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  • Cardiac Protection from Ischemia-Reperfusion Injury in Swimming Mice

    Author(s)
    Budiono, Boris P
    Vider, Jelena
    Peart, Jason N
    Headrick, John P
    Haseler, Luke J
    Griffith University Author(s)
    Peart, Jason N.
    Headrick, John P.
    Vider, Jelena
    Budiono, Boris P.
    Haseler, Luke J.
    Year published
    2015
    Metadata
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    Abstract
    PURPOSE:The purpose of this study was to determine whether cardiac protection from ischemia could be afforded with a forced-swimming as a higher intensity and stress model of exercise. We hypothesised was that higher-intensity training via forced swimming might invoke additional protective mechanisms or pathways than those previously reported in response to lower intensity voluntary activity such as wheel running. METHODS: Male C57Bl/6 mice swam for 90 min twice a day for 1 or 2 wk before randomly assigned to either 1) molecular analysis of cardiac pro-survival kinases with Phospho-Receptor Tyrosine Kinase (P-RTK) Proteome ...
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    PURPOSE:The purpose of this study was to determine whether cardiac protection from ischemia could be afforded with a forced-swimming as a higher intensity and stress model of exercise. We hypothesised was that higher-intensity training via forced swimming might invoke additional protective mechanisms or pathways than those previously reported in response to lower intensity voluntary activity such as wheel running. METHODS: Male C57Bl/6 mice swam for 90 min twice a day for 1 or 2 wk before randomly assigned to either 1) molecular analysis of cardiac pro-survival kinases with Phospho-Receptor Tyrosine Kinase (P-RTK) Proteome arrays and Western Immunoblotting, 2) transcriptional adaptations via qRT-PCR, or 3) global ischemia-reperfusion injury assessment via Langendorff isolated heart preparation with 25-min ischemia/45-min reperfusion. RESULTS: Hearts exhibited physiological hypertrophy (15.44% and 22% increase in Heart:Body weight ratio compared to sedentary controls in 1 and 2 wk groups respectively). Langendorff perfusion revealed left ventricular developed pressure (LVDP) improved (61.46% ± 5.7 vs. 44.35% ± 3.7, P<0.01) and end diastolic pressure was reduced (EDP mmHg: 12.68 ± 1.8 vs. 27.40 ± 1.8, P<0.01) following 2 wks of swim training. Subsequent gene and protein expression showed differential signaling in pro-survival kinases and other cardioprotective mechanisms. Pooled sample proteome arrays within the 2-week group showed exercised mice exhibited greater phosphorylation of various growth factors such as Insulin receptor, IGF-1R, FGF, HGF, PDGF. Protein expression of NFKB was reduced in exercised groups. CONCLUSIONS: These data indicate that swimming mice exhibited significant cardioprotection compared to the sedentary group after 2 weeks of exercise. Subsequent proteomic screening showed that in the 2-week group, a number of P-RTK growth factor receptors were activated in response to exercise. The anti-inflammatory and activation of pro-survival kinases due to the hormetic effect of exercise warrants further investigation.
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    Conference Title
    Medicine & Science in Sports & Exercise
    Volume
    47
    Issue
    5
    DOI
    https://doi.org/10.1249/01.mss.0000478903.50888.9f
    Subject
    Human Movement and Sports Sciences
    Medical Physiology
    Public Health and Health Services
    Science & Technology
    Life Sciences & Biomedicine
    Sport Sciences
    Publication URI
    http://hdl.handle.net/10072/388800
    Collection
    • Conference outputs

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