Abstract

During endurance and resistance exercise training, AMPK and mTOR signaling were known as selective pathways implicating the differentiation of exercise-induced phenotype in skeletal muscle. Among the previous studies, however, the differences in exercise protocol, the individuality and the genetic heterogeneity within species make it difficult to reach a consistent conclusion in the roles of AMPK and mTOR signaling. In this review, we aim not to reanalyze the previous articles and present the research progress of AMPK and mTOR signaling in exercise, but to propose an abstract general hypothesis for exercise-induced phenotype. Generally, exercise- induced skeletal muscle phenotype is independent of one and a few genes, proteins and signaling pathways. Convergent adaptation will better summarize the specificity of skeletal muscle phenotype in response to a single mode of exercise. Backward adaptation will open a new concept to illustrate the process of exercise-induced adaptation, such as mitochondrial quality control and muscle mass homeostasis.

Highlights

  • During endurance and resistance exercise training, AMPK and mammalian target of rapamycin (mTOR) signaling were known as selective pathways implicating the differentiation of exercise-induced phenotype in skeletal muscle

  • Endurance and resistance exercise represent extremes on exercise-induced adaptation and produce markedly different phenotypes that are mediated by a complex interplay between AMP-activated kinase (AMPK) and mammalian target of rapamycin signaling (Egan and Zierath, 2013)

  • While PKB/Akt and AMPKα2 activities are essential for Akt substrate of 160 kDa (AS160) phosphorylation during insulin- and Aminoimidazole-4- carboxamide1-β-Dribofuranoside (AICAR)-stimulated glucose uptake in L6 myotubes, neither kinase is indispensable for the effects of muscle contraction on AS160 phosphorylation (Kramer et al, 2006)

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Summary

Introduction

During endurance and resistance exercise training, AMPK and mTOR signaling were known as selective pathways implicating the differentiation of exercise-induced phenotype in skeletal muscle. Endurance and resistance exercise represent extremes on exercise-induced adaptation and produce markedly different phenotypes that are mediated by a complex interplay between AMP-activated kinase (AMPK) and mammalian target of rapamycin (mTOR) signaling (Egan and Zierath, 2013). Exercise-induced phenotype in physiology is accomplished by integrating gene, cell, tissue, organ and systems during chronic adaptations to different types of exercise such as resistance and endurance.

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Conclusion

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