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Regulation of Exercise-Induced Autophagy in Skeletal Muscle

  • Autophagy in Pathobiology (W-X Ding and H-M Shen, Section Editors)
  • Published:
Current Pathobiology Reports

Abstract

Purpose of Review

Physical exercise is a highly effective method to prevent several pathogenic conditions, such as obesity, type 2 diabetes, and cardiovascular diseases, largely due to metabolic adaptations induced by exercise in skeletal muscle. Yet how exercise induces the beneficial effects in muscle remains to be fully elucidated. Autophagy is a lysosomal degradation pathway that regulates nutrient recycling, energy production, and organelle quality control. The autophagy pathway is upregulated in response to stress during exercise and muscle contraction, and may be an important mechanism mediating exercise-induced health benefits.

Recent Findings

A number of studies have indicated that physical exercise induces non-selective autophagy and selective mitophagy in skeletal muscle in animal models and humans. The AMPK-ULK1 and the FoxO3 signaling pathways play an essential role in the activation of the upstream autophagy machinery in skeletal muscle during exercise. The autophagy activity is required for health benefits of exercise, as in different autophagy-deficient mouse lines exercise-induced effects are abolished.

Summary

This review aims to summarize and highlight the most recent findings on the role of autophagy in muscle maintenance, the molecular pathways that upregulate autophagy during exercise, and the potential functions of exercise-induced autophagy and mitophagy in skeletal muscle.

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Acknowledgments

This work was supported by NIH Grant R00DK094980.

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Correspondence to Congcong He.

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Altea Rocchi and Congcong He declare that they have no conflict of interest.

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This article does not contain any studies with human or animal subjects performed by any of the authors.

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This article is part of the Topical Collection on Autophagy in Pathobiology

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Rocchi, A., He, C. Regulation of Exercise-Induced Autophagy in Skeletal Muscle. Curr Pathobiol Rep 5, 177–186 (2017). https://doi.org/10.1007/s40139-017-0135-9

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