Abstract

Aging is associated with a decline in cardiac function. Exercise intervention has been suggested as a way to improve this decrement. Age-related decline in cardiac function is associated with decreases in fatty acid oxidation, mitochondrial function, and AMP-activated protein kinase (AMPK) activity. The molecular mechanisms involved with age-related changes in mitochondrial function and substrate metabolism are poorly understood. We determined gene expression differences in hearts of Young (6 mo), Old (33 mo), and old exercise trained (Old + EXE) (34 mo) FBN rats, using Qiagen PCR arrays for Glucose, Fatty acid, and Mitochondrial metabolism. Old rats demonstrated decreased (p < 0.05) expression for key genes in fatty acid oxidation, mitochondrial function, and AMPK signaling. There were no differences in the expression of genes involved in glucose metabolism with age. These gene expression changes occurred prior to altered protein translation as we found no differences in the protein content of peroxisome proliferator activated receptor gamma, coactivators 1 alpha (PGC-1α), peroxisome proliferator activated receptor alpha (PPARα), and AMPKα2 between young and old hearts. Four months of exercise training did not attenuate the decline in the gene expression in aged hearts. Despite this lack of change in gene expression, exercise-trained rats demonstrated increased exercise capacity compared to their sedentary counterparts. Taken together, our results show that differential expression of genes associated with fatty acid metabolism, AMPK signaling and mitochondrial function decrease in the aging heart which may play a role in age-related declines in fatty acid oxidation, AMPK activity, and mitochondrial function in the heart.

Highlights

  • Aging is associated with a decline in cardiac function in humans as well as rodents (Lakatta and Sollott, 2002)

  • We found that exercise training improved functional exercise capacity (Figure 4) despite either no changes in gene expression compared to Old hearts or in some cases, a further reduction in the expression of genes associated with energy metabolism and mitochondrial function in the heart

  • This study was the first to utilize a comprehensive approach in the study of age and exercise effects in aged hearts on substrate metabolism and mitochondrial function by an integration of gene expression, protein content, and protein activity

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Summary

Introduction

Aging is associated with a decline in cardiac function in humans as well as rodents (Lakatta and Sollott, 2002). Mitochondrial energetic deficiency with aging has been well-documented (McMillin et al, 1993; Fannin et al, 1999; Phaneuf and Leeuwenburgh, 2002; Chakravarti et al, 2008; VenturaClapier et al, 2008). The mechanisms of this mitochondrial dysfunction may include biogenesis. Several studies have documented age-dependent impairment in the mitochondrial respiratory capacity (Kumaran et al, 2005; Navarro and Boveris, 2007)

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