Metabolic benefits of resistance training and fast glycolytic skeletal muscle

Abstract

Skeletal muscle exhibits remarkable plasticity with respect to its metabolic properties. Recent work has shown that interventions such as resistance training, genetic alterations and pharmacological strategies that increase muscle mass and glycolytic capacity, and not necessarily oxidative competence, can improve body composition and systemic metabolism. We review here recent advances in our understanding of the signaling and transcriptional regulatory pathways of this strategy and review new evidence obtained from mice and humans that supports the notion that increasing muscle mass and glycolytic capacity may effectively counter insulin resistance and type 2 diabetes mellitus.

Fig. 1.

Multiple substrates of the PI 3-kinase/Akt pathway mediate growth and metabolic signals in skeletal muscle. As discussed in the text, the PI 3-kinase/Akt network carries a tremendous burden as a mediator of protein synthesis, protein degradation, glucose transport and glycogen synthesis. Many of PI 3-kinase/Akt effectors exhibit functional diversity; that is, instead of one substrate one function, most substrates regulate multiple physiological processes including but not limited to growth and metabolism (reviewed in Ref. 48). Of particular interest is better understanding how resistance training and resistance training-like mimetics (e.g., inhibitors of myostatin) that clearly impact skeletal muscle mass and fast glycolytic fibers enhance skeletal muscle's responsiveness to insulin, augment glucose use and storage, and improve systemic metabolism.