影响androgenic-anabolic类固醇的运动员。

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Hartgens F, Kuipers H

影响androgenic-anabolic类固醇的运动员。

运动医学。2004;34 (8):513 - 54。

PubMed ID
15248788 (在PubMed
]
文摘

Androgenic-anabolic类固醇(AAS)是合成雄性激素睾酮的衍生品。他们能对人体起到强有力的作用可能是有益的运动性能。回顾文献显示大部分实验室研究没有调查的实际剂量AAS目前滥用。因此,这些研究可能不能反映实际的(不良)影响类固醇。可用的科学文献描述了短期政府这些药物的运动员可以增加力量和体重。强度增长5 - 20%的初始强度和增加2 - 5公斤体重,这可能归因于增加瘦体重,曾被观察到。减少脂肪量似乎并没有发生。尽管AAS政府可能会影响红细胞生成和血液血红蛋白浓度,没有观察到疲劳性能的影响。小数据的影响,原子吸收光谱法对代谢反应在运动训练和恢复可用,因此,不允许公司的结论。短期和长期的主要不利后果AAS滥用,男运动员经常自我报告增加性欲,寻常痤疮的发生,增加身体攻击性行为的头发和增量。 AAS administration will disturb the regular endogenous production of testosterone and gonadotrophins that may persist for months after drug withdrawal. Cardiovascular risk factors may undergo deleterious alterations, including elevation of blood pressure and depression of serum high-density lipoprotein (HDL)-, HDL2- and HDL3-cholesterol levels. In echocardiographic studies in male athletes, AAS did not seem to affect cardiac structure and function, although in animal studies these drugs have been observed to exert hazardous effects on heart structure and function. In studies of athletes, AAS were not found to damage the liver. Psyche and behaviour seem to be strongly affected by AAS. Generally, AAS seem to induce increments of aggression and hostility. Mood disturbances (e.g. depression, [hypo-]mania, psychotic features) are likely to be dose and drug dependent. AAS dependence or withdrawal effects (such as depression) seem to occur only in a small number of AAS users. Dissatisfaction with the body and low self-esteem may lead to the so-called 'reverse anorexia syndrome' that predisposes to the start of AAS use. Many other adverse effects have been associated with AAS misuse, including disturbance of endocrine and immune function, alterations of sebaceous system and skin, changes of haemostatic system and urogenital tract. One has to keep in mind that the scientific data may underestimate the actual untoward effects because of the relatively low doses administered in those studies, since they do not approximate doses used by illicit steroid users. The mechanism of action of AAS may differ between compounds because of variations in the steroid molecule and affinity to androgen receptors. Several pathways of action have been recognised. The enzyme 5-alpha-reductase seems to play an important role by converting AAS into dihydrotestosterone (androstanolone) that acts in the cell nucleus of target organs, such as male accessory glands, skin and prostate. Other mechanisms comprises mediation by the enzyme aromatase that converts AAS in female sex hormones (estradiol and estrone), antagonistic action to estrogens and a competitive antagonism to the glucocorticoid receptors. Furthermore, AAS stimulate erythropoietin synthesis and red cell production as well as bone formation but counteract bone breakdown. The effects on the cardiovascular system are proposed to be mediated by the occurrence of AAS-induced atherosclerosis (due to unfavourable influence on serum lipids and lipoproteins), thrombosis, vasospasm or direct injury to vessel walls, or may be ascribed to a combination of the different mechanisms. AAS-induced increment of muscle tissue can be attributed to hypertrophy and the formation of new muscle fibres, in which key roles are played by satellite cell number and ultrastructure, androgen receptors and myonuclei.

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