Nitric oxide and muscle weakness
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Muscle weakness and fatigue are cardinal features of muscle disease, occurring in inherited and sporadic muscle disorders, and also in neurogenic disorders of muscle. Although many neuromuscular disorders cause muscular atrophy, weakness is not necessarily related to reduced muscle bulk, implying that contractile power depends on other intrinsic metabolic properties of muscle fibers. Therefore, a search for the factors regulating muscle force in neuromuscular disease should be directed to metabolic, energy-dependent processes, in addition to structural changes in muscle fiber morphometry, or in muscle fibrils, or even in muscle innervation. Metabolic disturbances in muscle are primary features of glycogenopathies, e.g., in muscle phosphorylase deficiency and in mitochondrial cytopathies, but the resulting deficits in muscle function even in these disorders are not entirely clear.
In this issue of Neurology®, in an important study, Finanger Hedderick et al.1 draw attention to the potential importance of abnormal sarcolemmal neuronal nitric oxide synthase (nNOS) activity as a factor leading to muscle weakness in a variety of different neuromuscular disorders. They reviewed nNOS immunofluorescence staining in 161 muscle biopsies from patients with inherited myopathies excluding dystrophinopathies and acquired neuromuscular disorders, and also studied mouse models of steroid myopathy and starvation-induced cachexia. …
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