Exercise Mitigates the Loss of Muscle Mass by Attenuating the Activation of Autophagy during Severe Energy Deficit
| Autor: | David Morales-Alamo, Miriam Gelabert-Rebato, Hans-Christer Holmberg, Pedro de Pablos-Velasco, Mario Perez-Valera, Jose A. L. Calbet, Ismael Perez-Suarez, Antonio Pérez-López, Marcos Martin-Rincon, Miriam Martinez-Canton, Sergio Perez-Regalado, Julian W. Juan-Habib |
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| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male Time Factors medicine.medical_treatment Autophagy-Related Proteins Muscle Proteins Skeletal muscle Quadriceps Muscle 0302 clinical medicine autophagy-lysosome Testosterone Nutrition and Dietetics Middle Aged Hälsovetenskaper Exercise Therapy Protein catabolism medicine.anatomical_structure Treatment Outcome protein degradation caloric restriction lcsh:Nutrition. Foods and food supply Muscle Contraction Signal Transduction Autophagy-lysosome ubiquitin-proteasome Adult medicine.medical_specialty Proteasome Endopeptidase Complex Diet Reducing Caloric restriction lcsh:TX341-641 Protein degradation Article 03 medical and health sciences Internal medicine Health Sciences medicine Autophagy Humans Ubiquitin-proteasome skeletal muscle Catabolism business.industry Insulin AMPK Overweight 030104 developmental biology Endocrinology Proteolysis business Energy Metabolism Lysosomes 030217 neurology & neurosurgery Food Science |
| Zdroj: | Nutrients, Vol 11, Iss 11, p 2824 (2019) Nutrients Volume 11 Issue 11 |
| ISSN: | 2072-6643 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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