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Autophagy is essential to support skeletal muscle plasticity in response to endurance exercise

Sanchez, Anthony M. J., Bernardi, Henri, Py, Guillaume, Candau, Robin B.·2014·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology

DOI 10.1152/ajpregu.00187.2014

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Abstract

Physical exercise is a stress that can substantially modulate cellular signaling mechanisms to promote morphological and metabolic adaptations. Skeletal muscle protein and organelle turnover is dependent on two major cellular pathways: Forkhead box class O proteins (FOXO) transcription factors that regulate two main proteolytic systems, the ubiquitin-proteasome, and the autophagy-lysosome systems, including mitochondrial autophagy, and the MTORC1 signaling associated with protein translation and autophagy inhibition. In recent years, it has been well documented that both acute and chronic endurance exercise can affect the autophagy pathway. Importantly, substantial efforts have been made to better understand discrepancies in the literature on its modulation during exercise. A single bout of endurance exercise increases autophagic flux when the duration is long enough, and this response is dependent on nutritional status, since autophagic flux markers and mRNA coding for actors involved in mitophagy are more abundant in the fasted state. In contrast, strength and resistance exercises preferentially raise ubiquitin-proteasome system activity and involve several protein synthesis factors, such as the recently characterized DAGK for mechanistic target of rapamycin activation. In this review, we discuss recent progress on the impact of acute and chronic exercise on cell component turnover systems, with particular focus on autophagy, which until now has been relatively overlooked in skeletal muscle. We especially highlight the most recent studies on the factors that can impact its modulation, including the mode of exercise and the nutritional status, and also discuss the current limitations in the literature to encourage further works on this topic.

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Authors: Sanchez, A. M. J., Bernardi, H., Py, G., & Candau, R. B.
Affiliations: Department of Critical Care, McGill University Health Centre and Meakins-Christie Laboratories, Department of Medicine, McGill University, Montreal, Quebec, Canada;
Institut National de la Recherche Agronomique, UMR 866 Dynamique Musculaire et Métabolisme, Montpellier, France; and
Faculty of Sport Sciences, University of Montpellier 1, Montpellier, France
Venue: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher: American Physiological Society
Published: 2014-10-15
Volume: 307
Issue: 8
Pages: R956-R969
ISSN: 0363-6119
1522-1490
DOI: 10.1152/ajpregu.00187.2014
Cited by: 125
References: 46
Language: en

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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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Autophagy is essential to support skeletal muscle plasticity in response to endurance exercise

Abstract

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Integrity signals

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Claims other papers make about this one

Citations

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Cited by

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