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Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion.

Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. Research Abstract Details 

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  • Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. Abstract Text:

    john m lawlerJohn M Lawler,hyo-bum kwakHyo-Bum Kwak,wook songWook Song,janet l parkerJanet L Parker,

    Oxidative stress is associated with muscle fatigue and weakness in skeletal muscle of ischemic heart disease patients. Recently, it was found that endurance training elevates protective heat shock proteins (HSPs) and antioxidant enzymes in skeletal muscle in healthy subjects and antioxidant enzymes in heart failure patients. However, it is unknown whether coronary ischemia and mild infarct without heart failure contributes to impairment of stress proteins and whether exercise training reverses those effects. We tested the hypothesis that exercise training would reverse alterations in muscle TNF-alpha, oxidative stress, HSP70, SOD (Mn-SOD, Cu,Zn-SOD), glutathione peroxidase (GPX), and catalase (CAT) due to chronic coronary occlusion of the left circumflex (CCO). Yucatan swine were divided into three groups (n = 6 each): sedentary with CCO (SCO); 12 wk of treadmill exercise training following CCO (ECO); and sham surgery controls (sham). Forelimb muscle mass-to-body mass ratio decreased by 27% with SCO but recovered with ECO. Exercise training reduced muscle TNF-alpha and oxidative stress (4-hydroxynonenal adducts) caused by CCO. HSP70 levels decreased with CCO (-45%), but were higher with exercise training (+348%). Mn-SOD activity, Mn-SOD protein expression, and Cu,Zn-SOD activity levels were higher in ECO than SCO by 72, 82, and 112%, respectively. GPX activity was 177% greater in ECO than in SCO. CAT trended higher (P = 0.059) in ECO compared with SCO. These data indicate that exercise training following onset of coronary artery occlusion results in recovery of critical stress proteins and reduces oxidative stress.

    Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. Publishing Authors By Initials

    jm lawlerJM Lawler,hb kwakHB Kwak,w songW Song,jl parkerJL Parker,

    For similar animals: chordata: vertebrates: mammals: artiodactyla: swine: sus scrofa: swine, miniature research abstracts see: animals: chordata: vertebrates: mammals: artiodactyla: swine: sus scrofa: swine, miniature research

    PUBMED ID PMID:

    MEDLINE DATE:

    Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: American journal of physiology. Regulatory, integr

    VOLUME: 291

    Page Numbers: R1756-63

    Journal Abbreviation: Am. J. Physiol. Regul. Integr.

    ISSN: 0363-6119

    DAY: 27

    MONTH: 07

    YEAR: 2006

    Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901230

    Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. Keywords Mesh Terms:

    KEYWORDS: Swine, Miniature

    MESH TERMS: methods

    Chemical & Substance for Abstract: Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion. Information

    Substance Name: HSP70 Heat-Shock Proteins

    Registry Number: 0

    Grant and Affiliation Information for Exercise training reverses downregulation of HSP70 and antioxidant enzymes in porcine skeletal muscle after chronic coronary artery occlusion.

    AFFILIATION: Redox Biology and Cell Signaling Laboratory, Department of Health and Kinesiology, Texas A&M University, College Station, TX 77843-4243, USA. jml2621@neo.tamu.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: R01 HL 64931

    ACRONYM: HL

    MEDLINETA: Am J Physiol Regul Integr Comp

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