Premium
Chronic Interval Exercise Modifies the Myocardial Lipid Profile in a Miniature Swine Model of Heart Failure with Preserved Ejection Fraction
Author(s) -
Emter Craig Allen,
Rector R. Scott,
Baines Christopher P.,
Ford Kaitlin D.,
Ford David A.
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.1192.14
Subject(s) - cardiolipin , heart failure , medicine , lipidomics , endocrinology , ejection fraction , cardiology , ceramide , lipid profile , heart failure with preserved ejection fraction , chemistry , phospholipid , biochemistry , cholesterol , apoptosis , membrane
Manipulation of dietary lipid intake and exercise has demonstrated beneficial effects in preventing the progression of heart failure (HF). We have previously shown chronic exercise prevents mitochondrial dysfunction characterized by increased mitochondrial permeability transition. Recent studies examining impaired mitochondrial function have focused on cardiolipin, a mitochondria‐localized phospholipid that decreases during HF. Our purpose was to examine the effect of chronic exercise on myocardial lipid phenotype in aortic‐banded mini‐swine with compensated HF. Shotgun lipidomics was used to examine alterations in ventricular lipids in male control (n=7), sedentary HF (n=4), and exercise trained HF (HF‐TR, n=7) animals. Total cardiolipin was significantly increased in the HF‐TR animals. Specific modifications in the cardiolipin pool were found in the tetralinoleoyl cardiolipin molecular species. Differences in triacylglycerol and ceramide molecular species were also observed. In conclusion, our novel results demonstrate the efficacy of exercise in modulating myocardial lipid profile in a large animal model of HF. We propose that our previous observation of exercise‐dependent preservation of normal mitochondrial function may be mediated via modification of myocardial lipid phenotype. Research support: NIH HL074214 , HL111906 (DAF), HL093982 ‐01, HL101332 (CAE), and VA‐CDA2 (RSR).