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  • Title: [Physical training of patients with high grade compromise of heart pumping function].
    Author: Schuler G, Hambrecht R.
    Journal: Z Kardiol; 1996; 85 Suppl 6():253-61. PubMed ID: 9064974.
    Abstract:
    Regular exercise is regarded as a mainstay of physical fitness and endurance; it remains to be determined, however, whether patients with severe impairment of left ventricular performance derive profit from this treatment to the same extent as patients with normal myocardial contractility. Irrespective of the underlying cause profound changes are initiated by heart failure with respect to neurohumoral factors, ultrastructure of skeletal muscle, and peripheral vascular resistance. Initially these changes are set in motion by the inability of the heart to provide sufficient flow to the peripheral organs; eventually, however, they attain a role of their own and contribute to the disease independently. Intolerance of physical exercise, in particular, is not so much the result of pulmonary congestion and low cardiac output. Reduction of oxidative capacity of skeletal muscle, excessive peripheral vascular resistance, and impairment of vasodilatation in response to metabolic needs seem to contribute more to this incapacitating symptom. Until recently, physical exercise was regarded as harmful in patients with severe impairment of left ventricular performance; in order to prevent further deterioration patients were frequently treated by bedrest. Controlled trials, however, have shown that regular physical exercise in these patients may favourably influence the course of this disease, or even reverse some harmful changes. The following results were obtained in a group of 12 patients with depressed left ventricular ejection fraction (LV-EF 25 +/- 10%) participating in an ambulatory training program: 1) Left ventricular end-diastolic dimension was significantly reduced from 70 +/- 5 mm to 66 +/- 3 mm (p < 0.05). 2) There was significant improvement of skeletal muscle perfusion and oxygen uptake during submaximal and maximal exercise resulting in delayed onset of anaerobic metabolism and increased exercise capacity. 3) Intrinsic change of skeletal muscle ultrastructure were in part corrected; mitochondrial volume density increased significantly. There was a close correlation between changes in maximal oxygen uptake and changes of cytochrome-C-oxidase positive mitochondrial volume density. 4) Cardiac output and left ventricular ejection fraction in response to exercise, however, remained unchanged, indicating that no significant central effects were achieved by regular exercise.
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