کراتین که منشاء عمده تولید انرژی در عضلهاست. روزانه تقریبا ۲ درصد کراتین بدن به کراتینین تبدیل میشود. کراتینین محصول کاتابولیک کراتین فسفات است که در انقباض عضله اسکلتی مصرف میشود و سپس با جریان خون به کلیهها میرود.
کراتین در متابولیسم عضلات اهمیت فراوانی دارد، زیرا از طریق سنتز فسفوکراتین؛ ملکول پرانرژی ایحاد مینماید. این ماده طی دومرحله ساخته میشود، ابتدا سنتز گلیکو سیامین میباشد که از واکنش بین گلیسین و آرژنین در کلیه ها؛ مخاط روده؛ لوزالمعده و احتمالا درکبد صورت میگیرد وحاصل آن بعنوان اثر مهاری تولید از طریق فید بک منفی عمل میکند، سپس گلیکوسیامین (گوانیدواستات) به کبد انتقال مییابد وپس از متیله شدن تبدیل به کراتین میشود، و کراتین حاصل وارد خون شده، درتمام بدن خصوصا بافتهای عضلانی گسترش مییابد زیرا بافتهای عضلانی بیشترین مصرف کننده کراتین بوده ومعمولا مقدار کراتین باتوده عضلانی نسبتی متعادل دارد. ودرنهایت کراتینین دراثر دهیدراتاسیون (ازدست دادن آب) کراتین درعضله ایجاد میشود. کراتینین آزاد شده دیگردرمتابولیسم بدن مورد استفاده قرار نمیگیرد و از کلیه دفع میشود.
کراتین مونوهیدرات باعث افزایش سنتز پروتئیین و افزایش احتباس آب و املاح و افزایش جذب آمینو اسیدها در عضلات اسکلتی شده که این اتفاق باعث افزایش قوای جسمانی بدنساز میشود. در ضمن این مکمل به انجام تمرینات سخت کمک کرده و باعث افزایش حجم و توده عضلانی میإشود.
با توجه به عوارض سایر مکملها میتوان گفت که کراتین مونوهیدرات عوارض محسوسی ندارد. اما در هر حال توجه شود مصرف طولانی مدت با افزایش فشار به کبد وکلیهها میتواندایجاد مشکل کند. استفاده مکملها در سنین نوجوانی (قبل از ۱۸ سال) با ایجاد اختلال در وضع طبیعی بدن ، باعث ناهنجاریهای رشدی و آسیب به اندامهای داخلی مانند کلیهها و کبد و دستگاه گوارشی میشود.
For the use of creatine to increase athletic performance, see Creatine supplements.
Not to be confused with creatinine.
Creatine (// or //) is a nitrogenous organic acid that occurs naturally in vertebrates and helps to supply energy to all cells in the body, primarily muscle. This is achieved by increasing the formation of adenosine triphosphate (ATP). Creatine was identified in 1832 when Michel Eugène Chevreul isolated it from the basified water-extract of skeletal muscle. He later named the crystalized precipitate after the Greek word for meat, κρέας (kreas). Early analysis showed that human blood is approximately 1% creatine, and the highest concentrations are found in animal blood, brain (0.14%), muscle (0.50%), and testes (0.18%). The liver and kidney contain approximately 0.01% creatine. Today, creatine content (as a percentage of crude protein) can be used as an indicator of meat quality.
Creatine is a derivative of the guanidinium cation.
Creatine is naturally produced in the human body from amino acids primarily in the kidney and liver. It is transported in the blood for use by muscles. Approximately 95% of the human body's total creatine is located in skeletal muscle.
In humans and animals, approximately half of stored creatine originates from food (about 1 g/day, mainly from meat). A study, involving 18 vegetarians and 24 non-vegetarians, on the effect of creatine in vegetarians showed that total creatine was significantly lower than in non-vegetarians. Since vegetables are not the primary source of creatine, vegetarians can be expected to show lower levels of directly derived muscle creatine. However, the subjects happened to show the same levels after using supplements. Given the fact that creatine can be synthesized from the above mentioned amino acids, protein sources rich in these amino acids can be expected to provide adequate capability of native biosynthesis in the human body.
The enzyme L-arginine:glycine amidinotransferase (AGAT) is a mitochondrial enzyme responsible for catalyzing the first rate-limiting step of creatine biosynthesis, and is primarily expressed in the kidneys and pancreas.
Genetic deficiencies in the creatine biosynthetic pathway lead to various severe neurological defects. Clinically, there are three distinct disorders of creatine metabolism. Deficiencies of the two synthetic enzymes can cause L-arginine:glycine amidinotransferase deficiency and guanidinoacetate methyltransferase deficiency. 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.
The phosphocreatine system
Creatine, synthesized in the liver and kidney, 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. Fortunately, 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 with 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. 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. For a review of the creatine kinase system and the pleiotropic actions of creatine and creatine supplementation see.
Use as a supplement
Main article: Creatine supplements
Creatine has been shown to be an effective antioxidant with supplementation alone and also when associated with resistance training.
Creatine supplements are used by athletes, bodybuilders, wrestlers, sprinters, 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.[unreliable source?] The Mayo Clinic states that creatine has been associated with asthmatic symptoms and warns against consumption by persons with known allergies to creatine.
There are reports of kidney damage with creatine use, such as interstitial nephritis; patients with kidney disease should avoid use of this supplement. In similar manner, liver function may be altered, and caution is advised in those with underlying liver disease, although studies have shown little or no adverse impact on kidney or liver function from oral creatine supplementation. In 2004 the European Food Safety Authority (EFSA) published a record which stated that oral long-term intake of 3g pure creatine per day is risk-free. The reports of damage to the kidneys by creatine supplementation have been scientifically refuted.
Long-term administration of large quantities of creatine is reported to increase the production of formaldehyde, which has the potential to cause serious unwanted side effects. However, this risk is largely theoretical because urinary excretion of formaldehyde, even under heavy creatine supplementation, does not exceed normal limits.
Extensive research has shown that oral creatine supplementation at a rate of five to 20 grams per day appears to be very safe and largely devoid of adverse side-effects, while at the same time effectively improving the physiological response to resistance exercise, increasing the maximal force production of muscles in both men and women.
A meta analysis performed in 2008 found that creatine treatment resulted in no abnormal renal, hepatic, cardiac, or muscle function.
While some research indicates that supplementation with pure creatine is safe, a survey of 33 commercially available supplements 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. 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.
A study in 1999 with males ages 22 (+- 2.9) found that males given creatine and males given placebo showed no drastic difference in body mass with the creatine group having a 2kg change in mass due to higher body water content 
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.
Pregnancy and breastfeeding
There is a lack of scientific information on the effects of creatine supplementation during pregnancy and breastfeeding. Pasteurized cow's milk contains higher levels of creatine than human milk.
Treatment of diseases
Creatine has been demonstrated to cause modest increases in strength in people with a variety of neuromuscular disorders. Creatine supplementation has been, and continues to be, investigated as a possible therapeutic approach for the treatment of muscular, neuromuscular, neurological and neurodegenerative diseases (arthritis, congestive heart failure, Parkinson's disease, disuse atrophy, gyrate atrophy, McArdle's disease, Huntington's disease, miscellaneous neuromuscular diseases, mitochondrial diseases, muscular dystrophy, and neuroprotection), and depression.
A study demonstrated that creatine is twice as effective as the prescription drug riluzole in extending the lives of mice with the degenerative neural disease amyotrophic lateral sclerosis (ALS, or Lou Gehrig's disease). The neuroprotective effects of creatine in the mouse model of ALS may be due either to an increased availability of energy to injured nerve cells or to a blocking of the chemical pathway that leads to cell death. A similarly promising result has been obtained in prolonging the life of transgenic mice affected by Huntington's disease. Creatine treatment lessened brain atrophy and the formation of intranuclear inclusions, attenuated reductions in striatal N-acetylaspartate, and delayed the development of hyperglycemia.
Treatment of muscle disorders
A meta analysis found that creatine treatment increased muscle strength in muscular dystrophies, and potentially improved functional performance. It has also been implicated in decreasing mutagenesis in DNA
Improved cognitive ability
A placebo-controlled double-blind experiment found that a group of subjects composed of vegetarians and vegans who took 5 grams of creatine per day for six weeks showed a significant improvement on two separate tests of fluid intelligence, Raven's Progressive Matrices, and the backward digit span test from the WAIS. The treatment group was able to repeat longer sequences of numbers from memory and had higher overall IQ scores than the control group. The researchers concluded that "supplementation with creatine significantly increased intelligence compared with placebo." A subsequent study found that creatine supplements improved cognitive ability in the elderly. A study on young adults (0.03 g/kg/day for six weeks, e.g., 2 g/day for a 70-kilogram (150 lb) individual) failed to find any improvements.