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Creatine Monohydrate

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What is it?

Creatine is formed in the human body from the amino acids methionine,

glycine, and arginine. Creatine is stored in the human body as creatine

phosphate (CP) or phosphocreatine. The average person’s body contains

approximately 120 grams of creatine stored as creatine and creatine phos-

phate.

Creatine can also be supplied by foods. Certain foods such as beef, her-

ring, and salmon, are fairly high in creatine, but a person would have to eat

pounds of these foods daily to equal what can be found in one teaspoon of

powdered creatine from a supplement.

What is it supposed to do?

During short maximal bouts of exercise such as weight training or sprint-

ing, stored adenosine triphosphate (ATP) is the dominant energy source.

However, stored ATP is depleted rapidly. To give energy, ATP loses a phos-

phate and becomes adenosine diphosphate (ADP). At this point, the ADP

must be converted back to ATP to derive energy from this energy produc-

ing system.

When ATP is depleted, it can be recharged by creatine, in the form of cre-

atine phosphate. That is, the CP donates a phosphate to the ADP making it

ATP again. An increased pool of CP means faster and greater recharging of

ATP and, therefore, more work can be performed for a short duration, such

as sprinting, weight lifting and other explosive anaerobic endeavors.

Other e ects of creatine may be increases in protein synthesis and increased

cell hydration, though researchers are still elucidating the mechanisms.

What does the research say?

The above is, of course, an immensely oversimpli ed review of an excep-

tionally complex system, but the basic explanation is correct. To date, re-

search has shown ingesting creatine can increase the total body pool of CP

which leads to greater generation of force with anaerobic forms of exercise,

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such as weight training, sprinting, etc.

Early research with creatine showed it can increase lean body mass and

improve performance in sports that require high intensity intermittent ex-

ercise such as sprinting, weight lifting, football, etc.

Creatine has had spotty results in research that examined its e ects on en-

durance oriented sports such as swimming, rowing and long distance run-

ning, with some studies showing no positive e ects on performance with

endurance athletes.

Whether or not the failure of creatine to improve performance with endur-

ance athletes was due to the nature of the sport or the design of the stud-

ies is still being debated. But one thing is for sure; the research is stronger

in high intensity sports of short duration.

Recent ndings with creatine monohydrate have con rmed previous re-

search showing it’s a safe and e ective supplement. More recent research

has focused on exactly how it works, and has looked deeper into its poten-

tial medical uses.

Several studies have shown it can reduce cholesterol by up to 15%, and

may be useful for treating wasting syndromes such as HIV. Creatine is also

being looked at as a supplement that may help with diseases a ecting the

neuromuscular system, such as muscular dystrophy (MS) and others.

A plethora of recent studies suggest creatine may have therapeutic ap-

plications in aging populations, muscle atrophy, fatigue, gyrate atrophy,

Parkinson’s disease, Huntington’s disease, and other mitochondrial cytopa-

thies, neuropathic disorders, dystrophies, myopathies and brain patholo-

gies.

The importance of creatine is underscored by creatine de ciency disorders:

inborn errors of metabolism that prevent creatine from being manufac-

tured. People born without the enzyme(s) responsible for making creatine

su er from a variety of neurological and developmental symptoms which

are mitigated with creatine supplementation.

As for safety, some have suggested that creatine might increase the need

for extra uid intake to avoid potential dehydration and muscle pulls. Still,

creatine has not been shown to increase either dehydration or muscle pulls

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in the research. In some people, creatine may increase a by-product of cre-

atine metabolism called creatinine, which is a crude indicator but not a

cause of kidney problems.

Some doctors have mistakenly thought that high creatinine levels (in

athletes using creatine) are a sign of kidney problems, but that is not the

case.

Creatinine is not toxic to the kidneys and most doctors are not aware that

creatine may raise creatinine levels with no toxicity to the kidneys. People

with pre-existing kidney problems might want to avoid creatine due to the

e ects it can have on this test, though creatine supplementation has never

been shown to be toxic to the kidneys and the vast number, of studies to

date have found creatine to be exceedingly safe.

It’s interesting to note that there has been a concerted e ort by many

groups and ignorant medical professionals to portray creatine as being

somehow poorly researched ( atly untrue) and unsafe for long term use.

They systematically ignore the dozens of studies that exist showing it’s

both safe and e ective. Even more bizarre, they ignore the recent studies

that are nding creatine may help literally thousands of people with the

aforementioned diseases. This is unscienti c, unethical, and just plain im-

moral, in my view.

One question that often comes up regarding creatine is whether or not the

loading phase is required. Originally, the advice for getting optimal results

was to load up on creatine followed by a maintenance dose thereafter. This

advice was based on the fact that the human body already contains ap-

proximately 120 grams of creatine (as creatine and creatine phosphate)

stored in tissues and to increase total creatine stores, one had to load for

several days in order to increase those stores above those levels.

The idea also seemed to work well, in practice, with people noticing con-

siderable increases in strength and weight during the loading phase. All

was not perfect however as many people found the loading phase to be a

problem, with gastrointestinal upset, diarrhea and other problems. At the

very least, loading was inconvenient and potentially expensive.

The need for a loading phase was a long held belief, but is it really needed

to derive the bene ts of creatine? The answer appears to be no, as both

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research and real world experience have found the loading phase may not

be needed after all. A 1996 study compared a loading phase vs. no loading

phase among 31 male subjects.

to creatine load

human skeletal

muscle is to ingest

20 g of creatine

for 6 days. This

elevated tissue

concentration can

then be maintained

by ingestion of 2

g/day thereafter.

The ingestion of 3

g creatine/day is,

in the long term,

likely to be as ef-

fective at raising

tissue levels as this

higher dose.

The subjects loaded for 6 days using 20 g/day and a maintenance dose 2

g/day for a further 30 days. As expected, tissue creatine levels went up ap-

proximately 20 percent and the participants got stronger and gained lean

mass. Nothing new there! And, not surprisingly, without a maintenance

dose creatine levels went back to normal after 30 days.

Then the group was given 3g of creatine without a loading dose. The study

found a similar -– but more gradual -– increase in muscle creatine concen-

trations over a period of 28 days. The researchers concluded:

“...a rapid way to creatine load human skeletal muscle is to ingest 20 g of cre-

atine for 6 days. This elevated tissue concentration can then be maintained by

ingestion of 2 g/day thereafter. The ingestion of 3 g creatine/day is, in the long

term, likely to be as e ective at raising tissue levels as this higher dose.”

A more recent study done in 1999 found that 5 g of creatine per day with-

out a loading phase in 16 athletes signi cantly increased measures of

strength, power, and increased body mass without a change in body fat

levels (whereas the placebo group showed no signi cant changes).

”

The researcher of this 1999 study concluded:

“...these data also indicate that lower doses of creatine monohydrate may be

ingested (5 g/d), without a short-term, large-dose loading phase (20 g/d), for

an extended period to achieve signi cant performance enhancement.”

So, if you have su ered through the loading phase in the past thinking it

was the only way to maximize the e ects of your creatine supplement, it

appears you can rest assured you don’t have to go through all that hassle.

A 3 - 5 gram per day dose over an extended period of time will probably do

the same thing.

What does the real world have to say?

What can I say? Creatine monohydrate is one of the most widely used sup-

plements in bodybuilding, and I know of very few people who feel that

they haven’t gotten good results from using it.

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“ ...a rapid way

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Chapter 5/Creatine Monohydrate

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Recommendations:

“ ...these data

Creatine can be found in the form of creatine monohydrate, creatine ci-

trate, creatine phosphate, tri-creatine malate, creatine-magnesium chelate

and even liquid “creatine serum”. The newest form being touted as the best

invention since the discovery of testosterone is creatine ethyl ester. How-

ever, the vast majority of research to date showing creatine e ects on mus-

cle mass and performance used the monohydrate form and most creatine

found in supplements is in the monohydrate form.

also indicate that

lower doses of cre-

atine monohydrate

may be ingested

(5 g/d), without a

short-term, large-

dose loading phase

(20 g/d) for an

extended period to

achieve significant

performance en-

hancement.

There are many and surprisingly complicated problems with the above

forms, but I will do my best to cover the essential issues. For one thing,

these forms have little or no research supporting any of their claims, some

of which are either totally outlandish, or biologically impossible. Many

companies selling these products make claims, for example, that creatine

monohydrate is poorly absorbed and or poorly metabolized by the body.

This is simply untrue: research has found that creatine monohydrate is

highly absorbable. Some claim less “bloating” or other supposed e ects of

monohydrate, but don’t have a drop of data to support the claim, or even

a feasible theory as to why their form would not have the e ect vs. the

monohydrate form.

”

They often claim dramatically improved absorption over monohydrate

(without data), fewer side e ects (without data), the ability to reduce the

number of non-responders to creatine (without data), etc. Are you starting

to see a theme here?!

Now, it’s not impossible for example, that a creatine citrate or malate (both

of which are simply creatine bound to a TCA cycle intermediate) may work

for a higher percentage of people than the monohydrate form, thus reduc-

ing the number of non-responders, but it has yet to be proven.

It may be that the creatine-magnesium chelate form – the most interest-

ing form of the group in my view – may be superior to the monohydrate

form for adding LBM or strength, but there has yet to be a single head-to-

head study that compared one version to the other. That people are get-

ting some results from these new forms is all well and ne, but are those

results above and beyond that of monohydrate? If so, is it simply from the

malate, citrate, or magnesium? If a study was to nd that an equal amount

of creatine-malate, citrate, etc. was 10 percent more e ective than mono-

hydrate, but was 4 times as expensive, would you get the same results just

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