The use of Anabolic-androgenic
steroid (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
levels (Viru, Karelson, & Smirnova, 1992), this is accompanied
by an increase 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 decreases 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. Evens 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, &
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 an 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.