Since the discovery of creatine in 1832, it has fascinated scientists
with its central role in skeletal muscle metabolism. In humans, over 9
5% of the total creatine (Cr(tot)) content is located in skeletal musc
le, of which approximately a third is in its free (Cr(f)) form. The re
mainder is present in a phosphorylated (Cr(phos)) form. Cr(f) and Cr(p
hos) levels in skeletal muscle are subject to individual variations an
d are influenced by factors such as muscle fibre type, age and disease
, but not apparently by training or gender. Daily turnover of creatine
to creatinine for a 70kg male has been estimated to be around 2g. Par
t of this turnover can be replaced through exogenous sources of creati
ne in foods, especially meat and fish. The remainder is derived via en
dogenous synthesis from the precursors arginine, glycine and methionin
e. A century ago, studies with creatine feeding concluded that some of
the ingested creatine was retained in the body. Subsequent studies ha
ve shown that both Cr(f) and Cr(phos) levels in skeletal muscle can be
increased, and performance of high intensity intermittent exercise en
hanced, following a period of creatine supplementation. However, neith
er endurance exercise performance nor maximal oxygen uptake appears to
be enhanced. No adverse effects have been identified with short term
creatine feeding. Creatine supplementation has been used in the treatm
ent of disease where creatine synthesis is inhibited.