Abstract
PURPOSE Chronic exercise training elicits adaptations in the heart that improve pump function and confer cardioprotection. To identify molecular mechanisms by which exercise training stimulates this favorable phenotype, a proteomic approach was employed to test the hypothesis that rat cardiac proteins would be differentially expressed or modified after exercise training. METHODS Exercise-trained rats (n=8) underwent six weeks of progressive treadmill training, five days per week, with high intensity sprints interspersed periodically with running at a moderate speed. Sedentary control rats (n=8) were age-matched and weight-matched to exercise-trained rats. Hearts were harvested and quick-frozen in liquid nitrogen at various times (0–72 hr) after the last bout of exercise and were subsequently used to generate 2-dimensional electrophoretic (2-DE) proteome maps. PDQuest software was used to analyze 2-DE gels, quantify spot densities, and compare expression levels between groups. Protein spots were identified with mass spectrometry of trypsin digests. RESULTS Exercise-trained rats exhibited a 14% greater left ventricular weight-to-body weight ratio than sedentary rats (p < 0.05). Compared with hearts of sedentary rats, 26 protein spot intensities were significantly altered in hearts of exercise-trained rats (p < 0.05), and 15 additional spots appeared exclusively on gels from the exercise-trained rats. Among candidate proteins with increased levels of expression in hearts of exercise-trained rats were a heat shock protein, a mitochondrial elongation factor, a proteasome subunit, desmin, and two steroid modifying enzymes. Proteins that exhibited decreased expression levels in the hearts of exercise-trained rats included a mitochondrial ATP synthase and a myosin heavy chain fragment. CONCLUSIONS Exercise training alters the cardiac proteome of the rat. The proteome changes include several candidate proteins that require further study to determine their role in the adaptation of the heart to exercise training. Supported by American Heart Association Midwest Affiliate and NIH R03 AG022625.
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