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Open AccessArticle

Exercise Mitigates the Loss of Muscle Mass by Attenuating the Activation of Autophagy during Severe Energy Deficit

1
Department of Physical Education and Research Institute of Biomedical and Health Sciences (IUIBS), University of Las Palmas de Gran Canaria, Campus Universitario de Tafira, s/n, 35017 Las Palmas de Gran Canaria, Canary Islands, Spain
2
Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, University of Alcalá, Ctra. Madrid-Barcelona, km 33,600, 28871 Alcalá de Henares, Madrid, Spain
3
Department of Endocrinology and Nutrition, Hospital Universitario de Gran Canaria Doctor Negrín, Calle Plaza Barranco de la Ballena, s/n, 35010 Las Palmas de Gran Canaria, Canary Islands, Spain
4
Department of Health Sciences, Mid Sweden University, SE-83140 Östersund, Sweden
5
School of Kinesiology, Faculty of Education, The University of British Columbia, Vancouver, BC V6T 1Z, Canada
6
Department of Physical Performance, The Norwegian School of Sport Sciences, Postboks, 4014 Ulleval Stadion, 0806 Oslo, Norway
*
Author to whom correspondence should be addressed.
Nutrients 2019, 11(11), 2824; https://doi.org/10.3390/nu11112824
Received: 6 October 2019 / Revised: 30 October 2019 / Accepted: 14 November 2019 / Published: 19 November 2019
(This article belongs to the Special Issue Nutrition and Exercise Metabolism)
The loss of skeletal muscle mass with energy deficit is thought to be due to protein breakdown by the autophagy-lysosome and the ubiquitin-proteasome systems. We studied the main signaling pathways through which exercise can attenuate the loss of muscle mass during severe energy deficit (5500 kcal/day). Overweight men followed four days of caloric restriction (3.2 kcal/kg body weight day) and prolonged exercise (45 min of one-arm cranking and 8 h walking/day), and three days of control diet and restricted exercise, with an intra-subject design including biopsies from muscles submitted to distinct exercise volumes. Gene expression and signaling data indicate that the main catabolic pathway activated during severe energy deficit in skeletal muscle is the autophagy-lysosome pathway, without apparent activation of the ubiquitin-proteasome pathway. Markers of autophagy induction and flux were reduced by exercise primarily in the muscle submitted to an exceptional exercise volume. Changes in signaling are associated with those in circulating cortisol, testosterone, cortisol/testosterone ratio, insulin, BCAA, and leucine. We conclude that exercise mitigates the loss of muscle mass by attenuating autophagy activation, blunting the phosphorylation of AMPK/ULK1/Beclin1, and leading to p62/SQSTM1 accumulation. This includes the possibility of inhibiting autophagy as a mechanism to counteract muscle loss in humans under severe energy deficit. View Full-Text
Keywords: autophagy-lysosome; caloric restriction; protein degradation; skeletal muscle; ubiquitin-proteasome autophagy-lysosome; caloric restriction; protein degradation; skeletal muscle; ubiquitin-proteasome
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Martin-Rincon, M.; Pérez-López, A.; Morales-Alamo, D.; Perez-Suarez, I.; de Pablos-Velasco, P.; Perez-Valera, M.; Perez-Regalado, S.; Martinez-Canton, M.; Gelabert-Rebato, M.; Juan-Habib, J.W.; Holmberg, H.-C.; Calbet, J.A.L. Exercise Mitigates the Loss of Muscle Mass by Attenuating the Activation of Autophagy during Severe Energy Deficit. Nutrients 2019, 11, 2824.

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