A leg cramp is maddening but repeated leg pain on exertion halts an athlete’s progress and performance. Such is the case with chronic exertional compartment syndrome (CECS), the topic of today’s feature article. Physiotherapist Chris Mallac highlights this frustrating syndrome, including the theories about why it happens in the first place. Although several theories of etiology... MORE
Vastus Medialis Obliquus: Part II
In part one of this series, Chris Mallac explained the anatomy and complex biomechanics of the VMO and its role in relation to the patellofemoral joint. In part 2, he argues that regardless of cause and effect of the VMO on patellofemoral pain, VMO dysfunction in the presence of pain is very real, and thus exercises to rehabilitate the function of this muscle are necessary.
By and large, the majority of the research suggests that VMO is an important patella stabiliser for the knee, as it moves during flexion and extension movements. However, many of these findings relate the role that VMO plays on the patella in a non weight-bearing situation, and the function of not only the patellofemoral joint, but also 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, valgus knee collapse, foot pronation postures as well as inherent tibial torsions, femoral anterversions and genu valgus postures. These all impact on the patellofemoral alignment and thus may possibly 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 knee1 (PFPS included), particularly atrophy of the VMO2. 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 (PFP) syndrome3.
The exact mechanisms that cause a morphological change in the muscle during atrophy is still a subject of debate. It may be either a decrease in muscle fibre diameter/area (atrophy) and/or a decrease in the numbers of muscle fibres (hypoplasia)4 5. Furthermore, it is unclear whether atrophy of the VMO precedes a patella injury or develops secondarily as a consequence of pain inhibition and physical inactivity following recurrent injuries6.
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 for certain is that in the presence of PFPS some manner of morphological change and alteration in activation in the VMO co-exists.
Finally, the exact cause of this morphological change is also debatable. The most common explanation is that the quadriceps atrophy is caused by reflex inhibition leading to loss of muscle contractility and thus muscle size over time1. This phenomenon is commonly referred to as ‘autogenic muscle inhibition’ or AMI2.
AMI is described as 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 still persist after the acute stage of the injury, leading to barriers in the rehabilitation process. It has been suggested that the cause of the AMI is altered afferent input from the joint mechanoreceptors that then modulates the outgoing efferent output from the spinal motor neurones to the muscle. This alpha motorneurone modulation (inhibition) results in an inability to fully activate the muscle3.
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 full weight bearing1 2. 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 small 3.38% difference in CSA of the quadriceps between affected and non-affected limbs in patients with chronic PFPS. Interestingly, the same researchers did find a more pronounced loss of peak extension torque on the affected side that was not correlated to CSA loss. It may be that PFPS leads to greater loss of strength in the quadriceps compared with loss of CSA.
Finally, some researchers believe that delayed activation of the VMO is possibly the more significant variable rather than gross muscle strength loss of the VMO3 4 5. Therefore, the muscle may look the same as the unaffected side (CSA), it may be as strong or close to the same strength, but it may activate in a different manner, or have delays in activation, in a similar way that transversus abdominus has been found to have a delayed activation in patients with low back pain6 7 (see activation ratios above).
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:
- Weight bearing vs. non weight bearing exercises.
- Hip rotation position – external vs. internal vs. neutral
- Knee joint angles of flexion
- Facilitation with electrical stimulation
- Biofeedback awareness
- Stable vs. unstable surfaces
- 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 exercise8. Indeed, all these approaches provided no additional benefit over quadriceps exercise alone. However, they did not elaborate 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 in fact be more selective in activation of the VMO.
What needs to be considered in the selection of exercises are the following points;
- Patellofemoral joint stress is minimised from 90 to 45 degrees of knee flexion during non-weight bearing exercises9.
- PF stress is minimised from 45 degrees to 0 degrees of knee flexion when the limb is weight-bearing10.
- EMG feedback can increase a client’s awareness of VMO to VL activation within 5 days of biofeedback facilitated training11.
- Resistance used in rehabilitation is also important. Leroux et al (1999) found when using electrical stimulation, the VMO contributed only 6.31% of the total torque produced during a maximum voluntary isometric knee extensor contraction12. It is therefore likely that VMO will not respond to high load resistive exercises.
- Hip rotation positions seems to have no beneficial effect on VMO:VL activation13 14.
- Strengthening work on the hip abductors and external rotators has a positive effect on patients with PFPS, without any specific exercises for VMO15.
- Squat exercises performed on unstable surfaces with high levels of instability can enhance the activity of the VMO, and that squatting exercises performed on foam surfaces with low levels of instability or hard surfaces are not as effective for the selective activation of the VMO16.
- Despite some landmark research many years ago demonstrating the interconnections between the VMO and adductor mass and the idea that hip adduction may preferentially activate the VMO17, the idea that hip adduction can preferentially activate the VMO has been refuted by many other studies18 19.
With these above points in mind, below are some examples of exercises that incorporate the following parameters to preferentially activate the VMO and/or assist in the relief of 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.
a. 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.
b. Place the other foot on a bench behind you. The focus is to hold as much of the weight as possible on the front foot.
c. The distance between the front foot and hip joint needs to be reasonably small as to closely approximate the running posture. For sports that need greater lunge type positions such as hockey, the front foot can be placed further out in front.
d. 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 that then requires the quadriceps to work harder to counteract. The band can be under slight tension when the knee is flexed and it will then stretch and create tension as the knee extends.
e. 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.
f. Bend/flex the knee so that the knee follows the third toe and minimise the knee flexion to a maximum of 45 degrees.
g. 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 purpose of the exercise is to stimulate the quadriceps so the knee needs to be allowed to come forward.
h. Perform three sets of 15 repetitions and light weight can be added as strength and control improves. This can be a barbell on the shoulders or holding two dumbbells in the hands.
i. To further increase the stability challenge, the arms can be held above the head to increase the height of the centre of mass of the body (with or without dumbbells overhead).
2. Baby squat
a. 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.
b. 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.
c. The other foot is placed on a bench so that the hip is in flexion, abduction and external rotation.
d. 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.
e. Keeping the spine vertical, slowly bend the knee to no more than 45 degrees. If the trunk is allowed to come forward and create too much hip flexion, force will shunt away from the quadriceps and onto the hip extensors.
f. Keep the kneecap tracking in line with the third toe.
g. Perform three sets of 15 repetitions slowly.
3. Wall slider squat
a. Using the same slant board and foam block as in the ‘baby squat’, stand on this, with the foot belonging to knee with the affected VMO.
b. The other leg is held up in hip flexion.
c. Place the opposite shoulder in contact with the wall.
d. Hold a light weight overhead on the stance leg side. The arm will be in vertical flexion.
e. Slowly bend the knee and allow the opposite shoulder to slide down the wall.
f. The bending knee again should follow the third toe.
g. The opposite hip can now start drop out of full flexion.
h. As the knee now extends straight during 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 swing phase of running.
i. The friction of the shoulder against the wall acts as a resistance.
j. Perform three sets of 15 repetitions slowly.
Injuries to the knee are a common occurrence in sports. Ligament injuries, patellofemoral pain syndromes and meniscal tears can all create autogenic muscle inhibition, and this can shut down the excitability of the quadriceps muscles – particularly the VMO. The VMO has for a long time been thought to be the main controller of the patellar alignment in the trochlear groove and thus weakness in this muscle has been thought to be 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. It may be that 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 fully rehabilitate the PFPS affected athlete.
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