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Exercise and Training Regulation of Autophagy Markers in Human and Rat Skeletal Muscle.
Botella, Javier; Jamnick, Nicholas A; Granata, Cesare; Genders, Amanda J; Perri, Enrico; Jabar, Tamim; Garnham, Andrew; Lazarou, Michael; Bishop, David J.
Afiliación
  • Botella J; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC 3011, Australia.
  • Jamnick NA; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC 3011, Australia.
  • Granata C; Metabolic Research Unit, Institute for Mental and Physical Health and Clinical Translation (IMPACT), School of Medicine, Deakin University, Waurn Ponds, VIC 3011, Australia.
  • Genders AJ; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC 3011, Australia.
  • Perri E; Department of Diabetes, Central Clinical School, Monash University, Melbourne, VIC 3011, Australia.
  • Jabar T; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC 3011, Australia.
  • Garnham A; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC 3011, Australia.
  • Lazarou M; Department of Biomedical Sciences for Health, University of Milan, 20122 Milan, Italy.
  • Bishop DJ; Institute for Health and Sport (iHeS), Victoria University, Melbourne, VIC 3011, Australia.
Int J Mol Sci ; 23(5)2022 Feb 27.
Article en En | MEDLINE | ID: mdl-35269762
Autophagy is a key intracellular mechanism by which cells degrade old or dysfunctional proteins and organelles. In skeletal muscle, evidence suggests that exercise increases autophagosome content and autophagy flux. However, the exercise-induced response seems to differ between rodents and humans, and little is known about how different exercise prescription parameters may affect these results. The present study utilised skeletal muscle samples obtained from four different experimental studies using rats and humans. Here, we show that, following exercise, in the soleus muscle of Wistar rats, there is an increase in LC3B-I protein levels immediately after exercise (+109%), and a subsequent increase in LC3B-II protein levels 3 h into the recovery (+97%), despite no change in Map1lc3b mRNA levels. Conversely, in human skeletal muscle, there is an immediate exercise-induced decrease in LC3B-II protein levels (-24%), independent of whether exercise is performed below or above the maximal lactate steady state, which returns to baseline 3.5 h following recovery, while no change in LC3B-I protein levels or MAP1LC3B mRNA levels is observed. SQSTM1/p62 protein and mRNA levels did not change in either rats or humans following exercise. By employing an ex vivo autophagy flux assay previously used in rodents we demonstrate that the exercise-induced decrease in LC3B-II protein levels in humans does not reflect a decreased autophagy flux. Instead, effect size analyses suggest a modest-to-large increase in autophagy flux following exercise that lasts up to 24 h. Our findings suggest that exercise-induced changes in autophagosome content markers differ between rodents and humans, and that exercise-induced decreases in LC3B-II protein levels do not reflect autophagy flux level.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Condicionamiento Físico Animal / Autofagia Límite: Animals / Humans Idioma: En Revista: Int J Mol Sci Año: 2022 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Suiza
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Condicionamiento Físico Animal / Autofagia Límite: Animals / Humans Idioma: En Revista: Int J Mol Sci Año: 2022 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Suiza