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  • Title: Metabolic myopathy as a cause of the exercise limitation in lung transplant recipients.
    Author: Tirdel GB, Girgis R, Fishman RS, Theodore J.
    Journal: J Heart Lung Transplant; 1998 Dec; 17(12):1231-7. PubMed ID: 9883765.
    Abstract:
    BACKGROUND: Cardiopulmonary exercise (CPEx) studies of lung transplant (LTx) recipients have found low maximum oxygen consumptions because of an as yet unexplained mechanism. Although it is likely that a significant problem resides within the mitochondria, this study determines whether a defect in oxygen uptake or utilization is present. METHODS: Six LTx recipients and six age- and sex-matched, healthy control subjects were studied to assess the possibility of a mitochondrial myopathy in LTx recipients. We used standard CPEx testing in conjunction with near-infrared spectroscopy (NIRS), a noninvasive optical technique to assess peripheral oxygen uptake in exercising muscle. NIRS analyzes the absorption spectra of hemoglobin and myoglobin at 760 and 850 nm to determine the relative oxygen saturation of these compounds during exercise with respect to baseline values. Relative changes in oxygen saturation are determined from the application of Beers law to changes in absorbance to compute changes in optical density (deltaOD). The LTx recipients and control subjects performed maximal noninvasive CPEx studies with NIRS analysis of the vastus lateralis muscle. RESULTS: All subjects had a circulatory limitation to exercise. The LTx group had a significantly lower percent predicted maximum oxygen consumption than the control group (45.3%+/-14% vs 100.8%+/-15.6%, [mean +/- SD] P < .001) and earlier onset of the anaerobic threshold (30.3%+/-7.6% vs 60.3%+/-8.0% of predicted VO2max, P < .0001) The LTx recipients demonstrated a significantly smaller deltaOD at maximum exercise as determined by NIRS analysis (0.024+/-0.005 deltaOD vs 0.054+/-0.03 deltaOD, P < .05). CONCLUSIONS: LTx recipients have an impaired maximal exercise capacity because of a disorder of peripheral oxygen utilization. This may be caused by a cyclosporine-induced mitochondrial myopathy.
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