Hartgens Fred, Kuipers Harm
Department of Surgery, Outpatient Clinic Sports Medicine, University Hospital Maastricht, and Sports Medicine Center Maastricht, Maastricht, The Netherlands.
Sports Med. 2004;34(8):513-54. doi: 10.2165/00007256-200434080-00003.
Androgenic-anabolic steroids (AAS) are synthetic derivatives of the male hormone testosterone. They can exert strong effects on the human body that may be beneficial for athletic performance. A review of the literature revealed that most laboratory studies did not investigate the actual doses of AAS currently abused in the field. Therefore, those studies may not reflect the actual (adverse) effects of steroids. The available scientific literature describes that short-term administration of these drugs by athletes can increase strength and bodyweight. Strength gains of about 5-20% of the initial strength and increments of 2-5 kg bodyweight, that may be attributed to an increase of the lean body mass, have been observed. A reduction of fat mass does not seem to occur. Although AAS administration may affect erythropoiesis and blood haemoglobin concentrations, no effect on endurance performance was observed. Little data about the effects of AAS on metabolic responses during exercise training and recovery are available and, therefore, do not allow firm conclusions. The main untoward effects of short- and long-term AAS abuse that male athletes most often self-report are an increase in sexual drive, the occurrence of acne vulgaris, increased body hair and increment of aggressive behaviour. 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.
雄激素-同化类固醇(AAS)是雄性激素睾酮的合成衍生物。它们可对人体产生强大作用,这可能对运动表现有益。文献综述显示,大多数实验室研究并未调查该领域目前滥用的AAS实际剂量。因此,这些研究可能无法反映类固醇的实际(不良)影响。现有科学文献表明,运动员短期使用这些药物可增加力量和体重。已观察到力量增加约为初始力量的5%-20%,体重增加2-5千克,这可能归因于瘦体重的增加。脂肪量似乎并未减少。尽管使用AAS可能会影响红细胞生成和血液血红蛋白浓度,但未观察到对耐力表现有影响。关于AAS对运动训练和恢复期间代谢反应影响的数据很少,因此无法得出确凿结论。男性运动员最常自我报告的短期和长期滥用AAS的主要不良影响包括性欲增强、寻常痤疮的出现、体毛增多以及攻击性行为增加。使用AAS会干扰睾酮和促性腺激素的正常内源性分泌,停药后这种干扰可能会持续数月。心血管危险因素可能会发生有害改变,包括血压升高以及血清高密度脂蛋白(HDL)、HDL2和HDL3胆固醇水平降低。在对男性运动员的超声心动图研究中,AAS似乎并未影响心脏结构和功能,尽管在动物研究中已观察到这些药物对心脏结构和功能有有害影响。在运动员研究中,未发现AAS会损害肝脏。心理和行为似乎受到AAS的强烈影响。一般来说,AAS似乎会导致攻击性和敌意增加。情绪障碍(如抑郁、[轻]躁狂、精神病性特征)可能与剂量和药物有关。AAS依赖或戒断效应(如抑郁)似乎仅在少数AAS使用者中出现。对身体的不满和低自尊可能会导致所谓的“反向厌食综合征”,这易引发AAS使用行为。AAS滥用还与许多其他不良反应有关,包括内分泌和免疫功能紊乱、皮脂腺系统和皮肤改变、止血系统和泌尿生殖道变化。必须牢记,由于这些研究中使用的剂量相对较低,未接近非法类固醇使用者的剂量,科学数据可能低估了实际不良影响。由于类固醇分子的差异以及对雄激素受体的亲和力不同,AAS的作用机制在不同化合物之间可能存在差异。已认识到几种作用途径。5-α还原酶似乎通过将AAS转化为双氢睾酮(雄烷醇酮)发挥重要作用,双氢睾酮作用于靶器官(如男性附属腺体、皮肤和前列腺)的细胞核。其他机制包括芳香化酶介导的作用,芳香化酶将AAS转化为雌性激素(雌二醇和雌酮)、对雌激素的拮抗作用以及对糖皮质激素受体产生竞争性拮抗作用。此外,AAS刺激促红细胞生成素合成和红细胞生成以及骨形成,但会抵消骨吸收。对心血管系统的影响被认为是由AAS诱导的动脉粥样硬化(由于对血清脂质和脂蛋白的不利影响)、血栓形成、血管痉挛或对血管壁的直接损伤介导的,或者可能归因于不同机制的组合。AAS诱导的肌肉组织增加可归因于肥大和新肌纤维的形成,其中卫星细胞数量和超微结构、雄激素受体和肌核起着关键作用。