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Endurance exercise training attenuates fibrosis and collagen cross‐linking in myocardium of aged F344BNF1 rats
Author(s) -
Wright Kathryn Jean,
Betik Andrew,
Thomas Melissa,
Hepple Russell,
Belke Darrell
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1129.5
Subject(s) - mmp1 , timp1 , pentosidine , fibrosis , senescence , glycation , matrix metalloproteinase , endocrinology , medicine , collagenase , gene expression , endurance training , chemistry , biochemistry , gene , enzyme , diabetes mellitus
The objective of the study was to determine if endurance exercise training (ET) could attenuate the age‐related increase in fibrosis and collagen cross‐linking in the myocardium of the heart, which is thought to be a cause of the age‐related decline in diastolic function. Fisher 344 × Brown Norway F1 rats underwent ET from late middle age into senescence. Genes for collagen synthesis and degradation were assessed by polymerase chain reaction. Matrix metalloproteinase (MMP) activity was assessed using EnzChek Gelatinase/Collagenase Assay kit, and collagen cross‐linking was determined indirectly by immunohistochemical staining for advanced glycation end‐products. Tissue inhibitor of matrix metalloproteinase‐1 (TIMP1) gene expression, TIMP and MMP1 protein expression, and MMP activity increased with age but with no ET effect. ET attenuated the age‐related increase in fibrosis and collagen cross‐linking, while increasing survival rate. This could have attenuated the age‐related decline in myocardial compliance and in turn have helped attenuate the decrease in diastolic function generally seen with aging. This work was supported by an operating grant from CIHR (MOP 57808).