Creatine helps create essential adenosine triphosphate (ATP). This is the energy source of muscle contractions. By upping your levels, you can increase the amount of energy available to your muscles, boosting your performance. Because your muscle strength and size increases when you add weight and reps, improving your performance can be a game changer in terms of increasing your muscle mass. If you’re able to lift longer and harder, your muscles will grow. Creatine is certainly a winner among muscle building supplements.
ZMA: This supplement is a combination of zinc, magnesium and vitamin B-6. Some research shows that this combination can help raise testosterone levels. In the trial, subjects took a daily dose of ZMA (which included 30 mg zinc monomethionine, 450 mg magnesium aspartate and 10.5 mg vitamin B-6) at night during 7 weeks. Other hormones like IGF also increased, while the stress hormone, cortisol was reduced, creating an overall more favorable hormone profile. Not surprisingly, muscle performance also improved. (n) This paper is surrounding in controversy, however, because one of the scientists involved also holds the trademark for ZMA, and the research is company-funded.
The pancreas is one of the extrahepatic (beyond the liver) organs that can synthesize creatine, alongside the kidneys. Freshly prepared pancreatic β-cells will normally secrete insulin in response to glucose stimulation, and it appears that phosphocreatine is required for this effect, since phosphocreatine is increased in response to glucose alongside an increase of the ADP:ATP ratio. They appear to close ATP sensitive potassium channels (KATP channels), causing a release of insulin secondary to calcium release. Both phosphocreatine and ADP are implicated, but it seems that despite the channel being sensitive to ATP, the concentration of ATP in a pancreatic cell (3-5mM) is already above the activation threshold (in the micromolar range) and thus a further increase would not have an appreciable effect.
The main storage area of creatine in the human body is the skeletal (contractile) muscle, which holds true for other animals. Therefore, consumption of skeletal muscle (meat products) is the main human dietary source of creatine. Since vegetarians and vegans lack the main source of dietary creatine intake, which has been estimated to supply half of the daily requirements of creatine in normal people, both vegetarians and vegans have been reported to have lower levels of creatine. This also applies to other meat-exclusive nutrients, such as L-Carnitine.
Myotonic Dystrophy type I (DM1) is an inhereted muscular disorder caused by an expanded CTG repeat in the DMPK gene on chromosome 19q13.3 (genetic cause of the disorder) resulting in muscular degeneration and myotonia. The related myopathy, Myotonic Dystrophy type II (DM2) which is also known as proximal myotonic myopathy (PROMM) is due to a CCTG repeat on 3q, and is less affected by myotonia and more by muscular pain and weakness. There is no cure for either because they are genetic disorders, so current therapies are aimed at reducing side-effects. Therapies include modafinil for the somnolence and perhaps creatine for the reduction in strength and functionality.
In regard to the blood brain barrier (BBB), which is a tightly woven mesh of non-fenestrated microcapillary endothelial cells (MCECs) that prevents passive diffusion of many water-soluble or large compounds into the brain, creatine can be taken into the brain via the SLC6A8 transporter. In contrast, the creatine precursor (guanidinoacetate, or GAA) only appears to enter this transporter during creatine deficiency. More creatine is taken up than effluxed, and more GAA is effluxed rather than taken up, suggesting that creatine utilization in the brain from blood-borne sources is the major source of neural creatine. However, “capable of passage” differs from “unregulated passage” and creatine appears to have tightly regulated entry into the brain in vivo. After injecting rats with a large dose of creatine, creatine levels increased and plateaued at 70uM above baseline levels. These baseline levels are about 10mM, so this equates to an 0.7% increase when superloaded. These kinetics may be a reason for the relative lack of neural effects of creatine supplementation in creatine sufficient populations.
One pilot study using 150mg/kg creatine monohydrate for a five day loading phase followed by maintenance (60mg/kg) for the remainder of the five weeks noted that supplementation was associated with fewer muscle symptoms and complaints alongside improved muscular function, yet a later trial trying to replicate the obsevations using 150mg/kg daily for five weeks noted the opposite, that creatine supplementation exacerbated symptoms.