Exercise and training regulation of autophagy markers in human and rat skeletal muscle
Journal article
Botella, Javier, Jamnick, Nicholas A., Granata, Cesare, Genders, Amanda J., Perri, Enrico, Jabar, Tamim, Garnham, Andrew, Lazarou, Michael and Bishop, David J.. (2022). Exercise and training regulation of autophagy markers in human and rat skeletal muscle. International Journal of Molecular Sciences. 23(5), p. Article 2619. https://doi.org/10.3390/ijms23052619
Authors | Botella, Javier, Jamnick, Nicholas A., Granata, Cesare, Genders, Amanda J., Perri, Enrico, Jabar, Tamim, Garnham, Andrew, Lazarou, Michael and Bishop, David J. |
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Abstract | 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. |
Keywords | autophagy; exercise; LC3; skeletal muscle |
Year | 2022 |
Journal | International Journal of Molecular Sciences |
Journal citation | 23 (5), p. Article 2619 |
Publisher | Multidisciplinary Digital Publishing Institute (MDPI AG) |
ISSN | 1661-6596 |
Digital Object Identifier (DOI) | https://doi.org/10.3390/ijms23052619 |
PubMed ID | 35269762 |
Scopus EID | 2-s2.0-85125404948 |
PubMed Central ID | PMC8910616 |
Open access | Published as ‘gold’ (paid) open access |
Page range | 1-15 |
Funder | Australian Research Council (ARC) |
National Health and Medical Research Council (NHMRC) | |
Publisher's version | License File Access Level Open |
Output status | Published |
Publication dates | |
Online | 27 Feb 2022 |
Publication process dates | |
Accepted | 25 Feb 2022 |
Deposited | 30 Oct 2023 |
ARC Funded Research | This output has been funded, wholly or partially, under the Australian Research Council Act 2001 |
Grant ID | DP140104165 |
1106471 | |
DP200100347 |
https://acuresearchbank.acu.edu.au/item/8zxq2/exercise-and-training-regulation-of-autophagy-markers-in-human-and-rat-skeletal-muscle
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Publisher's version
OA_Botella_2022_Exercise_and_training_regulation_of_autophagy.pdf | |
License: CC BY 4.0 | |
File access level: Open |
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