The use of Anabolic-androgenic steroids (AAS) have been associated with numerous changes in physiological function (Yesalis et al 1989; Kleiner 1991). Anabolic steroids can increase strength and muscle mass when accompanied by adequate protein, calories and intense training (Freed, Banks, Longson & Burley, 1975; Kleiner, 1991; Landry & Primos, 1990; American College of Sport Medicine, 1987). Anabolic steroids improve nitrogen utilization and promote positive nitrogen balance by the reversal of catabolic processes. Anabolic steroids can improve nitrogen balance and increase the concentration of total plasma amino acids. This seems to be due to an amino acid saving mechanism with a renal site of action (Kleiner, 1991; Hausmann, Nutz, Rommelsheim, Caspari & Mosebach, 1990). Intense training can serve to maintain a relative state of chronic catabolism. Therefore, the requirements for protein and calories appear to increase when training with the aid of anabolic steroids (Freed, Banks, Longson & Burley, 1975; Kleiner, 1991). A protein intake of 12% to 20% of the total calories has been recommended for athletes (Paul, 1989). The protein and calorie requirements for bodybuilders using steroids are unknown (Kleiner, 1991; Kleiner, Bazzarre & Litchford, 1990).
Anabolic-androgenic steroids may play a physiological role in the regulation of fatty acid oxidation in liver and fast twitch muscle mitochondria even in the absence of intense physical training (Guzman, Saborido, Castro, Molano, & Megias, 1991).
Anabolic-androgenic steroid use may alter glucose tolerance, and induce hyperinsulinism (Yesalis, Wright, & Bahrke, 1989). Powerlifters using anabolic steroids have been shown to develop insulin resistance and diminished glucose tolerance (Cohen, & Hickman, 1987). Although chronic exercise generally decreases serum insulin levels (Viru, Karelson & Smirnova, 1992), this is accompanied by an increased peripheral insulin sensitivity (Richter, Mikines, Galbo & Keins, 1989).
The mechanical stresses encountered from the rapid increases in muscular performance when using Anabolic-androgenic steroids have been suggested to increase the risk of tendon tears in athletes particularly when combined with rapid increases in training intensity and volume (Hoffman & Ratamess 2006, Butt 2015). Studies in mice and rats suggest anabolic-androgenic steroids may lead to decrease in collagen synthesis, degradation of collagen, and a potential compromise of tensile strength (Hoffman & Ratamess 2006). However, human studies are lacking (Hoffman & Ratamess 2006). Parssinen (2000) reported high doses of anabolic steroids decrease the degradation and increase the synthesis of type I collagen. Evans (1998) performed an ultrastructural analysis on ruptured tendons from anabolic steroid users and non-users. Evans concluded that anabolic steroids did not induce any ultrastructural collagen changes that would increase the risk of tendon ruptures (Evans 1998).
Men have been shown to be more susceptible to gynecomastia as a result of using aramatizing anabolic-androgenic steroid (Yesalis, Wright & Bahrke, 1989). Gynecomastia in athletes has been associated with the increase of serum estradiol concentrations during the use of particular anabolic-androgenic steroids (Alen, Reinila, Vihko & Reijo, 1985).
Alen, Reinila & Reijo (1985) observed that serum testosterone level tended to increase throughout a 26 week cycle of various AAS until abruptly dropping below normal levels during cessation. When athletes discontinue the use of AAS they experience a refractory period where they do not produce physiological amounts of endogenous testosterone (Di Pasquale, 1992a). Anabolic-androgenic steroid can reduce endogenous testosterone, gonadotrophic hormones and sex hormone-binding globulin (Yesalis, Wright & Bahrke, 1989). Weight trained athletes have been shown to have low serum testosterone concentrations immediately after cessation of an AAS cycle but return to normal within weeks (Alen, Reinila & Reijo, 1985).
Hurley, Seals, Hagberg, Goldberg, Ostrove, Holloszy, Wiest & Goldberg (1984) found that oral AAS significantly decreased both free and total serum testosterone levels. In contrast, injectable AAS significantly increased free and total serum testosterone level when taken alone or in combination with the oral form.
In young and older men treated with graded doses of testosterone, myostatin levels were significantly higher on day 56 than baseline. Changes in myostatin levels were significantly correlated with changes in total and free testosterone in young men.