Molecular adaptation to resistance exercise

Abstract

In Chapter seven, we defined the signal transduction theory of exercise adaptation. The present chapter builds on this theory and focuses specifically on the molecular responses to resistance exercise and adaptation to training. In summary, resistance exercise training uses different strategies to increase muscle mass and strength. Loading to failure at any weight increases muscle mass, in part by increasing mTORC1 pathway activity in almost all the fibres within the muscle, resulting in increased myofibrillar protein synthesis and muscle hypertrophy. Adding leucine-rich protein with training augments the increase in muscle size by activating mTORC1 using a distinct mechanism. Beyond mTORC1, load to failure results in muscle-specific inhibition of myostatin signalling through the cleavage of Notch, and the activation of Akt and the production of E3 ubiquitin ligases that increase protein turnover and the addition of sarcomeres in parallel. Lifting a heavy weight is needed to maximise strength changes since this increases neural drive to the muscle and improves force transfer through the load-dependent activation of the ERK/Egr1 pathway. Resistance exercise can induce muscle injury, and serious muscle injury requires resident stem cells (satellite cells) to fully repair. Furthermore, when muscle fibres increase in cross-sectional area beyond ˜1,000 µm2, these same satellite cells are recruited to provide the greater transcriptional and translational capacities needed to support the larger cells. Together, these molecular effectors (mTORC1, myostatin, Akt, ERK and satellite cells) transduce the signal of high load from resistance exercise into a coordinated increase in muscle size and strength.