Clenbuterol is a β2 agonist with certain structural and pharmacological similarities to ephinphrineand Albuterol, but its effects are more potent and longer-lasting as a stimulant and thermogenic
drug than any other drug in its category. Clen causes an increase in aerobic capacity, central nervous system stimulation, and an increase in blood pressure and oxygen transportation. It increases the rate at which body fat is metabolized while increasing the body’s body’s metabolic rate which basically allows your body to break down macronutrients MUCH EASIER. It is commonly prescribed by doctors it’s for smooth muscle relaxant properties. It used as bronchodilator by people who suffer from breathing disorders like as asthma.  When it comes to beta-2 agonists Like Celn, Albuterol, and ephedrine everyone reacts differently. Half of my article will explain what clenbuterol looks like on paper, in studies, and how it should work and has worked for many people. However Through my many years in dealing with real life people as well as my own experiences I have learned No two people are exactly alike. Everyone reacts differently to different compounds from the side effects they experience to the results they get from them.  I can only explain to you what studies have shown me, what information I have gathered from various literature/resources, what I have learned through my own experiences,  and lastly what I have learned through helping others use these chemicals.  I have used clenbuterol  several different times in several different ways.  I did not get great results with clenbuterol and I did not like the side effects I experienced.  Nonetheless I personally know thousands of people who loved both the results and the experience of using clenbuterol. This may or may not be the right research chemical for you.. My job is to Arm you with as much information as I can so that you can experience clenbuterol for your self. In the safest  possible way and knowing everything there is to know about how your experience may turn out. So that you will be ready for whatever comes your way. So that You can Kill that Sh*t the right way..

What Beta 2 adrenegic agonists?

They promote smooth muscle relaxation, resulting in the dilation of bronchial pathways, vasodilation in liver and muscle, they also cause the relaxation of uterine muscle in women, and the release of insulin where its anabolic properties begin. Beta-adrenergic receptors are stacked together to stimulate G protein. The alpha subunit of the G protein activates adenylyl cyclase, which then catalyzes the production of cyclic adenosine monophosphate  aka cAMP. In the lung, cAMP produces a decrease in the intracellular calcium plasma concentrationd through activation of protein kinase A.  In addition, beta-2 agonists open large conductance calcium-activated potassium channels and thereby tend to hyperpolarize airway smooth muscle cells. The combination of decreased intracellular calcium and increased membrane potassium conductance, with decreased myosin light chain kinase activity leads to smooth muscle relaxation and bronchodilation.  This is the reason the body gets so dehydrated and cramped during a Clen run. We will dive into further in a bit.

Clen improves body composition

In this study I came across twenty-three unfit Standard bred mares were divided into four experimental groups. The one group was give 2.4 mcg per kg of clen body weight twice daily plus exercise. The exercise routine was 50 of their max oxygen utilization at three times a week.  Booty fat thickness was measured at 2 week intervals by using B-mode ultrasound, and percent body fat (%fat) was calculated by using previously published methods. Results indicated body fat decreased 9.3% at week 4 and 6.9% at week 6, and fat-free mass) increased by 3.2% at week 8. On the other hand, Clen had significant changes in %fat (-15.4%), fat mass (-14.7%), and FFM (+4.3%) at week 2. ClenEx had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen; however, this group had a different fat free mass response, which significantly increased moer than 4.4% at week 6. That is amazing when you consider this was only a period 8 weeks (2months). Most people are happy if they can lose 2 percent bodyfat in 12 weeks. The fact that fat free mass INCREASED shows that this drug is not only thermogenic but also ANABOLIC. Again this has to be attributed to the fact that Clen increases insulin release, remember insulin is the most anabolic hormone in the body.  (J Appl Physiol. 2001 Nov;91(5):2064-70)

Thought I never would say this, CLen is good for the liver LOL

In a study I came upon, Clenbuterol minimized LPS-induced liver damage, as represented by significantly lowered concentrations of several parameters for liver-failure (AST, ALT, Bilirubin), and improved hepatic tissue morphology. Clenbuterol administration after LPS challenge failed to inhibit TNF alpha-release but reduced liver-damage. Simultaneous use of the beta(2)-AR antagonist propranolol augmented LPS-induced liver failure, suggesting a role of endogenous adrenoceptor-agonists in prevention of organ-failure during systemic inflammation. The results indicate that a selective beta(2)-AR agonist might be used as an additional therapeutic agent in the clinic for the treatment of (acute) systemic inflammatory disorders in order to reduce or prevent subsequent liver failure.  Am I telling you guys to use this as liver protectant on cycle, NOOOOOOOO! All I am getting at is that it’s not liver toxic like others mentioned unless you do not treat your electrolyte levels with care, which can lead other problems besides liver issues, such as heart failure, brain malfunction and so on. (Inflamm Res. 2004 Mar;53(3):93-9. Epub 2004 Feb 16.)

Clen can aid in endurance, well at least for those who have asthma

Already it has been mentioned that Clen aids those with asthma as it breaks of the congested passageways, so that air flows freely. This in turn will allow the individual to do more anaerobic and aerobic activity. In this study, the protective effect of clenbuterol on exercise-induced asthma was studied in 14 patients with a specific bronchial hyperreactivity. The selectivity of clenbuterol for beta 2-receptors was also looked at during this study. Patients were selected according to spirometric criteria: reduced dynamic indexes of respiratory function after exercise and, particularly, forced expiratory volume at 1 s (FEV1) decreased by at least 20% compared with initial values. A polycardiographic study was simultaneously carried out for the evaluation of systolic time intervals and polycardiographic indexes. After the preliminary measurements (C1), oral clenbuterol was taken at 0.02 mg twice a day and measurements were repeated after 30 (CII) and 60 days (CIII) of therapy. During treatment, physical exercise did not significantly influence the indexes of respiratory function (FEV1 decreased by 4.7 +/- 5.8 and 9.8 +/- 10.5% in CII and CIII with respect to initial values). Similarly systolic time intervals and polycardiographic indexes did not change significantly with respect to the initial values. A small increase in heart rate at rest was observed in CII (+ 7%, p less than 0.05): however, no significant changes were recorded in CIII compared with the initial values. Clenbuterol thus seems to offer an effective protection against exercise-induced asthma without the negative effects on the cardiovascular system which may arise from activation of beta 1-adrenergic receptors.  The key is to take the proper dosage with clen, as too much causes respiratory issues which we will dive into. (Respiration. 1987;51(3):205-13.)

Clebuterol improves athletic performance?

Unlike inhaled beta 2-agonists, more studies  and human trials need to be performed before the action of systemic beta 2-agonists on athletic performance can be assessed accurately. Experiments in animals with oral clenbuterol have shown growth in muscle bulk across numerous species, but human studies cannot confirm similar muscle mass enlargement in healthy men at the moment. Of course the human studies demonstrate the potential for long-acting systemic beta 2-agonists such as Clen to increase muscle strength in certain muscle fiber types, it is difficult to judge the drugs’ effects on overall athletic performance, because athletic skill is more than strength, speed, and endurance. The effect of oral clenbuterol on athletic performance cannot be evaluated from its actions on muscle strength alone but effects on motor skill/ coordination. However, as evidence stands now, sports regulatory agencies are correct to ban systemic beta 2-agonists until the following 2 points can be proven: (1) oral forms provide a therapeutic benefit that cannot be obtained with aerosol or inhaled forms; and (2) oral forms do not give any unfair advantage to the competitor in muscle strength, power output, or endurance. Provided they are administered as prescribed, aerosol or inhaled beta-agonists do not impart an unfair advantage or enhance athletic performance and can continue to be used in competition by athletes with EIA. However, small studies have shown a small increase in power ouput. I know others such as myself receive a nice initial boost in lifts, for the first few weeks. Part of the reason the strength increase goes away is tolerance, but the other reason is probably tissue receptor saturation, meaning the B 2 receptors desensitized, thus no longer easily stimulated to give that nice pronounced effect. I will disagree with the article in stating that it is not known to whether Beta-2 agonists stimulate brain function, as it is clear that they stimulate the production of cAMP which definitely activates NMDA receptors. NMDA receptors are responsible for hormone production, cathelomine production and even other neurotransmitter production such as DOPAMINE. Both Dopamine and PEA are crucial for motor and coordination skills. Everytime I start taking Clen, I definitely notice more awareness, more MIND MUSCLE CONNECTION and so on.  I would NOT rule out Clen as performance enhancer by any means. For crying out loud, there are still researchers who do not find creatine monohydrate to be a performance enhancer. PFFTTT! (Ann Pharmacother. 1995 Jan;29(1):75-7.)

How to prevent down regulation

As you know Clen starts to lose its potency over a period of an estimated 14 days but I would say more 10 days LOL. Benedryl is one of the anti histamines people use help prevent toldernace. The other anti histamine is Ketofin which again does the same thing. Basically anit histamines inhibit phospholipase which brings the desensitization of beta 2 receptors to a hault. Thus, allowing one to have a longer effective Clen cycle. With these Anithistamines in your system, you can use Clen longer without the typical 1-2 week break in between. Most people will go 2 on and 2 off, but with these anti-histamines you could technically go 4 plus weeks straight. This is of course only one way of doing things and I personally Like a much different method which we will talk about later in my ” Clenbuterol dosage” segment of this write up.

Clenbuterol side effects 

Clebuterol depletes taurine from the body

If you want to read the study, I have the citation in paranthesis at the end of this paragraph. I can tell you this, that depletion of taurine can be really unsafe if not monitored. Taurine is responsible for storing electrolytes within their due tissues. Without a proper balance of electrolytes, the body WILL NOT FUNCTION PROPERLY. Be sure to supplement Taurine at least 950mg a day post work out or even as much as 3-6g daily.I recommend taking a dose of just Taurine  in the am, after your second dose of Clen, and post training . The reason Clenbuterol depletes taurine levels in the Liver , is because the body it stops the conversion of T4 to T3 within the Liver.  This is why many chemical using experts will suggest running T3 while on a Clen cycle. Since taurine will aid reducing electrolyte depletion, it will decrease overall cramps. I also recommend taking calcium as mentioned before, all B2 agonist will deplete calcium, so be sure to supplement at 500mg of Calcium while on Clen. Now you will need to supplement magnesium with Clen but it MUST be taken at a different time of the day then Calcium, as magnesium competes with calcium for the same receptors.  Potassium must also be taken during your clen cycle, you could always add some coconut water and bananas to your regime, as they are loaded with potassium and will be absorbed more efficiently than a potassium supplement.   (Adv Exp Med Biol. 1996;403:233-45.)

Not so good for cardio

Yes I know we discussed how the right amount of Clen could aid in endurance, but aerobic activitiy is a different part of your cardio conditioning, also think of it like this. I know people can lift more reps which requires more oxygen while on a cycle, yet; they cannot run the miles they were able to off of cycle. The difference here is merely aerobic verse anaerobic exercises. Anaerobic activity is based off of short bursts while aerobic activity is geared more the long haul. A power lifter would be a description of an anaerobic athlete, while a triathlon competitor would be a good description of an aerobic athlete. In a study I found, Clen Xdecreased O2max around 6.2% and velocity to O2max decreased 10.0%, whereas both CLENEX and CLEN decreased in time to exhaustion between 4 and 6 percent.  EX alone increased  O2max by more than 6.5%, velocity to O2max over 10.0%, velocity to produces lactate concentration of 4 mmol or plus 13.5%, and time to exhaustion slightly under 15%. Plasma volume was altered in CLENEX below 10% and EX over 27% but not in CLEN. Posttest recovery HR was higher at 2 min post-GXT in the CLENEX, CLEN, and CON compared with their pretest values; RVP remained elevated at 2 min of recovery in the CLEN and CON groups; however, in the EX, recovery HR and RVP had returned to pre-GXT levels by 2 min of recovery. There you notice that with other groups, their heart rate returned to normal, but with the pure clen group heart rate was still elevated, sure they were able to push beyond a normal rate but with the normal healthy body they would have recovered faster. I like to think of this like someone taking ephedrine before a fight, they would gas out in the first round due to such an elevated heart rate, the heart needs to be able to settle so that the body stays hydrated, and adrenaline to cortisol stay at proper levels, no one wants an adrenaline dump during competition, as their performance will suffer greatly.  (Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.)

Clen can cause Skin Cell Death of the Heart at least in Rats

We all know that high doses of Clen cause extremely elevated heart rate levels. But we all thought it was only from the increased metabolic rate, thyroid production, and depletion of potassium. Well in essence, in theory, the depletion of potassium could be the reason for myocyte necrosis within the heart. Of course more research would be warranted to prove this theory but I cannot affor to pay for it. LMAO! In this study, Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. This data shows significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term heart health.

It is my job to tell you the dangers of everything as well as the benefits my friends. Unlike the Media however I will only tell you the truth and not over hyped propaganda with an agenda behind it. No I will explain the side effects and dangers of using a chemical that are “real”..

Celnbuterol

Clenbuterol is a β2 agonist with certain structural and pharmacological similarities to ephinphrineand Albuterol, but its effects are more potent and longer-lasting as a stimulant and thermogenic
drug than any other drug in its category. Clen causes an increase in aerobic capacity, central nervous system stimulation, and an increase in blood pressure and oxygen transportation. It increases the rate at which body fat is metabolized while increasing the body’s body’s metabolic rate which basically allows your body to break down macronutrients MUCH EASIER. It is commonly prescribed by doctors it’s for smooth muscle relaxant properties. It used as bronchodilator by people who suffer from breathing disorders like as asthma.  When it comes to beta-2 agonists Like Celn, Albuterol, and ephedrine everyone reacts differently. Half of my article will explain what clenbuterol looks like on paper, in studies, and how it should work and has worked for many people. However Through my many years in dealing with real life people as well as my own experiences I have learned No two people are exactly alike. Everyone reacts differently to different compounds from the side effects they experience to the results they get from them.  I can only explain to you what studies have shown me, what information I have gathered from various literature/resources, what I have learned through my own experiences,  and lastly what I have learned through helping others use these chemicals.  I have used clenbuterol  several different times in several different ways.  I did not get great results with clenbuterol and I did not like the side effects I experienced.  Nonetheless I personally know thousands of people who loved both the results and the experience of using clenbuterol. This may or may not be the right research chemical for you.. My job is to Arm you with as much information as I can so that you can experience clenbuterol for your self. In the safest  possible way and knowing everything there is to know about how your experience may turn out. So that you will be ready for whatever comes your way. So that You can Kill that Sh*t the right way..

What Beta 2 adrenegic agonists?

They promote smooth muscle relaxation, resulting in the dilation of bronchial pathways, vasodilation in liver and muscle, they also cause the relaxation of uterine muscle in women, and the release of insulin where its anabolic properties begin. Beta-adrenergic receptors are stacked together to stimulate G protein. The alpha subunit of the G protein activates adenylyl cyclase, which then catalyzes the production of cyclic adenosine monophosphate  aka cAMP. In the lung, cAMP produces a decrease in the intracellular calcium plasma concentrationd through activation of protein kinase A.  In addition, beta-2 agonists open large conductance calcium-activated potassium channels and thereby tend to hyperpolarize airway smooth muscle cells. The combination of decreased intracellular calcium and increased membrane potassium conductance, with decreased myosin light chain kinase activity leads to smooth muscle relaxation and bronchodilation.  This is the reason the body gets so dehydrated and cramped during a Clen run. We will dive into further in a bit.

Clen improves body composition

In this study I came across twenty-three unfit Standard bred mares were divided into four experimental groups. The one group was give 2.4 mcg per kg of clen body weight twice daily plus exercise. The exercise routine was 50 of their max oxygen utilization at three times a week.  Booty fat thickness was measured at 2 week intervals by using B-mode ultrasound, and percent body fat (%fat) was calculated by using previously published methods. Results indicated body fat decreased 9.3% at week 4 and 6.9% at week 6, and fat-free mass) increased by 3.2% at week 8. On the other hand, Clen had significant changes in %fat (-15.4%), fat mass (-14.7%), and FFM (+4.3%) at week 2. ClenEx had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen; however, this group had a different fat free mass response, which significantly increased moer than 4.4% at week 6. That is amazing when you consider this was only a period 8 weeks (2months). Most people are happy if they can lose 2 percent bodyfat in 12 weeks. The fact that fat free mass INCREASED shows that this drug is not only thermogenic but also ANABOLIC. Again this has to be attributed to the fact that Clen increases insulin release, remember insulin is the most anabolic hormone in the body.  (J Appl Physiol. 2001 Nov;91(5):2064-70)

Thought I never would say this, CLen is good for the liver LOL

In a study I came upon, Clenbuterol minimized LPS-induced liver damage, as represented by significantly lowered concentrations of several parameters for liver-failure (AST, ALT, Bilirubin), and improved hepatic tissue morphology. Clenbuterol administration after LPS challenge failed to inhibit TNF alpha-release but reduced liver-damage. Simultaneous use of the beta(2)-AR antagonist propranolol augmented LPS-induced liver failure, suggesting a role of endogenous adrenoceptor-agonists in prevention of organ-failure during systemic inflammation. The results indicate that a selective beta(2)-AR agonist might be used as an additional therapeutic agent in the clinic for the treatment of (acute) systemic inflammatory disorders in order to reduce or prevent subsequent liver failure.  Am I telling you guys to use this as liver protectant on cycle, NOOOOOOOO! All I am getting at is that it’s not liver toxic like others mentioned unless you do not treat your electrolyte levels with care, which can lead other problems besides liver issues, such as heart failure, brain malfunction and so on. (Inflamm Res. 2004 Mar;53(3):93-9. Epub 2004 Feb 16.)

Clen can aid in endurance, well at least for those who have asthma

Already it has been mentioned that Clen aids those with asthma as it breaks of the congested passageways, so that air flows freely. This in turn will allow the individual to do more anaerobic and aerobic activity. In this study, the protective effect of clenbuterol on exercise-induced asthma was studied in 14 patients with a specific bronchial hyperreactivity. The selectivity of clenbuterol for beta 2-receptors was also looked at during this study. Patients were selected according to spirometric criteria: reduced dynamic indexes of respiratory function after exercise and, particularly, forced expiratory volume at 1 s (FEV1) decreased by at least 20% compared with initial values. A polycardiographic study was simultaneously carried out for the evaluation of systolic time intervals and polycardiographic indexes. After the preliminary measurements (C1), oral clenbuterol was taken at 0.02 mg twice a day and measurements were repeated after 30 (CII) and 60 days (CIII) of therapy. During treatment, physical exercise did not significantly influence the indexes of respiratory function (FEV1 decreased by 4.7 +/- 5.8 and 9.8 +/- 10.5% in CII and CIII with respect to initial values). Similarly systolic time intervals and polycardiographic indexes did not change significantly with respect to the initial values. A small increase in heart rate at rest was observed in CII (+ 7%, p less than 0.05): however, no significant changes were recorded in CIII compared with the initial values. Clenbuterol thus seems to offer an effective protection against exercise-induced asthma without the negative effects on the cardiovascular system which may arise from activation of beta 1-adrenergic receptors.  The key is to take the proper dosage with clen, as too much causes respiratory issues which we will dive into. (Respiration. 1987;51(3):205-13.)

Clebuterol improves athletic performance?

Unlike inhaled beta 2-agonists, more studies  and human trials need to be performed before the action of systemic beta 2-agonists on athletic performance can be assessed accurately. Experiments in animals with oral clenbuterol have shown growth in muscle bulk across numerous species, but human studies cannot confirm similar muscle mass enlargement in healthy men at the moment. Of course the human studies demonstrate the potential for long-acting systemic beta 2-agonists such as Clen to increase muscle strength in certain muscle fiber types, it is difficult to judge the drugs’ effects on overall athletic performance, because athletic skill is more than strength, speed, and endurance. The effect of oral clenbuterol on athletic performance cannot be evaluated from its actions on muscle strength alone but effects on motor skill/ coordination. However, as evidence stands now, sports regulatory agencies are correct to ban systemic beta 2-agonists until the following 2 points can be proven: (1) oral forms provide a therapeutic benefit that cannot be obtained with aerosol or inhaled forms; and (2) oral forms do not give any unfair advantage to the competitor in muscle strength, power output, or endurance. Provided they are administered as prescribed, aerosol or inhaled beta-agonists do not impart an unfair advantage or enhance athletic performance and can continue to be used in competition by athletes with EIA. However, small studies have shown a small increase in power ouput. I know others such as myself receive a nice initial boost in lifts, for the first few weeks. Part of the reason the strength increase goes away is tolerance, but the other reason is probably tissue receptor saturation, meaning the B 2 receptors desensitized, thus no longer easily stimulated to give that nice pronounced effect. I will disagree with the article in stating that it is not known to whether Beta-2 agonists stimulate brain function, as it is clear that they stimulate the production of cAMP which definitely activates NMDA receptors. NMDA receptors are responsible for hormone production, cathelomine production and even other neurotransmitter production such as DOPAMINE. Both Dopamine and PEA are crucial for motor and coordination skills. Everytime I start taking Clen, I definitely notice more awareness, more MIND MUSCLE CONNECTION and so on.  I would NOT rule out Clen as performance enhancer by any means. For crying out loud, there are still researchers who do not find creatine monohydrate to be a performance enhancer. PFFTTT! (Ann Pharmacother. 1995 Jan;29(1):75-7.)

How to prevent down regulation

As you know Clen starts to lose its potency over a period of an estimated 14 days but I would say more 10 days LOL. Benedryl is one of the anti histamines people use help prevent toldernace. The other anti histamine is Ketofin which again does the same thing. Basically anit histamines inhibit phospholipase which brings the desensitization of beta 2 receptors to a hault. Thus, allowing one to have a longer effective Clen cycle. With these Anithistamines in your system, you can use Clen longer without the typical 1-2 week break in between. Most people will go 2 on and 2 off, but with these anti-histamines you could technically go 4 plus weeks straight. This is of course only one way of doing things and I personally Like a much different method which we will talk about later in my ” Clenbuterol dosage” segment of this write up.

Clenbuterol side effects 

Clebuterol depletes taurine from the body

If you want to read the study, I have the citation in paranthesis at the end of this paragraph. I can tell you this, that depletion of taurine can be really unsafe if not monitored. Taurine is responsible for storing electrolytes within their due tissues. Without a proper balance of electrolytes, the body WILL NOT FUNCTION PROPERLY. Be sure to supplement Taurine at least 950mg a day post work out or even as much as 3-6g daily.I recommend taking a dose of just Taurine  in the am, after your second dose of Clen, and post training . The reason Clenbuterol depletes taurine levels in the Liver , is because the body it stops the conversion of T4 to T3 within the Liver.  This is why many chemical using experts will suggest running T3 while on a Clen cycle. Since taurine will aid reducing electrolyte depletion, it will decrease overall cramps. I also recommend taking calcium as mentioned before, all B2 agonist will deplete calcium, so be sure to supplement at 500mg of Calcium while on Clen. Now you will need to supplement magnesium with Clen but it MUST be taken at a different time of the day then Calcium, as magnesium competes with calcium for the same receptors.  Potassium must also be taken during your clen cycle, you could always add some coconut water and bananas to your regime, as they are loaded with potassium and will be absorbed more efficiently than a potassium supplement.   (Adv Exp Med Biol. 1996;403:233-45.)

Not so good for cardio

Yes I know we discussed how the right amount of Clen could aid in endurance, but aerobic activitiy is a different part of your cardio conditioning, also think of it like this. I know people can lift more reps which requires more oxygen while on a cycle, yet; they cannot run the miles they were able to off of cycle. The difference here is merely aerobic verse anaerobic exercises. Anaerobic activity is based off of short bursts while aerobic activity is geared more the long haul. A power lifter would be a description of an anaerobic athlete, while a triathlon competitor would be a good description of an aerobic athlete. In a study I found, Clen Xdecreased O2max around 6.2% and velocity to O2max decreased 10.0%, whereas both CLENEX and CLEN decreased in time to exhaustion between 4 and 6 percent.  EX alone increased  O2max by more than 6.5%, velocity to O2max over 10.0%, velocity to produces lactate concentration of 4 mmol or plus 13.5%, and time to exhaustion slightly under 15%. Plasma volume was altered in CLENEX below 10% and EX over 27% but not in CLEN. Posttest recovery HR was higher at 2 min post-GXT in the CLENEX, CLEN, and CON compared with their pretest values; RVP remained elevated at 2 min of recovery in the CLEN and CON groups; however, in the EX, recovery HR and RVP had returned to pre-GXT levels by 2 min of recovery. There you notice that with other groups, their heart rate returned to normal, but with the pure clen group heart rate was still elevated, sure they were able to push beyond a normal rate but with the normal healthy body they would have recovered faster. I like to think of this like someone taking ephedrine before a fight, they would gas out in the first round due to such an elevated heart rate, the heart needs to be able to settle so that the body stays hydrated, and adrenaline to cortisol stay at proper levels, no one wants an adrenaline dump during competition, as their performance will suffer greatly.  (Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.)

Clen can cause Skin Cell Death of the Heart at least in Rats

We all know that high doses of Clen cause extremely elevated heart rate levels. But we all thought it was only from the increased metabolic rate, thyroid production, and depletion of potassium. Well in essence, in theory, the depletion of potassium could be the reason for myocyte necrosis within the heart. Of course more research would be warranted to prove this theory but I cannot affor to pay for it. LMAO! In this study, Myocyte-specific necrosis in the heart and soleus muscle of adult male Wistar rats was investigated in response to a single subcutaneous injection of the anabolic beta(2)-adrenergic receptor agonist clenbuterol. Necrosis was immunohistochemically detected by administration of a myosin antibody 1 h before the clenbuterol challenge and quantified by using image analysis. Clenbuterol-induced myocyte necrosis occurred against a background of zero damage in control muscles. In the heart, the clenbuterol-induced necrosis was not uniform, being more abundant in the left subendocardium and peaking 2.4 mm from the apex. After position (2.4 mm from the apex), dose (5 mg clenbuterol/kg), and sampling time (12 h) were optimized, maximum cardiomyocyte necrosis was found to be 1.0 +/- 0.2%. In response to the same parameters (i.e., 5 mg of clenbuterol and sampled at 12 h), skeletal myocyte necrosis was 4.4 +/- 0.8% in the soleus. This data shows significant myocyte-specific necrosis in the heart and skeletal muscle of the rat. Such irreversible damage in the heart suggests that clenbuterol may be damaging to long-term heart health.

It is my job to tell you the dangers of everything as well as the benefits my friends. Unlike the Media however I will only tell you the truth and not over hyped propaganda with an agenda behind it. No I will explain the side effects and dangers of using a chemical that are “real”..

Clenbuterol dosage

When dosing clenbuterol you have several different ways of doing so however we have two main common dosing protocols. The first one being the 4 weeks on 4 weeks off clenbuterol dosage program, and the second being the 2 weeks on 2 weeks off clenbuterol dosage program.  Weather you decide to go with 2 weeks on 2 weeks off or 4 weeks on 4 weeks off the dosing will always start off the same and gradually increase/ramp up the same as well. When starting your clenbuterol program you will want to sart out with 3 20mcg doses a day and move up 20mcg every 2 to 3 days till you reach 140mcg max dosing for a man 100mcg for a woman IMO of course. Always spread the dosing out over 3 doses a day or more if you can and space them a couple of hours apart.  Never go above 140mcg and always only go up 20mcg every 2 to 3 days. You must access tolerance  first moving into clen easy to gauge how your body will react to this compound. Always live on the side of safety my friends.  Once you reach 140mcg stick to that dose for the rest of the time you are on the clen cycle. If you are a smaller person Ie below 175lb then you need not go above 100mcg at most. This should be plenty to see results and always remember that more is not always better. Here is what my dosing looked like over the first 10 days of my last clenbuterol program…

Day.  Morning/noon/night

1. 20mcg/20mcg/20mcg

2. 20mcg/20mcg/20mcg

3. 40mcg/20mcg/20mcg

4. 40mcg/20mcg/20mcg

5. 40mcg/40mcg/20mcg

6. 40mcg/40mcg/20mcg

7. 40mcg/40mcg/40mcg

8. 40mcg/40mcg/40mcg

9. 40mcg/40mcg/40mcg

10. 60mcg/40mcg/40mcg

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Therefore, in obese people, overeating may be the result of their brain signaling a huge biochemical reward for ingesting food, even when the body already has met its energergetic demands. This means your craving for food might not be a result of the body signaling a need for more energy, but rather a falsified impulse triggered by your pleasure center.

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Effect of Dietary Protein Content on Weight Gain, Energy Expenditure, and Body Composition During Overeating

A Randomized Controlled Trial

Abstract

Context The role of diet composition in response to overeating and energy dissipation in humans is unclear.

Objective To evaluate the effects of overconsumption of low, normal, and high protein diets on weight gain, energy expenditure, and body composition.

Design, Setting, and Participants A single-blind, randomized controlled trial of 25 US healthy, weight-stable male and female volunteers, aged 18 to 35 years with a body mass index between 19 and 30. The first participant was admitted to the inpatient metabolic unit in June 2005 and the last in October 2007.

Intervention After consuming a weight-stabilizing diet for 13 to 25 days, participants were randomized to diets containing 5% of energy from protein (low protein), 15% (normal protein), or 25% (high protein), which they were overfed during the last 8 weeks of their 10- to 12-week stay in the inpatient metabolic unit. Compared with energy intake during the weight stabilization period, the protein diets provided approximately 40% more energy intake, which corresponds to 954 kcal/d (95% CI, 884-1022 kcal/d).

Main Outcome Measures Body composition was measured by dual-energy x-ray absorptiometry biweekly, resting energy expenditure was measured weekly by ventilated hood, and total energy expenditure by doubly labeled water prior to the overeating and weight stabilization periods and at weeks 7 to 8.

Results Overeating produced significantly less weight gain in the low protein diet group (3.16 kg; 95% CI, 1.88-4.44 kg) compared with the normal protein diet group (6.05 kg; 95% CI, 4.84-7.26 kg) or the high protein diet group (6.51 kg; 95% CI, 5.23-7.79 kg) (P = .002). Body fat increased similarly in all 3 protein diet groups and represented 50% to more than 90% of the excess stored calories. Resting energy expenditure, total energy expenditure, and body protein did not increase during overfeeding with the low protein diet. In contrast, resting energy expenditure (normal protein diet: 160 kcal/d [95% CI, 102-218 kcal/d]; high protein diet: 227 kcal/d [95% CI, 165-289 kcal/d]) and body protein (lean body mass) (normal protein diet: 2.87 kg [95% CI, 2.11-3.62 kg]; high protein diet: 3.18 kg [95% CI, 2.37-3.98 kg]) increased significantly with the normal and high protein diets.

Conclusions Among persons living in a controlled setting, calories alone account for the increase in fat; protein affected energy expenditure and storage of lean body mass, but not body fat storage.

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Fish oil, for example, will help you burn fat…but did you know it will also help you build muscle? Researchers gave 22 subjects 4 capsules each containing 1 g fish oil (600 mg EPA and 200 mg DHA), daily, for six weeks (another group got a placebo). As you can see from the chart below, the fish oil  group lost about a pound of fat, but they also gained about the same amount of lean mass:

So fish oil is one of those fat-loss products that won’t just help you lose fat, but also helps build lean mass at the same time. And another study performed at Johannes Gutenberg University in Germany, showed that fish oil could sharpen mental focus. But perhaps even more interesting to bodybuilders is that fish oil has also been shown to be anti-estrogenic and can even elevate levels of IGF-1, a highly anabolic hormone. Dietary fatty acids , specifically those found in fish oil, have also been shown to be major biologic regulators and have properties that improve overall health. And Krill oil, has been shown to be at least equal, though perhaps better, than fish oil, in all areas that have been scientifically studies thus far.

And how about caffeine? Caffeine can help you burn fat by preferentially “telling” your body to use body fat for fuel instead of protein and carbohydrates – but it can also help improve focus, aid muscular contractions (thereby boosting strength levels, and even boost athletic performance. That’s why we have included it in every fat burner we make!

But what about creatine? We all know that it makes you bigger and stronger, but most people forget that it’s a wonderful fat loss agent. And not only does it help you lose fat, it can give a significant boost to your working memory and general intelligence. Yeah, believe it or not, creatine can turn dumb-jocks into smart-jocks. And it also helps aid general health by improving cardiovascular indexes and heart function.

We can’t forget testosterone either – it’s been shown in numerous studies to not only build muscle, but also to burn fat and although you can’t purchase testosterone legally without a prescription, there are plenty of great testosterone boosters on the market. But did you know that adequate testosterone levels can help everything from maintaining normal glucose (blood sugar) levels, to optimal thyroid levels,  to a healthy heart? And it’s been shown in some studies to help improve cognitive function as well.

But perhaps just as astonishing is Whey Protein – which we know builds muscle and burns fat like no other protein we’ve ever had in the bodybuilding market. In one study, performed on rodents, it protected them against versus tumors induced by the powerful carcinogen, dimethylhydrazine. And in vivo, research suggests it to be a potent weapon against breast cancer.  Some cancer patients have even seen reduced tumor size in a published study. Whey protein consumption has been linked to improved cholesterol levels, and furthermore to be a potent inhibitor of oxidized LDL cholesterol. And would you believe that whey can improve bone health too? Well it can – it has been shown to boost total protein synthesis and DNA content of bone cells. At the same time, it also has been proven to be an immunostimulator – it boosts your immune system. Unbelievable huh? Because it also helps you burn fat, just like the rest of the compounds here!

So although many people think of losing weight as being inherently “unhealthy” – the truth is that many of the best fat burners are also very healthy as well.

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Lymphatic malformation works on the lymphatic system, which is responsible for removing excess fluid from tissues and organs, and transporting white blood cells. But in lymphatic malformation, the vessels become clogged, and fluid builds up, creating large cysts of spongelike tissue that further impedes the transport of fluid and white blood cells.

sometimes these growths disappear after a few years, although many patients have them permanently. In some cases, the growths are simply cosmetic, but as with any type of tumor, they can put pressure on internal organs, as well as the eyes, tongue, and the throat, thereby leading to major complications including respiratory distress, heart failure, and even blindness. Treatment options include surgical removal or the injection of a drug; but these options aren’t effective for all types of the disease.

This unexpected use for Viagra is surprising, but perhaps seems less crazy when you consider that it was first developed to treat high blood pressure, and the chemical in Viagra, sildenafil, is also sold under the brand name Revatio, as a treatment for high blood pressure involving the lungs. The researchers stumbled on this new use for Viagra when an infant girl presented with a severe case of lymphatic malfunction that caused growth in her chest and resulted in high blood pressure – you guessed it – involving the lungs.

The pressure caused high blood pressure, so the girl was given Revatio. .The result was a massive reduction in growths, so it was given to two more patients, one of whom experienced a  ~25 percent reduction in a vision-obstructing growth, and , and another saw a ~75% reduction in growths on her back. Last month the highly prestigious New England Journal of Medicine published the findings. Since then, a fourth patient has been treated, and again improvement was seen.

Unfortunately, the growths come back upon cessation of treatment. And although the exact mechanism of action at work is yet-undiscovered, researchers are hopeful that this discovery will lead to an eventual cure.

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Hello,

I’m really happy you’re taking the time out of your day to read my bio.  Never in a million years did I dream I’d be placing myself on an inmate web site to find companionship, but here I am.

If you’re interested in who I am, or what I was all about, then Google me; I’m all over the internet.  Do not believe everything you read; some is true and some is not.  I used to be a professional athlete and now I’m in prison…it’s a long story and if you get to know me I’ll share it with you.  Just know that I’m a loyal Capricorn looking for a true friend in every sense of the word.

I work out five days a week to keep myself in shape.  I keep up on all current events.  I enjoy reading novels and listen to all types of music.

Please make sure to include your address when you write to me.  I cannot email you, you can only email me.  If you’d like to write me direct my current address is below.

I’m looking forward to hearing from you! (smile)

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If you’re considering steroid use or prohormone use, or are simply new to the steroid world, consider this a crash course; if you’re already an old hand at steroid use, consider this a refresher course; because for over two decades, with few exceptions, we’ve been in a relative drought for cutting-edge studies. It goes without saying that any steroid or prohormone cycle ought to be accompanied by something to support your health and something like HCGenerate to support a speedy return to normal hormone levels. N2 Guard is actually considered a “must have” supplement among health-conscious prohormone fans, for helping to keep them healthy while on a cycle.

During the early days of steroid research, thousands of different anabolic steroids were described by the pharmaceutical industry, in a seemingly endless attempt to formulate the Holy Grail – a completely side-effect free steroid, with ideal anabolic and androgenic properties. But very few of steroids ever made it through the testing phase and even fewer moved on to be patented.

That’s why, every so often, we see some new steroid showing up as an undetectable compound being used in doping circles, or on the nutritional market. The former arises from the inevitable demand athletes place on themselves to be the best in their given sport, while the latter comes from a poorly written law in the United States of America, that essentially make it legal to sell certain prohormones as dietary supplements (given that certain provisos are met). In many cases, specific prohormones have later been made illegal by new legislation (on the chopping block right now is Superdrol clones – like Beastdrol - so stock up!). And again, we’re not talking about new research here, we’re talking about very old research being recycled and repackaged.

Between 75 and 100 different steroids have washed up on the shores of the American dietary market, between the first Andro (4-Androstene-3,17-dione) bottle that appeared in Mark McGwire’s locker, to the more recent products like Helladrol, Dieselbolan, and Katanadrol.

There are three basic families of anabolic steroids, most of which will be familiar, or at least partially familiar, to the average steroid user.

Testosterone is, of course, the first anabolic steroid synthesized. It’s been rightly characterized as the gold standard for all anabolics, and is in fact the one against which all others are measured in terms of potency. Testosterone is the most important naturally occurring steroid. In men it is synthesized in the testes at the rate of roughly 4-10 milligrams per day, while another 0.5 mg per day comes from the adrenal coortex. Helladrol is a great example of a testosterone-based prohormone, but with an added 4-chloro attachment that prevents it from converting to estrogen.

You see, testosterone is naturally reduced to dihydrotestosterone (DHT) and oxidized to estradiol. We see this conversion to DHT in tissus such as the scalp, while oxidation takes place in adipose (fat) and other tissue.

Testosterone and dihydrotestosterone together are responsible for the typically male sex characteristics, but their function is different. In the adolescence testosterone induces the sex drive in men, enlargement of the penis, the production of sperm, increase of muscle mass and lowering of the voice, the so called anabolic effects.

While testosterone is responsible for the primary sexual maturation of males, Dihydrotestosterone is responsible for what we generally call secondary sexual effects during puberty, i.e. an increase in body and facial hair, acne, and a deeping of the voice. These effects are termed androgenic. Indeed, Dihydrotestosterone forms its own family of anabolic steroids, including Anadrol, Primobolan, Anavar, Masteron, Superdrol, and more. With the exception of the ‘drols, these steroids are generally used on cutting cycles. Beastdrol is an example of an incredibly popular and effective DHT-based prohormone (and while it’s still currently legal, that may change in the future). Katanadrol is also in this same family, and is a very potent prohormone used for cutting cycles.

D-Aspartic Acid is a very popular testosterone booster used after prohormone cycles.

Testosterone in the methylated form, as well as its esters, have been on the market for a very long time as anabolic preparations. Because it’s orally inactive in its natural form, it’s necessary to methylate it (as in methyltestosterone) or inject it. Methylated, it acts very quickly, as it does when injected, unless an ester is attached. After injecting a testosterone ester, a slowed release to the blood takes place, the length of which depends on the length of the attached ester. With this simple chemical alteration, we can inject once a week, instead of daily. Testosterons and its derivatives are the most versatile of anabolic steroids, seen in both bulking cycles, and they include Testosterone Cypionate (and Enanthate, Propionate, etc…), Dianabol, Clostebol (and it’s prohormone variant, Helladrol), Equipoise, and blends like Omnadren and Sustanon.

And finally, the third major family of anabolic steroids, is 19-nor, most famously represented by Deca-Durabolin (commonly known as just Deca, which is Nandrolone Decanoate). Nandrolone, especially in the Decanoate form (a long acting ester) is a wildly popular steroid with a very good ability to build muscle, help heal injuries, and possessing few side effects.

Like testosterone, nandrolone can convert to estrogen, but in principle it does so in such a miniscule amount so as to make it unnoticeable to most users. but this happens only under special circumstances and in small amounts. It can also convert to a dihydro version, just as we see with testosterone, but in this case, it’s converted to Dihydronandrolone. Again, this is a relatively minor conversion, and not noticeable to most users. And just as we see with the other two families, the 19-nor group generally shares many of the same properties with drugs it shares a familial bond with. Although I don’t consider this family to be as versatile as testosterone per se, we find that Deca can be used in both a cutting or bulking cycle, while other drugs in the category include Trenbolone, Nilevar, and Nandrolone Phenylpropionate – and are generally thought to be cutting drugs.

So while none of this is particularly new information, we can see that this old information is the stuff that makes up the foundation of tomorrow’s hottest designer undetectable steroid, the next prohormone, or the next trend in new-steroid-from the old (i.e. Masteron Enanthate, Trenbolone Enanthate, etc..).

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What is Testosterone?

Testosterone is a steroid hormone from the androgen group and is also the MAIN hormone in a male’s body.  In mammals, testosterone is primarily secreted  by the testes of males and by the ovaries of females, while a tiny amounts is also secreted by the adrenal glands. It is the main male sex hormone and an anabolic steroid. Testosterone plays a key role in the development of male reproductive tissues which are the testis and prostate . Testosterone also promotes secondary sexual characteristics such as increased muscle and bone mass and hair growth, sexual behavior, development of the male genitals, increased glands, and sperm production and maturation. The adult human male body produces about ten times more testosterone than an adult human female body, but females are more sensitive to the testosterone. The brain and the bones are two important tissues in humans where the main effect of testosterone is carried out by way of aromatization to estradiol. Testosterone in the bones allows estradiol to accelerate maturation of the cartilage into bone, leading to closure of the epiphyses and end of growth. This in short explains why when young girls reach menarche, their growth sort of stunts.  Estradiol serves as the most important feedback signal to the hypothalamus which triggers LH production.  Testosterone is derived from cholesterol which is why people who suffer from cholesterol issues usually have low testosterone. Testosterone is a hormone that is triggered through the HPTA(hypothalamus).  When the HPGA Axis is stimulated, the hypothalamus secretes gonadotropin-releasing hormone (GnRH), which on reaching the anterior pituitary, binds to the gonadotrophs and stimulates the release of both the luteinizing hormone (LH) and follicle stimulatinghormone (FSH) into the bloodstream. In the testes, testosterone is produced by the Leydig cells. The male generative glands additionally contain Sertoli cells which require testosterone for spermatogenesis. Like most hormones, testosterone is supplied to target tissues in the blood where much of it is transported bound to a specific plasma protein gondal called the sex hormone binding globulin (SHBG). In males, LH binds to Leydig cells, stimulating production of the principal Leydig cell hormone, testosterone. Testosterone is secreted to the plasma and also carried to Sertoli cells by androgen binding protein (ABP). In Sertoli cells the 4 double bond of testosterone is reduced, producing dihydrotestosterone. A little more than 5% of testosterone is reduced to 5a-dihydrotestosterone (DHT) by the cytochrome through the enzyme 5a reductase. The conversion of testosterone to DHT leads to more sebaceous glands which in turn leads to oily skin and acne. Less than 1% of testosterone is converted into estradiol by aromatase; also known as the CYP19A1 enzyme. Going back to the Sertoli Cells, in these cells it is regulated by FSH, again acting through a cAMP- and PKA-regulatory pathway. In addition, FSH stimulates Sertoli cells to secrete androgen-binding protein (ABP), which transports testosterone and DHT from Leydig cells to sites of spermatogenesis. There testosterone acts to stimulate protein synthesis and sperm development. Aromatase activity is also found in granulosa cells, but in these cells the activity is stimulated by FSH. Typically, the thecal cell androgens produced in response to LH distribute to granulosa cells, whereas granulosa cell aromatase converts these androgens to estrogens. As granulosa cells mature they develop capable large numbers of LH receptors in the plasma membrane and become increasingly receptive to LH, increasing the amount of estrogen created from these cells. If not controlled it could lead to problems such as suppressed testosterone or gynecomastia due to the excess E2 levels.   In a real short simplified expression; more SHBG leads to more Estrogen which leads to eventual negative effects. Testosterone biosynthesis involves the cleavage of the sidechain of cholesterol by CYP11A, a mitochondrial cytochrome P450 oxidase with the loss of six carbon atoms to become pregnenolone. Next, two additional carbon atoms are removed by the CYP17A enzyme in the endoplasmic reticulum to give up a variety of carbon 19 steroide. In addition, the 3-hydroxyl group is oxidized by 3-β-HSD to produce androstenedione. In the final step, the C-17 keto attached group androstenedione is reduced by 17-β hydroxysteroid dehydrogenase to give way to testosterone. (Journal of Clinical Endocrinology & Metabolism Vol. 37, No. 1 148-151
doi:10.1210/jcem-37-1-148)

Benefits of Test on cycle ((brain boost, libido boost, more glycogen retention, great sense of well being,

One obvious benefit of Testosterone is increases in muscle mass. Here is a study I came across: Seven hypogonadal men, 19-47 yr of age, after at least a 12-week washout from previous androgen therapy, were treated for 10 weeks with testosterone enanthate (100 mg/week) by im injections. Body weight, fat-free mass measured by underwater weighing and deuterated water dilution, and muscle size measured by magnetic resonance imaging were assessed before and after treatment. Energy and protein intake were standardized at 35 Cal/kg.day and 1.5 g/kg.day, respectively. Body weight increased significantly from 79.2 +/- 5.6 to 83.7 +/- 5.7 kg after 10 weeks of testosterone replacement therapy (weight gain, 4.5 +/- 0.6 kg; P = 0.0064). Fat-free mass, measured by underwater weighing, increased from 56.0 +/- 2.5 to 60.9 +/- 2.2 kg (change, +5.0 +/- 0.7 kg; P = 0.0004), but percent fat did not significantly change. Similar increases in fat-free mass were observed with the deuterated water method. The cross-sectional area of the triceps arm muscle increased from 2421 +/- 317 to 2721 +/- 239 mm2 (P = 0.045), and that of the quadriceps leg muscle increased from 7173 +/- 464 to 7720 +/- 454 mm2 (P = 0.0427), measured by magnetic resonance imaging. Muscle strength, assessed by one repetition maximum of weight-lifting exercises increased significantly after testosterone treatment. L-[1-13C]Leucine turnover, leucine oxidation, and nonoxidative disappearance of leucine did not significantly change after 10 weeks of treatment. There was no significant change in hemoglobin, hematocrit, creatinine, and transaminase levels. Replacement doses of testosterone increase fat-free mass and muscle size and strength in hypogonadal men. Whether androgen replacement in wasting states characterized by low testosterone levels will have similar anabolic effects remains to be studied. (J Clin Endocrinol Metab. 1997 Feb;82(2):407-13.)

According to another study I came across Testosterone boosts muscle function and IGF-1 production.  welve older men (> or =60 yr) with serum total testosterone concentrations <17 nmol/l (480 ng/dl) were randomly assigned in double-blind manner to receive either placebo (n = 5) or testosterone enanthate (TE; n = 7) injections. Weekly intramuscular injections were given for the 1st mo to establish increased blood testosterone concentrations at 1 mo and then changed to biweekly injections until the 6-mo time point. TE doses were adjusted to maintain nadir serum testosterone concentrations between 17 and 28 nmol/l. Lean body mass (LBM), muscle volume, prostate size, and urinary flow were measured at baseline and at 6 mo. Protein expression of androgen receptor (AR) and insulin-like growth factor I, along with muscle strength and muscle protein metabolism, were measured at baseline and at 1 and 6 mo of treatment. Hematological parameters were followed monthly throughout the study. Older men receiving testosterone increased total and leg LBM, muscle volume, and leg and arm muscle strength after 6 mo. LBM accretion resulted from an increase in muscle protein net balance, due to a decrease in muscle protein breakdown. TE treatment increased expression of AR protein at 1 mo, but expression returned to pre-TE treatment levels by 6 mo. IGF-I protein expression increased at 1 mo and remained increased throughout TE administration. The researchers conclude that physiological and near-physiological increases of testosterone in older men will increase muscle protein anabolism and muscle strength. (Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E601-7.)

Testosterone even acts like creatine according to another study I cam e across:

Androgens stimulate myogenesis, but we do not know what cell types within human skeletal muscle express the androgen receptor (AR) protein and are the target of androgen action. Because testosterone promotes the commitment of pluripotent, mesenchymal cells into myogenic lineage, they hypothesized that AR would be expressed in mesenchymal precursor cells in the skeletal muscle. AR expression was evaluated by immunohistochemical staining, confocal immunofluorescence, and immunoelectron microscopy in sections of vastus lateralis from healthy men before and after treatment with a supraphysiological dose of testosterone enanthate. Satellite cell cultures from human skeletal muscle were also tested for AR expression. AR protein was expressed predominantly in satellite cells, identified by their location outside sarcolemma and inside basal lamina, and by CD34 and C-met staining. Many myonuclei in muscle fibers also demonstrated AR immunostaining. Additionally, CD34+ stem cells in the interstitium, fibroblasts, and mast cells expressed AR immunoreactivity. AR expression was also observed in vascular endothelial and smooth muscle cells. Immunoelectron microscopy revealed aggregation of immunogold particles in nucleoli of satellite cells and myonuclei; testosterone treatment increased nucleolar AR density. In enriched cultures of human satellite cells, more than 95% of cells stained for CD34 and C-met, confirming their identity as satellite cells, and expressed AR protein. AR mRNA and protein expression in satellite cell cultures was confirmed by RT-PCR, reverse transcription and real-time PCR, sequencing of RT-PCR product, and Western blot analysis. Incubation of satellite cell cultures with supraphysiological testosterone and dihydrotestosterone concentrations (100 nm testosterone and 30 nm dihydrotestosterone) modestly increased AR protein levels. Researchers conclude that AR is expressed in several cell types in human skeletal muscle, including satellite cells, fibroblasts, CD34+ precursor cells, vascular endothelial, smooth muscle cells, and mast cells. Satellite cells are the predominant site of AR expression. These observations support the hypothesis that androgens increase muscle mass in part by acting on several cell types to regulate the differentiation of mesenchymal precursor cells in the skeletal muscle.

Testosterone also boosts glycogen according this other article I came upon: The purpose of the current study was to show that testosterone and estradiol act differentially on skeletal muscles from different regions, differentially with reference to glycogen metabolism. To study this hypothesis, healthy mature male Wistar rats (90-120 days of age, weighing about 180-200 g) were castrated (a bilateral orchidectomy was performed to test the significance of skeletal muscle glycogen metabolism in the absence of testosterone). One group of castrated rats was supplemented with testosterone (100 microg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards). To test whether estradiol has any effect on male skeletal muscle glycogen metabolism 17beta-estradiol (5 microg/100 g body weight, i.m., for 30 days from day 31 postcastration onwards) was administered to orchidectomized rats. To test whether these sex steroids have any differential effect on skeletal muscles from different regions, skeletal muscles from the temporal region (temporalis), muscle of mastication (masseter), forearm muscle (triceps and biceps), thigh muscle (vastus lateralis and gracilis), and calf muscle (gastrocnemius and soleus) were considered. Castration enhanced blood glucose levels and decreased glycogen stores in skeletal muscle from head, jaw, forearm, thigh, and leg regions. This was accompanied by diminished activity of glycogen synthetase and enhanced activity of muscle phosphorylase. Following testosterone supplementation to castrated rats, a normal pattern of all these parameters was maintained. Estradiol administration to castrated rats did not bring about any significant alteration in any of the parameters. The data obtained suggest a stimulatory effect of testosterone on skeletal muscle glycogenesis and an inhibitory effect on glycogenolysis. Estradiol did not play any significant role in the skeletal muscle glycogen metabolism of male rats. (Can J Physiol Pharmacol. 1999 Apr;77(4):300-4.)

Testosterone also boosts brain/neuron function leading to more spatial learning and motor skills. Testosterone also boosts red blood cell count along EPO levels. Testosterone will promote more energy, motivation and controlled aggression.  Obviously libido and sense of well being will be elevated due to the correlation of testosterone to dopamine. Dopamine as mentioned before in my articles, is the main reason you feel good and feel the need to spread your seed.HAHAHAHA

Different forms of Testosterone Injections

Test Prop

Testosterone propionate has probably the second shortest half life of all testosterone esters. With a 4.5 day half-life, it will not produce water retention to the degree of other testosterone forms such as Testosterone-Enanthate; which is a very desirable quality for many as it means the chances for blood pressure spikes are lower. After the use of Testosterone propionate the effects start showing in a snap. In a short period of time, an athlete/ bodybuilder will feel more aggressive and stronger. The individual will start to experience an increase in appetite; along with improved recovery time from post training. For those who have issues with injections, this is definitely not the steroid for you since injections are frequently expected. You will need to administer Testosterone propionate at a minimum of every 3 days but most choose to inject Test prop every other day for max results. There are some veterans that will even inject prop daily. The longer the ester bond attached to the testosterone is, the longer the actual steroid is active within your body, but the less actual test you will in turn have within the body. This is because, for every 100mgs of testosterone cypionate you inject, approximately only 69.90mgs of it is truly testosterone; the rest is the cypionate ester, which must be removed through bodily processes. On the other hand, with the propionate ester you will get 83.72mgs of pure Testosterone. The advantage to longer esters is that they need to be injected less frequently. The disadvantage to long estered steroid hormones is that they contain less of the actual steroid as just explained. Testosterone Propionate is usually the preffered form of testosterone when it comes to cutting cycles as it does not hold nowhere near as much water as other forms of testosterone, leaving you with a more toned look as opposed to a bloated and unattractive appeal. Women also prefer this form of testosterone as they can minimize side effects while on. Remember, Test prop’s effects begin to really drop the second day after injecting, so in my honest humble opinion, never go longer than 24 hours aka eod without injecting your prop for maximum gains. (J Clin Endocrinol Metab. 1986 Dec;63(6):1361-4.) The side effects of Testosterone propionate are much easier to control than many other forms of testosterone since one can control the flow of the hormone to a more efficient degree due to the short half-life. To make sure you have the maximum benefits of using Testosterone propionate, inject a little amount of this steroid into your system at any one time. Women can experience virilization with this form of testosterone just like any other form of testosterone, so caution is warranted when cycling prop. In case you are not sure what that means, it means the women’s voice will deepen, her clitoris will enlarge, and she will start to develop hair in the wrong places HAHAHAHHAHA.

Test Cyp

Testosterone cypionate, is testosterone with the cypionate ester bond attached to it; which is a slow-acting long ester added to it. Test cyp. Is a time released duration of testosterone thereby reducing the frequency of injections for hormone therapy patients permitting for monthly shots. A big reason; why, bodybuilders and athletes choose to run it with their cycles as no one wants to have to continuously inject themselves for what ever the reason may be. Like all forms of the androgen testosterone, this form of testosterone will provide great overall gains, increased sense of well being, and a steady libido, whereas test prop would give a surge of libido due its potent quick delivery.

Sustanon 250

Sustanon was developed by the pharmaceutical company Organon as a means of ideal Hormone Replacement Therapy treatment because it was thought at the time that these different esters would be able to provide a constant flow of Testosterone over a month’s time. Sustanon is a blend of four different estered testosterones which include: testosterone propionate  at 30 mg, testosterone propionate at 60 mg, testosterone isocaproate  at 60mg, and testosterone decanoate at 100 mg.  During the 80’s through 90’s this was the choice form of testosterone, everyone who was on wanted to include Sus 250 in their cycle. The main advantage to this form of testosterone, according to the Organon, is that it can be injected once a month, and the different esters would provide different timed releases over that month, and the patient would really only need to visit the doctor once a month for their Testosterone replacement therapy. For athletes or bodybuilders who are injecting 1000mg plus throughout the month, Sus 250 will make no true differences in delivery or benefits. I will say this, there are some people I know that had the most strength gains while on this form of testosterone than any other form, in theory I can only speculate that some of the remaining forms of testosterone with newer levels of testosterone engage to make androgenic attributes stronger.

Testosterone PhenylPropionate

When compared to other forms of testosterone phenyl propionate does not have a lot of popularity among most chemical athletes. Athletes ALWAYS want quick results from their anabolic androgenic steroids, and testosterone phenyl propionate is not able to give them the quick results they are expecting. Testosterone phenyl propionate has the shortest duration of all testosterone esters and this is the reason it has been called ineffective by many. With a 1-2 days duration within the body, it prevents water retention in the muscles of the body; a very desirable effect at that. After the use of testosterone phenyl propionate the effects start showing in a snap. In this little time, an athlete will feel more aggressive and stronger just as Test Prop. He will have an increased appetite; and so forth just as with Test Prop. However because of its terribly short half life it will HAVE to be injected daily, and for some that is just not going to happen. LMAO! Alternatively, you can inject it every two days if taken with other steroids like winstrol (oral) and Dianabol. The primary advantage of this stuff is that foreign underground manufacturers are not afraid to dose it at 200 mg per ml, unlike other short esters like propionate in which 100 mg per ml is the standard dosage.

Test Decanoate

Testosterone decanoate, is probably best known as one of the ingredients in Sustanon. Also known as Neotest 250 is testosterone with the decanoate ester, a slow-acting long ester bond attached to it. The Neotest 250 brand was developed in an oil solution form for intramuscular injection, and packaged in a 10 ml multi-dose vial containing 250 mg per ml of testosterone decanoate. The individual drug Neotest 250 is no longer available through manufacturer, and no other independent testosterone decanoate products are known to be in distrubution. At present, the decanoate version of testosterone can only be found within testosterone blends like Sus 250.

Cousin of Sus 250 aka Omnadren 250

Omnadren 250 is a combination of the 4 separate forms of testosterone esters just as Sus 250. Most commonly, people will correlate Omnadren 250 with its cousin Sustanon 250, since they are both a blend of 4 testosterone esters. The only difference between the two lies in the last and most concentrated- ester. While Omnadren contains the caproate ester, Sustanon contains the decanoate ester in the same concentration amount. Really, except for price, theres no real notable difference nor  benefits.  Financnially speaking,  youre going to be paying as much for Omnadren as you would for Sustanon 250. So it really does not matter which one you use per your cycle but rather which you can obtain through your source, pretty much it’s like comparing Test Cyp To Test E.

The small concentrations of the shorter acting esters like propionate and phenylpropionate are rendered practically useless when Omnadren is injected once or twice per week. Furthermore, when injecting only a few times per week the peaks and valleys of concentration in the blood are not desirable. We want our blood concentration of the drugs to be as high as they can be relative to dose to produce maximum results. Obviously, this is not the case when fast acting esters are introduced and subsequently dissolute before another injection is given. As the longest ester in Omnadren (caproate) is slightly faster acting than the longest ester in Sustanon (decanoate), users will notice an increase in their testosterone levels sooner with Omnadren than with Sustanon. This has a few consequences which we shall examine now. First of all, since testosterone aromatizes into estradiol, a buildup of this female hormone will occur more rapidly which could lead to the onset of gyno. With the estrogen increase follows the inevitability of increased water retention. This is significant for 3 reasons: First, the users strength will increase. Secondly, the user’s size will increase, and finally, definition in the muscles will begin to dissipate. As a clear observation, Omnadren is clearly used more so for bulking than cutting.

Test Ethanate

Testosterone Ethanate is the European version of Testosterone Cypionate and by far the most worldwide used form of testosterone, especially recreational usage. Remember most TRT patients will receive either the androgel or Test cyp.  Another problem about the administration of Testosterone Enanthate is the fact that this form of testosterone aromatazes in estradiol very quickly. Many aspects of course depend from person to person because in most cases the reactions are correlated with the fact that these individuals are predisposed to them. There are athletes that even at a dose of 100mg/day or even more aren’t affected by the feminization process, they don’t stock fats and retain only an insignificant quantity of water.  Usual dosing for Test E. is usually 250-1000mg, but some hardcore vets will go up to Dan Duchaine’s crazy advice of 2000mgs.

Test Suspension

Testosterone Suspension is water base form of testosterone that was developed and used for decades by many chemical athletes. It is actually the first anabolic androgenic steroid used for performance and muscle enhancement. For the purpose of building mass, Testosterone Suspension has never been surpassed since it was first developed in the 1930’s. Many underground labs also suspend this product in propylene glycol or oil as well resulting in a very painful injection compared to its original water base. It has no ester bond attached to it; as a result no ester is calculated into the weight. This is extremely beneficial to the user since 100mg of testosterone suspension will yield 100mg of pure testosterone unlike the other esterfied testosterones such as testosterone enanthate which only yields 72mg of actual testosterone per 100mg of total weight. Testosterone suspension considerably raises the storing of glycogen in the muscle cells and because it is dissolved in water it becomes effective immediately. Also making it different from other esterfied hormones is that it only keeps sustained and elevated testosterone levels for 2-3 days due to its short half life. This forces the individual to inject on a daily basis, with better results coming from twice-three time a day use due to its short active-life with the effective dose ranging from 350-1000mg per week or 50-140mg per day. One should practice site rotation and should practice injecting in the same spot only once per week at most to avoid muscle bruising. It should be noted that test suspension is usually a very painful shot, so it is often cut with something else, such as B-12, or other anabolic androgenic steroids. And yes, you can mix a water based steroid with an oil based steroid in the same syringe to try to dampen the pain of the injeciton. Again I repeat if you are not a fan of injections, then this form of Testosterone is NOT for you BWHAH AHAHAAHA!

Test CHP

Testosterone CHP, is a French made Testosterone preparation. See, this form of testosterone comes in 296mgs, 148mgs, and 37mgs ampules, of one milliliter each. Why the akward dosing? Well, actually, its much less strange than you think. . See those amps provide a very sensible 200mgs, 100mgs, and 25mgs respectively with this particular ester, combined with testosterone, at those available doses. As we all know, esters delay the release of a hormone, and Test-CHP has 9 carbons, which hints that it is a long acting ester comparable cypionate, (8 carbons) or decanoate, (10 carbons) with an active life of about 13.5 days. Obviously, this is a very long acting version of testosterone, and anecdotally, the longer esters, tend to produce more water retention. This stuff would be good for bulking, therefore, and not really for cutting.

TestoVirion

Testoviron is a blend of two foms of testosterone. Usually testosterone with the propionate ester bond attached, and testosterone with the Enanthate ester bond attached. Intesting but contradicting, Schering, who produces this product, also has a pure testosterone Enanthate product of the same name. “Frontloading” is employed with products like this one, since it contains both testosterone propionate, and Enanthate. This is where double or triple the intended dose for the cycle is injected for the first two weeks, and the propionate ester gives a very quick rise in blood plasma levels of testosterone, and then the Enanthate ester is relied on for a more even blood level in the ensuing weeks. The reasoning behind this is presumably to get the blood levels of the drug up quickly in the hopes of seeing results more quickly, and then have the blood levels even out and stay constant.

Of all testosterones available on the market today, blended ester products like this one are the most unjustifiably expensive. This is both because they are in high demand, as well as more rare than single estered products. You can only find Testoviron overseas at 135mg per ml. Expect to pay up to $5-7 for an amp of this stuff, and if your source is asking for more, don’t bother as the price is not worth the bite. When the price of other forms of testosterone is so low, there is no justification purchasing a blended product for any more than you would purchase a single estered testosterone.

Balco’s “Cream”

The Cream is the slang name given by Victor Conte to a transdermal designer steroid, containing testosterone and epitestosterone, designed by BALCO to avoid detection on drug tests. While testosterone is certainly an anabolic steroid, epitestosterone is simply an inactive epimer of the parent steroid hormone. The reason the latter would be included in the cream along with testosterone is to beat doping tests based on the testosterone:epitestosterone ratio.  It’s pretty much a ploy to keep using other stronger substances without getting caught. Now of course it is detectable thanks to WADA LOL.

Testosterone Undecanoate

This testosterone ester has been developed and used clinically in many countries possessing the desired profile. Testosterone undecanoate, marketed under the brand name Aveed^®, Nebido^®, and others, has a decade plus worth of research and use in treating male hypogonadism. Being that it has 10 carbon tail rather than an 11 carbon tail, it’s more likely to slowly release within the muscle tissue cells. It is the preferred form of hormone replacement for many men’s health specialists, due to its pharmacokinetic properties. Test Undecanoate is capable of maintaining a steady concentration of testosterone for 12 weeks in most users, up to 14 weeks in some. To reach a steady state, a 4 ml depot of TU in castor oil is injected, with a follow-up injection six weeks later; from then on, testosterone concentration is typically maintained with a 4 ml depot injected every 12 weeks. For American AAS users, or men receiving testosterone therapy, this sounds like testosterone perfection, one shot every three months, rather than 12 or more. Unfortunately, the FDA is being uncharacteristically slow in approving TU, due to the rare report of shortness of breath that has occurred when the depot is improperly injected. Proper intramuscular injection technique requires that the plunger of the syringe be pulled back slightly to ensure that the drug is not being injected into a blood vessel, as this could allow the large globule to enter the bloodstream. If injected into a large vein, the globule could enter the pulmonary circulation (lungs) fairly intact, causing the sensation noted, until it is dispersed in the general circulation. Most AAS injections are limited to 2 ml or less. One issue with TU that may affect compliance is a greater frequency or severity of injection-related pain. Four ml may not seem like a large volume, a teaspoon has 5 ml. However, when injected into the glute, 4 ml of an oil-filled depot can feel like one is sitting on a golf ball. Recently, a study was performed measuring relative pain associated with a 4 ml Test Undecanoate injection, and how long the pain can last. This will likely be of interest to many men, as TU could quickly become the hormone replacement of choice in the U.S. when approved. Those considering high-volume injections of other AAS, or hoping to acquire TU for recreational purposes, will likely find this worthy of note as well. Certain AAS, particularly veterinary preparations, are administered in low concentrations. In the study, recently published in the Asian Journal of Andrology, Australian clinicians followed 125 hypogonadal men receiving TU, administered as a single 4 ml intramuscular injection every 12 weeks; 43 returned during the study period for a scheduled injection, and their data were included in the analysis. In reviewing these results, it is important to consider that the injections were provided in the clinic, by experienced nurses using proper injection protocol. The injections were provided slowly, over 3-5 minutes, through a 1½-inch, 21-gauge needle, the standard needle size used by doctors and bodybuilders for intramuscular injections. These results likely represent “best-case scenario” as a legitimate drug, properly injected, in a clinical setting by experienced practitioners. In the “real world,” the outcome is likely to be worse, with increased risk of other injection-related complications (ex. bleeding, infection, injecting into a vein, tissue damage, and scarring). The results indicated that the worst pain was immediately post-injection (58 percent), and resolved fairly quickly. In fact, none of the subjects reported that pain interfered with normal activities; in all cases, the pain resolved in three days or less.  The authors compared this to an earlier study examining pain associated with a 1 ml intramuscular injection of testosterone enanthate (TE). In this, most men did not experience reportable pain; only 29 percent noted any injection-related discomfort. The difference between the TE and TU experience is likely related to the volume of the injection (1 ml versus 4 ml). Two traits were noted that were associated with less pain were age and obesity. Older men reported less pain than their younger counterparts; this may be due to reduced pain sensitivity that occurs with aging, or they may just have more pain threshold capabilities. Obese men have a much thicker subdermal fat pad. In some men, this may be thicker than the length of the needle, causing the 4 ml depot to be dispersed among the less reactive fat tissue, as opposed to the deep sensitive muscle. Though this has been noted to be an issue, it appears drug delivery may be equally effective when injected as an oil depot into fat or muscle. Most normal-weight or lean men would not find the visible bulge from the injection comfortable or at tolerable. (Journal of Andrology, Vol. 23, No. 3, May/June 2002)  I don’t understand why over such little insignicant issues such as injection pain would the United States not allow such a wonderful form of Testosterone to hit the TRT market, seriously what a SHAME!  If few you think a few days of muscle soreness is a problem, then you need to man up. LOL

Andriol

Andriol is the oral version of the anabolic androgenic steroid testosterone undecanoate developed by the pharmaceutical company Organon. This testosterone preparation is encapsulated and sealed in an oil base in a 40 mg capsule taken orally. According to the makers of Andriol, the oil esterfied tablet bypasses the liver, preventing it from being decimated by the liver and from adding harmful stresses to the liver found in other forms of testosterone. It is also supposed to enter the body as a fat through the lymphatic system. Even at 240 mg per day, the results are mediocre at best with the exemption of the first hour where you get the surge of energy. Increasing the dose will not do much either which tells us that oral testosterone is limited and is a waste.  The advantage to using Andriol is its lack of side effects such as minimal estrogen conversion, mimimal to no blood pressure spikes, no water retention,

Androgel

Androgel is the more common and FDA approved testosterone treatment here in the US. Androgel is a topical testosterone cream or more aptly a Transdermal Testosterone. One of the primary forms of treatment of low-testosterone Androgel unlike many testosterone medications does not need to be injected but as a transdermal cream is applied directly to the skin. Beyond the form in-which it comes there are not too many differences between Androgel and typical injectable testosterone but differences do exist. In the end, by topical application or injection, either way you are receiving the same testosterone hormone but the most notable difference is in the efficiency rating.  When we use injectable testosterone much more of the hormone is made available to the body; while no injectable testosterone with the exemption of Testosterone Suspension provides a 100% absorption rating many are close; Androgel however can only report a 10% usable amount from each dosing therapy provided. To give understanding; one of the most common forms of testosterone used in hormone replacement therapy is that of Testosterone Propionate and injections of 50mg are the usual dosing protcols. For the Androgel users to receive the same amount of usable testosterone by application of this transdermal cream one would need to apply approximately 5 grams of the solution in-order to reach the same end.  ONE BIG REASON; why I told my doc that I MUST have injections over topical delivery.  When some transdermal testosterone preparations have been examined, they have shown that the plasma concentration of testosterone increased very rapidly, and reached the peak level within 3-6 hours of application of the experimental patch. This is comparable with some of the better oral products out there, let’s be real anybody would rather swallow a tablet over having to inject themselves constantly. This is the reason why so many orals have even become popular in the sports world in the first place, athletes are busy people who don’t have time to mess around. Basically, you can expect all of the benefits of injectable testosterone with the transdermals providing that you dose them the same, which on average most doctor’s will not leading to less significant improvements with the patch compared to the shots. An example would be Androderm, which is a patch containing 12.2mgs of testosterone, and androgel, which gives you about 10% of the total active testosterone. So if its 100mg per serving, you only are getting 10mgs, UMMM I think I will pass. The main problem with this method is that if the individual has a high amount of aromatizing enzymes within the body, the androstendione will convert to estradiol without even giving full accesss to testosterone. This is why you will see if you search that scientists realized that leaner men handle supraphsiological levels of androgens much better than over weight men. A good way of knowing that you have high aromatizing enzymes within your body is checking to see if you have a floppy chest, significant lower belly fat, significant tricep fat, fatty shoulders, round face, overly emotional, and thigh/lower body fat. Any of these may be a high indicator of elevated aromatase enzymes along with high estrogen levels.

Side effects to consider while on Testosteorne

Here is a list of sides that are commonly noted with the use of Testosterone: Acne; bitter or strange taste in mouth; change in sex drive; fatigue; gum or mouth irritation; gum pain; gum tenderness or swelling; hair loss; headache. Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); breast growth or pain; change in the size or shape of the testicles; dark urine or light-colored bowel movements; depression or mood changes; dizziness; gingivitis; interrupted breathing while sleeping; loss of appetite; nausea; painful or prolonged erection; stomach pain; swelling of the ankles or legs; urination problems; weight gain; yellowing of the skin or eyes. (drugs.com)

As you can see many of these forms of testosterone offer their own benefits whether it is for Testosterone Replacement Therapy or anabolic cycle. I really like Ronnie’s belief that you can never have too much testosterone. LONG LIVE TESTOSTERONE AND ALL IT’S FORMS!!!!!

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GW-501516 is a PPARδ modulator compound is currently being investigated for drug use by GlaxoSmithKline. It activates the same pathways activated through exercise, including PPARδ and AMP-activated protein kinase. It is being trialed as a potential treatment for a few conditions consisting mainly of obesity, diabetes, dyslipidemia and heart disease. GW-501516 has a synergistic effect when combined with the AMP-K agonist AICAR: the combination has been shown to significantly increase exercise endurance in animal studies more than 40%. And from My own experience yes it works my friends.

GW-50156 regulates fat burning through a number of different pathways which includes exercise mimetic effects.  It increases glycogen retention in skeletal muscle tissue while increasing muscle gene expression. This shift changes the body’s metabolism to allow for more fat burning and for energy instead of carbohydrates or protein as the source of fuel. This is why the main reason why it’s being looked into as a treatment for diabetes.  As it will not allow the patients to endure and overly catabolic state, thus allowing energy levels and health to be stable at all times. GW-501516 clearly demonstrates that it increases muscle mass while keeping glucose from touching the adipose tissue sort of like Need2Slin but need2slin does much more then just this. Treatments with GW-501516 have been shown to increase HDL cholesterol by up to 79% and the compound is now undergoing Phase II trials to improve HDL cholesterol in humans. We dive into its attributes further later in the article But again let me speak from personal experience. I did a test with this drug and Winstrol. I know for my self when I take wonstrol it always kills my cholesterol levels. Last time I took it I ended up with an HDL of ten and a LDL over two hundred and it only took less then 2 weeks for this to happen. So knowing this I took wintrol for 4 weeks and also took GW-501516 along with it and I was amazed at the results. My cholesterol levels were BETTER at the end of the 4 week trial. So if cholesterol is of concern for you then you need to get some of this stuff my friend because trust me it works.

Concerns had been raised right before the 2008 Beijing Olympics that GW-501516 could be used by athletes as a performance enhancing drug which was not detectable nor tested for during the doping test. The main reason why athletes would use it is because of the increase in endurance through the increase of glycogen storage leading to increased muscular endurance, again ring a bell. Need2Slin does THE SAME THING! GW-501516 has yet to be label a controlled or banned substance by any national drug enforcement agency including Wada. Obviously no one will test positive for this drug, so if I were an Olympic athlete looking for a boost; this would be at the top of the list considering its much outweighed pros over cons. Any Athletes looking for a edge can use this drug and never have to worry about popping hot. They can not test for it my friends so you are golden. Some new testing is coming out in the next 3-5 years that will allow them to basically test your DNA to see if your bosy as been drug altered in anyway but this is years in the making. For now you are safe to take GW-501516 and not have to worry about popping hot.

Injecting GW501516 is like injecting a cardio session LOL

The benefits of endurance exercise on general health make it desirable to identify orally active agents that would mimic or potentiate the effects of exercise to treat metabolic diseases. Although certain natural compounds, such as reseveratrol, have endurance-enhancing activities, their exact metabolic targets remain elusive. We therefore tested the effect of pathway-specific drugs on endurance capacities of mice in a treadmill running test. Researchers found that PPARbeta/delta agonist and exercise training synergistically increase oxidative myofibers and running endurance in adult mice. Because training activates AMPK and PGC1alpha, they then tested whether the orally active AMPK agonist AICAR might be sufficient to overcome the exercise requirement. Unexpectedly, even in sedentary mice, 4 weeks of AICAR treatment alone induced metabolic genes and enhanced running endurance by 44%. These results demonstrate that AMPK-PPARdelta pathway can be targeted by orally active drugs to enhance training adaptation or even to increase endurance without exercise.  Now how does this peptide cause mice to lose weight without activity? Simple, the Activation of PPARβ/δ by GW501516 in skeletal muscle cells induces the expression of genes involved in preferential lipid utilization, β-oxidation, cholesterol efflux, and energy uncoupling. In addition, the treatment of muscle cells with GW501516 increases apolipoprotein-A1 specific efflux of intracellular cholesterol, thus identifying this tissue as an important target of PPARβ/δ agonists. Interestingly, fenofibrate induces genes involved in fructose uptake, and glycogen formation. In contrast, rosiglitazone-mediated activation of PPARγ induces gene expression associated with glucose uptake, fatty acid synthesis, and lipid storage. Furthermore, we show that the PPAR-dependent reporter in the muscle carnitine palmitoyl-transferase-1 promoter is directly regulated by PPARβ/δ, and not PPARα in skeletal muscle cells in a PPARγ coactivator-1-dependent manner. This study demonstrates that PPARs have distinct roles in skeletal muscle cells with respect to the regulation of lipid, carbohydrate, and energy homeostasis. Overall the peptide GW501516 (PPARβ/δ agonists) would increase fatty acid catabolism, cholesterol efflux, and energy expenditure in muscle, and speculate selective activators of PPARβ/δ may have therapeutic utility in the treatment of hyperlipidemia, atherosclerosis, and obesity.  (Dressel et al. 17 (12): 2477).. However I would advice only using this drug orally IMO..

Proof that GW5010516 increases insulin sensitivity

Elevated plasma free fatty acids cause insulin resistance in skeletal muscle through the activation of a constant chronic inflammatory process. This process involves nuclear factor (NF)-kappaB activation as a result of diacylglycerol (DAG) accumulation and following protein kinase Ctheta (PKCtheta) phosphorylation. At present, it is unknown whether peroxisome proliferator-activated receptor-delta (PPARdelta) activation prevents fatty acid-induced inflammation and insulin resistance in skeletal muscle cells. In C2C12 skeletal muscle cells, the PPARdelta agonist GW501516 prevented phosphorylation of insulin receptor substrate-1 at Ser(307) and the inhibition of insulin-stimulated Akt phosphorylation caused by exposure to the saturated fatty acid palmitate. This latter effect was reversed by the PPARdelta antagonist GSK0660. Treatment with the PPARdelta agonist enhanced the expression of two well known PPARdelta target genes involved in fatty acid oxidation, carnitine palmitoyltransferase-1 and pyruvate dehydrogenase kinase 4 and increased the phosphorylation of AMP-activated protein kinase, preventing the reduction in fatty acid oxidation caused by palmitate exposure. In agreement with these changes, GW501516 treatment reversed the increase in DAG and PKCtheta activation caused by palmitate. Consistent with these findings, PPARdelta activation by GW501516 blocked palmitate-induced NF-kappaB DNA-binding activity. These findings indicate that PPARdelta attenuates fatty acid-induced NF-kappaB activation and the subsequent development of insulin resistance in skeletal muscle cells by reducing DAG accumulation. The results of the study clearly demonstrate that PPARdelta activation is a pharmacological target to prevent insulin resistance. (Endocrinology 2010 Apr; 151(4) :1560-9.)

The peroxisome proliferator-activated receptor δ (PPARδ) regulates the expression of genes involved in cellular lipid and cell energy metabolism in many metabolically active tissues, such as liver, muscle, and fat, and plays a role in the cellular response to stress and environmental stimuli. The particular role of PPARδ in insulin-secreting β-cells, however, is not well understood; we recently identified the cell-specific role of PPARδ on mitochondrial energy metabolism and insulin secretion in lipotoxic β-cells. After treatment of HIT-T15 cells, a syrian hamster pancreatic β-cell line, with high concentrations of palmitate and/or the specific PPARδ agonist GW501516, we detected the gene expression changes for transcripts, such as peroxisome proliferator-activated receptor gamma co-activator 1 (PGC-1α), nuclear respiratory factor 1 (NRF-1), mitochondrial transcription factor A (mtTFA), the protein levels of the mitochondria uncoupling protein 2 (UCP2), mitochondrial morphology, the insulin secretion capacity and ATP/ADP ratio. Our results show that GW501516 treatment promoted generation of mitochondrial ATP, as well as expression levels of PGC-1α, NRF-1 and mtTFA, decreased basal insulin secretion, but had no effect on glucose-stimulated insulin secretion (GSIS), increased amounts of UCP2 and changed ATP-to-ADP ratio, improved mitochondrial morphology in palmitate-treated β-cells. GW501516-induced activation of PPARδ enhanced mitochondrial energy metabolism, but also promoted a concomitant mitochondrial uncoupling and resulted in decreased basal insulin secretion and restricted GSIS; this observation indicated the possible action of a protective mechanism responding to the alleviation of excessive lipid load and basal insulin secretion in lipotoxic β-cells. (Volume 343, Numbers 1-2, 249-256, DOI: 10.1007/s11010-010-0520-8) As you can see this peptide has a profound effect on the liver and pancreas resulting in lower blood sugar and controlled insulin output.

GW501516 prevents brain aging.

Brain inflammation plays a central role in numerous brain pathologies, including multiple sclerosis (MS). Microglial cells and astrocytes are the effector cells of neuroinflammation. They can be activated also by agents such as interferon-γ (IFN-γ) and lipopolysaccharide (LPS). Peroxisome proliferator-associated receptor (PPAR) pathways are involved in the control of the inflammatory processes, and PPAR-β seems to play an important role in the regulation of central inflammation. In addition, PPAR-β agonists were shown to have trophic effects on oligodendrocytes in vitro, and to give partial protection in experimental autoimmune encephalomyelitis (EAE), an animal model of MS. In the present work, a three-dimensional brain cell culture system was used as in vitro model to study antibody-induced demyelination and inflammatory responses. GW 501516 is a specific PPAR-β agonist that researchers chose to  examine for its capacity to protect from antibody-mediated demyelination and to prevent inflammatory responses induced by IFN-γ and LPS. GW 501516 decreased the IFN-γ-induced up-regulation of TNF-α and iNOS in accord with the proposed anti-inflammatory effects of this PPAR-β agonist. However, it increased IL-6 m-RNA expression. In demyelinating cultures, reactivity of both microglial cells and astrocytes was observed, while the expression of the inflammatory cytokines and iNOS remained unaffected. Furthermore, GW 501516 did not protect against the demyelination-induced changes in gene expression.  This suggests that the protective effects of PPAR-β agonists observed in vivo can be attributed to their anti-inflammatory properties rather than to a direct protective or trophic effect on oligodendrocytes.  We all know that both alzheimer’s and Dementia are caused by chronic inflammation within the brain. Further research is still needed but this peptide displays promise in preventing the aging of the brain. (Journal of Neuroinflammation 2009, 6:15 doi:10.1186/1742-2094-6-15)

GW501516 helps prevent the onset of Diabetes

In contrast to the well-established roles of PPARgamma and PPARalpha in lipid metabolism, little is known for PPARdelta in this process. We show here that targeted activation of PPARdelta in adipose tissue specifically induces expression of genes required for fatty acid oxidation and energy dissipation, which in turn leads to improved lipid profiles and reduced adiposity. Importantly, these animals are completely resistant to both high-fat diet-induced and genetically predisposed (Lepr(db/db)) obesity. As predicted, acute treatment of Lepr(db/db) mice with a PPARdelta agonist depletes lipid accumulation. In parallel, PPARdelta-deficient mice challenged with high-fat diet show reduced energy uncoupling and are prone to obesity. In vitro, activation of PPARdelta in adipocytes and skeletal muscle cells promotes fatty acid oxidation and utilization. Our findings suggest that PPARdelta serves as a widespread regulator of fat burning and identify PPARdelta as a potential target in treatment of obesity and its associated disorders. (Cell. 2003 Apr 18;113(2):159-70. PMID:12705865)

PPAR Agonist help prevent Dyslipidemia

In vitro and in vivo genetic and pharmacological studies have demonstrated PPARα regulates lipid catabolism. In contrast, PPARγ regulates the conflicting process of lipid storage. However, relatively little is known about PPARβ/δ in the context of target tissues, target genes, lipid homeostasis, and functional overlap with PPARα and -γ. PPARβ/δ, a very low-density lipoprotein sensor, is abundantly expressed in skeletal muscle, a major mass peripheral tissue that accounts for approximately 40% of total body weight. Skeletal muscle is a metabolically active tissue, and a primary site of glucose metabolism, fatty acid oxidation, and cholesterol efflux. Surprisingly, the role of PPARβ/δ in skeletal muscle has not been investigated. We utilize selective PPARα, -β/δ, -γ, and liver X receptor agonists in skeletal muscle cells to understand the functional role of PPARβ/δ, and the complementary and/or contrasting roles of PPARs in this major mass peripheral tissue. Activation of PPARβ/δ by GW501516 in skeletal muscle cells induces the expression of genes involved in preferential lipid utilization, β-oxidation, cholesterol efflux, and energy uncoupling. Furthermore, we show that treatment of muscle cells with GW501516 increases apolipoprotein-A1 specific efflux of intracellular cholesterol, thus identifying this tissue as an important target of PPARβ/δ agonists. Interestingly, fenofibrate induces genes involved in fructose uptake, and glycogen formation. In contrast, rosiglitazone-mediated activation of PPARγ induces gene expression associated with glucose uptake, fatty acid synthesis, and lipid storage. Furthermore, we show that the PPAR-dependent reporter in the muscle carnitine palmitoyl-transferase-1 promoter is directly regulated by PPARβ/δ, and not PPARα in skeletal muscle cells in a PPARγ coactivator-1-dependent manner. This study demonstrates that PPARs have distinct roles in skeletal muscle cells with respect to the regulation of lipid, carbohydrate, and energy homeostasis. Moreover, we surmise that PPARβ/δ agonists would increase fatty acid catabolism, cholesterol efflux, and energy expenditure in muscle, and speculate selective activators of PPARβ/δ may have therapeutic utility in the treatment of hyperlipidemia, atherosclerosis, and obesity.  (Dressel et al. 17 (12): 2477)

GW5015016 decreases chances of Heart Disease

The peroxisome proliferator-activated receptors (PPARs) are dietary lipid sensors that regulate fatty acid and carbohydrate metabolism. The hypolipidemic effects of the fibrate drugs and the antidiabetic effects of the glitazone drugs in humans are due to activation of the alpha (NR1C1) and gamma (NR1C3) subtypes, respectively. In macrophages, fibroblasts, and intestinal cells, GW501516 increases expression of the reverse cholesterol transporter ATP-binding cassette A1 and induces apolipoprotein A1-specific cholesterol efflux. When dosed to insulin-resistant middle-aged obese rhesus monkeys, GW501516 causes a dramatic dose-dependent rise in serum high density lipoprotein cholesterol while lowering the levels of small-dense low density lipoprotein, fasting triglycerides, and fasting insulin. These results suggest that PPARdelta agonists may be effective drugs to increase reverse cholesterol transport and decrease cardiovascular disease which is typically associated with the metabolic syndrome X. (Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5306-11. Epub 2001 Apr 17. PMID:11309497)

As for as dosing is concerned, I recommend 5-20mgs once a day, and research on HUMANS has clearly shown that 5mg is sufficient to elicit its intended effects. I really don’t understand why this peptide is not as common as it should be. Its exercise in a vial LMAO.

Now onto the fun stuff guys. Dosing, stacking and uses for this drug. Many people would start out at a 5mg a day dose and I think this is fine but I would also add in another 5mg dose pre work out as well on work out days at the very least if not just run it 10mg every day IMO. IMO one could use this during pct allow you to keep calories high and not gain to much fat which is often what happens. I think its also great in combo with Sarms S4 as a bridge between cycles but I am against using S4 during pct. SO only use it after pct and you are sure you have recovered. Now here is the best part GW-501516 can be used with Drugs like winstrol, Beastdrol, and other orals that would cause problems with cholesterol and this would help keep the numbers to a minimum. High blood pressure, nose bleeds and high cholesterol is common with a lot of oral steroids and this drug will help in the sense that it will lower cholesterol levels..

That is all for now my friend. Always remember to Keep Killing that sh*t!!!!!

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