Mechanisms of exercise- and training-induced fatty acid oxidation in skeletal muscle
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Exercise has acute and chronic effects on fat burning. Concerning the acute effect, observed during and after a single exercise session, the enzymes responsible for burning fat increase. Carnitine palmitoyltransferase 1 (CPT1), which regulates the β-oxidation of fatty acids in mitochondria, is believed to play an important role in the acute effect. The activation of AMP-activated protein kinase (AMPK), which detects the energy state of muscles, may contribute to the exercise-induced activation of CPT1. In the chronic effect observed with ongoing exercise training, physiological changes in muscle function are seen. In particular, an increase in the number of mitochondria and enhancement of fatty acid metabolism are observed after endurance training. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) plays an important role in adaptive thermogenesis and mitochondrial biogenesis. Exercise enhances the expression of PGC-1α, and the increase in PGC-1α mediates the physiological changes observed in skeletal muscle after endurance training. Recently, several isoforms of PGC-1α were identified. Different signaling pathways regulate the expression of each isoform. In this review, we discuss the regulation of lipid metabolism during physical activity. We also describe the PGC-1α isoforms and the signaling pathways that regulate their expression in relation to the effects of exercise training on skeletal muscle. Finally, we introduce two studies that may explain the systemic effect of endurance training.
- 一般社団法人日本体力医学会の論文
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