitamin D receptor allele. In subjects that had this specific allele a significant elevation in bone resorption markers were present in the urine following 4-weeks of protein supplementation, while in subjects without this specific allele had no increase in N-telopeptide (Harrington et al., 2004). The effect of protein on bone health is still unclear, but it does appear to be prudent to monitor the amount of animal protein in the diet for susceptible individuals. This may be more pronounced in individuals that may have a genetic endowment for this. However, if animal protein consumption is modified by other nutrients (e.g. calcium) the effects on bone health may be lessened.

Protein Intake and Liver Disease RiskThe American Heart Association has suggested that high protein diets may have detrimental effects on liver function (St. Jeor et al., 2001). This is primarily the result of a concern that the liver will be stressed through metabolizing the greater protein intakes. However, there is no scientific evidence to support this contention. Jorda and colleagues (1988) did show that high protein intakes in rats produce morphological changes in liver mitochondria. However, they also suggested that these changes were not pathological, but represented a positive hepatocyte adaptation to a metabolic stress.

Protein is important for the liver not only in promoting tissue repair, but to provide lipotropic agents such as methionine and choline for the conversion of fats to lipoprotein for removal form the liver (Navder and Leiber, 2003a). The importance of high protein diets has also been acknowledged for individuals with liver disease and who are alcoholics. High protein diets may offset the elevated protein catabolism seen with liver disease (Navder and Leiber, 2003b), while a high protein diet has been shown to improve hepatic function in individuals suffering from alcoholic liver disease (Mendellhall et al., 1993).