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Skeletal formula of creatine
Ball and stick model of creatine
Systematic IUPAC name
2-[Carbamimidoyl(methyl)amino]acetic acid
Other names
N-Carbamimidoyl-N-methylglycine; Methylguanidoacetic acid
3D model (JSmol)
ECHA InfoCard 100.000.278
EC Number
  • 200-306-6
MeSH Creatine
RTECS number
  • MB7706000
Molar mass 131.135 g·mol−1
Appearance White crystals
Odor Odourless
Melting point 255 °C (491 °F; 528 K)
13.3 g L−1 (at 18 °C)
log P −1.258
Acidity (pKa) 3.429
Basicity (pKb) 10.568
Isoelectric point 8.47
171.1 J K−1 mol−1 (at 23.2 °C)
189.5 J K−1 mol−1
−538.06–−536.30 kJ mol−1
−2.3239–−2.3223 MJ mol−1
C01EB06 (WHO)
3 hours
GHS pictograms GHS07: Harmful
GHS Signal word Warning
H315, H319, H335
P261, P305+351+338
Related compounds
Related alkanoic acids
Related compounds
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is ☑Y☒N ?)
Infobox references

Creatine (/ˈkrətn/ or /ˈkrətɪn/)[1] is an organic compound with the nominal formula (H2N)(HN)CN(CH3)CH2CO2H. This species exists in various modifications (tautomers) in solution. Creatine is found in vertebrates where it facilitates recycling of adenosine triphosphate (ATP), the energy currency of the cell, primarily in muscle and brain tissue. Recycling is achieved by converting adenosine diphosphate (ADP) back to ATP via donation of phosphate groups. Creatine also acts as a buffer.[2]


Creatine was first identified in 1832 when Michel Eugène Chevreul isolated it from the basified water-extract of skeletal muscle. He later named the crystallized precipitate after the Greek word for meat, κρέας (kreas). In 1928, creatine was shown to exist in equilibrium with creatinine.[3] Studies in the 1920s showed that consumption of large amounts of creatine did not result in its excretion. This result pointed to the ability of the body to store creatine, which in turn suggested its use as a dietary supplement.[4]

In 1912, Harvard University researchers Otto Folin and Willey Glover Denis found evidence that ingesting creatine can dramatically boost the creatine content of the muscle.[5][non-primary source needed] In the late 1920s, after finding that the intramuscular stores of creatine can be increased by ingesting creatine in larger than normal amounts, scientists discovered creatine phosphate, and determined that creatine is a key player in the metabolism of skeletal muscle. The substance creatine is naturally formed in vertebrates.[6]

The discovery of phosphocreatine[7][8] was reported in 1927.[9][10][8] In the 1960s, creatine kinase (CK) was shown to phosphorylate ADP using phosphocreatine (PCr) to generate ATP. It follows that ATP, not PCr is directly consumed in muscle contraction. CK uses creatine to "buffer" the ATP/ADP ratio.[11]

While creatine's influence on physical performance has been well documented since the early twentieth century, it came into public view following the 1992 Olympics in Barcelona. An August 7, 1992 article in The Times reported that Linford Christie, the gold medal winner at 100 meters, had used creatine before the Olympics. An article in Bodybuilding Monthly named Sally Gunnell, who was the gold medalist in the 400-meter hurdles, as another creatine user. In addition, The Times also noted that 100 meter hurdler Colin Jackson began taking creatine before the Olympics.[12][13]

Phosphocreatine relays phosphate to ADP.

At the time, low-potency creatine supplements were available in Britain, but creatine supplements designed for strength enhancement were not commercially available until 1993 when a company called Experimental and Applied Sciences (EAS) introduced the compound to the sports nutrition market under the name Phosphagen.[14] Research performed thereafter demonstrated that the consumption of high glycemic carbohydrates in conjunction with creatine increases creatine muscle stores.[15]

The cyclic derivative creatinine exists in equilibrium with its tautomer and with creatine.


Creatine synthesis primarily occurs in the liver and kidneys.[2][16] On average, it is produced endogenously at an estimated rate of about 8.3 mmol or 1 gram per day in young adults.[16][17] Most of the human body's total creatine and phosphocreatine stores are found in skeletal muscle, while the remainder is distributed in the blood, brain, and other tissues.[17][18] Creatine is also obtained through the diet at a rate of about 1 gram per day from an omnivorous diet.[16][18] Some small studies suggest that total muscle creatine is significantly lower in vegetarians than non-vegetarians, as expected since foods of animal origin are the primary source of creatine. However, subjects happened to show the same levels after using supplements.[19]

Creatine is not an essential nutrient[20] as it is naturally produced in the human body from the amino acids glycine and arginine, with an additional requirement for methionine to catalyze the transformation of guanidinoacetate to creatine. In the first step of the biosynthesis these two amino acids are combined by the enzyme arginine:glycine amidinotransferase (AGAT, EC: to form guanidinoacetate, which is then methylated by guanidinoacetate N-methyltransferase (GAMT, EC:, using S-adenosyl methionine as the methyl donor. Creatine itself can be phosphorylated by creatine kinase to form phosphocreatine, which is used as an energy buffer in skeletal muscles and the brain.


Phosphocreatine system[edit]

Creatine, which is synthesized in the liver and kidneys, is transported through the blood and taken up by tissues with high energy demands, such as the brain and skeletal muscle, through an active transport system. The concentration of ATP in skeletal muscle is usually 2–5 mM, which would result in a muscle contraction of only a few seconds.[21] During times of increased energy demands, the phosphagen (or ATP/PCr) system rapidly resynthesizes ATP from ADP with the use of phosphocreatine (PCr) through a reversible reaction catalysed by the enzyme creatine kinase (CK). In skeletal muscle, PCr concentrations may reach 20–35 mM or more. Additionally, in most muscles, the ATP regeneration capacity of CK is very high and is therefore not a limiting factor. Although the cellular concentrations of ATP are small, changes are difficult to detect because ATP is continuously and efficiently replenished from the large pools of PCr and CK.[21] Creatine has the ability to increase muscle stores of PCr, potentially increasing the muscle's ability to resynthesize ATP from ADP to meet increased energy demands.[22][23][24]

Genetic deficiencies[edit]

Genetic deficiencies in the creatine biosynthetic pathway lead to various severe neurological defects.[25] Clinically, there are three distinct disorders of creatine metabolism. Deficiencies in the two synthesis enzymes can cause L-arginine:glycine amidinotransferase deficiency caused by variants in GATM and guanidinoacetate methyltransferase deficiency, caused by variants in GAMT. Both biosynthetic defects are inherited in an autosomal recessive manner. A third defect, creatine transporter defect, is caused by mutations in SLC6A8 and inherited in a X-linked manner. This condition is related to the transport of creatine into the brain.[26]

Supplement health effects[edit]


Creatine use can increase maximum power and performance in high-intensity anaerobic repetitive work (periods of work and rest) by 5 to 15%.[27][28][29] Creatine has no significant effect on aerobic endurance, though it will increase power during short sessions of high-intensity aerobic exercise.[30][31]

A survey of 21,000 college athletes showed that 14% of athletes take creatine supplements to improve performance.[32] Non-athletes report taking creatine supplements to improve appearance.[32]

Creatine is reported to increase cognitive performance,[33] especially in individuals with inadequate intakes in their diet and is claimed by some sources [34][35] to be a nootropic supplement.

Nutritional supplement[edit]

Creatine-monohydrate is suitable for vegetarians and vegans, as the raw materials used for the production of the supplement have no animal origin.[36]

Therapeutic use[edit]

According to a clinical study focusing on people with various muscular dystrophies, using a pure form of creatine monohydrate can be beneficial in rehabilitation after injuries and immobilization.[37]

Medical use[edit]

A clinical study has shown that the intake of pure, high-quality creatine alone, or in combination with exercise, may reduce and delay age-related muscle atrophy, by improving fat-free body mass, muscle strength and endurance, while simultaneously improving bone density.[38]

Adverse effects[edit]

Side effects include:[39][40]

  • Weight gain due to extra water retention to the muscle
  • Potential muscle cramps / strains / pulls
  • Upset stomach
  • Diarrhea
  • Dizziness
  • High blood pressure due to extra water consumption

Use of creatine by healthy adults in normal dosages does not harm kidneys; its effects on the kidney in elderly people and adolescents were not well understood as of 2012.[41] Both the American Academy of Pediatrics and the American College of Sports Medicine recommend that individuals younger than 18 years old not use creatine.[42][43]

One well-documented effect of creatine supplementation is weight gain within the first week of the supplement schedule, likely attributable to greater water retention due to the increased muscle creatine concentrations.[44]

A 2009 systematic review discredited concerns that creatine supplementation could affect hydration status and heat tolerance and lead to muscle cramping and diarrhea.[45][46]


Creatine taken with medications that can harm the kidney can increase the risk of kidney damage:[47]

A National Institutes of Health study suggests that caffeine interacts with creatine to increase the rate of progression of Parkinson's Disease.[48]


A 2011 survey of 33 supplements commercially available in Italy found that over 50% of them exceeded the European Food Safety Authority recommendations in at least one contaminant. The most prevalent of these contaminants was creatinine, a breakdown product of creatine also produced by the body.[49] Creatinine was present in higher concentrations than the European Food Safety Authority recommendations in 44% of the samples. About 15% of the samples had detectable levels of dihydro-1,3,5-triazine or a high dicyandiamide concentration. Heavy metals contamination was not found to be a concern, with only minor levels of mercury being detectable. Two studies reviewed in 2007 found no impurities.[43]

Food safety[edit]

When creatine is mixed with protein and sugar at high temperatures (above 148 °C), the resulting reaction produces carcinogenic heterocyclic amines (HCAs).[50] Such a reaction happens when grilling or pan-frying meat.[51] Creatine content (as a percentage of crude protein) can be used as an indicator of meat quality.[52]


Creatine is a derivative of the guanidinium cation. A cyclic form of creatine, called creatinine, exists in equilibrium with its tautomer and with creatine. Creatine undergoes phosphorylation, by the action of creatine kinase to give phosphocreatine. The phosphate group is attached to an NH center of the creatine. The P-N bond is highly reactive.

Creatine supplements are marketed in ethyl ester, gluconate, monohydrate, and nitrate forms.[41]


This graph shows the mean plasma creatine concentration (measured in μmol/L) over an 8-hour period following ingestion of 4.4 grams of creatine in the form of creatine monohydrate (CrM), tri-creatine citrate (CrC), or creatine pyruvate (CrPyr).[53]

Endogenous serum or plasma creatine concentrations in healthy adults are normally in a range of 2–12 mg/L. A single 5 g (5000 mg) oral dose in healthy adults results in a peak plasma creatine level of approximately 120 mg/L at 1–2 hours post-ingestion. Creatine has a fairly short elimination half-life, averaging just less than 3 hours, so to maintain an elevated plasma level it would be necessary to take small oral doses every 3–6 hours throughout the day. After the "loading dose" period (1–2 weeks, 12–24 g a day), it is no longer necessary to maintain a consistently high serum level of creatine. As with most supplements, each person has their own genetic "preset" amount of creatine they can hold. The rest is eliminated as waste. A typical post-loading dose is 2–5 g daily.[54][55][56]

Creatine supplementation appears to increase the number of myonuclei that satellite cells will 'donate' to damaged muscle fibers, which increases the potential for growth of those fibers. This increase in myonuclei probably stems from creatine's ability to increase levels of the myogenic transcription factor MRF4.[57]



It is ineffective as a treatment for amyotrophic lateral sclerosis.[58]

Muscle disorders[edit]

A meta-analysis found that creatine treatment increased muscle strength in muscular dystrophies, and potentially improved functional performance.[59] Creatine treatment does not appear to improve muscle strength in people who have metabolic myopathies.[59] High doses of creatine lead to increased muscle pain and an impairment in activities of daily living when taken by people who have McArdle disease.[59]

Parkinson's disease[edit]

Creatine's impact on mitochondrial function has led to research on its efficacy and safety for slowing Parkinson's disease. As of 2014, the evidence did not provide a reliable foundation for treatment decisions, due to risk of bias, small sample sizes, and the short duration of trials.[60]

See also[edit]


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    Creatine synthesis (mmol/day)   8.3
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External links[edit]