There is a genetic condition known as gyrate atrophy of the choroid and retina, which is associated with a high level of Ornithine in the blood and a relative decrease in Arginine, which causes a relative creatine deficiency due to L-arginine being required to make creatine and because high ornithine can suppress creatine synthesis (AGAT) in the glial cells of the retina. This condition can be attenuated by either reducting ornithine in the diet or by supplementing creatine, which is, in this instance, therapeutic.
It is prudent to note that creatine supplementation has been shown to reduce the body’s endogenous production of creatine, however levels return to normal after a brief period of time when supplementation ceases [1,6]. Despite this creatine supplementation has not been studied/supplemented with for a relatively long period. Due to this, long term effects are unknown, therefore safety cannot be guaranteed. Whilst the long term effects of creatine supplementation remain unclear, no definitive certainty of either a negative or a positive effect upon the body has been determined for many health professionals and national agencies [19,78]. For example the French Sanitary Agency has banned the buying of creatine due to the unproven allegation that a potential effect of creatine supplementation could be that of mutagenicity and carcinogenicity from the production of heterocyclic amines . Long term and epidemiological data should continue to be produced and collected to determine the safety of creatine in all healthy individuals under all conditions .
It is equally important, if not more so, to ensure that you supply your body with more protein than it is breaking down each day. Your body uses protein for many things daily, and when you are working out, your body may start to break down proteins to provide extra energy. But your body also requires proteins to create new muscle cells and repair damaged ones. Many bodybuilding supplements contain large amounts of protein to ensure that your body has plenty for all required processes. Jump to Our 10 Best Bodybuilding Supplement List
I'm 6'1" 175 pounds 27 years old. I would like to increase my general muscle mass and reduce my stomach fat. I would consider myself and ectomorph (hard gainer) as I have never really developed much muscle while I've always been very active in sports and periodic weight training. Over the past year I lost about 30 pounds (nearly all fat) by reducing my caloric intake effectively and regular whole body exercises. I was on my way to my ideal body composition until I became a bike courier. I've been a bike messenger for 9 months and recently my stomach fat has started to return. I'm riding 50+ miles each weekday riding for 9 hours a day. How many calories should I be eating? I've tried everywhere between 2400-3,500 cal/day. Is it possible for me to be eating too few calories while still accumulating stomach fat? Is it realistic for me to be able to maintain or even build muscle mass in this scenario? Please help, thanks.
After supplementation of creatine monohydrate (loading phase, followed by 19 weeks maintenance), creatine precursors are decreased by up to 50% (loading) or 30% (maintenance), which suggests a decrease in endogenous creatine synthesis during supplementation. This appears to occur through creatine’s own positive feedback and suppression of the l-arginine:glycine amidinotransferase enzyme, the rate-limiting step in creatine synthesis, as levels of intermediates before this stage are typically elevated by up to 75%.
But muscle can’t turn into fat, just like mud can’t turn into gold. If you quit lifting, your muscles mass will decrease over time because there’s no training to stimulate your body to keep it. And your body-fat level will increase if you don’t start eating less (since you burn less). The obvious solution when you stop lifting is to also stop eating so much.
In regard to practical interventions, concurrent glycogen loading has been noted to increase creatine stores by 37-46% regardless of whether the tissue was exercised prior to loading phase. It is important to note, however, that creatine levels in response to the creatine loading protocol were compared in one glycogen-depleted leg to the contralateral control leg, which was not exercised. This does not rule out a possible systemic exercise-driven increase in creatine uptake, and the increase in creatine noted above was larger than typically seen with a loading protocol (usually in the 20-25% range). Consistent with an exercise-effect, others have reported that exercise itself increases creatine uptake into muscle, reporting 68% greater creatine uptake in an exercised limb, relative to 14% without exercise.
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.