CFC
Bluelight Crew
- Joined
- Mar 9, 2013
- Messages
- 18,171
Am J Physiol Heart Circ Physiol. 2007 Dec;293(6):H3575-83. Epub 2007 Sep 28.
Anabolic steroids induce cardiac renin-angiotensin system and impair the beneficial effects of aerobic training in rats.
Rocha FL, Carmo EC, Roque FR, Hashimoto NY, Rossoni LV, Frimm C, Anéas I, Negrão CE, Krieger JE, Oliveira EM.
Abstract
We evaluated the effects of swimming and anabolic steroids (AS) on ventricular function, collagen synthesis, and the local renin-angiotensin system in rats. Male Wistar rats were randomized into control (C), steroid (S; nandrolone decanoate; 5 mg/kg sc, 2x/wk), steroid + losartan (SL; 20 mg.kg(-1).day(-1)), trained (T), trained + steroid (T+S), and trained + steroid + losartan (T+SL; n = 14/group) groups. Swimming was performed 5 times/wk for 10 wk. Serum testosterone increased in S and T+S. Resting heart rate was lower in T and T+S. Percent change in left ventricular (LV) weight-to-body weight ratio increased in S, T, and T+S. LV systolic pressure declined in S and T+S. LV contractility increased in T (P < 0.05). LV relaxation increased in T (P < 0.05). It was significantly lower in T+S compared with C. Collagen volumetric fraction (CVF) and hydroxyproline were higher in S and T+S than in C and T (P < 0.05), and the CVF and LV hypertrophy were prevented by losartan treatment. LV-ANG I-converting enzyme activity increased ( 28 % ) in the S group ( 33 % ), and type III collagen synthesis increased ( 56 % ) in T+S but not in T group. A positive correlation existed between LV-ANG I-converting enzyme activity and collagen type III expression (r(2) = 0.88; P < 0.05, for all groups). The ANG II and angiotensin type 1a receptor expression increased in the S and T+S groups but not in T group. Supraphysiological doses of AS exacerbated the cardiac hypertrophy in exercise-trained rats. Exercise training associated with AS induces maladaptive remodeling and further deterioration in cardiac performance. Exercise training associated with AS causes loss of the beneficial effects in LV function induced by exercising. These results suggest that aerobic exercise plus AS increases cardiac collagen content associated with activation of the local renin-angiotensin system.
http://www.ncbi.nlm.nih.gov/pubmed/17906098
Med Sci Sports Exerc. 2011 Oct;43(10):1836-48. doi: 10.1249/MSS.0b013e318217e8b6.
Anabolic steroid associated to physical training induces deleterious cardiac effects.
Do Carmo EC, Fernandes T, Koike D, Da Silva ND Jr, Mattos KC, Rosa KT, Barretti D, Melo SF, Wichi RB, Irigoyen MC, de Oliveira EM.
Abstract
Cardiac aldosterone might be involved in the deleterious effects of nandrolone decanoate (ND) on the heart. Therefore, we investigated the involvement of cardiac aldosterone, by the pharmacological block of AT1 or mineralocorticoid receptors, on cardiac hypertrophy and fibrosis.
METHODS:
Male Wistar rats were randomized into eight groups (n = 14 per group): Control (C), nandrolone decanoate (ND), trained (T), trained ND (TND), ND + losartan (ND + L), trained ND + losartan (TND + L), ND + spironolactone (ND + S), and trained ND + spironolactone (TND + S). ND (10 mg·kg(-1)·wk(-1)) was administered during 10 wk of swimming training (five times per week). Losartan (20 mg·kg(-1)·d(-1)) and spironolactone (10 mg·kg(-1)·d(-1)) were administered in drinking water.
RESULTS:
Cardiac hypertrophy was increased 10% by using ND and 17% by ND plus training (P < 0.05). In both groups, there was an increase in the collagen volumetric fraction (CVF) and cardiac collagen type III expression (P < 0.05). The ND treatment increased left ventricle-angiotensin-converting enzyme I activity, AT1 receptor expression, aldosterone synthase (CYP11B2), and 11-β hydroxysteroid dehydrogenase 2 (11β-HSD2) gene expression and inflammatory markers, TGFβ and osteopontin. Both losartan and spironolactone inhibited the increase of CVF and collagen type III. In addition, both treatments inhibited the increase in left ventricle-angiotensin-converting enzyme I activity, CYP11B2, 11β-HSD2, TGFβ, and osteopontin induced by the ND treatment.
CONCLUSIONS:
We believe this is the first study to show the effects of ND on cardiac aldosterone. Our results suggest that these effects may be associated to TGFβ and osteopontin. Thus, we conclude that the cardiac aldosterone has an important role on the deleterious effects on the heart induced by ND.
http://www.ncbi.nlm.nih.gov/pubmed/21407130
** I have another paper that I prefer that uses Losartan to reverse the harms caused by AAS, a little older than these. It was the first paper to get me interested in harm reduction of cardiovascular sides. I can't find it via a search but I do have it downloaded. I'll add it on when I find it.
We've also talked in drips and drabs about AAS and cardiovascular health (and how to lessen harm) loads of times on here. Some of the threads I can remember include:
http://www.bluelight.org/vb/threads/760319-AAS-and-Cardiovascular-Health-Case-Study
http://www.bluelight.org/vb/threads/732223-AAS-Bodybuilders-and-heart-ventricle-function
http://www.bluelight.org/vb/threads/755959-Another-Study-on-AAS-and-Cardiac-Risk
Anabolic steroids induce cardiac renin-angiotensin system and impair the beneficial effects of aerobic training in rats.
Rocha FL, Carmo EC, Roque FR, Hashimoto NY, Rossoni LV, Frimm C, Anéas I, Negrão CE, Krieger JE, Oliveira EM.
Abstract
We evaluated the effects of swimming and anabolic steroids (AS) on ventricular function, collagen synthesis, and the local renin-angiotensin system in rats. Male Wistar rats were randomized into control (C), steroid (S; nandrolone decanoate; 5 mg/kg sc, 2x/wk), steroid + losartan (SL; 20 mg.kg(-1).day(-1)), trained (T), trained + steroid (T+S), and trained + steroid + losartan (T+SL; n = 14/group) groups. Swimming was performed 5 times/wk for 10 wk. Serum testosterone increased in S and T+S. Resting heart rate was lower in T and T+S. Percent change in left ventricular (LV) weight-to-body weight ratio increased in S, T, and T+S. LV systolic pressure declined in S and T+S. LV contractility increased in T (P < 0.05). LV relaxation increased in T (P < 0.05). It was significantly lower in T+S compared with C. Collagen volumetric fraction (CVF) and hydroxyproline were higher in S and T+S than in C and T (P < 0.05), and the CVF and LV hypertrophy were prevented by losartan treatment. LV-ANG I-converting enzyme activity increased ( 28 % ) in the S group ( 33 % ), and type III collagen synthesis increased ( 56 % ) in T+S but not in T group. A positive correlation existed between LV-ANG I-converting enzyme activity and collagen type III expression (r(2) = 0.88; P < 0.05, for all groups). The ANG II and angiotensin type 1a receptor expression increased in the S and T+S groups but not in T group. Supraphysiological doses of AS exacerbated the cardiac hypertrophy in exercise-trained rats. Exercise training associated with AS induces maladaptive remodeling and further deterioration in cardiac performance. Exercise training associated with AS causes loss of the beneficial effects in LV function induced by exercising. These results suggest that aerobic exercise plus AS increases cardiac collagen content associated with activation of the local renin-angiotensin system.
http://www.ncbi.nlm.nih.gov/pubmed/17906098
Med Sci Sports Exerc. 2011 Oct;43(10):1836-48. doi: 10.1249/MSS.0b013e318217e8b6.
Anabolic steroid associated to physical training induces deleterious cardiac effects.
Do Carmo EC, Fernandes T, Koike D, Da Silva ND Jr, Mattos KC, Rosa KT, Barretti D, Melo SF, Wichi RB, Irigoyen MC, de Oliveira EM.
Abstract
Cardiac aldosterone might be involved in the deleterious effects of nandrolone decanoate (ND) on the heart. Therefore, we investigated the involvement of cardiac aldosterone, by the pharmacological block of AT1 or mineralocorticoid receptors, on cardiac hypertrophy and fibrosis.
METHODS:
Male Wistar rats were randomized into eight groups (n = 14 per group): Control (C), nandrolone decanoate (ND), trained (T), trained ND (TND), ND + losartan (ND + L), trained ND + losartan (TND + L), ND + spironolactone (ND + S), and trained ND + spironolactone (TND + S). ND (10 mg·kg(-1)·wk(-1)) was administered during 10 wk of swimming training (five times per week). Losartan (20 mg·kg(-1)·d(-1)) and spironolactone (10 mg·kg(-1)·d(-1)) were administered in drinking water.
RESULTS:
Cardiac hypertrophy was increased 10% by using ND and 17% by ND plus training (P < 0.05). In both groups, there was an increase in the collagen volumetric fraction (CVF) and cardiac collagen type III expression (P < 0.05). The ND treatment increased left ventricle-angiotensin-converting enzyme I activity, AT1 receptor expression, aldosterone synthase (CYP11B2), and 11-β hydroxysteroid dehydrogenase 2 (11β-HSD2) gene expression and inflammatory markers, TGFβ and osteopontin. Both losartan and spironolactone inhibited the increase of CVF and collagen type III. In addition, both treatments inhibited the increase in left ventricle-angiotensin-converting enzyme I activity, CYP11B2, 11β-HSD2, TGFβ, and osteopontin induced by the ND treatment.
CONCLUSIONS:
We believe this is the first study to show the effects of ND on cardiac aldosterone. Our results suggest that these effects may be associated to TGFβ and osteopontin. Thus, we conclude that the cardiac aldosterone has an important role on the deleterious effects on the heart induced by ND.
http://www.ncbi.nlm.nih.gov/pubmed/21407130
** I have another paper that I prefer that uses Losartan to reverse the harms caused by AAS, a little older than these. It was the first paper to get me interested in harm reduction of cardiovascular sides. I can't find it via a search but I do have it downloaded. I'll add it on when I find it.
We've also talked in drips and drabs about AAS and cardiovascular health (and how to lessen harm) loads of times on here. Some of the threads I can remember include:
http://www.bluelight.org/vb/threads/760319-AAS-and-Cardiovascular-Health-Case-Study
http://www.bluelight.org/vb/threads/732223-AAS-Bodybuilders-and-heart-ventricle-function
http://www.bluelight.org/vb/threads/755959-Another-Study-on-AAS-and-Cardiac-Risk
