| Exercise training normalizes sympathetic outflow by central antioxidant mechanisms in rabbits with pacing-induced chronic heart failure. | |
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MedLine Citation:
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PMID: 17548725 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: In a recent study, we demonstrated that an increase in oxidative stress in the rostral ventrolateral medulla plays a critical role in the sympathoexcitation observed in chronic heart failure (CHF). Growing evidence indicates that exercise training evokes an antioxidative effect in CHF. In the present study, we therefore hypothesized that long-term exercise exerts its beneficial effect on autonomic activity in CHF via central antioxidative mechanisms. METHODS AND RESULTS: Experiments were performed on New Zealand White rabbits. All rabbits were instrumented to measure mean arterial pressure, heart rate, and renal sympathetic nerve activity and to test baroreflex sensitivity. Exercise training significantly decreased baseline renal sympathetic nerve activity (65.8+/-5.2% to 41.3+/-3.9% of Max [where "Max" is the maximum renal sympathetic nerve activity induced by a 50-mL puff of smoke directed to the external nares of the rabbit], P<0.05) and increased the maximal gain of the baroreflex curves for heart rate (2.2+/-0.2 to 4.6+/-0.7 bpm per mm Hg, P<0.01) and renal sympathetic nerve activity (1.9+/-0.2% to 4.5+/-0.4% of Max per mm Hg, P<0.01) in CHF rabbits. Exercise training increased expression of CuZn superoxide dismutase (0.3+/-0.1 to 1.5+/-0.3 [ratio of CuZn superoxide dismutase to tubulin], P<0.01) and decreased NAD(P)H oxidase subunit gp91(phox) protein expression (1.9+/-0.2 to 1.2+/-0.1 [ratio of gp91(phox) to tubulin], P<0.05) in the rostral ventrolateral medulla of CHF rabbits. Central overexpression of CuZn superoxide dismutase dose-dependently decreased baseline renal sympathetic nerve activity (control, 68.5+/-7.1% of Max; 10(10) particles of adenovirus, 53.2+/-4.4% of Max; and 10(11) particles of adenovirus, 33.7+/-3.5% of Max; P<0.05) in CHF rabbits. CONCLUSIONS: These results suggest that an upregulation in central antioxidative mechanisms and suppressed central prooxidant mechanisms may contribute to the exercise training-induced beneficial effects on autonomic activity in CHF. |
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Authors:
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Lie Gao; Wei Wang; Dongmei Liu; Irving H Zucker |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2007-06-04 |
Journal Detail:
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Title: Circulation Volume: 115 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 2007 Jun |
Date Detail:
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Created Date: 2007-06-19 Completed Date: 2007-07-10 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: United States |
Other Details:
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Languages: eng Pagination: 3095-102 Citation Subset: AIM; IM |
Affiliation:
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Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, NE 68198-5850, USA. lgao@unmc.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antioxidants / metabolism* Baroreflex / physiology Blotting, Western Body Weight Chronic Disease Disease Models, Animal Echocardiography Exercise Therapy / methods* Free Radicals / metabolism Gene Expression Regulation, Enzymologic Gene Transfer Techniques Heart Failure / metabolism*, physiopathology, therapy*, ultrasonography Male Myocardium / pathology NADPH Oxidase / genetics, metabolism Organ Size Oxidative Stress Pacemaker, Artificial Rabbits Superoxide Dismutase / genetics, metabolism Sympathetic Nervous System / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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P0-1-HL-62222/HL/NHLBI NIH HHS; R0-1-HL-38690/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antioxidants; 0/Free Radicals; EC 1.15.1.1/Superoxide Dismutase; EC 1.6.3.1/NADPH Oxidase |
| Comments/Corrections | |
Comment In:
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Circulation. 2007 Jun 19;115(24):3042-4
[PMID:
17576880
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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