Question about Clen

png12977

New Member
I just got back from a cruise that stopped in Mexico and bought some clen at the pharmacy. It says the pills are 0.02mg. Is that 20mcg? Also, on the days you take 40, 60, 80 mcg etc, do you take it all at once or break up the dosage into 2 or 3 times a day? When do you start taking benadryl? Should it be taken 1st thing in the morning?
 
I just got back from a cruise that stopped in Mexico and bought some clen at the pharmacy. It says the pills are 0.02mg. Is that 20mcg? Also, on the days you take 40, 60, 80 mcg etc, do you take it all at once or break up the dosage into 2 or 3 times a day? When do you start taking benadryl? Should it be taken 1st thing in the morning?


0.02mg = 20mcg (you can google conversion amounts for future reference, Sir)

Take the Clenbuterol all at once first thing in the morning, or if you work out in the upon waking in the morning, take it immediately AFTER your work out.

Take the Benedryl before going to bed, between 50-100mg. Ketotifen however is a better choice though than Benedryl in pertinence to Clenbuterol.

...IMO, Clenbuterol is a garbage drug w/ minimal positive attributes combined w/ negative health implications and harsh side effects. Why are you taking it and what is your dosing protocol consist of?
 
I'm still researching cycles for it, as there are many theories. Are you saying it's not going to make much of a difference if it's added to a clean diet and cardio? I've heard that it helps keep muscle while you are on a lower calorie diet. Is there something you suggest that's better?
 
I'm still researching cycles for it, as there are many theories. Are you saying it's not going to make much of a difference if it's added to a clean diet and cardio? I've heard that it helps keep muscle while you are on a lower calorie diet. Is there something you suggest that's better?


A consistent & clean diet on top of an appropriate weight training/cardio regime in addition to proper recovery will get you to where you would be at w/ clen. The muscle retaining properties and potential skeletal muscle anabolism that claim come w/ it have not ever been seen in human studies, only in animal models. IMO, certain AAS (particularly strong androgens) are superior to muscle retention while on a calorie deficit to just about anything else out there.
 
I just got back from a cruise that stopped in Mexico and bought some clen at the pharmacy. It says the pills are 0.02mg. Is that 20mcg? Also, on the days you take 40, 60, 80 mcg etc, do you take it all at once or break up the dosage into 2 or 3 times a day? When do you start taking benadryl? Should it be taken 1st thing in the morning?

Start out at 20mcg a day, I tried 40mcg my first go at it on a sunday a couple of months ago, and yeah, it was way to much, didn't even fall asleep that night, got out of bed and went to work. My heart was pounding all night too.
 
The muscle retaining properties and potential skeletal muscle anabolism that claim come w/ it have not ever been seen in human studies, only in animal models,
That's not true. Anticatabolic effects have been shown numerous times in humans, corroborating the animal data.


This paper was pretty explicit, titled "Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure." They found that "Clenbuterol was well tolerated and led to a significant increase in both lean mass and the lean/fat ratio."

In another human study, they slowly titrated the dose by 20mcg/wk for three months. They found that "clenbuterol therapy increased skeletal muscle mass and strength."

This study, titled "Oral albuterol dosing during the latter stages of a resistance exercise program" found that "A higher lean body mass trend also occurred with albuterol from weeks 10-13."

Finally, this study give albuterol for 12 weeks to boys with muscular dystrophy. Outcome measurements included lean body mass and fat mass. They found that "Lean body mass was significantly higher for subjects following albuterol treatment compared to placebo treatment, while fat mass was significantly lower."

While there is definitely more evidence in animals showing anabolic/anti-catabolic effects from beta-agonists, there is plenty of evidence supporting the existence of the same effect in human skeletal muscle.
 
Start out at 20mcg a day, I tried 40mcg my first go at it on a sunday a couple of months ago, and yeah, it was way to much, didn't even fall asleep that night, got out of bed and went to work. My heart was pounding all night too.
Or even better, bite the tabs in half and start at 10 mcg/day. Increase the dose by only 10mcg every 3-4 days.
 
Here is something you might try for a 20 week cycle. Notice the break in the 9th week. It seems like your off for a while but in all actuality your only off for a week.

Week 1- On(20-40mcg)
Week 2- Off
Week 3- On(20-40mcg)
Week 4- Off
Week 5- On(40-60mcg)
Week 6- Off
Week 7- On(60-80mcg)
Week 8- Off
Week 9- Off
Week 10- Off
Week 11- On(20-40mcg)
Week 12- Off
Week 13- On(20-40mcg)
Week 14- Off
Week 15- On(40-60mcg)
Week 16- Off
Week 17- On(60-80mcg)
Week 18- Off
Week 19- Off
Week 20- Off
Repeat if needed...

You can adjust your clen dosage depending on how you feel. This is a generic cycle that I have used with good results.

Hope this helps,

mands
 
That's not true. Anticatabolic effects have been shown numerous times in humans, corroborating the animal data.


This paper was pretty explicit, titled "Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure." They found that "Clenbuterol was well tolerated and led to a significant increase in both lean mass and the lean/fat ratio."

In another human study, they slowly titrated the dose by 20mcg/wk for three months. They found that "clenbuterol therapy increased skeletal muscle mass and strength."

This study, titled "Oral albuterol dosing during the latter stages of a resistance exercise program" found that "A higher lean body mass trend also occurred with albuterol from weeks 10-13."

Finally, this study give albuterol for 12 weeks to boys with muscular dystrophy. Outcome measurements included lean body mass and fat mass. They found that "Lean body mass was significantly higher for subjects following albuterol treatment compared to placebo treatment, while fat mass was significantly lower."

While there is definitely more evidence in animals showing anabolic/anti-catabolic effects from beta-agonists, there is plenty of evidence supporting the existence of the same effect in human skeletal muscle.

The first two studies you give relate to ppl w/ heart failure which are more than likely in an untrained state, so IMO those needs to be thrown out since individuals who have heart failure on top of being an in untrained state should not be compared 2 ppl who are healthy subjects, let alone avid weight trainers like ppl on this forum. Also, the next 2 studies you give acutally use the drug Albuterol, NOT Clenbuterol, so IMO those 2 can be thrown out too. Now, I understand that both of these drugs are beta-2 agonists, but that shouldn't give ppl to say that they are indeed the same drug. They may have different agonist, antagonist, and/or inverse agonist properties on various receptors we simply do not know about yet. Furthermore, although researchers have theories on why Clenbuterol (and various other beta 2 agonists) may promote skeletal muscle anabolism and/or prevent catabolism, but no one really know's for sure. With minimal to zero effects in these regards in most ppl that use the drugs, until researchers know FOR SURE as to what mechanism of action(s) (MOA) Clenbuterol has to do possibly do this, I will still hold the thought that there really is none whatsoever.
 
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Ok, we all know that the effectiveness of AAS as well as the amount of side effects experienced vary person to person. On a personal experience level, I think Clen is at the top of the list when it comes to varying greatly between users. I personally love Clen when used with Keto and Taurine for about 6-8 weeks. I can cut off a considerable amount of fat in just that short time with this simple cycle. However, I have friends who do not use Clen because they say it doesn't work. I have not monitored their intake, workout routines sleeping habits, etc., like you would see in a clinical study. But, I think this just shows that it's one of those drugs that you have to give a go to really know if it's going to work for you or not.

Always take your Clen in the morning. if you take it before you go to bed you will not sleep even 1minute during the night.

Always take Ketotifen with Clen. As some of you know, I am a huge Keto supporter. Nothing helps me sleep better while on Clen. When I have forgotten to take my Keto dose before bed I get way too hot and have a rather "itchy" feeling from the Clen.

Always take Taurine with Clen. Cramps out the ass if you don't...seriously.

Give it at least 2 weeks before you say it doesn't work. It starts showing signs of working right away for me. But the weight loss really starts to kick in around week 2. I have had friends who lose 10 lbs or more in the first week (some over 20). Diet has a lot to do with this as well, of course.

The main point here is that Clen illicits very different reactions based on individual subjective usage. So, give it a shot if you really think you can commit to it with a solid diet.

Cheers
 
The first two studies you give relate to ppl w/ heart failure which are more than likely in an untrained state, so IMO those needs to be thrown out since individuals who have heart failure on top of being an in untrained state should not be compared 2 ppl who are healthy subjects, let alone avid weight trainers like ppl on this forum.
Instead of showing appreciation for the correction and further knowledge, you're demonstrating cognitive dissonance with a silly denial of my contradictory evidence. The fact is, you were wrong to say that the "potential skeletal muscle anabolism" has "not ever been seen in human studies, only in animal models." Can you admit you were wrong. Further, it's foolish to throw out these human studies simply because the subjects weren't lifting weights. There's absolutely no reason to think that training would interfere with the anabolic/anticatabolic effects or otherwise oppose the beta-2 agonism.
Also, the next 2 studies you give acutally use the drug Albuterol, NOT Clenbuterol, so IMO those 2 can be thrown out too. Now, I understand that both of these drugs are beta-2 agonists, but that shouldn't give ppl to say that they are indeed the same drug. They may have different agonist, antagonist, and/or inverse agonist properties on various receptors we simply do not know about yet.
The only beta subtype found in skeletal muscle in beta-2. These two studies on albuterol corroborate the two studies on clenbuterol. Both beta-2 agonists (and others) have been shown to increase muscle mass in several different populations IN HUMANS.
 
Furthermore, although researchers have theories on why Clenbuterol (and various other beta 2 agonists) may promote skeletal muscle anabolism and/or prevent catabolism, but no one really know's for sure.
This is also incorrect. http://jap.physiology.org/cgi/content/full/102/2/740 (This study) examined clen's mechanism of action. It's worth noting that early in the paper they state that "CHRONIC ADMINISTRATION OF clenbuterol and other synthetic compounds that activate beta-adrenergic receptors has been shown to induce skeletal muscle growth in multiple mammalian species, including rats, cows, sheep, pigs, and humans." Just like I said before, this is a feature of beta-agonists generally (including clen, albuterol, metaproterenol, etc), in humans.

The study found that clen not only increases muscle mass through the well established cAMP -> PKA pathway, but also the PI3K -> Akt -> mTOR pathway. To say that "no one really knows for sure" how clen promotes skeletal muscle anabolism is incorrect. While you can play semantic games over what it means to "know for sure", there's no question that researches have a very good understanding of the pathways that clen operates through.
With minimal to zero effects in these regards in most ppl that use the drugs...
Not so fast. Clen produces minimal to zero effects according to who? You? Sorry, but the human studies I already posted contradict that. Also, keep in mind that most bodybuilders take clen while dieting, an environment where muscle loss is the norm. They're in a poor position to assess the anabolic/anti-catabolic effects of clen when a positive result would likely manifest itself as a slowing of muscle loss. Ask yourself how easy is it to quantify that, let alone identify it. Even if bodybuilders did take clen while bulking, it's laughable to think that an individual would be in any position to assess the extent of clen's additive effect with nothing more than uncontrolled anecdote.
until researchers know FOR SURE as to what mechanism of action(s) (MOA) Clenbuterol has to do possibly do this, I will still hold the thought that there really is none whatsoever.
You can be obstinate and hold the thought for as long as you want. You can ignorantly keep asserting that there are no human studies, that no one knows what the mechanism of action is. I can see you're eager to stay ignorant, so be my guest.
 
Wow, I would love to sit you 2 down in a political type platform and have you debate. I'll be the moderator...that would be very intriguing I believe
 
Instead of showing appreciation for the correction and further knowledge, you're demonstrating cognitive dissonance with a silly denial of my contradictory evidence. The fact is, you were wrong to say that the "potential skeletal muscle anabolism" has "not ever been seen in human studies, only in animal models." Can you admit you were wrong. Further, it's foolish to throw out these human studies simply because the subjects weren't lifting weights. There's absolutely no reason to think that training would interfere with the anabolic/anticatabolic effects or otherwise oppose the beta-2 agonism.
The only beta subtype found in skeletal muscle in beta-2. These two studies on albuterol corroborate the two studies on clenbuterol. Both beta-2 agonists (and others) have been shown to increase muscle mass in several different populations IN HUMANS.


Yes, the studies you gave concluded that beta 2 agonists do show to have muscle building properties in humans. However, you do have to admit though that we would rather see these results to ppl that fit the bill on this forum more than on ppl w/ heart failure or individuals w/ muscle disorders, correct?. Also, on the last part of your comments, you missed the point about the clenbuterol & albuterol comparisions. I meant thinking outside of the box than to more of them being beta 2 agonists, as they might have different MOA other than that, as we see this with many other drugs. One of the best examples I can think of off the top of my head is the antidepressant Remeron as it is known to display agonist (though BOTH inverse & indirect) and antagonist properties on all types of various receptors giving it many different MOA. I was referring to w/ the Clen and Albuterol that maybe there are different MOA that we don't know about them yet which would distinquish between them much more than we already do now.
 
This is also incorrect. http://jap.physiology.org/cgi/content/full/102/2/740 (This study) examined clen's mechanism of action. It's worth noting that early in the paper they state that "CHRONIC ADMINISTRATION OF clenbuterol and other synthetic compounds that activate beta-adrenergic receptors has been shown to induce skeletal muscle growth in multiple mammalian species, including rats, cows, sheep, pigs, and humans." Just like I said before, this is a feature of beta-agonists generally (including clen, albuterol, metaproterenol, etc), in humans.

The study found that clen not only increases muscle mass through the well established cAMP -> PKA pathway, but also the PI3K -> Akt -> mTOR pathway. To say that "no one really knows for sure" how clen promotes skeletal muscle anabolism is incorrect. While you can play semantic games over what it means to "know for sure", there's no question that researches have a very good understanding of the pathways that clen operates through.
Not so fast. Clen produces minimal to zero effects according to who? You? Sorry, but the human studies I already posted contradict that. Also, keep in mind that most bodybuilders take clen while dieting, an environment where muscle loss is the norm. They're in a poor position to assess the anabolic/anti-catabolic effects of clen when a positive result would likely manifest itself as a slowing of muscle loss. Ask yourself how easy is it to quantify that, let alone identify it. Even if bodybuilders did take clen while bulking, it's laughable to think that an individual would be in any position to assess the extent of clen's additive effect with nothing more than uncontrolled anecdote.
You can be obstinate and hold the thought for as long as you want. You can ignorantly keep asserting that there are no human studies, that no one knows what the mechanism of action is. I can see you're eager to stay ignorant, so be my guest.


First of all, the study you mention is in rats. Terminator, while we can both go round and round about rats studies vs humans, just let it be known that many studies which seem excellent in rats, when it comes to humans, its not more as clear cut. A perfect example is w/ the studies involving the hormone "resistin" in mice almost a decade ago. Researchers thought they found exactly what causes insulin resistance, but still now they are debate whether resistin may even cause a negative effect, neutral, or even possibly a positive effect in regards to insulin function in the human body.

So, back to the study you give. Govenor, Idk if you actually read the WHOLE STUDY, just skimmed through it, or simply read the abstract, but your previous posts contradict what you state. In the study it says verbatim... "The findings illustrate that the actions of clenbuterol are likely mediated through multiple pathways and underscore the necessity to examine multiple muscles under a variety of conditions to establish a complete understanding of clenbuterol and its mode of action. The growth and muscle-sparing effects of clenbuterol could be mediated through a single or multiple pathway(s) that affects protein synthesis or degradation processes."

...even the researchers in the study DO NOT know for sure the exact mechanism of actions that Clenbuterol has in regards to skeletal muscle, though they at least feel they know somewhat and are at least on to something.

Here is something else for you in the study, Detective John Kimbell, verbatim...
"The growth and muscle-sparing effects of clenbuterol could be mediated through a single or multiple pathway(s) that affects protein synthesis or degradation processes. The reported effects of clenbuterol and other 2-adrenergic agonists on muscle protein turnover have been contradictory (23). A number of studies utilizing radioisotopically labeled amino acids have reported increases in the fractional synthesis rates in skeletal muscles after treatment with 2-adrenergic agonists (18, 26, 29). However, other studies have found no change in protein synthesis rates (28, 35). The conflicting results could be because of differences in the muscles studied and the timing of the measurements. In general, the growth effects induced by 2-adrenergic agonists are more pronounced in predominantly fast-twitch muscle than slow-twitch muscle (18, 23, 31, 38). Increases in fractional synthesis rates have been observed at 1–3 days after the start of clenbuterol treatment, returning to normal within 7–10 days (18, 29). For example, Hesketh et al. (18) observed a 37% increase in the fractional rate of protein synthesis in the rat gastrocnemius after 1 day of clenbuterol treatment, which returned to control levels by 4 days."

...so you used the term "chronic" in relation to using Clenbuterol to gain consistent quality muscle, but if you look at how on the sentence in the last study how protein synthesis rates returned to normal after 4 days. I really don't see this as 3 days of the body trying to increase muscle mass via protein synthesis as chronic. Furthermore, study #23 supports this notion as Clenbuterol ONLY supporting muscular growth for a very short time. The link is provided below is ppl want to look at it...

Beta-adrenergic agonists and hypertrophy of skelet... [Life Sci. 1992] - PubMed result

...the study provided in the link above along with the study I have already quoted verbatim have also talked about the beta 2 agonist property of Clenbuterol only works well in "type II fast twitch". The study also gives 2 other studies that show no change in protein synthesis with the possible reason for this being differences in muscles being studied. So w/ me saying it doesn't give some ppl the results they want (zero to minimal) is correct. Also, back to the point of Clenbuterol's action on skeletal muscle fading away quickly. I guess you might say to up the dose slowly all the way to 720 micrograms like they do in the 1 study you give regarding ppl who built muscle using that much Clenbuterol. Do you SERIOUSLY consider this a study of merit pertaining to the ppl on this forum. SERIOUSLY, Conan, do you REALLY consider that safe?! Here is the link for ppl who might not believe me...

Effect of clenbuterol on cardiac and skeletal musc... [J Heart Lung Transplant. 2006] - PubMed result

,,,also here is a link to a study that contradicts using Clenbuterol for bodybuilding purposes in the first place...

Elsevier
 
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Yes, the studies you gave concluded that beta 2 agonists do show to have muscle building properties in humans.
I'm glad you can admit you were mistaken.,
However, you do have to admit though that we would rather see these results to ppl that fit the bill on this forum more than on ppl w/ heart failure or individuals w/ muscle disorders, correct?
Sure, and we'd all like a free pony too. Unfortunately, you're usually going to be straight out of luck if what you want is an RCT in a resistance trained population.
Also, on the last part of your comments, you missed the point about the clenbuterol & albuterol comparisions. I meant thinking outside of the box than to more of them being beta 2 agonists, as they might have different MOA other than that, as we see this with many other drugs. One of the best examples I can think of off the top of my head is the antidepressant Remeron as it is known to display agonist (though BOTH inverse & indirect) and antagonist properties on all types of various receptors giving it many different MOA. I was referring to w/ the Clen and Albuterol that maybe there are different MOA that we don't know about them yet which would distinquish between them much more than we already do now.
You can postulate unknown MOAs all you want. But a lack of evidence is evidence of nothing. The mere possibility of an additional mechanism of action is irrelevant when there's already an established mechanism of action, with an established effect, that the substances have been established to work through.
 
First of all, the study you mention is in rats. Terminator, while we can both go round and round about rats studies vs humans, just let it be known that many studies which seem excellent in rats, when it comes to humans, its not more as clear cut. A perfect example is w/ the studies involving the hormone "resistin" in mice almost a decade ago. Researchers thought they found exactly what causes insulin resistance, but still now they are debate whether resistin may even cause a negative effect, neutral, or even possibly a positive effect in regards to insulin function in the human body.
OhNoYo, we know that the mechanism of action is mediated through transactivation of the beta-2 AR. Understanding the underlying biochemical cascades can be interesting, but is hardly necessary for one to say that the MOA is known. The MOA is beta-2 receptor transactivation. We know that because beta-2 blockade attenuates the anabolic effects. Further, even if you didn't know the mechanism of action at all, it changes nothing about the fact that we know clenbuterol has a positive effect on muscle mass.
So, back to the study you give. Govenor, Idk if you actually read the WHOLE STUDY, just skimmed through it, or simply read the abstract, but your previous posts contradict what you state. In the study it says verbatim... "The findings illustrate that the actions of clenbuterol are likely mediated through multiple pathways and underscore the necessity to examine multiple muscles under a variety of conditions to establish a complete understanding of clenbuterol and its mode of action. The growth and muscle-sparing effects of clenbuterol could be mediated through a single or multiple pathway(s) that affects protein synthesis or degradation processes."

...even the researchers in the study DO NOT know for sure the exact mechanism of actions that Clenbuterol has in regards to skeletal muscle, though they at least feel they know somewhat and are at least on to something.
It doesn't contradict anything I said. What you're not realizing is that the study is examining the biochemical cascades that follow from b2 activation. At a macro level, the mechanism of action is already clear. It's beta-2 agonism. In this study, they were examining the subsequent, underlying cascades. They found that in addition to the well known cAMP->PKA cascade (which b2-agonists have long been known to operate though), the effect was also seen to be mediated through mTOR.

But the cascade is irrelevant. Knowing that anabolism/anticatabolism from activation of the b2 receptor is mediated through cAMP or mTOR is just as irrelevant as knowing that activation of the androgen receptor is mediated through dimerization of the AR and binding to a hormone response element. At at a receptor level, the mechanism of action and the effects produced are already clear.

I would point out, though, that even if it weren't clear, that's fine, as the MOA at a receptor level is also irrelevant. If studies show that androgens or b2 agonists increase muscle mass as an end point in humans, it doesn't matter if you understand how. There are several pharmaceutical drugs that produce therapeutic effects and that went to market even though the MOA was a mystery (e.g. accutane).
 
Here is something else for you in the study, Detective John Kimbell, verbatim...

...so you used the term "chronic" in relation to using Clenbuterol to gain consistent quality muscle, but if you look at how on the sentence in the last study how protein synthesis rates returned to normal after 4 days. I really don't see this as 3 days of the body trying to increase muscle mass via protein synthesis as chronic. Furthermore, study #23 supports this notion as Clenbuterol ONLY supporting muscular growth for a very short time.
Two things. One, it appears you're ignorant of the fact that FSR (synthesis) is only one half the story when it comes to protein balance (the other being breakdown). Clen could increase FSR for only 3 days, but inhibit proteolysis (breakdown) for much longer, leading to a long-term, net increase in muscle mass.

Second, it doesn't matter what this study in rats found when long term (3 months+) anabolic effects have been observed in human studies.

...the study provided in the link above along with the study I have already quoted verbatim have also talked about the beta 2 agonist property of Clenbuterol only works well in "type II fast twitch". The study also gives 2 other studies that show no change in protein synthesis with the possible reason for this being differences in muscles being studied. So w/ me saying it doesn't give some ppl the results they want (zero to minimal) is correct.
No, that's a non sequitur. Just because clen doesn't increase FSR doesn't mean it doesn't increase muscle mass (which it could do by slowing breakdown). A net positive effect has been demonstrated in humans, despite whether or not some random person taking it is in a position to notice that positive effect.
Also, back to the point of Clenbuterol's action on skeletal muscle fading away quickly. I guess you might say to up the dose slowly all the way to 720 micrograms like they do in the 1 study you give regarding ppl who built muscle using that much Clenbuterol. Do you SERIOUSLY consider this a study of merit pertaining to the ppl on this forum. SERIOUSLY, Conan, do you REALLY consider that safe?! Here is the link for ppl who might not believe me...
Yes, I consider it perfectly safe to increase the dose by 20 mcg per week for weeks on end. When this happens, the dose is slowly being increased to keep pace with desensitization. The level of receptor activation is kept in balance with desensitization. The results at such a high dose are entirely relevant. You're ignorant to look at the dose and ignore the long period of time over which they slowly increased the dose. The absolute dose is essentially meaningless if you don't look at it in terms of the state of desensitization.

In fact, bodybuilders increase the dose much faster than in this study, producing more b2 action. They take a greater risk doing this, they experience greater side effects... and they're also likely to experience greater anabolism/anticatabolism.
,,,also here is a link to a study that contradicts using Clenbuterol for bodybuilding purposes in the first place...

Elsevier
No, it doesn't. The paper is on muscle quality, (that is, its functional characteristics), not muscle quantity, or hypertrophy.
 
Two things. One, it appears you're ignorant of the fact that FSR (synthesis) is only one half the story when it comes to protein balance (the other being breakdown). Clen could increase FSR for only 3 days, but inhibit proteolysis (breakdown) for much longer, leading to a long-term, net increase in muscle mass.

Second, it doesn't matter what this study in rats found when long term (3 months+) anabolic effects have been observed in human studies.

No, that's a non sequitur. Just because clen doesn't increase FSR doesn't mean it doesn't increase muscle mass (which it could do by slowing breakdown). A net positive effect has been demonstrated in humans, despite whether or not some random person taking it is in a position to notice that positive effect.
Yes, I consider it perfectly safe to increase the dose by 20 mcg per week for weeks on end. When this happens, the dose is slowly being increased to keep pace with desensitization. The level of receptor activation is kept in balance with desensitization. The results at such a high dose are entirely relevant. You're ignorant to look at the dose and ignore the long period of time over which they slowly increased the dose. The absolute dose is essentially meaningless if you don't look at it in terms of the state of desensitization.

In fact, bodybuilders increase the dose much faster than in this study, producing more b2 action. They take a greater risk doing this, they experience greater side effects... and they're also likely to experience greater anabolism/anticatabolism.
No, it doesn't. The paper is on muscle quality, (that is, its functional characteristics), not muscle quantity, or hypertrophy.


With being a former Mr. Olympia, I would think that you would NOT give out such dangerous advice. You gotta be kidding saying upping Clenbuterol dosages slowly to pretty much infinity is safe AND effective. First off, the use of Clenbuterol already poses a threat to the myocardium which may possibly result in arrythiamias, left ventricular hypertrophy, and even myocardial infarction. Using Clenbuterol for weeks, months, years, hell even decades on end it sounds like in your case would without question increase these bad side effects on top of possibly causing congestive heart failure (CHF). Secondly, with the desensitization effect, there would come a time that the minimal effects of upon muscular growth related to Clenbuterol would come to an end. This is already seen in Clenbuterol rather quickly anyway. We have already assessed this with a previous study mentioned, but if you already forgot, I will put if for you verbatim PLUS give you a link to the study provided below. Here is the sentence, verbatim... "The hypertrophic effect of beta-adrenergic agonists is transient, with the effect diminishing during prolonged treatment."

Beta-adrenergic agonists and hypertrophy of skelet... [Life Sci. 1992] - PubMed result

...also, out of all ppl on this forum, I would think YOU would appreciate the MOA of substances, Gov! Why talk NOW about who cares what Substance X does as long as it gets you HUGE, when all you talk about is how things work?

On an end note, ppl (including myself) look up to you and many take your words to heart. So plz, for the sake of ppls health on this forum, plz tell them upping the dose of clenbuterol every 20mcg and taking it for long time periods, weeks on end as you put it, is uneffective and extremely dangerous!
 
Also, if you could plz Detective Kimbell, show me the studies regarding Clenbuterol slowing muscle protein breakdown. Humans studies would be better, but I'm sure there aren't any out there. I was just wanting to see the data out there since you claim although Clenbuterol's MOA of increasing protein synthesis stops abruptly (in some studies it stops after the 1st day), you claim other MOA for Clenbuterol in terms of slowing muscle breakdown would ultimately cause anabolism.
 
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