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

Abstract

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.

Adaptation of motor unit contractile properties in rat medial gastrocnemius to treadmill endurance training: Relationship to muscle mitochondrial biogenesis

“…The elevated PGC-1α in the MGS has been observed also after 4 and 8 weeks of training ( Fig 9 ). This result is in agreement with our previous study showing that 8 weeks of endurance training up-regulates mitochondrial biogenesis markers such as Nrf2, PGC-1α as well as proteins involved in fatty acid metabolism [ 68 ]. On the other hand, an increase in mtDNA copy number was found at the final stage of training (8 weeks) in both the MGF and MGS ( Fig 7 ).…”

Physical resistance training-induced changes in lipids metabolism pathways and apoptosis in prostate

“…It is well established that the maximal rate of muscle fatty acid oxidation is higher during physical exercise. Physical resistance training induces expression of the fatty acid transporter cluster of differentiation 36 (CD36) in muscles [12,13]. Studies with pharmacological and immunologic CD-36 inhibitors have shown that the antiangiogenic signaling mediated by CD36 and thrombospondin 1 (TSP-1) is dependent on protein tyrosine kinases Fyn and Lyn, and Src kinases [14][15][16].…”

Comprehensive analysis of circular RNA profiles in skeletal muscles of aging mice and after aerobic exercise intervention

“…Intriguingly, miRNA-mRNA network analysis of circBBS9 annotated top genes in metabolic pathways from KEGG analysis as its potential target genes, which supported a possible regulatory role of circBBS9 in the metabolic programs in myocytes. For example, LDHA, AMD1, DNMT3A and ACADSB were reported to regulate muscle cell proliferation and muscle atrophy [28][29][30][31], while ACADS, CS, GATM, CHSY1 were related to muscle energy metabolism [32][33][34]. Thus, aging and aerobic training, two opposite processes impact muscle functionality, may exert their impacts by modulating the circBBS9-miRNA-mRNA network.…”