MITOCHONDRIA: Investigation of in vivo muscle mitochondrial function by 31P magnetic resonance spectroscopy |
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| Institution: | 1. Centro Cardiologico Monzino, IRCCS, Milan, Italy;2. Dept. of Clinical Sciences and Community Health, Cardiovascular Section, University of Milano, Milano, Italy;3. Cardiovascular Department, Division of Cardiology, Azienda Sanitaria Universitaria Integrata and University of Trieste, Trieste, Italy;4. Unità Operativa Cardiologia Riabilitativa, Multimedica IRCCS, Milano, Italy;5. SDN IRCCS, Naples, Italy;1. Department of Radiology and Nuclear Medicine, Radboud University Medical Center, Nijmegen, The Netherlands;2. Department of Targeted Therapeutics, MIRA Institute, University of Twente, Enschede, The Netherlands;3. Department of Experimental Molecular Imaging, University Clinic and Helmholtz Institute for Biomedical Engineering, RWTH-Aachen University, Aachen, Germany;4. Department of Pharmaceutics, Utrecht Institute for Parmaceutial Sciences, Utrecht University, Utrecht, The Netherlands;1. Department of Geology, Marshall University, Huntington, WV 25755, United States;2. West Virginia Geological and Economic Survey, 1 Mont Chateau Road, Morgantown, WV 26508, United States;3. Cliffs Natural Resources, Cliffs Mining Division, 550 E. Division Street, Ishpeming, MI 49849, United States;4. Penn-Virginia Resource Partners, L.P., 7 Sheridan Square, Suite 400, Kingsport, TN 37660, United States |
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| Abstract: | The most important function of mitochondria is the production of energy in the form of ATP. The socio-economic impact of human diseases that affect skeletal muscle mitochondrial function is growing, and improving their clinical management critically depends on the development of non-invasive assays to assess mitochondrial function and monitor the effects of interventions. 31P magnetic resonance spectroscopy provides two approaches that have been used to assess in vivo ATP synthesis in skeletal muscle: measuring Pi ⟶ ATP exchange flux using saturation transfer in resting muscle, and measuring phosphocreatine recovery kinetics after exercise. However, Pi ⟶ ATP exchange does not represent net mitochondrial ATP synthesis flux and has no simple relationship with mitochondrial function. Post-exercise phosphocreatine recovery kinetics, on the other hand, yield reliable measures of muscle mitochondrial capacity in vivo, whose ability to define the site of functional defects is enhanced by combination with other non-invasive techniques. |
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| Keywords: | Mitochondrial function Skeletal muscle Saturation transfer Phosphocreatine recovery |
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