VMO: An Update

The following is an article written for the online, video-based physical therapy continuing education company MedBridge

Patellofemoral pain syndrome (PFPS) is among the most common sports injuries and yet the current treatment protocols are not optimal. In particular, the latest research questions our ability to selectively recruit vastus medialis obliquus (VMO) and affect its timing and suggests that VMO may have nothing to do with the PFPS.

Prevalence of Patellofemoral Pain Syndrome

PFPS has an astounding prevalence according to a retrospective case-control analysis by Taunton et al. They analyzed 2,002 running-related injuries seen at a primary care sports injury facility – and 42.1% (842/2,002) were knee injuries. Of these knee injuries, 39.3% (331/842) were due to patellofemoral pain syndrome (PFPS), which made PFPS by far the most common diagnosis found in this large-scale study.

Similarly, in an older study (1984), Devereaux et al found that over a five year period, 137 patients presented with PFPS – accounting for 25% of all knee injuries seen at this sports injury clinic.

These two studies were conducted 17 years apart, giving support to the consistently high prevalence of this disorder. Now the most important question is, how are we treating these patients?

How are we treating patients with PFPS?

Imbalance of LV and VMO

The biomechanical study by Lieb et al made the VMO the mainstay of most physical therapy protocols and treatment approaches for PFPS.

Conducted in 1968, the study found that VMO’s fibers are oriented at 55° from the longitudinal axis of the femur. This orientation alone makes VMO the primary restraint to lateral subluxation of the patella. The study further postulated that VMO was able to counterballance the pull of the much larger vastus lateralis (VL) due to the discrepancy in mechanical advantages.

As a result of this study, an insufficient balance between the VL and VMO has long been considered the primary contributing factor in developing patellar subluxation, or maltracking.

VL:VMO timing

A study by Cowan et al found that subjects with PFPS have an imbalance of VL:VMO timing. The VL typically begins to fire approximately 15-20 ms prior to the VMO.

Due to this understanding of the biomechanics, the treatment strategy typically involved correcting the potential VMO atrophy, hypoplasia, inhibition, and impaired motor control.

Now, this all seems logical in theory, but can we actually selectively train the VMO? Is this relatively small muscle affected differently than the rest of the quadriceps musculature in the presence of pain?

New research questions…

Does VMO atrophy relative to the rest of quadriceps?

A recent study by Giles and colleagues refutes one of the cornerstones of the VMO theory; namely, that this small muscle tends to atrophy relative to the rest of the quadriceps during or following surgery. They performed a cross-sectional study of 35 participants diagnosed with PFPS.

The results showed atrophy of all portions of the quadriceps muscles – and no selective atrophy of the VMO – present in the affected limb of people with unilateral PFPS.

Can we selectively activate VMO?

Even if the atrophy was present, the literature is not very kind to the ability to preferentially activate this musculature either.

Cerny et al evaluated the ability to preferentially recruit the VMO during 22 different quadriceps exercises. Through electromyographic analysis, they determined that VMO activity was not higher in any exercise compared to VL.

In a randomized controlled trial, Song et al found no evidence that VMO can be activated separately. They compared the change in VMO cross-sectional area after 8 weeks of unilateral leg press and unilateral leg press with subsequent hip adduction. The two groups showed no significant difference between the change in VMO cross-sectional area (the standard leg press actually yielded better results).

Thus, selective isolation of the VMO in everyday clinical practice is highly unlikely. In all reality, if we consider inability to selectively recruit their target, most of the ‘VMO programs’ are merely strengthening the quadripceps as a whole. If we could selectively recruit these fibers, according to Grabiner et al, it would take approximately 60% of maximal voluntary contraction to stimulate hypertrophy of the VMO.

Does VMO training have advantages over general quadriceps strengthening?

In 2010, Bennell et al investigated how VMO retraining compares to a general quadriceps strengthening program in relation to vasti onset.

The VMO retraining group used EMG biofeedback during the following series of exercises:

  • isometric VMO contractions at 90° of knee flexion
  • standing mini squats to 40°
  • isometric contraction of the VMO in combination with hip abduction and hip external rotation during an isometric wall contraction in standing
  • step downs

The quadriceps group performed:

  • isometric quad sets
  • straight-leg raises
  • SAQs
  • side-lying hip abduction

At the conclusion of the training programs, the retraining group actually did create more significant changes in stair descent activation in the short-term. However, at the 8-week follow-up, both values were nearly identical. The initial improvement may have been due to the use of ‘step downs’ in the retraining group, which most closely simulates the functional and muscular demands of stair descent.

During stair ascent, on the other hand, the quadriceps strengthening group caused a much more significant alteration in VMO:VL timing and was the only group that caused the VMO to fire prior to the VL.

A study conducted by Laprade et al showed similar results using isometric exercise. This study compared the EMG activity in individuals with PFPS and asymptomatic controls during 5 isometric exercises. There was no significant difference in the ratio of VMO:VL firing between the two groups.

Given these results, I find it hard to support the use of VMO training in everyday clinical practice.

Does VMO strengthening make a difference for PFPS?

Suppose it was possible to selectively recruit the VMO. Would it reduce patellofemoral contact stress sufficiently to relieve the pain?

Sawatsky et al say no. They conducted a biomechanical study using New Zealand white rabbits. Although this is not a direct human study, the muscular alignment and pull of the quadriceps is very similar: the fibers of the VMO and VL are oriented at 45-50° and 14-19°, respectively, in relation to the longitudinal axis of the femur.

They transected VMO at varying levels of knee flexion (30°, 60°, and 90°), measuring patellofemoral joint contact pressures before and after the transections.

There were no significant differences between peak pressures, average pressures, contact areas, or contact shapes before and after transection.

If the contact area and pressure are not altered when the muscle is removed from the equation, then why do we continue thinking VMO training is the gold standard in PFPS treatment?

Should we stop blaming the glutes for everything?

Below is an article written for MikeReinold.com… 

Anterior cruciate ligament (ACL) rupture1,2 and patellofemoral pain syndrome (PFPS)3,4,5 are two of the most common lower extremity complaints that physicians or physical therapists will encounter. In addition to the high incidence of these pathologies, with regards to ACL injury, very high ipsilateral re-injury and contralateral injury have also been reported6,7,8. With the importance of treating and/or preventing these injuries, several researchers have taken it upon themselves to determine what movement patterns predispose athletes to developing these injuries. This research indicates that greater knee abduction moments9,10, peak hip internal rotation11 and hip adduction motion12 are risk factors for PFPS development. Whereas, for ACL injury, Hewett and colleagues13 conducted a prospective cohort study identifying Knee abduction angle at landing as predictive of injury status with 73% specificity and 78% sensitivity. Furthermore, as the risk factors for developing both disorders are eerily similar, Myer et al performed a similar prospective cohort study finding that athletes demonstrating >25 Nm of knee abduction load during landing are at increased risk for both PFPS and ACL injury14. With a fairly robust amount of research supporting a hip etiology in the development of these injuries, it would make sense that weakness of the hip musculature would also be a risk factor, right?

A recent systematic review found very conflicting findings on the topic. With regards to cross-sectional research, the findings were very favorable with moderate level evidence indicating lower isometric hip abduction strength with a small effect size (ES) and lower hip extension strength with a small ES15. Additionally, there was a trend toward lower isometric hip external rotation and moderate evidence indicates lower eccentric hip external rotation strength with a medium ES in individuals with PFPS15. Unfortunately, the often more influential prospective evidence told a different story. Moderate-to-strong evidence from three high quality studies found no association between lower isometric strength in hip abduction, extension, external rotation or internal rotation and the risk of developing PFPS15. The findings of this systematic review indicated hip weakness may be a potential consequence of PFPS, rather than the cause. This may be due to disuse or fear avoidance behaviors secondary to the presence of anterior knee pain. Regardless of its place as a cause or consequence, hip strengthening has proved beneficial in patients with both PFPS16,17,18 and following ACL Reconstruction19, but does it actually help to change the faulty movement patterns?

Gluteal strengthening can cause several favorable outcomes, from improved quality of life to decreased pain, unfortunately however marked changes in biomechanics is not one of the benefits. Ferber and colleagues20 performed a cohort study analyzing the impact of proximal muscle strengthening on lower extremity biomechanics and found no significant effect on two dimensional peak knee abduction angle. In slight contrast however, Earl and Hoch21 found a reduction in peak internal knee abduction moment following a rehabilitation program including proximal strengthening, but no significant change in knee abduction range of motion was found. It should be noted that this study included strengthening of all proximal musculature and balance training, so its hard to conclude that the results were due to the strengthening program. Potentially, gluteal endurance may be more influential than strength itself, so it would make sense that following isolated fatigue of this musculature, lower extremity movement patterns would deteriorate.

Once again, this belief is in contrast to the available evidence. While fatigue itself most definitely has an impact on lower extremity quality of movement, isolated fatigue of the gluteal musculature tells a different story. Following a hip abductor fatigue protocol, patients only demonstrated less than a one degree increase in hip-abduction angle at initial contact and knee-abduction angle at 60 milliseconds after contact during single-leg landings22. In agreement with these findings, Geiser and colleagues performed a similar hip abductor fatigue protocol and found very small alterations in frontal plane knee mechanics, which would likely have very little impact on injury risk23. The biomechanical explanation for why weakness or motor control deficits in the gluteal musculature SHOULD cause diminished movement quality makes complete sense, but unfortunately, the evidence at this time does not agree.

While the evidence itself does not allow the gluteal musculature to shoulder all of the blame, this does not mean we should abandon addressing these deficits in our patients. As previously stated, posterolateral hip strengthening has multiple benefits, but it is not the end-all-be-all for rehabilitation or injury prevention of lower extremity conditions. Proximal strength deficits should be assessed through validated functional testing in order to see its actual impact on lower extremity biomechanics on a patient-by-patient basis. Following this assessment, interventions should be focused on improving proximal stability, movement re-education, proprioception, fear avoidance beliefs, graded exposure, and the patient’s own values, beliefs, and expectations.

Strength Training Considerations for Patellofemoral Pain Syndrome

In my previous post regarding Patellofemoral Pain Syndrome (PFPS), I delved into its etiological understanding. Now that we are beginning to learn more about this syndrome and its subsequent biomechanical considerations, we can begin to develop a more effective and targeted strength training program.

Slide1

Posterolateral Hip Musculature

Last year, two systematic reviews were published that showed continued evidence for an association between weak hip abductors and PFPS. Lankhorst et al found significantly less hip abductor strength and less hip external rotator strength when adjusted to patient’s body weight in PFPS patients compared to the control subjects. Also, Barton et al investigated gluteal muscle activity and its association with those patients suffering from PFPS. They found that evidence indicates Gluteus Medius muscle activity is delayed and of shorter duration during stair ascent/descent and running. In contrast, Gluteus Maximus muscle activity is increased during stair descent in individuals with PFPS.

With these findings, logically, it makes sense to target both the hip abductors and external rotators, but is there evidence to support this?

In 2010, Fukuda et al conducted a randomized controlled trial (RCT) comparing the short-term effects of a combined hip abductor, lateral rotator, and quadriceps strengthening program (HKE) to that of a traditional quadriceps strengthening program alone (KE). After 4 weeks, those in the HKE group showed significantly superior improvements in function and reduced pain during stair negotiation. A previous study by Nakagowa et al found very similar results where one group focused on stretching the quadriceps, gastrocnemius, iliotibial band, and strengthening the quadriceps, whereas the experimental group program consisted of strengthening exercises for the transverse abdominal muscles, and the hip abductors/rotators. In this study, only the intervention group improved perceived pain symptoms during functional activities.

These studies show targeted hip strengthening as a viable option, but unfortunately, these early studies only provided outcomes between 4 and 6 weeks post-intervention. Khayambashi et al conducted a RCT looking at isolated hip abductor and external rotator strengthening 3 times per week for 8 weeks with a 6 month follow-up. At the conclusion of the study, the exercise group’s VAS Pain Scale decreased from 7.9 to 1.4 and maintained at 1.7 at the 6 month follow-up. This group’s WOMAC score showed similar improvements with a baseline rating of 54 and post intervention scores of 10.7 (8 week) and 10.8 (6 month). Both of these outcomes showed significantly superior results in comparison to both baseline and the control group. This study showed the utility of hip posterolateral musculature training in isolation from any other intervention. To build upon this study, Fukuda et al attempted to determine if adding hip strengthening exercises to a conventional knee exercise program produces better long-term outcomes than conventional knee exercises alone. Once again, the experimental group showed superior results in comparison to the traditional quadriceps strengthening program. The combined hip/knee strengthening program produced significant improvements in all outcome measures (LEPS, AKPS, Single-hop test, and NPRS ascending/descending stairs) at 3, 6, and 12 months post-treatment. In comparison, the traditional quadriceps program only showed decreases in pain at 3 and 6 months. The body of evidence supporting the targeted strengthening of the hip abductors and external rotators continues to grow with documented short and long-term functional and pain specific outcomes.

For further information regarding hip abductor (specifically gluteus medius) strength training, please read “Evidence-Based Strength Training: Gluteus Medius“.

squat-ass-to-grass

Quadriceps Musculature

As common sense would dictate, Lankhorst et al found quadriceps weakness to be a risk factor for developing PFPS. That being said, quadriceps strengthening with this patient population is an especially difficult task. As was discussed during my post on etiology, patellofemoral joint stress is of utmost importance during rehabilitation.

According to the research done by Steinkamp et al, patellofemoral joint stress increases with decreasing angles of knee flexion in the open kinetic chain (OKC). Whereas, stress increases with increasing levels of knee flexion in the closed kinetic chain (CKC). Based on this research, the most appropriate ranges for those with PFPS to exercise in are 0-45° in the CKC and 90-45° in the OKC. As chondral lesions and/or osteoarthritic changes are common within this population, you must be pay close attention where the joint contact area migrates during exercise. As knee flexion increases, the patella glides inferiorly on the femur, while contact on the patella gradually shifts from inferior to superior. This information aides us in exercise prescription, but it should not eliminate other ranges of motion during rehab. Pain is patient specific and can vary based on underlying pathology, experiences, and other biomechanical/neurophysiological factors. All exercises should be conducted within your individual patient’s tolerance and these ‘appropriate ranges’ should be used to help guide your prescription.

Slide1

Upon implementing a more functional approach to your rehabilitation program (which should be started as soon as possible), patellofemoral joint stress should continue to guide your program. Chinkulprasert et al conducted a controlled laboratory study trying to determine what exercises elicit the greatest patellofemoral joint stresses amongst the lateral step-up (LSU), forward step-up (FSU), and forward step-down (FSD). The FSD, FSU, and LSU were performed by 20 healthy subjects at the same step-height across exercises. Upon completion of the study, it was determined that during the FSD, significantly greater patellofemoral stresses and reaction forces were recorded than during either of the other two exercises. Early in rehabilitation, the FSD should be withheld in favor of the other less intense exercises. As patient tolerance increases, the FSD can be a viable option to improve eccentric quadriceps control during stair ascension. Slide1 Additionally, Dolak et al determined that prior to progressing to a functional strength program, those who completed a hip-specific strength program demonstrated increased pain reduction compared to those who completed a quadriceps-specific strength program. The hip-specific group’s VAS Pain Score decreased from 4.6 to 2.4, while the quadriceps-specific group only decreased from 4.2 to 4.1. In my opinion, this study shows the importance of controlling frontal and transverse plane movements prior to beginning an intensive functional strength program.

Notice how I left out the mystical VMO? Yep, me too.

It should be understood that PFPS is a multi-factorial condition and therefore warrants a multi-modal treatment strategy (NOT JUST STRENGTH TRAINING). I will continue to delve further into this topic as the year goes on, but in the meantime, I believe these two case reports will add some insight:

Mascal CL, et al. Management of patellofemoral pain targeting hip, pelvis, and trunk muscle function: 2 case reports. J Orthop Sports Phys Ther. 2003 Nov;33(11):647-60.

Lowry CD, et al. Management of patients with patellofemoral pain syndrome using a multimodal approach: a case series. J Orthop Sports Phys Ther. 2008 Nov;38(11):691-702.

Etiology of PFPS: A Biomechanical Perspective

So, my last post regarding patellofemoral pain syndrome (VMO? VM-No) stated its prevalence and its misdirected treatment. This next post will help to clear up some of the confusion amongst clinicians as to the cause of PFPS, which should in turn help to drive the most effective treatment strategies.

What causes PFPS? Now, this is a very loaded question. However, over the last couple decades, the etiology of this disorder has become a little more clear…

It all breaks down to a very simple formula: Patellofemoral Joint (PFJ) Reaction Force / PFJ Contact Area.

In general, as an individual goes into deeper ranges of knee flexion, their PFJ contact area increases. During OKC knee flexion the patella glides inferiorly to increase its contact with the femoral trochlea and during the CKC the femur rotates posteriorly causing increased contact with the patella. Due to this variation in loading, the PFJ experiences some of the highest stresses in the body especially during the lower ranges of knee flexion where the contact area is the smallest. In 2002, Heino et al attempted to show that individuals suffering from PFPS did demonstrate altered joint loading and subsequent joint stress. They compared the PFJ reaction force, joint stress, and utilized contact area during free and fast walking between subjects with PFPS and asymptomatic controls. They found that, on average, those with PFPS had increased joint stress, decreased utilized contact area, and decreased joint reaction forces. It was theorized that the decrease in joint reaction force may have been due to the patient’s unwillingness to forcefully load their effected limb. The increased joint stress and decreased contact area seem to implicate this improper loading as a probable cause of the anterior knee pain felt in these patients. This allows us to conclude that the general etiology of PFPS is decreased PFJ contact area and/or increased reaction force → increased chondral stress → increased subchondral bone stress → stimulation of pain receptors → Patellofemoral pain. This pain can be traced back to nociceptive afferent nerves located in the subchondral bone (Biedert et al). This theory of increased cartilage loading and subsequent degeneration was supported by Farrokhi et al in 2011 when they found that patella cartilage thickness was significantly decreased in comparison to asymptomatic controls. Additionally, they found that following an acute bout of exercise, those without PFPS exhibited decreased time to return to baseline cartilaginous thickness.

This is all well and good, but what causes this altered contact area?

This abnormal loading may be caused by non-modifiable morphological abnormalities. The first possible cause is patella alta (PA) which, according to Ward et al, increases the incidence of lateral displacement, lateral tilt, and decreased contact area. In regards to PFJ contact area, they found a statistically significant difference between subjects with PA and those with normal patella vertical displacement at all ranges tested (0°, 20°, 40°, and 60° of knee flexion). This does appear to make biomechanical sense due to the fact that the inferior pole of the patella is thought to make initial contact with the femoral trochlea at approximately 20° of knee flexion and if the patella is positioned more superiorly, initial contact will not occur until deeper ranges of knee flexion, thus decreasing overall PFJ contact area. Another non-modifiable factor is the lateral displacement and resulting decreased contact area caused by trochlear dysplasia. This bony morphological defect results in flattening of the lateral facet of the intercondylar groove, which is typically the most important local factor in controlling excessive lateral patella translation. This can result in not only abnormal loading, but also chronic patellar subluxation and/or dislocation. This flattening of the lateral intercondylar groove can result in up to a 55% decrease in medial patellar stability. Unfortunately, there is very little that we, as therapists, can do to correct these morphological abnormalities, however there are certain factors influencing abnormal patellar tracking that can be altered conservatively.

The static Q-angle has been implicated in patellofemoral pathology for countless years, but how does this correlate to alignment during functional activity? Massada et al found that dynamic Q-angle values were statistically significant in determining individuals who suffer from PFPS even in the absence of a increased static Q-angle. In this study, there was little correlation between static Q-angle and the presence of PFPS. This gives support to the use of this dynamic measure in lieu of its static counterpart. So what factors influence this dynamic Q-angle? This angle has both proximal influences at the hip (excessive adduction and femoral IR) and distal influences at the ankle/foot (excessive pronation and tibial IR). During weight bearing, the femur moves about a fixed patella and therefore excessive femoral IR results in increased contact directed primarily at the lateral facet of the patella (Powers et al). In fact, just 10° of IR can lead to a substantial decrease in PFJ contract area and a 50% increase in joint stress. The figure to the right demonstrates the lateral tilt of the patella during non-weight bearing (A) and the femoral IR resulting in altered contact area during weight bearing (B). Additionally, Souza et al found that females with PFPS demonstrated greater peak hip internal rotation compared to the control group during running, drop jump, and step down. The PFPS group also demonstrated 14% weaker hip abductor strength and 17% weaker hip extensor strength. Wilson et al, Noehren et al, and Nakagawa et al found that individuals presenting with PFPS demonstrated increased hip adduction during running, jumping, and single-leg squats. This adduction creates an increased valgus force about the knee joint, which in turn causes increased loading of the lateral PFJ. Distally, pronation at the subtalor joint can lead to IR of the tibia, which then once again creates an increase in valgus at the PFJ.

Last, but not least, quadriceps dominance (QD) has been shown to increase the incidence of PFPS due to the subsequent increased PFJ compression. When landing from a jump, a QD individual will have their knees in front of their toes, excessive dorsiflexion, heels off of the ground, and limited hip flexion. This posture puts significant stress on the quadriceps and PFJ while taking stress off of the back extensors and hip extensors. This compensation can be adopted by patients who demonstrate weak hip extensors relative to knee extensors. Compensating in this manner will, in time, lead to quadriceps overuse and increased knee loading, which will lead the patient down the previously mentioned cascade toward PFPS. Pollard et al helped to support this theory when they found that greater utilization of hip extensors during a drop jump activity was associated with decreased knee valgus angles and moments. They also found that individuals who landed in a QD position demonstrated increased knee valgus, increased knee adduction moments, and decreased energy absorption at the knee and hip. These individuals were unable to properly dissipate the high ground reaction forces and ultimately put unnecessary stress on the patellofemoral joint.

Now that we are beginning to better understand this pathology and its risk factors, we can begin to form more efficient and effective conservative treatment strategies. These treatments should be focused on decreasing laterally directed PFJ forces (locally, proximally, and distally), decreasing quadriceps dominance, and maximizing PFJ contact area. Each of these three treatment principles will be discussed in additional blog posts in the coming weeks.

Interested in learning more about PFPS in the meantime? Search for just about any article published by Christopher M. Powers, PhD, PT, FACSM, FAPTA and you should be in pretty good shape…

VMO? VM-No.

According to a retrospective case-control analysis by Taunton et al, of the 2,002 running-related injuries seen at a primary care sports injury facility, 42.1% (842/2,002) were knee injuries. Of these knee injuries, 39.3% (331/842) were due to patellofemoral pain syndrome (PFPS), which made PFPS far and away the most common disgnosis found in this large-scale study. Additionally, an older study done in 1984 showed similar results. Devereaux et al found that over a five year period, 137 patients presented with PFPS, which accounted for 25% of all knee injuries seen at this sports injury clinic. These two studies were conducted 17 years apart, giving support to the consistently high prevalence of this disorder, but the real question is, how are we treating these patients?

Based on a biomechanical study completed by Lieb et al in 1968, the vastus medialis obliquus (VMO) has been the mainstay of most physical therapy protocols for PFPS. This study helped to identify the fiber orientations of the quadriceps musculature and the functional significance of these orientations. It was found that the VMO’s fibers were oriented at 55° from the longitudinal axis of the femur which, based on orientation alone, makes it the primary restraint to lateral subluxation of the patella. Due to the discrepancy in mechanical advantages, it was postulated that the VMO was able to counterbalance the pull of the much larger vastus lateralis (VL). An insufficient balance between the VL and VMO has long been considered the primary contributing factor in developing patellar subluxation or maltracking. Additionally, Cowan et al found that subjects with PFPS have an imbalance in VL:VMO timing. They found that the VL typically begins to fire approximately 15-20 ms prior to the VMO. Due to this understanding of the biomechanics involved, the physical therapist’s treatment strategy typically involved correcting the potential VMO atrophy, hypoplasia, inhibition, and/or impaired motor control. Now, this all seems logical in theory, but can we actually selectively train the VMO? And does this relatively small muscle actually have the impact that we have all been led to believe?

Cerny et al evaluated the ability to preferentially recruit the VMO during 22 different quadriceps exercises. It was determined through electromyographic analysis that VMO activity was not higher in any exercise in relation to the VL. Song et al conducted a RCT that found the attempted isolation of this small segment of the quadriceps was not supported. They compared the change in VMO cross-sectional area (CSA) after 8 weeks of unilateral leg press and unilateral leg press with subsequent hip adduction. It was found that there was no significant difference between the change in VMO CSA between the two groups (the standard leg press actually yielded better results). Due to this fact, selective isolation of the vastus medialis obliquus in everyday clinical practice is highly unlikely. In all reality, based on the inability to selectively recruit their target, most of these ‘VMO programs’ are no more than a general quadriceps strengthening program. If it was actually possible to selectively recruit these fibers, according to Grabiner et al, it would take approximately 60% of maximal voluntary contraction to stimulate hypertrophy of the VMO. In 2010, Bennell et al investigated the efficacy of VMO retraining in relation to vasti onset compared to a general quadriceps strengthening program. The VMO retraining group used EMG biofeedback during isometric VMO contractions at 90° of knee flexion, standing mini squats to 40°, isometric contraction of the VMO in combination with hip abduction and hip external rotation during an isometric wall contraction in standing, and step downs (don’t get me started on step downs…). The quadriceps group performed isometric quad sets, straight-leg raises, SAQs, and side-lying hip abduction. At the conclusion of the training programs, the retraining group actually does create more significant changes in stair descent activation in the short-term, however at the 8-week follow-up both values are nearly identical. The initial improvement may have been due to the use of ‘step downs’ in the retraining group, which most closely simulates the functional and muscular demands of stair descent. During stair ascent, on the other hand, the quadriceps strengthening group caused a much more significant alteration in VMO:VL timing and was the only group that caused the VMO to fire prior to the VL. A study conducted by Laprade et al also showed similar results, but this time utilizing isometric exercise. This study looked at the EMG activity of individuals with PFPS compared to asymptomatic controls during 5 isometric exercises. There was no significant difference in the ratio of VMO:VL firing between the two groups. Given the results of these studies, I find it hard to support the use of VMO training during everyday clinical practice.

Lets say that, theoretically, it was possible to selectively recruit the fibers of the VMO… Would this result in sufficient reductions in patellofemoral contact stress to relieve the pain associated with this diagnosis? A study done by Sawatsky et al says no. This was a biomechanical study utilizing New Zealand white rabbits. While this is not a direct human study, the muscular alignment/pull of the quadriceps is very similar in that the fibers of the VMO are oriented at approximately 45-50° and the VL is oriented at approximately 14-19° with respect to the longitudinal axis of the femur. Measures of patellofemoral joint contact pressures were taken before and after transection of the VMO at varying levels of knee flexion (30°, 60°, and 90°). At the conclusion of the study, it was found that there was no significant difference between peak pressures, average pressures, contact areas, or contact shapes between pre and post transection. If contact area and pressure is not altered when the muscle is removed from the equation, then why do we continue thinking VMO training is the gold standard in PFPS treatment?

So… then what causes and what is effective in treating patellofemoral pain syndrome? Over the coming weeks, I will provide theories on underlying pathology/impairments and their subsequent treatment strategies… So stay tuned!