Figure 2.

Diagram of the major signalling pathways involved in the control of skeletal muscle hypertrophy and mitochondrial biogenesis. Voluntary exercise training activates kinases/phosphatases to mediate a specific exercise-induced signal. The cross talk among the numerous signalling pathways activated and the multiple site regulation produces a high sensitive and complex transduction network. Activation of AMPK by aerobic/endurance exercise training enhances mitochondrial biogenesis partly by directly phosphorylating and activating PGC-1α. Resistance training is a potent stimulus for the increase in skeletal muscle mass. Activation of FAK through integrins leads to the inhibition of TSC, thereby permitting activation of mTOR. In addition, hypertrophy is promoted by activation of IGF-1 activating PI3K/Akt/mTOR signaling pathway that leads to hypertrophy. AMPK, AMP-activated protein kinase; PGC-1α, PPAR-γ coactivator 1α; FAK, focal adhesion kinase; TSC, tuberous sclerosis complex; mTOR, mammalian target of rapamycin; IGF-1, insulin-like growth factor 1; PI3K, phosphatidylinositide 3-kinases.