Comparison of in vivo postexercise phosphocreatine recovery and resting ATP synthesis flux for the assessment of skeletal muscle mitochondrial function

• Published in: American Journal of Physiology: Cell Physiology Vol. 299; no. 5; pp. C1136 - C1143
• Main Authors: van den Broek, N. M. A., Ciapaite, J., Nicolay, K., Prompers, J. J.
• Format: Journal Article
• Language: English
• Published: United States American Physiological Society 01.11.2010
• Subjects: Adenosine Diphosphate - metabolism; Adenosine triphosphatase; Adenosine Triphosphate - biosynthesis; Animals; Enzyme Inhibitors - pharmacology; Hydrogen-Ion Concentration; Magnetic Resonance Spectroscopy; Male; Mitochondria; Mitochondria, Muscle - drug effects; Mitochondria, Muscle - metabolism; Muscle, Skeletal - metabolism; Muscle, Skeletal - ultrastructure; Musculoskeletal system; Onium Compounds - pharmacology; Oxidative Phosphorylation; Oxygen Consumption; Phosphocreatine - metabolism; Physical Conditioning, Animal - physiology; Physiology; Rats; Rats, Wistar; Rodents; Spectrum analysis
• ISSN: 0363-6143; 1522-1563; 1522-1563
• DOI: 10.1152/ajpcell.00200.2010

31 P magnetic resonance spectroscopy (MRS) has been used to assess skeletal muscle mitochondrial function in vivo by measuring 1) phosphocreatine (PCr) recovery after exercise or 2) resting ATP synthesis flux with saturation transfer (ST). In this study, we compared both parameters in a rat model of mitochondrial dysfunction with the aim of establishing the most appropriate method for the assessment of in vivo muscle mitochondrial function. Mitochondrial dysfunction was induced in adult Wistar rats by daily subcutaneous injections with the complex I inhibitor diphenyleneiodonium (DPI) for 2 wk. In vivo 31 P MRS measurements were supplemented by in vitro measurements of oxygen consumption in isolated mitochondria. Two weeks of DPI treatment induced mitochondrial dysfunction, as evidenced by a 20% lower maximal ADP-stimulated oxygen consumption rate in isolated mitochondria from DPI-treated rats oxidizing pyruvate plus malate. This was paralleled by a 46% decrease in in vivo oxidative capacity, determined from postexercise PCr recovery. Interestingly, no significant difference in resting, ST-based ATP synthesis flux was observed between DPI-treated rats and controls. These results show that PCr recovery after exercise has a more direct relationship with skeletal muscle mitochondrial function than the ATP synthesis flux measured with 31 P ST MRS in the resting state.