Fusion and beyond: Satellite cell contributions to loading-induced skeletal muscle adaptation
Open accessAbstract
Satellite cells support adult skeletal muscle fiber adaptations to loading in numerous ways. The fusion of satellite cells, driven by cell-autonomous and/or extrinsic factors, contributes new myonuclei to muscle fibers, associates with load-induced hypertrophy, and may support focal membrane damage repair and long-term myonuclear transcriptional output. Recent studies have also revealed that satellite cells communicate within their niche to mediate muscle remodeling in response to resistance exercise, regulating the activity of numerous cell types through various mechanisms such as secretory signaling and cell-cell contact. Muscular adaptation to resistance and endurance activity can be initiated and sustained for a period of time in the absence of satellite cells, but satellite cell participation is ultimately required to achieve full adaptive potential, be it growth, function, or proprioceptive coordination. While significant progress has been made in understanding the roles of satellite cells in adult muscle over the last few decades, many conclusions have been extrapolated from regeneration studies. This review highlights our current understanding of satellite cell behavior and contributions to adaptation outside of regeneration in adult muscle, as well as the roles of satellite cells beyond fusion and myonuclear accretion, which are gaining broader recognition.
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Satellite cell fusion is not an obligatory requirement at all stages of hypertrophy but becomes increasingly relevant when sustained loading pushes existing myonuclei toward their functional limits.
“Rather than acting as an obligatory requirement at all stages of hypertrophy, satellite cell fusion is better interpreted as a mechanism that becomes increasingly relevant when sustained loading pushes existing myonuclei toward their functional limits [22,68].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [68]
In “Matters of controversy—The necessity of satellite cells for load-induced muscle hypertrophy” (page unavailable), the review says adult muscle can grow without fusion and that an upper limit to the myonuclear domain may have been approached after eight weeks without it. That supports the proposed interpretation, but the review does not establish that sustained loading makes fusion increasingly necessary: it also says adult fibers can grow during prolonged loading without myonuclear addition, and attributes some limits on long-term growth to non-fusion satellite-cell functions. (LLM, conf=0.82)
Experimental — accuracy not yet measuredOnce initial gains supported by existing myonuclei are largely realized, further adaptation may require a slower phase of structural remodeling involving satellite cell participation and myonuclear expansion.
“Once the initial gains supported by existing myonuclei have been largely realized, further adaptation may require a slower phase of structural remodeling involving satellite cell participation and myonuclear expansion [66,68].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [68]
In “Matters of controversy—The necessity of satellite cells for load-induced muscle hypertrophy” (page unavailable), the review says resident myonuclei can support appreciable growth, while satellite-cell participation helps maximize growth and sustain adaptation. It does not establish a subsequent slower phase of structural remodeling requiring myonuclear expansion; it notes that myonuclear accretion had stabilized after four weeks in one training model. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIsolated single-fiber transcriptomics reporting absolute RNA content per isolated myofiber segment bypasses the tissue-denominator problem.
“Alternatively, emerging isolated single-fiber transcriptomics, which report absolute RNA content per isolated myofiber segment, entirely bypasses the tissue-denominator problem [68].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [68]
The retrieved passages from the review’s main text and References (page numbers unavailable) discuss myonuclear transcription and muscle adaptation, but none addresses isolated single-fiber transcriptomics, absolute RNA content per myofiber segment, or a tissue-denominator problem. Searches for those terms and related descriptions did not locate support for the attributed methodological claim. (LLM, conf=0.70)
Experimental — accuracy not yet measuredRNA:DNA is not a universally superior method but a useful adjunct whose interpretation depends on the experimental question and timeframe.
“RNA:DNA is therefore not a universally superior method but a useful adjunct whose interpretation depends on the experimental question and timeframe [37,68].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [68]
The supplied passages discuss satellite cells, myonuclei, and how experimental conditions affect their study, but do not address RNA:DNA as a measurement method. Searches for “RNA:DNA” and for an RNA-to-DNA ratio as a measure of muscle hypertrophy found no passage evaluating its usefulness, superiority, or dependence on the experimental question and timeframe. The copy is marked as complete. (LLM, conf=0.72)
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MUSCLE REGENERATION IN EXPERIMENTAL ANIMALS AND IN MAN
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Self-citationCell–cell contact and signaling in the muscle stem cell niche
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Self-citationAkt1 deficiency diminishes skeletal muscle hypertrophy by reducing satellite cell proliferation
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RhoA within myofibers controls satellite cell microenvironment to allow hypertrophic growth
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Muscle is a stage, and cells and factors are merely players
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YAP/TAZ as Molecular Targets in Skeletal Muscle Atrophy and Osteoporosis
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Self-citationGold nanoparticles modulate macrophage polarization to promote skeletal muscle regeneration
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The roles of miRNAs in adult skeletal muscle satellite cells
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GLUD1 determines murine muscle stem cell fate by controlling mitochondrial glutamate levels
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Protein Turnover in Skeletal Muscle: Looking at Molecular Regulation towards an Active Lifestyle
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Positional Context of Myonuclear Transcription During Injury-Induced Muscle Regeneration
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Self-citationCollagen-Based Scaffolds for Volumetric Muscle Loss Regeneration
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The pathogenesis of anti-signal recognition particle necrotizing myopathy: A Review
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AMPKα2 is a skeletal muscle stem cell intrinsic regulator of myonuclear accretion
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Tensile Loaded Tissue-Engineered Human Tendon Constructs Stimulate Myotube Formation
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Satellite cell-derived TRIM28 is pivotal for mechanical load- and injury-induced myogenesis
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MuSK-BMP signaling in adult muscle stem cells maintains quiescence and regulates myofiber sizePreprint
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Self-citationNEDD4-1 deficiency impairs satellite cell function during skeletal muscle regeneration
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ApoE isoform does not influence skeletal muscle regeneration in adult mice
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Resistance Training Diminishes Mitochondrial Adaptations to Subsequent Endurance TrainingPreprint
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Regenerate to “Rejuvenate”: Insights From Adult Resident Stem Cells of Aged Flatworms and Mice
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The role of MEGF10 in myoblast fusion and hypertrophic response to overload of skeletal muscle
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“Rather than acting as an obligatory requirement at all stages of hypertrophy, satellite cell fusion is better interpreted as a mechanism that becomes increasingly relevant when sustained loading pushes existing myonuclei toward their functional limits [22,68].”
InfluentialADAPTIVE CHANGES OF THE CIRCULATORY SYSTEM IN STRENGTH SPORTS ATHLETES
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GABA promotes myoblast fusion and prevents TNF-α-induced muscle protein degradation in C2C12 cells
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The Health Benefits of Exercise: Molecular and Cellular Mechanisms
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Transient MYC Mimicking the Exercise Response Orchestrates Multifaceted Skeletal Muscle AdaptationsPreprint
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- Authors
- Murach, K. A., Fry, C. S., Dupont‐Versteegden, E. E., McCarthy, J. J., & Peterson, C. A.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Murach, Kevin A.
- Peterson, Charlotte A.
- ORCID
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2021-09-04
- Volume
- 35
- Issue
- 10
- Pages
- e21893-e21893
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC9293230
- OpenAlex
- W3197320781
- Cited by
- 120
- References
- 234
- Citations by year
- 2026: 22 · 2025: 22 · 2024: 25 · 2023: 26 · 2022: 21 · 2021: 4
- FWCI
- 1.99
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The FASEB Journal (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Journal of the Arkansas Academy of Science (submittedVersion, cc-by-nc)
- UKnowledge (University of Kentucky) (submittedVersion, cc-by-nc)
- Funders
- National Institutes of Health
- National Institute on Aging (AG049086, AG063994)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- satellite cells, skeletal muscle adaptation, myonuclear accretion, muscle hypertrophy, resistance training, endurance exercise, muscle remodeling, extrinsic signaling, cell-cell contact, proprioception, muscle regeneration
- MeSH terms
- Adaptation, Physiological, Animals, Humans, Signal Transduction, Muscle Fibers, Skeletal, Satellite Cells, Skeletal Muscle
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