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. 2017 Aug 11;7:7894. doi: 10.1038/s41598-017-08480-2

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Autophagy is essential for the beneficial cardiac remodelling caused by exercise training in obesity and insulin resistance. Exercise training ameliorates diet-induced obesity and insulin resistance, and is very effective in preventing cardiac fibrosis and pathological hypertrophy when cardiac and skeletal autophagy is normal. Conversely, deficient skeletal and cardiac muscle autophagy dissociates the whole-body metabolic benefits of exercise (e.g., protection against obesity and insulin resistance) from cardioprotection. This phenomenon is driven primarily by the exercise training-mediated impairment of mitochondrial protein homeostasis, as well as exacerbation of ER stress, fibrosis and pathological hypertrophy in the hearts of mice with deficient autophagy. This unfavourable cardiac remodelling, however, potentiates the metabolic benefits of exercise in the periphery, at least in part, by elevating circulating FGF21 levels. Arrows represent stimulation, whereas T-shaped connectors represent inhibition. Thicker lines indicate stronger observed effects.