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1 Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA; Medicine, Duke University, Durham, NC, USA; Sarah W. Stedman Nutrition and Metabolism Center, Duke University, Durham, NC, USA
2 Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA
3 Exercise and Sport Science, College of Health and Human Performance, East Carolina University, Greenville, NC, USA
4 Medicine, Duke University, Durham, NC, USA; Pharmacology & Cancer Biology, Duke University, Durham, NC, USA; Sarah W. Stedman Nutrition and Metabolism Center, Duke University, Durham, NC, USA
5 Physiology, Brody School of Medicine, East Carolina University, Greenville, NC, USA; Exercise and Sport Science, College of Health and Human Performance, East Carolina University, Greenville, NC, USA
* To whom correspondence should be addressed. E-mail: cortrightr{at}mail.ecu.edu.
Skeletal muscle contains two populations of mitochondria that appear to be differentially affected by disease and exercise training. It remains unclear how these mitochondrial subpopulations contribute to fiber-type related and/or training-induced changes in fatty acid oxidation and regulation of carnitine palmitoyltransferase 1
(CPT1), the enzyme that controls mitochondrial fatty acid uptake in skeletal muscle. To this end, we found that fatty acid oxidation rates were 8.9-fold higher in subsarcolemmal mitochondria (SS) and 5.3-fold higher in intermyofibrillar mitochondria (IMF) that were isolated from red (RG) compared to white (WG) gastrocnemius muscle, respectively. Malonyl-CoA (10 µM), a potent inhibitor of CPT1, completely abolished fatty acid oxidation in SS and IMF mitochondria from WG, whereas oxidation rates in the corresponding fractions from RG were inhibited only 89% and 60%, respectively. Endurance training also elicited mitochondrial adaptations that resulted in enhanced fatty acid oxidation capacity. Ten weeks of treadmill running differentially increased palmitate oxidation rates 100% and 46% in SS and IMF mitochondria, respectively. In SS mitochondria, elevated fatty acid oxidation rates were accompanied by a 48% increase in citrate synthase (CS) activity but no change in CPT1 activity. Non-linear regression analyses of mitochondrial FAO rates in the presence of 0-100 µM MCA indicated that IC50 values were neither dependent on mitochondrial subpopulation nor affected by exercise training. However, in IMF mitochondria, training reduced the Hill coefficient (p<0.05), suggesting altered CPT1 kinetics. These results demonstrate that endurance exercise provokes subpopulation-specific changes in mitochondrial function that are characterized by enhanced fatty acid oxidation and modified CPT1-malonyl-CoA dynamics.
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