creatine final (1)

The Effects of Creatine as an Ergogenic Aid

Enoch Samraj

KINE 5320 –Advanced Exercise Physiology

Dr. Paul McDonough

December 6, 2011

Creatine as an Ergogenic Aid

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

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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

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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

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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

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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).

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,

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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,

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

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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

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

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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

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 (VO2

) 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 VO2

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,

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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 VO2

and performance during alternating bouts of exercise at different

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 VO2

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 VO2

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

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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 VO2

max. No effect of RA on maximal HR was exhibited, yet VO2 max

and duration of incremental

exercise were significantly higher versus BASE, however VO2 max

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.

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

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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.

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).

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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.

References

Andres LP, Sacheck J, Tapia ST. 1999. A review of Creatine supplementation: side

effects and improvements in athletic performance.Nutr Clin Care.2(2): 73-81.

Astrorino TA, Marrocco AC, Gross SM, Johnson DL, Brazil CM, Icenhower ME,

Kneessi RJ. 2005. Is running performance enhanced with creatine serum ingestion? J. Nat

Streng Cond Assoc. 19 (4): 730-734.

Bamben MG, Lamont HS. 2005. Creatine supplementation and exercise performance.

Sports Med. 35(2): 107-125.

Bloch K, Schoenheimer R.1941.The biological precursors of creatine. J Biol Chem.

138:167-194.

Harris RC, Viru M, Greenhaff PL, Hultman E.1993. The effect of oral Cr

supplementation on running performance during maximal short-term exercise in man. J.

Physiol. 467:74.

Jones AM, Carter H, Pringle JSM. 2002. Effect of creatine supplementation on oxygen

uptake kinetics during submaximal exercise. J Appl Physiol. 92: 2571-2577.

Mesa JLM, Ruiz JR, Gonzalez MM, Sainz AG, Garzon MJC. 2002. Oral creatine

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Rawson ES, Persky AM. 2007. Mechanisms of muscular adaptations to creatine

supplementation. Sports Med. 8(2): 43-53

Rico SJ, Marco MTM. 2000. Creatine enhances oxygen uptake and performance during

alternating intensity exercise. Med Sci Sport & Exerc.32:379-385.

Syrotuik DG, Game AB, Gillies EM.2001. Effects of creatine monohydrate

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creatine final (1)

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