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 counterbalance 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 mal-tracking.
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 the inability to selectively recruit their target, most of the ‘VMO programs’ are merely strengthening the quadriceps 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
- 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?