MESO-Rx
Anabolic Steroids
Clenbuterol.. How anti-catabolic is it?
- Thread starter Vgten
- Start date
Personally, I am not opposed to using it. But as with anything, it has to be a personal decision based on weighing the pros and cons.
As for the anti-catabolic properties of clen, I dont consider them to be much of anything.
As for the anti-catabolic properties of clen, I dont consider them to be much of anything.
hooker
New Member
Actually...clen's more appropriately (bear with me here) anti-antianabolic, I believe...and probably most useful for PCT....
Check this out...Hypogonadism increases glucocorticoid production(1), so after a cycle when you are hypgonadal, you should have more glucocorticoids floating around, right? Because you have stopped taking exogenous hormones and are now waiting for your own to begin production, so for that time, you are hypogonadal. Ergo you have more glucocorticoid production going on. Well, clen is a glucocorticoid antagonist (2), so it should stave off some of them...and you'll note that in one of the studies below, the researchers have also associated clen with an anti-anabolic effect (2); you will not necessarily synthesize protein into new muscle, but it's not being inhibited either, and thereby causing a halt in Fat Free Mass accrual potential.
A study by Sharpe et. al. (done in 1986 called "Control and Manipulation of Animal Growth") states that glucocorticoids are anti-anabolic and not catabolic. Basically, what I'm saying is that, in answer to Heywood's statement, Clen is probably anti-antianabolic, and not actually anti-catabolic (as many including myself) have thought before. It will, therefore, halt the glucocorticoid induced inhibition of protein synthesis (in humans), but probably not do anything to increase that synthesis to where new muscle is built....but on PCT when glucocorticoids will be produced in excessive amounts due to your hypogonadal state, it would seem that clen would be very (!) beneficial. Hence...clen can preserve your ability (potential) to build muscle, but is probably not anabolic or even anti-catabolic per se.
Things get confusing at this point, because different studies can show different things regarding clen and anabolism vs/ catabolic hormones. The most relevant one, however, was done on standardbred horses who were given clen and exercising vs those who were just exercising and not using clen (they had a drug tested bodybuilding competition coming up) and the control group was not taking clen, nor exercising (due to work and family comittments). In that study, the horses who took the clen had lower cortisol levels at all times than the other two groups (3). Horses, it should be noted, have a response to excersize which is similar to humans (3).
Finally, I think that any anabolic effect of clen would be dose dependant, and eventually rely on other mechanisms of action than cortisol inhibition, for this effect, as rodents given an anabolic dose of clen (hundreds of times what a human could reasonably take) actually experienced increased cortisol levels (4). Thus, the anabolic effect of clen, as relates to the cortisol reducing effects of it, experience an inversely proportionate U-Shaped curve relative to each other.
Endocr Pract. 1999 Sep-Oct;5(5):277-81.
[SIZE=+1]Glucocorticoid-induced muscle atrophy: mechanisms and therapeutic strategies.[/SIZE]
Salehian B, Kejriwal K.
Department of Medicine, Division of Endocrinology, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA.
OBJECTIVE: To analyze the mechanisms of action of glucocorticoids in causing muscle atrophy and to examine the therapeutic effect of testosterone as well as other treatment modalities in counteracting this adverse effect. METHODS: We reviewed selected publications to analyze the mechanisms of glucocorticoid-induced muscle atrophy in animal models and in humans. The pathophysiologic features of glucocorticoid-induced hypogonadism and the possible relationship to the muscle atrophy in patients receiving glucocorticoids were assessed. The beneficial effects of testosterone on the muscles of hypogonadal and eugonadal men were also reviewed. Other measures such as exercise and glutamine and their possible therapeutic and preventive effects were examined in the context of hypercortisolemia. RESULTS: Glucocorticoids induce rapid muscle breakdown and proximal muscle atrophy. The mechanism of glucocorticoid-induced muscle atrophy relies on the degradation of the myosin heavy chain (catabolic effect), the most important contractile protein in muscle, associated with a decrease of its synthesis (antianabolic effect). One of the contributing factors in the development of muscle atrophy is hypogonadism that is induced by long-term glucocorticoid use. Androgen possesses anabolic and anticatabolic effects in vitro and in animal models. Androgens can be used safely to counteract the catabolic effects of cortisol. Other measures such as exercise, glutamine, and alanyl-glutamine are promising in animal models of glucocorticoid-induced muscle atrophy. CONCLUSION: This study suggests the possible efficacy of testosterone and glutamine on glucocorticoid-induced muscle atrophy. Testosterone and glutamine are natural biologic products with safe pharmacologic profiles, and their bioefficacy merits active research in humans.
[SIZE=+1]Clenbuterol antagonizes glucocorticoid-induced atrophy and fibre type transformation in mice.[/SIZE]
Pellegrino MA, D'Antona G, Bortolotto S, Boschi F, Pastoris O, Bottinelli R, Polla B, Reggiani C.
Department of Experimental Medicine, Human Physiology Unit, University of Pavia, 27100 Pavia, Italy. map@unipv.it
Beta-agonists and glucocorticoids are frequently coprescribed for chronic asthma treatment. In this study the effects of 4 week treatment with beta-agonist clenbuterol (CL) and glucocorticoid dexamethasone (DEX) on respiratory (diaphragm and parasternal) and limb (soleus and tibialis) muscles of the mouse were studied. Myosin heavy chain (MHC) distribution, fibres cross sectional area (CSA), glycolytic (phosphofructokinase, PFK; lactate dehydrogenase, LDH) and oxidative enzyme (citrate synthase, CS; cytochrome oxidase, COX) activities were determined. Muscle samples were obtained from four groups of adult C57/B16 mice: (1) Control (2) Mice receiving CL (CL, 1.5 mg kg(-1) day(-1) in drinking water) (3) Mice receiving DEX (DEX, 5.7 mg kg(-1) day(-1) s.c.) (4) Mice receiving both treatments (DEX + CL). As a general rule, CL and DEX showed opposite effects on CSA, MHC distribution, glycolytic and mitochondrial enzyme activities: CL alone stimulated a slow-to-fast transition of MHCs, an increase of PFK and LDH and an increase of muscle weight and fibre CSA; DEX produced an opposite (fast-to-slow transition) change of MHC distribution, a decrease of muscle weight and fibre CSA and in some case an increase of CS. The response varied from muscle to muscle with mixed muscles, as soleus and diaphragm, being more responsive than fast muscles, as tibialis and parasternal. In combined treatments (DEX + CL), the changes induced by DEX or CL alone were generally minimized: in soleus, however, the effects of CL predominated over those of DEX, whereas in diaphragm DEX prevailed over CL. Taken together the results suggest that CL might counteract the unwanted effects on skeletal muscles of chronic treatment with glucocorticoids.
PMID: 15109214 [PubMed - indexed for MEDLINE]
[SIZE=+1]Effect of chronic clenbuterol administration and exercise training on immune function in horses.[/SIZE]
Malinowski K, Kearns CF, Guirnalda PD, Roegner V, McKeever KH.
Equine Science Center, Dept. of Animal Science, The State University of New Jersey, New Brunswick 08901, USA.
Effects of longitudinal exercise training and acute intensive exercise (simulated race test) on immune function have not been reported in horses. Clenbuterol, a beta2-adrenergic agonist, is used to manage inflammatory airway disease in horses. This study investigated the interaction of 8 wk of exercise training with or without 12 wk of clenbuterol administration in horses. Twenty-three untrained standardbred mares (10 +/- 3 yr, Mean +/- SE) were used and divided into four experimental groups. Horses given clenbuterol plus exercise (CLENEX; n = 6) and clenbuterol alone (CLEN; n = 6) received 2.4 microg/kg BW of clenbuterol twice daily (in an average volume of 20 mL) on a schedule of 5 d on and 2 d off for 12 wk. The CLENEX group was also aerobically trained 3 d/wk. Mares given exercise alone (EX; n = 5) were aerobically trained for 3 d/wk, and the control group (CON; n = 6) remained sedentary. Both EX and CON horses were administered similar volumes (approximately 20 mL) of molasses twice daily. A simulated race test (SRT) resulted in an elevation in lymphocyte number postexercise (P < 0.05). There was no significant difference after acute exercise in either monocyte or granulocyte number. Acute exercise resulted in a decrease (P < 0.05) in the percentage of CD4+ and an increase (P < 0.05) in the percentage of CD8+ cells. The SRT resulted in a decreased lymphoproliferative response to pokeweed mitogen (P < 0.05). A SRT had no effect on antibody production in response to equine influenza vaccine. The EX group demonstrated greater cortisol concentrations at rest and at all other time points postexercise after completing the training regimen compared with CLENEX horses (P < 0.05). Preexercise (SRT) peripheral blood monocyte number was lower in CLENEX horses than in other treatment groups (P < 0.05). Clenbuterol and exercise training did not significantly affect post-SRT changes in leukocyte numbers. Exercise training resulted in a decrease (P < 0.05) in the percentage of CD8+ cells post-SRT compared with other groups, but the percentage of CD4+ cells was not altered by either clenbuterol or exercise conditioning. Lymphocyte proliferative response was not affected by clenbuterol or exercise treatment. Horses demonstrated responses to bouts of acute exercise as noted with other species, namely humans and rodents.
[SIZE=+1]The effect of clenbuterol on adrenal function in rats.[/SIZE]
Illera JC, Silvan G, Blass A, Martinez MM, Illera M.
Departamento de Fisiologia Animal, Facultad de Veterinaria, Universidad Complutense de Madrid, Spain.
The use of anabolic agents is illegal in the European Community but the effect of these agents on animal welfare is not well documented. The aim of this study was to evaluate whether the administration of anabolic agents, such as clenbuterol, causes stressful effects in rats, as reflected by the adrenal function. Anabolic doses of clenbuterol (1 mg kg-1, 99% purity) were administered orally by stomach tube daily for 45 d to female Long Evans rats (250-300 g, n = 50). Twenty-five animals were used as controls. Blood samples were collected from the jugular vein in anaesthetised animals (ketamine and xylazine). At the end of the experiment, the animals were sacrificed and the adrenal glands were removed. Hormonal levels were measured by an enzyme immunoassay previously validated for this species. Hormonal levels of cortisol and corticosterone, and histopathological analysis, were used as indicators of the adrenal function. 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. Higher relative adrenal gland weight (adrenal gland-to-body weight ratio) was also found in the treated group (p < 0.01). The major histopathological finding was the presence of hyperplasia in the adrenocortical cells. It was concluded that the administration of an anabolic dose of clenbuterol causes a hyperstimulation of adrenal gland secretion that could adversely affect animal welfare.
Check this out...Hypogonadism increases glucocorticoid production(1), so after a cycle when you are hypgonadal, you should have more glucocorticoids floating around, right? Because you have stopped taking exogenous hormones and are now waiting for your own to begin production, so for that time, you are hypogonadal. Ergo you have more glucocorticoid production going on. Well, clen is a glucocorticoid antagonist (2), so it should stave off some of them...and you'll note that in one of the studies below, the researchers have also associated clen with an anti-anabolic effect (2); you will not necessarily synthesize protein into new muscle, but it's not being inhibited either, and thereby causing a halt in Fat Free Mass accrual potential.
A study by Sharpe et. al. (done in 1986 called "Control and Manipulation of Animal Growth") states that glucocorticoids are anti-anabolic and not catabolic. Basically, what I'm saying is that, in answer to Heywood's statement, Clen is probably anti-antianabolic, and not actually anti-catabolic (as many including myself) have thought before. It will, therefore, halt the glucocorticoid induced inhibition of protein synthesis (in humans), but probably not do anything to increase that synthesis to where new muscle is built....but on PCT when glucocorticoids will be produced in excessive amounts due to your hypogonadal state, it would seem that clen would be very (!) beneficial. Hence...clen can preserve your ability (potential) to build muscle, but is probably not anabolic or even anti-catabolic per se.
Things get confusing at this point, because different studies can show different things regarding clen and anabolism vs/ catabolic hormones. The most relevant one, however, was done on standardbred horses who were given clen and exercising vs those who were just exercising and not using clen (they had a drug tested bodybuilding competition coming up) and the control group was not taking clen, nor exercising (due to work and family comittments). In that study, the horses who took the clen had lower cortisol levels at all times than the other two groups (3). Horses, it should be noted, have a response to excersize which is similar to humans (3).
Finally, I think that any anabolic effect of clen would be dose dependant, and eventually rely on other mechanisms of action than cortisol inhibition, for this effect, as rodents given an anabolic dose of clen (hundreds of times what a human could reasonably take) actually experienced increased cortisol levels (4). Thus, the anabolic effect of clen, as relates to the cortisol reducing effects of it, experience an inversely proportionate U-Shaped curve relative to each other.
Endocr Pract. 1999 Sep-Oct;5(5):277-81.
[SIZE=+1]Glucocorticoid-induced muscle atrophy: mechanisms and therapeutic strategies.[/SIZE]
Salehian B, Kejriwal K.
Department of Medicine, Division of Endocrinology, Charles R. Drew University of Medicine and Science, Los Angeles, California, USA.
OBJECTIVE: To analyze the mechanisms of action of glucocorticoids in causing muscle atrophy and to examine the therapeutic effect of testosterone as well as other treatment modalities in counteracting this adverse effect. METHODS: We reviewed selected publications to analyze the mechanisms of glucocorticoid-induced muscle atrophy in animal models and in humans. The pathophysiologic features of glucocorticoid-induced hypogonadism and the possible relationship to the muscle atrophy in patients receiving glucocorticoids were assessed. The beneficial effects of testosterone on the muscles of hypogonadal and eugonadal men were also reviewed. Other measures such as exercise and glutamine and their possible therapeutic and preventive effects were examined in the context of hypercortisolemia. RESULTS: Glucocorticoids induce rapid muscle breakdown and proximal muscle atrophy. The mechanism of glucocorticoid-induced muscle atrophy relies on the degradation of the myosin heavy chain (catabolic effect), the most important contractile protein in muscle, associated with a decrease of its synthesis (antianabolic effect). One of the contributing factors in the development of muscle atrophy is hypogonadism that is induced by long-term glucocorticoid use. Androgen possesses anabolic and anticatabolic effects in vitro and in animal models. Androgens can be used safely to counteract the catabolic effects of cortisol. Other measures such as exercise, glutamine, and alanyl-glutamine are promising in animal models of glucocorticoid-induced muscle atrophy. CONCLUSION: This study suggests the possible efficacy of testosterone and glutamine on glucocorticoid-induced muscle atrophy. Testosterone and glutamine are natural biologic products with safe pharmacologic profiles, and their bioefficacy merits active research in humans.
[SIZE=+1]Clenbuterol antagonizes glucocorticoid-induced atrophy and fibre type transformation in mice.[/SIZE]
Pellegrino MA, D'Antona G, Bortolotto S, Boschi F, Pastoris O, Bottinelli R, Polla B, Reggiani C.
Department of Experimental Medicine, Human Physiology Unit, University of Pavia, 27100 Pavia, Italy. map@unipv.it
Beta-agonists and glucocorticoids are frequently coprescribed for chronic asthma treatment. In this study the effects of 4 week treatment with beta-agonist clenbuterol (CL) and glucocorticoid dexamethasone (DEX) on respiratory (diaphragm and parasternal) and limb (soleus and tibialis) muscles of the mouse were studied. Myosin heavy chain (MHC) distribution, fibres cross sectional area (CSA), glycolytic (phosphofructokinase, PFK; lactate dehydrogenase, LDH) and oxidative enzyme (citrate synthase, CS; cytochrome oxidase, COX) activities were determined. Muscle samples were obtained from four groups of adult C57/B16 mice: (1) Control (2) Mice receiving CL (CL, 1.5 mg kg(-1) day(-1) in drinking water) (3) Mice receiving DEX (DEX, 5.7 mg kg(-1) day(-1) s.c.) (4) Mice receiving both treatments (DEX + CL). As a general rule, CL and DEX showed opposite effects on CSA, MHC distribution, glycolytic and mitochondrial enzyme activities: CL alone stimulated a slow-to-fast transition of MHCs, an increase of PFK and LDH and an increase of muscle weight and fibre CSA; DEX produced an opposite (fast-to-slow transition) change of MHC distribution, a decrease of muscle weight and fibre CSA and in some case an increase of CS. The response varied from muscle to muscle with mixed muscles, as soleus and diaphragm, being more responsive than fast muscles, as tibialis and parasternal. In combined treatments (DEX + CL), the changes induced by DEX or CL alone were generally minimized: in soleus, however, the effects of CL predominated over those of DEX, whereas in diaphragm DEX prevailed over CL. Taken together the results suggest that CL might counteract the unwanted effects on skeletal muscles of chronic treatment with glucocorticoids.
PMID: 15109214 [PubMed - indexed for MEDLINE]
[SIZE=+1]Effect of chronic clenbuterol administration and exercise training on immune function in horses.[/SIZE]
Malinowski K, Kearns CF, Guirnalda PD, Roegner V, McKeever KH.
Equine Science Center, Dept. of Animal Science, The State University of New Jersey, New Brunswick 08901, USA.
Effects of longitudinal exercise training and acute intensive exercise (simulated race test) on immune function have not been reported in horses. Clenbuterol, a beta2-adrenergic agonist, is used to manage inflammatory airway disease in horses. This study investigated the interaction of 8 wk of exercise training with or without 12 wk of clenbuterol administration in horses. Twenty-three untrained standardbred mares (10 +/- 3 yr, Mean +/- SE) were used and divided into four experimental groups. Horses given clenbuterol plus exercise (CLENEX; n = 6) and clenbuterol alone (CLEN; n = 6) received 2.4 microg/kg BW of clenbuterol twice daily (in an average volume of 20 mL) on a schedule of 5 d on and 2 d off for 12 wk. The CLENEX group was also aerobically trained 3 d/wk. Mares given exercise alone (EX; n = 5) were aerobically trained for 3 d/wk, and the control group (CON; n = 6) remained sedentary. Both EX and CON horses were administered similar volumes (approximately 20 mL) of molasses twice daily. A simulated race test (SRT) resulted in an elevation in lymphocyte number postexercise (P < 0.05). There was no significant difference after acute exercise in either monocyte or granulocyte number. Acute exercise resulted in a decrease (P < 0.05) in the percentage of CD4+ and an increase (P < 0.05) in the percentage of CD8+ cells. The SRT resulted in a decreased lymphoproliferative response to pokeweed mitogen (P < 0.05). A SRT had no effect on antibody production in response to equine influenza vaccine. The EX group demonstrated greater cortisol concentrations at rest and at all other time points postexercise after completing the training regimen compared with CLENEX horses (P < 0.05). Preexercise (SRT) peripheral blood monocyte number was lower in CLENEX horses than in other treatment groups (P < 0.05). Clenbuterol and exercise training did not significantly affect post-SRT changes in leukocyte numbers. Exercise training resulted in a decrease (P < 0.05) in the percentage of CD8+ cells post-SRT compared with other groups, but the percentage of CD4+ cells was not altered by either clenbuterol or exercise conditioning. Lymphocyte proliferative response was not affected by clenbuterol or exercise treatment. Horses demonstrated responses to bouts of acute exercise as noted with other species, namely humans and rodents.
[SIZE=+1]The effect of clenbuterol on adrenal function in rats.[/SIZE]
Illera JC, Silvan G, Blass A, Martinez MM, Illera M.
Departamento de Fisiologia Animal, Facultad de Veterinaria, Universidad Complutense de Madrid, Spain.
The use of anabolic agents is illegal in the European Community but the effect of these agents on animal welfare is not well documented. The aim of this study was to evaluate whether the administration of anabolic agents, such as clenbuterol, causes stressful effects in rats, as reflected by the adrenal function. Anabolic doses of clenbuterol (1 mg kg-1, 99% purity) were administered orally by stomach tube daily for 45 d to female Long Evans rats (250-300 g, n = 50). Twenty-five animals were used as controls. Blood samples were collected from the jugular vein in anaesthetised animals (ketamine and xylazine). At the end of the experiment, the animals were sacrificed and the adrenal glands were removed. Hormonal levels were measured by an enzyme immunoassay previously validated for this species. Hormonal levels of cortisol and corticosterone, and histopathological analysis, were used as indicators of the adrenal function. 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. Higher relative adrenal gland weight (adrenal gland-to-body weight ratio) was also found in the treated group (p < 0.01). The major histopathological finding was the presence of hyperplasia in the adrenocortical cells. It was concluded that the administration of an anabolic dose of clenbuterol causes a hyperstimulation of adrenal gland secretion that could adversely affect animal welfare.
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