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

• Published in: PloS one Vol. 12; no. 12; p. e0189456
• Main Authors: Zoladz, Jerzy A, Koziel, Agnieszka, Broniarek, Izabela, Woyda-Ploszczyca, Andrzej M, Ogrodna, Karolina, Majerczak, Joanna, Celichowski, Jan, Szkutnik, Zbigniew, Jarmuszkiewicz, Wieslawa
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 12.12.2017; Public Library of Science (PLoS)
• Subjects: Acyl-CoA dehydrogenase; Animals; Bioenergetics; Biology and Life Sciences; Biosynthesis; Carbohydrates; Carnitine; Carnitine palmitoyltransferase; CD36 antigen; Durability; Endurance; Exercise; Fatty acid metabolism; Fatty acids; Fitness equipment; Fitness training programs; Fuels; Genetic aspects; Glycerol; Glycerol-3-phosphate; Hyperthermia; Hypothermia; Medicine and Health Sciences; Metabolism; Mitochondria; Muscle fatigue; Muscles; Musculoskeletal system; Neurosciences; Oxidation; Palmitoyltransferase; Phosphates; Physical education; Physical fitness; Physical Sciences; Physiological aspects; Physiology; Proteins; Rats; Rodents; Running; Signaling; Skeletal muscle; Temperature; Temperature effects; Training; Poland
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0189456

We studied the effects of various assay temperatures, representing hypothermia (25°C), normothermia (35°C), and hyperthermia (42°C), on the oxidation of lipid-derived fuels in rat skeletal muscle mitochondria of untrained and endurance-trained rats. Adult 4-month-old male Wistar rats were assigned to a training group (rats trained on a treadmill for 8 weeks) or a sedentary control group. In skeletal muscle mitochondria of both control and trained rats, an increase in the assay temperature from 25°C to 42°C was accompanied by a consistent increase in the oxidation of palmitoylcarnitine and glycerol-3-phosphate. Moreover, endurance training increased mitochondrial capacity to oxidize the lipid-derived fuels at all studied temperatures. The endurance training-induced increase in mitochondrial capacity to oxidize fatty acids was accompanied by an enhancement of mitochondrial biogenesis, as shown by the elevated expression levels of Nrf2, PGC1α, and mitochondrial marker and by the elevated expression levels of mitochondrial proteins involved in fatty acid metabolism, such as fatty acid transporter CD36, carnitine palmitoyltransferase 1A (CPT1A), and acyl-CoA dehydrogenase (ACADS). We conclude that hyperthermia enhances but hypothermia attenuates the rate of the oxidation of fatty acids and glycerol-3-phosphate in rat skeletal muscle mitochondria isolated from both untrained and trained rats. Moreover, our results indicate that endurance training up-regulates mitochondrial biogenesis markers, lipid-sustained oxidative capacity, and CD36 and CPT1A proteins involved in fatty acid transport, possibly via PGC1α and Nrf2 signaling pathways.