glycogen storage disease type v/väsymys

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Muscle fatigue in myophosphorylase deficiency: power spectral analysis of the electromyogram.

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It has been postulated that the power spectral shift in the surface EMG during fatigue is due to accumulation of muscle lactate. This hypothesis has been directly tested by measuring such shift in 3 patients with myophosphorylase deficiency who performed sustained isometric contractions of the

Phosphorylase re-expression, increase in the force of contraction and decreased fatigue following notexin-induced muscle damage and regeneration in the ovine model of McArdle disease.

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McArdle disease is caused by a deficiency of myophosphorylase and currently a satisfactory treatment is not available. The injection of notexin into, or the layering of notexin onto, the muscles of affected sheep resulted in necrosis followed by regeneration of muscle fibres with the expression of

Pharmacological and nutritional treatment for McArdle disease (Glycogen Storage Disease type V).

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BACKGROUND McArdle disease (Glycogen Storage Disease type V) is caused by the absence of the glycolytic enzyme, muscle phosphorylase. People present with exercise-induced pain, cramps, fatigue, and myoglobinuria, which can result in acute renal failure if it is severe. OBJECTIVE To systematically

Muscle fatigue in McArdle's disease. Muscle fibre conduction velocity and surface EMG frequency spectrum during ischaemic exercise.

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The origin of fatigue in McArdle's disease is still a matter of debate. Both a reduction of muscle membrane excitability and failure of excitation-contraction (E-C) coupling have been suggested as causes. We performed intermittent isometric biceps brachii contractions (80% maximal voluntary

Reflex sympathetic activation during static exercise is severely impaired in patients with myophosphorylase deficiency.

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During static exercise, metabolites accumulate in the muscle interstitium where they stimulate chemosensitive afferent nerves that reflexly increase efferent muscle sympathetic nerve activity (MSNA) and blood pressure. In experimental animals, lactic acid potently stimulates the muscle metaboreflex,

Recurrent Compartment Syndrome Leading to the Diagnosis of McArdle Disease: Case Report.

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Glycogen storage disorders are rare diseases of metabolism that are usually diagnosed when a patient presents with recurrent fatigue, muscle pains, and exercise intolerance. In this case report, we describe a patient who presented with the second episode of nontraumatic compartment syndrome over a

[Muscle phosphorylase deficiency in childhood. A case report].

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Myophosphorylase deficiency or McArdle's disease is rarely recognized in childhood. The onset is generally in adolescence or in adult age with exercise intolerance, muscle cramps and myoglobinuria. Two siblings of 6 and 2 years of age are described. The first patient showed early fatigue and both

McArdle Disease and Exercise Physiology.

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McArdle disease (glycogen storage disease Type V; MD) is a metabolic myopathy caused by a deficiency in muscle glycogen phosphorylase. Since muscle glycogen is an important fuel for muscle during exercise, this inborn error of metabolism provides a model for understanding the role of glycogen in

Anesthesia considerations in a patient with mcArdle disease: a case report.

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A patient with McArdle disease underwent bowel surgery with general anesthesia and was successfully managed. McArdle disease is a rare skeletal muscle disorder affecting approximately 1 in 100,000 people. McArdle disease, also known as type V glycogen storage disease, is an autosomal recessive

Muscle fatigue in McArdle's disease studied by 31P-NMR: effect of glucose infusion.

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In muscle phosphorylase deficiency (McArdle's disease) there is an abnormally rapid fatigue during strenuous exercise. Increasing substrate availability to working muscle can improve exercise tolerance but the effect on muscle energy metabolism has not been studied. Using phosphorus-31 nuclear

Physical training for McArdle disease.

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BACKGROUND McArdle disease is a rare metabolic myopathy caused by a complete absence of the enzyme muscle glycogen phosphorylase. Affected people experience symptoms of fatigue and cramping within minutes of exercise and are at risk for acute muscle injury (rhabdomyolysis) and acute renal failure.

Reduced levels of skeletal muscle Na+K+ -ATPase in McArdle disease.

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We evaluated the hypothesis that impaired sarcolemmal function associated with exaggerated potassium release, impaired potassium uptake, or both may contribute to exertional fatigue and abnormal circulatory responses to exercise in McArdle disease (MD). The cellular mechanism of exertional fatigue

Mechanisms of exertional fatigue in muscle glycogenoses.

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Exertional fatigue early in exercise is a clinical hallmark of muscle glycogenoses, which is often coupled with painful muscle contractures and episodes of myoglobinuria. A fundamental biochemical problem in these conditions is the impaired generation of ATP to fuel muscle contractions, which

A High Creatine Kinase Concentration Might Be a Sign of McArdle Disease in Patient With Type 1 Diabetes.

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Type 1 diabetes (the pancreas producing little or no insulin) is usually diagnosed in children and young adults and was previously known as juvenile diabetes. McArdle disease is a common metabolic defect caused by an inherited deficit of myophosphorylase. These 2 diseases might have some

Recurrent acute kidney failure due to McArdle disease.

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We present an adolescent with McArdle disease and recurrent acute kidney failure due to rhabdomyolysis. The patient was admitted with acute kidney failure for 3 times and due to a history of proximal weakness, fatigue, and muscular cramps after physical activities a glycogen-storage disease was

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