It’s time to switch to less boring language. I am that renowned Moris Silber, MD, PhD, research Professor that you might have been heard much of in the recent past, with respect to obtaining knowledge of how to quickly pump up your muscle safe and legally, just by proper nutrition, max-power brief workout and a absolutely unique “RUGENIX” formulation. I want now to address you directly - the broad health and fitness conscious audience. It’s time to unveil to my avid friends my lifelong Bio-Medical expertise in-the-field Elite Sports Medicine, which hugely more complicated and has much broader application, compared to its kid-sister orthopedic sports medicine. I plan doing this by meeting regularly with you on this webinar educational site of www.Rugenix.com. If there is a will, let’s find the way. Yet, in turn, I would request few (not many!) commitments on your parts:
• stay strongly motivated,
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• stay open-minded to new ideas for improvement health, physique, and psyche
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It is still largely accepted, that the main rout of Cr biosynthesis in humans involves formation of guanidinoacetae in the kidney, its transport through the blood and its methylation to Cr in the liver, though all the precurces of guanidinoacetate are formed in other tissues, for instance, a complete urea cycle operates actively only in liver, the main site of Arginine (Arg) biosynthesis is, however, the, kidney, Citrulline is synthesized in the liver or small intestine then taken up by the kidney to be converted into Arg.
An important practical aspect of Cr biosynthesis to add is that methyl groups (Methyonine and Choline) on a normal equilibrated diet, also Folic acid and/or vit B12 and B6 deficiency may substantially impair the Cr biosynthesis.
Although the pathway of Cr metabolism in humans seem simple, the situation is complicated by the fact that most tissues lack several enzymes required, thus necessitating transport of intermediates between the tissues through the blood to allow the whole cascade of reactions to proceed. This, on the other hand, gives us the perfect opportunity to monitor these events by available hands on biochemical tools in laboratory and in the field tests. With the assumption of an average content in muscle of 30mM of total Cr and a quantitative uptake of the compound by the digestive tract, this loss could be compensated by ingestion of 500gof raw meat per day. Because Crn is a very poor substrate of the Cr transporter, because no other specific saturable uptake mechanism exists for Crn, and because Crn, most likely due to its nonionic nature, is membrane permeable, Crn constantly diffuses out of the tissues into the blood and is excreted by the kidneys into the urine. Because the rate of non-enzymatic formation of Crn from Cr is nearly constant, and because near to 90% of the total bodily Cr is to be found in muscle tissue, 24-h urinary Crn excretion is frequently used as a rough measure of total muscle mass. However, this approach sufferers various limitations. Twenty to twenty five percent of the in vivo conversion of CP into Crn may proceed via phosphoril-creatinine (CrnP) as an intermediate.
The first tangible puzzle reflects Creatine (Cr) and Creatine Kinase System (CK). Very recently, a series of new discoveries have been made that are bound to have distinguished implications for bioenergetics, physiology, human pathology, and clinical diagnosis and that suggest that deregulation of the Creatine Kinase system is associated with most of it. Disturbances of the CK system have been observed in muscle, brain, cardiac, and renal diseases as well as in cancer. On the other hand, Cr by itself and Cr analogs such as Cyclocreatine were found to have antitumor, antiviral, and antidiabetic effects and to protect tissues from hypoxic, ischemic, neurodegenerative, or muscle damage. This said, one perceives it rational that ever since the discovery of Phosphorylcreatine (CP) in 1927 and particularly of its essential CK enzyme in 1934, research efforts focused mainly on biochemical, physiological, and pathological aspects of the CK reaction itself and on its involvement in “high-energy phosphate” metabolism of cells and tissues with high-energy demands. In contrast, Cr (from Greek kreas, flesh) metabolism of itself has attracted considerably less attention until 1972. Nevertheless, oral Cr ingestion has independently been introduced as ergogenic (quick energy supplier) aid in sports.
However, first Cr was used in sports as an overly ergogenic aid to the actively contracting striated muscle, mainly fast-twitch white myofibrils. At the same time independent observations has been reported on the simaltenuous increase under similar experimental condition in muscle protein. Then, a new era in Cr science has boldly declared itself.
The following important amino acids L-arginine, Glicine, and S-adenosil-L-methionine to yield guanidinoacetic acid, the immediate precursor of Cr after its methylation, are involved in biosynthesis of Cr in the body. The most part (up to 94%) of Cr is found in the muscular tissue. Yet muscle has virtually no Cr-synthesizing capacity, Cr has to be taken up from the blood against a large concentration gradient by a saturable, Na+ - and Cl-- -dependent Cr transporter that spans the plasma membrane. The daily demand for Cr is met either by intestinal absorption of dietary Cr or by de novo Cr biosynthesis. The first step of Cr biosynthesis probably occurs mainly in the kidney, whereas the liver is likely to be the principal organ accomplishing the subsequent methylation of guanidinoacetic acid to Cr. It is worthy to note that the detailed contribution of different organs (pancreas, kidney, liver, testicls) to total Cr synthesis is still rather unclear. The muscular Cr and CP are later nonenzymatically converted at an almost steady rate (approximately 2% of total Cr per day) to Crn, wich diffuses out of the cells and is excreted by the kidneys into the urine. The highest levels of Cr andCP are found in skeletal muscle, heart, spermatozoa, and photoreceptor cells of the retina. Intermediate levels are found in brain, brown adipose tissue, intestine, seminal vesicles, seminal vesicle fluid, endothelial cells, and macrophages. Resting type 2a and 2b skeletal muscle fibers (white fast twitch) contain around 33mM CP and 7mM C, whereas type 1 fibers (red slow) comprise about 16mM CP and 7mM Cr. Nevertheless, the concentration of total Cr seems to parallel the muscle glycolitic capacity in both muscle types. In serum and erythrocytes, as opposite extremes, Cr amounts to only 25-100uM and 270-400uM, respectively. An almost constant fraction of the body Cr (1.1% a day) and CP (2.6% a day) is converted nonenzymatically into Crn, giving a overall conversion rate for the total Cr pool (Cr and CP) of approximately 1.7% a day. Consequently, in a 70-kg man containing about 120g of total Cr, roughly 2g/day are converted into Crn, and have to be replaced by Cr from the diet or from de novo biosynthesis.
Beginning today we will be featuring a once a week post written my Dr. Silber regarding the world of sports performance and nutrition, specifically his product Rugenix. Dr Silber has been a pioneer in the world of sports performance and has offered to share some of this knowledge with our followers.
The next post will contain the first article of the series titled Metabolic Benchmarks. It intends to provide you with as much as possible up to date information reflecting the Metabolic Benchmarks of Maximal Power Output, and how to use it for your strictly individual unlimited merit. This first article or two may seem a bit dry, but if you stick with us the articles will continue to become easier to understand and apply to your lives.