OBJECTIVE: To characterize muscle metabolic anomalies associated with polymyalgia rheumatica (PMR) using P-31 magnetic resonance spectroscopy (MRS). METHODS: Seventeen patients with PMR and 9 age-matched control subjects were investigated. The forearm flexor muscles were examined by P-31 MRS in a 4.7 T superconducting horizontal magnet (Biospec Bruker 47/30) during a rest-exercise-recovery protocol. The intracellular pH and the relative concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), ATP, and phosphomonoesters were measured every minute during the protocol. Based on the PCr and pH time-dependent changes during exercise and recovery, the rates of ATP production from PCr hydrolysis, glycogenolysis, and aerobic metabolism were calculated for each minute of exercise. RESULTS: At rest, the metabolic parameters [PCr]:[Pi], pH, and [PCr]:[ATP] were not significantly different between the PMR patients and the control subjects. During exercise, the energetic cost and the contribution of anaerobic and oxidative pathways to energy supply were similar in the 2 groups, as were the recovery kinetics of the phosphorylated compounds and pH. CONCLUSION: Muscle MRS does not confirm the findings of histologic and biochemical studies that suggest an alteration of mitochondrial function in PMR. No other modifications in glycolytic or glycogenolytic pathways or in proton handling were found that could indicate an alteration of muscle energetics in patients with PMR.
OBJECTIVE: To characterize muscle metabolic anomalies associated with polymyalgia rheumatica (PMR) using P-31 magnetic resonance spectroscopy (MRS). METHODS: Seventeen patients with PMR and 9 age-matched control subjects were investigated. The forearm flexor muscles were examined by P-31MRS in a 4.7 T superconducting horizontal magnet (Biospec Bruker 47/30) during a rest-exercise-recovery protocol. The intracellular pH and the relative concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), ATP, and phosphomonoesters were measured every minute during the protocol. Based on the PCr and pH time-dependent changes during exercise and recovery, the rates of ATP production from PCr hydrolysis, glycogenolysis, and aerobic metabolism were calculated for each minute of exercise. RESULTS: At rest, the metabolic parameters [PCr]:[Pi], pH, and [PCr]:[ATP] were not significantly different between the PMR patients and the control subjects. During exercise, the energetic cost and the contribution of anaerobic and oxidative pathways to energy supply were similar in the 2 groups, as were the recovery kinetics of the phosphorylated compounds and pH. CONCLUSION: Muscle MRS does not confirm the findings of histologic and biochemical studies that suggest an alteration of mitochondrial function in PMR. No other modifications in glycolytic or glycogenolytic pathways or in proton handling were found that could indicate an alteration of muscle energetics in patients with PMR.