Enhanced Protein Synthesis primary desire with anabolics, trenbolone or testosterone

Iron Game

Veteran
Protein is the primary building block of muscle. It is not the only important factor but it is primary. Protein synthesis refers to the rate by which cells build proteins and as synthesis is increased more is available for work and production. This increases the body’s anabolic atmosphere, and also greatly improves the overall rate of recovery, which is essential to total progress. This is not only important during periods of growth, but essential to periods of weight loss in a preservation capacity.*
 
Lets Name the Best Steroids that have the highest rate of Protein Synthesis , anyone know what the best one would be? Testosterone maybe?
 
This is a great article for newbies and vets alike. :fyi: By: John Berardi
Do you remember back when your momma read bedtime stories to you? You know, illustrated children's books spinning tales of old Gepetto and Pinnochio, Jack and his Beanstalk, and Raskolnikov and his Crime and his Punishment. What's that?

No one ever read Crime and Punishment to you? Okay, just kidding about that one, but in all seriousness, one of the themes that makes a great children's story is the clear delineation between good and evil. When you're a kid, you know whom to love and you know whom to hate.

Thinking back, one of my favorite stories was the legend of Robin Hood. This story told of a daring outlaw who robbed from the rich and gave to the poor. In my youth I was enamored with his cunning and his loyalty to his friends. It was always satisfying when his quick wit allowed him to make a fool of the powerful Sheriff of Knottingham.

On one occasion, Robin and his men were able to sneak into an archery contest and win the first prize, a golden arrow. Although this contest was a trap set by Knottingham, Robin and his merry men had good on their side and were able to win the arrow and escape capture. I've liked the underdog ever since.

Unfortunately in today's supplement market, a modern day Sherwood Forest if you will, a story is being told that's the antithesis of the Robin Hood story. You see, in this bedtime tale, the rich Knottinghams of the industry are robbing from the consumer, and they're doing so with promises of golden arrows.

So, true to my love of the underdog, you know where this article is headed. Just call me Robin Hood (and no, I don't wear tights!).


A Little Knowledge Is Dangerous


Weight lifters today are more informed about training and nutrition than they were a decade ago. But as often is the case, a little information can be dangerous. Unfortunately, you and your wallet are the ones in danger in this case.

Take the phenomenon of overnight catabolism, for example. First, you learn what the word catabolic means. It's the opposite of anabolic and has to do with muscle wasting. Then you learn that you become catabolic during sleep at night. As a result, you make it your goal to prevent this catabolism at any cost.

Now here comes the dangerous part. The big bad Knottinghams of the supplement world realize your unnecessary desperation and begin to use this information against you, spinning scientific-sounding tales based on spurious assumptions and false promises.

They come as a wolf dressed in sheep's clothing and, unlike the fairy tales of our youth, it becomes difficult to distinguish the heroes from the villains.

Keeping with the overnight catabolism theme, Knottingham's new golden arrow is his so-called "nighttime anti-catabolic protein formula." He's been trying to convince would-be supplement consumers that his super expensive, slow-released protein blends are the only way to prevent wasting away to nothing overnight.

Using fancy words and a couple of inappropriate references, he claims that the conventional protein powders on the market today are useless for overnight consumption and that only his special high-tech blend will make you huge.

With furrowed brow, I unsheath my arrow.


What Happens When the Lights Go Out


When tucking into bed at night, you're about to embark on a six to eight hour journey of rest and repair. After all, it's been a long day in the forest. However, during this time you aren't feeding the body. We call this the post-absorptive period. If you haven't heard of this post-absorptive period before, let me explain.

Throughout the day, the first hour or two after eating is referred to as the post-prandial period. During this time, the body digests and absorbs nutrients. When you eat and even during the post-prandial period, the body's maintenance needs for blood glucose and energy are met. At this time it begins to synthesize proteins and glycogen in the liver and muscle.

Once this period is over, the post-absorptive period sets in. After the absorption of the nutrients from your last meal is complete and the nutrients in the blood have been delivered, the body begins using those stored nutrients for energy.

Then, in order to maintain blood glucose and tissue metabolism, the liver and muscle start metabolizing and sending glucose and amino acids out into the blood.

If you're eating frequently during the day, the overnight period is your longest post-absorptive period. It should be no surprise that after an overnight fast and a long post-absorptive period, some of the muscle glycogen and muscle protein will have been depleted. In fact, research has verified this hypothesis and shown specifically that after the overnight fast, muscle protein breakdown exceeds muscle protein synthesis.

Interestingly, the opposite is true in the splanchnic region (gut, liver, etc) because in these tissues, synthesis exceeds breakdown. Therefore during the night, muscle is broken down to feed the gut/liver/etc and presumably other tissues as well (1).


Feeding For Increased Muscle Mass: Nuts And Berries Of The Forest Won't Do It


Understanding what happens after an overnight fast, I'm sure you're now wondering how you might keep out of the post absorptive period and prevent overnight muscle losses. Well, the secret is in understanding how the body handles protein and amino acids under normal conditions. Remember, net muscle-protein status (anabolism or catabolism) is determined by a simple equation: protein synthesis minus protein breakdown.

Large increases in blood amino acid levels (100-200% above the fasted baseline) are necessary for increasing protein synthesis. Therefore a protein meal containing at least 20-30 grams of fast-digesting protein (like whey) can accomplish such a goal.

Interestingly, to inhibit protein breakdown we only need small increases in blood amino-acid levels (25-50% above fasted baseline). However, these small increases must be prolonged (4-5 hours) in order to realize this inhibition of protein breakdown. In this situation, a slow-digesting protein like casein is necessary.

So, at this point you might be asking why you can't simply consume whey protein every few hours in order to maintain super-high levels of blood amino acids. It makes sense that this would keep amino acid levels high for a very long period of time, thus stimulating protein synthesis and preventing protein breakdown, right? Well, not so fast, Little John.

Unfortunately, when large increases in blood amino acid levels (+100%) are achieved via intravenous infusion for a prolonged period of six hours, protein synthesis only increases from the 30 minute to the two-hour mark. After two hours, protein synthesis rates almost immediately return to baseline.

Unbelievably, protein synthesis rates remain at baseline levels from the two hour to the six hour marks, even with the same level of hyperaminoacidemia (2).

So it's clear that keeping amino acid levels elevated all day won't keep protein synthesis rates racing along. It's my guess that if you were to try to do this, breakdown would simply balance synthesis and you wouldn't get any bigger.

It's my theory that you need those phasic bursts in amino-acid levels to stimulate protein synthesis.

If you're keeping up, this presents a confusing picture as to how to time your meals for optimal protein growth. In my opinion, large bursts of hyperaminoacidemia every four hours or so (to stimulate synthesis in a phasic manner), coupled with a prolonged low-level hyperaminoacidemia (to chronically inhibit breakdown) may be the best way to coerce the muscles into getting huge.

So how can you accomplish this? That's easy, at least when you're awake.

Consider the "pros" and "cons" of the bodybuilder's two main sources of protein:


Whey protein intake (30g) produces large transient hyperaminoacidemia. After an hour, blood amino acids are elevated by about 300%. After two hours, about 92%. After four hours, you're back to baseline. This is ideal for increased protein synthesis but does nothing for protein breakdown (3,4).

Casein protein intake (30g) produces moderate but prolonged hyperaminoacidemia. After two hours, blood amino acids are elevated by about 32% and after four hours by about 35%. After seven hours, blood amino acids are still elevated. This is ideal for prevention of protein breakdown but does nothing for protein synthesis (3,4).
The next question is, where the heck are you gonna find whey and casein protein in Sherwood Forest? Well, if you can find a cow or a goat, you're in luck.

Milk protein is composed of 80% casein and 20% whey. Milk is interesting in that, believe it or not, the whey and casein fractions are absorbed separately. In one study, subjects consumed skimmed milk and were evaluated over the course of eight hours.

With milk-protein ingestion, there's a rapid rise in blood amino acids within one hour (probably as a result of the whey fraction), a plateau from one to three hours (a combination of simultaneous whey and casein absorption), and then there's a progressive decline over the course of the next eight hours.

However, blood amino acids are still elevated at the eight hour point as a result of the casein fraction. (5).

While this discussion has only dealt with milk proteins, it may be safe to say that most animal proteins are probably similar to casein in their slow digestion and absorption profiles. So, during the day, eating a combination of fast digesting and slow-digesting proteins every four hours or so is probably the best way to maintain a highly positive daily protein status.

Again, this can be done with milk proteins alone or with a combination of whey or milk protein and animal protein at each meal.

In the end, though, don't get too obsessed with seeking out your favorite cow every four hours. Research has shown that eating animal protein alone does a nice job of increasing post-prandial protein synthesis, too.


Don't Let The Sheriff's Men Steal Your Muscles Overnight


All these recommendations are interesting for the waking hours while you're robbing from the rich, but what about at night when bedding down with the lovely Maid Marian?

Well, if I had an ideal nighttime protein shake to set by the bed, it would include a combination of ingredients that promotes two large bursts of hyperaminoacidemia every four hours (leading to two bursts of synthesis - one at bedtime and one four hours later) and a prolonged low-level hyperaminoacidemia (to inhibit breakdown).

Now, part of this can be accomplished with a milk-isolate blend taken immediately before bed. There are many such blends on the market.

At this point, you might be asking yourself why I simply don't recommend milk. Well, I'm hesitate to suggest milk as a result of the recent data showing that unfermented, intact milk (skim or whole) may not be all that great for you. The high incidence of milk allergies and lactose intolerance coupled with a huge insulin index makes me hesitant to give my endorsement to the moo juice.

However, milk products like cottage cheese behave differently than milk and are another solid choice. The whey content of cottage cheese could use some beefing up though, so don't be afraid to throw in some whey or milk isolates.

Although quite effective, unfortunately this route doesn't allow for the second burst of fast protein and hyperaminoacidemia that we want about four hours into our slumber. So the simplest way to do this would be to make a big shake/meal before bed, consume half at bedtime and the other half in the middle of the night.


The Golden Arrows


You can certainly wake up in the middle of the night to provide the body with some protein nutrition, but some people believe doing so will disturb sleep patterns and in the long run, you'll be worse for the waking.

So why not formulate a special high-tech protein powder that will accomplish our goal of two large bursts of hyperaminoacidemia every four hours (two bursts of synthesis - one at bedtime and one four hours later) and a prolonged low-level hyperaminoacidemia (to inhibit breakdown) without having to wake up to get it?

Such a formula might contain 15g of regular whey protein, 30g of casein, and 15g of time-released, encapsulated whey protein that sits around in the gut for four hours and is magically released during one big digestive burst at that time.

With such a formula, the 60g protein dose would definitely keep you covered for the overnight fast and might help you pack on a little extra muscle.

Excited yet? Well, don't fall for the trap. I'm sorry to tell you that such a formula is probably impossible to make. First of all, I'm not aware of any technology that will allow such a precision release of protein at a predetermined time. Secondly, if there were a way to do this, the costs would certainly be prohibitive.

But what about the current crop of overnight protein formulas popping up in magazine ads? What are they supposed to do? Well, unfortunately they don't even claim to accomplish the goals I set out above.

All they claim to do is provide you with a slow released protein that keeps blood levels of amino acids low and stable all night, thus minimizing protein breakdown. Considering that plain old cottage cheese can accomplish this goal, these formulations aren't so revolutionary.

In fact, either milk protein blends or homemade whey/casein combinations may even be superior to slow digesting proteins alone, as indicated above. The combination of fast and slow may be best for both increasing muscle protein synthesis and preventing muscle protein breakdown.

So why the need for fancy overnight protein products? At a price of four to seven bucks per 50g of protein (based on the brands I've looked at), I can't see one. All I can see is the rich robbing from the misinformed poor.


A Happy Ending


To summarize this little bedtime story:


About halfway through the night your body runs out of muscle-building fuel and leaves you in a catabolic state. To prevent this, it's a good idea to get some protein before bed.
The so-called "nighttime anti-catabolic protein formulas" hitting the market are overpriced, overhyped, and aren't even ideal for battling catabolism.
A better and more-affordable choice is plain old cottage cheese and/or a blend of proteins like those found in Low-Carb Grow! (Milk itself isn't a good choice however.)
Armed with these arrows of information, I'll now let you go do battle with catabolism and all those unscrupulous Sheriff of Knottinghams out there. Now, where'd that little muffin Maid Marian run off to?
 
ANAVAR RESEARCH
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. [email protected]

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.

Quote:
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 & Surgery, University of Texas Medical Branch, UTMB, USA. [email protected]

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.

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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. [email protected]

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. [email protected]

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.

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Treatment with an anabolic agent is associated with improvement in respiratory function in persons with tetraplegia: a pilot study.Spungen AM, Grimm DR, Strakhan M, Pizzolato PM, Bauman WA.
Rehabilitation Medicine, Mount Sinai School of Medicine, New York, NY, USA.

BACKGROUND: Pulmonary complications are a major cause of morbidity and mortality among individuals with cervical spinal cord lesions. Strengthening of the respiratory musculature may reduce these complications. Anabolic steroids have been used to increase muscle mass and improve muscle performance. Oxandrolone, an anabolic steroid, may have beneficial effects on breathing in persons with tetraplegia. METHODS: The effect of one-month treatment with oxandrolone on weight gain and pulmonary function was studied in ten subjects with complete motor tetraplegia. Spirometry, maximal inspiratory and expiratory pressures, and resting self-rating of dyspnea (Borg Scale) were measured at baseline and repeated again at the end of one month of oxandrolone therapy (20 mg/day). Serum lipid profiles and liver function tests were performed before and after treatment. A paired t-test was used to determine pre- and post-treatment differences on the dependent variables. Percent change from baseline was calculated for each variable and tested using a one-sample t-test. RESULTS: On average, the subjects gained 1.4+/-1.5 kg, a 2+/-2% increase in weight (p=0.01). A significant, 9+/-2% improvement was found in the combined measures of spirometry (p<0.005). Maximal inspiratory pressure improved an average of 10+/-7% (p<0.001). Maximal expiratory pressure improved 9+/-13% (non-significant). Subjective self-rating of dyspnea decreased an average of 37+/-28% (p<0.01). CONCLUSIONS: In healthy subjects with tetraplegia, the use of oxandrolone was associated with significant improvements in weight and pulmonary function, and a subjective reduction in breathlessness. Therefore, oxandrolone may be indicated to strengthen respiratory musculature in individuals who have tetraplegia and ventilatory insufficiency aggravated by superimposition of pneumonia or other such conditions. However, long-term use of oxandrolone may not be indicated, due to the adverse complications associated with this class of agents.
 
yeah probably tren ace for sure , as well as divorce synthesis, anger synthesis , break shit synthesis and so on and so forth lol
 
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