Since its discovery in 1832, creatine has fascinated scientists with its
central role in skeletal muscle metabolism (Balsom, Soderlund and Ekblom, 1994).
Creatine isn't solely used as a supplement for exercise performance. It has been used in a variety of areas since its discovery.
Creatine has been used in the treatment of some disorders namely gyrate atrophy of the thyroid, inborn errors of metabolism and as a
potential lipid lowering agent. (Roberts, 1977).
Humans have creatine available for use in the body and approximately 95% of this is found in skeletal muscle. The total amount
of creatine in the body is made up of approximately 33% in its natural
form whilst the remainder is in the phosphorylated form phosphocreatine. High levels of creatine are also found elsewhere in
the body namely in the heart, brain and testes.
The immediate energy source for skeletal muscle contraction is
adenosine triphosphate (ATP). During muscle contraction, ATP is hydrolysed to adenosine diphosphate (ADP) and must be continuously
replenished. With rapid increases in energy demands, phosphocreatine is degraded and the phosphate donated to the ADP
to regenerate ATP. This reaction is catalysed by creatine kinase and
leads to an accumulation of free creatine in the active muscles which,
during recovery from exercise, is rephosphorylated back to phosphocreatine.
Creatine is turned over in the body at the rate of about 2 grams
per day (in a 70kg male) or at the rate of around 2% of body weight.
(Balsom et al, 1994). As creatine can be used in the resynthesis of ATP,
stores need to be identified so the body may replenish its creatine
pool. This can be done in two ways.
Firstly, exogenously in which the creatine can be found in the diet.
Creatine is available in foods such as fish, up to 10g/kg, and meat, up
to 5g/kg (Roberts, 1997) but this can be diminished in the cooking
process (Greenhaff, 1995). Creatine is "stored" by the body after consumption of food. This realisation was confirmed by Chanutin in
1926 when he observed that a major portion of ingested creatine was
retained by the body. If creatine is taken orally, usually in the form of
creatine monohydrate, then its ingestion depresses its biosynthesis but
this response is reversible when supplementation ceases (Walker, 1979).
The second source of creatine comes endogenously from the synthesis of the amino acids arginine, glycine and methionine in the
liver pancreas and kidneys (Balsom et al, 1994). The endogenous synthesis of creatine is believed to be at least partly regulated by
exogenous intake, most likely by a feedback mechanism (Balsom et al,
1994). It is difficult for the body to take in much creatine on a daily
basis. The average creatine from a mixed diet has been estimated to
be only 1g/day (Hoogwerf, Laine and Greene, 1986), so while part of
the daily creatine requirement can be fulfilled by the diet, this needs to
be complemented by endogenous synthesis.
Vegetarians seem to be the most vulnerable groups of people who don't take in enough creatine in their diet. In these cases daily
needs are then met exclusively by way of endogenous synthesis (Delanghe, De Slypere and De Buyzere, 1989).
The creatine that is produced endogenously by the liver, kidneys
and pancreas is transported to the muscle via the bloodstream. The
exact mechanism by which creatine enters human skeletal muscle is not clear (Balsom et al,1994). It is present in skeletal muscle at about
125 mmol/kg dm and is normally distributed with most values ranging
from 90 to 160 mmol/kg dm. Interestingly there does seem to be some
difference in opinion as to whether there are differences in levels
between males and females. Balsom et al (1994) reported no significant difference (p>0.05) but Forsberg, Nilsson, Werneman,
Bergstrom and Hultman (1991) reported that females have a slightly
higher creatine content than do males. The reasons for this were unknown.
The phosphocreatine and creatine exist in equilibrium in about a
2:1 ratio. This ratio seems to change as we get older perhaps due to
inactivity. Moller and Brandt (1981) reported that the elderly have a
lower level of phosphocreatine and a higher level of free creatine
compared with younger subjects.
Implications for exercise
It has been postulated that the availability of phosphocreatine is
one of the most likely limitations to muscle performance during brief,
high intensity power exercise (Katz, Sahlin, Henriksson, 1986). This is due
to the depletion of phosphocreatine resulting in an inability to
resynthesise ATP at the rate required. In the past, the levels of creatine
and phosphocreatine had to be determined by muscle biopsy but this
was invasive on the body and also led to unreliable results being obtained. This occurred as the levels of
phosphocreatine rise in the time between the muscle fragment being removed from the body
and analysis. These levels can now be determined by non-invasive methods using Nuclear Magnetic Resonance spectroscopy (NMR)
(McNully, Kent and Chanve, 1988). If there is enough free creatine
available then it plays a central role in the resynthesis of ATP (Greenhaff, 1995).
A great deal of research has been done on the rate that ATP can
be resynthesised from phosphocreatine. The research indicates that
the phosphocreatine rates decline within 1-2 seconds of the muscle
contracting (Hultman, Greenhaff, Ren and Soderlund, 1991). These rates of decline have also shown to be higher in type II versus type I
fibres (Soderlund, Greenhaff and Hultman, 1992).
If the rate of phosphocreatine resynthesis can be improved then
more ATP can be produced and more energy provided. The rate that phosphocreatine resynthesis will occur from creatine has a slow and
fast component (Roberts, 1997). Almost half of the phosphocreatine is
restored to pre-exercise levels after 1 minute but the rest may take up
to 10 minutes depending on the exercise intensity (Sahlin, Harris and
Hultman, 1979). This is further illustrated by the difference in rates
between fibres where type I fibres have shown to be faster in their
resynthesis compared with type II fibres (Tesch, Thorsson and Fujitsuka,
1989). This was thought to be due to the higher aerobic potential of
type I fibres and also because the type I fibres had undergone a smaller change in pH during exercise (Tesch and Wright, 1983).
However, improvements in performance have been seen in type II fibres as a result of improved ATP resynthesis from the increased
availability of phosphocreatine (Casey, Constantin-Teodosiu, Howell,
Hultman and Greenhaff, 1996).
Supplementation studies
It has now been shown that ingestion of creatine can increase
the stores in the body by 20-30%. This was evident in a group of healthy
subjects following creatine supplementation with 20g/day for five days.
Up to 20% of this increase was in the form of phosphocreatine
(Greenhaff, Bodin, Soderlund and Hultman, 1994).
Creatine absorption is also improved when insulin is present.
Therefore creatine should be taken with some form of glucose (usually
an orange drink) to stimulate insulin release (Balsom et al, 1994).
The amount of creatine retained in the body is dependent on the
initial levels of creatine before supplementation begins. This explains
why vegetarians have the greatest uptake of creatine during supplementation (Balsom et al, 1994). The amount of creatine retained
will be high in the initial stages, but as the dose is increased, less is
retained (Greenhaff, 1994). Creatine intake has also been found to be
increased in an exercised muscle, at submaximal levels, over a sedentary one (Harris, Soderlund and Hultman, 1992).
Urinary analysis is used to determine how much creatine is retained by the body and how much is excreted. This analysis has
been used to indicate that there seems to be an upper level of retention in the body, around 160mmol/kg dm for most people
(Balsom et al, 1994). Therefore continuing high doses for prolonged
periods will be of little benefit (Greenhaff, 1994).
Once the initial supplementation period is over, only small amounts (2-3g/day) need to be taken in order to keep the skeletal
muscle levels up (Balsom et al, 1994). The only adverse side effects of
creatine supplementation have been weight gain (Greenhaff et al, 1994). A mean increase of 1kg was found by Balsom et al (1994) in 17
participants who consumed 20g/day for 6 days. Explanations for this
weight gain seem to point to water retention as the likely answer.
Other research indicates that creatine may stimulate protein synthesis
(Ingwall, 1976). This may lead to increased muscle size and therefore
increased body weight (Balsom et al, 1994). This would seem disadvantageous in sports where low body weight is important.
The benefits of creatine supplementation on exercise performance have been seen in numerous studies across a variety of
sporting modes. Greenhaff, Casey, Short, Harris, Soderlund and Hultman (1993) have demonstrated that during five bouts of thirty
seconds maximal knee extensions, with 1 minute recovery, torque production was increased by 5-7% (particularly in bouts two, three and
four) in the creatine ingested (20g/day for 5 days) subjects. The placebo group showed no improvement at all.
It appears that creatine supplementation can increase the ability
to sustain a high power output for a longer period of time during repeated, short, maximal bouts of exercise (Roberts, 1997). Balsom,
Soderlund, Sjodin and Ekblom (1995) also illustrated that after creatine
supplementation, performance on five maximal efforts on a cycle ergometer of six seconds duration, produced a lower muscle lactate
level and helped to maintain power output for longer. This suggests
that higher initial creatine levels, following creatine supplementation,
led to a lesser dependence on anaerobic glycolysis for the resynthesis
of ATP. Therefore the improvements in performance seen in high intensity exercise of short duration may be partly explained by a
greater supply of phosphocreatine in the active muscle before each
exercise period as a result of higher pre-exercise concentrations, a
smaller decrease in muscle pH and a higher rate of resynthesis during
recovery periods (Balsom et al, 1994).
Brannon, Adams, Conniff and Baldwin (1997) also postulate that
gains in high intensity running performance following creatine supplementation are a combined result of increased aerobic (citrate
synthase) and anaerobic (creatine and phosphocreatine) energy buffering capacity of the muscle.
Rossiter, Cannell and Jakeman (1996) suggest that increasing the
total amount of creatine in the body (as occurs with supplementation)
may increase the buffering capacity of the muscle. Chemical buffers
(such as the breakdown of phosphocreatine) within the cell provide
resistance to lowering of the pH (Roberts, 1997). Therefore an increased availability of phosphocreatine to breakdown will potentially
improve the buffering capacity and delay the point at which pH reaches low levels and affects exercise performance (Jones and
Round, 1993).
The benefits of creatine supplementation at high intensity are
clear but does this also apply to exercise at submaximal intensity? Most
of the research tends to indicate that creatine supplementation will
have little or no benefit on performance in submaximal exercise (Green, Greenhaff, McDonald, Bell, Holliman and Stroud, 1994). This
seems logical as phosphocreatine isn't the major fuel for endurancebased
exercise. Similar results were seen in 6km cross-country running trials. The results were in fact worse than
pre-supplementation and this has partly been attributed to the increased body weight associated
with creatine ingestion (Balsom, Harridge, Soderlund, Sjodin and Ekblom, 1993).
Conclusion
Research indicates that benefits in short term maximal exercise
can be seen following creatine supplementation. The exact mechanism that provides the benefit is still not clear but increasing the
total creatine pool in the body seems to provide more phosphocreatine available for ATP resynthesis. Increased
phosphocreatine availability may also have the potential to increase
the intramuscular buffering capacity (Roberts,1997). Furthermore,
creatine supplementation may improve athletic performance in the long term as the training done can be more "quality" based.
Some individuals may experience greater benefits over others
during creatine supplementation. The amount of benefit is directly
related to the concentration of creatine in the skeletal muscle before
the onset of supplementation (Greenhaff,1995).
The only adverse side effect reported is weight gain possibly as a
result of water retention or increased protein synthesis. This may be
disadvantageous in some sports but beneficial to "put on some size" in
others.
The ideal dose for creatine supplementation still needs to be
determined especially in relation to body weight and the amount that
needs to be taken after the initial loading period has finished.
Future studies will also need to examine what are the risks of long
term creatine ingestion, what determines whether individuals have high or low creatine levels (excluding dietary influences), is there a
difference in creatine levels between the sexes, and if so why, and the
actual mechanism by which creatine enters human skeletal muscle.
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