For testosterone, dihydrotestosterone is the principle androgenic product; estradiol is the major estrogenic metabolite. Thus, high endogenous concentrations of testosterone may confer both psychological and physiological advantage in sports. Additionally, testosterone has been linked to increased risk-taking in economic domains (Stanton et al., 2011; van Honk et al., 2004, but see also Stanton, Mullette-Gillman et al. 2011) and social domains (Mazur, 1995). Basal testosterone is positively correlated with power motivation in men (Schultheiss et al, 2003; Schultheiss et al, 2005), whereas basal estradiol is positively correlated with power motivation in women (Stanton & Edelstein, 2009; Stanton & Schultheiss, 2007). In addition to their androgenic (masculinizing) effects, testosterone, and indeed all androgens, also have anabolic (muscle-building) actions. Furthermore, testosterone may promote athletic performance, not only through its long-term anabolic actions, but also through rapid effects on behavior. Testosterone and other anabolic-androgenic steroids enhance athletic performance in men and women. Agnathans (jawless vertebrates) such as lampreys do not produce testosterone but instead use androstenedione as a male sex hormone. In women, mean levels of total testosterone have been reported to be 32.6 ng/dL. Androgen receptors occur in many different vertebrate body system tissues, and both males and females respond similarly to similar levels. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects. These independent partial syntheses of testosterone from a cholesterol base earned both Butenandt and Ruzicka the joint 1939 Nobel Prize in Chemistry. The chemical synthesis of testosterone from cholesterol was achieved in August that year by Butenandt and Hanisch. The Organon group in the Netherlands were the first to isolate the hormone, identified in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)". He reported in The Lancet that his vigor and feeling of well-being were markedly restored but the effects were transient, and Brown-Séquard's hopes for the compound were dashed. Testosterone has been detected at variably higher and lower levels among men of various nations and from various backgrounds, explanations for the causes of this have been relatively diverse. Testosterone's bioavailable concentration is commonly determined using the Vermeulen calculation or more precisely using the modified Vermeulen method, which considers the dimeric form of sex hormone-binding globulin. Gender verification for all female competitors was finally dropped from Olympic competition in 1999 (Dickinson et al, 2002). Later tests screened female athletes for the presence of a Y chromosome, and subsequently for the SRY gene on the Y chromosome (Simpson et al, 2000). Such tests would have potential to identify as males both XX athletes with masculinization due to CAH, and XY competitors with incomplete AIS or partial genital masculinization due to 5a-reductase deficiency. In the 1930's, concerns were raised about the masculine appearance of several female athletes, most notably two competitors in the 100 meter event at the 1936 Olympic games in Berlin (Ritchie et al, 2008). Lacking DHT, the external genitalia of XY males are feminized at birth, although the testes descend into the labia majora under the influence of testosterone (Wilson et al, 1993). The use of testosterone in sports has been banned by the World Anti-Doping Agency (WADA) and other sports organizations due to its performance-enhancing effects and potential health risks. Understanding how hormone levels, such as testosterone, growth hormone, estradiol and others correlate with performance indicators including speed and strength is crucial for optimizing athletic abilities. By Barr body screening, male competitors with Klinefelter's syndrome or female athletes with CAH are identified as female, but women with AIS are identified as male. The 6β-hydroxylation of testosterone is catalyzed mainly by CYP3A4 and to a lesser extent CYP3A5 and is responsible for 75 to 80% of cytochrome P450-mediated testosterone metabolism. In addition to conjugation and the 17-ketosteroid pathway, testosterone can also be hydroxylated and oxidized in the liver by cytochrome P450 enzymes, including CYP3A4, CYP3A5, CYP2C9, CYP2C19, and CYP2D6. A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD. In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively. During puberty, elevated levels of testosterone induce virilization and male secondary sexual characteristics. This is consistent with current policy for athletes with DSD, which allows participation by women with "conditions that may accord some advantages", including congenital adrenal hyperplasia, androgen-secreting tumors, and polycystic ovarian syndrome (IAAF, 2006). Most experimental studies of post-competition changes in testosterone have used serum or salivary sampling, and it is well established that serum and salivary testosterone levels are highly correlated (Ellison, 1988; Riad-Fahmy et al., 1982; Smith et al., 1979). Furthermore, disorders of sexual differentiation (DSD) can produce elevated concentrations of endogenous androgens, potentially creating a competitive advantage for female athletes with DSD. Athletes aim to maximize their performance through the anabolic effects of testosterone and AAS, while limiting androgenic actions. In women, excess production of endogenous testosterone due to inborn disorders of sexual development (DSD) may convey a competitive advantage. They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. Suffering the ridicule of his colleagues, he abandoned his work on the mechanisms and effects of androgens in human beings. A testicular action was linked to circulating blood fractions – now understood to be a family of androgenic hormones – in the early work on castration and testicular transplantation in fowl by Arnold Adolph Berthold (1803–1861).
