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  • Title: Phosphorus 31 nuclear magnetic resonance spectroscopy suggests a mitochondrial defect in claudicating skeletal muscle.
    Author: Pipinos II, Shepard AD, Anagnostopoulos PV, Katsamouris A, Boska MD.
    Journal: J Vasc Surg; 2000 May; 31(5):944-52. PubMed ID: 10805885.
    Abstract:
    OBJECTIVE: Decreased oxygen supply is generally accepted as the primary cause of muscle dysfunction in patients with peripheral arterial occlusive disease (PAOD) and intermittent claudication, although reported morphologic changes in the mitochondria of claudicating muscle suggest that impaired energy utilization may also play a role. With the measurement of the phosphate-rich compounds of muscle energy metabolism (adenosinetriphosphate [ATP], adenosinediphosphate [ADP], and phosphocreatine [PCr]) and pH, phosphorus P 31 magnetic resonance spectroscopy ((31)P MRS) provides a unique, noninvasive method to investigate this hypothesis further. METHODS: Calf muscle bioenergetics were studied in 12 men with moderate claudication (ankle-brachial index >/=0.5 and </=0.8) and 14 normal control subjects with the use of (31)P MRS and standard treadmill testing. Phosphorus MRS evaluation of the superficial posterior calf muscles was carried out with a 90-second submaximal isometric plantar flexion exercise. This mild exercise was chosen to permit in-magnet testing and to allow study of intrinsic mitochondrial efficiency under conditions of unchallenged blood flow. Phosphocreatine and ADP recovery time constants (t.c.), two very sensitive measures of oxidative mitochondrial function, as well as intracellular pH and ATP production via anaerobic glycolysis were determined during three exercise sessions and the results averaged and compared to known values obtained from a control population. RESULTS: During the (31)P MRS protocol, the end exercise intracellular pH (7.11 +/- 0.01 vs 7.11 +/- 0.01) and ATP production by anaerobic glycolysis (0.13 +/- 0.05 vs 0.14 +/- 0.03 mmol/L per second) were no different in PAOD patients versus control subjects, confirming that the protocol exercise did not significantly reduce oxygen supply. Phosphocreatine and ADP recovery t.c. (137 +/- 41 vs 44 +/- 3 seconds and 60 +/- 10 vs 29 +/- 2 seconds, respectively) were significantly slower than normal (P <.05, t test). There was, however, no correlation between these measures of mitochondrial function and any treadmill parameter (P >.5, Pearson moment correlation). CONCLUSIONS: Phosphorus 31 MRS provides the first direct evidence of defective energy metabolism in the mitochondria of claudicating calf muscle. This defect appears to be independent of both arterial flow and the severity of occlusive disease in patients with mild to moderate claudication. Coupled with documented ultrastructural and DNA abnormalities in the mitochondria of claudicating skeletal muscle, these data provide evidence for a secondary cause of muscle dysfunction in intermittent claudication.
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