Jump to content
Forum All Steroids

Cure Clenbuterol / MK 2866


leratz
 Share

Recommended Posts

Je suis d'accord que le risque existe mais sous certaines conditions

J Appl Physiol. 2004 Dec 10; [Epub ahead of print] Related Articles, Links

{beta}2-Adrenergic receptor stimulation in vivo induces apoptosis in the rat heart and soleus muscle.

Burniston JG, Tan LB, Goldspink DF.

Research Institute for Sports and Exercise Sciences, Liverpool John Moores University, Liverpool, United Kingdom.

High doses of the beta2-adrenergic receptor (AR) agonist, clenbuterol, can induce necrotic myocyte death in the heart and slow-twitch skeletal muscle of the rat. However, it is not known if this agent can also induce myocyte apoptosis and whether this would occur at a lower dose than previously reported for myocyte necrosis. Male Wistar rats were given single subcutaneous injections of clenbuterol. Immunohistochemistry was used to detect myocyte specific apoptosis (detected on cryosections using a caspase 3 antibody and confirmed using annexin V, single-strand DNA labelling and TUNEL). Myocyte apoptosis was first detected at 2 h, and peaked 4 h after clenbuterol administration. The lowest dose of clenbuterol to induce cardiomyocyte apoptosis was 1 microg kg(-1), with peak apoptosis (0.35 +/- 0.005 %; P<0.05) occurring in response to 5 mg kg(-1) . In the soleus, peak apoptosis (5.8 +/- 2 %; P<0.05) was induced by the lower dose of 10 microg kg(-1). Cardiomyocyte apoptosis occurred throughout the ventricles, atria and papillary muscles. However, this damage was most abundant in the left ventricular subendocardium at a point 1.6 mm, that is, approximately one-quarter of the way from the apex towards the base. beta-AR antagonism (involving propranolol, bisoprolol or ICI 118,551) or reserpine was used to show that clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte beta1-AR, whereas in the soleus direct stimulation of the myocyte beta2-AR was involved. These data show that when administered in vivo, beta2-AR stimulation by clenbuterol is detrimental to cardiac and skeletal muscles even at low doses, by inducing apoptosis through beta1- and beta2-AR, respectively.

Link to comment
Share on other sites

NB: Les effets sur le long terme ne sont pas connu. Il a été dit que suivre le traitement sur le long terme peut engendrer une infiltration de fibres collagène dans les parois cardiaques entrainant un raidissement des muscles cardiaques augmentant les risques d’arythmies ou d’arrêts cardiaques.

voici le premier jet pour le coeur le reste c'était sur le net si je trouve l'étude je te la pose , mais il faut pas oublier que le clen est pour les chevaux ..

EDIT je suis un merde en anglais mais je crois que some t'a rep .

Link to comment
Share on other sites

Je suis d'accord avec toi Jonas sur les effets à long terme sur lesquels nous n'avons pas de recul, du moins pour des sujets sains. Car il semble que chez des sujets malades (asthme) il y a un interet

Le papier que je cite c'est chez l'humain et la conclusion est que :

Even the highest dose of clenbuterol caused only a marginal increase in tremor, not statistically different from that induced by placebo.

Que faut il en conclure, que l'on peut consommer du Clen sans problème...certainement pas !

Pediatr Pulmonol. 1987 Jan-Feb;3(1):34-7.

Bronchodilating activity of oral clenbuterol in asthmatic children after single administration of different dosages.

Boner AL, Bennati D, Castellani C, Sette L, Schiassi M.

Abstract

The dose-response activity of clenbuterol, a new long-acting beta 2-agonist, was evaluated in 12 children aged 5 to 11 years with moderate to severe asthma. The study was a double-blind cross-over comparison of three oral dose levels: 0.5, 1.0, and 1.5 micrograms/kg and placebo all in the form of syrup. Pulmonary function, heart rate, blood pressure, and tremor were evaluated at 30, 60, 90, and 120 min, then hourly for 8 hr, following the ingestion of the drug. The bronchodilating effect of clenbuterol, evaluated as percentage changes in expiratory flow rates was significantly different from placebo. The overall fall-off in the effect of 1.0 micrograms/kg and 1.5 micrograms/kg doses after 8 hr was small. The results of the 1.0 micrograms/kg dose often overlapped those of the 1.5 micrograms/kg dose, suggesting that a single 1.0 micrograms/kg dose of clenbuterol is most advisable in children, assuring the most favorable risk/benefit ratio. Even the highest dose of clenbuterol caused only a marginal increase in tremor, not statistically different from that induced by placebo.

PMID: 3588048 [PubMed - indexed for MEDLINE]

Link to comment
Share on other sites

Guest Somebody

ET je me répète encore pour ceux qui la flemme de lire TOUT le paragraphe!!!!

High doses of the beta2-adrenergic receptor (AR) agonist, clenbuterol, can induce necrotic myocyte death in the heart and slow-twitch skeletal muscle of the rat. However, it is not known if this agent can also induce myocyte apoptosis and whether this would occur at a lower dose than previously reported for myocyte necrosis. Male Wistar rats were given single subcutaneous injections of clenbuterol. Immunohistochemistry was used to detect myocyte specific apoptosis (detected on cryosections using a caspase 3 antibody and confirmed using annexin V, single-strand DNA labelling and TUNEL). Myocyte apoptosis was first detected at 2 h, and peaked 4 h after clenbuterol administration. The lowest dose of clenbuterol to induce cardiomyocyte apoptosis was 1 microg kg(-1), with peak apoptosis (0.35 +/- 0.005 %; P<0.05) occurring in response to 5 mg kg(-1) . In the soleus, peak apoptosis (5.8 +/- 2 %; P<0.05) was induced by the lower dose of 10 microg kg(-1). Cardiomyocyte apoptosis occurred throughout the ventricles, atria and papillary muscles. However, this damage was most abundant in the left ventricular subendocardium at a point 1.6 mm, that is, approximately one-quarter of the way from the apex towards the base. beta-AR antagonism (involving propranolol, bisoprolol or ICI 118,551) or reserpine was used to show that clenbuterol-induced myocardial apoptosis was mediated through neuromodulation of the sympathetic system and the cardiomyocyte beta1-AR, whereas in the soleus direct stimulation of the myocyte beta2-AR was involved. These data show that when administered in vivo, beta2-AR stimulation by clenbuterol is detrimental to cardiac and skeletal muscles even at low doses, by inducing apoptosis through beta1- and beta2-AR, respectively.

Et je traduit même!!! Apoptosis: http://fr.wikipedia.org/wiki/Apoptose

1mcg par 1kg/de poids, c'est exactement les doses que l'on prend, c'est à dire genre 80mcg par jour

Link to comment
Share on other sites

 Share

×
×
  • Create New...