Lateral patellar tracking has been proposed as a contributing factor to chronic anterior knee pain (13), a common condition particularly in active populations (37,18). Coordination of the activity of the medial (vastus medialis obliquus, VMO) and lateral (vastus lateralis, VL) components of the quadriceps femoris muscle influences patellar tracking (16). While still contentious, there is evidence of disrupted vasti motor control in individuals with anterior knee pain with delayed onset of VMO EMG activity compared with VL, whereas normally, the two onsets occur either simultaneously or with VMO onset earlier (4). Such motor control changes may be important in the initiation (35) and perpetuation of anterior knee pain because they can increase lateral patellofemoral joint loading (27). Therefore, physiotherapy treatment for anterior knee pain often aims to restore normal vasti motor control with specific retraining for VMO advocated (9,25). This retraining approach uses the principles of specificity of training, practice, and feedback. Surface EMG biofeedback is often incorporated to provide augmented feedback of the activity of VMO relative to VL during exercise progression.
We have shown that deficits in VMO timing during stair stepping in people with anterior knee pain can be reversed by a 6-wk multimodal physiotherapy program that included motor control retraining (MCR) for VMO (5). However, the changes in muscle timing may have resulted from the other physiotherapy modalities such as knee taping (7) or from the pain reduction with treatment, independent of the techniques used. A small, uncontrolled study also showed that a 6-wk rehabilitation program comprising stretching, balance, and weight-bearing strengthening exercises of the quadriceps and hip abductor muscles improved timing of VMO (2).
It is unclear whether MCR is needed to alter vasti activation or whether a generalized quadriceps strengthening (QS) program could achieve similar outcomes. QS exercises such as isometric contraction, non-weight-bearing knee extension, and straight-leg raises are still widely used to treat anterior knee pain (10,23,36). This is because quadriceps strength is reduced in people with anterior knee pain (17,28), and cadaveric studies describe lower patellofemoral joint contact forces and pressures in inner range (17). A recent randomized controlled trial comparing general QS with VMO retraining found that both exercise programs improved pain and function to a similar extent (32). However, whether both exercise programs similarly address impairments in vasti motor control has not been evaluated.
Thus, we intended to compare the effects of a VMO MCR program with a QS program on vasti onset timing. To eliminate confounding effects of simultaneous pain reduction with treatment, we will use individuals who have previously experienced anterior knee pain but are currently pain-free. Furthermore, the cohort will be limited to those with a delay in the onset of VMO relative to those with a delay in the onset of VL because our aim was to evaluate the restoration of normal motor control. Given the tenets underlying MCR and evidence showing that such training can lead to greater improvements in aspects of motor control than strengthening exercise (22), we hypothesize that an MCR program will induce greater improvements in EMG onset timing of VMO compared with a general QS program and that improvements will be maintained in the short term after cessation of training.
Participants were a community sample recruited from the university and from the metropolitan region via print media advertisements, posted flyers, web site notices, electronic newsletters, pay slips, and e-mails to sporting clubs, libraries, and pharmacies. The institutional human research ethics committee approved the study, and all participants provided written informed consent. One subject was younger than 18 yr, and in this case, written informed consent was obtained from a parent.
The inclusion criteria were as follows: (i) aged between 16 and 40 yr, with the upper limit to reduce likelihood of patellofemoral joint osteoarthritis; (ii) self-reported history of anterior knee pain of insidious onset and with at least one episode of pain in the past 12 months aggravated by at least two of the following: prolonged sitting, stairs, squat, running, kneeling, and hopping/jumping; (iii) currently asymptomatic for at least 8 wk; and (iv) delay in the onset of VMO EMG relative to that of VL of greater than 10 ms during either the ascent or descent of a stair stepping task (see measurement section) (6). The exclusion criteria were as follows: (i) history of knee surgery or other knee injury in previous 12 months, (ii) physiotherapy treatment for knee pain in previous 12 months, (iii) history of patellar dislocation/subluxation, (iv) clinical evidence of other knee pathological diagnosis or spinal referred pain, (v) lower limb pathology affecting ability to complete the testing or exercise protocol, and (vi) current use of nonsteroidal anti-inflammatory or corticosteroid drugs.
This single-blind randomized controlled trial comprised a 6-wk intervention with an 8-wk follow-up (Fig. 1). Participants were assessed immediately before treatment (baseline), after treatment (final), and then 8 wk after reassessment (follow-up) by a blinded assessor who was an experienced musculoskeletal physiotherapist (M.D.) skilled in the measurement procedures.
After baseline assessment, participants were randomly assigned to the MCR program or the QS program. Simple randomization was used through a computer-generated table of random numbers. An independent researcher kept the assignment scheme concealed in opaque envelopes in a locked cupboard. Allocation was revealed to the treating physiotherapist by telephone at the time the participant presented for treatment.
Six musculoskeletal physiotherapists located across the metropolitan region implemented both standardized interventions. It was not possible to blind the therapists. The therapists underwent training and were provided with a treatment manual. Treatments were individual sessions lasting 45-60 min. Two sessions occurred during the first week the following four sessions spread for 5 wk (a single weekly visit omitted at week 5). A standardized home exercise sheet with diagrams and written instructions was provided to each participant as well as ankle weights for those in the QS group. Compliance with the home exercises was monitored by asking participants to complete a daily logbook that was checked by the physiotherapist. During the follow-up period, participants were asked to cease the specific exercise program.
The MCR program was based on that devised by McConnell and used in our previous trial of anterior knee pain (9). The program incorporated four exercises including three performed in weight-bearing positions (Table 1). As the emphasis was on activating the VMO, therapists provided participants with an explanation of the vasti relationships and the concepts behind the training program including the need for participants to concentrate on activating the VMO muscle during each exercise. To assist with this, dual-channel surface EMG biofeedback units (Pathway MR-20 (The Prometheus Group, Dover, NH) or NeuroTrac ETS) were used with the electrodes placed over VL and VMO. These biofeedback units provide a visual display of the amount of VMO and VL muscle activity. The visual display can be set as either two bars side-by-side representing the absolute activity of VMO and VL or as one bar representing the ratio of VMO to VL activity. The choice of visual display was at the discretion of the therapist depending on the participant's preference. The participants used the biofeedback unit to ensure that they were attaining a VMO contraction and with the specific aim of achieving greater VMO than VL activation during the exercises. Biofeedback units were used during the physiotherapy treatment sessions but were not provided for the home exercises. The therapist also provided feedback about the alignment of the entire lower limb and trunk during the performance of the weight-bearing exercises to ensure correct alignment with the knees positioned over the feet, the pelvis level, and the trunk upright. The therapist determined the dosage for each exercise with an emphasis on the quality of the contraction and movement and not the quantity. Exercises 1, 2, and 4 were conducted for up to three sets of 10 repetitions, whereas up to three sets of 4 repetitions were conducted for each leg for exercise 3 (Table 1). The exercises were performed twice daily.
Generalized QS program.
The QS program was based on exercises used in clinical practice for anterior knee pain (36) (Table 1). It comprised three quadriceps exercises all performed in non-weight-bearing, nonfunctional positions. In addition, an exercise to strengthen the hip abductor muscles was included in non-weight-bearing to control for the standing isometric hip abduction exercise performed as part of the MCR program. The aim of the QS program was to gain increases in strength using the overload principle. Before the program commenced, a 10-repetition maximum (10RM) was determined for each exercise. Resistance was commenced at 60% of 10RM in the first week and was then progressively increased by the therapist using ankle weights to maintain 10RM. Each exercise was performed for three sets of 10 repetitions with a 6-s isometric hold (Table 1). Given the emphasis on strengthening, the exercises were performed once daily in contrast to the more frequent dosage of the MCR program.
Onset of VMO and VL EMG activity.
EMG activity of VMO and VL was recorded using Ag/AgCl surface electrodes (Graphics Control Corporation, c/o Medical Equipment Services Pty, Ltd., Richmond, Australia) placed over the muscle bellies of VMO and VL with an interelectrode distance of 22 mm. The electrode for VMO was placed over the muscle belly approximately 4 cm superior and 3 cm medial to the superomedial patella border and was oriented 55° to vertical. The electrode for VL was placed 10 cm superior and 6-8 cm lateral to the superior border of the patella and was oriented 15° to vertical (1,14). The ground electrode was placed over the tibial tubercle.
Participants ascended and descended stairs at a rate of 96 steps per minute paced by a metronome. The stairs comprised a 60-cm platform with two steps of 20-cm height on both sides (6,8,14). After at least five practice trials, recordings of EMG activity of VMO and VL were made for five consecutive trials during the stance phase on the first stair during ascent (concentric contraction) and descent (eccentric contraction).
EMG data were preamplified (10×) distal to the surface electrodes, band-pass-filtered between 20 and 500 Hz, sampled at 1000 Hz, and 12-bit A-D converted (Associative Measurement Pty, Ltd., North Ryde, NSW, Australia). EMG data were full-wave-rectified and low-pass-filtered at 50 Hz (sixth-order Butterworth filter). A computer algorithm was used to identify the onset of EMG activity of each muscle. It identified the point at which the EMG signal deviated by more than 3 SD, for a minimum of 25 ms, above the baseline level (averaged for 200 ms before the commencement of the trial) (19). The rectified unfiltered EMG data were visually checked by a blinded assessor to verify the EMG onsets identified by the computer. The EMG sampling rate allowed a resolution of 1 ms.
EMG onsets were identified from individual trials and averaged during the five repetitions. The relative difference in the time of EMG onset of VMO and VL was quantified during stair ascent and stair descent by subtracting the onset of VMO EMG from that of VL. Our reliability for this protocol is excellent (ICC = 0.91 and 0.96 for stair ascent and descent, respectively) (6).
Quadriceps strength was measured using a KinCom dynamometer (Chattecx Corp., Chattanooga, TN). Participants were in a sitting position and were secured using stabilization straps. Concentric and eccentric quadriceps activity through the range of 0°-90° of knee flexion was assessed at 60°·s−1. Participants performed three maximal contractions with a rest interval of ∼60 s between each. Isometric quadriceps strength was then assessed at 60° knee flexion in a sitting position. The test consisted of three maximal 5-s contractions with a 60-s rest interval. The highest peak torque of the three trials, normalized to body weight, was used.
The primary outcome measure was the difference in onset timing of VMO and VL and sample size calculations were based on our previous research (5). Here, physiotherapy treatment induced a mean ± SD change of 27 ± 26 ms, whereas there was no change with a placebo treatment. Although the effect of a QS program on VMO-VL onset timing is unknown, a sample size of 60 patients (30 per group) had 80% power (α level, P < 0.05) to detect a difference in VMO and VL EMG onset timing difference of at least 17 ms between the two treatment groups if the SD is ≤26 ms. An onset timing difference of this magnitude was chosen to exceed the SEM of our test procedure (6). Although a clinically relevant difference in VMO-VL onset timing is not known, a biomechanical modeling study showed that a difference of as little as 5 ms is associated with an increase in patellofemoral stress (27).
Statistical analyses were performed using SPSS on an intention-to-treat basis and a conservative method for replacing missing values. For each participant, the change in VMO-VL timing scores was calculated by subtracting the final and follow-up values from that of the baseline. For missing values in the QS participant who dropped out, the mean values of the MCR group were used. Data were first examined to ensure that they were normally distributed. Mean change scores within groups, difference in change scores between groups, together with 95% confidence intervals, were calculated. Paired t-tests were used to evaluate the change after treatment in each group, whereas independent t-tests were used to compare the amount of change between the two groups. Relationships between baseline EMG onset difference and change after treatment was examined within each group using Pearson r correlation coefficients. A significance level of P < 0.05 was set.
Between May 2002 and December 2004, 346 volunteers were screened by telephone. Of these, 104 underwent physical screening, 91 were eligible for assessment of their vasti EMG onset and of these, 28 did not have a VMO timing delay ≥ 10 ms in either stair ascent or descent. Sixty participants were enrolled into the trial (Fig. 1). Groups were comparable at baseline for demographic features except height; the MCR group was significantly taller (Table 2). There was no baseline difference between groups for EMG and strength measures (Table 3). The 6-wk program was completed by 59 participants (28 QS and 31 MCR) with 1 (4%) dropped out from the QS group. Compliance with the home exercise sessions was similar between groups with the mean ± SD percentage of sessions completed being 71% ± 17% in the MCR group and 78% ± 20% in the QS group (P > 0.05). Follow-up was completed by 57 (95%) participants (28 QS and 29 MCR).
Change immediately after intervention.
During stair ascent, there was a significant change in VMO-VL onset timing after treatment in the MCR group (P = 0.04) with a reduced delay in VMO EMG onset relative to that of VL. There was no significant change in VMO-VL EMG onset timing in the QS group (P > 0.05). However, there was no difference between groups in the amount of change in VMO-VL EMG onset timing (P > 0.05; Table 3 and Fig. 2A), and this result was not altered when the baseline EMG value was included as a covariate in the analysis (P = 0.99).
During stair descent, there was a significant change in VMO-VL EMG onset timing in both groups after treatment (MCR, P < 0.0001; QS, P = 0.003) with earlier onset of VMO EMG relative to that of VL. The MCR group demonstrated a greater change in timing than the QS group (P = 0.02). After treatment, the EMG onset of VMO was approximately 9 ms earlier than that of VL in the MCR group, whereas VMO EMG onset occurred at approximately the same time as that of VL in the QS group (Table 3 and Fig. 2B). This difference in change in onset timing between groups was even greater when the baseline EMG value was included as a covariate in the analysis (P = 0.003).
After training, the QS group had a 20% increase in eccentric quadriceps strength (P < 0.0001), a 12% increase in concentric strength (P = 0.005), and a 14% increase in isometric strength (P < 0.0001). In contrast, there was no increase in strength for the MCR group with changes of 3% (P = 0.48), 4% (P = 0.41), and 6% (P = 0.059), respectively. The change in eccentric strength was significantly greater in the QS group compared with the MCR group (P = 0.004) with no difference between groups for changes in concentric strength (P = 0.18) or isometric strength (P = 0.06; Table 3).
Relationship between baseline VMO-VL onset timing difference and changes with treatment.
There was a significant relationship between the baseline EMG onset timing difference and change in EMG onset timing difference in both the MCR group (r = −0.67 stair ascent and r = −0.58 stair descent, both P < 0.001) and the QS group (r = −0.70 stair ascent and r = −0.60 stair descent, both P < 0.001). This indicates that the greater the initial deficit in VMO EMG onset, the greater the change after treatment.
Change at follow-up.
During stair ascent, there was a significant improvement in VMO-VL EMG onset timing compared with baseline in both the MCR (P = 0.007) and the QS (P = 0.004) groups. There was no difference in the amount of change from baseline comparing the MCR and QS groups (P = 0.85; Table 3 and Fig. 2A), and this result was not altered when the baseline EMG value was included as a covariate in the analysis (P = 0.38).
During stair descent, there was a significant difference in VMO-VL timing compared with baseline in both the MCR (P = 0.001) and the QS (P < 0.001) groups. There was no difference in the amount of change from baseline comparing groups (P = 0.81; Table 3 and Fig. 2B), and this result was not altered when the baseline EMG value was included as a covariate in the analysis (P = 0.76).
At follow-up, the QS group had a 16% increase in eccentric strength (P = 0.002), a 15% increase in concentric strength (P = 0.007), and a 14% increase in isometric strength (P < 0.0001) compared with baseline. This compared with a 5% (P = 0.18), 12% (P = 0.002), and 11% (P = 0.003) increase in the MCR group for the strength measures, respectively. There was no difference between groups for the change in strength measures compared with baseline (eccentric, P = 0.14; concentric, P = 0.99; isometric, P = 0.76; Table 3).
Because impairments in vasti motor control may play a role in anterior knee pain, this study compared whether two different exercise programs that are commonly used in clinical practice and which have both been shown to reduce pain, can alter these impairments. The MCR program used exercises with a focus on activation of the VMO during weight-bearing eccentric activities and incorporated EMG biofeedback. Quadriceps strength gains were not a target of the intervention. The QS program used non-weight-bearing exercises designed to elicit quadriceps strength increases without specific attention to coordination of the vasti muscles. Improvements immediately after the interventions were generally related to the target of the interventions; that is, improvements in motor control, albeit only during stair descent, in the MCR group and improvements in strength in the QS group. In contrast, at follow-up, 8 wk after cessation of formal training, both groups had improved relative timing of VMO EMG activity in both stair ascent and descent and quadriceps strength gains by amounts that did not differ between training groups.
Immediate changes in motor control and in strength were relatively specific to the intervention group.
Although it is clear that strength should increase after the strength training protocol, the mechanism for the greater changes in motor control during stair descent after the MCR intervention requires consideration. We did not include a control group who received no treatment or who received placebo treatment. However, our previous research using the same EMG testing protocol showed that VMO onset timing did not change during 6 wk of a placebo treatment in people with anterior knee pain (5). Thus, it is unlikely that the changes in motor control we observed during stair descent were the result of spontaneous improvements occurring over time.
We have shown that experimentally induced knee pain causes a deficit in motor control of VMO and VL in normal individuals (20) that is similar to that observed in clinical populations of people with anterior knee pain (8). Although the mechanism for these changes is not completely understood, pain can affect motor output at any level of the central nervous system (e.g., spinal cord (31), motor cortex (34), and premotor areas (11)). Thus, improved VMO timing after treatment may simply result from reduced pain rather than a specific direct result of the treatments (2,5). However, in the present study, pain relief is not a plausible explanation for the improvements because the cohort was pain-free. Furthermore, our present findings cannot be explained by strength changes alone because the MCR group did not show a significant increase in strength immediately after the intervention in any of the measured contraction modes. Other factors must explain the greater improvement in VMO timing during stair descent immediately after the MCR intervention.
Recent studies have reported improved timing of EMG activity of other postural muscles after MCR programs. Timing of activation of the deep abdominal muscle, transversus abdominis, improves immediately after a single session of repeated skilled activation of the muscle (33) and after 8 wk of training (33) in people with low back pain. Timing did not change after other interventions such as simple sit up training for the abdominal muscles (33) or a neck flexor strength training protocol (Jull, unpublished data). Recent work has attempted to identify mechanisms underlying such changes in motor control. For instance, changes in the representation of the abdominal muscle at the motor cortex accompany changes in timing of activity of these muscles (Tsao and Hodges, unpublished data). This suggests that plastic changes at the motor cortex may contribute to the restoration of control. These changes were induced only by MCR and not by other exercise interventions such as a walking program.
A number of other studies have reported greater plasticity of the motor pathway with skill training than with strength training. Animal studies show greater changes in the motor cortex after skill training than after strength training (29). Furthermore, research has shown that 4 wk of visuomotor skill training of the biceps brachii is associated with increased response to corticospinal volleys excited by transcranial magnetic stimulation over the motor cortex (suggesting increased excitability of motor cortical cells or motoneurons) but no change in strength (22). In contrast, a strength training protocol increased strength but not the response to transcranial magnetic stimulation (3,21,22). Taken together, these findings suggest that plastic changes in the motor pathway underlie the changes in motor control and that, at least immediately after treatment, the changes depend on specific training of motor skill.
This specificity of training may also partly explain why greater changes in VMO-VL onset timing seen in the MCR group compared with the QS group were confined to stair descent. The differential response may reflect the specificity of the training program relative to the stair ascent and descent outcome measures. The MCR program was primarily weight-bearing, involved a greater emphasis on eccentric quadriceps contraction, and included a stair descending exercise similar to the measurement task. This closer approximation of the MCR training to the stair descent measurement task than to the stair ascent task may have yielded a better training effect for this outcome measure. Because both training programs involved concentric quadriceps contractions, this may explain why no group differences were found in the stair ascent task.
Three components of the MCR program could be responsible for the greater plastic changes seen in vasti motor control during stair descent compared with the QS program. First, EMG biofeedback was used to provide augmented feedback of contraction of VMO and VL during the exercises consistent with common clinical practice. There is some evidence from a few randomized trials that the incorporation of EMG biofeedback into a physiotherapy exercise program improves the magnitude of activation of VMO and VL in patients with anterior knee pain (12,38). However, these studies did not measure relative timing of onset of vasti EMG.
Second, the MCR program also included an exercise that encouraged VMO activation while performing isometric hip abduction and external rotation to train gluteus medius in weight-bearing. Altered hip muscle function has been noted in individuals with patellofemoral pain (3,21). It is hypothesized that retraining hip external rotation control may reduce the valgus force acting at the knee and improve VMO activation. Although the present study and another (2) included hip strengthening exercises and reported normalization of VMO onset timing, the specific contribution of hip exercise to the VMO onset timing changes cannot be elucidated because both programs involved additional treatment components. However, gains in hip strength are unlikely to have explained our results. Because we were most interested in assessing the effects of specific VMO retraining and recognizing that one particular exercise in the MCR program had the potential to simultaneously improve hip strength, we also included a hip strengthening exercise into the QS program to ensure a similar component between programs and thus control for this aspect.
Third, there is evidence that weight-bearing exercises as used in our MCR program may alter the activity of the vasti muscles (26,30). For example, studies have found that in weight-bearing tasks, the synchronization of motor unit discharge between the medial and lateral vasti was higher (26) and that the onset of EMG activity of the different vasti was more simultaneous compared with during non-weight-bearing tasks (26). Thus, training in weight-bearing may generate more closer onsets between VMO and VL than non-weight-bearing exercise.
In the present study, timing of the vasti muscles was also changed during stair descent after the QS program but to a lesser extent than after the MCR program. This may be because of some of the features of the QS program. It is possible that the type of strengthening exercises may have had some effects on motor control. Although studies have generally failed to find a specific exercise that results in a preferential activation of VMO relative to VL during performance of the exercise (15,24,39), it is possible that one or more of the tasks may drive at least some degree of plasticity in the motor pathway over time. One other uncontrolled study also showed improved vasti EMG onset timing during both stair ascent and descent in people with anterior knee pain after a rehabilitation program that did not include specific VMO retraining (2). Although this program included strength training, it also included other components such as weight-bearing exercise that may influence coordination between the vasti. The fact that changes in vasti onset timing were only seen in stair descent and not ascent in our QS group could be because of the greater increase in eccentric compared with concentric strength (20% vs 12%) because this approximates more closely the contraction mode used during the stair descent task.
Improvements in motor control and strength after cessation of training were not specific to the interventions.
The improvement in motor control and strength in both groups at 8 wk after treatment cessation was unexpected. Although we can only speculate, there are several potential mechanisms. First, we did not control or record any changes in activity level or function at the completion of training. It is plausible that the increased knee control and quadriceps strength attained with the interventions, as well as increased confidence of the participants in their exercise ability after the 6-wk exercise program may have led to changes in function or exercise tolerance. Improved functional use of the knee may have induced gains in the untrained parameters. Second, as stated above, the interventions included multiple components, some of which may have contaminated the outcomes. For instance, the weight-bearing component of the MCR program may have induced changes in quadriceps strength but at a slower rate than the targeted QS program. In contrast, as described above, some elements of the QS program may have been sufficient to induce plasticity in the motor pathway. Although it is clear that early gains in motor control and strength are dependent on specific interventions, it is unclear whether specificity is needed for longer-term outcomes. It is also possible that periodic treatments will be needed to maintain improvements after an MCR program. However, clinical decisions about the most appropriate exercise program should be made on comparison of outcomes related to parameters that have direct meaning to a patient, such as pain and function. A recent randomized controlled trial comparing an MCR and a QS program in 69 people with patellofemoral pain found that both exercise programs equally improved pain, function, and quality of life (32) in the short term. Whether such improvements are maintained over time equally in both groups needs to be investigated particularly given the episodic and recurrent nature of the condition.
This work was funded by the National Health and Medical Research Council (project grant no. 209064).
ClinicalTrials.gov identifier: NCT00662493.
There are no conflicts of interests identified.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
The authors thank the therapists who conducted the treatments: Andrew Briggs, Elin Wee, Debbie Virtue, Sue Hogarth, Angus Bell, and Randall Cooper.
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