Fig. 5
Proposed mechanism for the high-intensity interval training (HIIT) effects on cardiac fibroblast. HIIT induces an increased DNA methyltransferase 1 (DNMT1) level in cardiac fibroblasts and results in hypermethylation (
) on the
acyl-CoA dehydrogenase very long chain (ACADVL) gene. Silencing of the gene impairs mitochondrial function by downregulating very long-chain acyl-CoA dehydrogenase (VLCAD) expression and facilitates the release of cytochrome C (Cyto C) into the cytoplasm. This regulation activates caspase cascade-associated actin filament disassembly and possibly permeabilizes (broken arrow) the nuclear envelope by decreasing lamin B1 (LMNB) to reduce cardiac fibrosis. \(\normalsize \tt V\)O2peak, peak oxygen consumption; Arp2, actin-related protein 2