The DOI matches its Crossref record; 56 of the 57 references it cites were found in a registry or an index.
Myonuclei acquired by overload exercise precede hypertrophy and are not lost on detraining
Open accessAbstract
Effects of previous strength training can be long-lived, even after prolonged subsequent inactivity, and retraining is facilitated by a previous training episode. Traditionally, such "muscle memory" has been attributed to neural factors in the absence of any identified local memory mechanism in the muscle tissue. We have used in vivo imaging techniques to study live myonuclei belonging to distinct muscle fibers and observe that new myonuclei are added before any major increase in size during overload. The old and newly acquired nuclei are retained during severe atrophy caused by subsequent denervation lasting for a considerable period of the animal's lifespan. The myonuclei seem to be protected from the high apoptotic activity found in inactive muscle tissue. A hypertrophy episode leading to a lasting elevated number of myonuclei retarded disuse atrophy, and the nuclei could serve as a cell biological substrate for such memory. Because the ability to create myonuclei is impaired in the elderly, individuals may benefit from strength training at an early age, and because anabolic steroids facilitate more myonuclei, nuclear permanency may also have implications for exclusion periods after a doping offense.
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“The pre-existing, expanded nucleolar templates are immediately available to rapidly transcribe massive amounts of 45S pre-rRNA”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [115]
In the citing paper
“Consequently, when an individual resumes training, the muscle fiber bypasses the initial, slow, and energetically demanding process of satellite cell proliferation [115].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [115]
In the citing paper
“explaining the accelerated rate of “re-growth” universally observed in previously trained humans [115,117]”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [115]
In the citing paper
“Studies by Bruusgaard et al. [115] and Kadi et al. [116] utilizing advanced single-fiber techniques demonstrated that prolonged unloading leads to a slow decay in total RNA, whereas newly acquired myonuclei (donated via satellite cell fusion) are not eliminated via apoptosis.”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [115]
In the citing paper
“Research shows that in addition to hormone concentrations, the number of myonuclei can affect skeletal muscle training [79, 80].”
From Integrating Transwomen and Female Athletes with Differences of Sex Development (DSD) into Elite Competition: The FIMS 2021 Consensus Statement (2021) · cites this paper as [80]
In the citing paper
“However, detraining does not diminish the myonuclei number,27”
In the citing paper
“Hence, it is possible that strength advantages gained when training in a high-testosterone environment may not be fully reversed by testosterone suppression.”
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Metadata
- Authors
- Bruusgaard, J. C., Johansen, I. B., Egner, I. M., Rana, Z. A., & Gundersen, K.
- Affiliations
- University of Oslo (NO)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-08-16
- Volume
- 107
- Issue
- 34
- Pages
- 15111-15116
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2930527
- OpenAlex
- W2057868246
- Cited by
- 327
- References
- 57
- Citations by year
- 2026: 11 · 2025: 21 · 2024: 14 · 2023: 22 · 2022: 25 · 2021: 43 · 2020: 27 · 2019: 22 · 2018: 18 · 2017: 13 · 2016: 26 · 2015: 15 · 2014: 20 · 2013: 17 · 2012: 17
- FWCI
- 6.52
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Norges Forskningsråd (rcn-foriss-191730, rcn-foriss-182717)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Health Sciences › Medicine › Genetics (clinical) › Neurogenetic and Muscular Disorders Research
- Keywords
- myonuclei, muscle hypertrophy, detraining, muscle memory, resistance training, denervation atrophy, disuse atrophy, apoptosis, myonuclear domain, aging, anabolic steroids
- MeSH terms
- Animals, Cell Nucleus, Female, Humans, Hypertrophy, Male, Models, Biological, Muscle Denervation, Muscular Atrophy, Physical Conditioning, Animal, Rats, Wistar, Apoptosis, Muscle Fibers, Skeletal, Models, Animal, Mice, Rats, Resistance Training
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