The use of AAS have
been associated 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 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 increase peripheral insulin sensitivity
(Richter, Mikines, Galbo, & Keins, 1989).
Men have been shown to be more susceptible to gynecomastia
as a result of anabolic-androgenic steroid use (Yesalis, Wright,
& Bahrke, 1989). Gynecomastia in athletes has been associated
with the increase of serum estradiol concentrations during the
use of 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 a
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 an the oral form.
Interestingly, serum testosterone levels have been linked to
aggressive behavior in animals and humans (Bahrke, Barke, &
Strauss, 1990).
