Testosterone and its AAS derivatives increase muscle protein synthesis (MPS) and accretion, satellite cell activation and possibly decrease catabolic pathways via genomic and non-genomic mechanisms (Fig. However, the significantly higher prevalence rates in the Middle East may be due to the majority of studies relying on self-reports from athletes rather than general populations įull size table Effects on skeletal muscle The Middle East has relatively significantly high levels of AAS use while use in South America, Europe, North America, Oceania and Africa ranges from 5–2% of the population, highlighting the global issue at hand. Although it is common for individuals to use AAS for multiple reasons, the greatest motivation to use AAS is primarily to improve body image, while competitive bodybuilding and athletic performance (non-bodybuilding) are secondary and tertiary respectively. It is currently estimated that 6.4% of males and 1.6% of females use AAS globally, with recreational sportspeople being the highest users. The world anti-doping agency was created in 1999 to protect athletes from the detrimental health risks of AAS use and to ensure maintenance of the integrity of sport globally. Due to this rise in use and the associated adverse effects of AAS, many countries changed their legislation to incorporate AAS to regulate its use and distribution in the 1990s. Due to advancements in technology and pharmacology, a range of anabolic androgenic steroids (AAS) (Table 1, ) began to be commonly used by the recreational gym-user in the 1980s, primarily by young men to improve body image. The use of testosterone and its derivatives were later banned by the International Olympics Committee in 1974. Shortly thereafter, the hormone started to be used by competitive athletes to increase muscle mass and performance, however, the British Association of Sports Medicine and the American College of Sports Medicine continued to deny its potential benefits until the 1970s. Although research into sex hormones existed in the early 19th century, it was only in the 1930s when the anabolic effects of testosterone were demonstrated. The fine margins of winning and losing in athletic competitions has always encouraged innovative techniques to help athletes gain a competitive advantage with little regard to the potential negative consequences. Research is currently lacking on effective treatments for withdrawal symptoms and further long-term research is warranted on the effects of AAS use on metabolic health in males and females. While cessation of AAS use can restore normal lipid levels, it may lead to withdrawal symptoms such as depression and hypogonadism that can increase CVD risk. Chronic AAS use also appears to cause higher fasting insulin levels and impaired glucose tolerance and possibly higher levels of VAT however, research is currently lacking on the effects of AAS use on glucose metabolism. AAS use markedly decreases high-density lipoprotein cholesterol (HDL-C) and increases low-density lipoprotein cholesterol (LDL-C). Therefore, the aim of this review is to explore the impact of AAS use on mechanisms of muscle hypertrophy and markers of MetS. This clustering of interconnected abnormalities is often referred as metabolic syndrome (MetS). Much research has focused on AAS effects on blood lipids and lipoproteins, with abnormal concentrations of these associated with insulin resistance, hypertension and increased visceral adipose tissue (VAT).
However, chronic AAS use also has a detrimental effect on metabolism ultimately increasing the risk of cardiovascular disease (CVD). Primarily through binding to the androgen receptor, AAS exert their hypertrophic effects via genomic, non-genomic and anti-catabolic mechanisms. In combination with resistance exercise, AAS use increases muscle protein synthesis resulting in skeletal muscle hypertrophy and increased performance. It is estimated 6.4% of males and 1.6% of females globally use anabolic-androgenic steroids (AAS), mostly for appearance and performance enhancing reasons.
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