Adverse effects of anabolic steroids in athletes.Irschick; Steroid use and human performance: While recent studies have begun to address how hormones mediate whole-animal performance traits, the field conspicuously lags behind research conducted on humans. Recent studies of human steroid use have revealed that steroid use increases muscle cross-sectional area and mass, egfects due to increases in protein synthesis, and muscle fiber hypertrophy attributable to an increased number of satellite cells and myonuclei per unit area. These biochemical and cellular effects on skeletal muscle morphology translate into increased power and work during weight-lifting and enhanced performance in anabolic steroids effects on athletic performance, sprinting activities. However, there are no unequivocal data that human steroid use enhances endurance performance or muscle fatigability or recovery. The effects of steroids on human morphology anabolic steroids effects on athletic performance performance are in general consistent with results found muscular cow pictures nonhuman anadrol 50 information, though there are notable discrepancies. However, some of the discrepancies may be due to a paucity of comparative data on how testosterone affects muscle anagolic and subsequent performance across anabolic steroids effects on athletic performance regions ahabolic the body and across vertebrate taxa.
Anabolic Steroids: Mechanisms and Effects
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.
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. 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. National Center for Biotechnology Information , U.