How To Take Creatine

Creatine Practical Guide.

Creatine: A practical guide evolved from the thousands of questions asked by professional and amateur athletes from around the globe. Learn How To Most Effectively Combine Exercise, Nutrition And Smart Creatine Use For Explosive Muscle Growth And Improved Overall Health. Here is just a small sampling of the many questions addressed by this e-book How long can I keep creatine on the shelf? Will I lose muscle after I stop supplementing? Not all creatine brands recommend the same amount. What gives? Is mixing creatine with protein powder a bad idea? Why do so many creatine brands contain so much dextrose? Is loading really necessary? Im currently taking Accutane for nodular acne. Is it safe for me to supplement? Will creatine stunt my growth? Im training twice as much these days and Im still not making any gains! Why? If creatine isnt a steroid, then how come it gave me a positive doping result? Will creatine shrink my package?! Continue reading...

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The Diagnostic Use of Isoenzymes

For example, creatine kinase (CK) occurs in different forms in different cells. An elevated serum level of CK-1 indicates a breakdown of skeletal muscle and is one of the signs of muscular dystrophy. An elevated CK-2 level indicates heart disease, because this isoenzyme comes only from cardiac muscle. There are five isoenzymes of lactate dehydrogenase (LDH). High serum levels of LDH-1 may indicate a tumor of the ovaries or testes, while LDH-5 may indicate liver disease or muscular dystrophy. Different isoenzymes of phosphatase in the blood may indicate bone or prostate disease.

General Suppression of Reaction Rates

The fundamental basis of all biologic and chemical processes is molecular activity and mobility, which are governed by thermal energy. This means that as temperature is lowered molecular motion is slowed.15 The removal of heat from a system slows down both physical and chemical processes in proportion to the loss of heat and therefore to the fall in temperature. Physical phenomena such as osmotic pressure depend solely on the rate of molecular motion so that the decrease in the rate of the process is proportional to the fractional change in absolute temperature. Many chemical reactions, however, depend upon an energy of activation, which is the minimum energy required for molecules to react. This results in a special relationship between the rate of reaction and temperature described originally by Arrhenius and outlined below (see15). Since the processes of deterioration associated with ischemia and anoxia are mediated by chemical reactions, it has proved well founded to attempt to...

Glucose Uptake And Energy Metabolism

Endoneurial glucose, fructose, sorbitol, and myo-inositol were measured in sciatic nerve and L5 DRG. ATP, creatine phosphate, and lactate were measured in sciatic nerve and superior cervical ganglion. a-Lipoic acid had no significant effect on either energy metabolism or polyol pathway of normal nerves. In contrast, it significantly increased glucose, fructose, and sorbitol but paradoxically increased, rather than reduced, endoneurial myo-inositol. a-Lipoic acid prevented the reduction in superior cervical ganglion creatine phosphate. We conclude that glucose uptake is reduced in EDN and that this deficit is dose-dependently reversed by a-lipoic acid, a change associated with an improvement in peripheral nerve function, possibly by improving energy metabolism in ischemic nerve and by increasing endoneurial myo-inositol.

What agents may be used for maintenance anesthesia

Neuromuscular blocking agents with a benzylisoquinolinium nucleus such as d-tubocurarine, atracurium, and mivacurium release histamine from mast cells on injection. They also may bind directly to muscarinic receptors on ganglia, nerve endings, and airway smooth muscle. Both mechanisms theoretically may increase airway resistance. Relaxants with an aminosteroid nucleus such as pancuronium and vecuronium continue to be used safely in asthmatic patients. In patients with bronchospasm neuromuscular blocking agents improve chest wall compliance, but smooth muscle airway tone and lung compliance remain the same. Prolonged use of muscle relaxants in ventilated asthmatic patients is associated with increases in creatine kinase and clinically significant myopathy.

Targeting Nonhepatic Hmgcoa Reductase

Statins are now widely used in clinical practice and have proven to be well-tolerated and safe. As detailed above, the widespread use of statins has led to observations of anecdotal benefit unrelated to their inhibition of hepatic HMG-CoA reductase. The principal adverse effects are recognised to be liver and muscle toxicity 137 . Elevated hepatic transaminase has been observed in 0.5-2 of cases and is dose-dependent being reversible with a reduction in dose. Myopathy is recognised to be the major significant adverse effect for statins. This is frequently a non-specific, mild myalgia comprising muscle aches and cramps without elevation of creatine kinase. Rarely, statin treatment can lead to a myositis with muscle soreness and weakness associated with an elevated creatine kinase. This can lead to rhadomyolysis with myoglobinuria and acute renal necrosis. This side effect, although very rare, resulted in the voluntary withdrawal of cerivastatin in 2001. Understanding the mechanism of...

Eother motor diseases

Hypermetabolism of skeletal muscle leads to hydrolysis of adenosine triphosphate, glycolysis, glycogenolysis, uncoupled oxidative phosphorylation, increase in oxygen consumption, and heat production. The earliest symptom is often unexplained tachycardia. The sine qua non of MH is an unexplained rise in end-tidal CO2. Patients may demonstrate peculiar rigidity, even after nondepolarizing relaxants have been administered. If untreated, the patient develops numerous metabolic abnormalities, including metabolic acidosis, respiratory acidosis, hypoxemia, hyperthermia, rhabdomyolysis, hyperkalemia, hypercalcemia, hyperphosphatemia, elevations in creatine kinase, myoglobinuria, acute renal failure, cardiac dysrhythmias, and disseminated intravascular coagulation. Death is common if the problem is unrecognized and untreated. Data from the North American Malignant Hyperthermia Registry (NAMHR) have determined a rate of cardiac arrest of 2.7 and of death 1.4 . Interestingy, although the malady...

Transmethylation Reactions

A second cluster of methyl group acceptors are involved with energy metabolism (Fig. 1). Trimethyllysine is used to make carnitine which transports fatty acids into mitochondria for the production of ATP and acetyl CoA via beta oxidation. Creatine can accept phosphate from ATP when it is present in excess and provides a reservoir of high energy phosphate in muscle cells to maintain activity when energy demands exceed the amount of ATP that can be provided by the glucose in muscle. This maintains muscle activity as cellular metabolism adjusts to draw on glycogen for additional ATP and mobilize glucose from the liver. Epinephrine is a hormone that enables the cell to respond to stress by increasing glycogen utilization. In addition, it modulates the flow of fatty acids to and from cells (Montgomery et al., 1990).

Physics of Magnetic Resonance Spectroscopy

Magnetic resonance spectroscopy (MRS) actually predates MRI, and early efforts focused on characterizing uniform samples of substances in test tubes. As with conventional imaging, most MRS work in humans is focused on proton signals, but it is possible to get spectroscopic signals from other elements. In the brain, the primary signal-producing molecules on proton spectroscopy are N-acetyl aspartate (NAA), choline, creatine, myoinositol, glutamine and glutamate, lactate as well as some lipids and amino acids. Figure 4 shows both a sample spectrum of normal white matter and a demyelinating lesion. The NAA peak is located at 2.02 parts per million (ppm) shift (the standard way that MRS spectra are described) and is a marker for healthy neurons 36 . However, its exact role in the neuron is not known. Choline is located at 3.2 ppm and is primarily found in membranes. It reflects more white matter than gray matter and tends to reflect myelin concentration, although many other diseases can...

Prospects For Future Research

In MRS, most studies have focused on changes in NAA, a neuronal marker that is expected to decrease in degenerative disorders, and on choline and creatine, which are considered indicators of cell membranes turnover and energy supply in the tissue, respectively. Since gliosis is often prominent in various degenerative disorders, short TE techniques (such as STEAM with TE 34 ms) should be used more widely in order to evaluate myoinositol, a putative marker of gliosis.

Magnetic Resonance Spectroscopy

MRS provides chemical information on tissue metabolites (3,4). The molecules that can be studied by MRS in human brain tissue are hydrogen 1 ( H) and phosphorus 31 (31P). Magnetic resonance sensitivity is far greater for protons than it is for phosphorus (3). Therefore, most commercial MR scanners are capable of only proton MRS. Spectra are usually obtained from localized brain regions. The brain region is defined on a single slice by placing a small voxel, on the order of 1 or 2 cm2, in the area of interest. The compounds that can be observed in proton spectra are primarily identified by their frequency (i.e., their position in the spectrum), expressed as the shift in frequency in pars per million (ppm) relative to a standard. A normal spectrum shows peaks from N-acetyl groups, especially N-acetylaspartate (NAA) at 2.0 ppm, creatine (Cr), and phosphocreatine at 3.0 ppm, and cho-line-containing phospholipids (Ch) at 3.2 ppm (3). An additional peak at 1.3 ppm arises from the methyl...

Role Of Acetaldehydeprotein Adducts And Free Radicals

The increase in malondialdehyde-acetaldehyde protein adducts supports previous suggestions that alcohol induces cardiac lipid peroxidation 83,84 concomitant with endogenous cardiac-derived acetaldehyde formation, possibly via alcohol dehydrogenase (ADH) or cytochrome P450 actions. However, although the activity of cardiac alcohol dehydrogenase is low, catalase may also generate acetaldehyde 85-88 , The importance of these studies relates to the observation that malondialdehyde-acetaldehyde adducts are cytotoxic, inducing the release ofTNF-alpha and up-regulating ICAM-1 in endothelial cells in vitro 89 , Reactive oxygen free radical species may play a prominent role in alcohol-induced heart muscle damage. Cardiac tissue from chronic alcohol misusers shows increased 'agepigments indicative of damage by reactive oxygen species 90 , Involvement of reactive oxygen species damage is also implicated by studies showing that in alcohol-fed rats, the resulting shift in fatty acid profile is...

Roles in Biological Processes

PARs are single-use receptors that rely on proteolytic cleavage for activation. Trypsin and thrombin cleave PAR to expose the tethered ligand domain (SLIGRL-NH2 or SLIGKV-NH2) causing receptor activation 77 . Cleavage is dependent on the presence of associated proteins that anchor the proteases to the plasma membrane promoting localization on the cell surface. For example, tissue factor is needed for coagulation Factor Viia to cleave PAR2. Following injury, cell proliferation and differentiation increase after serine protease exposure. Cell synthesis is activated through the p38 mitogen-activated protein kinase (MAPK) activation, protein kinase A and B (PKA, PKB) signaling 78, 80 . Signal transduction occurs through phospholipase C for MAPK and PKB and adenyl cyclase for PKA. Additionally, the intracellular C-terminus of PAR interacts with creatine kinase activating Rho kinase.

Multiple System Atrophy

Olivopontocerebellar Atrophy Pathology

A few proton MR spectroscopy (MRS) studies have demonstrated that N-acetylaspartate (NAA) and choline (Cho) were reduced in the lentiform nucleus of MSA patients (32,33). The NAA creatine (Cr) ratio was particularly decreased in MSA-P patients, probably reflecting putaminal neuronal loss (32). MRS, however, has not been widely used to help differentiate patients with MSA from patients with PD.

Nonclassical Estrogen Signaling

WAY-169916 (42) has been described as the first representative of a new class of pathway selective-ER ligands for the treatment of rheumatoid arthritis (RA) 73 . This series of 4-(indazole-3-yl)phenols was discovered by screening for in vitro activity using an assay developed in HAECT-1 cells transfected with human ERa and a reporter gene NF-kB-luciferase 74 . WAY-169916 blocks the transcription of NF-kB induced by IL-1 p with an IC50 of 93 nM and 93 inhibition compared to E2. Since 42 is active only when ER is coexpressed with NF-kB-luc, the inhibition is ER dependent. WAY-169916 has demonstrated inhibition of NF-kB target genes in vivo, but does not increase uterine wet weight after five days of dosing in female mice. This result indicates it does not inhibit transcriptional pathways classically associated with ERa in uterine tissues. It is orally active in an adjuvant-induced model of RA 75 and in models of IBS 74 . It also demonstrated activity after SC administration...

Magnetic Resonance Imaging and Spectroscopy Evidence 321 Atrophy

For example, the ratio of NAA to creatine was reduced by 20 in the cortex of the wobbler mutant mouse concomitant with increased immunohistochemical evidence of axonal injury 193 . Likewise, the ratio of NAA to choline was reduced by 30 in the guinea pig brain during acute EAE induced by whole spinal cord homogenate, but this change preceded the development of significant neurologic deficits 38 . In contrast, a significant accumulation of swollen axons correlated with suppression of absolute NAA values was observed in monkeys 4 weeks after induction of EAE with MBP 209 . Unfortunately, no detailed analysis of NAA spectroscopy has been correlated to APP accumulation, spheroid formation, or other markers of axon injury in either the TMEV model of MS or in an EAE model with progressive axonal injury and neurologic deficit. sections while NAA as measured by HPLC was reduced by more than 50 as compared to non-lesion white matter in MS patients and by more than 60 as compared to healthy...

What is the significance of masseter muscle rigidity

After surgery patients should be admitted and followed for signs of MH (tachycardia, blood pressure lability, hyperthermia which is usually a late symptom , urine myoglobin). If creatine phosphokinase (CPK) is 20,000, the patient should be considered to have MH. If the CPK is

Skeletal Muscle Disorders Duchenne Muscular Dystrophy

A characteristic biochemical feature of DMD is an elevated level of crea-tine phosphokinase (CPK) in the serum, ranging from 10 to 10,000 times normal levels. CPK is a muscle enzyme responsible for releasing the energy stored in creatine phosphate during muscle contraction. The presence of large amounts of CPK in the blood system reflects muscle degeneration but does not necessarily represent the severity of the damage to the muscles.

Conclusions and Future Directions

26 McLaurin MD, Apple FS, Voss EM, Herzog CA, Sharkey SW. Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease Evidence of cardiac troponin T expression in skeletal muscle. Clin Chem 1997 43 976-982. 55 McLaurin MD, Apple FS, Voss EM, Herzog Ca, Sharkey SW. Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease Evidence of cardiac troponin T expression in skeletal muscle. Clin Chem 1997 43 976-982. 79 Adams JE, Abendschein DR, Jaffe AS. Biochemical markers of myocardial injury. Is MB creatine kinase the choice for the 1990s Circulation 1994 88 750-763. 90 Adams JE, Schechtman KB, Landt Y, Ladenson JH, Jaffe AS. Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I. Clin Chem 1994 40 1291-1295. 92 Jernberg T, Lindahl B, James S, et al. Comparison between strategies using creatine kinase-MB (mass), myoglobin and...


We found that acute moderate alcohol exposure directly protected cardiac myocytes from ischemia-induced damage 32 , Under normoxic conditions over 3 hours of incubation, 10 of cells demonstrated osmotic fragility, indicating that isolated myocytes remained healthy. Under simulated ischemic conditions over 3 hours of incubation, 75 of myocytes demonstrated osmotic fragility. Ten minute exposure of myocytes to 50 mM ethanol before, but not during, simulated ischemia reduced cell damage by 35 . Exposure of cardiac myocytes tojust 10 mM ethanol throughout simulated ischemia reduced cell damage by 56 . Furthermore, 20 minute Langendorff perfusion of isolated rat heart with 10 mM ethanol reduced creatine kinase release after 45 minutes of ischemia and 30 minutes of reperfusion by 70 . Therefore, brief exposure to physiological levels of ethanol induced powerful

Skeletal Muscle

Deficiencies of either alpha-tocopherol or selenium also occur naturally leading to, for example, white muscle disease which is seen in farm animals or horses where a combination of inadequate soil selenium is combined with poor dietary ATC 217-226 , Concomitant changes in this disorder include reduced plasma glutathione peroxidase activities and increased serum creatine kinase activities 221,227 ,


HC-Ad vectors encoding the dystrophin cDNA were developed by several groups 5, 8, 14 . Two groups incorporated a muscle-specific muscle creatine kinase (MCK) promoter 5, 8 , allowing demonstration of striated muscle-specific expression of dystrophin from the vector. Direct intramuscular injection of these dystrophin-encoding HC-Ad vectors in the dystrophin-deficient mdx mouse model resulted in expression of recombinant dystrophin that properly localized to the muscle sarcolemma 7, 14 . Furthermore, dystrophin-associated proteins, which are lost in DMD and mdx muscle secondary to the primary absence of dystrophin, were restored in muscle fibers expressing HC-Ad vector-delivered dystrophin 54 . The prevention of dystrophic morphologic changes in muscle of mdx mice receiving an intramuscular injection of dystrophin-encoding HC-Ad vector was a second indicator of normal function provided by the recombinant dystrophin that was expressed from the HC-Ad vector 7 .

Laboratory Markers

A number of biochemical markers of brain injury have been studied, including cerebrospinal fluid creatine kinase BB and serum levels of the cytoplasmic enzyme neuron-specific enolase and the astroglial protein S100 (32,33). These proteins are assayed in the blood or cerebrospinal fluid, and high levels at specific times after CA suggest extensive brain injury and correlate with poor outcome. Tirschwell et al. reported the finding that cerebrospinal fluid creatine kinase BB level of 205 U L had 100 specificity and positive predictive value for predicting poor outcome but a sensitivity of only 48 (32). However, combining median nerve SSEP studies with cerebrospinal fluid creatine kinase BB levels maintained 100 specificity but increased sensitivity to 78 (34). Some concern was noted, however, in performing lumbar puncture after CA in patients who may be developing cerebral edema.

Immediate Energy

Creatine kinase (CREE-uh-tin KY-nase) obtains Pj groups from an energy-storage molecule, creatine phosphate (CP), and donates them to ADP to make ATP. This is a fast-acting system that helps to maintain the ATP level while other ATP-generating mechanisms are being activated.


Binding of telbivudine to human plasma proteins is low (3.3 ). Telbivudine is not a substrate or inhibitor of the CYP450 isozymes, and it is minimally metabolized. Renal excretion in a bi-exponential manner is the predominant route of elimination, with approximately 42 of the dose unchanged. The elimination half-life of telbivudine was between 40 and 49 h. The clinical efficacy of telbivudine was evaluated in 1367 HBV patients in a phase III study, which included a lamivudine arm. The primary efficacy endpoint was therapeutic response at one year, a composite endpoint coupling viral suppression (serum HBV DNA suppression

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