Regulation of nitric oxide production in limb and  ventilatory muscles during chronic exercise training

Vassilakopoulos, T.; Deckman, G.; Kebbewar, Moustafa; Rallis, George; Harfouche, Rania; Hussain, Sabah N. A.

doi:10.1152/ajplung.00270.2002

Cited by 69 publications

(74 citation statements)

References 28 publications

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“…nNOSμ expression and activity increased in the hindlimb and respiratory muscles of rats subjected to long-term treadmill running or swimming (Balon and Nadler 1997;TatchumTalom et al 2000;Vassilakopoulos et al 2003). Skeletal muscle nNOSμ expression declines with age in rats, suggesting that sarcopenia may be linked with the downregulation of nNOSμ (Song et al 2009), but long-term treadmill running has been found to reverse this age-related decrease in nNOSμ expression (Song et al 2009).…”

Section: Nnos and Skeletal Muscle Adaptation To Exercisementioning

confidence: 99%

nNOS regulation of skeletal muscle fatigue and exercise performance

Percival

2011

Biophys Rev

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Neuronal nitric oxide synthases (nNOS) are Ca 2+ /calmodulin-activated enzymes that synthesize the gaseous messenger nitric oxide (NO). nNOSμ and the recently described nNOSβ, both spliced nNOS isoforms, are important enzymatic sources of NO in skeletal muscle, a tissue long considered to be a paradigmatic system for studying NO-dependent redox signaling. nNOS is indispensable for skeletal muscle integrity and contractile performance, and deregulation of nNOSμ signaling is a common pathogenic feature of many neuromuscular diseases. Recent evidence suggests that both nNOSμ and nNOSβ regulate skeletal muscle size, strength, and fatigue resistance, making them important players in exercise performance. nNOSμ acts as an activity sensor and appears to assist skeletal muscle adaptation to new functional demands, particularly those of endurance exercise. Prolonged inactivity leads to nNOS-mediated muscle atrophy through a FoxO-dependent pathway. nNOS also plays a role in modulating exercise performance in neuromuscular disease. In the mdx mouse model of Duchenne muscular dystrophy, defective nNOS signaling is thought to restrict contractile capacity of working muscle in two ways: loss of sarcolemmal nNOSμ causes excessive ischemic damage while residual cytosolic nNOSμ contributes to hypernitrosylation of the ryanodine receptor, causing pathogenic Ca 2+ leak. This defect in Ca 2+ handling promotes muscle damage, weakness, and fatigue. This review addresses these recent advances in the understanding of nNOS-dependent redox regulation of skeletal muscle function and exercise performance under physiological and neuromuscular disease conditions.

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Section: Nnos and Skeletal Muscle Adaptation To Exercisementioning

confidence: 99%

nNOS regulation of skeletal muscle fatigue and exercise performance

Percival

2011

Biophys Rev

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“…In rat skeletal muscle myoblasts, the IL-1β-mediated iNOS induction was reduced by blocking ERK1/2 activation and completely abolished by the inhibition of NFκB. Increased iNOS mRNA level after an acute bout of exercise in rat skeletal muscles has been reported by some authors [117,132] , but not others [134] . However, the role of iNOS is controversial because it is often coexpressed with pro-inflammatory cytokines and adhesion molecules causing muscle inflammation and wasting.…”

Section: Exercise Activation Of Redox Signaling Pathwaysmentioning

confidence: 85%

Hormesis and Exercise: How the Cell Copes with Oxidative Stress

Radák

Goto

2008

American J. of Pharmacology and Toxicology

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Contraction-induced production of reactive oxygen and nitrogen species has been shown to cause oxidative stress to skeletal muscle, heart and other organs. As an adaptive response, muscle antioxidant defense systems are upregulated in response to exercise to restore intracellular prooxidantantioxidant homeostasis. Thus, both young and old animals and humans involved in regular exercise have shown reduced oxidative damage during acute physical exertion at accustomed or excessive intensity, or under oxidative challenges otherwise deemed detrimental. The current article provides a brief review of this exercise-induced hormesis with the emphasis on the role of redox sensitive signal transduction pathways (mainly nuclear factor κB and mitogen-activated protein kinase) that can activate the gene expression of antioxidant enzymes and proteins. Molecular mechanisms and gene targets for these signaling pathways, as well as the biological significance of the adaptations, are discussed.

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“…The role of NO is commonly related to vasodilation of the endothelium to facilitate the coming of nutrients distribution to the active muscles as well as the removal and transport of metabolites, maintaining cellular homeostasis 43,44 . Studies using animals showed that 4 and 8 weeks of treadmill running training 47,48 as 4 weeks of swimming training 49 can upregulate nNOS levels in the skeletal muscle of trained mice. On the other hand, studies with humans are not clear in showing if there is an increase in the levels of nNOS and NO in skeletal muscle in response to exercise 45,46 .…”

Section: Physical Exercise Nitric Oxide Synthesis and Glucose Uptakementioning

confidence: 99%

Molecular mechanisms of glucose uptake in skeletal muscle at rest and in response to exercise

Pereira

Moura

Muñoz

et al. 2017

Motriz: rev. educ. fis.

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-Glucose uptake is an important phenomenon for cell homeostasis and for organism health. Under resting conditions, skeletal muscle is dependent on insulin to promote glucose uptake. Insulin, after binding to its membrane receptor, triggers a cascade of intracellular reactions culminating in activation of the glucose transporter 4, GLUT4, among other outcomes. This transporter migrates to the plasma membrane and assists in glucose internalization. However, under special conditions such as physical exercise, alterations in the levels of intracellular molecules such as ATP and calcium act to regulate GLUT4 translocation and glucose uptake in skeletal muscle, regardless of insulin levels. Regular physical exercise, due to stimulating pathways related to glucose uptake, is an important non-pharmacological intervention for improving glycemic control in obese and diabetic patients. In this mini-review the main mechanisms involved in glucose uptake in skeletal muscle in response to muscle contraction will be investigated.

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Regulation of nitric oxide production in limb and ventilatory muscles during chronic exercise training

Cited by 69 publications

References 28 publications

nNOS regulation of skeletal muscle fatigue and exercise performance

nNOS regulation of skeletal muscle fatigue and exercise performance

Hormesis and Exercise: How the Cell Copes with Oxidative Stress

Molecular mechanisms of glucose uptake in skeletal muscle at rest and in response to exercise

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