A regimented exercise schedule serves to modify cell molecular components leading to muscle adaptation. These modifications are driven by transcriptional processes under the control of several epigenetic paradigms. Metabolism is an emerging factor in cell epigenetic modifications, of which alpha-ketoglutarate (α-KG), Acetyl-CoA, and reactive oxygen species (ROS) are considered key metabolites. ROS, particularly following high-intensity exercise, leads to the oxidative modification of DNA, and potentially to the oxidation of the epigenetic mark 5-methylcytosine. ROS can also interfere with several epigenetic modifying enzymes and cofactors, highlighting the important interrelationship between cell metabolism and reprogramming of gene transcription through a state of disrupted epigenetics. While our understanding of the influence of exercise-induced oxidative stress and redox biochemistry in epigenetics is in its infancy, the ensuing chapter should be viewed as a starting point to explore the multidirectional connections between exercise, oxidative stress/redox biology in the epigenetic landscape. To this end, we will initially outline the relationship between metabolism and the epigenetic nexus, prior to outlining how exercise stress can influence the epigenetics. An overview of the potential interplay between exercise-induced oxidative stress/redox biology and epigenetics will be outlined, before offering a brief review of the interactions between exercise and noncoding RNAs.

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Exercise-Epigenetic Axis: Metabolic Alignment to Oxidative Stress and Redox Status

  • Gareth W. Davison,
  • Aya Mohammed,
  • Rachelle Irwin,
  • Diane Lees-Murdock,
  • Colum P. Walsh

摘要

A regimented exercise schedule serves to modify cell molecular components leading to muscle adaptation. These modifications are driven by transcriptional processes under the control of several epigenetic paradigms. Metabolism is an emerging factor in cell epigenetic modifications, of which alpha-ketoglutarate (α-KG), Acetyl-CoA, and reactive oxygen species (ROS) are considered key metabolites. ROS, particularly following high-intensity exercise, leads to the oxidative modification of DNA, and potentially to the oxidation of the epigenetic mark 5-methylcytosine. ROS can also interfere with several epigenetic modifying enzymes and cofactors, highlighting the important interrelationship between cell metabolism and reprogramming of gene transcription through a state of disrupted epigenetics. While our understanding of the influence of exercise-induced oxidative stress and redox biochemistry in epigenetics is in its infancy, the ensuing chapter should be viewed as a starting point to explore the multidirectional connections between exercise, oxidative stress/redox biology in the epigenetic landscape. To this end, we will initially outline the relationship between metabolism and the epigenetic nexus, prior to outlining how exercise stress can influence the epigenetics. An overview of the potential interplay between exercise-induced oxidative stress/redox biology and epigenetics will be outlined, before offering a brief review of the interactions between exercise and noncoding RNAs.