Physiology of nitric oxide in skeletal muscle.

By J. Stamler, G. Meissner. Physiological Reviews, 2001

1,109 citations recorded by the source corpus.

Subfields: Ecology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/539a7fa7c9470890db43f18c9a25bd2fe181148b

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Citations in the corpus

• Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans. (2009, background): “10), but there is also evidence that NO has the potential to modulate other aspects of mitochondrial and muscle contractile function (11, 57, 58).”
• Dietary nitrate supplementation enhances muscle contractile efficiency during knee-extensor exercise in humans. (2010, background): “A slight shift in substrate utilization toward a relatively greater use of carbohydrate, perhaps as a consequence of a NO-mediated increase in myocyte glucose uptake (64), might provide a partial explanation for this effect.”
• Effects of dietary nitrate on oxygen cost during exercise (2007, background): “NO increases blood flow to the muscles and modulates muscular contraction and glucose uptake (for review see Stamler & Meissner 2001).”
• Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force Production (2008, background): “ditions, but it does not play a significant role in normal muscle (373).”
• Neuronal nitric oxide synthase: structure, subcellular localization, regulation, and clinical implications. (2009, positive): “However, caveolin-3 by inhibiting CaCaM binding suppresses NO synthesis in skeletal muscle, and consequently this inhibition is reversed by Ca-CaM [10].”
• Protein Oxidation: Basic Principles and Implications for Meat Quality (2013, background): “Three isoforms of NOS, which include neuronal NOS (NOS1 or nNOS), macrophage (immune)/calcium calmodulinindependent or inducible NOS (NOS2 or iNOS), and endothelial NOS (eNOS or NOS) have been identified (Stamler and Meissner, 2001).”
• Respiratory care of the patient with Duchenne muscular dystrophy: ATS consensus statement. (2004, background): “In addition, the recently discovered protective mechanism of nitric oxide release in exercising muscle may be defective in children with DMD (44, 45).”
• Regulatory role for the arginine-nitric oxide pathway in metabolism of energy substrates. (2006, background): “The target cells for NO action can be the NO-producing cell itself, the neighboring cells via its direct release or the distant cells via transport by glutathione and red blood cells [25].”