Exercise and exercise training-induced increase in autophagy markers in human skeletal muscle
Open accessAbstract
Moderately trained male subjects (mean age 25 years; range 19–33 years) completed an 8-week exercise training intervention consisting of continuous moderate cycling at 157 ± 20 W for 60 min (MOD; n = 6) or continuous moderate cycling (157 ± 20 W) interspersed by 30-sec sprints (473 ± 79 W) every 10 min (SPRINT; n = 6) 3 days per week. Sprints were followed by 3:24 min at 102 ± 17 W to match the total work between protocols. A muscle biopsy was obtained before, immediately and 2 h after the first training session as well as at rest after the training session. In both MOD and SPRINT, skeletal muscle AMPKThr172 and ULKSer317 phosphorylation was elevated immediately after exercise, whereas mTORSer2448 and ULKSer757 phosphorylation was unchanged. Two hours after exercise LC3I, LC3II and BNIP3 protein content was overall higher than before exercise with no change in p62 protein. In MOD, Beclin1 protein content was higher immediately and 2 h after exercise than before exercise, while there were no differences within SPRINT. Oxphos complex I, LC3I, BNIP3 and Parkin protein content was higher after the training intervention than before in both groups, while there was no difference in LC3II and p62 protein. Beclin1 protein content was higher after the exercise training intervention only in MOD. Together this suggests that exercise increases markers of autophagy in human skeletal muscle within the first 2 h of recovery and 8 weeks of exercise training increases the capacity for autophagy and mitophagy regulation. Hence, the present findings provide evidence that exercise and exercise training regulate autophagy in human skeletal muscle and that this in general was unaffected by interspersed sprint bouts.
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Physical activity stimulates mitophagy.
“was recently shown to stimulate mitophagy [57,153,167,168]”
From Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging (2021) · cites this paper as [168]
Physical activity increases Parkin expression in the skeletal muscles of rodents and humans.
“and increase Parkin expression in the skeletal muscles of rodents [153] and humans [57,168]”
From Mitochondrial Dynamics and Mitophagy in Skeletal Muscle Health and Aging (2021) · cites this paper as [168]
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Retracted
- Authors
- Brandt, N., Gunnarsson, T. P., Bangsbo, J., & Pilegaard, H.
- Affiliations
- University of Copenhagen (DK)
- Corresponding author
- Pilegaard, Henriette
- Venue
- Physiological Reports
- Publisher
- Wiley
- Published
- 2018-04
- Volume
- 6
- Issue
- 7
- Pages
- e13651
- ISSN
- 2051-817X (ISSN-L)
- PMC
- PMC5889490
- OpenAlex
- W2796408712
- Cited by
- 120
- References
- 28
- Citations by year
- 2026: 12 · 2025: 11 · 2024: 16 · 2023: 15 · 2022: 13 · 2021: 29 · 2020: 9 · 2019: 10 · 2018: 5
- FWCI
- 10.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Physiological Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (publishedVersion, cc-by)
- Funders
- Sundhed og Sygdom, Det Frie Forskningsråd (4181-00078)
- Natur og Univers, Det Frie Forskningsråd (0602-02281B)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- exercise training, autophagy, skeletal muscle, mitophagy, AMPK, ULK1, mTOR, Beclin-1, LC3, BNIP3, Parkin, oxidative phosphorylation, sprinting, cycling, post-exercise recovery
- MeSH terms
- High-Intensity Interval Training, Adult, Autophagy, Humans, Male, Exercise, Muscle, Skeletal, Young Adult
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