Vastus Medialis Obliquus: Part II

Most of the research suggests that VMO is an important patella stabilizer for the knee, as it moves during flexion and extension movements. However, many of these findings relate to the role that VMO plays on the patella in a non-weight-bearing situation, and the function of the patellofemoral joint and the VMO may change as we assume a weight-bearing position.

In weight-bearing, the limb is subject to so many more kinetic variables such as pelvic position, hip joint flexion/ adduction, hip rotation postures, dynamic knee valgus, foot pronation postures, as well as inherent tibial torsions, femoral anteversions, and genu valgus postures. These all impact the patellofemoral alignment and thus may play a bigger role in patella dysfunction rather than VMO dysfunction.

VMO dysfunction in the presence of knee pain

Atrophy of the quadriceps is a common observable clinical feature following injury to the knee (PFPS included), particularly atrophy of the VMO^(1,2). Atrophy of the VMO, imbalance of the VMO/vastus lateralis (VL) strength, and altered neuromuscular timing of the different parts of the quadriceps muscle have all been described in patellofemoral pain syndrome⁽³⁾.

The exact mechanisms that cause a morphological change in the muscle during atrophy are still debatable. It may be either a decrease in muscle fiber diameter/area (atrophy) or a decline in the number of muscle fibers (hypoplasia)^(4,5). Furthermore, it is unclear whether atrophy of the VMO precedes a patella injury or develops secondarily due to pain inhibition and physical inactivity following recurrent injuries⁽⁶⁾.

Clinically, what is observed is that the PFPS patient presents with a painful knee, usually some swelling and observable atrophy of the VMO or inability to activate the VMO. However, this is not to suggest conclusively that the lack of VMO has caused the PFPS. All that can be said is that in the presence of PFPS, some manner of morphological change and alteration in activation in the VMO co-exist.

Finally, the exact cause of this morphological change is also debatable. The most common explanation is that quadriceps atrophy is caused by reflex inhibition, leading to loss of muscle contractility and, thus, muscle size over time⁽¹⁾. This phenomenon is called‘arthrogenic muscle inhibition (AMI)⁽⁷⁾.

Arthogenic Muscle Inhibition

Arthrogenic muscle inhibition (AMI) is a reflexive ‘shut down’ of the musculature surrounding a joint. It is initially designed to protect an injured joint; however, the inability to fully activate the muscles may persist after the acute stage, leading to barriers in the rehabilitation process. It has been suggested that the cause of AMI is altered afferent input from the joint mechanoreceptors that then modulate the outgoing efferent output from the spinal motor neurons to the muscle. This alpha motor neuron modulation (inhibition) results in an inability to activate the muscle fully⁽⁸⁾.

Cross-sectional area (CSA)

Very few studies have measured the actual CSA of the quadriceps under imaging. However, it has been found that after traumatic injury resulting in an inability to weight bear, quadriceps atrophy is more pronounced than in sufferers of more chronic knee pain who have been fully weight-bearing^(1,9). This suggests that even modified weight bearing has some benefits in maintaining muscle mass.

However, the actual effect of knee pain on quadriceps atrophy and CSA may not be as significant as once thought. Callaghan and Oldham (2004) found only a tiny 3.38% difference in CSA of the quadriceps between affected and non-affected limbs in patients with chronic PFPS. Interestingly, the same researchers saw a more pronounced loss of peak extension torque on the affected side that was not correlated to CSA loss. PFPS leads to a more significant loss of strength in the quadriceps than CSA loss.

Finally, some researchers believe that delayed activation of the VMO is the more significant variable than gross muscle strength loss of the VMO^(10-12). Therefore, the muscle may look the same as the unaffected side (CSA) and may be as strong or close to the same strength. Still, it may activate differently or have delays in activation in a similar way that transverses abdominus has been found to have a delayed activation in patients with low back pain (see activation ratios above)⁽¹³⁾.

Retraining VMO function

The selection of effective exercises to strengthen and activate the VMO has also received widespread attention in the form of research into the ‘best’ exercises and positions to produce VMO firing. The variables that can be considered and manipulated, and which have been the subject of greatest research are:

1. Weight-bearing vs. non-weight-bearing exercises.
2. Hip rotation position – external vs. internal vs. neutral
3. Knee joint angles of flexion
4. Facilitation with electrical stimulation
5. Biofeedback awareness
6. Stable vs. unstable surfaces
7. Concurrent adductor contraction with quadriceps activation

However, in a systematic review of the literature on exercise therapy in the conservative management of PFPS, Bolga and Boling (2011) found no difference in pain response and exercise therapy if it incorporated quadriceps electrical stimulation, biofeedback, or simultaneous hip adductor activation with exercise⁽¹⁴⁾. Indeed, none of these approaches provided any additional benefit over quadriceps exercise alone. However, they did not elaborate on whether or not the interventions shown in these studies demonstrated greater VMO activation compared with a control exercise. Although the interventions may not change the response and improvements in pain, they may be more selective in activating the VMO.

What needs to be considered in the selection of exercises are the following points;

1. Patellofemoral joint stress is minimized from 90-45 degrees of knee flexion during non-weight-bearing exercises⁽¹⁵⁾.
2. PF stress is minimized from 45 to 0 degrees of knee flexion when the limb is weight-bearing⁽¹⁵⁾.
3. EMG feedback can increase a client’s awareness of VMO to VL activation within five days of biofeedback-facilitated training⁽¹⁶⁾.
4. Resistance used in rehabilitation is also essential. Leroux et al. (1999) found that when using electrical stimulation, the VMO contributed only 6.31% of the total torque produced during a maximum voluntary isometric knee extensor contraction⁽¹⁷⁾. Therefore, VMO will likely not respond to high-load resistive exercises.
5. Hip rotation positions seem to have no beneficial effect on VMO:VL activation(^16,17).
6. Strengthening work on the hip abductors and external rotators positively affects patients with PFPS without any specific exercises for VMO⁽¹⁸⁾.
7. Squat exercises performed on unstable surfaces with high levels of instability can enhance the activity of the VMO, and squatting exercises performed on foam surfaces with low levels of instability or hard surfaces are not as effective for the selective activation of the VMO⁽¹⁹⁾.
8. Despite some landmark research many years ago demonstrating the interconnections between the VMO and adductor mass, the notion that hip adduction can preferentially activate the VMO has been refuted by many other studies^(20-22).

VMO exercises

With these points in mind, below are some exercises that incorporate the following parameters to preferentially activate the VMO and assist in relieving PFPS. The key features of these exercises are small ranges of movement in safe positions for the PF joint, unstable surfaces, high repetition and low load, external force to incorporate the hip external rotators and hip abductors, and EMG feedback used if available.

Split squat

1. 1. Stand on an unstable surface, such as a BOSU ball or two foam pads. The lead foot on the unstable surface belongs to the VMO you wish to retrain.
   2. Place the other foot on a bench behind you. The focus is to hold as much weight as possible on the front foot.
   3. The distance between the front foot and hip joint must be reasonably small to closely approximate the running posture. For sports requiring greater lunge-type positions, such as hockey, the front foot can be placed further out in front.
   4. Place a theraband or powerband around the knee so that the direction of pull is from the front. This induces a flexion moment on the knee, requiring the quadriceps to work harder to counteract. The band can be under slight tension when the knee is flexed, stretching and creating tension as the knee extends.

An inside band provides a medially directed force

5. Place another band around the upper shin (below the patella) so that the direction of pull attempts to pull the knee inwards, thus creating hip adduction/internal rotation. This will then activate the hip abductors and external rotators to counteract this force.

6. Bend/flex the knee so that the knee follows the third toe and minimize the knee flexion to a maximum of 45 degrees.

7. The direction of knee flexion should be so that the patella is pushed forward towards the toes and the tibia creates a positive angle. If the tibia is kept upright, then this directs force away from the quadriceps and towards the hip extensors. The exercise aims to stimulate the quadriceps, so the knee must be allowed forward.

The front band provides an additional knee flexion force

8. Perform three sets of 15 repetitions, and lightweight can be added as strength and control improves. This can be a barbell on the shoulders or holding two dumbbells in the hands.
9. To further increase the stability challenge, the arms can be held above the head to raise the height of the body’s center of mass (with or without dumbbells overhead).

Additional balance challenge with arms above head

Baby squat

1. Place a slant board on a foam mat. Stand on this slant board with the foot that belongs to the VMO you wish to retrain.
2. The purpose of the slant board is that it encourages the knees to come forward during knee flexion, thus working the quadriceps over the hip extensors, and the slight plantarflexed position takes away passive tension of the soleus during dorsiflexion that can ‘steal’ force away from the quadriceps.
   
   

Start position: Notice the band attempts to pull the knee in a medial direction

3. The other foot is placed on a bench so that the hip is in flexion, abduction, and external rotation.
4. Place a band around the working knee and then stand on the band with the foot on the bench. Wrap the band over the thigh and hold onto it. This band creates an adduction and internal rotation force on the hip, requiring the hip abductors and external rotators to work harder.

Finish position: Notice the small range of knee flexion to minimize the patellofemoral joint compression

5. Keeping the spine vertical, slowly bend the knee to no more than 45 degrees. If the trunk can come forward and create too much hip flexion, the force will shunt away from the quadriceps and onto the hip extensors.
6. Keep the kneecap tracking in line with the third toe.
7. Perform three sets of 15 repetitions slowly.

Finish position: Notice vertical trunk posture to ensure the movement becomes quad loading.

Wall slider squat

1. Using the same slant board and foam block as in the ‘baby squat,’ stand on this, with the foot belonging to the knee with the affected VMO.
2. The other leg is held up in hip flexion.
3. Place the opposite shoulder in contact with the wall.
4. Hold a lightweight overhead on the stance leg side. The arm will be in vertical flexion.
5. Slowly bend the knee and allow the opposite shoulder to slide down the wall.
6.The bent knee should again follow the third toe.

Start position

7. The opposite hip can now start to drop out of complete flexion.
8. As the knee extends straight during the ascent of the body, the opposite shoulder will slide up the wall. Drive the opposite hip back into full flexion. This will mimic the running action of the opposite leg during the swing phase of running.
9. The friction of the shoulder against the wall acts as a resistance.
10. Perform three sets of 15 repetitions slowly.

Finish position

Summary

Injuries to the knee are a common occurrence in sports. Ligament injuries, patellofemoral pain syndromes, and meniscal tears can all create arthrogenic muscle inhibition, which can shut down the excitability of the quadriceps muscles – particularly the VMO. For a long time, the VMO has been thought to be the central controller of the patellar alignment in the trochlear groove, and thus, weakness in this muscle has been considered the causative factor in PFPS.

However, the majority of scientific opinion is still divided as to the exact role that the VMO plays in creating PFPS. VMO dysfunction is the consequence of PFPS, and other biomechanical and load variables can be implicated in the creation of PFPS.

Irrespective of the cause and effect of VMO dysfunction and PFPS, it is clinically observed (and the literature supports the notion) that VMO dysfunction and PFPS are related. Therefore, strength and control exercises for the VMO will be needed to rehabilitate the PFPS-affected athlete.