The BFR Hype

TAGS: muscle growth, blood flow restriction, Jennifer Petrosino

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At this point, I’m sure you have either 1) heard of blood flow restriction training (BFR) or 2) seen people in the gym training with knee wraps or elastic bands wrapped around their limbs and cutting off their circulation. You should know that this is likely being done as a way to increase muscle mass. And after watching the massive pump that these BFR users get throughout the durations of their workouts, you might have even thought, “Maybe I should give this thing a shot.” If you have had those thoughts, this article is for you. Full disclosure: I’m writing this about using BFR as a stimulus to make your muscle grow bigger (hypertrophy), not about its many benefits as a therapeutic modality.

How To Do BFR

When you lift, blood flow gets freely shunted into the working muscle. That is, unless you are doing BFR. With BFR, you wrap something around the limb you are training so that the blood flow into the limb (arterial) is restricted and the blood flow out of the limb (venous) is blocked. Once you are wrapped up tight, you do a few sets at a light load for some high reps. Together, these effects result in a super-pumped muscle, and in the longterm, it can result in increases in muscle strength and mass1-6.


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This means that to set up your BFR training, you will need to get some elastic bands, knee wraps, or a tourniquet and apply them to the top of the limb you are working (under your armpit for arms, and high up on your thigh for legs). You need to wrap it tight enough that you feel a lot of pressure (just don’t go overboard and actually do it like a real-life I’m-bleeding-out tourniquet). Then, figure out what weight you need to be at for 20-30% or your one rep max for an exercise, and do 3-4 sets of 30+ reps, resting for around 30 seconds between each set. Then, get ready to have an epic pump!

What’s Going on in Your Muscles When You Do BFR Training?

As you work through those high-rep BFR sets, blood is getting pushed into the limb, and due to the occlusion, it’s unable to get out. This results in your muscles looking SUPER PUMPED. It’s also why the hypertrophy people get all excited about BFR after the first session, because who doesn't like looking full and vascular. When you remove the occlusion, your muscles immediately get flooded with O2 (what we call hyperemia), the metabolic byproducts that have accumulated get cleared, and protein synthesis is stimulated6, 7. Additionally, this type of training causes increases in circulating levels of growth hormone, cortisol, norepinephrine, and epinephrine8, 9.

And while there is some debate as to if the protein synthesis stimulated is a result of an increase in O2 and nutrient shunting to the muscle, it is really clear that BFR training is efficient at stimulating acute protein synthesis and eventual muscle growth. Which brings us to the question that many people ask next: “How does BFR work?” To be honest, we know a lot about what’s going on when it comes to BFR, but there is also still A LOT to be learned.

mTOR Activation/Protein Synthesis

A protein called mammalian target of rapamycin complex 1 (mTORC1) is an essential regulator of protein synthesis that gets activated following a lifting session. When mTOR is inhibited, muscle protein synthesis and hypotrophy are blunted. We know that BFR training also stimulates protein synthesis 7, 101118, and there are studies where people do BFR training and mTOR is blocked, just like protein synthesis is blocked with normal training 11. Early on, this was important to prove because it demonstrated that the effects of BFR on protein synthesis weren’t working through some wild and crazy new pathway. Instead, they were working through the tried-and-true mTOR pathway.

Lactate Hypothesis

Many studies have observed that large amounts of lactate accumulate with BFR. This, of course, makes sense considering that restricting blood flow out of the working muscles results in intramuscular lactate accumulation and thus a decreasing muscle pH. As muscle pH declines, so does the force generated by your super-strong fast-twitch fibers. In this situation, you eventually call on your slow-twitch ones to help you to move the load. This is possibly why BFR stimulates the hypertrophy of both fast and slow fibers, whereas traditional strength training predominantly stimulates the faster ones to grow12. In fact, researchers have found that just a systemic injection of lactate is sufficient to activate pathways involved in stimulating protein synthesis13. Furthermore, others have found that seven days of lactate injections following an acute muscle injury are capable of stimulating muscle hypertrophy after a month of recovery14. But I wouldn't start injecting lactate just yet, as the results in muscle cell cultures are less clear, with some studies showing that giving muscle cells lactate has no effect on muscle protein synthesis and hypertrophy, whereas others show that it does14, 15.

The Oxygen Hypothesis

Some researchers out there believe that it's the act of causing the muscle to be in a low-O2 environment and then reperfusing it that is responsible for BFR’s effects. See, BFR creates a transiently hypoxic (low oxygen) environment for the muscle, which is partially why lactate is being produced (the muscle is working in an anaerobic environment). Researchers who believe that it’s the oxygen rather than the lactate that is responsible for BFR’s effects have asked the question, “What happens to muscle growth in a low-oxygen environment?” For example, a group of researchers had people do knee extensions in either normal oxygen conditions or hypoxic conditions, then collected muscle biopsies 15 minutes and five hours after training on the excercised and non-exercised quad. The researchers found that there was a delay in the immediate amounts of protein synthesis with hypoxia and that by four hours post training, the hypoxic training group had more activated protein synthesis pathways than the training-alone group did16. This result is similar to what has been shown in studies where BFR stimulates a larger increase in protein synthesis post training than training alone does. Additionally, in rats, researchers looked at the effects of performing venous occlusion on muscle growth. These researchers found that 14 days of venous occlusion (the rodent form of BFR) was sufficient for inducing a large amount of muscle hypertrophy17, thus supporting the idea that limiting oxygen to the muscle but then reperfusing it has some potent effects on muscle growth. Of course, there are also those who disagree with the idea that first occluding and then reperfusing the muscle during BFR is what is responsible for increases in muscle hypertrophy. So, to disprove this, those researchers have looked at the role of forcing increases in muscle blood and oxygen using pharmacological vasodilators, and they have asked the question, “Is training and taking a vasodilator as effective as training with BFR when it comes to stimulating muscle protein synthesis?” To get at this question, they had a group of men do either 1) lifting with BFR or 2) lifting with a vasodilator drug (sodium nitroprusside). What they found was this: immediately following exercise, arterial blood flow and lactate were way higher in the group doing BFR than in the one taking the vasodilator. Protein synthesis levels were higher following BFR training, as was the stimulation of the mTOR pathway. Hence, at first glance, it seems pretty convincing that it’s not the increase in O2 that causes hypertrophy but rather something else intrinsic to BFR. But that’s where we have to stop and really think about it18. Acute, drug-induced increases in O2 levels are not the same thing as the occlusion-perfusion that occurs with BFR.


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At rest, muscle blood flow is low, but when you lift, the increasing oxygen demand can increase it nearly 100X19. This type of functional hyperemia, like what BFR induces, and then some following reperfusion cause micro-vascular shear stress. And over-repeated or chronic exposure causes increases in angiogenesis. Muscle stretch from continuous overload (think about high-rep training) can also induce angiogenesis20, 21. But the changes that occur in muscle capillary density during weighted hypertrophic stimuli don’t just occur after one session (just like you don't get a massive amount of hypotrophy following one BFR session, the growth you see is a pump LOL). These adaptations take weeks to occur 22, 23. Stimulating an increase in O2 in the muscle via pharmacological manipulation may not be capable of recreating the benefits of BFR. However, I think that we need to consider that the compensatory stimulation of angiogenesis, and thus more eventual capillarization to the muscle, could be why BFR is working. Look at it like this: in lifting, you lift heavier or for more reps to elicit adaptions to muscle size and strength. BFR occluding and reperfusing probably elicit adaptations to the muscle’s vasculature. And this is no small adaption, as O2 diffusion across the muscle determines its food source (oxygen), and this can block its hypertrophic potential when limited.

Summing It Up

Although the specifics of how BFR works aren’t really nailed down, we do know that it works. We know that it stimulates protein synthesis and that it allows you to use high-rep, light loads to get muscle strength and hypertrophy gains. We also know that it gives you one hell of a workout pump. So, for those no longer able to lift heavy, or those who want something fun to try, grab some knee wraps and give it a try!

References

  1. Abe, T., Kearns, C.F. & Sato, Y. Muscle size and strength are increased following walk training with restricted venous blood flow from the leg muscle, Kaatsu-walk training. Journal of applied physiology 100, 1460-1466 (2006).
  2. Behringer, M. & Willberg, C. Corrigendum: Application of Blood Flow Restriction to Optimize Exercise Countermeasures for Human Space Flight. Frontiers in physiology 10, 276 (2019).
  3. Behringer, M. & Willberg, C. Application of Blood Flow Restriction to Optimize Exercise Countermeasures for Human Space Flight. Frontiers in physiology 10, 33 (2019).
  4. Burgomaster, K.A. et al. Resistance training with vascular occlusion: metabolic adaptations in human muscle. Medicine and science in sports and exercise 35, 1203-1208 (2003).
  5. Evans, C., Vance, S. & Brown, M. Short-term resistance training with blood flow restriction enhances microvascular filtration capacity of human calf muscles. Journal of sports sciences 28, 999-1007 (2010).
  6. Takarada, Y., Sato, Y. & Ishii, N. Effects of resistance exercise combined with vascular occlusion on muscle function in athletes. European journal of applied physiology 86, 308-314 (2002).
  7. Fujita, S. et al. Blood flow restriction during low-intensity resistance exercise increases S6K1 phosphorylation and muscle protein synthesis. Journal of applied physiology 103, 903-910 (2007).
  8. Takano, H. et al. Hemodynamic and hormonal responses to a short-term low-intensity resistance exercise with the reduction of muscle blood flow. European journal of applied physiology 95, 65-73 (2005).
  9. Takarada, Y. et al. Rapid increase in plasma growth hormone after low-intensity resistance exercise with vascular occlusion. Journal of applied physiology 88, 61-65 (2000).
  10. Fry, C.S. et al. Blood flow restriction exercise stimulates mTORC1 signaling and muscle protein synthesis in older men. Journal of applied physiology 108, 1199-1209 (2010).
  11. Gundermann, D.M. et al. Activation of mTORC1 signaling and protein synthesis in human muscle following blood flow restriction exercise is inhibited by rapamycin. American journal of physiology. Endocrinology and metabolism 306, E1198-1204 (2014).
  12. Nielsen, J.L. et al. Proliferation of myogenic stem cells in human skeletal muscle in response to low-load resistance training with blood flow restriction. The Journal of physiology 590, 4351-4361 (2012).
  13. Cerda-Kohler, H. et al. Lactate administration activates the ERK1/2, mTORC1, and AMPK pathways differentially according to skeletal muscle type in mouse. Physiological reports 6, e13800 (2018).
  14. Tsukamoto, S., Shibasaki, A., Naka, A., Saito, H. & Iida, K. Lactate Promotes Myoblast Differentiation and Myotube Hypertrophy via a Pathway Involving MyoD In Vitro and Enhances Muscle Regeneration In Vivo. International journal of molecular sciences 19 (2018).
  15. Oishi, Y. et al. Mixed lactate and caffeine compound increases satellite cell activity and anabolic signals for muscle hypertrophy. Journal of applied physiology 118, 742-749 (2015).
  16. Gnimassou, O. et al. Environmental hypoxia favors myoblast differentiation and fast phenotype but blunts activation of protein synthesis after resistance exercise in human skeletal muscle. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 32, 5272-5284 (2018).
  17. Kawada, S. & Ishii, N. Skeletal muscle hypertrophy after chronic restriction of venous blood flow in rats. Medicine and science in sports and exercise 37, 1144-1150 (2005).
  18. Gundermann, D.M. et al. Reactive hyperemia is not responsible for stimulating muscle protein synthesis following blood flow restriction exercise. Journal of applied physiology 112, 1520-1528 (2012).
  19. Andersen, P. & Saltin, B. Maximal perfusion of skeletal muscle in man. The Journal of physiology 366, 233-249 (1985).
  20. Degens, H., Turek, Z., Hoofd, L.J., Van't Hof, M.A. & Binkhorst, R.A. The relationship between capillarisation and fibre types during compensatory hypertrophy of the plantaris muscle in the rat. Journal of anatomy 180 ( Pt 3), 455-463 (1992).
  21. Tomanek, R.J. & Torry, R.J. Growth of the coronary vasculature in hypertrophy: mechanisms and model dependence. Cellular & molecular biology research 40, 129-136 (1994).
  22. Egginton, S. Physiological factors influencing capillary growth. Acta physiologica 202, 225-239 (2011).
  23. Olfert, I.M., Baum, O., Hellsten, Y. & Egginton, S. Advances and challenges in skeletal muscle angiogenesis. American journal of physiology. Heart and circulatory physiology 310, H326-336 (2016).

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