Fig. 1.
Schematic figure representing the regulation of mitochondrial biogenesis by endurance exercise (
). Endurance exercise acutely increases Ca2+, ADP, AMP and epinephrine. In addition exercise reduces skeletal muscle glycogen (
) in the contracting muscles which in turn activates the sensing proteins AMPK and p38 MAPK. Especially elevated AMP and ADP trigger an increased phosphorylation of AMPK at Thr172 and the increased Ca2+ concentration via calmodulin causes CaMK II autophosphorylation. Both AMPK and p38 MAPK activate and translocate the transcriptional co-activator PGC-1α to the mitochondria and nucleus. The kinases AMPK, p38 MAPK and SIRT 1 then might phosphorylate PGC-1 α and reduce the acetylation of PGC-1 α, which increases its activity. Thus, endurance exercise leads to more PGC-1 α which over time results in mitochondrial biogenesis