# Acute Inflammatory Responses to Blood Flow Restriction Training: A Systematic Review

## TL;DR

Blood flow restriction training causes short-term increases in inflammation markers like leukocytes and macrophages, similar to heavy resistance training.

## Contribution

This systematic review quantifies acute inflammatory responses to BFR training and compares them to high-load resistance training.

## Key findings

- BFR training leads to transient increases in leukocytes and lymphocytes in blood.
- Macrophage activity in muscle tissue increases significantly after BFR.
- Inflammatory responses after BFR are comparable to those after high-load resistance training.

## Abstract

The effects of Blood Flow Restriction (BFR) training are well-established, but its impact on the inflammatory response remains unclear. This systematic review evaluates whether BFR training induces acute inflammation by analyzing changes in inflammatory parameters.

This review was conducted according to PRISMA guidelines. The literature search was performed across PubMed, Web of Science, BISp-Surf and Google Scholar up to July 2025. Studies were included if they reported acute changes in inflammatory markers within 72 h after BFR training, as well as macrophage presence up to 14 days. Only trials involving healthy adults with inflammatory parameters assessed via peripheral blood or muscle biopsy were considered. Risk of bias was assessed using RoB 2 and ROBINS-I. Standardized mean differences (SMDs) were calculated to quantify within-study changes. In addition, relative percentage changes were calculated to enable a comparison of the magnitude of inflammatory responses across studies. An effect direction plot was created to summarize the direction of inflammatory marker changes (SWiM 2020).

Nine studies involving 189 healthy adults were included in the systematic review. Transient increases in total leukocytes (18–33%) and lymphocytes (37–43%) were consistently observed in peripheral blood following exercise. Significant increases in total tissue macrophages (200%) were also reported. Findings on neutrophils (up to + 40%), cytokines (up to + 340%), and lymphocyte subpopulations (TCD4⁺: +25%, TCD8⁺: +39%) varied across studies.

The findings suggest that BFR training induces acute inflammation, characterized by transient leukocytosis, lymphocytosis, and increased macrophage activity. However, the variability in neutrophil and cytokine responses, as well as in lymphocyte subsets, may be attributed to variations in training parameters and methodological approaches. Overall, these responses appear comparable to those observed following high-load resistance training (HL-RT). Further research is needed to clarify the underlying mechanisms and their potential contribution to muscle adaptation.

The online version contains supplementary material available at 10.1186/s40798-025-00926-6.

BFR training can induce acute changes in inflammatory markers, including transient increases in circulating total leukocyte and lymphocyte counts and a sustained presence of macrophages in muscle tissue. Neutrophil and cytokine responses, as well as lymphocyte subsets, showed variability across studies.The magnitude of immune cell responses following BFR training appear similar to that observed after HL-RT, where immune cell recruitment has been linked to regenerative processes. These responses, particularly the sustained presence of M2 macrophages, raise the possibility that inflammation following BFR training may also contribute to muscle regeneration.Further research is needed to clarify the underlying mechanisms and potential role of BFR-induced inflammation in muscle adaptation. Standardized training and measurement protocols are also required to improve comparability.

BFR training can induce acute changes in inflammatory markers, including transient increases in circulating total leukocyte and lymphocyte counts and a sustained presence of macrophages in muscle tissue. Neutrophil and cytokine responses, as well as lymphocyte subsets, showed variability across studies.

The magnitude of immune cell responses following BFR training appear similar to that observed after HL-RT, where immune cell recruitment has been linked to regenerative processes. These responses, particularly the sustained presence of M2 macrophages, raise the possibility that inflammation following BFR training may also contribute to muscle regeneration.

Further research is needed to clarify the underlying mechanisms and potential role of BFR-induced inflammation in muscle adaptation. Standardized training and measurement protocols are also required to improve comparability.

The online version contains supplementary material available at 10.1186/s40798-025-00926-6.