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?! Read more here...

Creatine Practical Guide Summary


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Creatine is one of the most common nutritional supplements employed for possible ergogenic benefits. The Metzl et al71 survey of high school students reported use by as many as 44 of high school senior athletes, which parallels estimates of collegiate use. Creatine has become generally accepted to provide benefit in short, maximally anaerobic events, likely through enhancement of adenosine triphosphate regeneration.72 There is also some evidence suggesting a possible direct effect of creatine on muscle development through increased expression of mRNA and growth factors specific to muscle.73 Whether by direct effect or through increased capacity for resistance training, creatine has been linked with increases in muscle mass, including by direct measurements such as ultrasonography.74 As to the effects of creatine on actual strength and sports performance, the supplement has had mixed results at best. Some authors have demonstrated improvement in short-duration events like repeated...

Biochemical pathways of ATP generation

The store of ATP is limited and must therefore be continuously replenished. Regeneration of ATP occurs through aerobic and anaerobic processes by which energy-rich chemical substances (carbohydrates, fat and phosphocreatine) are transformed into compounds with less stored energy (lactate, H2O, CO2 and creatine). This is achieved by sequences of chemical reactions by which part of the change in free energy is used for the synthesis of ATP through a reversal of reaction (1). The ATP-ADP cycle constitutes a basic feature of energy metabolism in all cells and is an intermediate between energy-utilizing and energy-consuming processes.

Evaluation Guidelines Table31

Routine blood tests to assess for metabolic disorders are required for all patients with behavioral abnormalities. Sodium, glucose, creatine, blood urea nitrogen, calcium, liver function tests, and thyroid hormone levels are mandatory. Depending on the situation, other blood studies such as serum ammonia, ceruloplasmin, porphobilinogen, drug levels, prolactin and other hormones, toxicology screens, vasculitic studies, and HIV and syphilis serologic tests may be appropriate. Gastric lavage is useful in patients with suspected drug ingestion and possibly when one is looking for blood as a source of hepatic encephalopathy. Genetic testing can be done when Huntington's disease is considered likely. Because of the putative biological nature of many depressions, certain research-related tests have been developed, including the dexamethasone suppression test, measurement of urinary

Hypercholesterolemia Statins

Hypercholesterolemia contributes significantly to overall cardiovascular morbidity and mortality. Statins are the number one class of anticholesterol medications. They are well known for side effects of gastrointestinal disturbance, headache, and rash. For athletes, myalgias and, rarely, rhabdomyolysis are possible complications of significant import. Baseline creatine kinase levels prior to onset of statin therapy may be useful in case these complications arise.15 Most changes in creatine kinase levels with statin use and or exercise are asymptomatic. Rhabdomyolysis

Clinical Implications

Perioperative MI, whether clinically apparent or silent, is associated with increased mortality in both the short and long term. Most perioperative infarctions are asymptomatic and detected only by serial ECG and myocardial enzyme monitoring. Likewise, in-hospital mortality is uncommon in the setting of perioperative MI, with hospital survival rates typically greater than 90 , similar to rates for MI in the nonoperative setting. However, in a manner analogous to clinically silent MI detected after PCI, even smaller infarcts detected after noncardiac surgery are associated with striking increases in medium- to late-term mortality. In one series of 229 patients who had routine serial myocardial enzyme determinations performed over a 3-day period after major vascular surgery, elevated serum troponin levels were detected in 12 of the patients. Whereas increased troponin levels were not associated with a greater likelihood of in-hospital mortality, by 6 months those patients with...

Adverse Events after Percutaneous Coronary Intervention

Has been widely debated, several studies using data from large-scale clinical trials demonstrate an excess risk of mortality with creatine kinase MB fraction (CK-MB) elevations of greater than three times the upper limit of normal. However, other studies have observed an excess in mortality only at higher degrees of myonecrosis, such as more than five times the upper limit of normal or when there is the development of Q waves. In an analysis of patients enrolled in the Randomized Evaluation in PCI Linking Angio-max to reduced Clinical Events 2 (REPLACE-2) study, a CK-MB elevation greater than or equal to three times the upper limit of normal was associated with a 3.5-fold excess risk of mortality at 12 months and accounted for 13.2 of all mortality seen by 12 months (Fig. 10-4).4 This forms the threshold definition for periprocedural (within 48 hours) MI within many PCI trials of adjunctive pharmacotherapy. In contrast, weighing the clinical significance of bleeding events reductions...

Comparative milk genomics

The folate requirements of lactating dairy cows have been extensively reviewed by Girard et al., (2005). Lactation increases the demands both for methylated compounds (synthesis of milk choline, creatine, creatinine and carnitine) and for methionine to support milk protein synthesis (Xue and Snoswell, 1985 Girard and Matte, 2005). The high demand for folate during lactation is demonstrated by the observation that total serum folates decrease by 40 across the lactation period in dairy cows (Girard et al, 1989).

Intensive Statin Therapy For Acute Coronary Syndrome

Simvastatin group experienced the primary end point, compared with 14.4 in the simvastatin only group (40 mg 80 mg), reflecting a hazard ratio of 0.89 (P .14). Myopathy (i.e., creatine kinase 10 times the upper limits of normal with muscle symptoms) occurred in 9 patients (0.4 ) receiving 80 mg of sim-vastatin, in no patients receiving lower doses of simvastatin, and in 1 patient receiving placebo (P .02).

Neuroimaging Studies and Macroscopic Appearance

Phous foci of calcium in approximately 50 of cases. MRI of central neurocytomas reveals a well-circumscribed, intraven-tricular mass that is heterogeneous but overall isointense, commonly with a lobulated pattern on Tl-weighted sequences with heterogeneously moderate to marked vascular enhancement by gadolinium. T2-weighted sequences have a variable signal intensity ranging from low to hyperintense, compared with cerebral cortex.48,55,92 Neuroimaging of biologic parameters of these tumors is limited. Proton magnetic resonance spec-troscopy (H-MRS) and thallium-201 SPECT (TI-SPECT) of several tumors demonstrated high choline peaks, compared with -acetyl aspartate and creatine phosphate, and significant thallium uptake in all tumors irrespective of MIB-1 immuno-histochemical proliferative indices.48 The high choline in the tumors is confirmed by high-pressure liquid chromatography (HPLC) in frozen tissue.99 FDG uptake with PET is typically low, but increased FDG uptake has been detected...

Magnetic Resonance Spectroscopy

Magnetic resonance imaging is based on the nuclear magnetic resonance (NMR) signal from water protons. Magnetic resonance spectroscopy (MRS) uses high field magnets to detect intracellular NMR signals from carbon-13, phosphorus-31, sodium-23, and fluorine-19.49 This biochemical assay, which compares regions of interest, has a spatial resolution of 1-2 cm3 and requires rather long imaging times. It measures compounds found in gray and white matter. The more interesting ones for neuro-rehabilitation include N-acetylaspartate (NAA), found only in neurons and axons, as well as choline, creatine, and myo-inositol. Choline compounds are involved in membrane metabolism and often increase in brain tumors. In-ositol is asociated with glial cells and glial swelling. Lactate is associated with ischemia. Creatine levels are usually stable, so the other compounds may be described as a ratio of the creatine peak.

Percutaneous Coronary Intervention versus Reoperation

The PCI cohort, 30 underwent PCI of the left main coronary artery, 38 had at least one graft treated, 77 received at least one stent, and 7.7 experienced a non-Q MI (creatine kinase-myocardial band isoenzyme CK-MB level four times the upper limit of normal). At 5 years, unadjusted survival was 79.5 for CABG and 75.3 for PCI (P .008). At 5 years, after adjustment for propensity score, PCI was associated with a hazard ratio for death of 1.47 (P .09). The interpretation of excess mortality with PCI was hampered by the marked difference in baseline characteristics and small number of patients who could be matched. The only randomized comparison of PCI and CABG in patients after bypass surgery was reported by Morrison and colleagues,208 who randomized 143 patients (67 to PCI and 75 to CABG). At 3 years, the survival rate was approximately 75 , comparable to the 5-year survival rate in the Cleveland Clinic study there was no significant advantage of one procedure over the other.

Saphenous Vein Graft Percutaneous Coronary Intervention

Impact of embolic protection device use on periprocedural myocardial infarction (PMI) in vein graft PCI. Left, The Saphenous Vein Graft Angioplasty Free of Emboli Randomized (SAFER) trial cumulative distribution function curve of peak cardiac enzyme values after assignment to placebo (395 patients), GuardWire (406 patients), and the per-protocol subgroup with technically successful GuardWire use (366 patients). The creatine phosphokinase-myocardial band isoenzyme (CPK-MB) level is represented as multiples of the upper limit of normal. There is a significantly lower incidence of PMI of any size with GuardWire use. Right, The FilterWire EX Randomized Evaluation (FIRE) trial a similar plot for patients randomized to distal protection with the FilterWire EX or to the GuardWire, showing noninferiority of the FilterWire. (Data from Baim DS, Wahr D, George B, et al Randomized trial of a distal embolic protection device during percutaneous intervention of saphenous vein...

Chronic Exertional Compartment Syndrome

Chronic exertional compartment syndrome (CECS) is another cause of athletic lower leg pain. Patients with CECS complain of cramping, burning, or aching lower leg pain with pain or numbness that may radiate to the foot and ankle. The pain is clearly associated with exertion. Pain onset is characteristically at a fixed point in the patient's activity, with progressively increasing pain if the exercise continues and a dramatic reduction in pain within minutes of rest. The pathophysiology of CECS involves elevated intracom-partmental pressure, which causes relative ischemia of the involved muscles and pressure on neurovascular structures. The diagnosis of CECS can be confirmed by compartment pressure testing after exercise demonstrating increased intra-compartmental pressure correlated with symptom reproduction. Patients with CECS should be questioned about the use of nutritional supplements, such as creatine, that may increase muscle water content and overall muscle mass and contribute...

Adverse Cardiac Events

In earlier RCTs of CEA versus medical therapy, MI was not included in the outcomes analysis. However, the importance of MI as a component of the primary composite end point is underscored by the increased risk of death in patients who experience MI in the perioperative period after vascular surgery.43,44 For this reason, the incidence of MI, as determined by preprocedural and postprocedural electrocardiograms and serial creatine kinase CK CK-MB measurements, has been included in the end point of most high-risk CAS registries and trials. In this patient cohort, the 30-day incidence of MI is the range of 1 to 2.4 .31-33,43,44 More than 80 of these are non-Q-wave in type. There appears to be significant and consistent reduction in MI with CAS versus CEA (2.4 vs. 6.1 P . 04 in the SAPPHIRE trial33). The risk of MI in low-risk patients undergoing CAS is likely to be even lower, a contention that is supported by data from the CAVATAS trial, which reported no cases of MI in the endovascular...

The Dgc And Sarcoglycan Function As A Mechanosignaling Complex

Mand and Campbell 2000 Heydemann et al. 2001). Mice with a targeted deletion of y-sarcoglycan were generated first and revealed that sarcoglycan loss is independent of dystrophin (Hack et al. 1998). Moreover, y-sarcoglycan mutant muscle displayed a similar phenotype to dystrophin mutant muscle, although y-sarcoglycan mutant muscle was more severely affected. The characteristic finding in dystrophin or sarcoglycan mutant muscle is focal degeneration or focal necrosis (Fig. 2) that is characterized in its earliest stages by regional uptake of the vital tracer Evans blue dye (EBD) (Hack et al. 1998). Normal muscle is impermeable to EBD, whereas sarcoglycan mutant muscle readily takes up EBD focally. EBD uptake is also seen in dystrophin mutant muscle where sarcoglycan is secondarily reduced (Matsuda et al. 1995 Straub et al. 1997). The mechanism responsible for membrane permeability defects in sarcoglycan-deficient muscle is not well understood. Electron microscopy of sarcoglycan mutant...

Skeletal Muscle Disease

For gene replacement therapy, the level and tissue specificity of sarcoglycan expression must also be considered (Cordier et al. 2000, 2001). In a transgenic approach, we expressed high levels of Y-sarcoglycan using the muscle creatine kinase (MCK) promoter (Zhu et al. 2001). The MCK promoter drives expression in both skeletal and cardiac muscle, although it typically leads to greater levels of expression in skeletal muscle (Gossett et al. 1989 Johnson et al. 1989). High-level overexpression of Y-sarcoglycan in a wild-type background resulted in severe muscle wasting and weakness. Interestingly, the

Anticomplement Therapy In

Of C1s-INH-248 interaction with the early components of the lectin pathway remains unclear. Administration of C1s-INH-248 prior to reperfusion caused a significant reduction in infarct size-associated cardiac damage as measured by cardiac creatine kinase (CK) activity and a reduction in neutrophil infiltration into the infarct zone (96). CGS 32359, a C5a receptor antagonist, is a recombinant form of C5a which binds to the C5 receptor without activating subsequent inflammatory functions of neutrophils(97). In a porcine model of MI R, animals treated prior to reperfusion with CGS 32359 demonstrated a significant reduction in infarct size and PMN infiltration (98). To date, there are no clinical data available on the efficacy or safety of CGS 32359 or the other complement inhibitors addressed in this paragraph.

Table 552 Neuroleptic Neurotoxicity

The principal features of NMS are hyperthermia, muscle rigidity, autonomic dysfunction, and mental status changes. Laboratory findings include elevated creatine kinase, polymorphonuclear leukocytosis, elevated aldolase, alkaline phosphatase, lactic dehydrogenase (LDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), hypocalcemia, hypomagnesemia, low iron, proteinuria, and myoglobinuria. y Approximately 40 percent of patients with NMS develop medical complications that may be life threatening. NMS is a clinical diagnosis based on the presence of the proper historical setting and the characteristic constellation of signs. Disorders with similar features include malignant hyperthermia, heat stroke induced by neuroleptics, lethal catatonia, other drug reactions, and vascular,

Mixed Connective Tissue Disease

The diagnosis of MCTD is made in patients with symptoms and signs of more than one connective tissue disease and the characteristic serologic markers. CNS manifestations are evaluated with MRI, which may demonstrate signs of vascular disease. In patients with seizures, EEG shows focal or generalized slowing and often epileptiform activity. y CSF in patients with headaches or aseptic meningitis may be normal or show a lymphocytic pleocytosis or increased protein. Elevations of serum creatine phosphokinase occur in about half of those with myopathic symptoms. Electromyographic changes may confirm the presence of myopathy, and biopsy may show inflammatory myositis.y

Forearm Exercise Testing

Although muscle contraction is ATP-consuming, the ATP content of a contracting muscle changes little during a sustained contraction. Interestingly, muscle ATP stores are incapable of sustaining a muscle contraction for more than a single second. Phosphocreatine, a high-energy compound with an intramuscular concentration approximately four- to five-fold that of ATP, permits rapid ATP regeneration through the rephosphorylation of adenosine diphosphate (ADP). This reaction is catalyzed by creatine kinase, an enzyme found in large quantities in skeletal muscle tissue. Nevertheless, this anaerobic energy source is depleted in less than a minute, and even when combined, these two sources of readily available energy are incapable of maintaining high-intensity exercise. For this reason, skeletal muscle tissue must rely on other energy sources when sustained exertion is necessary.

Evaluation Guidelines Table156

MRI, Magnetic resonance imaging CT, computed tomography EMG, electromyography CSF, cerebrospinal fluid WBC, white blood count RBC, red blood count GABA, gamma aminobutyric acid GAD, glutamic acid decarboxylase DNA, deoxyribonucleic acid NCV, nerve conduction velocity MUAP, motor unit action potential FBS, fasting blood sugar SR, sedimentation rate ANA, antinuclear antibodies SPEP, serum protein electrophoresis eSr, erythrocyte sedimentation rate B12 , vitamin B12 T4 TSH, thyroxine-thyroid-stimulating hormone VDRL, Venereal Disease Research Laboratory CK, creatine kinase IgG, immunoglobulin G N A, not applicable.

Pharmacologic Interventions Statins

Knee Plica Exercises

Although there is some concern about the potential toxicity of statins, their benefits significantly outweigh their risks. Liver toxicity can occur and is defined as an alanine transaminase (ALT) elevation of three times or more the upper limit of normal (ULN) on two occasions at least 1 month apart. The average risk of hepatotoxicity from statin therapy is approximately 1 , but risk increases as a function of increasing doses. Mild elevations in serum transaminase levels early during the course of therapy are relatively common and usually resolve spontaneously. If hepatotoxicity develops, statin therapy should be discontinued until transaminase levels normalize and therapy with a different statin can be initiated. There is no documented evidence that the statins increase risk for liver failure. The most important adverse event associated with statin therapy is rhabdomyolysis, myoglobinuria, and renal failure. The risk for rhabdomyolysis is less than 0.1 . Symptoms of rhabdomyolysis...

Question 3 Were unbiased criteria used to detect the outcome in all patients

A diagnosis of myocardial infarction was made if the following conditions were met creatine kinase or creatine kinase-MB more than twice the upper limit of normal or troponin I or T more than twice the upper limit of normal (if neither creatine kinase or crea-tine kinase-MB were available) or troponin I or T more than three times the upper limit of normal for the same markers within 24 h of percutaneous transluminal coronary angioplasty or troponin I or T more than five times the upper limit of normal for the same markers within 24 h of coronary artery bypass grafting surgery. In addition to these marker criteria, a patient had to have experienced electrocardiographic changes in two or more contiguous leads showing new Q waves (or R waves in V1 or V2), left bundle branch block, or ischaemic ST-T wave changes, or typical clinical presentation consistent with myocardial infarction defined as one of the following cardiac ischaemic-type pain lasting more than 20 min, pulmonary oedema, or...

Neuronal Migration Defects

Type II lissencephaly occurs in a group of disorders associated with congenital muscular dystrophy, often involving the eyes as well. The Walker-Warburg syndrome, the Finnish muscle-eye-brain disease (MEB), and Fukuyama congenital muscular dystrophy (FCMD) are entities within this group. The Walker-Warburg syndrome (WWS) is the most severe of these, and the syndrome has a high proportion of neonatal lethality. The brain malformation often is complex with hydrocephalus, cerebellar hypoplasia (and occasionally Dandy-Walker malformation), and sometimes an occipital encephalocele associated with the cortical malformation. Clinically, it is characterized by profound hypotonia in the neonatal period due to the combined muscle and CNS involvement. The eyes can be affected in a number of ways, of which retinal dysplasia is the most consistent. Anterior chamber malformations, cataracts, choroidal colobomata, optic nerve hypoplasia, and microphthalmia can occur. Serum creatine kinase levels are...

Posterior Fossa Anomalies

A patient with one of the brainstem syndromes needs to be evaluated in an effort to rule out disorders that may mimic the syndrome (see differential diagnosis), and also to define the extent of the abnormalities and establish the presence of any associated malformations. In patients with Mobius' syndrome, this may require (in addition to a careful neurological and ophthalmological examination) brain stem auditory evoked responses creatine-kinase determination imaging of the brain,

Evaluation of Joint and Other Musculoskeletal Symptoms

Musculoskeletal Scleroderma

Myalgias can be caused by localized trauma or overuse, systemic infection, metabolic disorder, or primary muscle disease. Multiple tender sites in an otherwise healthy patient suggest fibromyalgia. An elevated creatine kinase (CK) level with proximal weakness may be caused by an inflammatory myopathy.

Prognostic Implications of Periprocedural Myocardial Infarction

Top, The Kaplan-Meier curves for 6 months' unadjusted mortality after percutaneous coronary intervention (PCI) for increments of post-PCI creatine kinase-myocardial band isoenzyme (CK-MB). Bottom, Continuous unadjusted relationship between peak CK-MB (as times the upper limit of normal ULN ) and 6 months' mortality. The thin lines represent the 95 confidence intervals. (From Roe MT, Mahaffey KW, Kilaru R, et al Creatine kinase-MB elevation after percutaneous coronary intervention predicts adverse outcomes in patients with acute coronary syndromes. Eur Heart J 2004 25 313-321.)

Spontaneous Cerebellar Astrocytoma

Of children, such as PNET and ependymoma. Therefore histo-logic examination is necessary to establish a definitive diagnosis. Recently, magnetic resonance spectroscopy (MRS) has been used to distinguish pediatric cerebellar tumors based on differential levels of tumor metabolites and macromolecules. Pilocytic astrocytomas demonstrate increased choline N-acetyl-aspartate (Cho NAA) ratios and elevated lactate levels when compared with normal brain but similar to many other tumor types.25,59 In one study, low-grade astrocytomas had higher NAA Cho ratios than PNET but lower ratios than ependymoma, whereas creatine-to-Cho ratios were highest for ependymoma and lowest for PNET.25,59 Other metabolites differentially detected in PNET and astrocytoma in vitro include glutamate, glycine, taurine, and myoinositol. Elevated lactate levels in pilocytic astrocytoma carry no indication of malignancy and may reflect aberrant glucose utilization in these tumors.59 At present, MRS cannot replace tissue...

Positron Emission Tomography or PET Scanning

Will leak from the damaged or dying heart muscle. Some of these enzymes are very specific to the heart and help determine whether a patient is having a heart attack. One of these is called creatine kinase, or CK. Another is called lactate dehydrogenase, or LDH. Troponin is a type of protein that leaks from the damaged heart muscle and can also help diagnose a heart attack.

Kennedy syndrome spinobulbar muscular atrophy SBMA

A rare inherited neurodegenerative disease, Kennedy syndrome or spinobulbar muscular atrophy (SBMA), is characterized by progressive neuromuscular weakness resulting from a loss of motor neurons in the spinal cord and brain stem. The onset of this disease occurs in the third to fifth decades of life and is often preceded by muscular cramps on exertion, tremor of the hands and elevated muscle creatine kinase (Kennedy etal. 1968). The initial description of Kennedy syndrome also contains one case with gynaecomastia. Subsequent reports confirmed the presence of androgen insensitivity in men with SBMA, showing various degrees of gynaecomas-tia, testicular atrophy, disorders of spermatogenesis, elevated serum gonadotropins and diabetes mellitus (Arbizu et al. 1983 Shimada et al. 1995). An alteration in the AR was regarded as a pathophysiological sign for SBMA and the expansion of a CAG tract encoding a polyglutamine (polyQ) stretch within the N-terminal region of the receptor was...

Kennedy syndrome a pathological expansion of the AR gene CAG repeats

X-linked spinobulbar muscular atrophy (X-SBMA) or Kennedy syndrome, is a rare inherited neurodegenerative disease characterized by progressive neuromuscular weakness being caused by a loss of motor neurons in the brain stem and spinal cord. Disease onset developing in the third to fifth decade of life is likely to be preceded by muscular cramps on exertion, tremor of the hands and elevated muscle creatine kinase. The initial description of one of the individuals affected with Kennedy syndrome also includes gynaecomastia, a hypoandrogenic symptom (Kennedy et al. 1968). Subsequent reports emphasized the presence of symptoms indicating the development of androgen insensitivity in men with X-SBMA exhibiting varying degrees of gynaecomastia, testicular atrophy, disorders of spermatogenesis, elevated serum gonadotropins and also diabetes mellitus (e.g. Arbizu et al. 1983). Thus, the AR was regarded as candidate gene for X-SBMA and the expansion of the polyglutamine repeat within the...

Effects of Heat Stress on the Cell Kinetics of the Germ Cells

Heat Stress Fertility Decline

Nonenzymatic antioxidant molecules include a-tocopherol (vitamin E), b-carotene (vitamin A), ascorbate (vitamin C), glutathione, estrogens, creatine (related to carotene) flavonoids (aromatic oxygen heterocyclic compounds widely distributed in higher plants), resveratrol (a botanical antioxidant), metallothionein (cadmium-binding protein involved in heavy metal detoxification), taurine (an aminosulfonic acid) and its precursors, and other thiols such as nonstructural polyunsaturated lipids and melatonin. Oral administration of vitamin E reduced the level of testicular-free radicals in a rat experimental model of varicocele 119 , and the effectiveness of anti-oxidants to treat infertile men has been previously demonstrated in randomized trials 120 . Therefore, antioxidants can be effectively applied to treat heat-inducible oxidative stress in humans.

Clinical Assessment and Diagnosis

Routine laboratory testing of patients with AHF includes electrolytes and blood glucose, as well as serum creatinine and blood urea nitrogen to assess renal function. CBC count is measured to determine if anemia or infection is present. Creatine kinase and or troponin concentrations are used to diagnose ischemia, and hepatic transaminases are measured to assess hepatic congestion. Thyroid function tests are measured to assess hyperthyroidism or hypothyroidism as causes of AHF. A urinalysis is obtained in patients with an unknown history of renal disease to rule out nephrotic syndrome. Lastly, a toxicology screen is obtained in patients in whom use of illicit drugs is suspected.

Emergency Department Treatment and Disposition

Patients with major burns must be assessed for airway protection and adequate circulation. Clinicians should also remember to cover the burned areas with a clean, dry sheet administer aggressive pain control to patients and aggressively address fluid resuscitation. The Parkland formula is commonly used to estimate fluid requirements. The patient's weight in kilograms is multiplied by the percent BSA involved this number is multiplied by 4 mL of lactated Ringers solution. Half of this amount is given during the first 8 hours and the remaining amount is given over the next 16 hours of resuscitation. It is recommended to keep urine output approximately 0.5 to 1.0 mL kg h. In order to monitor for effects of cell breakdown, urinalysis, creatine kinase, and an EKG should be obtained. Circumferential burns of the extremities may compromise circulation. If distal pulses are decreased, an escharotomy should be considered to prevent compartment syndrome.


Beta-hydroxy-beta-methylbutyrate (HMB) is a relatively new product marketed as an anti-catabolic compound. Use of HMB has been associated with increased lean muscle mass and decreased CPK levels after exercise, but the mechanism of these effects is unclear.72 In a separate study, brief use of HMB did not prevent common effects of exercise such as muscle soreness or swelling.88 Other studies have shown HMB does not have an androgenic effect nor does it have a significant impact beyond resistance training alone on strength and body composition among athletes.89-91 Used either alone or with creatine, HMB has not shown ergogenic effects on either aerobic or anaerobic exercise, although one isolated study did demonstrate an increased time to peak lactate production with its use.92,93 Again, no clear mechanism exists to explain this effect. No major risks have been associated with HMB use. In fact, HMB may impart favorable cardiovascular effects via lipid metabolism.94 In summary, no clear...

Muscle fatigue and metabolism

The cause of muscle fatigue (i.e. inability to maintain a defined exercise intensity) is considered to be multifactorial. The classic hypothesis is that muscle fatigue is caused by failure of the energetic processes to generate ATP at a sufficient rate. The evidence for this hypothesis is that interventions which increase the power (i.e. aerobic training, hyperoxia, blood doping) or capacity (i.e. CHO loading, creatine supplementation, glucose supplementation) of the energetic processes result in increased performance and delayed onset of fatigue. Similarly, factors that impair the energetic processes (i.e. depletion of muscle glycogen, intracellular acidosis, hypoxic conditions, reduced muscle blood flow) have a negative influence on performance. The evidence is, however, circumstantial and a direct cause and effect relationship remains to be established.

Legal substances or procedures

One of the most debated substances lately has been creatine (Cr), and its performance-enhancing effects. Research indicates that Cr supplementation (initially 20 g day followed by 3-4 g day) can increase muscle PCr content in some individuals. Exercise performance involving short periods of extremely powerful activity can be enhanced, especially during repeated bouts of activity 15 , whereas performance in aerobic exercise is not influenced. Furthermore, it has been demonstrated that Cr results in increased improvement of muscle strength with strength training but the mechanism behind this has not been discovered 16 . So far there are no documented gastrointestinal, renal or muscle side-effects associated with Cr intake.

Influence of muscle mass on power and capacity of wholebody energy production

The power of anaerobic energy production appears to be limited by the activities of key enzymes such as myosin ATPase, creatine kinase and PFK. On a whole-body level an increased working muscle mass will result in a proportional increase in the total enzyme activities and therefore an increased anaerobic energy production ability. However, aerobic power is largely limited by cardiac output and will not therefore be influenced by the working muscle mass. The capacity of both aerobic and anaerobic energy production is limited by intrinsic muscular factors such as amount of glycogen, amount of PCr, and the volume available to distribute inhibitory metabolic end-products. An increased working muscle mass will increase the total available amount of glycogen and PCr and will therefore increase the amount of energy that can be produced by these processes. An increased working muscle mass, achieved either by training-induced hypertrophy or by increased recruitment of fast-twitch muscle...

Anaerobic processes of ATP generation

Although the aerobic processes dominate during sustained exercise regeneration of ATP can also occur through anaerobic processes. Three different ATP-generating anaerobic processes exist Breakdown of PCr ADP+PCr+H+ ATP + creatine PCr is a high-energy phosphate compound stored in muscle tissue at a concentration three times that of ATP. Creatine kinase (CK) is a highly active enzyme and catalyzes an equilibrium reaction ADP + PCr+H+ ATP + creatine a work rate of 50 of Vo2m PCr is reduced to 79 of the initial level and at a work rate of 80 of Vo2m PCr is reduced to 32 of the initial level 3 . During recovery from exercise ADP decreases and the reaction is shifted back to the left. The half-time for PCr resynthesis is about 30 s and after 2-4 min recovery PCr is restored to the initial level. An overshoot in PCr above the pre-exercise level has been observed in fast-twitch muscle fibers after high-intensity exercise 4 and in slow-twitch fibers after prolonged exercise at moderate...

Acute Coronary Syndromes

Women who present with ACS are older and have higher incidences of diabetes and hypertension compared to men. They also have less severe CAD, with greater absence of critical obstructions and more preserved LV function. In ACS, women were more likely to have elevated C-reactive protein (CRP) and brain natriuretic peptide (BNP), whereas men were more likely to have elevated creatine kinase-MB (CK-MB) and troponin.33

Other Forms of Chorea

Neuroacanthocytosis (NA) is a rare disorder with autosomal dominant, recessive, or even X-linked inheritance and is manifested by chorea, tics, dystonia, parkinsonism, self-mutilatory behavior, amyotrophy, areflexia, elevated creatine phosphokinase (CK), and other symptoms. y One of the most distinguishing features of NA is an eating dysfunction that is due to orolingual dystonia and is manifested by expulsion of food from the mouth by a protruding tongue. Involuntary vocalizations and parkinsonism also occur. Although the mechanism of acanthocyte formation in NA is unknown, abnormal protein to fatty acid ratios and in some cases abnormal erythrocyte surface antigens have been found. It is possible that, as in the periodic ataxias, some of the paroxysmal dyskinesias represent abnormalities of the calcium channel or other channelopathies. Acanthocytes in most patients can be seen in fresh blood smears, but erythrocytes may require incubation in normal saline for 3 to 5 minutes prior to...

Lethal Infantile Mitochondrial Disease or Congenital Lactic Acidosis

Important tests to order include blood levels of amino acids urine levels of organic acids serum and CSF levels of lactate, pyruvate, and ammonia liver and renal function tests, blood creatine kinase (skeletal and cardiac fractions) ultrasound evaluation of the heart neuroimaging of the brain and electroencephalography to document a toxic metabolic encephalopathy.

General Management Goals

Cardiac monitoring is recommended for the first 24 to 48 hours after stroke due to the high frequency of cardiac dysfunction associated with stroke. In approximately 3 percent of cases, concomitant cerebral and myocardial ischemia can occur. A variety of cardiac arrhythmias can occur after ischemic or hemorrhagic stroke and subarachnoid hemorrhage (SAH), including tall P waves, longer or shorter PR and QT intervals, ST segment elevation or depression, peaked or inverted T waves, U waves, sinus bradycardia, wandering atrial pacemaker, paroxysmal atrial pacemaker, nodal bradycardia, AV block, premature atrial or ventricular contractions, atrial fibrillation and flutter, and AV dissociation. These abnormalities have generally been attributed to increased circulating levels of catecholamines. If ischemic ECG changes occur, serial creatine kinase and lactate dehydrogenase isoenzymes are indicated. Ventricular wall motion abnormalities have been demonstrated by echocardiography in patients...

Congenital Myopathies

Creatine kinase levels are normal or only mildly elevated in patients with the congenital myopathies. Neurophysiological studies are useful in excluding the neuropathies and myasthenias. In the congenital myopathies, nerve conduction studies are normal, and the EMG may show only mild, nonspecific myopathic features. Definitive diagnosis of a congenital myopathy rests on the morphological characteristics seen on muscle biopsy. These morphological abnormalities must be present in substantially increased numbers to make the diagnosis. Any of the pathological findings may be nonspecific findings in other neuromuscular disorders. In some cases of congenital myopathy, the muscle biopsy may show only minor nonspecific myopathic features. This may reflect a selectivity of muscle involvement, and when other causes have been excluded, a label of nonspecific congenital myopathy may be applied.

Carnitine Palmitoyl Transferase II Deficiency

Ihere are two presentations the adult muscular form, in which prolonged exercise induces weakness and myoglobinuria, and a severe infantile form, in which nonketotic hypoglycemic coma without dicarboxylicaciduria, seizures, hepatomegaly, cardiomegaly, and cardiac arrhythmia are accompanied by low plasma and tissue levels of carnitine with increase in long-chain acylcarnitines. Ihe classic adult form is autosomal recessive and usually affects males between 15 and 30 years of age. Ihe serum creatine kinase value is normal between episodes, carnitine levels are usually normal in plasma and tissues, and long-term muscle weakness is rare, although lipid storage may be seen on muscle biopsy. Ihe differential diagnosis includes other carnitine cycle disorders. Management involves supportive treatment of the renal failure and measures to remove the myoglobin from kidney and avoidance of triggering factors-prolonged exercise, exposure to cold, infections, and fasting. Presentation in the...

Outcomes of Drug Eluting Stent Implantation

The procedural success rate was 100 in the SES and BMS groups. Periprocedural creatine kinase MB fraction (CK-MB) level elevation of three or more times normal developed in 7 SES patients (6.9 ) and in 10 BMS patients (8.3 ) (P . 69). There were no incidents of death, stent thrombosis, Q-wave MI, or emergent bypass surgery during hospitalization in either group. Quantitative angiographic and IVUS results after the procedures showed that the MLD (4.08 0.57 versus 3.36 0.47 mm, P .001) and IVUS lesion lumen area (12.41 3.20 versus 9.62 2.57 mm2, P .001) after the procedure were larger because of greater acute lumen gain (2.73 0.73 versus 2.06 0.56 mm, P .001) in the BMS group compared with the SES group. However, at follow-up angiography, lumen loss (0.05 0.57 versus 1.27 0.90 mm, P .001) and the overall angiographic restenosis rate (7.0 versus 30.3 , P .001) were significantly lower in the SES group than the BMS group. At 1 year, there were no deaths or acute MIs in either group....


With this in mind, biologic imaging studies are taking an increasing role in GBM patient management. In particular, they can be a useful adjunct when evaluating new enhanced areas of uncertain significance in previously treated patients. Fluo-rodeoxyglucose positron emission tomography (FDG-PET) scans can be useful to distinguish metabolically active areas such as tumor from inactive areas such as necrosis. However, PET scans require a cyclotron to generate appropriate isotopes, and access to these scans can be limited in some areas. Increasingly, MRI techniques that are potentially more universally available are being used to provide similar biologic information. Proton magnetic resonance spectroscopy (MRS) can be used to detect metabolites in normal and abnormal brain tissue.22 Common metabolite peaks generated include choline (Cho), creatine (Cr), -acetyl aspartate (NAA), lactate (Lac), and lipid (Lip). Active tumor will often show increased choline and decreased NAA compared with...

Colorado Tick Fever

Colorado tick fever is an acute viral infection transmitted by the bite of the Dermacentor andersoni tick (Figure 16-10). The disease is limited to the western United States and is most prevalent from March to September. Symptoms start about 3 to 6 days after the tick bite. Fever continues for 3 days, stops, and then recurs 1 to 3 days later for another few days. Other symptoms include excessive sweating, muscle aches, joint stiffness, headache, photophobia, nausea, vomiting, weakness, and an occasional faint rash. Routine blood tests might show a low WBC count, mildly elevated liver function, and mildly elevated creatine phosphokinase (CPK). Diagnosis is confirmed by testing blood for complement fixation immu-nofluorescent antibody staining to Colorado tick virus. Treatment is removal of the tick and treatment of symptoms.

Force Scaling

NCV, Nerve conduction velocity VER visual evoked responses VDRL, Venereal Disease Research Laboratories CSF, cerebrospinal fluid HIV, human immunodeficiency virus ACh, acetylcholine EMG, electromyography MRI, magnetic resonance imaging RA factor, rheumatoid arthritis factor ESR, erythrocyte sedimentation CK, creatine kinase ANA, antinuclear antibody WBC, white blood cells SSEP, somatosensory evoked potentials HD, Huntington's disease EEG, electroencephalography BAER, brain stem auditory evoked response Ab, antibody MSA, multiple system atrophy ENG, electronystagmography CT, computed tomography N A, not applieable.

Embolic Protection

Tions were shown to have prognostic implications.257 Even when mostly straightforward single-lesion, single-stent SVG PCI procedures were carried out before the availability of embolic protection, significant creatine kinase elevations were observed in 20 of patients.258,259 The rate of MI and procedural risk were shown to increase with lesion complexity, length, and estimated plaque volume,260 and when MI occurred, there was an increased 30-day mortality rate approaching 15 .261 In more than 1000 patients who underwent SVG stenting, CK-MB elevation was the most powerful predictor of late mortality.262 Potential approaches to reduce embolic myocardial infarction occurring during SVG PCI include strategies to remove thrombus before PCI, capturing debris that is liberated by filters or occlusion-aspiration techniques, or exclusion of debris by use of a covered stent (discussed later).


The definition of periprocedural myocardial infarction (PMI) has been a subject of debate and has evolved over the past decade. Traditionally, PMI was defined along the same lines as acute MI not related to revascularization, using at least two of three criteria prolonged chest pain, electrocardiographic q waves, and rise in the levels of serum markers. Subsequently, numerous publications demonstrated that creatine kinase (CK) and creatine kinase-myocardial band isoenzyme (CK-MB) elevations had prognostic implications, even in absence of pathologic q waves. The cutoff values of CK and CK-MB used to define PMI in these studies varied widely. Numerous investigators used the cutoff value of three times the upper limit of normal (ULN) of CK or CK-MB as the defining threshold of PMI, although it has been traditional to report more than one times the ULN, more than five times the ULN, and occasionally, more than eight times the ULN values.4,5 Later studies used tro-ponin and myoglobin...

Muscular Dystrophy

The most common of the dystrophies and the first to be described was that delineated by French neurologist Guillaume Duchenne in 1868. Duchenne muscular dystrophy (DMD) is a sex-linked recessive disorder. Consequently, it affects only males and is inherited through female carriers of the gene. Affected boys have abnormally elevated concentrations of muscle-cell enzymes such as creatine phosphokinase in their blood this abnormality is also found in about three-fourths of female carriers. DMD appears to have a rather uniform incidence worldwide of 15-33 cases per 100,000. A family history of DMD is identified in only about one-third of cases. Others are attributed to either a previously unexpressed carrier state or a new mutation.


The principal symptom of myotonia is that of muscle stiffness and an inability to relax contracted muscle (usually sodium channel myotonia is not painful). Stiffness may be confused with increased muscle tone related to spasticity or rigidity. Muscle cramps, which must be distinguished from this stiffness, are often a feature of a peripheral nerve disorder and are readily differentiated on EMG. Dystonia should be considered in these patients, but this disorder results in abnormal postures and is the result of discharges of whole motor units rather than individual muscle fibers. Painless but electrically silent contractures may be a feature of metabolic myopathy such as McArdle's disease and may be mistaken for myotonia. In patients who are taking neuroleptics or those who have been withdrawn from levodopa, neuroleptic malignant syndrome should be considered in the presence of muscle rigidity or stiffness with fever, an elevated creatine kinase (CK)...

Inorganic Mercury

Differential Diagnosis and Evaluation. Serum concentrations of mercury are unreliable indicators of inorganic and organic mercury toxicity because blood levels vary greatly between individuals and in the same individual. The threshold biological exposure index (BEI) for blood is 15 pg L, and for urine it is 35 pg g creatine. However, urinary excretion is not a good measure of toxicity, since there seems to be little correlation between symptomatology and the amount of mercury excreted in the urine. Although the early differential diagnosis might include Parkinson's disease, the tremor seen with mercurial intoxication is not solely a resting tremor and is usually coarser than that found in patients with Parkinson's disease. Because the signs of mercury intoxication may mimic those of some common neurological syndromes, the correct diagnosis is dependent on a good occupational history, clinical symptomatology, and documentation of mercury in the patient's blood, urine, or hair.


Gelastic seizures appear to originate from the hamartoma itself. Depth electroencephalogram (EEG) recordings within HHs have demonstrated focal seizure origin from the hamar-toma, and electrical stimulation has reproduced typical gelas-tic seizures.7 Spectroscopy in patients with gelastic seizures and HH demonstrates no abnormalities of N-acetyl aspartate (NAA)-to-creatine ratios in the temporal lobes but decreased NAA creatine levels within the hamartomas. In addition, although surface EEG recordings may indicate a temporal lobe focus, temporal lobectomies in such patients may improve seizures briefly, rarely providing long-term seizure control.


This is a metabolite of creatine, which stores energy in muscles. It is freely filtered by the glomeruli of the kidney and the clearance of creatinine from the plasma can be used to provide an approximation of the glomerular filtration rate. Like BUN, it is not a very accurate indicator of kidney function, as approximately 75 of the kidney tissue must be nonfunctional before elevated levels are seen.


The most common hereditary myopathy is DMD with its dystrophin deficiency. Dys-trophin reinforces the sarcolemmal membrane of muscle fibers, so mechanical stress from an eccentric contraction could injure fibers. Strengthening is feasible, however, without inducing much of a rise in creatine kinase muscle enzyme. In DMD, weakness evolves in the hip flexors and gluteal muscles and leads to a lordotic stance, The plantar flexors are stronger than the tibialis anterior, so children walk on their toes. Tendon shortening gradually increases across all joints. Gait becomes unsafe. Some patients choose to use a wheelchair, whereas others choose to use a polypropylene knee-ankle-foot orthosis (KAFO) to prolong ambulation for 1 or 2 years. Contractures may require tendon lengthening or casting before fitting the braces, however. A spinal fusion for scoliosis is less likely to be used for DMD than for patients with spinal muscular atrophy, a congenital myopathy, or poliomyelitis, because of the...

Anaerobic training

Anaerobic training results in an increase in the activity of creatine kinase (CK) and glycolytic enzymes such an increase implies that a certain change in an activator results in a higher rate of energy production of the anaerobic pathways. Intense training does not appear to influence the total creatine phosphate (CP) pool, but it allows the muscle glycogen concentration to be elevated, which is of importance for performance during repeated high-intensity exercise 63 . The capacity of the muscles to release and neutralize H+ (buffer capacity) is also increased after a period of anaerobic training 64 . This will lead to a lower reduction in pH for a similar amount of lactate produced during high-intensity exercise. Therefore, the inhibitory effects of H+ within the muscle cell are smaller, which may be one of the reasons for a better performance in high-intensity tests after a period of anaerobic training. Another important effect of the anaerobic training is an increased activity of...


If baseline BP is more than 20 10 mm Hg above target level, initial therapy should consist of two antihypertensive agents (one of which should be a thiazide diuretic unless there is a contraindication) started simultaneously. The majority of patients with HTN will need two or more drugs to achieve adequate control of BP. As demonstrated in the Hypertension Optimization Trial (Hansson et al., 1998), diabetic patients require, on average, 3.4 medications to achieve adequate control. In uncomplicated HTN the BP target is less than 140 90 mm Hg. In patients with diabetes or chronic kidney disease (GFR 1.5 mg dL in men or 1.3 mg dL in women, or albuminuria defined as 300 mg day on 24-hr urine specimen or 200 mg albumin g creatine on urine spot check), the BP target is less than 130 80 mm Hg.

Injury and repair

Quadriceps Contusions

Following muscle damage several proteins are released into serum. One of the most commonly used markers of muscle injury is creatine kinase (CK) which is generally detectable 1-2 days post injury and can remain elevated for 5-6 days after prolonged strenuous exercise. Most of the measured CK is caused by the muscle-specific isoenzyme CK-MM. Carbonic anhy-drase III (CA-III) and myoglobin (Mb) are more specific to muscle than total CK is, and the profile differs. CA-III is present in type I fibers only and Mb peaks immediately after long-distance running, making them suitable for markers of acute events. It must be acknowledged that a large variability exists with regard to interindividual differences in responses of

Alcoholic Myopathy

There are two forms of alcoholic muscle disease (1) an acute, painful myopathy associated with weakness, cramps, swollen and tender muscles, high creatine kinase, and rhabdomyolysis with or without myoglobinuria and (2) a chronic myopathy that is painless and often unnoticed by the patient, causing proximal weakness and type II fiber atrophy on nerve biopsy. In addition to skeletal muscle involvement, patients may have an associated cardiomyopathy. y Acute necrotizing myopathy and rhabdomyolysis cause severe painful swelling of one or more muscles with induration of the skin and soft tissues. Creatine kinase levels may be elevated, and myoglobinuria may result in acute renal failure. Acute attacks resolve in days to weeks after abstaining and long-term disability is uncommon unless the patient has repeated attacks.y Chronic myopathy is painless weakness of proximal muscles. A cardiomyopathy, peripheral and autonomic neuropathies, and other complications of alcohol abuse may be...

Reyes Syndrome

Overall, mortality currently is 30 to 35 percent. Predictors of poor outcome appear to be young age, especially infants younger than 2 years old high clinical stage at the time of hospital admission rapid progression from vomiting to coma maximal clinical stage high creatine kinase levels and ammonia levels above 300 pg dl at the time of hospital admission. In those surviving, hepatic recovery is full but nervous system residua are many. Behavioral problems include attention difficulties, retardation, and aggressive impulsivity. Neurological problems include hemiparesis and quadriparesis, dysarthria, cortical blindness, and seizures. Even among children believed to have full recovery, 34 percent had measurable deficits in school achievement, visuomotor integration, sequencing, and problem solving. y

Takotsubo syndrome

Takotsubo syndrome (TTS), also known as apical ballooning, is a reversible neuromyocardial failure which resembles acute myocardial infarction clinically and electrophysiologically in patients with normal coronary arteries 63 . TTS is clinically characterized by sudden onset of anginal chest pain, dyspnea or syncope. Initially, the ECG shows ST elevation, which turns into negative T-waves a few hours or days later, which may persist for months 64, 65 . Reversible akinesia or hypokinesia affects most frequently the left ventricular apex but rarely also the midventricular segments the non-affected ventricular segments show hyper-contractility. Cardiac enzymes such as creatine phosphokinase and troponin might be slightly elevated. Coronary angiography shows no stenoses of the coronary arteries. The cause and pathogenesis of TTS are unknown, but it may be triggered by physical or emotional stress and catecholamine tox-icity 66 . TTS has been described in association with pheochromocytoma,...

Spectrum of ACSs

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Approximately two-thirds of all MIs are NSTE MI, whereas one-third of patients with MI present with STE. NSTE MI differs from UA in that ischemia is severe enough to produce myocardial necrosis resulting in the release of a detectable amount of biomarkers, mainly troponins T or I, but also creatine kinase (CK) myocardial band (MB), from the necrotic myocytes in the bloodstream. The clinical significance of serum markers will be discussed in greater detail in later sections of this chapter. FIGURE 8-1. Evaluation of the ACS patient. aAs described in Table 8-1. bPositive above the myocardial infarction decision limit. cNegative below the myocardial infarction decision limit. (ACSs, acute coronary syndromes CABG, coronary artery bypass graft CAD, coronary artery disease CKMB, creatine kinase myocardial band ECG, electrocardiogram min, minute PCI, percutaneous coronary intervention.) Refer to Figure 9-2 for further details regarding ECG interpretation. (From...

Ergogenic substances

Some of these are included in the list of doping drugs, such as caffeine (max 12 mg mL is allowed in urine) and alcohol. Among the (still) legal and most often used diet supplements are creatine, Q10, antioxidants and ginseng. The daily need of creatine is approximately 2 g day and it is covered through both the diet and the body's own production (through the amino acids argi-nine and methionine). In the diet, creatine is found especially in meat (c. 5 g kg), fish and to a smaller extent in milk (80-100 mg L). If the intake of creatine is increased, the muscle tissue will reach a saturation limit after approximately 4 days whereafter the surplus is excreted in the urine. An increased intake of creatine may have a positive effect, especially after short-term explosive exercise 89 . Athletes who consume a well-balanced diet do not, however, need a creatine supplement.

CP resynthesis

Postexercise CP resynthesis occurs rapidly with a halftime of 50-60 s and is important for the recovery of power-generating capacity following intense exercise 15 . It is critically dependent upon oxygen availability 16,17 and CP resynthesis is faster in individuals with a high muscle oxidative capacity. Dietary creatine supplementation increases muscle CP levels and postexercise CP resynthesis and is associated with enhanced high-intensity exercise performance 18 . For these reasons there has been considerable interest in this compound as an ergogenic aid. The resynthesis of CP and restoration of myoglobin oxygen stores contribute to the elevated oxygen consumption during postexercise recovery. Other potential factors include elevated heart rate and ventilation, increased body temperature, elevated catecholamines, glycogen synthesis and uncoupling of mitochondrial respiration. The longheld view that lactate oxidation contributes to an increase in postexercise oxygen consumption does...

Breakdown of PCr

It is well established that due to its high power and rapid recruitment PCr breakdown is an important energy source during high-intensity exercise and at the onset of exercise. However, there is evidence that the CK reaction also has a role in aerobic metabolism. CK is located both in the intermembrane space of the mitochondria (CKmit) and at sites of ATP utilization in the cytosol. During exercise PCr will regenerate ATP at the site of ATP utilization and creatine will diffuse to mitochondria. PCr is then regenerated by CKmit and diffuses back to the sites of ATP utilization. Through the action of this creatine shuttle the concentration of ADP in the vicinity of mitochondria will be high and oxidative phosphorylation will be stimulated. Experiments with permeabilized fibers have shown that creatine is an important activator of mitochondrial respiration in cardiac tissue and slow-twitch fibers of skeletal muscle 11 , and recently creatine supplementation was shown to enhance aerobic...

Subjective Objective

The combination of a low T4 level and an elevated thyroid-stimulating hormone (TSH) level is virtually diagnostic of primary hypothyroidism, because TSH elevation does not occur in central hypothyroidism. Further delineation between primary and secondary hypothyroidism is dependent on history, examination, and other laboratory studies. In addition to TFTs, other laboratory abnormalities have been described, including anemia (normocytic-normochromic, microcytic-hypochromic, or macrocytic) and hyponatremia (factitious due to hyperlipidemia or secondary to impaired free water excretion), as well as elevated serum creatine kinase, myoglobin,1 and prolactin. Because of the possibility of concomitant adrenal insufficiency, a serum cortisol level should also be obtained. The EEG may show slowing of the posterior dominant rhythm and a generalized voltage decrease, as well as triphasic waves that disappear with replacement therapy. 'eel CSF analysis may reveal an elevated protein...

Muscle Biopsy

The decision to proceed with a muscle biopsy is made after a thorough medical and neurological history, examination, laboratory evaluation, and electromyogram study, thereby permitting the formulation of a preliminary diagnosis and, hence, dictating the studies required of the muscle biopsy specimen. The history characterizes the weakness (e.g., its rate of onset, distribution, time course, precipitants e.g., exercise-induced , associated symptoms, and family pedigree). The clinical examination quantifies the weakness and identifies any associated features (e.g., myotonia). The laboratory assessment (e.g., serum creatine kinase, urine myoglobin) screens for abnormalities of the blood and urine, and electromyography provide information typically not obtainable in other ways, including (1) the identification of a disorder other than a myopathy (e.g., motor neuron disease, neuromuscular junction defect), thereby avoiding an unnecessary muscle biopsy (2) further characterization of the...

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