Adolescent idiopathic scoliosis (AIS) can lead to ventilatory restriction, respiratory muscle weakness and exercise limitation. However, both the causes and the extent of muscle dysfunction remain unclear. The aim of our study is to describe muscle weakness and its relationship to lung function and tolerance to exercise in AIS patients.Lung and muscle function, together with exercise capacity, were assessed in 60 patients with pronounced spinal deformity (.40u) and in 25 healthy volunteers.Patients with AIS had only mild to moderate abnormal ventilatory patterns, the most frequent of which were restrictive abnormalities. The function of respiratory and limb muscles and exercise capacity were below normal limits in AIS patients, and were significantly lower than in controls. Exercise capacity was found to correlate with the function of inspiratory, expiratory, upper limb and lower limb muscles which, in addition, were reciprocally interrelated. Multivariate analysis showed that lower limb muscle function is the main contributor to exercise intolerance. There appeared to be no connection between spinal deformity and lung function, muscle function or exercise capacity.We conclude that AIS patients show generalised muscle dysfunction which contributes to the reduction in their exercise capacity, even in the absence of severe ventilatory impairment.
Modification of tyrosine residues and formation of 3-nitrotyrosine is one of the most commonly identified effects of reactive nitrogen species on proteins. In this study we evaluated the presence and localization of tyrosine nitration in various ventilatory and limb muscles. We also assessed the contribution of the neuronal (nNOS), the endothelial (eNOS), and the inducible (iNOS) isoforms of nitric oxide synthase (NOS) to tyrosine nitration in skeletal muscles both under normal conditions and in response to severe sepsis. In normal rats and mice, muscle tyrosine nitration was detected at 52, 48, 40, 30, 18, and 10 kD protein bands. Tyrosine nitration of the majority of these protein bands was significantly reduced within 1 h of in vivo NOS inhibition in rats. Diaphragmatic protein tyrosine nitration in mice deficient in the inducible NOS (iNOS-/-) averaged ~ 50% of that detected in wild-type (iNOS+/+) mice. Injection of bacterial lipopolysaccharides (LPS) in rats produced a significant rise in protein tyrosine nitration in the mitochondrial and membrane fractions but not in the cytosol of ventilatory muscles. Absence of iNOS expression (iNOS-/-), but not nNOS (nNOS-/-) or eNOS (eNOS-/-), in genetically altered mice resulted in a significant reduction in LPS-mediated rise in diaphragmatic nitrotyrosine. We conclude that tyrosine nitration of proteins occurs in normal muscle fibers and is dependent mainly on the activity of the iNOS isoform. Sepsis-mediated increase in protein tyrosine nitration is limited to the mitochondria and cell membrane and is highly dependent on the activity of the iNOS but not the nNOS or eNOS isoforms.
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