Blood Flow Restriction Training Post ACLR: What is it and why is it useful?

Within non-professional sport settings, low levels of return to performance rates and high levels of reinjury rates are common issues amongst current anterior cruciate ligament reconstruction (ACLR) rehabilitation. In current practice, whilst approximately 84% of athletes expect to return to sport by 12 months, only 24% achieve this goal (Webster & Feller 2019). ACL reinjury rates also remain high with graft failure rates at up to 14% for adults and 28% for young athletes (Raines et al 2017).

Quadriceps weakness and atrophy is a common issue post ACLR (Charles et al, 2020). The loss of thigh muscle mass is a contributing factor to disability during the acute stages post ACLR whilst persistent quadriceps weakness is known to have a role to play in higher re- injury rates as well as poor long term health outcomes (Grindem et al, 2016). Blood flow restriction training (BFR) is a novel intervention that has shown promise in increasing muscular strength and hypertrophy (Loenneke et al, 2012). BFR training aims to target a metabolic stress mechanism, inducing hypertrophic changes within muscle (Pearson & Hussain, 2014).

Theories behind the use of BFR for improving quadriceps mass and function post ACLR

To understand how BFR training may be effective at producing muscular hypertrophy it is important to understand how this process occurs. When analysing the methods for inducing muscular hypertrophy, historically it has been suggested that in order to increase muscle mass and strength, type II muscle fibres need to be heavily activated during training, since these fibres have been shown to be more responsive to hypertrophy than type I fibres (Pearson & Hussain, 2014). In order to facilitate this, moderate-high intensity strength training with loads of >65% 1RM has been preferable in strength training prescription (Pearson & Hussain, 2014).

Although a common procedure, ACLR surgery remains a complex and technically demanding surgical intervention that typically leaves athletes in considerable levels of pain, with limited range of motion and high levels of muscle atrophy (Bliss, 2017). For this reason, it is unrealistic to believe that the athlete may be able to load their knee at levels of >65% 1RM in the acute to sub-acute stages post operatively and therefore alternative methods for creating hypertrophic gains must be considered (Bliss, 2017).

Recent literature has suggested that BFR training methods can be effective in producing these changes within skeletal muscle at training loads <50%1RM (Pearson & Hussain, 2014). Typically, this is achieved via placing a torniquet, pressurised cuff, or elastic bandage around the proximal portion of upper or lower extremities (Pearson & Hussain, 2014). It is believed that the pressure is maintained at a level that allows sufficient arterial inflow whilst restricting venous outflow, creating an ischaemic or hypoxic environment enhancing the training effect by accelerating metabolic stress. This allows the ability to perform low load resistance training (LL-RT) and produce similar outcomes to high load resistance training (HL-RT) (Pearson & Hussain, 2014).

One of the main priorities of rehabilitation after ACLR surgery is the restoration of knee extensor muscle strength (Buckthorpe et al, 2019). Deficits in knee extensor muscle size and strength post ACLR are linked to reduced knee function, increased risk of osteoarthritis and heightened risk of re-injury when returning to sport along with reduced performance (Buckthorpe et al, 2019). Limb Symmetry Indexes (LSI) are useful outcome measures for knee extensor strength comparing both the operated and non-operated limb (Buckthorpe et al, 2019). Low LSI scores have been reported as a risk factor for re-injury, individuals with LSI scores less than 90% have been shown to be up to three times more likely to sustain a subsequent knee injury than those who achieved more than 90% LSI. Additionally, for every 1%-point increase in quadriceps symmetry there is up to 3% reduction in re-injury rates (Grindem et al 2016). This highlights the importance of restoring thigh muscle mass and strength post ACLR in order to optimise patient outcomes and reducing re-injury rates.

Whilst athletes of all levels and sports may be subject to the possibility of requiring ACLR, it is known that non-professional athletes participating in multi-directional sports requiring cutting, jumping, landing and pivoting are placed at greater risk of injury (Gianotti et al,

2009). As the primary stage for muscle strength loss and atrophy occurs in the acute to sub- acute stage post-surgery, this is the chief focus of where this intervention may be most effective. High numbers of sub-elite athletes don’t achieve LSI at the 6-month mark post- surgery, and this may give insight as to how pivotal being able to enhance early loading can be (Buckthorpe et al, 2019). Given that the average annual cost of ACL reconstructions is upward of 1 billion US dollars (Raines et al, 2017) and that re-injury rates range from 2-30% there is an inherent need to improve rehabilitation following primary reconstructions (Raines et al, 2017).

BFR & Hypertrophy: What are the physiological mechanisms?

A recent 2020 systematic review highlighted that BFR training may have a positive effect in restoring quadriceps muscle cross sectional area post ACLR (Charles et al, 2020). Another 2019 systematic review of randomised controlled trials highlighted that short durations of BFR training (<2 weeks) has no effect on muscle cross sectional area however a moderate – long duration (~15 weeks) may have a positive effect on muscle hypertrophy (Lipker et al, 2019). To better understand how and why it may be effective it is imperative to understand how BFR training may interact with the primary mechanisms of muscular hypertrophy. The primary mechanisms that facilitate muscular hypertrophy are mechanical tension, metabolic stress and muscle damage (Pearson & Hussain, 2014). The role that BFR may have in these mechanisms are:

Mechanical Tension

Mechanical tension refers to the maximal strain that is placed upon a muscle when it is loaded, this is primarily induced with high loads and causes upregulation of mechanotransduction, localised hormone production and fast twitch fibre recruitment (Pearson & Hussain, 2014). It is unclear whether BFR training has a large impact on mechanical tension due to the low load nature of the resistance training performed.

Metabolic Stress

Metabolic stress refers to the accumulation of metabolites within muscle cells as a result of training (Pearson & Hussain, 2014). It has been reported that metabolic stress is as important if not more important than mechanical tension in promoting muscle growth (Pearson & Hussain, 2014). Levels of metabolic stress have been shown to increase under ischemic conditions such as that which is performed in BFR training (Pearson & Hussain, 2014). Studies implementing BFR where a period of low-intensity resistance exercise (~30– 50 % 1RM) with BFR (~110–200 mmHg) was found to result in a significantly greater increase in muscle cross sectional area than similar programmes performed without BFR (Pearson & Hussain, 2014). Proposed physiological components that link metabolic stress to increased muscular hypertrophy include elevated systemic hormone production, type II fibre recruitment and cell swelling.

Muscle Damage

The theory regarding exercise induced muscle damage (EIMD) and its link with muscular hypertrophy is centred on the role that eccentric contractions have on the facilitation of

muscle damage. Currently there is mixed evidence regarding the role that BFR has on facilitating this mechanism with limited evidence promoting muscle damage for only up to 24 hours post training. A greater link between muscle damage and increased mechanical tension can be seen (Pearson & Hussain, 2014).

Additional Mechanisms

Arthrogenic muscle inhibition (AMI) is theorised to be a primary determinant of the loss of muscle mass and reduction in muscle strength post ACLR. As AMI impedes the recruitment of high threshold motor units it prevents adequate muscular activation from occurring during exercise (Buckthorpe et al, 2019). As with Henneman’s size principle, BFR has been theorised to promote high threshold motor unit activation due to the exhaustion of lower threshold motor units. Therefore BFR can be a proposed mechanism to overcome this deficit without the need for high mechanical tension (Ellefsen et al, 2015).

Secondary mechanisms behind muscle hypertrophy that BFR is linked with include up regulation of systemic and localised hormones, muscle cell swelling, nitric oxide production, reactive oxygen species production, heat shock protein production and muscle fibre recruitment (Pearson & Hussain, 2014). Detail of these secondary mechanisms goes beyond the scope of this blog.

Conclusion:

Reducing knee extensor weakness and thigh muscle atrophy is pivotal in promoting optimal outcomes post ACL reconstruction (Thomas et al, 2016). Fundamental mechanisms that promote muscular strength and hypertrophy include mechanical tension, metabolic stress and muscle damage. During the acute stages post ACLR, patients are limited in their ability to tolerate high levels of mechanical tension and muscle damage due to pain, limited range of motion, swelling and AMI that prevent the knee from being heavily loaded. BFR training may provide a solution to ongoing quadriceps muscle weakness and thus improve return to performance and re-injury rates. This can be achieved by allowing maximal levels of metabolic stress to occur within the muscle at very low loads which is practically achievable in the acute ACLR patient.

References:

Webster, K. E., & Feller, J. A. (2019). Expectations for Return to Preinjury Sport Before and After Anterior Cruciate Ligament Reconstruction. The American journal of sports medicine, 47(3), 578–583. https://doi.org/10.1177/0363546518819454

Raines, B. T., Naclerio, E., & Sherman, S. L. (2017). Management of Anterior Cruciate Ligament Injury: What's In and What's Out?. Indian journal of orthopaedics, 51(5), 563–575. https://doi.org/10.4103/ortho.IJOrtho_245_17

Charles, D., White, R., Reyes, C., & Palmer, D. (2020). A SYSTEMATIC REVIEW OF THE EFFECTS OF BLOOD FLOW RESTRICTION TRAINING ON QUADRICEPS MUSCLE ATROPHY AND CIRCUMFERENCE POST ACL RECONSTRUCTION. International Journal Of Sports Physical Therapy, 15(6), 882-891. doi: 10.26603/ijspt20200882

Grindem, H., Snyder-Mackler, L., Moksnes, H., Engebretsen, L., & Risberg, M. (2016). Simple decision rules can reduce reinjury risk by 84% after ACL reconstruction: the Delaware-Oslo ACL cohort study. British Journal Of Sports Medicine, 50(13), 804-808. doi: 10.1136/bjsports- 2016-096031

Loenneke, J., Abe, T., Wilson, J., Ugrinowitsch, C., & Bemben, M. (2012). Blood Flow Restriction: How Does It Work?. Frontiers In Physiology, 3. doi: 10.3389/fphys.2012.00392

Pearson, S., & Hussain, S. (2014). A Review on the Mechanisms of Blood-Flow Restriction Resistance Training-Induced Muscle Hypertrophy. Sports Medicine, 45(2), 187-200. doi: 10.1007/s40279-014-0264-9

Bliss, J. (2017). Anterior cruciate ligament injury, reconstruction, and the optimization of outcome. Indian Journal Of Orthopaedics, 51(5), 606. doi: 10.4103/ortho.ijortho_237_17

Buckthorpe, M., La Rosa, G., & Villa, F. (2019). RESTORING KNEE EXTENSOR STRENGTH AFTER ANTERIOR CRUCIATE LIGAMENT RECONSTRUCTION: A CLINICAL COMMENTARY. International Journal Of Sports Physical Therapy, 14(1), 159-172. doi: 10.26603/ijspt20190159

Gianotti, S., Marshall, S., Hume, P., & Bunt, L. (2009). Incidence of anterior cruciate ligament injury and other knee ligament injuries: A national population-based study. Journal Of Science And Medicine In Sport, 12(6), 622-627. doi: 10.1016/j.jsams.2008.07.005

Lipker, L. A., Persinger, C. R., Michalko, B. S., & Durall, C. J. (2019). Blood Flow Restriction Therapy Versus Standard Care for Reducing Quadriceps Atrophy After Anterior Cruciate Ligament Reconstruction. Journal of sport rehabilitation, 28(8), 897–901. https://doi.org/10.1123/jsr.2018-0062

Ellefsen, S., Hammarström, D., Strand, T. A., Zacharoff, E., Whist, J. E., Rauk, I., Nygaard, H., Vegge, G., Hanestadhaugen, M., Wernbom, M., Cumming, K. T., Rønning, R., Raastad, T., &

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Thomas, A. C., Wojtys, E. M., Brandon, C., & Palmieri-Smith, R. M. (2016). Muscle atrophy contributes to quadriceps weakness after anterior cruciate ligament reconstruction. Journal of science and medicine in sport, 19(1), 7–11. https://doi.org/10.1016/j.jsams.2014.12.009