When creatine supplementation is combined with heavy resistance training, muscle insulin like growth factor (IGF-1) concentration has been shown to increase. Burke et al  examined the effects of an 8 week heavy resistance training protocol combined with a 7 day creatine loading protocol (0.25 g/d/kg lean body mass) followed by a 49 day maintenance phase (0.06 g/kg lean mass) in a group of vegetarian and non-vegetarian, novice, resistance trained men and women. Compared to placebo, creatine groups produced greater increments in IGF-1 (78% Vs 55%) and body mass (2.2 Vs 0.6 kg). Additionally, vegetarians within the supplemented group had the largest increase of lean mass compared to non vegetarian (2.4 and 1.9 kg respectively). Changes in lean mass were positively correlated to the modifications in intramuscular total creatine stores which were also correlated with the modified levels of intramuscular IGF-1. The authors suggested that the rise in muscle IGF-1 content in the creatine group could be due to the higher metabolic demand created by a more intensely performed training session. These amplifying effects could be caused by the increased total creatine store in working muscles. Even though vegetarians had a greater increase in high energy phosphate content, the IGF-1 levels were similar to the amount observed in the non vegetarian groups. These findings do not support the observed correlation pattern by which a low essential amino acid content of a typical vegetarian diet should reduce IGF-1 production . According to authors opinions it is possible that the addition of creatine and subsequent increase in total creatine and phosphocreatine storage might have directly or indirectly stimulated production of muscle IGF-I and muscle protein synthesis, leading to an increased muscle hypertrophy .
Creatine is old school and definitely hit a pop culture zenith, but that doesn’t make it out-dated or irrelevant today. Creatine supplementation gets results. For starters, one study from Medicine and Science in Sports and Exercise confirms that creatine supplementation can enhance physical performance, claiming that it “exhibits small but significant physiological and performance changes.”
Different forms of creatine in combination with other sports supplements as well as varying doses and supplementation methodology should continue to be researched in an attempt to understand further application of creatine to increase sports and exercise performance of varying disciplines. It is important to remain impartial when evaluating the safety of creatine ingested as a natural supplement. The available evidence indicates that creatine consumption is safe. This perception of safety cannot be guaranteed especially that of the long term safety of creatine supplementation and the various forms of creatine which are administered to different populations (athletes, sedentary, patient, active, young or elderly) throughout the globe.
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Older women with knee osteoarthritis given supplemental creatine at 20g for five days followed by 5g for the rest of the twelve week trial experienced improvements in stiffness (52% reduction), pain (45%), and physical function (41%) as assessed by WOMAC, despite no improvements in physical power output relative to placebo. This study paired supplementation and placebo with a mild exercise regimen.
The creatine transporter (CrT) is positively regulated by proteins known to be involved in sensing and responding to the cellular energy state, including the mammalian target of rapamycin (mTOR). Upon activation, mTOR stimulates SGK1 and SGK3 to act upon PIKfyve and subsequently PI(3,5)P2 to increase CrT activity. Beyond mTOR, SGK1 also is stimulated by intracellular calcium and a lack of oxygen (ischemia). Because transient ischemia is associated with increased reactive oxygen species (ROS) production after blood flow is restored (reperfusion) it has been hypothesized that muscle contraction may increase creatine uptake through a similar ROS-mediated mechanism.
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It is known that intracellular energy depletion (assessed by a depletion of ATP) stimulates AMPK activity in order to normalize the AMP:ATP ratio, and when activated AMPK (active in states of low cellular energy and colocalizes with creatine kinase in muscle tissue) appears to inhibit creatine kinase via phosphorylation (preserving phosphocreatine stores but attenuating the rate that creatine buffers ATP). While phosphocreatine technically inhibits AMPK, this does not occur in the presence of creatine at a 2:1 ratio. It seems that if the ratio of phosphocreatine:creatine increases (indicative of excess cellular energy status) that AMPK activity is then attenuated, since when a cell is in a high energy status, there is less AMP to directly activate AMPK.