High Oxidative Capacity Due to Chronic Exercise Training Attenuates Lipid-Induced Insulin Resistance
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Figures
- FIG. 1.
Mitochondrial oxygen flux (pmol ⋅ mg−1 ⋅ s−1) measured in permeabilized muscle fibers in trained (black bars) and untrained (white bars) subjects (A) and normalized to mitochondrial content (B). *P < 0.05, trained vs. untrained subjects. mtDNA copy number calculated as the ratio ND1/LPL in arbitrary units (C). All data are expressed as mean ± SE. cytc, cytochrome c; FCCP, fluoro-carbonyl cyanide phenylhydrazone; M, malate; MG3, malate glutamate and ADP; MGS3, MG3 and succinate; MO, malate octanoyl-carnitine; MO3, MO and ADP; MOG3, MO3 and glutamate; MOGS3, MOG3 and succinate; O4, oligomycin.
- FIG. 2.
Insulin sensitivity expressed as insulin-stimulated change of ΔRd (A), carbohydrate oxidation (B), and NOGD (C) (all parameters expressed as μmol ⋅ kg−1 ⋅ min−1) in trained (black bars) and untrained (white bars) subjects during a hyperinsulinemic-euglycemic clamp with simultaneous infusion of glycerol or lipid. Data expressed as mean ± SE. *P < 0.05.
- FIG. 3.
The expression level of insulin receptor (A), pGSK3β (B), GS (C), phosphorylation of FOXO1 (pFOXO1) (D), and phosphorylation of PDK4 (E) in trained and untrained subjects before and after glycerol (white and light gray bars, respectively) as well as before and after lipid infusion (black and dark gray bars, respectively). Representative Western blots under baseline conditions (b), after glycerol (g), and after lipid (l) infusion, with (+) and without (−) insulin stimulation (F). Data expressed as mean ± SE. AU, arbitrary units.
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