ArticleBasic research in cardiology2013
Neuronal nitric oxide synthase is indispensable for the cardiac adaptive effects of exercise.
Article in Basic research in cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Hyperbaric oxygenation applied before or after mild or hard stress: effects on the redox state in the muscle tissue.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Antiquated ejection fraction: Basic research applications for speckle tracking echocardiography.Frontiers in physiology · 2022Review
- Non-neuronal cardiac acetylcholine system playing indispensable roles in cardiac homeostasis confers resiliency to the heart.The journal of physiological sciences : JPS · 2021Article
- A Novel Endocrine Role for the BAT-Released Lipokine 12,13-diHOME to Mediate Cardiac Function.Circulation · 2021Article
- Proteomic Analysis of Cardiac Adaptation to Exercise by High Resolution Mass Spectrometry.Frontiers in molecular biosciences · 2021Article
- Molecular Mechanisms Mediating Adaptation to Exercise.Advances in experimental medicine and biology · 2020Review
- Aerobic exercise protects against pressure overload-induced cardiac dysfunction and hypertrophy via β3-AR-nNOS-NO activation.PloS one · 2017Article
- CXL-1020, a Novel Nitroxyl (HNO) Prodrug, Is More Effective than Milrinone in Models of Diastolic Dysfunction-A Cardiovascular Therapeutic: An Efficacy and Safety Study in the Rat.Frontiers in physiology · 2017Article
- Insulin-like growth factor 1 prevents diastolic and systolic dysfunction associated with cardiomyopathy and preserves adrenergic sensitivity.Acta physiologica (Oxford, England) · 2016Article
- Compromised redox homeostasis, altered nitroso-redox balance, and therapeutic possibilities in atrial fibrillation.Cardiovascular research · 2016Review
- Article
- Obligatory role of neuronal nitric oxide synthase in the heart's antioxidant adaptation with exercise.Journal of molecular and cellular cardiology · 2015Article
- Abnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balance.Antioxidants & redox signaling · 2014Review
- Aerobic exercise inhibits sympathetic nerve sprouting and restores β-adrenergic receptor balance in rats with myocardial infarction.PloS one · 2014Article
- Expression levels of sarcolemmal membrane repair proteins following prolonged exercise training in mice.Indian journal of biochemistry & biophysics · 2013Article
- Fibronectin contributes to pathological cardiac hypertrophy but not physiological growth.Basic research in cardiology · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Exercise results in beneficial adaptations of the heart that can be directly observed at the ventricular myocyte level. However, the molecular mechanism(s) responsible for these adaptations are not well understood. Interestingly, signaling via neuronal nitric oxide synthase (NOS1) within myocytes results in similar effects as exercise. Thus, the objective was to define the role NOS1 plays in the exercise-induced beneficial contractile effects in myocytes. After an 8-week aerobic interval training program, exercise-trained (Ex) mice had higher VO(2max) and cardiac hypertrophy compared to sedentary (Sed) mice. Ventricular myocytes from Ex mice had increased NOS1 expression and nitric oxide production compared to myocytes from Sed mice. Remarkably, acute NOS1 inhibition normalized the enhanced contraction (shortening and Ca(2+) transients) in Ex myocytes to Sed levels. The NOS1 effect on contraction was mediated via greater Ca(2+) cycling that resulted from increased phospholamban phosphorylation. Intriguingly, a similar aerobic interval training program on NOS1 knockout mice failed to produce any beneficial cardiac adaptations (VO(2max), hypertrophy, and contraction). These data demonstrate that the beneficial cardiac adaptations observed after exercise training were mediated via enhanced NOS1 signaling. Therefore, it is likely that beneficial effects of exercise may be mimicked by the interventions that increase NOS1 signaling. This pathway may provide a potential novel therapeutic target in cardiac patients who are unable or unwilling to exercise.
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