cypssk

hi my wife his taking clenbuterol 0.02mg nihfi wk1 1 a day 2 days on 1 day off wk 2/3/4/ 2 a day 2 days on 1 day off but when i took clens before they use to make my hands shake but they dont make her hands shake do you think she needs to increace the dose

Geo

Some people are Immune to them dude, i know i am, i get no sides from Clen at all, i used to do 4 a day, 2 morning, 2 before training, or cardio. But i know some people who just take 1 and they start shaking like a leaf.

Try taking 2 , and see how she responds. Id also go for 2 weeks on, 2 weeks off.

Geo

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Rob070886

My girlfriend is taking them at the moment, when she first started them she was taking 2 a day and was shaking like crazy, now she is taking 6 a day and doesnt shake at all. she says she doesnt think shes lost anything yet, i think she has lost a bit though. does anybody know at all how long ti takes to start noticing?

Geo

Clen only aids fat loss to a certain point, her diet and cardio must be up to scratch.

Its got a half life on 36-39 hrs dude.

Geo

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Ziricote

How long has she been on it?

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diaita

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DEFICIT "the amount by which an actual sum is lower than that expecteed or required"

Rob070886

hey all,
she has been on it for about 12 days now, her cardio and diet are good but diet could be better (hope she doesnt see this haha) she doesnt need to lose any weight but she wants to get leaner.

R

Rob070886

forgot to mention, as geo said she is cycling 2 weeks on 2 weeks off

Pscarb

why on earth are your women using a potentially very hrmful drug if their diets could be better??

do you know what clen could do to the heart?

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Lost Soul

DNP, bath, death spring to mind .......which is a worrying assessment of the 'get rich quick' syndrome we have managed to adopt in other areas of our lives in the 21st century....shame

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phzend

What risks are there to the heart in humans at mcg doses? I'm aware of the Uni of Melbourne study that showed heart enlargement and stiffening of the heart in mice (same as heart failure) but that was at a dose of 1mg per 1kg of body weight. That dose would probably kill a human. Many years ago some idiot put clenbuterol in the Anabol tabs at the lab and we all know what happened there, I believe Paul Borrensen (RIP) (if my memory serves me well) ended up in hospital due to this, didn't some folks die from it?

What evidence is there that Clen at typical doses used by bb'ers causes heart enlargement and HF in humans?

I'm not suggesting there aren't any side effects but just curious as to the evidence. Before I moved away from the 'dark side' I had my fair share of Clen, I hope I haven't laid the seeds for HF in years to come. My Dad died of HF last year and it isn't a nice way to go.

I would be more concerned about ephedrine, I wonder how many guys are banging in ephedrine day in and day out and not realising they are hypertensive, surely that is more of a danger than Clen, unless you happen to be a mouse in Melbourne!

If we all followed Vince Gironda bb'ing would be drug free and in a better place right now

Tatyana

It is not heart enlargement or heart attacks, by cardio myocyte death and necrosis.

I don't think that the dose has to be all that high either.

The body up-regulates the beta-2 receptors in response to clen quite quickly, about 2 weeks on average for most.

Edit: Actually, there is the possibility of enlargement of a few organs

http://jap.physiology.org/cgi/content/full/93/5/1824

Myotoxic effects of clenbuterol in the rat heart and soleus muscle

J Appl Physiol 93: 1824-1832, 2002; doi:10.1152/japplphysiol.00139.2002

Abstract

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 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. These data show 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 health.


Introduction

THE ANABOLIC AND LIPOLYTIC EFFECTS of the 2-adrenergic receptor (AR) agonist clenbuterol have been widely investigated, principally at doses ranging from 1 to 5 mg/kg in a variety of sedentary laboratory and livestock animals (6, 12, 25, 29). In response to such doses, the size of the heart, skeletal muscle, bone, lung, and kidney all increase, whereas the liver (35) and adipose tissue decrease in mass (6, 30). However, not all investigations have been able to demonstrate clenbuterol's anabolic effects, particularly when low doses are used (5), which suggests a dose-response relationship between clenbuterol and muscle hypertrophy.

Clenbuterol administration has been shown to be beneficial in some animal models of Duchenne muscular dystrophy (14, 15) but not in others (21). It has yet to be proven, however, that clenbuterol-induced muscle hypertrophy is of any functional significance in normal populations, whether the dose administered is low (5) or high (20). More recent animal studies using doses (1-5 mg/kg) known to promote anabolism and investigating the combined effects of clenbuterol administration and exercise have shown a decrease in exercise performance (17, 26) and a high incidence of sudden cardiac failure (11). This suggests that clenbuterol administration may be antagonistic to the muscular and/or cardiovascular adaptation to exercise, although the mechanism by which this occurs is not yet understood.

It is conceivable that, like the less selective -AR agonist isoproterenol (3, 27), clenbuterol may induce cell death and necrosis in the heart. Indeed, clenbuterol has previously been shown to induce general histological damage in the soleus muscle of the rat in response to a dose of 2 mg/kg administered via drinking water (36). We have, therefore, tested the hypothesis that clenbuterol administration may induce myocyte damage in the heart as well as the soleus. This may then provide a possible mechanism for the adverse effects of clenbuterol on the adaptation to exercise (17, 26) and for the increased collagen deposition found in the heart after its long-term administration (11).

Not surprisingly, the aforementioned anabolic and lipolytic (i.e., repartitioning) effects of clenbuterol have attracted the attention of many athletes, despite clenbuterol being banned by the World Anti-Doping Agency. Body builders in particular take high doses of this 2-AR agonist (28). The protocol for determining an individual's optimal dose is crude and involves ever-increasing daily doses until the side effects can no longer be tolerated (10). The doses employed during clenbuterol abuse, therefore, vary widely, with men being better able than women to tolerate the side effects, which include tachycardia, hypokalemia, arrhythmia, muscle cramps, and muscle tremors (19). An average daily dose for males can be eight tablets or ~2 µg clenbuterol/kg body wt. In addition, because of its lack of androgenic side effects, clenbuterol is also popular among sedentary as well as athletic women for use as a repartitioning agent. Scientific investigations into the effects of clenbuterol in humans are far less numerous than those pertaining to livestock or laboratory animals. Nonetheless, clenbuterol has been shown to have some therapeutic potential in speeding up the rehabilitation of postoperative muscle wasting in humans (23) and has been proposed for the pharmacological amelioration of cachexia in chronic diseases such as cancer (4) and Duchenne muscular dystrophy (15). The present finding that even a single administration of clenbuterol induces necrosis in cardiac and skeletal myocytes demonstrates that, before clenbuterol can be properly considered for clinical use, its potential myotoxic effects need to be more closely investigated.

The pharmacokinetics of chronic clenbuterol administration are likely to be complex, with the possibility of tachyphlaxis or the accumulation of unmetabolized clenbuterol in the plasma. To avoid these complications, we have used only a single administration (enteral or parenteral) of clenbuterol and investigated the incidence of myocyte-specific necrosis in response to this in the heart and soleus muscle of the rat.

Clenbuterol is lipophilic and is known to have direct intracellular actions (1). Although the anabolic effects of clenbuterol administration have previously been shown to be 2-AR mediated (6), the same cannot be assumed for clenbuterol's myotoxic effects. To investigate whether clenbuterol-induced necrosis was receptor mediated or a direct action of clenbuterol, selective -AR antagonists have been used. In addition, the norepinephrine (NE) depleting agent reserpine was also used to investigate the possible neuromodulation of the sympathetic nervous system (SNS) by clenbuterol.

The present study presents data on clenbuterol-induced necrosis in the heart and soleus muscle of the rat at doses commonly employed to demonstrate its anabolic effects. The dose dependency and time course of cardiac and skeletal myocyte necrosis has been investigated in detail. To achieve meaningful quantification in the heart, a study of the topographical distribution of this cellular damage was crucial. Furthermore, by scaling the data provided in the current rat model, it was found that doses commonly abused by athletes fall within the range capable of inducing myocyte death and loss.

Tatyana

http://www.pubmedcentral.nih.gov/art...?artid=1831534

Published in final edited form as:
Muscle Nerve. 2005 December; 32(6): 767–774.



Dose-dependent apoptotic and necrotic myocyte death induced by the β₂-adrenergic receptor agonist, clenbuterol
Jatin G Burniston, PhD,¹ Neil Chester, PhD,¹ William A Clark, PhD,² Lip-Bun Tan, DPhil,³ and David F Goldspink, DSc¹

Abstract
We have investigated the dose- and time-dependency of myocyte apoptosis and necrosis induced by the β₂-adrenergic receptor agonist, clenbuterol, with the aim of determining whether myocyte apoptosis and necrosis are two separate processes or a continuum of events. Male Wistar rats were administered subcutaneous injections of clenbuterol, and immunohistochemistry was used to detect myocyte specific apoptosis and necrosis. Myocyte apoptosis peaked 4 h after, and necrosis 12 h after, clenbuterol administration. In the soleus, peak apoptosis (5.8 ± 2.0 %; P<0.05) was induced by 10 μg and peak necrosis (7.4 ± 1.7 %; P<0.05) by 5 mg of clenbuterol kg^-1. Twelve hours after clenbuterol administration, 73 % of damaged myocytes labelled as necrotic, 27 % as apoptotic and necrotic and none labelled as purely apoptotic. Bi-daily administrations of 10 μg of clenbuterol kg^-1 induced cumulative myocyte death over 8 days. These data show that the phenotype of myocyte death is dependent on the magnitude of the insult and the time at which it is investigated. Only very low doses induced only apoptosis, in most cases apoptotic myocytes lysed and became necrotic and the magnitude of necrosis was greater than that of apoptosis. Thus, it is important to investigate both apoptotic and necrotic myocyte death, this being contrary to the current trend of only investigating apoptotic cell death.

Introduction

The β₂-adrenergic receptor (AR) agonist, clenbuterol, has been widely reported as an anabolic agent capable of inducing pronounced muscle hypertrophy ^{6, 11, 28, 36, 37}. However, data from our laboratory has revealed that this agent is also capable of inducing significant myocyte apoptosis ⁴ and necrosis ³ in the heart and slow-twitch soleus muscle of rats. Furthermore, the onset of myocyte death occurs at doses lower than those commonly used to demonstrate the hypertrophic effects of this agent ^{6, 11, 28, 36, 37}. Our data regarding the myotoxic effects of clenbuterol provide a reasonable explanation for the detrimental effects of this drug when used as an anabolic agent to improve exercise performance ^{10, 17, 22, 31}, and the previously reported increase in collagen in the hearts of animals treated with β-agonists ^{10, 14}.
Cell death has been characterised as either apoptotic or necrotic, based on morphological features ²³. Two prominent morphological changes distinguish apoptosis from necrosis: (1) the formation of apoptotic bodies, and (2) the maintenance of cell membrane integrity. When studied in vitro, apoptotic cells often lyse and become necrotic ¹⁶, a phenomenon termed “secondary necrosis” or “apoptosis-necrosis” ²⁷. Based on observations of developmental/programmed cell death, it was originally assumed that apoptotic cells or apoptotic bodies in vivo would be phagocytosed before lysis occurred ^{1, 24}, the principal mechanism for this process being externalisation of phosphatidylserine ³⁵. However, recent work ^{12, 13} has shown that the capacity for solid tissues, such as the heart and skeletal muscles, to remove apoptotic cells in vivo may be overwhelmed and in many instances myocyte necrosis is the predominant form of death. Apoptosis and necrosis may co-exist in the heart both clinically ¹⁸ and in response to experimental interventions ²¹. Whether this is an initiation of two separate processes or a continuum of events is not known.
Our previous work has investigated apoptosis and necrosis separately, in response to single administrations of clenbuterol. In the current work, both apoptosis and necrosis were measured simultaneously and the myotoxic effects of chronic administration was investigated. The pharmacobiodynamics of repeated administrations are complex. Clenbuterol has a long half-life (~33 h in the rat) in the plasma ³⁹ and other tissues ³², and the β₂-AR is known to be particularly sensitive to desensitization and downregulation ¹⁹. To minimize these effects, clenbuterol was administered at 48-h intervals and myocyte death was investigated at the optimum time after the last injection.