Blood Flow Restriction Therapy

Where We Are and Where We Are Going

Bryan G. Vopat, MD; Lisa M. Vopat, MD; Megan M. Bechtold, DPT; Kevin A. Hodge, MD


J Am Acad Orthop Surg. 2020;28(12):e493-e500. 

In This Article

Mechanism of Action

The process in which BFRT generates muscle development when low-load resistance training alone has not shown results is not completely understood. The proposed mechanism is based on the combination of two primary factors, metabolic and mechanical stress. These factors act synergistically to signal a number of secondary mechanisms including tissue hypoxia, build-up of metabolites, and cellular swelling. Subsequently, this promotes autocrine and paracrine signaling pathways that lead to protein synthesis, type 2 muscle fiber recruitment, local and systemic anabolic hormone synthesis, and stimulation of myogenic stem cells.[4]

Resistance exercise relies on the recruitment of motor units. Type 2, or fast twitch, muscle fibers have a relatively larger diameter and higher stimulation threshold. They receive energy mainly from the glycolytic pathway instead of oxidative metabolism, so they are preferentially recruited in a hypoxic environment. Tissue hypoxia from BFRT has been demonstrated to cause a preferential recruitment of type 2 motor units, which typically are only recruited with high-load training.[6] Takarada et al[9] determined through the use of electromyography that BFRT stimulated 1.8 times greater muscle recruitment than volume-matched controls. Therefore, muscle fiber recruitment may play a role in the effects of BFRT on muscle development.

Blood pooling caused by venous occlusion has been theorized to be an important factor in the effect of BFRT. Through the combined process of increased extracellular fluid and metabolite accumulation, including lactate and reactive oxygen species, a pressure gradient is created which drives fluid into the muscle fibers. The resulting increased cell volume has been shown to alter the structure of the cells and drive anabolic signaling pathways. Evidence has shown that cellular swelling promotes increased protein synthesis in many different cell types including hepatocytes, osteocytes, and muscle fibers.[4,6]

Tissue hypoxia also may cause an increase in localized and systemic hormone synthesis. Takarada et al[9] determined systemic growth hormone levels to be 290 times greater in BFRT patients compared with matched controls. Despite several investigations reporting elevated anabolic hormones after BFRT, the effect of systemic anabolic hormones on muscle development has been debated and is not completely understood at this time.[4,6]

BFRT has also been shown to have an effect on vasculature by promoting postexercise blood flow, oxygen delivery, and angiogenesis. Studies have found increased angiogenetic factors after BFRT, such as vascular endothelial growth factor, hypoxia-inducible factor 1 alpha, and neuronal nitric oxide synthase.[10] This potentially improves blood supply to musculature, thus improving performance through enhanced aerobic capacity and endurance.[11] Although the mechanism of BFRT remains incompletely understood at this time, the literature has consistently shown that BFRT increases muscle strength, hypertrophy, and angiogenesis (Figure 1).

Figure 1.

Diagram of the proposed mechanism of action for BFRT. BFRT = blood flow restriction therapy, ROS = reactive oxygen species