Cardiovascular effects of androgenic-anabolic steroids

Melchert, Russell B.; Welder, Allison A.

doi:10.1249/00005768-199509000-00004

Cited by 167 publications

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“…Anabolic androgenic steroids have been associated with myocardial ischemia, sudden cardiac death, and hypertension in athletes, leading to the view that androgens are detrimental to the cardiovascular system. 4 However, anabolic androgenic steroids consist of a variety of different steroids with differing pharmacological properties. No clinical study has yet demonstrated a conclusive link between physiological testosterone and fatal cardiovascular events.…”

Section: Discussionmentioning

confidence: 99%

“…1,2 Androgens have been associated with an increased cardiovascular risk by adversely affecting the plasma lipid and lipoprotein profile, thrombosis, cardiac hypertrophy, and suspected proatherogenic effects. 3,4 However, beside these genetic, mainly testosterone receptor-mediated pathways, recent studies demonstrate another, genomic-independent way of testosterone action. Short-term administration of testosterone acutely induces vasodilation in the systemic, coronary, and pulmonary vascular beds.…”

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confidence: 99%

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Testosterone Induces Cytoprotection by Activating ATP-Sensitive K ⁺ Channels in the Cardiac Mitochondrial Inner Membrane

Michels

Gassanov

et al. 2004

Circulation

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Background-Whereas in the past, androgens were mainly believed to exert adverse effects on the cardiovascular system, recent experimental data postulate a benefit of testosterone for recovery of myocardial function after ischemia/ reperfusion injury. Thus, we examined whether testosterone might improve myocardial tolerance to ischemia due to activation of mitochondrial (mitoK ATP ) and/or sarcoplasmatic (sarcK ATP ) K ATP channels. Methods and Results-In a cellular model of ischemia, testosterone significantly decreased the rate of ischemia-induced death of cardiomyocytes that could be prevented by 5-hydroxydecainoic acid but was unaffected by the sarcK ATP blocker HMR1098 and the testosterone receptor antagonist flutamide. To index mitoK ATP , mitochondrial flavoprotein fluorescence was measured. Testosterone induced a highly significant increase in mitochondrial flavoprotein fluorescence in intact myocytes and isolated mitoplasts that could be abolished by 5-hydroxydecainoic acid. Testosteronemediated flavoprotein oxidation of mitoplasts was K ϩ dependent and ATP sensitive. In mitoplast-attached singlechannel recordings, testosterone directly activated an ATP-sensitive K ϩ channel of the inner mitochondrial membrane. Addition of the K ATP channel opener diazoxide and pinacidil to the cytosolic solution activated the ATP-sensitive K

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Testosterone Induces Cytoprotection by Activating ATP-Sensitive K ⁺ Channels in the Cardiac Mitochondrial Inner Membrane

Michels

Gassanov

et al. 2004

Circulation

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“…Our data clearly indicate that AAS-induces negative cardiac effects. Although experimental data obtained from animals correlates well with data from human subjects, the pathophysiology of adverse cardiovascular effects of AAS use is still poorly understood [42]. Changes in hepatic tissue are typical following druginduced liver dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Endocrinological and Pathological Effects of Anabolic-androgenic Steroid in Male Rats

2004

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Abstract. Many athletes use drugs, especially anabolic androgenic steroids (AAS), but there are few reports on the endocrinological and pathological changes in AAS abusers. In this study we reported the results of endocrinological examinations in rats administered AAS and also physical changes. We separated 37 male Wistar rats (7 weeks old) into 3 groups: Group A was medicated with nandrolone decanoate, metenolone acetate, and dromostanolone; Group B with nandrolone decanoate and saline; and Group C was given only saline. They were given subcutaneous injections of the medications or the control vehicle once a week for 6 weeks. Medications were stopped for 4 weeks, and then resumed for another 6 weeks. After that, rats were sacrificed. Serum testosterone level in Group A was significantly higher than that in Group C. Serum dihydrotestosterone in Group A was significantly higher than that in both Groups B and C. Serum estradiol-17b levels in Groups A and B were significantly higher than that in Group C. In pathological evaluation, heart, testis, and adrenal gland were severely damaged. These findings indicate that there is a high degree of risk related to the use of AAS.

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“…The CH induced by the AAS may occur by its interaction with nuclear receptors, directly acting in the DNA increasing the protein synthesis or, by affecting specific enzymes, ion flow and structural matrix in the myocardium as well (25) . However, the exact mediators of these effects are diverse and vary from mechanical stimuli to humoral circulating factors released by the heart and peripheral organs (26) ; however, the real mechanisms through which the AAS causes CH and increase of interstitial collagen are not well-known until the present moment.…”

Section: Discussionmentioning

confidence: 99%

A associação de esteroide anabolizante ao treinamento físico aeróbio leva a alterações morfológicas cardíacas e perda de função ventricular em ratos

Carmo

Rosa

Koike

et al. 2011

Rev Bras Med Esporte

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Introduction: Anabolic-androgen steroids (AAS) associated with physical training induce changes from physiological cardiac hypertrophy (CH) to pathological hypertrophy. However, these studies were performed with strength athletes, and the AAS effects associated with aerobic training are still poorly understood. Thus, the aim of this study was to evaluate the effects of aerobic training and AAS on the cardiac structure and function. Methods: 28 Wistars rats divided in 4 groups were used: sedentary control (SC), sedentary anabolic (SA), trained control (TC) and trained anabolic (TA). The AAS was administered twice a week (10mg/Kg/week). The swimming training was conducted 5 sessions per week during 10 weeks. We evaluated blood pressure and heart rate by tail plethysmography, ventricular function by echocardiography, cardiomyocyte diameter and collagen volumetric fraction by histological methods. Results: There were no differences in BP. TC group showed reduction in rest heart rate after the experimental period, which did not occur in TA group. CH of 38% in SA group; 52% in TC group and 64% in TA group compared to SC group was observed. TA group presented decrease in diastolic function in relation to other groups. The trained groups showed significant increases in cardiomyocytes diameter. SA and TA groups showed increase in collagen volumetric fraction in relation to SC and TC groups. Conclusion: The results show that AAS treatment associated to swimming training induces CH, mainly by the increase in interstitial collagen, which can lead to loss of diastolic function.

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Cardiovascular effects of androgenic-anabolic steroids

Cited by 167 publications

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Testosterone Induces Cytoprotection by Activating ATP-Sensitive K ⁺ Channels in the Cardiac Mitochondrial Inner Membrane

Testosterone Induces Cytoprotection by Activating ATP-Sensitive K ⁺ Channels in the Cardiac Mitochondrial Inner Membrane

Endocrinological and Pathological Effects of Anabolic-androgenic Steroid in Male Rats

A associação de esteroide anabolizante ao treinamento físico aeróbio leva a alterações morfológicas cardíacas e perda de função ventricular em ratos

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Cardiovascular effects of androgenic-anabolic steroids

Cited by 167 publications

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Testosterone Induces Cytoprotection by Activating ATP-Sensitive K + Channels in the Cardiac Mitochondrial Inner Membrane

Testosterone Induces Cytoprotection by Activating ATP-Sensitive K + Channels in the Cardiac Mitochondrial Inner Membrane

Endocrinological and Pathological Effects of Anabolic-androgenic Steroid in Male Rats

A associação de esteroide anabolizante ao treinamento físico aeróbio leva a alterações morfológicas cardíacas e perda de função ventricular em ratos

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Testosterone Induces Cytoprotection by Activating ATP-Sensitive K ⁺ Channels in the Cardiac Mitochondrial Inner Membrane

Testosterone Induces Cytoprotection by Activating ATP-Sensitive K ⁺ Channels in the Cardiac Mitochondrial Inner Membrane