I started hearing about blood flow restriction training several years ago, but never really gave it much credence. I thought it was mostly a gimmick to give people that sought-after ‘pump’ which isn’t actually a useful marker of efficacy. I have begun to see blood-flow restriction being implemented more and more frequently in the gym and hear about it fairly regularly on podcasts that I listen to. I didn’t understand the mechanism behind it or in what instances it might be most applicable. My 10,000 ft view was that it enabled adaptations to be achieved at a lower work capacity. While the notion of experiencing performance improvements in less time and with less effort was intriguing, I had heard that blood-flow restriction could be misapplied and even dangerous. I’m really not one to go for the latest and greatest technology so I never experimented with it myself despite the curiosity to better understand its role in performance.
Just the other day, I came across a really neat lecture series on YouTube by Dr. Andy Galpin (https://www.youtube.com/@drandygalpin) wherein he discussed a paper detailing the influence of metabolites on muscle fiber recruitment and subsequent muscle hypertrophy (1). This concept caught my attention and I went looking for the paper to learn more about it. I had no idea the paper would also touch on blood flow restriction training. I wanted to take the time to resume my thoughts and understanding following reading it, so here we are.
The first mention of blood-flow restriction training in the paper is in how it compares to low load training to volitional failure with regard to muscular hypertrophy (1). Both appear to instigate similar amounts of muscle growth. The paper begins with a brief overview of the mechanisms governing muscle hypertrophy, which is probably an equally valid jumping-off point here.
Mechanotransduction is the process through which muscle contraction induces a mechanical stress that is consequently converted into a chemical signal (1). Mechanotransduction is implicated as the predominant stimulus eliciting resistance-training associated muscle hypertrophy. Focal adhesions, characterized by focal adhesion proteins bound together, attach to integrin receptors. Focal adhesions purportedly facilitate the transfer of tension within the muscle cell from the extracellular matrix to the cell nucleus (1). Within the nucleus, the mechanistic target of rapamycin complex 1 (mTORC1) is activated. mTORC1 is hugely involved in stimulating protein synthesis and thereby contributing to muscle hypertrophy.
Returning to blood flow restriction training… Because the load used during this form of exercise is so low, the tension placed on the muscle cell is relatively small (1). Thus, there is currently doubt that mechanotransduction is the driving force behind muscular hypertrophy in this context. The idea that metabolite accumulation from blood-flow restriction might be mediating muscle hypertrophy has gained some favor, serving as a metabolic as opposed to mechanical sensor. However, research is lacking that demonstrates a true causative relationship between metabolite production and muscle hypertrophy, merely an association (1). The metabolic environment in these studies is not adequately controlled as many training variables are being manipulated simultaneously.
What is consistently represented in research is that local fatigue is critical to muscle hypertrophy (1). Fatigue is highly correlated with muscle activation, with increased activation inciting a greater degree of fatigue development. Fatigue also contributes to an elevated number of muscle fibers being recruited. Metabolites are produced consequent to higher metabolic demand resulting from a rise in muscle activation. The takeaway here is that metabolites are likely a symptom of activation and do not directly influence muscle growth (1). What metabolites may be doing is promoting muscle activation. Until it is shown that metabolites can elicit muscle growth independent of muscle contraction, the jury is still out on their overall impact.
What is plausible is that metabolite accumulation magnifies muscle fatigue (1). Both inorganic phosphate and hydrogen ion accumulation seem to impair cross-bridge formation that leads to muscular contraction. In repetition-matched, low-load exercises, blood flow restriction outperforms non-blood flow restriction in terms of muscle growth, although this outcome is negated when both are performed to volitional failure. This stands in contrast to high load resistance exercise whereby blood flow restriction provides no hypertrophic benefit (1). It is likely that, in the first scenario, muscle fatigue is reached more quickly with blood flow restriction, in part due to enhanced fiber recruitment consequent to fatigue, while in the second scenario muscle activation is equated and thus fatigue is generally similar. Note that load and fatigue dictate fiber recruitment such that either a high load or a high fatigue will cause more higher-threshold fibers to become activated (1). These observations potentially invalidate the notion that metabolites directly influence muscle growth but instead instigate greater recruitment and activation.
Both high and low load training, when completed to volitional failure, seem to produce similar muscle fiber recruitment patterns owing to a similar level of fatigue being met (1). The authors actually performed an experiment in which blood flow restriction was initiated post-exercise to essentially hold the metabolites in place, which showed a detrimental effect in women of the study and a neutral effect on the men. They went on to point out that magnitude of force does not dictate the twitch force of a motor unit because motor neuron firing always incites maximal force production by the muscle fiber (1). Fatigue can interfere with this force generation, but load cannot. The number of motor units recruited ultimately influences the force produced by the entire muscle. A higher percentage of muscle fibers recruited, or a larger quantity of the muscle activated, will elicit a greater force. This negates the point made initially that low loads cannot drive hypertrophy through mechanotransduction as each muscle fiber recruited is under maximum tension.
To wrap this up and tie it with a bow, my interpretation is that blood-flow restriction would be most useful for those who do not have the desire or the capacity to use high loads in their training. If one is injured, elderly, or has some other reason for wanting to implement low-load training, blood-flow restriction might be an interesting protocol to experiment with. Nevertheless, I would be very careful to work with a professional who can monitor pressure throughout the use of the blood-flow restriction cuffs to mitigate injury risk.
References
- Dankel SJ, Mattocks KT, Jessee MB, Buckner SL, Mouser JG, Loenneke JP. Do Metabolites That Are Produced during Resistance Exercise Enhance Muscle hypertrophy? European Journal of Applied Physiology. 2017;117(11):2125-2135. doi:https://doi.org/10.1007/s00421-017-3690-1