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Aerobic exercise prevents cardiomyocyte damage caused by oxidative stress in early cardiovascular disease by increasing vascularity while L-arginine supplementation prevents it by increasing activation of the enzyme nitric oxide synthase

Brazilian journal of medical and biological research, 2023-01, Vol.56 (1), p.e12533-e12533 [Peer Reviewed Journal]

COPYRIGHT 2023 Associacao Brasileira de Divulgacao Cientifica (ABDC) ;This work is licensed under a Creative Commons Attribution 4.0 International License. ;ISSN: 0100-879X ;ISSN: 1414-431X ;EISSN: 1414-431X ;DOI: 10.1590/1414-431X2023e12533

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  • Title:
    Aerobic exercise prevents cardiomyocyte damage caused by oxidative stress in early cardiovascular disease by increasing vascularity while L-arginine supplementation prevents it by increasing activation of the enzyme nitric oxide synthase
  • Author: Bertoldi, J.M.C.R.J ; Kindlovits, R ; Rocha, H.N.M ; Fernandes-Santos, C ; Gomes, J.L.P ; Oliveira, E.M ; Muniz, I.C ; Santos, M.M ; Pereira, J.F ; Rocha, N.G ; da Nobrega, A.C.L ; Medeiros, R.F
  • Subjects: Aerobic exercises ; Arginine ; BIOLOGY ; Cardiovascular disease ; Cardiovascular diseases ; Care and treatment ; Enzyme activation ; Exercise ; Fructose ; Health aspects ; Heart cells ; MEDICINE, RESEARCH & EXPERIMENTAL ; Oxidative stress ; Oxidoreductases ; Physiological aspects
  • Is Part Of: Brazilian journal of medical and biological research, 2023-01, Vol.56 (1), p.e12533-e12533
  • Description: L-Arginine and chronic exercise reduce oxidative stress. However, it is unclear how they affect cardiomyocytes during cardiovascular disease (CVD) development. The aim of this research was to investigate the possible effects of L- arginine supplementation and aerobic training on systemic oxidative stress and their consequences on cardiomyocytes during cardiometabolic disease onset caused by excess fructose. Wistar rats were allocated into four groups: control (C), fructose (F, 10% fructose in water), fructose training (FT; moderate running, 50-70% of the maximal velocity), and fructose arginine (FA; 880 mg/kg/day). Fructose was given for two weeks and fructose plus treatments for the subsequent eight weeks. Body composition, blood glucose, insulin, lipid profile, lipid peroxidation, nitrite, metalloproteinase-2 (MMP-2) activity, left ventricle histological changes, microRNA-126, -195, and -146, eNOS, p-eNOS, and TNF-[alpha] expressions were analyzed. Higher abdominal fat mass, triacylglycerol level, and insulin level were observed in the F group, and both treatments reversed these alterations. Myocardial vascularization was impaired in fructose-fed groups, except in FT. Cardiomyocyte hypertrophy was observed in all fructose-fed groups. TNF-[alpha] levels were higher in fructose-fed groups than in the C group, and p-eNOS levels were higher in the FA than in the C and F groups. Lipid peroxidation was higher in the F group than in the FT and C groups. During CVD onset, moderate aerobic exercise reduced lipid peroxidation, and both training and L-arginine prevented metabolic changes caused by excessive fructose. Myocardial vascularization was impaired by fructose, and cardiomyocyte hypertrophy appeared to be influenced by pro-inflammatory and oxidative environments. Key words: Cardiovascular disease; Exercise; Arginine; Fructose; Oxidative stress
  • Publisher: Associacao Brasileira de Divulgacao Cientifica (ABDC)
  • Language: English;Portuguese
  • Identifier: ISSN: 0100-879X
    ISSN: 1414-431X
    EISSN: 1414-431X
    DOI: 10.1590/1414-431X2023e12533
  • Source: SciELO
    GFMER Free Medical Journals
    PubMed Central
    DOAJ Directory of Open Access Journals

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