Sirui Wang, Taiwei Guo, Yating Zhang
BFR is a mechanistically distinct and broadly applicable modality whose clinical value depends on rigorous individualization, careful safety stratification, and continued mechanistic investigation.
BACKGROUND: Blood flow restriction (BFR) exercise combines low-intensity contractions with partial arterial inflow restriction and venous occlusion to generate a localized hypoxic, metabolite-rich milieu that activates a broad spectrum of molecular pathways.
AIM: To synthesize contemporary (2020-2026) evidence on the systemic molecular effects of BFR across skeletal-muscle, endocrine, cardiovascular, immune, and neuromuscular systems, and to connect these mechanisms to clinical practice.
APPROACH: Narrative review supported by a structured PubMed/Web of Science/Scopus search prioritizing randomized trials and recent systematic reviews and meta-analyses.
KEY FINDINGS: BFR engages mTORC1 signaling, myostatin suppression, satellite-cell proliferation, HIF-1α stabilization, and angiogenic gene expression to produce hypertrophic and functional outcomes broadly comparable to high-load resistance training; it elicits acute endocrine (growth hormone, IGF-1, testosterone, catecholamines) and metabolic (lactate, reactive oxygen species, AMPK) responses, together with cardiovascular, immune, and neural adaptations whose systemic clinical magnitude is modest and population-dependent. It is worth noting that the hypertrophic and signaling effects described arise from low-load contraction performed under occlusion; neither section implies an anabolic effect of passive occlusion without contraction.
CONCLUSION: BFR is a mechanistically distinct and broadly applicable modality whose clinical value depends on rigorous individualization, careful safety stratification, and continued mechanistic investigation.