BFR Research

Using BFR and performing low-level exercise leads to immense​​​​​​ increase in lactate production1
  • There is also increased motor recruitment as a muscle continues to exercise under BFR, further perpetuating an increased blood lactate production

An accumulation of lactate and hydrogen ions within the muscle results in an augmented growth hormone (GH) release.2,3
  • So if we can increase lactate production, there will be a subsequent rise in GH


The rise in GH after performing BFR was 290% higher than baseline measurements. This is 1.7x higher than what has been reported for high-intensity training (HIT).3,4
  • Even though it is widely believed that GH plays a role in muscle anabolism and athletic performance, a recent systematic review found no effect of GH on athletic performance.5


It appears that the role of GH is to protect our tendon and muscle collagen structure after exercise -- GH is for recovery, not for building muscle. Thus, the correlation of increased GH release as the exercise intensity increases may be the body's protective response to help our tendons and other collagen-rich matrix recover.

The body's reaction to more and more strenuous exercise is to increase GH response in preparation for the subsequent collagen breakdown. The low loads associated with BFR do not cause this breakdown and you end up with a positive collagen turnover.

Insulin-like growth factor 1 or IGF-1 is a protein in humans that has been linked to muscle growth. In fact, clear cause-effect relationship between IGF-1 and muscle hypertrophy has been established and some feel that it is the regulator of muscle mass.6,7
  • IGF-1 is stimulated by GH -- thus, the larger the influx of GH, the more IGF-1 is stimulated, leading to larger increases in muscle size and strength.


Increased blood lactate levels facilitates GH production, which leads to activation of IGF-1

By increasing GH, muscle stem cells are activated; IGF-1 helps chaperone these cells into muscles fibers to create a new myocyte.  
  • The number of myocytes is the limiting factor for muscle growth -- thus, the more myocytes per muscle fiber, the larger the increase in muscular hypertrophy and strength.


A recent study confirmed that muscle satellite cells were incorporated into muscle fiber (chaperoned by IGF-1), which translates into addtional myonuclei (muscle cells). The gains in the number of satellite cells were 280% at mid-training, 250% 3 days post-training and 140% percent at 10 days post.8
  • The gains typically seen after heavy resistance training are 30-50%.9,10,11

The same study examined muscle fiber size via biopsy. The increase in muscle fiber area in the BFR group was 30-40% during and after training. To put this into perspective, 12 - 16 weeks of heavy resistance training has demonstrated a 15-20% increase in muscle fiber area in untrained men.10,11,12​​

1Yasuda T, Abe T, Brechue WF, et al. Venous blood gas and metabolite response to low-intensity muscle contractions with external limb compression. Metabolism 2010;59:1510–9

2Goto, K., Ishii, N., Kizuka, T., & Takamatsu, K. (2005). The impact of metabolic stress on hormonal responses and muscular adaptations. Med Sci Sports Exerc, 37(6) 955-963.

3Takarada Y, Nakamura Y, Aruga S, Onda T, Miyazaki S, Ishii N. Rapid increase in plasma growth ​hormone after low-intensity resistance exercise with vascular occlusion. J Appl Physiol (1985). 2000; 88:61-65. 

4Kraemer, W. J., Marchitelli, L., Gordon, S. E., Harman, E., Dziados, J. E., Mello, R., Fleck, S. J. ​(1990). Hormonal and growth factor responses to heavy resistance exercise protocols. J Appl Physiol (1985), 69(4), 1442-1450.

5Liu H, Bravata DM, Olkin I, Friedlander A, Liu V, Roberts B, Bendavid E, Saynina O, Salpeter SR, Garber ​AM, Hoffman AR (May 2008). "Systematic review: the effects of growth hormone on athletic performance". Ann. Intern. Med. 148 (10): 747–58. 

6Haddad F, Adams GR. Inhibition of MAP/ERK kinase prevents IGF-I-induced hypertrophy in rat muscles. J Appl Physiol. 2004;96(1):203–10.

7Point: IGF is the major physiological regulator of muscle mass. J Appl Physiol. 2010;108(6):1820,1; discussion 1823-4; author reply 1832. Stewart CE, Pell JM. Point:Counterpoint: IGF is/is not the major physiological regulator of muscle mass.

8​​Nielsen, J. L., Aagaard, P., Bech, R. D., Nygaard, T., Hvid, L. G., Wernbom, M., . Frandsen, U. (2012).Proliferation of myogenic stem cells in human skeletal muscle in response to low-load resistance training with blood flow restriction. J Physiol, 590(Pt 17), 4351-4361. 773–782. 

9Kadi F, Schjerling P, Andersen LL, Charifi N, Madsen JL, Christensen LR & Andersen JL (2004). Theeffects of heavy resistance training and detraining on satellite cells in human skeletal muscles. J Physiol 558, 1005–1012. 

10Kadi F & Thornell LE (2000). Concomitant increases in myonuclear and satellite cell content in female trapezius muscle following strength training. Histochem Cell Biol 113, 99–103.

11 Olsen S, Aagaard P, Kadi F, Tufekovic G, Verney J, Olesen JL, Suetta C & Kjaer M (2006). Creatine supplementation augments the increase in satellite cell and myonuclei number in human skeletal muscle induced by strength training. J Physiol 573, 525–534

12Aagaard P, Andersen JL, Dyhre-Poulsen P, Leffers AM,Wagner A, Magnusson SP, Halkjaer-Kristensen J & Simonsen EB (2001). A mechanism for increased contractile strength of human pennate muscle in response to strength training: changes in muscle architecture. J Physiol 534, 613–623.