No change in myonuclear number during muscle unloading and reloading
Abstract
Muscle fibers are the cells in the body with the largest volume, and they have multiple nuclei serving different domains of cytoplasm. A large body of previous literature has suggested that atrophy induced by hindlimb suspension leads to a loss of "excessive" myonuclei by apoptosis. We demonstrate here that atrophy induced by hindlimb suspension does not lead to loss of myonuclei despite a strong increase in apoptotic activity of other types of nuclei within the muscle tissue. Thus hindlimb suspension turns out to be similar to other atrophy models such as denervation, nerve impulse block, and antagonist ablation. We discuss how the different outcome of various studies can be attributed to difficulties in separating myonuclei from other nuclei, and to systematic differences in passive properties between normal and unloaded muscles. During reload, after hindlimb suspension, a radial regrowth is observed, which has been believed to be accompanied by recruitment of new myonuclei from satellite cells. The lack of nuclear loss during unloading, however, puts these findings into question. We observed that reload led to an increase in cross sectional area of 59%, and fiber size was completely restored to the presuspension levels. Despite this notable growth there was no increase in the number of myonuclei. Thus radial regrowth seems to differ from de novo hypertrophy in that nuclei are only added during the latter. We speculate that the number of myonuclei might reflect the largest size the muscle fibers have had in its previous history.
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Nuclei acquired during training may persist during subsequent unloading, contributing to muscle memory and facilitating more rapid re-expansion of translational capacity during retraining.
“Importantly, nuclei acquired during training may persist during subsequent unloading, contributing to the cellular basis of muscle memory and facilitating a more rapid re-expansion of translational capacity during retraining [67,69]”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [69]
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- Authors
- Bruusgaard, J. C., Egner, I. M., Larsen, T. K., Dupre-Aucouturier, S., Desplanches, D., & Gundersen, K.
- Affiliations
- University of Oslo (NO)
- Université Lyon 1, CNRS UMR 5534, Centre de Génétique et de Physiologie Moléculaire et Cellulaire, Villeurbanne, France; and
- Corresponding author
- Gundersen, K.
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2012-07-15
- Volume
- 113
- Issue
- 2
- Pages
- 290-296
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2137752780
- Cited by
- 107
- References
- 76
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 3 · 2023: 4 · 2022: 5 · 2021: 5 · 2020: 9 · 2019: 11 · 2018: 7 · 2017: 9 · 2016: 11 · 2015: 14 · 2014: 11 · 2013: 8 · 2012: 2
- FWCI
- 4.50
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Spaceflight effects on biology
- Health Sciences › Medicine › Complementary and alternative medicine › Cardiovascular and exercise physiology
- Keywords
- myonuclear number, muscle atrophy, muscle unloading, hindlimb unloading, muscle reloading, apoptosis, satellite cells, muscle fiber hypertrophy, fiber cross-sectional area, denervation atrophy
- MeSH terms
- Animals, Cell Nucleus, Female, Weight-Bearing, Rats, Wistar, Muscle Fibers, Skeletal, Hindlimb Suspension, Rats
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