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mitochondrial myopathies/fatiga muscular

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Mitochondrial Myopathy in Follow-up of a Patient With Chronic Fatigue Syndrome.

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Introduction. Symptoms of mitochondrial diseases and chronic fatigue syndrome (CFS) frequently overlap and can easily be mistaken. Methods. We report the case of a patient diagnosed with CFS and during follow-up was finally diagnosed with mitochondrial myopathy by histochemical study of muscle

Microdialysis and electromyography of experimental muscle fatigue in healthy volunteers and patients with mitochondrial myopathy.

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Consecutive 60-min microdialysis samples were taken from the tibial anterior muscle in 11 healthy subjects and 4 patients with mitochondrial myopathy before (2-3 samples) and after (3-4 samples, 2 controls and 1 patient excluded) sustained isometric foot dorsiflexions. Before exercise, mean

Fatigue and neuromuscular diseases.

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OBJECTIVE To identify the role of fatigue, its evaluation and its causes in the pathophysiology context of acquired or hereditary neuromuscular diseases of the spinal anterior horn cell, peripheral nerve, neuromuscular junction and muscle. METHODS A literature review has been done on Medline with

Mitochondrial myopathy presenting as fibromyalgia: a case report.

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BACKGROUND To the best of our knowledge, we describe for the first time the case of a woman who met the diagnostic criteria for fibromyalgia, did not respond to therapy for that disorder, and was subsequently diagnosed by biochemical and genetic studies with a mitochondrial myopathy. Treatment of

Recognition, diagnosis, and treatment of mitochondrial myopathies in endurance athletes.

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Endurance athletes complaining of muscle pains concomitant with fatigue and exercise intolerance provide a diagnostic challenge. When the most common causes have been ruled out, the presence of metabolic myopathies, including mitochondrial myopathies (MMs), should be considered. MMs are a group of

Fatigue and myalgia in AIDS patients.

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Fatigue and myalgia are common in patients with acquired immunodeficiency syndrome (AIDS). To determine whether altered muscle metabolism or impaired activation of muscle might account for these symptoms, we utilized three different exercise protocols to produce fatigue in nine AIDS patients who

Pregnancy with cytochrome oxidase-deficient mitochondrial myopathy.

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BACKGROUND Cytochrome oxidase-deficient mitochondrial myopathies represent a heterogeneous group of muscle disorders. Physical stress can cause life-threatening risks related to rhabdomyolysis or respiratory compromise. METHODS A 21-year-old primigravida with cytochrome C oxidase-deficient

Mitochondrial myopathies: disorders of the respiratory chain and oxidative phosphorylation.

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Mitochondrial myopathies are a clinical condition characterized by muscle weakness and fatigue in which the primary defect is localized at the level of the mitochondria. Microscopic examination shows accumulations of mitochondria at the fibre periphery (ragged red fibres) and in some cases
Chronic administration of the NADH-CoQ reductase inhibitor, diphenyleneiodonium to rats at two dose levels, 1.0 and 1.5 mg/kg per day, caused a 40% and 60% reduction, respectively, in the in vitro rate of NAD-linked respiration by skeletal muscle mitochondria. At the highest dose, muscle fatigue,

[Effect of sodium pyruvate on exercise intolerance and muscle weakness due to mitochondrial myopathy: a case report].

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We report the case of a 19-year-old woman who had been suffering from general fatigue and exercise intolerance since 15 years old. At 18 years old, she experienced muscle weakness and myalgia of the calves. Six months later, she was admitted to our hospital. She showed muscle weakness of the neck

Increased sensitivity to rocuronium and atracurium in mitochondrial myopathy.

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OBJECTIVE To describe the prolonged effect of the intermediate-acting, non-depolarising neuromuscular blocking agents rocuronium and atracurium in a 29-yr-old apparently healthy woman. METHODS Because of abdominal pain the patient was scheduled for explorative laparoscopic pelvic examination.

Advances in primary mitochondrial myopathies.

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Although mitochondrial diseases impose a significant functional limitation in the lives of patients, treatment of these conditions has been limited to dietary supplements, exercise, and physical therapy. In the past few years, however, translational medicine has identified potential

Effects of aerobic training in patients with mitochondrial myopathies.

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We studied the physiologic adaptation of patients with mitochondrial myopathies to aerobic training. Ten patients underwent individually supervised, moderate-intensity aerobic training on a treadmill for 8 weeks. Biochemical and functional measures improved with training. Estimated aerobic capacity

Metabolic profiles of exercise in patients with McArdle disease or mitochondrial myopathy.

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McArdle disease and mitochondrial myopathy impair muscle oxidative phosphorylation (OXPHOS) by distinct mechanisms: the former by restricting oxidative substrate availability caused by blocked glycogen breakdown, the latter because of intrinsic respiratory chain defects. We applied metabolic

Increased mitochondrial mass in mitochondrial myopathy mice.

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We have generated an animal model for mitochondrial myopathy by disrupting the gene for mitochondrial transcription factor A (Tfam) in skeletal muscle of the mouse. The knockout animals developed a myopathy with ragged-red muscle fibers, accumulation of abnormally appearing mitochondria, and
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