If you wander through health-food stores, you may
see muscular bodybuilders checking out
creatine supplements. Many
athletes now consume them to build strength and enhance athletic
performance, especially for physical efforts requiring energy bursts.
Since English Olympians initially brought attention to creatine’s
performance-enhancing benefits at the 1992 Barcelona games, creatine’s
popularity has skyrocketed. Its
effectiveness is now supported by numerous scientific studies, including
those suggesting benefits for people with physical disabilities,
including spinal cord injury (SCI).
Furthermore, animal studies
indicate that creatine supplementation exerts a neuroprotective effect
after SCI and traumatic brain injury (TBI) and with amyotrophic lateral
sclerosis (i.e., Lou Gerhig’s Disease).
Our bodies contain more than 100 grams (28 grams =
1 ounce) of creatine,
mostly in our muscles, heart, brain, and testes. Physical activity
stimulates primarily the liver to produce about two grams of creatine
daily from three key amino acids: glycine, arginine, and methionine. The
creatine is then sent through the blood and transported into muscle
Creatine can also be provided by diet, especially
one rich in meat and fish. Vegetarian diets, however, often lack not
only creatine, but also the methionine precursor needed for internal
production. For comparison’s sake, a pound of meat contains about
40-times more creatine (two grams) than a pound of milk.
Most muscle creatine is converted into the
energetically powerful creatine-phosphate. The high-energy molecular
bond connecting the creatine to the phosphate group is an energy source
that can quickly fuel muscle activity. This fueling, however, is
mediated through the creation of yet another powerhouse molecule called
adenosine triphosphate (ATP).
ATP is extremely important because it is the
body’s energy currency, expended to drive most biochemical processes.
Like creatine-phosphate, ATP’s terminal phosphate group is connected
by a high-energy bond that when severed provides energy needed for
Under more constant or endurance working
conditions, the body obtains ATP by metabolizing carbohydrates and fats,
a relatively slow process that cannot generate immediately needed ATP
When energy bursts are required, the body uses
instead creatine-phosphate. Specifically, the phosphate group on this
molecule is transferred to replenish spent ATP, transforming it into its
energetically powerful form. During
rest periods, creatine-phosphate is then replenished by the ATP
generated by the slower metabolic processes.
If intracellular creatine-phosphate levels can be
increased, for example, through supplementation, it will take longer
before the short-term energy source is depleted and a switchover to
slower carbohydrate or fat metabolism is needed.
This process can be visualized as if you have a
large wad of cash (i.e. creatine-phosphate) in your wallet. It’s
there, ready to be used to meet your immediate needs. The more you
supplement this wad, the more energy purchases you can quickly make.
In contrast, generating your energy through carbohydrate or fat
metabolism is the equivalent of writing a check that must clear the
system, a more time-consuming process better suited to meet your
long-term, larger needs.
Strength & Muscles:
Creatine supplementation is most useful for
physical activities that require intense bursts of energy - e.g., a
bench press, a sprint, or games requiring energy bursts. It is less
useful for endurance events, except when such events are enhanced by
building-up muscle strength through creatine-stimulated weightlifting.
Creatine can build muscle mass by several
mechanisms. For example, because weightlifting is exactly the sort of
short-term, intense physical activity fostered by creatine, more
repetitions and harder workouts can be achieved, building up muscle. In
addition, however, creatine increases water uptake into the muscle, a
process called cell volumizing that bulks up the muscles in a fashion
that may not add much real strength.
In one commonly used, creatine-supplementation
cycle, four 5-gram doses of creatine are consumed daily for five days.
These are often dissolved in a sweetened solution to enhance uptake.
After this loading phase, the daily dose is reduced to two grams for a
month, after which supplementation is discontinued for an additional
month. The cycle then starts over.
The washout period is recommended because increased
creatine levels will eventually trigger the body to shut down its
creatine production and transport into muscle from the blood. After the
washout period, the body regains these functions. Although some physical
gains may be lost, because more intense workouts were achieved during
the earlier supplementation phase, the next cycle will start at a higher
In addition to potential transient gastrointestinal
disturbances, chronic creatine supplementation may stress kidneys and
increase exposure to potential, manufacturing-process contaminants.
Although risk appears low given its extensive history of use, normal
metabolic patterns are affected to obtain the desired benefits, which
over time may have yet undefined deleterious effects.
Studies suggest that creatine can enhance strength
compromised by physical disability.
First, investigators at the Miami Project have
shown that creatine promotes upper-extremity work capacity in
quadriplegics (Jacobs, et al, Arch Phys Med Rehabil, 83, January
2002, pp. 18-23).
In this study, 16 male quadriplegics with complete
cervical C5-7 injuries were randomly assigned to receive either 20
grams/day of creatine or placebo maltodextrin (a common food ingredient)
for seven days. Treatment was then discontinued for a three-week washout
period, after which the treatment groups were reversed for another seven
days - i.e., the initial placebo group now received creatine, and the
initial creatine group now was given maltodextrin.
Work capacity was assessed before and after each
dosing period using arm ergometry, a common SCI-rehabilitation exercise.
Specifically, subjects faced a series of two-minute,
increasing-intensity work stages with one-minute, intervening recovery
After creatine supplementation, improvements were
noted in various respiratory measurements, including oxygen uptake,
carbon dioxide production, tidal volume (amount of air that enters the
lungs), and breathing rate. For example, 14 of the 16 subjects
demonstrated increased oxygen uptake, averaging an impressive 18.6 %.
Improvements were also noted in peak power output and increased time to
Second, Dr. Kenneth Adams and colleagues,
University of Texas, Southwestern Medical Study Center, Dallas carried
out a creatine-loading study in 10 subjects with SCI. The subjects had
their peak-power production tested on an upper extremity exercise
machine before and after creatine supplementation. Eighty-eight percent
improved their peak-power production, with quadriplegics and paraplegics
averaging 21and 13% improvement, respectively (Adams, et al, Arch
Phys Med Rehabil, 81, September 2000, p. 1263).
Third, Drs. Stephen Burns and Richard Kendall,
University of Washington have also evaluated the effects of creatine
supplementation on arm strength in C-6 quadriplegics (personal
communication). In this study, however, preliminary analyses indicated
no major benefits. Burns speculates that creatine supplementation
provides to both SCI and neurologically intact individuals similar
modest benefits in response to repeated maximal efforts on
short-duration exercises. However, these benefits may be offset by
weight gains attributed to non-strength-associated water uptake. In
other words, you may be hauling around more weight that will enhance
neither sporting nor transfer ability.
Finally, investigators have shown that creatine can
increase handgrip, knee-extension, and ankle strength in individuals
with various forms of neuromuscular disease (Tarnopolsky, M. &
Martin, J., Neurology, 52, 1999, pp 854-7).
The differences in the indicated benefits between
studies are not surprising because results can be affected by many
interacting factors, including, in these cases, the selected outcome
measures, dosing regimens, and sample sizes (e.g., more subjects may
statistically demonstrate subtler effects).
Animal studies indicate that creatine exerts a
neuroprotective effect in SCI and TBI. For example, Sullivan et al. (U.
Kentucky) demonstrated that creatine supplementation ameliorated the
extent of experimentally induced brain injury 36% in mice and 50% in rats
(Ann Neurol,48(5), 2000, pp 723-729). Hausmann et al. (2002, U.
Zurich) demonstrated that 4-weeks of creatine supplementation before
experimental spinal cord injury reduced glial scar formation and enhanced
functional recovery in rats (Spinal Cord, 40(9), 2002, pp 449-456).
Finally, Rabchevsky and colleagues (2003, U. Kentucky) showed that
creatine supplementation spared spinal cord gray matter in injured rats
(gray matter contains neuronal cell bodies and dendrites and glial cells;
white matter consists mainly of axons). The investigators felt that the
neuroprotective effects were less for SCI than TBI because the latter
affects gray matter to a much greater degree (J Neurotrauma., 20(7), 2003,
These studies suggest that dietary supplementation
with creatine may be a promising approach for reducing neurological damage
after TBI or SCI.
Concerning ALS, in a mouse model of the disorder,
Klivenyi et al (Harvard U.) showed that creatine supplementation protected
mice from neuronal loss and suggested that such supplementation may be a
new therapeutic strategy for ALS (Nat med, 5(3), 1999, pp 347-350).
In conclusion, although more definitive studies are
needed, creatine’s potential benefits have important ramifications for
many with physical disabilities because the enhancement of residual
strength, even to a limited degree, often can have profound
quality-of-life implications. Furthermore, creatine supplementation may
exert neuroprotective effects after TBI and SCI and also with ALS.
Resources: An excellent review of creatine
studies has been posted on http://carecure.rutgers.edu
(click on CareCure Community and scroll down to the creatine article).
Adapted from article appearing in Paraplegia News, November 2002.