What is the role of lipid metabolism during muscle work?
Lipids, especially long-chain fatty acids (L-cFA), constitute the major substrate for energy production (ATP) during fasting intervals, at rest, and with muscular activities of low intensity and long duration (>40–50 minutes).
L-cFA from adipose tissues move through the bloodstream bound to albumin. These, plus medium- and small-chain fatty acids, move across the endothelial cells and into the muscle cells (called fibers), where they are available for energy production, storage, or synthesis into membrane components. A L-cFA transporter protein (3 in Fig. 72.3 ) facilitates the entry of L-cFA into the muscle fiber. To be processed for energy, the free fatty acid must enter the mitochondria. Short- and medium-chain fatty acids cross freely into the mitochondria. L-cFA must combine with carnitine to enter the inner mitochondrial matrix. The combination of L-cFA with carnitine and their release into the mitochondrial matrix are catalyzed by CPT I and CPT II, respectively (1 and 2 in Fig. 72.3 ), which are located on the inner mitochondrial membrane. Once in the mitochondria, the fatty acids are converted to their respective CoA esters and sequentially shortened by the process of β-oxidation, which release acetyl CoA that then enters the TCA or Krebs cycle. CPT deficiency, trifunctional protein deficiency, and very long-chain acyl-CoA dehydrogenase deficiency are the most common fatty acid oxidation defect disorders.