Does Clenbuterol have a rebound effect?

Cdilly93

Bluelighter
Joined
Feb 6, 2014
Messages
358
Just wondering if clenbuterol has a fat gain rebound like effect, or maybe make you bloat a couple days after use? And another question is the effects it has on the heart? Thanks :)
 
Not really no. Beta receptors will downregulate on clen, but you won't get fat in the few days it takes them to recover.

With regards to the cardiac effects, what exactly is it you want to know?
 
The only rebound effect I found so to speak is my breathing went back to being shitty on tren. That's about it. Also some lethargy after being on for a long time at high doses. No fat gain, but glycogen and water will come back a bit.
 
Good question that something I never thought about but then again I've never used it, would expect it to have a rebound after losing fat quickly if I thought about it but fully trust cfcs knowledge
 
Not really no. Beta receptors will downregulate on clen, but you won't get fat in the few days it takes them to recover.

With regards to the cardiac effects, what exactly is it you want to know?
More specifically the heart valves, because i take mdma about once a month and use 5-htp inbetween to recover my serotonin and from the research ive done, i can be doing some damage concerning my heart valves (causes thickening, or something like that) So if clen will add more dangers in that aspect, i should probobably stay away.
 
More specifically the heart valves, because i take mdma about once a month and use 5-htp inbetween to recover my serotonin and from the research ive done, i can be doing some damage concerning my heart valves (causes thickening, or something like that) So if clen will add more dangers in that aspect, i should probobably stay away.

There is a possibility the use of MDMA and its metabolites could induce negative heart valve issues via its effects on 5-HT2b receptors...

Clenbuterol induced hypertension would not help matters...

[h=1]3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") induces fenfluramine-like proliferative actions on human cardiac valvular interstitial cells in vitro.[/h]Setola V1, Hufeisen SJ, Grande-Allen KJ, Vesely I, Glennon RA, Blough B, Rothman RB, Roth BL.
[h=3]Author information[/h]
  • 1Department of Biochemistry, Case Western Reserve University, 2109 Adelbert Road, Cleveland, OH 44106-4935, USA.


[h=3]Abstract[/h]Recent findings have implicated the 5-hydroxytryptamine 2B (5-HT2B) serotonin receptor in mediating the heart valve fibroplasia [valvular heart disease (VHD)] and primary pulmonary hypertension observed in patients taking the now-banned appetite suppressant fenfluramine (Pondimin, Redux). Via large-scale, random screening of a portion of the receptorome, we have discovered that the amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") and its N-demethylated metabolite 3,4-methylenedioxyamphetamine (MDA) each preferentially bind to and activate human recombinant 5-HT2B receptors. We also demonstrate that MDMA and MDA, like fenfluramine and its N-deethylated metabolite norfenfluramine, elicit prolonged mitogenic responses in human valvular interstitial cells via activation of 5-HT2B receptors. We also report that pergolide and dihydroergotamine, two drugs recently demonstrated to induce VHD in humans, potently activate 5-HT2B receptors, thus validating this assay system for its ability to predict medications that might induce VHD. Our discovery that MDMA and a major metabolite, MDA, induce prolonged mitogenic responses in vitro similar to those induced by fenfluramine and norfenfluramine in vivo (i.e., valvular interstitial cell fibroplasia) predict that long-term MDMA use could lead to the development of fenfluramine-like VHD. Because of the widespread abuse of MDMA, these findings have major public health implications. These findings also underscore the necessity of screening current and future drugs at h5-HT2B receptors for agonist actions before their use in humans.

Full Paper:

http://molpharm.aspetjournals.org/content/63/6/1223.long
 
More specifically the heart valves, because i take mdma about once a month and use 5-htp inbetween to recover my serotonin and from the research ive done, i can be doing some damage concerning my heart valves (causes thickening, or something like that) So if clen will add more dangers in that aspect, i should probobably stay away.

The valvular issues are, as you say, mostly related to seratonergic effects. They seem to be generally reversible but you may want to consider discontinuing the supplemental 5-htp.

Clen's cardiac effects are unrelated to that specific valvular issue. The main concern (with chronic administration) is cardiac hypertrophy and altered cardiac function, caused directly (by the drug itself) and indirectly by its potential side-effects (eg: elevated BP, heart rate, peripheral resistance, atrial fibrillation etc).

Clen also appears to be mildly toxic to cardiac myocytes, though most of these experiments have been performed on rats/mice, at high doses, and sometimes inference to humans is flawed from these models. However, I would always err on the side of caution.

Realistically, a typical cycle of clen is unlikely to do much harm although any stimulant should be considered an additive/synergistic risk to those already resulting from of AAS use. I'm not personally a fan of mixing stimulants of any kind with AAS, especially if other precautions haven't been taken (eg BP lowering medications, venesection etc).
 
The only rebound effect I found so to speak is my breathing went back to being shitty on tren. That's about it. Also some lethargy after being on for a long time at high doses. No fat gain, but glycogen and water will come back a bit.

It's interesting that you should notice this side effect Sero. I do wonder if it's related to the findings from this paper:

Effects of the beta 2-adrenergic agonist clenbuterol on capillary geometry in cardiac and skeletal muscles in young and middle-aged rats.

Suzuki J, Gao M, Xie Z, Koyama T.

Abstract

The effects of 10 day clenbuterol administration on cardiac and skeletal muscle capillarities were studied, particularly in terms of the distribution of arteriolar and venular capillaries and their capillary density, in young (10-week-old) and middle-aged (37-week-old) male Wistar rats. Rats of the treated groups were fed a diet containing 2 mg kg-1 clenbuterol hydrochloride. In both young and middle aged rats, clenbuterol treatment increased the body wt and the weights of the heart and hindlimb muscles. The mean fibre cross-sectional area was significantly increased after the treatment in the left ventricle, soleus, plantaris and both deep and superficial portions of gastrocnemius (P < 0.01). In the left ventricle, the total capillary density and the density of venular capillaries were decreased after the treatment in both young (9 and 13%, respectively) and middle-aged rats (10 and 11%, respectively). A decrease in total capillary density was also observed in all skeletal muscles examined. In both young and middle-aged rats, the capillary-to-fibre (C:F) ratio and the proportion of each capillary did not change after the treatment in both the left ventricle and skeletal muscles. Clenbuterol significantly decreased the activity of succinate dehydrogenase in all skeletal muscles examined (P < 0.01). These results suggest that clenbuterol increased the diffusion distance for oxygen in the left ventricle and skeletal muscles. These changes may reduce the oxygen supply to tissues and increase muscle fatigability.


http://www.ncbi.nlm.nih.gov/pubmed/9401584
 
It's interesting that you should notice this side effect Sero. I do wonder if it's related to the findings from this paper:

Effects of the beta 2-adrenergic agonist clenbuterol on capillary geometry in cardiac and skeletal muscles in young and middle-aged rats.

Suzuki J, Gao M, Xie Z, Koyama T.

Abstract

The effects of 10 day clenbuterol administration on cardiac and skeletal muscle capillarities were studied, particularly in terms of the distribution of arteriolar and venular capillaries and their capillary density, in young (10-week-old) and middle-aged (37-week-old) male Wistar rats. Rats of the treated groups were fed a diet containing 2 mg kg-1 clenbuterol hydrochloride. In both young and middle aged rats, clenbuterol treatment increased the body wt and the weights of the heart and hindlimb muscles. The mean fibre cross-sectional area was significantly increased after the treatment in the left ventricle, soleus, plantaris and both deep and superficial portions of gastrocnemius (P < 0.01). In the left ventricle, the total capillary density and the density of venular capillaries were decreased after the treatment in both young (9 and 13%, respectively) and middle-aged rats (10 and 11%, respectively). A decrease in total capillary density was also observed in all skeletal muscles examined. In both young and middle-aged rats, the capillary-to-fibre (C:F) ratio and the proportion of each capillary did not change after the treatment in both the left ventricle and skeletal muscles. Clenbuterol significantly decreased the activity of succinate dehydrogenase in all skeletal muscles examined (P < 0.01). These results suggest that clenbuterol increased the diffusion distance for oxygen in the left ventricle and skeletal muscles. These changes may reduce the oxygen supply to tissues and increase muscle fatigability.


http://www.ncbi.nlm.nih.gov/pubmed/9401584

Bad news if you're a Wistar rat....!!
 
Clen and tren was like God mode for me. I had 0 cardio issues. I work with dogs and woukd chase them around the play yard for a good hour every day. Now I get winded just having sex or doing faster paced pump work outs especially leg press and squats where I just do some masochistic retarded 30 rep sets.
 
I wouldn't say I experienced a legitimate rebound effect. I know people advice to supplement T3 on top of clen if one was to extend longer durations passed the cliche 2week/2week off scenario.

What I experienced on it? People thought I had the early signs of Parkinson's Disease from how much I shaked after day 8 at 120mcg. No real bad side effects besides outrageous shaking and overzealous body heat.

Everyone else pretty much covered the possible dangers from serotonin interactions with the various receptors located within the heart.
 
I don't have time to get detailed right this moment, but part of what you might be referring to could be related to loss of myostatin suppression post clenbuterol cycle, not to the suppression and subsequent re-expression of the beta adrenergic receptors. Myostatin inhibits muscle growth and acts as a sort of negative allosteric modulator; clenbuterol (to a cetrain extent because of the subtype of beta adronergic receptors it stimulates) is responsible for mildly suppressing myostatin. Thus, when you stop taking clenbuterol your myostatin levels return to whatever is physiologically normal for you, which results in (ever so slight) degradation of muscle tissue. Loss of muscle tissue, by nature, is followed by a rise in bodyfat... (oversimplified but muscle burns fat).
 
^^ Good point pharm, if used long enough and at high enough doses, this might cause some rebound effect/catabolism.
 
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