clenbuterol gebruik bij naturals
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soulreaver zei:
Daar heb je gelijk in, je hoeft ook niet alles zomaar klakkeloos over te nemen. En ik zou nooit zeggen dat ik me beter dan een ander vind. Ik probeer dit weekend wel even de pagina in te scannen waar het in vermeldt staat. En geloof me ook maar dan dat niet alles wat Chad zijn atleten voorschrijft ergens gepubliceerd staat
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D. zei:BumP along....
anyhow, de kern van mijn vraag IS eigenlijk. Als je gewoon afvalt een halve a een kilo in de week, en je gebruikt clen (je eet dus ook iets meer) ben je dan minder catabool dan wanneer je het niet zou gebruiken?
Clenbuterolzorgt er inderdaad voor dat je lichaam in een minder catabole fase komt. Het zorgt bovendien voor een positieve stikstofbalans. (dus een grotere opname van proteine in de spiercel dan dat deze uitscheid) De werking van clen alleen is echter niet sterk genoeg om in combinatie met een kcal arm dieet een klein verlies aan spiermassa te voorkomen
Soulreaver
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Koolhoven zei:
Nopez, dat mag duidelijk zijn, alhoewel Chad wel heel open is mbt. roids, gh, slin, enz. alleen hij zegt op zijn forum ook heel duidelijk, het is zijn werk, hij moet er van leven van het begeleiden van mensen, dus als hij klakkeloos alles vrijgeeft is dat in zijn eigen nadeel. En ik denk dat het laatste wat we moeten doen is elkaar afzeiken of de grond in boren. Laten we eerlijk zijn, de grote buitenwereld probeert bodybuilders al genoeg in een hokje te plaatsen als agressieve opgefokte domme testo monsters. laten wij onderling het respect dan voor elkaar bewaren
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marcos zei:
Ja want zoals ik al zei is de werking van clen alleen in een laag kcal dieet niet voldoende om behoud van spiermassa te garanderen. Om gewonnen massa te behouden na een kuur in een kcal rijk dieet echter wel
Soulreaver
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Along with the reversing of the effects of insulin (and inhibiting the action of insulin) which results in a release of glycogen back into the blood stream as glucose and an inability to store or use more glycogen, it will increase the rate of protein and fat being burned in the body. For bodybuilders that appears to be the primary use of the drug. This thermogenisis and an increase in the rate of fat being burned usually has as a result that the metabolic rate of the subject its much higher and he burns more calories. This in turn results in loss of adipose tissue (the shedding of fat in other words) revealing a leaner physique with cuts and striations. The downside to this effect is that there is a concomitant rise in the rate of protein being burned. Where fat is robbed from the fatty tissue in the body, protein is generally robbed from the muscle. As with all catabolic hormones, in time muscle loss can and will occur. Which is why many opt to use this compound during a cycle of anabolic steroids that will help preserve the lean body mass while reducing the fat.
http://www.bodybuilding.com/fun/catclen.htm
http://www.bodybuilding.com/fun/catclen.htm
Clenbuterol is a very interesting and remarkable compound. It is not a steroid hormone but a beta-2-symphatomimetic. Clenbuterol, above all, has a strong anti-catabolic effect, which means it decreases the rate at which protein is reduced in the muscle cell, consequently causing an enlargement of muscle cells. For this reason, numerous athletes use Clenbuterol after steroid treatment to balance the resulting catabolic phase and thus obtain maximum strength and muscle mass. A further aspect of Clenbuterol is its distinct fat-burning effect. Clenbuterol burns fat without dieting because it increases the body temperature slightly, forcing the body to burn fat for this process. Due to the higher body temperature Clenbuterol magnifies the effect of anabolic/androgenic steroids taken simultaneously, since the protein processing is increased.
http://www.anabolicreview.com/drugprofiles.php?steroid=89
http://www.anabolicreview.com/drugprofiles.php?steroid=89
Soulreaver
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(1)Analyst 1998 Dec;123(12):2521-4 Related Articles, Links
The effect of clenbuterol on adrenal function in rats.
Illera JC, Silvan G, Blass A, Martinez MM, Illera M.
Increased corticosterone and cortisol secretion was found in the treated group (p < 0.001), both in adrenal homogenates and peripheral blood samples, compared with control animals
(2)Psychoneuroendocrinology 1990;15(5-6):391-9 Related Articles, Links
Influence of clenbuterol, a beta-adrenergic agonist, on desipramine induced growth hormone, prolactin and cortisol stimulation.
Laakmann G, Munz T, Hinz A, Voderholzer U.
Psychiatric Hospital, University of Munich, Germany.
We report herein the effects of the beta-adrenergic agonist clenbuterol on desipramine (DMI)-induced growth hormone (GH), prolactin (PRL) and cortisol secretion in healthy male subjects. In the first study, nine subjects were treated with either clenbuterol (0.04 mg, p.o.) or placebo. In the second study, 12 subjects received either DMI (50 mg, i.v.) alone or in combination with clenbuterol (0.04 mg, p.o.) given 60 min prior to DMI administration. Clenbuterol alone had no influence on GH, PRL, or cortisol concentrations, compared to placebo. DMI alone caused GH stimulation (mean maximum = 15.7 +/- 3.4 ng/ml), which was significantly lower after combined administration of DMI and clenbuterol (mean maximum = 7.7 +/- 1.6 ng/ml) (p less than or equal to 0.01). DMI-induced PRL and cortisol stimulation was not influenced by clenbuterol pretreatment. These results indicate the inhibiting influence of noradrenergic beta-receptors on GH stimulation.
(3)J Anim Sci 1992 Sep;70(9):2809-21 Related Articles, Links
Responses of calves to treadmill exercise during beta-adrenergic agonist administration.
Bruckmaier RM, Blum JW.
Division of Nutrition Pathology, University of Berne, Switzerland.
Calves perorally administered the beta-adrenergic agonist (beta-A) clenbuterol for 28 d were studied before, during, and after a 12-min treadmill exercise. During exercise on d 1 of clenbuterol administration, respiratory rate, respiratory minute volume, and heart rate and blood glucose, lactate, and insulin concentrations increased more in beta-A-treated calves than in controls. Oxygen extraction rate and growth hormone concentrations were lower in clenbuterol-treated calves, whereas oxygen consumption, carbon dioxide production, and blood cortisol concentration increased similarly in the absence and presence of the beta-A. After 2 wk of daily clenbuterol administration, respiratory rate and respiratory minute volume during exercise were still higher and oxygen extraction was still lower, whereas all other measures were similar to those in controls. The increased heart rate in response to isoproterenol after 3 wk of clenbuterol administration was reduced markedly in resting but only slightly in exercising animals, whereas heart rate reduction by propranolol during exercise was similar to that in controls. Seven days after withdrawal of clenbuterol, newly administered clenbuterol evoked the same effects as on d 1. In conclusion, there were marked reactions to the first clenbuterol treatment that were in part enhanced during treadmill exercise. After 2 wk of beta-A administration, animals responded much less to the beta-A and changes were not different from those in controls.
Resensitization to the beta-A was observed 7 d after its withdrawal.
The effect of clenbuterol on adrenal function in rats.
Illera JC, Silvan G, Blass A, Martinez MM, Illera M.
Increased corticosterone and cortisol secretion was found in the treated group (p < 0.001), both in adrenal homogenates and peripheral blood samples, compared with control animals
(2)Psychoneuroendocrinology 1990;15(5-6):391-9 Related Articles, Links
Influence of clenbuterol, a beta-adrenergic agonist, on desipramine induced growth hormone, prolactin and cortisol stimulation.
Laakmann G, Munz T, Hinz A, Voderholzer U.
Psychiatric Hospital, University of Munich, Germany.
We report herein the effects of the beta-adrenergic agonist clenbuterol on desipramine (DMI)-induced growth hormone (GH), prolactin (PRL) and cortisol secretion in healthy male subjects. In the first study, nine subjects were treated with either clenbuterol (0.04 mg, p.o.) or placebo. In the second study, 12 subjects received either DMI (50 mg, i.v.) alone or in combination with clenbuterol (0.04 mg, p.o.) given 60 min prior to DMI administration. Clenbuterol alone had no influence on GH, PRL, or cortisol concentrations, compared to placebo. DMI alone caused GH stimulation (mean maximum = 15.7 +/- 3.4 ng/ml), which was significantly lower after combined administration of DMI and clenbuterol (mean maximum = 7.7 +/- 1.6 ng/ml) (p less than or equal to 0.01). DMI-induced PRL and cortisol stimulation was not influenced by clenbuterol pretreatment. These results indicate the inhibiting influence of noradrenergic beta-receptors on GH stimulation.
(3)J Anim Sci 1992 Sep;70(9):2809-21 Related Articles, Links
Responses of calves to treadmill exercise during beta-adrenergic agonist administration.
Bruckmaier RM, Blum JW.
Division of Nutrition Pathology, University of Berne, Switzerland.
Calves perorally administered the beta-adrenergic agonist (beta-A) clenbuterol for 28 d were studied before, during, and after a 12-min treadmill exercise. During exercise on d 1 of clenbuterol administration, respiratory rate, respiratory minute volume, and heart rate and blood glucose, lactate, and insulin concentrations increased more in beta-A-treated calves than in controls. Oxygen extraction rate and growth hormone concentrations were lower in clenbuterol-treated calves, whereas oxygen consumption, carbon dioxide production, and blood cortisol concentration increased similarly in the absence and presence of the beta-A. After 2 wk of daily clenbuterol administration, respiratory rate and respiratory minute volume during exercise were still higher and oxygen extraction was still lower, whereas all other measures were similar to those in controls. The increased heart rate in response to isoproterenol after 3 wk of clenbuterol administration was reduced markedly in resting but only slightly in exercising animals, whereas heart rate reduction by propranolol during exercise was similar to that in controls. Seven days after withdrawal of clenbuterol, newly administered clenbuterol evoked the same effects as on d 1. In conclusion, there were marked reactions to the first clenbuterol treatment that were in part enhanced during treadmill exercise. After 2 wk of beta-A administration, animals responded much less to the beta-A and changes were not different from those in controls.
Resensitization to the beta-A was observed 7 d after its withdrawal.
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Ik denk er hetzelfde over als Soulraver.
Na het gebruik van AAS, helpt clenbuterol niet om spiermassa te beschermen tegen de lage waarde van androgene middelen op dat moment. Dat idee is van jaren geleden en is foutief gebleken.
Het kan daarentegen misschien wel indirect positieve effecten hebben. Ten eerste stimuleert clenbuterol het centrale zenuwstelsel. Dit kan ervoor zorgen dat je minder last heb van overtraining veroorzaakt door de kuur in combinatie met lage androgene waardes na de kuur.
Wat ik een hele tijd geleden ook eens gelezen heb, is dat beta agonisten misschien het herstel versnellen. Clen is een beta agonist en beta agonisten hebben waarschijnlijk invloed op de hpta. Dus dat zou een sneller herstel kunnen betekenen.
Maar aangezien ephedrine ook een beta agonist is, kunnen beide van deze effecten ook gerealiseerd worden door ephedrine.
Na het gebruik van AAS, helpt clenbuterol niet om spiermassa te beschermen tegen de lage waarde van androgene middelen op dat moment. Dat idee is van jaren geleden en is foutief gebleken.
Het kan daarentegen misschien wel indirect positieve effecten hebben. Ten eerste stimuleert clenbuterol het centrale zenuwstelsel. Dit kan ervoor zorgen dat je minder last heb van overtraining veroorzaakt door de kuur in combinatie met lage androgene waardes na de kuur.
Wat ik een hele tijd geleden ook eens gelezen heb, is dat beta agonisten misschien het herstel versnellen. Clen is een beta agonist en beta agonisten hebben waarschijnlijk invloed op de hpta. Dus dat zou een sneller herstel kunnen betekenen.
Maar aangezien ephedrine ook een beta agonist is, kunnen beide van deze effecten ook gerealiseerd worden door ephedrine.
Soulreaver
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Zorgwekkender is echter nog, niet geheel op het cortisol verhaal gericht, en ik geef toe het is in ratten onderzocht, maar toch:
J Appl Physiol. 2002 Nov;93(5):1824-32. Related Articles, Links
Myotoxic effects of clenbuterol in the rat heart and soleus muscle.
Burniston JG, Ng Y, Clark WA, Colyer J, Tan LB, Goldspink DF.
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET, United Kingdom. hhsjburn@livjm.ac.jp
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 beta(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.
J Appl Physiol. 2002 Nov;93(5):1824-32. Related Articles, Links
Myotoxic effects of clenbuterol in the rat heart and soleus muscle.
Burniston JG, Ng Y, Clark WA, Colyer J, Tan LB, Goldspink DF.
Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 2ET, United Kingdom. hhsjburn@livjm.ac.jp
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 beta(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.
