albuterol cycle. Advice please.
- 02-03-2011, 08:32 AM
albuterol cycle. Advice please.
Currently on EC, how long should I before transitioning, do not want to destroy my receptors.
Planning on running it for 20 days at 3x4g
Again how effective is it in comparison? I know it is anabolic and people have gained muscle mass, but is it worth it in comparison of running EC on keto diet.
Or would albuterol with keto (the chemical not the diet), along with clean eating be a better combo?
- 02-03-2011, 09:34 AM
I will probably get most of the answers through searching im just running on no sleep, so if you can help, thanks. If not, all is well
- 02-03-2011, 10:31 AM
albuterol is not anabolic.Test e/dbol/epi/winnie
02-03-2011, 11:18 AM
02-03-2011, 12:13 PM
02-03-2011, 12:23 PM
02-03-2011, 02:34 PM
There is some really good information at the following link:
Credit to the original author. I just copied from the link.
Beta-2 Agonists & Muscle Growth: The Latest Research
Although traditionally used for the treatment of bronchial ailments, especially asthma, it quickly became apparent to the medical community that some beta(b)-adrenoceptor agonists had the ability to increase skeletal muscle mass and decrease body fat (i.e., the so-called “repartitioning effect”). Bodybuilders have long used clenbuterol a few weeks before competition as a “cutting drug” because it stimulates lipolysis and thermogenesis, but researchers are investigating the effects of b-2 agonists for other reasons…muscle hypertrophy! Clenbuterol is one of these compounds with important anti-catabolic and anabolic effects in animal models. However, the toxicity of the drug in humans has not favored the undertaking of clinical trials. There are very few human clenbuterol studies designed for muscle mass enhancement, but in a recent study in the Journal of Heart and Lung Transplant, researchers reported that clenbuterol increased lean muscle mass and reduced fat mass in sedentary patients with chronic heart failure. Patients were given oral clenbuterol or placebo for a total of 12 weeks in addition to their standard congestive heart failure therapy. Clenbuterol was initiated at a dose of 20 micrograms twice daily and uptitrated to 40 micrograms twice daily after seven days.
This dose— used in the treatment of asthma— has been shown to improve performance in athletes and after orthopedic procedures. At the end of three months, clenbuterol given at 80 micrograms per day did not change bodyweight, however, even though the patients were sedentary, lean mass increased in conjunction with a decrease in fat mass— consistent with the anabolic effect of clenbuterol on skeletal muscle. There was also a 27 percent increase in maximal strength; however, clenbuterol was associated with a decrease in endurance performance. Safety aspects of clenbuterol were well tolerated, as they saw no effect on cardiac function and importantly, no change in heart mass with clenbuterol. The researchers demonstrated an increase in lean mass and strength without improvement in endurance performance, yet there was minimal effect on the heart at this dose.1 The study is a follow-up study from 2006, when they administered 720 micrograms a day to heart patients. It was reported that 12 weeks of clenbuterol administration resulted in a 13.5 percent increase in muscle quad mass and a total-body mass increase of 11.8 percent. This study also reported that clenbuterol was well tolerated, and no serious side effects occurred.13 Clenbuterol is a b-2 agonist that is used for treatment of asthma in Europe, but is currently not approved in the United States. Clenbuterol possesses increased oral absorption and is a more selective and potent b-2 agonist than albuterol.2 The mechanisms in which b-2 agonists induce muscle hypertrophy are thought to occur via direct effects on muscle and not through endogenous stimulation of endocrine hormones such as insulin, growth hormone or thyroid.3
B-2 Receptor Mediates The Increase In Muscle Mass
Skeletal muscle contains a significant proportion of b-adrenoceptors, which are mostly of the b-2 subtype. Slow-twitch muscles have a greater density of b-adrenoceptors than fast-twitch muscles.6 B-2 adrenoceptors mediate the anabolic effects of clenbuterol; this was originally confirmed by the actions of the selective b-2 antagonist drug (blocks the actions of clenbuterol), which has a ~100-fold greater affinity for b-2 adrenoceptors than for b-1 adrenoceptors. The b-2 antagonist drug reduced the anabolic effects of clenbuterol when administered together and when the b-2 antagonist drug was administered alone, it caused muscle atrophy.10 Further confirmation was provided when researchers administered clenbuterol to control, b-1 or b-2 knockout mice and demonstrated that only control and b-1 adrenoceptor knockout mice exhibited skeletal muscle hypertrophy. These studies confirmed that b-2 adrenoceptors mediated the pharmacological effects of clenbuterol and that they were involved in the control of muscle growth.
Intramuscular B-2 Agonists Increase Muscle Mass and Repair
As mentioned previously, b-2 agonists have direct action on muscle, which facilitates repair and improves skeletal muscle regeneration. However, high-dose oral administration for lengthy treatment periods required to elicit skeletal muscle hypertrophy has been associated with cardiovascular side effects (especially cardiac hypertrophy) that have so far limited their clinical applicability. A recent study in the Journal of Applied Physiology reported that local intramuscular injection of b-2 agonists (formoterol) increased muscle mass and had minimal effects on the cardiovascular system. Rats received 0.01, 0.1, 1.0, 10, or 100 micrograms of formoterol (in 0.1-ml saline) via a single intramuscular injection into the right leg muscle. Interestingly, muscle mass was increased in the right leg at all doses of formoterol tested. The maximal hypertrophic response was seen at the highest dose— 100 micrograms. Researchers then injured the rats’ leg muscle and injected the injured leg with 100 micrograms of formoterol and found that compared to the control leg, the leg treated with formoterol had an increase in force production and muscle mass with a single injection of formoterol. One surprising finding of the study was that a single dose of formoterol increased muscle mass. One of the major factors limiting the use of b-2 agonists for treating muscle wasting and weakness relates to their cardiovascular effects. Chronic oral systemic b-2 agonist administration has been associated with cardiac hypertrophy and altered cardiovascular function.4, 5 In the study, neither single nor successive intramuscular injections were associated with cardiac hypertrophy.
B-2 Agonists Increase Muscle Mass Through Multiple Pathways
The basis for the effectiveness of clenbuterol as an anabolic agent has been attributed to its ability to promote muscle protein synthesis, as well as reduce muscle protein breakdown. There has been much debate as to whether the clenbuterol-induced increase in muscle mass is due preferentially to one mechanism or the other. Several genes for muscle hypertrophy have been identified in processes important to skeletal muscle growth, including mediators of cell-signaling pathways.
A. Reducing Myostatin: B-2 agonists have the ability to reduce myostatin levels. For example, b-2 agonists increase the expression of NOR-1. NOR-1 is part of the orphan nuclear receptors within the steroid/thyroid receptor “super” family. Not much is known about how NOR-1 regulates muscle, but when NOR-1 is inhibited, there is a dramatic increase (~65-fold) in the levels of myostatin cells.7 How the hell do you keep NOR-1 from dropping? B-2 agonists’ activation causes increases in NOR-1 expression and may inhibit myostatin expression and thus, promote skeletal muscle growth. One study reported that NOR-1 mRNA expression was significantly increased (>100-fold) by a B2-AR agonist. It is interesting to note that myostatin knockout mice appear resistant to the anabolic effects of B2-AR agonists on skeletal muscle, suggesting that the anabolic effects of B2-AR agonists may involve modulation of myostatin expression.7 These findings may provide an insight into the molecular mechanisms that mediate the metabolic and anabolic changes associated with chronic B2-adrenoceptor agonist-induced skeletal muscle hypertrophy.
B. Increasing mTOR/AKT and IGF-1: One signaling pathway involved in regulating skeletal muscle hypertrophy is the AKT/mTOR pathway. mTOR pathway activity increases in response to muscle activity during hypertrophy and decreases in activity during atrophy. IGF-1 activates both AKT and mTOR to promote hypertrophy. Multiple skeletal muscle AKT pathways are activated following b-2 adrenoceptor stimulation and these lead predominantly to skeletal muscle hypertrophy. For example, it was reported that stimulation of the b-2 adrenoceptor-signaling pathway resulted in AKT phosphorylation and subsequent activation of mTOR.8, 9 Additionally, when the researchers administered the mTOR antagonist rapamycin with clenbuterol, the anabolic actions of clenbuterol were inhibited.8 Finally, changes in skeletal muscle expression of IGF-1 mRNA have been observed shortly after the administration of clenbuterol, suggesting the regulation of these growth factors may be important in the initial response of skeletal muscle to the b-2 adrenoceptor-signaling pathway.
C. Reducing Catabolic Gene Expression: Researchers have determined that the catabolic actions of cortisol are mediated through the expression of MuRF1 (The MuRF1 protein was identified as an atrophy-specific factor, whose expression is upregulated in atrophying muscle) and atrogin-1 (atrogin-1 is very strongly induced in many catabolic states). B-2 adrenoceptor activation has been found to reduce the expression of muRF1 and atrogin-1 in skeletal muscle, an effect possibly mediated via AKT.8 Clenbuterol has been shown to reduce the anti-catabolic actions of cortisol.
The New Generation Of B-2 Agonists
“Newer” generation beta-agonists (formoterol and salmeterol) exert significant anabolic actions on skeletal muscle even at micromolar doses, compared with the millimolar doses required to elicit the same responses with older generation b-2 agonists such as fenoterol or clenbuterol. So what makes formoterol different from clenbuterol? Formoterol is said to be a full agonist of the beta-receptor; that is, formoterol mediates a greater cellular response (production of cAMP) than stimulation by clenbuterol (a partial agonist). If you compare a similar dose of formoterol to clenbuterol in animals, clenbuterol increased muscle size by 6 percent, however formoterol increased muscle size by 20 percent.12 The dosages of clenbuterol and other b-2 agonists to induce muscle hypertrophy have been supraphysiological dosages, which far exceed the estimated safe dosage in humans. The use of low-dose formoterol has some advantages over clenbuterol, as low dosages of formoterol treatment cause muscle hypertrophy without increasing the susceptibility of muscle fatigue. The promising aspect of formoterol is that it can be used at micromolar dosages, yet still produce muscle hypertrophy without cardiac hypertrophy.11 Formoterol has been recently reported to reduce the catabolic effects of muscle-wasting diseases like cancer; specifically, formoterol treatment resulted in a decrease in the mRNA content of catabolic gene expressions (ubiquitin and proteasome) in gastrocnemius muscles; this, together with the decreased proteasome activity observed, suggests that the main anti-proteolytic action of the drug may be based on an inhibition of the ATP-ubiquitin-dependent proteolytic system.14 Formoterol may be the perfect competition drug, because it has anti-catabolic actions on muscle as well as anabolic actions, yet minimal effects on cardiac hypertrophy.
1. Kamalakkannan G, Petrilli CM, George I, LaManca J, McLaughlin BT, Shane E, Mancini DM, Maybaum S. Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure. J Heart Lung Transplant, 2008 Apr;27(4):457-61.
2. Pasotti C, Capra A, Vibelli C. NAB 365 (clenbuterol) and salbutamol in asthmatics: a double-blind clinical trial. Int J Clin Pharmacol Biopharm, 1979;17:176–80.
3. Emery PW, Rothwell NJ, Stock MJ, Winter PD. Chronic effects of beta-2 adrenergic agonists on body composition and protein synthesis in the rat. Biosci Rep, 1984 Jan;4(1):83-9
4. Ryall JG, Gregorevic P, Plant DR, Sillence MN, Lynch GS. B-2 agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol. Am J Physiol Regul Integr Comp Physiol, 283: R1386-1394, 2002.
5. Ryall JG, Plant DR, Gregorevic P, Sillence MN, Lynch GS. B-2 agonist administration reverses muscle wasting and improves muscle function in aged rats. J Physiol, 555: 175-188, 2004.
6. Martin WH 3rd, Murphree SS, Saffitz JE. Beta-Adrenergic receptor distribution among muscle fiber types and resistance arterioles of white, red, intermediate skeletal muscle. Circ Res, 64: 1096–1105, 1989.
7. Pearen MA, Ryall JG, Maxwell MA, Ohkura N, Lynch GS, Muscat GE. The orphan nuclear receptor, NOR-1, is a target of b-adrenergic signaling in skeletal muscle. Endocrinology, 147: 5217–5227, 2006.
8. Kline WO, Panaro FJ, Yang H, Bodine SC. Rapamycin inhibits the growth and muscle-sparing effects of clenbuterol. J Appl Physiol, 102: 740–747, 2007.
9. Sneddon AA, Delday MI, Steven J, Maltin CA. Elevated IGF-II mRNA and phosphorylation of 4E-BP1 and p70S6k in muscle showing clenbuterol-induced anabolism. Am J Physiol Endocrinol Metab, 281: E676–E682, 2001.
10. Sillence MN, Matthews ML, Spiers WG, Pegg GG, Lindsay DB. Effects of clenbuterol, ICI118551 and sotalol on the growth of cardiac and skeletal muscle and on b-2 adrenoceptor density in female rats. Naunyn-Schmiedebergs Arch Pharmacol, 344: 449– 453, 1991.
11. Ryall JG, Schertzer JD, Lynch GS. Attenuation of age-related muscle wasting and weakness in rats after formoterol treatment: therapeutic implications for sarcopenia. J Gerontol A Biol Sci Med Sci, In press.
12. Ryall JG, Gregorevic P, Plant DR, Sillence MN, Lynch GS. Beta-2 agonist fenoterol has greater effects on contractile function of rat skeletal muscles than clenbuterol. Am J Physiol Regul Integr Comp Physiol, 2002 Dec;283(6):R1386-94.
13. George I, Xydas S, Mancini DM, Lamanca J, DiTullio M, Marboe CC, Shane E, Schulman AR, Colley PM, Petrilli CM, Naka Y, Oz MC, Maybaum S. Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support. J Heart Lung Transplant, 2006 Sep;25(9):1084-90.
14. Busquets S, Figueras MT, Fuster G, Almendro V, Moore-Carrasco R, Ametller E, Argilés JM, López-Soriano FJ. Anticachectic effects of formoterol: a drug for potential treatment of muscle wasting. Cancer Res, 2004 Sep 15;64(18):6725-31.
02-03-2011, 02:57 PM
02-03-2011, 02:59 PM
clearly they are not androgenic, but exert some anticatabolic effects
however in a roundabout way if you reduce catabolism you increase anabolism in the body
so i guess in an indirect way it is anabolic hmmm interesting
02-03-2011, 04:27 PM
Does anyone think this would be a good idea to use during PCT or would that just be dumb?
02-03-2011, 09:37 PM
02-04-2011, 12:50 PM
Good for PCT, if used as a muscle saver, but I suggest do not use to lose weight during PCT.
Last edited by grega60438; 02-04-2011 at 07:46 PM. Reason: spelling error
04-06-2011, 10:22 AM
From my experience I have tried it by itself with whey protein and a clean diet and Strength, size and vascularity was Pro-Hormone like...It feels like running EPI at 20mg ED...I was running it at 12mg a day...I used the pill form at 4mg per dose every 3 1/2 hours...This is a little bit of the log I did elsewhere:
(Keep in mind that this is only Albuterol run by itself with whey protein)
And I thought that being asthmatic as a child will suck forever!
I know that we can't talk about cost but this is totally cool, I just got mine for what I pay for a kid combo at Burger King (60 pills of 4mg).
Well, yes it gave me :
more air: I felt like my chest was opened from the inside.
more blood flow: The pump was amazing and my veins were everywhere.
I felt a lot stronger and my recovery time was up a bunch.
I was sweating a lot.
Lowered my LDL cholesterol about 20 points
A little shaky the first week.
Hot as Hell while working out.
Cramps, thirsty all the time
I’m taking two for now. Next week I will try to squeeze 1 more and see what happen, so far is Gooooooood!!!
P.D. Before Albuterol, I drop from 18” to 16.5” on biceps and from 205 to 190 in 4 weeks with only diet and exercise. I felt like ****. I was benching 255X6 at 205 and at 190 I was weak like a mofo! I could only make 4 bench reps with 205. This week I started Albu and increased carbs a just a little bit on Monday and at my first chest day with Albu I pushed 225 x 6 with no help. Maybe is mental but I can only say what I experimented and the gain in strength was really there.
Today I hit my biceps and shoulders. My biceps was 16.5” at the start and last measure was 17” pump. Today is my first bicep/shoulder day with Albu and biceps score 17.5” and shoulders were round and tight.
I will keep you updated with this.
So far it’s all GOOOOOOOOOD!!!!!
I'm planning to use it once I start PCT to keep gains and strength...It has worked for me before so I'm not saying it because I have read about it or a friend of a friend use it and told me...I have use it and it is gooood!!!
04-13-2011, 07:23 PM
04-16-2011, 03:56 AM
04-16-2011, 09:11 AM
04-16-2011, 10:42 AM
B2 agonist tend to **** muscle tissue from slow twitch type 1 to fast twitch type 2a, which is necessary for strength which in turn helps build muscle..
but to the OP you realize EPHEDRINE and ALBUTEROL hit the same receptors correct, Ephedrine is less selective in which one it hits and tends to leave them "open" as dan duchaine would say, but albuterol is more selective but not a pure beta2 like clen.
04-16-2011, 04:53 PM
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