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      Effects of Carnitine Supplementation on Muscle Metabolism by the Use of Magnetic Resonance Spectroscopy and Near-Infrared Spectroscopy in End-Stage Renal Disease

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          Background/Aim: A defect in skeletal muscle mitochondrial metabolism develops in patients with chronic renal failure on haemodialysis. Treatment with carnitine, a compound essential for normal mitochondrial function, has been suggested to have significant benefits in such patients, so we carried out a study to see if carnitine acts by improving muscle bioenergetics and function. Methods: In a phase II randomised double-blind trial, patients with end-stage renal disease received placebo or intravenous L-carnitine (20 mg/kg dry body weight three times weekly after haemodialysis) for 16 weeks (n = 13 in each group). <sup>31</sup>P magnetic resonance spectroscopy, <sup>1</sup>H magnetic resonance imaging and near-infrared spectroscopy were used to measure muscle bioenergetics and function at baseline and at 16 weeks. Results: There were no significant differences between groups at baseline. Mean plasma carnitine rose 10-fold in the carnitine group but was unchanged in the placebo group. L-Carnitine had no statistically significant effect on any of the parameters measured. The rate of proton efflux from muscle, as a measure of tissue perfusion, was low in both groups and was not affected by treatment. Conclusions: The study failed to show any significant effect of 16 weeks’ L-carnitine supplementation on these objective measures of muscle metabolism and function. Slow proton efflux from muscle provides evidence supporting low blood flow and, therefore, decreased oxygen availability, as an underlying mechanism for muscle mitochondrial dysfunction in this disorder.

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          Most cited references 4

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          Bioenergetics of skeletal muscle in mitochondrial myopathy.

          31Phosphorus nuclear magnetic resonance spectroscopy was used to examine skeletal muscle in 29 patients with mitochondrial myopathy, 9 male and 20 female. Gastrocnemius was investigated in 15 patients and 30 normal subjects and finger flexor muscle (flexor digitorum superficialis, fds) in 24 patients and 35 normal controls. Both muscles were studied in 10 of the patients. Results were abnormal (outside the full range of normal values) in all but 2 patients. In 86% of patients (25/29) abnormalities were detected in resting muscle. In most cases there was a low phosphocreatine/ATP ratio, high calculated free [ADP] and low phosphorylation potential. At rest, abnormality was detected with equal ease in fds and gastrocnemius. Exercise and recovery increased the sensitivity of MRS in detecting abnormal metabolism. Finger flexion was better tolerated by patients than plantar flexion and gave bigger changes in metabolite concentrations and intracellular pH. Thus, results from fds were more easily differentiated from normal. Exercise duration was significantly shorter than in controls while phosphocreatine depletion was more rapid than normal, consistent with a shortfall in mitochondrial ATP synthesis. Nearly all patients (25/27, 93%) showed abnormalities during recovery from exercise. [ADP] was high during exercise and its recovery was delayed, providing increased drive for oxidative phosphorylation. Phosphocreatine resynthesis during recovery (which reflects oxidative ATP synthesis) was slow both in absolute terms and in relation to [ADP]. Recovery of intracellular pH after exercise was significantly more rapid than normal, consistent with an upregulation of proton efflux.(ABSTRACT TRUNCATED AT 250 WORDS)
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            Carnitine deficiency in haemodialysed patients

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              Skeletal muscle mitochondrial function is preserved in young patients with chronic renal failure


                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                June 2004
                17 November 2004
                : 97
                : 2
                : c41-c48
                aOxford Kidney Unit, Churchill Hospital, Headington; bMRC Biochemical and Clinical Magnetic Resonance Unit, John Radcliffe Hospital, Headington, and cDepartment of Biochemistry, University of Oxford, Oxford, UK
                78399 Nephron Clin Pract 2004;97:c41–c48
                © 2004 S. Karger AG, Basel

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                Figures: 2, Tables: 2, References: 47, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/78399
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