Rationale and objectives: The aim of the authors' prospective study was to explore therapy-induced changes of muscular metabolism in arterial occlusive disease (AOD).
Materials: Before and after vascular therapy, respectively, 31 patients with AOD were examined by dynamic phosphorus-31 (31P) magnetic resonance spectroscopy (MRS) at 1.5 T; in the magnet, the quadriceps muscle was stressed by an isometric and an isotonic form of exercise until exhaustion, respectively. Twenty-three patients were treated by standardized percutaneous transluminal angioplasty; eight patients underwent a vascular operation.
Results: Vascular therapy induced a marked improvement of clinical and angiographic results. At the same work load, exercise-induced metabolic changes of the quadriceps muscle were significantly less pronounced after the vascular therapy: maxima of the ratio inorganic phosphate (Pi)/phosphocreatine (PCr) (isometric exercise: 0.34 [after therapy] versus 0.44 [before therapy]; isotonic exercise: 0.36 [after therapy] versus 0.51 [before therapy]) as well as minima of pH (isometric exercise: 7.00 [after therapy] versus 6.93 [before therapy]; isotonic exercise: 7.00 [after therapy] versus 6.93 [before therapy]). In relation to maximal values of Pi/PCr, the extent of acidosis was smaller after vascular therapy, resulting in a flatter slope of the regression line between these parameters (b = -0.24 +/- 0.10 versus b = -0.31 +/- 0.09). After both of the exercises, time of half recovery of Pi/PCr was significantly shorter after vascular therapy (isometric exercise: 43 seconds [after therapy] versus 83 seconds [before therapy]; isotonic exercise: 42 seconds [after therapy] versus 57 seconds [before therapy]).
Conclusions: After effective vascular therapy, minor exercise-induced metabolic changes (increased "work/energy cost-index"), a decreased contribution of anaerobic glycolysis to total adenosine triphosphate production as well as a markedly increased recovery rate of Pi/PCr are unequivocal spectroscopic proofs of an improved oxidative metabolism of muscle cells because of increased tissue perfusion.