will dig up the link later but here is a brief summary
scientists studied high dosages of clen in rats for a short period. the results were very shocking in that even though the duration of administration was short, like a week or so, dosing done daily, heart muscle was damaged beyond repair, particularly the left ventricular area via apoptosis. this is quite interesting news, since permanent damage of heart muscle is a no-no. even with a trained, enlarged, heart, damaged tissue will stress the heart more, creating heart failure sooner. the left ventricle is responsible for filling your heart with blood then ejecting through the rest of the circulation path. enlargement effects this greatly in that if you heart "overfills" or cant eject the blood properly, hypertrophy begins, and heart disease/failure will occur
cant remember off hand the doses of clen, but they were no where near the LD50 values for humans or rats, they were shockingly lower.
just some fyi stuff for you guys, evaluate your goals and reach them safely, you dont want to be a heart transplant candidate at any point in your life. will post the study later or at least a link
article summary
Dose-dependent apoptotic and necrotic myocyte death induced by the beta(2)-adrenergic receptor agonist, clenbuterol.
Burniston JG, Chester N, Clark WA, Tan LB, Goldspink DF.
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Webster Street, Liverpool L3 2ET, UK.
We have investigated the dose- and time-dependency of myocyte apoptosis and necrosis induced by the beta(2)-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 mug and peak necrosis (7.4 +/- 1.7%; P < 0.05) by 5 mg.kg(-1) clenbuterol. Twelve hours after clenbuterol administration, 73% of damaged myocytes labeled as necrotic, 27% as apoptotic and necrotic, and 0% as purely apoptotic. Administrations of clenbuterol (10 mug.kg(-1)) at 48-h intervals 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 apoptosis alone; 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, contrary to the current trend of only investigating apoptotic cell death. Muscle Nerve, 2005.
PMID: 16007677 [PubMed - as supplied by publisher]
scientists studied high dosages of clen in rats for a short period. the results were very shocking in that even though the duration of administration was short, like a week or so, dosing done daily, heart muscle was damaged beyond repair, particularly the left ventricular area via apoptosis. this is quite interesting news, since permanent damage of heart muscle is a no-no. even with a trained, enlarged, heart, damaged tissue will stress the heart more, creating heart failure sooner. the left ventricle is responsible for filling your heart with blood then ejecting through the rest of the circulation path. enlargement effects this greatly in that if you heart "overfills" or cant eject the blood properly, hypertrophy begins, and heart disease/failure will occur
cant remember off hand the doses of clen, but they were no where near the LD50 values for humans or rats, they were shockingly lower.
just some fyi stuff for you guys, evaluate your goals and reach them safely, you dont want to be a heart transplant candidate at any point in your life. will post the study later or at least a link
article summary
Dose-dependent apoptotic and necrotic myocyte death induced by the beta(2)-adrenergic receptor agonist, clenbuterol.
Burniston JG, Chester N, Clark WA, Tan LB, Goldspink DF.
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Webster Street, Liverpool L3 2ET, UK.
We have investigated the dose- and time-dependency of myocyte apoptosis and necrosis induced by the beta(2)-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 mug and peak necrosis (7.4 +/- 1.7%; P < 0.05) by 5 mg.kg(-1) clenbuterol. Twelve hours after clenbuterol administration, 73% of damaged myocytes labeled as necrotic, 27% as apoptotic and necrotic, and 0% as purely apoptotic. Administrations of clenbuterol (10 mug.kg(-1)) at 48-h intervals 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 apoptosis alone; 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, contrary to the current trend of only investigating apoptotic cell death. Muscle Nerve, 2005.
PMID: 16007677 [PubMed - as supplied by publisher]
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