This document summarizes research on creatine as an ergogenic aid. It discusses how creatine occurs naturally and helps supply energy to cells, especially muscle cells. It reviews studies showing that creatine supplementation can benefit performance in short, powerful activities by increasing ATP and PCr levels but may not improve endurance. The document also examines creatine synthesis and transport in the body, the roles of creatine and PCr in energy production and muscle contraction, and the effects of creatine on muscle fiber type, age, and training status.

1. The Effects of Creatine as an Ergogenic Aid
Enoch Samraj
KINE 5320 –Advanced Exercise Physiology
Dr. Paul McDonough
December 6, 2011

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Abstract
This paper looks at the ergogenic effect of creatine. Although many studies have been
conducted, it is still not very clear as to what extent creatine effects the performance of the
human body, but studies clearly indicate that creatine supplementation with a loading phase
followed by the maintaining phase can benefit the athlete in short powerful activities but research
is not conclusive about its effect on aerobic endurance activities such as cross country cycling.
This paper looks at the potential benefits of creatine supplementation and the process of creatine
synthesis, creatine degradation, and its utilization in the body.

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CHAPTER 1
Introduction
“There’s no magic bullet out there. But creatine is about the closest thing “says Rob
Zatchetka, New York Giants offensive lineman (Williams et al. 1999).Although creatine had
been identified as a natural substance for over 150 years, only as recent as the 1990’s has it been
under the scanner for researchers to study, because of its potential ergogenic effect with creatine
supplementation.
Creatine is a nitrogenous organic acid that occurs naturally in vertebrates and helps to
supply energy to all cells in the body, primarily muscle, by increasing the formation of
Adenosine triphosphate (ATP). Creatine was identified in 1832 by Michel Eugène Chevreul.
Creatine supplements are sometimes used by athletes, bodybuilders, and others who wish to gain
muscle mass, typically consuming 2 to 3 times the amount that could be obtained from a very-
high-protein diet (Williams et al. 1999).
The theoretical ergogenic benefits of creatine supplementation are related to the role of
creatine and PCr in muscle energetics. Although creatine supplementation may, theoretically, be
ergogenic for very high intensities, short term exercise performance depends upon the ATP-PCr
energy system, it may also theoretically; benefit performance in less intense, longer-duration
exercise bouts (Williams et al. 1999).
Although creatine supplementation may be ergogenic for certain exercises or sport
endeavors, some suggest that it may also be ergolytic (may impair performance in other type of
events) Theoretically, creatine supplementation may impair exercise or sport performance by
increasing body mass; this may decrease metabolic efficiency in tasks in which the body mass
needs to be moved efficiently from one point to another (Clark 1996, cited in Williams et al.
1999).
According to Williams et al. (1999), creatine supplementation theoretically may benefit
performance in a variety of exercise or sport endeavor’s such as very high intensity sprint
performance, high intensity exercises, repetitive tasks, longer anaerobic exercise tasks, and any
type of resistance-type sport task that is dependent on increased body mass, increased muscle
mass, and any associated gains in strength and power.

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Creatine Synthesis
About half of the body’s need for creatine comes from our diet; the remainder is
synthesized in the body through endogenous creatine synthesis. This happens especially when
dietary availability of creatine is insufficient to meet the daily demands. Creatine is not
considered an essential nutrient because it can be synthesized in the body from amino acids
(Williams et al. 1999).
The endogenous synthesis of creatine is 1-2 g/d, (Walker 1979, cited in Mesa et al. 2002)
and occurs mainly in the liver and secondarily in the pancreas and kidney. An additional 1-2g/d
of creatine are obtained from dietary intake, mainly fish and meat (Balsom et al.1994, cited in
Mesa et al. 2002). Endogenous creatine synthesis is downregulated by diet and therefore reduced
after enhanced creatine ingestion, (Walker 1960, cited in Mesa et al. 2002) but normal secretion
rates return upon termination of supplementation (Persky and Brazeau 2001, cited in Mesa et al.
2002).
After production or absorption from the gut, creatine travels through the blood-stream in
the plasma at a concentration of 20 to 100 micromols per liter (μmol/L) to be delivered to
various tissues (Volek & Kraemer 1996, cited in Andres et al. 1999). Approximately 98% of th4e
creatine in the whole body is found in skeletal muscle, 40% as free creatine, and 60% as PCr.
About 1.6% of the total creatine pool (TCr) is degraded per day to creatinine and excreted
through the kidney (Volek & Kraemer 1996, cited in Andres et al. 1999).
Creatine Transport into Muscle Cells
Muscle fibers are unable to synthesize creatine; therefore it must be taken up from the
blood stream. The daily demand for creatine is met both by intestinal absorption of dietary
creatine and by the novocreatine biosynthesis. Creatine is therefore exported from both liver and
gut and gets accumulated in creatine kinase (CK) containing tissues. Over 92% of creatine enters
skeletal muscle by binding to a specific transporter protein (Wallimann et al. 1992, cited in Mesa
et al. 1999). Two specific transporters, present in muscle fiber membranes, take up creatine from
the blood stream, they are creatine transporter 1 (CRT1) and choline transporter 1 (CHOt1).
Creatine is an osmotically active substance; thus an increase in intracellular creatine

5. Creatine as an Ergogenic Aid
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concentration is likely to induce the influx of water into the cell (Volek et al. 1997, cited in
Williams et al. 1999).
Creatine Degradation
In muscle cells at rest, creatine is phosphorylated by CK to form PCr within 25 minutes
upon arrival. For this purpose, the ATP formed by glycolysis and oxidative phosphorylation
reacts with creatine to form ADP and PCr. Large negative charges on PCr prevent diffusion
across biological membranes thus locking PCr in the muscle cell (Greenhaff 1997), during
exercise, when muscle ATP is being consumed, the high energy phosphoryl group of PCr is
transferred to ADP to restore ATP. Creatine is then recycled or transformed to creatinine (Crn).
Crn cannot be reutilized and is excreted in the urine (Greenhaff 1997).
The daily demand for creatine is met both by intestinal absorption of dietary creatine (1-
2g) and by de novocreatine biosynthesis. Because muscle has virtually no creatine synthesizing
capacity, creatine has to be taken up from the blood against a large concentration gradient by a
saturable [Na+] and [Cl−] dependent creatine transporter that spans the plasma membrane (Mesa
et al.2002).
During very high intensity exercise, the phosphate from the PCr is cleaved off to provide
energy for re-synthesis of ATP as follows; PCr +ADP↔ ATP +Cr. The energy thus derived from
the degradation of PCr allows the ATP pool to be turned over several dozen times during an all
out high intensity exercise. Phosphocreatine serves as a temporary energy buffer during periods
of intense muscle contraction, when ATP consumption exceeds synthesis (Deursen et al. 1993,
cited in Williams et al. 1999). From an ergogenic standpoint, the resynthesis of PCr is the most
critical factor during sustained high intensity exercises. In addition to its role as an energy buffer,
it has been proposed that the CK-PCr system functions in energy transport on the basis of the
functional and physical associations of CK iso-enzymes with subcellular sites of ATP production
and hydrolysis (Williams et al. 1999).

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Creatine Influence in Muscle Fiber type
Creatine and PCr concentrations correlate with the glycolytic capacity of the different
skeletal muscles. In this regard, the resting PCr content is 5-30% higher in type II versus type I
muscle fibers (Wyss and Wallimann 1994, cited in Mesa et al. 2002). This correlates with the
fact that sprinters have been observed to have higher levels of muscle PCr, whose muscles also
contain a higher proportion of type II fibers (Saltin et al. 1974, cited in Mesa et al. 2002). Thus
phosphocreatine is considered to be a possible limiting factor from maintaining muscle force,
especially in type II fibers (Greenhaff 1997, cited in Andres et al. 1999).
Creatine Influence on Age and Training Status
Total creatine in skeletal muscle can be measured via muscle biopsy or nuclear magnetic
resonance (NMR) spectroscopy. Although some differences have been reported, the literature
generally shows that sex, aging, and training status have no effect on creatine levels (Balsom et
al. 1994, cited in Andres et al. 1999). However Forsberg et al found higher muscle total creatine
levels in females, and Smith et al found that younger subjects had higher PCr contents.
A study using nuclear magnetic resonance spectroscopy failed to show any significant
difference between trained and untrained individuals in muscle PCr content (Gariod et al. 1994,
cited in Mesa et al. 2002). However, since sprinters have more type II muscle fibers than long
distance runners, and the resting PCr content is higher in type II than in type I muscle fibers
(Tesch et al.1989, cited in Mesa et al. 2002), these differences may be mainly caused by fiber
type and not training effects.
Creatine in Muscle Cells
The primary mechanism for the acute ergogenic effect of creatine supplementation is the
greater pre-exercise PCr availability that allows for rapid resynthesis of ATP during ATP-
depleting, high-intensity exercise. This mechanism would result in a decreased dependence on
anaerobic glycolysis, a process that can the buildup of lactate and hydrogen ion concentration,
which promotes the onset of fatigue and decreases muscular performance (Hultman et al. 1967,
cited in Andres et al. 1999). Furthermore, if there is an increase in pre-exercise creatine

7. Creatine as an Ergogenic Aid
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availability, there will be a greater flux of creatine through the creatine kinase reaction enhancing
PCr resynthesis between maximal intermittent exercises. This mechanism serves to enhance
muscular performance, but at the same time, will also act as a proton buffer to delay the onset of
fatigue (Andres et al. 1999). Another possible mechanism by which creatine improves exercise
performance involves the increase in creatine and PCr in muscle to increase the hydration levels
of the cell (Haussinger et al. 1993, cited in Andres et al. 1999). Creatine is an osmotically active
substance that may induce cell swelling if there is an increase in creatine concentration. This
increase in hydration levels could serve to stimulate protein synthesis thereby increasing the
diameter of type II fibers and increasing fat-free mass (Haussinger et al. 1993, cited in Andres et
al. 1999). This would allow for greater training intensity and increased muscular performance.
There is some indication that creatine supplementation reduces muscle damage and
enhances recovery from stressful exercise (Eric and Adam 2007). Reports of fewer muscle
dysfunctions (cramping, muscle tightness, strains, injuries, etc.) between creatine and non-
creatine users (Greenwood et al. 2003, cited in Eric and Adam 2007). And anecdotal reports
indicate that exogenous creatine and phosphocreatine decrease muscle soreness and increase
recovery between workouts. Exogenous phosphocreatine reduces muscle damage in cardiac
tissue by stabilizing the membrane phospholipid bilayer, decreasing membrane fluidity, and
turning the membrane into a more ordered state (Saks et al. 1996, cited in Eric and Adam 2007).
In cardiac tissue, this would decrease the loss of cardiac muscle proteins, which indicates less
muscle tissue damage (Saks and Strumia 1993).
During short period of intense physical exercise, muscle ATP content may be partially
buffered and restored after muscle activity has ceased. During physical inactivity, muscle ADP
content is buffered. In fact, the formation of CK- mediated PCr allows the conversion of ATP to
ADP, maintaining the substrate for new phosphorylation reactions. A large pool of PCr is
available in type II fibers for immediate regeneration of ATP hydrolyzed during short periods of
intense work (Bloch and Schoenheimer 1941).
While several mechanisms have been associated with muscle fatigue, it is clear that PCr
levels are correlated with force production (Volek and Kraemer 1996, cited in Andres et al.
1999). In addition, researchers have associated the loss of PCr as a contributor to fatigue due to

8. Creatine as an Ergogenic Aid
8
changes in excitation-contraction coupling from increased ADP levels (Williamann et al 1992,
cited in Andres et al. 1999).
One study demonstrated that immediately after either dynamic or isometric exhaustive
exercise, PCr content in the quadriceps femoris was 15-16% of resting muscle levels (Harris et
al. 1974, cited in Andres et al. 1999). The resynthesis of PCr during recovery appears to be
biphasic, expressing both a fast and a slow component (Harris et al. 1974, cited in Andres et al.
1999). The half-time of the fast component in this study was between 21-22 seconds, while the
slow component was more than 170 seconds, with the PCr levels resynthesizing faster after the
dynamic exercise.
This PCr hydrolysis buffers, at least in part, muscle ATP content during physical exercise
in both type I and type II muscle fibers. Nevertheless, after 10-30 seconds of maximal exercise,
the PCr hydrolysis mediated diminution of muscle PCr is higher in type II than in type I muscle
fibers (Karatzaferi et al. 2001, cited in Mesa et al. 2002). Since ATP turnover rates occur in
muscle up to 10-15 mmol/kg/sec and the PCr content is limited (70-90 mmol/kg dm), the relative
importance of PCr hydrolysis as a source of ATP regeneration falls off dramatically as the
exercise duration lasts beyond a few seconds (Terjung et al. 2000, cited in Mesa et al. 2002).
In periods of muscle inactivity, less ATP is needed by muscles (Mesa et al. 2002). In
these situations, CK catalyzes the reversible transfer of the γ-phosphate group of ATP to the
guanidino group of creatine, to yield ADP, PCr and H
. Therefore, the formation of PCr allows
the conversion of ATP to ADP, maintaining the substrate for new phosphorylation reactions.
Because of the high cytosolic CK activity in these muscles, the CK reaction remains in a near-
equilibrium state, keeps muscle ADP and ATP contents almost constant (over several seconds),
and thus ‘buffers’ the cytosolic phosphorylation potential that seems to be crucial for the
adequate functioning of a variety of cellular ATPases (Wyss and Daouk 2000).
Creatine and Recent Genomics
Recent advances in laboratory techniques and the surge of interest in genomics have
benefited creatine researchers. It has been hypothesized that, if creatine itself causes muscular
adaptations; perhaps, these changes occur at the molecular level (Rawson and Persky 2007).

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Creatine supplementation (6g/day for 12 weeks) plus resistance training results in a
significantly greater increase in fat free mass (4%), muscle volume (21.9%), strength (65%),
myofibrillar protein (58%), Type I (33%), Type IIa (31%), and Type IIx (36%) myosin heavy
chain mRNA expression and Type I (17%) and Type IIx (16%) myosin heavy chain protein
expression than resistance training alone (Willoughby and Rosene 2001,cited in Rawson and
Persky 2007). In a subsequent study these researchers demonstrated that creatine
supplementation (6g/day for 12 weeks) plus resistance training increased creatine kinase,
myogenin, and MRF-4 mRNA expression, and myogenin and MRF-4 protein expression
compared with resistance training and placebo ingestion.
Another study conducted by (Olsen et al.2006, cited in Rawson and Persky 2007)
demonstrated that 16 weeks of creatine supplementation, combined with resistance training,
increases the number of satellite cell and myonucleic concentration in healthy males. These
studies indicate that creatine alone, or in combination with resistance training, causes to skeletal
muscle hypertrophy (Rawson and Persky 2007).
Creatine Administration as an Ergogenic Aid
(Rawson and Volek 2003) reported that creatine supplementation and concurrent
resistance training result in an 8% greater increase in strength and an increase in muscular
endurance by 12%. It could be hypothesized that chronic creatine supplementation does not
directly affect skeletal muscle but could simply enhance the ability to train harder, via increased
basa muscle phosphocreatine and glycogen, and faster phosphocreatine resynthesis. In this
manner, creatine supplementation acts as a training aid, by allowing athletes to train at higher
intensities and volume over time.
Creatine supplementation protocols involve a loading phase and a maintenance phase.
The most common used creatine loading protocol is to ingest a daily total of 20-30 g of creatine,
usually creatine monohydrate, in four equal doses of 5-7 g dissolved in about 250 ml of fluid,
over the course of the day, for a period of 5 to 7 days (Williams et al. 1999). Creatine
supplementation can also be done based on body weight. Here the recommended loading dose is
0.3 g/kg body mass per day for a period of 5 to 6 days. Following the creatine loading phase,

10. Creatine as an Ergogenic Aid
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recommended maintenance dosages are about 2-5 g of creatine per day (Hultman et al. 1996,
cited in Williams et al. 1999).
Reports of improved performance and weight gain along with increase in strength and
size after creatine ingestion dates back to the early 1900s, and after a hundred years of study,
creatine remains one of the most popular and effective ergogenic aid available in the market. A
world wide phenomenon, it is used for recreational purposes but more importantly in the world
of athletics, and strength and conditioning. The question to be asked is, to what extent does
creatine enhance anaerobic and aerobic performance?
Creatine supplementation and High-Intensity Anaerobic Exercise
Several studies have supported the notion that creatine supplementation works as an
ergogenic aid in activities that require the use of PCr as an energy source and that rely heavily on
the rapid resynthesis rate of ATP during recovery. The types of exercise that would benefit from
PCr resynthesis would be of short duration, high intensity, and intermittent in nature. Studies
examining this use of creatine often use weight or power lifting protocols and / or non-weight
bearing high intensity cycling protocols with short rest periods between bouts. Faster sprint times
and increase in strength, power output, total work, and peak torque were found in several studies
using repeated bouts after only 5-7 days of creatine supplementation (Andres et al. 1999).
Creatine supplementation of 20 g/day for 5 days increases the maximal accumulated
oxygen deficit by increasing TCr and PCr levels. This effect has been seen to persist for at least 1
week after treatment (Jacobs et al. 1997, cited in Andres et al. 1999). Furthermore, creatine
supplementation has been shown to lessen the accumulation of hypoxanthine and ammonia
(markers of adenine nucleotide degradation) following a brief maximal exercise, indicating an
enhanced ability to supply ATP upon demand (Greenhaff 1993, cited in Andres et al. 1999).
Changes in lactate concentration with high-intensity exercise due to creatine supplementation
have been inconsistent, either decreasing or having no change (Soderlund et al. 1992, cited in
Andres et al. 1999).
In a classical study, (Sipila et al. 1981, cited in Mesa et al. 2002) seven patients ingested
daily 1.5g of creatine for one year. The patients increased body mass by about 10% and several

11. Creatine as an Ergogenic Aid
11
individuals improved their strength. One of the seven patients, who was an active runner,
improved his 100m mark by above 10%, reducing it from 17 seconds to 15 seconds. By contrast,
there are several studies that do not show any ergogenic effect on high-intensity exercise after
creatine supplementation. A study which tested the effect of oral creatine monohydrate
supplementation on running velocity, results proved that there was no increase in running
velocity with creatine supplementation (Redondo et al. 1996, cited in Mesa et al. 2002).
Another study proved to have no acute effects of short-term creatine supplementation on
muscle properties and sprint performances (Deutekom et al. 2000, cited in Mesa et al. 2002). In
these studies, there is a possibility that, muscle TCr content did not increase in excess of
20mmol/kg dm. Based on his most recent work Greenhaff strongly believes that it is necessary to
increase muscle TCr concentration by close to 20 mmol/kg dm to see any kind of ergogenic
benefits in exercise performance (Greenhaff 1996, cited in Williams et al. 1999). This may be
because subjects who increase muscle TCr by 20 mmol/kg dm may also increase the rate of PCr
resynthesis during the recovery period (Greenhaff et al. 1994, cited in Mesa et al. 2002).
It is clear that subjects vary in the amount of creatine accumulation during
supplementation; furthermore the magnitude of improvement in exercise performance following
creatine supplementation is significantly associated with the extent of muscle creatine
accumulation during supplementation. These findings give us some light as to why some
individuals do not show any ergogenic benefit with creatine supplementation (Greenhaff 1996,
cited in Mesa et al. 2002).
However, it is well known that muscle PCr content is increased after creatine
supplementation. If PCr is increased 10-20% after creatine supplementation, the energy supply
will be increased by 5-10% and 2.5-5%, for the 30- and 6-second sprints, respectively (Terjung
et al. 2000, cited in Mesa et al. 2002). Thus, creatine supplementation may be of potential benefit
in energy provision during short-term high-intensity exercise, this theory is currently accepted
and it has been advocated as an explanation for the success of some sprinters (Williams and
Branch 1998, cited in Mesa et al. 2002).
Creatine supplementation and Aerobic Exercise

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Phosphocreatine is not considered a primary energy substrate during endurance exercise.
However, some studies have shown that PCr levels still decrease during high-intensity aerobic
activity, but it does not decrease to the extent as during high-intensity exercise (Andres et al.
1999). Other researchers have shown that there is no effect of creatine ingestion on oxygen
uptake, respiratory gas exchange, and blood lactate concentrations during and after submaximal
treadmill exercise in physically active males (Stroud et al. 1994, cited in Andres et al. 1999).
Such research is consistent with PCr not being a limiting factor for this type of exercise (Andres
et al. 1999).
The potential benefits of Cr in endurance exercises is not conclusive, there has been
extensive studies done on the ergogenic benefits of short term and anaerobic performance, and
most research concludes with positive ergogenic benefits of Cr supplementation. On the other
hand the potential positive ergogenic effects that Cr might have on endurance performance have
been addressed in only a few papers. In a study conducted by Jones et al. (2002), they
investigated the effects of Cr loading on oxygen extraction (VO 2 ) kinetics during submaximal
exercise. Five subjects received Cr (20g/day for 5 days followed by 5 g/day maintenance dose)
while four subjects served as controls. Following all testing conditions, 35-50 days later the five
subjects initially supplemented with Cr now served as controls and the initial four subjects were
now supplemented with Cr. The results drawn from paired t-tests revealed that there were no
significant differences between groups for the VO 2 kinetic response during the moderated
exercise protocol and that Cr had no ergogenic effect.
Similar results were obtained by Syrotuik et al. (2001), by examining the effect of Cr
supplementation (0.3 g/kg, ingested in four equal proportions throughout the day, for 5 days,
then a maintenance phase of 0.03 g/kg for 5 weeks) on training volume for male rowers. The
initial 5 day loading period of Cr did not improve repeated interval rowing performance, 2000m
rowing times, or any strength measures. Following an additional 5 weeks of Cr supplementation,
still no differences were noted between the two groups relative to any of the performance
parameters.
In contrast to the two previous studies, Sanz and Marco (2000) investigated the effects of
Cr supplementation on VO 2 and performance during alternating bouts of exercise at different

13. Creatine as an Ergogenic Aid
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intensities. Fourteen males subjects were randomly assigned to either a Cr group (n=7; 20 g/day
for 5 days) or a placebo group (n=7). Cycling tests were carried out at intensities equal to 30%
and 90% of peak power until exhaustion. After a standardized warm up, the subjects then cycled
for a total of five, three minute stages alternating 30% and 90% of peak power output. After
which, blood samples were taken at four separate time points i.e. at rest, just before the end of
each cycling load, at exhaustion, and at five minutes post exercise. The results showed that there
was a greater VO 2 for the Cr group and a lower blood ammonia concentration. Plasma uric acid
was also found to be lower for the Cr group at the end of the exercise and five minutes post-
exercise. From an endurance performance standpoint, the Cr group increased their time to
exhaustion from 29.9 ± 3.8 minutes, to 36.5 ± 5.7 minutes, while there were no changes seen in
the placebo group. This study showed that Cr supplementation was able to increase the total
amount of work that could be performed during alternating bouts of different intensity exercise
by effecting oxygen utilization and enhancing oxidative phosphorylation at these varying
intensities.
Astorino et.al. (2005) studied the effect of creatine serum supplementation and its effect
on running performance. The subjects ingested Runners Advantage (RA) creatine serum, to test
the ergogenic properties of RA, then, cross country runners completed baseline testing (BASE),
an outdoor 5,000 meter run followed by treadmill VO 2 max testing on the same day. Subjects
were then tested after ingesting 5 ml of RA (n=13) containing 2.5 g of Cr or placebo (n=11).
Heart rate (HR), rating of perceived exertion (RPE), and run time were recorded. The group with
the RA recorded 56.48 ± 8.93 ml/kg/min, which was higher than the BASE score of 54.07 ±
9.36 ml/kg/min, yet the magnitude of the increase was within the coefficient of variation of VO 2
max. No effect of RA on maximal HR was exhibited, yet VO max2 and duration of incremental
exercise were significantly higher versus BASE, however VO max2 was similar in the placebo
group (58.85 ± 6.67 ml/kg/min) and BASE (57.28 ±7.22 ml/kg/min). Therefore, with RA
(creatine serum) ingestion, the 5,000 meter time was unchanged, and RPE was lower when
compared with the BASE. However this data does not support the ergogenic properties of
creatine supplementation in running performance.

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A possible explanation for the above result can be found from a previous study where
muscle biopsies from the vastus lateralis were obtained from 40 men. After randomized ingestion
of low and high dose, 2.5 and 20 g of Cr monohydrate powder for 5 days, the results
demonstrated a significant increase in muscle PCr, free Cr, and total creatine with Cr
monohydrate ingestion, which suggests Cr retention. In contrast, Cr serum ingestion did not
significantly alter concentrations of these phosphogens and it was found that these products did
not contain creatine. Therefore this data suggests that ingestion of this Cr serum does not
promote Cr retention. Because the ergogenic potential of Cr is dependent on its ability to
enhance muscle PCr and total creatine, the inability of Cr serum to be fully utilized by a muscle
may prevent any ergogenic benefit (Kreider et al. 2003, cited in Astorino et al. 2005).
Ground breaking work by Harris et al. (1993), demonstrated enhanced running
performance with creatine ingestion. In this study, middle distance runners completed 4 X 300 m
and 4 X 1000 m runs before and after ingestion of 30g of Cr monohydrate for 6 days. The results
demonstrated significant reductions in run time for the last 300 and 1,000 m, as well as overall 4
X 1,000 m time. This data suggests that performance of repeated bouts at shorter distances, as
well as interval training, may be enhanced with Cr monohydrate ingestion.
Side Effects of Creatine Supplementation
Creatine supplementation has been used for scientific experimentation for a number of
years and the only side effect that has been documented is an increase in body mass (Andres et
al. 1999). Many studies have used about 25 g/day as the short term creatine supplementation and
in some of these studies, screening of the blood before and after creatine supplementation, have
shown no adverse side effects (Greenhaff 1996, cited in Andres et al. 1999), although there have
been anecdotal reports of gastrointestinal distress for both men and women from creatine
supplementation (Ganesan et al. 1997, cited in Andres et al. 1999). Some athletic trainers have
reported an increase in muscle spasms and muscle pulls which might be related to creatine
supplementation and the increased water content in the muscle cell (Clarkson 1998, cited in
Andres et al. 1999). But overall, it is well tolerated.

15. Creatine as an Ergogenic Aid
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Conclusion
Research shows that dietary creatine supplementation of about 20 grams for about 5-7
days raises the TCr and PCr in skeletal muscle, after which these elevated levels are maintained
with a far less dose of about 3-5 g/day. This elevation of PCr results in an improved capacity to
maintain power output during high-intensity exercise, especially when the exercise is dependent
on the ATP-PCr energy system.
In regard to the ergogenic benefits of creatine in aerobic endurance exercises, few studies
have shown potential ergogenic benefits with creatine supplementation, however most studies
have proved otherwise, nevertheless its benefits are mainly seen in interval training methods,
which encompasses alternate bouts of high and low intensity exercises, and also another research
has shown to alter the rate of perceived exertion (RPE) which could lead to an increased
performance in an aerobic event. Further research needs to be done specially regarding its effects
on aerobic and endurance exercises. Little is known about the correlation of age, gender, sport
and creatine supplementation, this study can give insight into different factors that could cause
an impact in the ergogenic properties. Further research is also needed for specialized
populations, including children, pregnant women, adolescents, and people with diabetes or renal
disease (Andres et al. 1999).
Since most creatine loading studies have used absolute doses of creatine, not basing the
amount supplemented on body weight (Hultman et al. 1996, cited in Williams et al. 1999)
recommends a loading dose of 0.3 g/kg per day for a period of 5-6 days. Because creatine
appears to accumulate primarily in the muscle tissue, some researchers have advocated the
dosage on fat free mass or lean body mass. These are techniques that could provide additional
information and possible develop new theories especially in aerobic endurance and anaerobic
endurance testing.

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