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- 13 okt 2007
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Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure.
Kamalakkannan G, Petrilli CM, George I, LaManca J, McLaughlin BT, Shane E, Mancini DM, Maybaum S.
Division of Cardiology, Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, USA.
Comment in:
Clenbuterol, a beta(2)-agonist with potent anabolic properties, has been shown to improve skeletal muscle function in healthy subjects, and in high doses, promotes cardiac recovery in patients with left ventricular assist devices. In a small, randomized controlled study, we investigated the effect of clenbuterol on skeletal muscle function, cardiac function, and exercise capacity in patients with chronic heart failure. Clenbuterol was well tolerated and led to a significant increase in both lean mass and the lean/fat ratio. Maximal strength increased significantly with both clenbuterol (27%) and placebo (14%); however, endurance and exercise duration decreased after clenbuterol. Prior data support combining exercise training with clenbuterol to maximize performance, and on-going studies will evaluate this approach.
PMID: 18374884 [PubMed - indexed for MEDLINE]
Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support.
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.
Department of Surgery, Division of Cardiothoracic Surgery, Columbia College of Physicians and Surgeons, New York, New York 10032, USA. isaacgeorge@hotmail.com
BACKGROUND: High-dose clenbuterol (a selective beta2-adrenergic agonist) has been proposed to promote myocardial recovery during left ventricular assist device (LVAD) support, but its effects on cardiac and skeletal muscle are largely unknown. METHODS: Seven subjects with heart failure (5 ischemic, 2 non-ischemic) were started on oral clenbuterol 5 to 46 weeks post-LVAD implantation and up-titrated to daily doses of 720 microg. The following procedures were performed at baseline and after 3 months of therapy: echocardiography at reduced support (4 liters/min); cardiopulmonary exercise testing; body composition analysis; and quadriceps maximal voluntary contraction (MVC). Myocardial histologic analysis was measured at device implantation and explantation. RESULTS: There were no serious adverse events or arrhythmias. Creatine phosphokinase (CPK) was elevated in 4 subjects, with no clinical sequelae. No change in ejection fraction was seen. End-diastolic dimension increased significantly (4.73 +/- 0.67 vs 5.24 +/- 0.66; p < 0.01), despite a trend toward increased LV mass. Body weight and lean mass increased significantly (75.5 +/- 17.9 vs 79.2 +/- 25.1 kg, 21.1 +/- 8.9 vs 23.6 +/- 9.7 kg, respectively; both p < 0.05). Exercise capacity did not change, but MVC improved significantly from 37.0 +/- 15.7 to 45.8 +/- 20.6 kg (p < 0.05). No significant change in myocyte size or collagen deposition was seen. CONCLUSIONS: Cardiac function did not improve in this cohort of LVAD patients treated with high-dose clenbuterol. However, clenbuterol therapy increased skeletal muscle mass and strength and prevented the expected decrease in myocyte size during LVAD support. Further study will clarify its potential for cardiac and skeletal muscle recovery.
PMID: 16962470 [PubMed - indexed for MEDLINE]
Was wat aan het googlen waarom zoveel atleten (sprinters en zwemmers) zo graag clenbuterol gebruiken. Kwam toevallig hier op uit.
Dat clen anabool is mag onderhand wel duidelijk zijn, maar uit onderzoek blijkt dat de vergroting van het hart door clen dezelfde is als diegene die ontstaat bij getrainde atleten. Maw de vergroting van het hart is een 'goede' vergroting.
Kan iemand dit verzoenen met bijvoorbeeld dit onderzoek:
Myotoxic effects of clenbuterol in the rat heart and soleus muscle
Jatin G. Burniston1, Yeelan Ng1, William A. Clark2, John Colyer3, Lip-Bun Tan4, and David F. Goldspink1 1 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET; Departments of 3 Biochemistry and Molecular Biology and 4 Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom; and 2 Michael Reese Hospital and Medical Center, Chicago, Illinois 60616-3990
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 [Afbeelding niet meer beschikbaar]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.
Het verschil dat ik zie is dat de celdood die hier veroorzaakt wordt het geval is bij extreem hoge dosissen, + dat de dosis bij mensen langzaam omhoog geschroeft wordt en deze dieren zonder tolerantie ineens een monsterdosis krijgen.
Kamalakkannan G, Petrilli CM, George I, LaManca J, McLaughlin BT, Shane E, Mancini DM, Maybaum S.
Division of Cardiology, Department of Medicine, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, New York, USA.
Comment in:
Clenbuterol, a beta(2)-agonist with potent anabolic properties, has been shown to improve skeletal muscle function in healthy subjects, and in high doses, promotes cardiac recovery in patients with left ventricular assist devices. In a small, randomized controlled study, we investigated the effect of clenbuterol on skeletal muscle function, cardiac function, and exercise capacity in patients with chronic heart failure. Clenbuterol was well tolerated and led to a significant increase in both lean mass and the lean/fat ratio. Maximal strength increased significantly with both clenbuterol (27%) and placebo (14%); however, endurance and exercise duration decreased after clenbuterol. Prior data support combining exercise training with clenbuterol to maximize performance, and on-going studies will evaluate this approach.
PMID: 18374884 [PubMed - indexed for MEDLINE]
Effect of clenbuterol on cardiac and skeletal muscle function during left ventricular assist device support.
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.
Department of Surgery, Division of Cardiothoracic Surgery, Columbia College of Physicians and Surgeons, New York, New York 10032, USA. isaacgeorge@hotmail.com
BACKGROUND: High-dose clenbuterol (a selective beta2-adrenergic agonist) has been proposed to promote myocardial recovery during left ventricular assist device (LVAD) support, but its effects on cardiac and skeletal muscle are largely unknown. METHODS: Seven subjects with heart failure (5 ischemic, 2 non-ischemic) were started on oral clenbuterol 5 to 46 weeks post-LVAD implantation and up-titrated to daily doses of 720 microg. The following procedures were performed at baseline and after 3 months of therapy: echocardiography at reduced support (4 liters/min); cardiopulmonary exercise testing; body composition analysis; and quadriceps maximal voluntary contraction (MVC). Myocardial histologic analysis was measured at device implantation and explantation. RESULTS: There were no serious adverse events or arrhythmias. Creatine phosphokinase (CPK) was elevated in 4 subjects, with no clinical sequelae. No change in ejection fraction was seen. End-diastolic dimension increased significantly (4.73 +/- 0.67 vs 5.24 +/- 0.66; p < 0.01), despite a trend toward increased LV mass. Body weight and lean mass increased significantly (75.5 +/- 17.9 vs 79.2 +/- 25.1 kg, 21.1 +/- 8.9 vs 23.6 +/- 9.7 kg, respectively; both p < 0.05). Exercise capacity did not change, but MVC improved significantly from 37.0 +/- 15.7 to 45.8 +/- 20.6 kg (p < 0.05). No significant change in myocyte size or collagen deposition was seen. CONCLUSIONS: Cardiac function did not improve in this cohort of LVAD patients treated with high-dose clenbuterol. However, clenbuterol therapy increased skeletal muscle mass and strength and prevented the expected decrease in myocyte size during LVAD support. Further study will clarify its potential for cardiac and skeletal muscle recovery.
PMID: 16962470 [PubMed - indexed for MEDLINE]
Was wat aan het googlen waarom zoveel atleten (sprinters en zwemmers) zo graag clenbuterol gebruiken. Kwam toevallig hier op uit.
Dat clen anabool is mag onderhand wel duidelijk zijn, maar uit onderzoek blijkt dat de vergroting van het hart door clen dezelfde is als diegene die ontstaat bij getrainde atleten. Maw de vergroting van het hart is een 'goede' vergroting.
Kan iemand dit verzoenen met bijvoorbeeld dit onderzoek:
Myotoxic effects of clenbuterol in the rat heart and soleus muscle
Jatin G. Burniston1, Yeelan Ng1, William A. Clark2, John Colyer3, Lip-Bun Tan4, and David F. Goldspink1 1 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET; Departments of 3 Biochemistry and Molecular Biology and 4 Medicine, University of Leeds, Leeds LS2 9JT, United Kingdom; and 2 Michael Reese Hospital and Medical Center, Chicago, Illinois 60616-3990
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 [Afbeelding niet meer beschikbaar]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.
Het verschil dat ik zie is dat de celdood die hier veroorzaakt wordt het geval is bij extreem hoge dosissen, + dat de dosis bij mensen langzaam omhoog geschroeft wordt en deze dieren zonder tolerantie ineens een monsterdosis krijgen.
