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A Review on the Mechanisms of Blood-Flow Restriction Resistance Training-Induced Muscle Hypertrophy
Open accessAbstract
It has traditionally been believed that resistance training can only induce muscle growth when the exercise intensity is greater than 65% of the 1-repetition maximum (RM). However, more recently, the use of low-intensity resistance exercise with blood-flow restriction (BFR) has challenged this theory and consistently shown that hypertrophic adaptations can be induced with much lower exercise intensities (<50% 1-RM). Despite the potent hypertrophic effects of BFR resistance training being demonstrated by numerous studies, the underlying mechanisms responsible for such effects are not well defined. Metabolic stress has been suggested to be a primary factor responsible, and this is theorised to activate numerous other mechanisms, all of which are thought to induce muscle growth via autocrine and/or paracrine actions. However, it is noteworthy that some of these mechanisms do not appear to be mediated to any great extent by metabolic stress but rather by mechanical tension (another primary factor of muscle hypertrophy). Given that the level of mechanical tension is typically low with BFR resistance exercise (<50% 1-RM), one may question the magnitude of involvement of these mechanisms aligned to the adaptations reported with BFR resistance training. However, despite the low level of mechanical tension, it is plausible that the effects induced by the primary factors (mechanical tension and metabolic stress) are, in fact, additive, which ultimately contributes to the adaptations seen with BFR resistance training. Exercise-induced mechanical tension and metabolic stress are theorised to signal a number of mechanisms for the induction of muscle growth, including increased fast-twitch fibre recruitment, mechanotransduction, muscle damage, systemic and localised hormone production, cell swelling, and the production of reactive oxygen species and its variants, including nitric oxide and heat shock proteins. However, the relative extent to which these specific mechanisms are induced by the primary factors with BFR resistance exercise, as well as their magnitude of involvement in BFR resistance training-induced muscle hypertrophy, requires further exploration.
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“low-load BFR exercise has been shown to activate mTORC1/p70S6K1 signalling to a degree comparable with high-load resistance training [155,156]”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [156]
In the citing paper
“likely due to the compensatory increase in cellular swelling and localized metabolic stress [156].”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [156]
In the citing paper
“While BFR may provide a theoretically viable alternative for preserving or stimulating translational-capacity-related processes in these cohorts [155,156]”
From Ribosome Biogenesis as a Putative Bottleneck to Skeletal Muscle Hypertrophy: Mechanisms, Human Evidence, and Practical Modulators (2026) · cites this paper as [156]
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Koc, B. B., Jansen, E. J. P., de Jong, O., Ehlen, T., van Rijn, L., de Bie, R. A., & Schotanus, M. G. M. (2025) · International Journal of Sports Physical Therapy · doi:10.26603/001c.143781
Metadata
- Authors
- Pearson, S. J., & Hussain, S. R.
- Affiliations
- University of Salford (GB)
- Corresponding author
- Pearson, Stephen John
- Venue
- Sports Medicine
- Published
- 2014-09-24
- Volume
- 45
- Issue
- 2
- Pages
- 187-200
- ISSN
- 0112-1642 (ISSN-L)
- 1179-2035
- OpenAlex
- W2087307311
- Cited by
- 592
- References
- 169
- Citations by year
- 2026: 86 · 2025: 103 · 2024: 62 · 2023: 64 · 2022: 65 · 2021: 47 · 2020: 52 · 2019: 35 · 2018: 36 · 2017: 22 · 2016: 13 · 2015: 6
- FWCI
- 3.77
- Type
- journal article
- Language
- en
- Open access
- green
- usir.salford.ac.uk
- Licence
- Locations
- Sports Medicine (publishedVersion)
- PubMed (publishedVersion)
- University of Salford Institutional Repository (University of Salford) (submittedVersion, cc-by)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Sports Performance and Training
- Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
- Keywords
- blood flow restriction, resistance training, muscle hypertrophy, metabolic stress, mechanical tension, mechanotransduction, muscle damage, hormone production, reactive oxygen species, nitric oxide, heat shock proteins, cell swelling, autocrine and paracrine signaling, low-intensity exercise
- MeSH terms
- Adaptation, Physiological, Energy Metabolism, Hemodynamics, Humans, Regional Blood Flow, Muscle, Skeletal, Resistance Training
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