This becomes a focus of several interventions in the patient's care plan. The goal of VMO isolation is to improve the tracking of the patella and medial "pull" of the quads. This would, theoretically, affect patellofemoral strain. Due to the controversial state of this case, we thought we would do a review on the isolation of the vastus medialis muscle. Let's start out with reviewing a little anatomy. The quadriceps is made up of four parts: rectus femoris, vastus lateralis, vastus medialis, and vastus intermedius
Quadricep Muscles Origin, Insertion, Innervation
-Tibial tubersoity (patella acts as sesamoid bone, but some call patella the insertion and then the attachment of patella to tibial tuberosity is known as the patellar ligament)
Can You Isolate Part of a Muscle?
One way of analyzing this controversial issue is anatomically. Hubbard et al reviewed the anatomy of cadavers to enhance the interpretation of VMO isolation. The vastus medialis is commonly broken down into two components: vastus medialis longus (VML) and vastus medialis oblique (VMO). It is thought that the VMO is responsible for medial patellar tracking, due to its oblique fiber orientation. In the study, the VMO was unable to be found separated from the VML, meaning the VMO was not found to be a muscle independently. Any attempted separation required destruction of muscle fibers. Upon review of innervation, many studies in the past have come across independent innervation, leading to the hypothesis that the VMO was a separate muscle. However, these nerves have been found to be superficial separations from the femoral nerve leading to distal motor units, sensory contribution from the saphenous nerve, or penetrating innervation for the knee capsule. The authors argue that without isolated innervation, the VMO cannot be activated independently (the patella cannot solely be pulled medially); it is the activity of the femoral nerve the stimulates the entire vastus medialis to contract and extend the knee while pulling the patella medially.
Historically, many people were under the impression that the rectus femoris was the prime knee extensor. They thought the vastus medialis was responsible for the final 15 degrees of knee extension due to the inadequacies of the rectus femoris (Lieb & Perry, 1968). Boucher et al looked at the vastus medialis activity in patients with patellofemoral pain syndrome. They found that the vastus medialis and vastus lateralis were not more active in terminal extension. However, they did find that in patients with PFPS, there was a decreased VM:VL ratio compared to the control group. These differences were found to be attributable to a mechanical disadvantage (greater Q-angle); when the Q-angle was decreased, the ratio returned to normal. This same difference in VM and VL ratio was found in another study to be related to mechanical factors as well (Souza & Gross, 2001). Additionally, the authors discovered that isotonic quadriceps contractions elicited larger VM:VL EMG activity compared to isometric contractions. This may influence the treatment plan for patients with pathologies, such as patellofemoral pain syndrome. Ng et al. and Cowan et al. also came across this difference in VM and VL ratio with EMG activity. In fact, the authors were able to normalize the EMG activity with use of therapeutic exercise + biofeedback. Biofeedback has been found to be a useful component in motor retraining, especially regarding earlier activation of the VMO (Cowan et al., 2002). A delay of as little as 5 ms of the VMO relative to the VL can increase the compression forces on the lateral patellafemoral joint (Boling et al, 2006). Powers described a difference between VM and VL activity as well; however, it was attributed to patellar malalignment. Decreased VM activity was not found to be the cause of abnormal patellar tracking or patellar tilt.
Some convincing evidence has been found that the vastus medialis cannot be isolated. One study discussed the fact that the decrease in knee extensor strength in the last 15 degrees is due to a loss in mechanical advantage (Lieb & Perry, 1968). Following surgery, many practitioners have noted increased atrophy at the vastus medialis. This decreased prominence has been found to be associated with the obliquity of fibers, lowness of insertion, and thinness of fascial covering compared to the rest of the quadriceps. The "atrophy" noted in the vastus medialis is actually representative of general quadriceps weakness. On the other hand, the vastus medialis was shown to have a selective role in patellar tracking. Another proposed component to PFPS is a difference in onset between the VM and VL. Gilleard et al and Powers et al were unable to reproduce any difference in timing of activation, cessation, or intensity between the VM and VL, while Smith et al. was able to show that the differences that were found in VM and VL activity were due to the effect pain has on EMG activity (this was noted in individuals with PFPS). One of the focal points of the study was to see the effect taping had on VMO activation. With taping, vastus medialis activation was shown to occur prior to vastus lateralis activation. The authors were unsure if the cause was through mechanical means or pain reduction.
A systematic review we looked at included 20 different studies. The authors concluded that the VMO cannot be preferentially activated and strengthened (Smith et al., 2009). Only 3 of the studies were able to display any preferential VMO activation. Each of the 3 were in different knee angles, however, and had several methodological issues, such as poor electrode placement, noise from other muscle activity, and more. Other studies, not included in the systematic review, have been prone to methodological inconsistencies when compared to each other as well. One such method involves measuring EMG activity between OKC and CKC. A lack of evidence has been shown in both OKC and CKC for delayed onset and decreased amplitude of the VM for individuals with PFPS (Stensdotter, 2007).
As it has probably become obvious, VMO isolation is a controversial issue with many conflicting studies. Thein Brody & Hall do an excellent job summarizing the research, while offering their own opinion. Regarding measuring EMG amplitude, they point out that EMG measures electrical activity, not force production. To truly assess the effects the VMO has on the patella, one must consider fiber orientation, and cross-sectional area. The authors then return back to an anatomical discussion, stating an isolated VMO contraction has never been displayed. This suggests training the VMO independently to improve timing may not be possible. In fact, VMO:VL timing has been shown to improve after training the quadriceps muscle as a whole.
In our opinion, the research shows pretty heavily that it is not possible to isolate the VMO. That being said, exercises that have a focus of "VMO isolation" may still serve a purpose, whether through focusing on improving end-range mobility into extension or general quad strengthening, both often are common goals in rehab. The only concern may lie in possibly training into a dysfunctional motion (some may try to improve VMO activity by working hip adduction - this may reinforce the impairment of femoral adduction/IR). Our advice, overall, is to focus on your impairments and movement pattern. Often, those with knee pain improve with quad and glute strengthening, but be sure to assess each case.
So what are your thoughts and what have your experiences been on this issue? Should we be spending so much time trying to isolate the VMO for rehabilitation or focus on a more general method? Let us know!
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