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Title: Exercise Mitigates the Loss of Muscle Mass by Attenuating the Activation of Autophagy during Severe Energy Deficit
Authors: Martin Rincon, Marcos 
Pérez-López, Alberto
Morales Álamo, David 
Perez Suárez,Ismael 
De Pablos Velasco, Pedro Luis 
Pérez Valera, Mario 
Perez-Regalado, Sergio
Martinez-Canton, Miriam
Gelabert Rebato, Miriam 
Juan-Habib, Julian William
Holmberg, Hans-Christer
López Calbet, José Antonio 
UNESCO Clasification: 241106 Fisiología del ejercicio
Keywords: Autophagy-lysosome
Caloric restriction
Protein degradation
Skeletal muscle
Issue Date: 2019
Project: Viabilidad y Sostenibilidad Del Adelgazamiento Mediante Tratamiento Intensificado en Pacientes Con Sobrepeso U Obesidad: Mecanismos Neuroendocrinos y Moleculares 
Journal: Nutrients 
Abstract: 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.
ISSN: 2072-6643
DOI: 10.3390/nu11112824
Source: Nutrients [ISSN 2072-6643], v. 11 (11), 2824
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