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. 2016 Aug 23;7:352. doi: 10.3389/fphys.2016.00352

Figure 2.

Figure 2

Fold changes in gene expression Old and Old + EXE hearts relative to young hearts (Values are the Means ±S.E.M, n = 5 per group). (A) Genes involved in fatty acid transport and oxidation decline with age and this attenuation is not mitigated with exercise. (CPT1c, Carnitine-palmitoyl transferase 1c; CPT2, Carnitine palmitoyl transferase 2; FATP, Fatty acid transporter; FABP3, Fatty acid binding protein 3; HADHA, Hydroxyacyl-Coenzyme A dehydrogenase/3-ketoacyl-Coenzyme A thiolase/enoyl-CoA hydratase (trifunctional protein); LPL, Lipoprotein lipase). (B) AMPK signaling decrements with age involve changes in the gene expression of AMPK subunits and upstream kinases. (AMPKα2, Protein kinase; AMP, activated alpha 2 catalytic subunit; AMPKβ1, Protein kinase; AMP, activated beta 1 non-catalytic subunit; AMPKγ1, Protein kinase; AMP, activated gamma 1 non-catalytic sununit; Camkk2, Calcium/calmodulin-dependent protein kinase kinase 2 beta; LKB1, Liver kinase B 1). (C) Mitochondrial biogenesis and maintenance of mitochondrial function decline with age and exercise does not appear to improve the attenuation. (PGC1α, Peroxisome proliferator—activated receptor gamma, coactivator 1 alpha; PGC1β, Peroxisome proliferator—activator receptor gamma, coactivator 1 beta; Mfn1, Mitofusin 1; Mfn2, Mitofusin 2; HSP78, Heat shock protein 78). aP < 0.05 vs. Young, bP < 0.05 vs. Old + EXE.