Moderate exercise training decreases aortic superoxide production in myocardial infarcted rats

Myocardial infarction (MI) has been associated with increases in reactive oxygen species (ROS). Exercise training (ET) has been shown to exert positive modulations on vascular function and the purpose of the present study was to investigate the effect of moderate ET on the aortic superoxide producti...

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Bibliographic Details
Published in:European journal of applied physiology 2008-12, Vol.104 (6), p.1045-1052
Main Authors: Zanchi, Nelo Eidy, Bechara, Luiz Roberto Grassmann, Tanaka, Leonardo Yuji, Debbas, Victor, Bartholomeu, Teresa, Ramires, Paulo Rizzo
Format: Article
Language:English
Subjects:
Animal euthanasia
Animals
Aorta, Thoracic - metabolism
Bioavailability
Biochemistry
Biomedical and Life Sciences
Biomedicine
Coronary vessels
Disease Models, Animal
Endothelium
Endothelium, Vascular - metabolism
Endothelium, Vascular - physiopathology
Exercise
Fitness training programs
Heart attacks
Human Physiology
Male
Myocardial Infarction - metabolism
Myocardial Infarction - physiopathology
NADPH Oxidases - metabolism
Norepinephrine - pharmacology
Occupational Medicine/Industrial Medicine
Original Article
Oxidative stress
Physical Conditioning, Animal - physiology
Physical education
Physical fitness
Rats
Rats, Wistar
Sports Medicine
Superoxide Dismutase - metabolism
Superoxides - metabolism
Vasoconstriction - drug effects
Vasoconstrictor Agents - pharmacology
Vasodilation - physiology
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Summary:Myocardial infarction (MI) has been associated with increases in reactive oxygen species (ROS). Exercise training (ET) has been shown to exert positive modulations on vascular function and the purpose of the present study was to investigate the effect of moderate ET on the aortic superoxide production index, NAD(P)H oxidase activity, superoxide dismutase activity and vasomotor response in MI rats. Aerobic ET was performed during 11 weeks. Myocardial infarction significantly diminished maximal exercise capacity, and increased vasoconstrictory response to norepinephrine, which was related to the increased activity of NAD(P)H oxidase and basal superoxide production. On the other hand, ET normalized the superoxide production mostly due to decreased NAD(P)H oxidase activity, although a minor SOD effect may also be present. These adaptations were paralleled by normalization in the vasoconstrictory response to norepinephrine. Thus, diminished ROS production seems to be an important mechanism by which ET mediates its beneficial vascular effects in the MI condition.
ISSN:1439-6319
1439-6327
DOI:10.1007/s00421-008-0861-0