ACL tears are one of the most common injuries in athletics that lead to surgical intervention. The rate at which ACL reconstructions (ACLR) are performed has risen 22% from 2002 to 2014; with the highest rates occurring in adolescents.1 Unfortunately, far fewer return to their prior level of sport participation vs. anticipated (~65%2 vs ~84%3). During the immediate post-injury and post-op periods, and due to a number of factors, the quadriceps can atrophy quite rapidly. Accompanying this loss of muscle is an associated decrease in strength. Addressing this loss of size and strength is an important target for us in rehab, and one we need a deeper understanding of to help us intervene more effectively.
Restoring muscle quality and quantity is our responsibility. Unfortunately, the data consistently shows we are not meeting this goal. In order to safely return to sport, and to reduce the risk of second injury, it is generally accepted that one needs to achieve a Limb Symmetry Index (LSI) of 90% in the quad and hamstring muscle groups. However, at 6 months only 34% had a LSI of 90%4, with a small increase to 43.5% at 8 months5. When strength was assessed at 9 months post ACLR, 53% met a LSI of 90%.4 Although the LSI is commonly used and recommended, it does not account for strength loss in the uninvolved limb due to disuse. To elaborate on this potential discrepancy, Wellsandt and colleagues assessed individual’s strength prior to ACL reconstruction and at 6 months post-op.9 When comparing strength at 6 months post-op only, 57% achieved a LSI of 90%. When comparing this to the uninvolved side prior to surgery though, only 28% had a LSI of 90%.9
Welling’s group found a similar over estimation of strength when they compared LSI to knee extensor torque normalized to bodyweight. Although 34% and 53% met a LSI index of 90% at 6 and 9 months respectively, only 27% and 40% met a peak torque of 3.0 Nm/kg at 6 and 9 months.4 These discrepancies have even been identified in high level athletics as Herrington’s group found a chronic decrement in knee extensor torque (2.76 Nm/kg) amongst professional soccer players at 8 months following an ACLR.10 Collectively, these findings indicate a disuse effect of strength on the contralateral side, and that LSI may overestimate knee extensor strength. Thus, using established normalized values may be more representative of whether or not an athlete has achieved the necessary quadriceps strength for RTP.11–14 The silver lining from these papers is, the longer we rehab, the better quad strength becomes. Nevertheless, the majority of athletes return to sport prior to 9 months,5,6 resulting in a loss of self-reported function and an inability to return to their previous level of sport participation, out to 2 years.7,15–17
What causes these strength deficits?
Too often, management of the acute post-injury is somewhat of an afterthought. The default is to manage pain and edema via RICE; gradually increasing ROM and weight bearing activity as the joint tolerates. Recent evidence, however, indicates this is a critical time point for muscle. For example, 14 days of knee immobilization lead to vastus lateralis atrophy of >3% at 5 days, progressing to 8.4% after 14 days. This corresponded to 6.8 and 18kg decreases in quad strength respectively.18 To help explain these rapid muscle changes, the authors also showed a 68% increase in the gene expression of myostatin at 5 days.18 Myostatin is a theoretical light switch that controls muscle function by inhibiting differentiating muscle stem cells,19,20 while down regulating muscle protein synthesis and upregulating muscle protein breakdown.21,22 Along with negatively impacting the muscle’s ability to grow and repair, myostatin also contributes to an increase in fibrosis/scar tissue development following an injury.25
In accordance with this, it has been shown that myostatin gene and protein expression is upregulated 2-fold in the involved quadriceps following an ACL injury.23 This has been shown to extend into the acute postop phase.24 Prior to surgery, increased myostatin levels contributed to a 51% reduction in muscle stem cells per fiber, a 30% decrease in quad muscle volume, and a 46% increase in fibrotic area compared to the contralateral quad.26 Importantly, six months of rehab failed to improve any of these variables. In fact, quad size decreased an additional 18%; contributing to a 49% deficit in LSI.26
What can be done to address this?
Initially, performing a period of preoperative rehabilitation focused on normalizing quadriceps size and strength needs to be required prior to surgery. Preoperative atrophy has been shown to explain 46% of the decrement in quadriceps strength;27 with preoperative strength explaining 15% of the deficit.28 The Delaware-Oslo cohort showed that just 10 visits of pre-op physical therapy over 5 weeks significantly increased quadriceps strength and peak knee extensor torque.29 The use of BFR during this period is indispensable. Not only are BFR exercises well tolerated, low intensity BFR exercises have been shown to significantly reduce knee pain when compared to traditional low-intensity30, and moderate-intensity quadriceps strengthening exercises.31 In addition to addressing pain, 8 sessions of knee extensor training led to a 290% increase in muscle stem cells, which lead to a 30% increase in muscle fiber area in 3 weeks.32 BFR training for 8 weeks, decreased myostatin by 46% which may explain the aforementioned changes in muscle.33 Additionally, Kacin’s lab showed 5 prehab sessions consisting of unilateral knee extensions with or without BFR in the week leading up to an ACLR led to a 50% increase in quadriceps blood flow in the BFR group, which corresponded to a 5% increase isometric knee extensor endurance.34 Kacin had previously identified quad muscle endurance was more protective of atrophy than strength.27
In the immediate post-op period, passive use of BFR has been shown to significantly attenuate knee extensor atrophy by over 60%.35 When combined with low intensity NMES, passive BFR led to a 3.9% increase in muscle thickness and a 7-8% increase in isokinetic strength.36 As soon as the individual is able to tolerate resistance exercise, BFR at low loads is initiated. A recent paper by Luke Hughes showed similar changes in muscle thickness between traditional post-op rehab combined with either low intensity BFR leg press exercise biweekly or moderate-high intensity leg press.37 In addition to changes in muscle thickness, both groups demonstrated a significant increase in vastus lateralis pennation angle compared (BFR: 4.1%; HIT: 3.1%).37 Of equal importance, these findings indicate that two months of traditional PT plus one BFR exercise can produce greater muscle changes compared to six months of traditional PT.26 The significance of these results extend beyond changes in muscle; the BFR group also achieved greater improvements in joint ROM, greater reductions in joint swelling, and greater self-reported functional improvements compared to the moderate-high intensity leg press group.38
Muscle changes following an injury occur extremely fast and continue to fester late into the post-op period. The typical strategy to reduce pain and increase ROM during this critical period is not enough and emphasis must be placed on addressing the disuse state of muscle that ensues. Current evidence indicates low intensity BFR exercises can suppress myostatin levels to a similar extent as performing high load lifting, helping to combat post injury / surgery loss of quad muscle size and strength. Additionally BFR following ACLR may produce significantly greater improvements in pain, joint ROM, and joint swelling making it a clinically viable alternative to high load training.