23 research outputs found

    Effect of temperature on fatty acid metabolism in skeletal muscle mitochondria of untrained and endurance-trained rats - Fig 2

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    <p><b>Determination of protein levels in skeletal muscle homogenates (A) and mitochondria (B) from control (</b>c<b>) and trained (t) rats. A</b>, Representative Western blots and analyses of the protein expression of PGC1α, mitochondrial marker (Mito marker), Nrf2, CD36, β-actin and GADPH. <b>B</b>, Representative Western blots and analyses of the protein expression of ACADS, CPT1A, CD36, COXII, (Mito marker). Expression levels were normalized for β actin or GADPH (<b>A</b>, <i>right panel</i>) and mito marker or COXII (<b>B</b>, <i>right panel</i>). The data (± SD, <i>n</i> = 6) is from six independent homogenate or mitochondrial preparations from six different animals from each group. ***<i>P</i> < 0.001, **<i>P</i> < 0.01, *<i>P</i> < 0.05 vs. value obtained for control rats.</p

    Effect of temperature on fatty acid metabolism in skeletal muscle mitochondria of untrained and endurance-trained rats - Fig 1

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    <p><b>The influence of endurance training on mitochondrial oxidation of palmitoylcarnitine (A) and glycerol-3-phosphate (B) at 25</b>°<b>C, 35</b>°<b>C and 42</b>°<b>C.</b> Respiratory rates were measured in mitochondria isolated from control (c) and trained (<b>t</b>) rats in the presence of 150 μM ADP (state 3, phosphorylating respiration) with 0.5 mM palmitoyl-DL-carnitine (<b>A</b>) or 5 mM glycerol-3-phosphate (<b>B</b>). Mean values (± SD) for six mitochondria preparations from six different animals from each group (<i>n</i> = 6) are shown. <sup>###</sup><i>P</i> < 0.001, <sup>##</sup><i>P</i> < 0.01, <sup>#</sup><i>P</i> < 0.05 vs value obtained at 35°C for a given group of animals, i.e., within control rats or trained rats. ***<i>P</i> < 0.001, **<i>P</i> < 0.01, *<i>P</i> < 0.05 vs. value obtained for control rats for a given assay temperature.</p

    Experimental V’O<sub>2</sub> and simulated muscle V’O<sub>2</sub>, metabolite concentrations and ATP usage/supply fluxes during low-intensity (baseline) and high-intensity cycling exercise in untrained and trained muscle.

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    <p>(A) Experimental and simulated V’O<sub>2</sub>, simulated ADP and pH. (B) Simulated PCr, P<sub>i</sub> and ATP. (C) Simulated ATP usage (UT), ATP supply by OXPHOS (OX), ATP supply by anaerobic glycolysis (GL), ATP supply by creatine kinase (CK). Experimental baseline-heavy-intensity exercise transition: after 3 min. Simulated baseline-heavy-intensity exercise transition: after 3.4 min (the delay by 24 s corresponds to the cardio-dynamic phase of the pulmonary V’O<sub>2</sub> on-kinetics). The muscle V’O<sub>2</sub> is calculated based on the assumption that during baseline-intensity exercise (20 W) muscle V’O<sub>2</sub> constitutes ~75% and during heavy-intensity exercise ~85% of the pulmonary V’O<sub>2</sub> (see Ref. [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0154135#pone.0154135.ref040" target="_blank">40</a>]).</p
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