Abstract
Although circulating fatty acids are utilized as energy substrates, they also function as ligands to the peroxisome-proliferator activated receptors (PPARs), a family of fatty acid sensing transcription factors. Exercise training leads to various adaptations in the muscle such as elevation of glycogen content, mitochondrial number as well as upregulation of fatty acid uptake and utilization through downstream transcriptional adaptations. In line with this, CD36 has been shown to be critical in controlling fatty acid uptake and consequently, fatty acid oxidation. We show that exercise training could not ameliorate impaired endurance performance in CD36 KO mice despite intact adaptations in muscle glycogen storage and mitochondrial function. Changes in whole-body metabolism at rest and during exercise were also suppressed in these animals. Furthermore, there was inefficient upregulation of PPAR and PPAR-related exercise-responsive genes with chronic training in CD36 KO mice despite normal upregulation of Pgc1a and mitochondrial genes. Our findings supplement previous observations and emphasize the importance of CD36 in endurance performance, energy production and efficient downstream transcriptional regulation by PPARs.