Activation of vastus medialis oblique is not delayed in patients with osteoarthritis of the knee...

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Manual Therapy 12 (2007) 219–225 Original article Activation of vastus medialis oblique is not delayed in patients with osteoarthritis of the knee compared to asymptomatic participants during open kinetic chain activities John Dixon a, , Tracey E. Howe b a Teesside Centre for Rehabilitation Sciences, University of Teesside, The James Cook University Hospital, Marton Road, Middlesbrough, UK b HealthQWest, Glasgow Caledonian University, Cowcaddens Road, Glasgow, UK Received 7 July 2005; received in revised form 23 February 2006; accepted 1 June 2006 Abstract This study investigated whether the onset of electromyographic (EMG) activity of vastus medialis oblique (VMO) was delayed relative to that of vastus lateralis (VL) in patients with osteoarthritis (OA) of the knee compared to asymptomatic participants during open kinetic chain activities. An exploratory observational cross sectional study was carried out. Two groups were tested, symptomatic OA knee patients, diagnosed by an orthopaedic surgeon, ðn ¼ 17Þ, mean (SD) age 66.0 (7.6) years, and asymptomatic participants ðn ¼ 17Þ, 56.7 (8.6) years. Surface EMG activity of VMO and VL was measured, during concentric contractions extending the knee from 901 flexion, and during maximal voluntary isometric contractions at 601 knee flexion. The EMG onset times of VMO and VL were determined visually and by algorithm. The onset timing difference (OTD) between the two muscles was calculated for each subject, by subtracting the onset time of VL from VMO. Mann–Whitney U-tests revealed that the OTD between VMO and VL was not significantly different between the groups during either contraction type (both p40.05). The results of this exploratory study may have implications for rehabilitation programmes aimed at developing preferential activation of VMO compared to VL in OA knee patients. r 2006 Elsevier Ltd. All rights reserved. Keywords: Electromyography; Knee; Quadriceps; Osteoarthritis 1. Introduction Osteoarthritis (OA) is a common cause of disability in adults (Badley and Tennant, 1993). Although previously thought of being solely due to joint wear and tear, it is now believed that muscle dysfunction is an important factor in OA knee (Shrier, 2004). Impairments that may increase joint damage over time, such as arthrogenous muscle inhibition, quadriceps weakness, and slowed protective reflexes have been implicated (Hurley, 1999). Clinicians observe what appears to be selective atrophy of muscle vastus medialis oblique (VMO) in OA knee patients. There is evidence to suggest that VMO may be preferentially affected in patellofemoral pain syndrome patients, and its activation delayed relative to that of vastus lateralis (VL) when compared to healthy subjects (Witvrouw et al., 1996; Cowan et al., 2001, 2002). Theoretically this could lead to a biomechanical imbalance at the knee joint. Despite the prevalence of OA knee, there is a scarcity of research about VMO activation in OA knee patients. This has been studied during stair climbing (Hinman et al., 2002), and during the patellar tendon reflex response (Dixon et al., 2004). In both studies the activation timing of VMO relative to VL did not differ in OA knee patients compared to asymptomatic participants. However, it has been proposed that muscle activation order may be affected by the type of muscle contraction ARTICLE IN PRESS www.elsevier.com/locate/math 1356-689X/$ - see front matter r 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.math.2006.06.012 Corresponding author. Tel.: +44 1642 384125. E-mail address: [email protected] (J. Dixon).

Transcript of Activation of vastus medialis oblique is not delayed in patients with osteoarthritis of the knee...

Page 1: Activation of vastus medialis oblique is not delayed in patients with osteoarthritis of the knee compared to asymptomatic participants during open kinetic chain activities

ARTICLE IN PRESS

1356-689X/$ -

doi:10.1016/j.m

�CorrespondE-mail add

Manual Therapy 12 (2007) 219–225

www.elsevier.com/locate/math

Original article

Activation of vastus medialis oblique is not delayed in patients withosteoarthritis of the knee compared to asymptomatic participants

during open kinetic chain activities

John Dixona,�, Tracey E. Howeb

aTeesside Centre for Rehabilitation Sciences, University of Teesside, The James Cook University Hospital, Marton Road, Middlesbrough, UKbHealthQWest, Glasgow Caledonian University, Cowcaddens Road, Glasgow, UK

Received 7 July 2005; received in revised form 23 February 2006; accepted 1 June 2006

Abstract

This study investigated whether the onset of electromyographic (EMG) activity of vastus medialis oblique (VMO) was delayed

relative to that of vastus lateralis (VL) in patients with osteoarthritis (OA) of the knee compared to asymptomatic participants

during open kinetic chain activities. An exploratory observational cross sectional study was carried out. Two groups were tested,

symptomatic OA knee patients, diagnosed by an orthopaedic surgeon, ðn ¼ 17Þ, mean (SD) age 66.0 (7.6) years, and asymptomatic

participants ðn ¼ 17Þ, 56.7 (8.6) years. Surface EMG activity of VMO and VL was measured, during concentric contractions

extending the knee from 901 flexion, and during maximal voluntary isometric contractions at 601 knee flexion. The EMG onset times

of VMO and VL were determined visually and by algorithm. The onset timing difference (OTD) between the two muscles was

calculated for each subject, by subtracting the onset time of VL from VMO. Mann–Whitney U-tests revealed that the OTD between

VMO and VL was not significantly different between the groups during either contraction type (both p40.05). The results of this

exploratory study may have implications for rehabilitation programmes aimed at developing preferential activation of VMO

compared to VL in OA knee patients.

r 2006 Elsevier Ltd. All rights reserved.

Keywords: Electromyography; Knee; Quadriceps; Osteoarthritis

1. Introduction

Osteoarthritis (OA) is a common cause of disability inadults (Badley and Tennant, 1993). Although previouslythought of being solely due to joint wear and tear, it is nowbelieved that muscle dysfunction is an important factor inOA knee (Shrier, 2004). Impairments that may increasejoint damage over time, such as arthrogenous muscleinhibition, quadriceps weakness, and slowed protectivereflexes have been implicated (Hurley, 1999). Cliniciansobserve what appears to be selective atrophy of musclevastus medialis oblique (VMO) in OA knee patients. There

see front matter r 2006 Elsevier Ltd. All rights reserved.

ath.2006.06.012

ing author. Tel.: +441642 384125.

ress: [email protected] (J. Dixon).

is evidence to suggest that VMO may be preferentiallyaffected in patellofemoral pain syndrome patients, and itsactivation delayed relative to that of vastus lateralis (VL)when compared to healthy subjects (Witvrouw et al., 1996;Cowan et al., 2001, 2002). Theoretically this could lead toa biomechanical imbalance at the knee joint. Despite theprevalence of OA knee, there is a scarcity of researchabout VMO activation in OA knee patients. This has beenstudied during stair climbing (Hinman et al., 2002), andduring the patellar tendon reflex response (Dixon et al.,2004). In both studies the activation timing of VMOrelative to VL did not differ in OA knee patients comparedto asymptomatic participants.

However, it has been proposed that muscle activationorder may be affected by the type of muscle contraction

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ARTICLE IN PRESSJ. Dixon, T.E. Howe / Manual Therapy 12 (2007) 219–225220

(Grabiner et al., 1994; Stensdotter et al., 2003), andvoluntary muscle activation during open kinetic chain(OKC) activities remain to be investigated in this kneepathology. This type of activity is often used to evaluatequadriceps function in rehabilitation. Hence the aim ofthis study was to investigate onset of VMO and VLEMG activity in OA knee patients and asymptomaticparticipants during two OKC activities, seated non-weightbearing knee extensions (concentric contractions)extending the knee from 901 flexion, and duringmaximal voluntary isometric contractions (MVIC) at601 knee flexion. We tested the hypothesis that onset ofVMO EMG activity, relative to that of VL, would bedelayed in OA knee patients when compared to similarlyaged asymptomatic participants. We also measuredtorque produced by the quadriceps during MVICs usinga load cell to allow a comparison with previouslypublished studies (Tan et al., 1995; Cheing and Hui-Chan, 2001) reporting deficits in maximal quadricepsstrength in patients with OA knee.

2. Methods

An exploratory observational cross sectional studywas carried out, in conjunction with a study into reflexEMG activity (Dixon et al., 2004).

2.1. Participants

Ethical approval was granted by local research ethicscommittees. All subjects gave written and verbal in-formed consent before taking part in the study. Twosubject groups were tested, a group of symptomatic OAknee patients, and a group of similarly aged asympto-matic participants. Asymptomatic participants compriseda convenience sample from the local area and OApatients were recruited from South Tees Hospitals NHSTrust, UK outpatients orthopaedic clinics. Diagnosis ofOA knee was made by an orthopaedic surgeon, accordingto the American College of Rheumatology criteria(Altman et al., 1986), using clinical signs and symptomsand the presence of osteophytes determined by weight-bearing radiographs. Asymptomatic participants wereindividuals who reported having no history of knee pain.Participants were excluded if they presented withsignificant cognitive, cardiorespiratory, neurological, ormusculoskeletal impairments (excepting OA knee in thepatient group) that limited functional ability, or reporteduse of medication affecting neuromuscular function, or ifthey could not carry out the activities.

2.2. Procedure

For testing, each participant was seated on anadjustable padded ‘quadriceps chair’ (Tornvall, 1963;

Edwards et al., 1977; Dixon et al., 2004) with theposterior aspect of the knee positioned at the front edgeof the seat and arms folded across the chest. The chairback-rest was set at 701 of hip flexion (Doxey andEisenman, 1987). In bilateral OA knee patients andasymptomatic participants, data were recorded from thedominant limb, which was defined as the limb withwhich they would kick a ball (Cheing and Hui-Chan,2001). The symptomatic limb of patients with unilateralOA was tested.

After cleaning the skin with isopropyl alcohol, andshaving the area if necessary, active surface EMGrecording electrodes (BIOPAC Inc., USA, TSD150B,Ag/Ag Cl, diameter 11.4mm, electrode spacing 20mmcentre to centre, with a built in 350� amplification anda 3 dB bandpass of 12–500Hz) were placed on VMOand VL at standardized sites. The electrodes wereoriented in the estimated direction of the muscle fibres(Lieb and Perry, 1968). The VL electrode was sited onthe muscle belly, at one-third the distance from thesuperior border of the patella to the greater trochanter(Mannion and Dolan, 1996), oriented 12–151 laterallyfrom the long axis of the femur. For VMO placementwas on the muscle belly 5 cm from the superior medialborder patella border (Callaghan et al., 2001), oriented50–551 medially from the long axis of the femur.Hypoallergenic conductive gel (Lectron II, Pharmaceu-tical Innovations Inc., USA) was applied to theelectrodes to facilitate electrical contact with the skinsurface. All electrodes were taped to the skin to preventmovement artifacts. A ground electrode (Red dot TM,3M Healthcare, USA) was attached to the patella of theuntested leg.

2.2.1. Concentric contraction

An electrogoniometer (Type SG150, Biometrics Ltd,UK) was used to measure knee angle during theconcentric contraction. This was calibrated prior touse, and attached to the knee joint of the participantwith doubled sided tape. Each participant was asked toperform extension of the knee joint, from 901 kneeflexion to full extension (or as far as possible) and back.The instruction ‘‘straighten your leg’’ was given. Thiswas followed by ‘‘and relax’’ when the participantreached full extension. This was carried out ten times,each contraction separated by 20 s to minimize fatigueeffects.

2.2.2. Maximal voluntary isometric contraction (MVIC)

Force was measured using a load cell (TC601, AmberInstruments Ltd, UK). The load cell output was fed to achannel of the BIOPAC system and the voltage outputwas pre-calibrated by hanging known weights verticallyfrom the load cell. The MVIC activity was carried out atleast 3min after the concentric contraction. The kneewas positioned at 601 flexion (Kannus et al., 1987;

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Powers et al., 1996). This position has been shown toproduce a higher torque than other knee angles (Lieband Perry, 1971). This leg position was standardized bythe attachment to the chair of an adjustable arm thatsupported the leg of the subject at mid-calf level. Theangle of flexion was verified with a goniometer and theleg support adjusted accordingly. A comfortable non-extensible ankle strap was attached to the leg of thesubject at the level of the lateral malleolus. The load cellunder the chair was adjusted so that the chain passedfrom the leg at an angle of 901. The length of the lever-arm, being the distance from the centre of the knee jointto the load cell strap at the lateral malleolus, wasmeasured to allow torque calculations.

Participants carried out five maximal isometric con-tractions of the quadriceps with 30 s rest between eachcontraction to minimize fatigue. Each participant wasasked to straighten the leg as forcefully as possibleagainst the resistance of the chain for 3 s (Soderberg andKnutson, 2000) and then told to relax. The investigatorgave standardized instructions of ‘ready, steady, push,push, push, relax’ to elicit a contraction of 3 s. It wasconfirmed that participants understood the instructionsand they were given practice attempts to ensurefamilarization with the procedure. Verbal encourage-ment was given, as encouragement has been shown toincrease maximal voluntary contraction values (McNairet al., 1996). The peak force was utilized as the MVICfor the purposes of the study.

All data were sampled at 2048Hz using a physiolo-gical data acquisition system (BIOPAC Inc., USA)comprising an MP100 workstation with a high-leveltransducer HLT100 and dedicated analysis software(AcqKnowledge 3.5.3).

2.3. Onset timing determination

Onset of EMG activity, the ‘earliest rise beyond thesteady state’ of the raw EMG signal (Hodges and Bui,1996), was evaluated both visually and by computeralgorithm. Both methods were used because of age-related changes that affect the quality of the EMG signalin older people and which could affect onset timesdetermined by algorithm, e.g. lower amplitude andpoorer signal to noise ratio than younger people. Forvisual evaluation, the peak or trough of the first spike ofthe raw EMG was identified as the point of onset, byviewing the digitally stored data in the AcqKnowledgesoftware.

For computerized evaluation, an algorithm based onthe work of Hodges and Bui (1996) was used to identifythe EMG onset time for each electrode site (Dixon,2004). Here, EMG data was saved as an ASCII text filewith a resting baseline prior to contraction of 500msduration, and imported into Microsoft Excel. In Excel,the raw EMG data were full wave rectified and 50Hz

low-pass filtered using a single pole first order digitalfilter. The algorithm calculated the mean and standarddeviation (SD) of the first 100 data points (the baselinewindow, 48.83ms). The SD value was then used as thethreshold to determine EMG onset time. The algorithmidentified onset as the time point at which the meanvalue of a moving window of 50 data points (24.41ms)exceeded the mean of the baseline by 1SD of the baselinewindow. The mid-point of the moving window was thetime determined as onset. The algorithm was also testedwith 2 and 3 SDs as the threshold value, but it wasfound that the 1 SD threshold had best agreement withvisually determined onset times using Bland and Altmanlimits of agreement (Dixon, 2004). The 1SD algorithmonset times were therefore used, as in previous literature(Karst and Willett, 1995). On the few occasions whenthe baseline window contained a marked artifact, itsposition was moved to ensure that artifacts did notartificially increase the SD and hence the threshold.

The EMG onset time difference (OTD) between theVMO and VL was then calculated for both visually andcomputer evaluated results, by subtraction of the timefor VL from that of VMO. A negative value thereforeindicates that VMO onset is before that of VL. Themedian OTD (of 10 concentric and 5 MVICs) was thencalculated for each subject for both activities. This wasused in preference to the mean, as data for someparticipants were skewed.

For the concentric contraction, data were excludedfor one asymptomatic participant due to an electrodeproblem. Concentric and MVIC EMG data for one OAknee patient were excluded due to the poor signalquality possibly arising from obesity (Marks et al.,1994), which prevented successful onset determination.However this patient could perform the MVIC and theirtorque data were not excluded from the torque results.

2.4. Statistical analysis

Data were analysed using SPSS V 10. The Mann–Whitney U-test was used to test for between groupdifferences, as the data sets displayed either differencesin variance or non-normal distributions, as has beendescribed in other work (Karst and Willett, 1995).Values of po0.05 were regarded as statistically sig-nificant.

3. Results

Descriptive characteristics of the groups are shown inTable 1. The groups were significantly different in age,mass and body mass index (Mann–Whitney U-test, allpo0.05), but not in height ðp ¼ 1:00Þ, with the OA kneegroup being on average 9.3 years older, 9.4 kg heavierand having greater body mass index by 3.4 kg/m2.

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Table 1

Description of participants

Group Age (years) Height (m) Mass (kg) BMI (kg/m2) Sex

Mean (SD) Mean (SD) Mean (SD) Mean (SD) (M:F)

Asymptomatic 56.7 (8.6) 1.68 (0.09) 74.4 (10.9) 26.3 (2.7) 8:9

OA knee 66.0 (7.6) 1.67 (0.09) 83.8 (12.9) 29.7 (3.8) 11:6

150

100

50

0

-50

-100

Ons

et ti

min

g di

ffere

nce

(ms)

N- 16 16 16 16visual algorithm

Onset determination method

150

100

50

0

-50

-100N- 17 16

visual17 16algorithm

Onset determination method

Groupasymptomatic

OA knee

(a) (b)

Fig. 1. Onset timing difference during initiation of concentric contraction (1a) and MVIC (1b). Negative value indicates VMO activated before VL.

Table 2

Median (interquartile range) onset timing differences (ms) by contrac-

tion type and evaluation method

Group Concentric MVIC

Visual Algorithm Visual Algorithm

Asymptomatic 2.7 (23.9) 2.5 (38.7) �4.6 (21.2) �13.6 (44.3)

OA knee 7.9 (52.4) 3.6 (87.9) 1.5 (27.5) 5.3 (45.1)

p valuea 0.41 0.50 0.06 0.07

aMann–Whitney U-test.

J. Dixon, T.E. Howe / Manual Therapy 12 (2007) 219–225222

Fig. 1 shows the results for OTD, onset of VMOEMG activity relative to that of VL, for the concentriccontraction and for the MVIC, in graphic format. Themedian and interquartile range values are also presentedin Table 2. For both contraction types, the differencesbetween the groups in the OTD were not statisticallysignificant for either visual or computerized evaluationmethods (Mann–Whitney U-test, all p40.05). We notedgreater variability in the OA knee patients than in theasymptomatic participants in both contraction types, ascan be seen clearly in Fig. 1.

The MVIC torque produced by the OA knee patientswas on average 30% less than the asymptomaticparticipants (120.6Nm compared to 84.6Nm). Thisdifference was statistically significant (Mann–WhitneyU-test, po0.05).

We were not able to report confidence intervals forthe differences between the groups because the databreached the assumptions of normality and non-para-metric tests were used (Bland, 2000).

4. Discussion

Our aim was to investigate whether the onset of EMGactivity of VMO was delayed relative to that of VL in

OA knee patients compared to similarly aged asympto-matic participants, during maximal voluntary isometricand concentric muscle contractions of the quadriceps.We did this by calculating the OTD by subtracting theEMG onset time of VL from VMO. We found thatOTD was not significantly different between the OAknee patients and the asymptomatic participants ineither activity. This agrees with the small amount ofliterature in this area on OA knee patients during othertasks (Hinman et al., 2002; Dixon et al., 2004). We alsofound that MVIC torque of OA knee patients wassignificantly less than the similarly aged asymptomaticgroup, as has been shown in previous studies (Tan et al.,

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1995; Fisher and Pendergast, 1997; Cheing and Hui-Chan, 2001), and our torque data are comparable withthese reports.

We observed marked variability both within andbetween subjects (Fig. 1) in the VMO-VL OTD, whichhas been mentioned in some patellofemoral painsyndrome literature (Karst and Willett, 1995; Cowanet al., 2001) but not in great detail. We believe that thismay be firstly related to the OKC activities studied here,which have been shown to elicit greater variability inonset times than closed chain type activities (Stensdotteret al., 2003). Secondly, this may also be because of age-related changes that affect the quality of the EMG signalin older people. As the EMG signals of older peopleoften have a lower amplitude and poorer signal to noiseratio than that of younger people, due to muscle atrophyand increased subcutaneous fat, onset determinationmay be more difficult. Possibly we could have usedgreater smoothing than a 50Hz low pass filter, butexcess smoothing can cause loss of information (Karst,1998). Very few studies have evaluated EMG in olderpeople, and it would be preferable if more work werecarried out here. There is no universally accepted bestmethod for computerized onset determination (Hodgesand Bui, 1996; Staude and Wolf, 1999), but becausethese computerized methods have set standards orparameters, subjectivity is reduced. The algorithm usedhere is based on a well-used technique (Hodges and Bui,1996). Some studies have used variations, such as havingthe threshold exceeded for a minimum of 25ms (Hin-man et al., 2002) rather than the point where the meanof the window exceeds threshold, as used here. Also, weused a first order low pass filter compared to somestudies using higher order filters. However, we believethat this should produce very little difference in results,as at 50Hz filtering the phase lag is approximately 3ms.In addition the standard moving window technique thatfollows the low pass filtering averaged the data over24ms periods, and the VL onset times were subtractedfrom those of VMO, to produce a relative OTD.

The lack of a significant difference between the groupscould be attributable to several explanations. Firstly, thesample size ðn ¼ 17Þ could possibly result in an under-powered study. We did not carry out post hoc powercalculations as it is known that any analysis finding nosignificant difference will be shown to have beenunderpowered when post hoc power calculations arecarried out (Goodman and Berlin, 1994), and researchmust start somewhere (Bacchetti, 2002). However, wedid carry out an estimation of how many participantswould be required to adequately power a future study todetect differences between the groups in OTD. Thesepost hoc calculations were carried out with a significancelevel of 0.05 using the larger of the group SDs from thevisually evaluated results, but it should be noted thatbecause the data breached the assumptions of normality,

these calculations were approximations only, and maybe overestimates. Due to the variability observed, it wasdecided to use a value of 20ms as the difference to bedetected between the groups. The calculations showedthat a study with 95 participants in each group wouldhave 80% power to detect a difference of 20ms in OTDfor the concentric contraction. However, 142 partici-pants in each group would be required to provide 80%power for detection of a 20ms difference for MVIC.Further research with a larger sample size is thereforerecommended, and this study provides information thatwill assist future studies. To avoid making a type II errorfrom the results observed, future studies should use amuch larger total sample size, and our estimations showthat approximately 90–140 participants may be requiredper group for this type of OKC activity. The smallsample size in this study is a limitation and therefore theresults must be interpreted with caution. However, thiswas an exploratory study from which the results haveenabled sample size calculations to be undertaken forsubsequent studies.

It is possible that the OA knee patients in this studycould be a heterogeneous group, as the general OA kneepopulation is understood to display considerable hetero-geneity (Hurley, 1999). No attempt was made tocategorize patients in terms of aspects of OA kneeclassification, or duration or level of symptoms. If thiswas the case in future studies, sub-group analysis couldreveal whether specific sub-groups of the OA kneepopulation do exhibit an impairment in OTD that couldbe clinically important. In addition, an assumption wasmade that the asymptomatic participants did not haveradiographic OA. Although radiographs were not takenfrom the asymptomatic participants for ethical reasons,it is possible that they could have exhibited asympto-matic radiographic changes at the knee joint (Felson etal., 1987) which may have affected muscle activation.

The OKC type muscle contraction tested here maynot be representative of normal functional movementthat tends to occur in the weight bearing closed kineticchain manner (Callaghan and Oldham, 1996; Stensdot-ter et al., 2003). However, this is a standard method ofevaluating quadriceps function. Future studies shouldattempt to use both open and closed kinetic chaintesting. In addition, it was noticed that the MVICactivity often generated anticipatory muscle contractionin some subjects. As this anticipatory muscle activitygenerated force (measured by the load cell), these EMGonsets could not be validly excluded. Interestingly, usingthe computerized method, onset was often detected forVMO and not VL, or vice-versa, which could haveadded to the variability discussed above.

Nevertheless, we believe that this exploratory studyadds to the evidence base about neuromuscular impair-ments in OA knee, and will inform future researchand practice. Much of our understanding of muscle

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dysfunction in OA knee remains speculative (Hurley,1999). This study and those already published indicatethat the timing of VMO muscle activation relative tothat of VL in OA knee patients does not differ from thatof asymptomatic participants, in contrast to evidence inPFPS. However there are some published studiesreporting that experimental knee effusion can preferen-tially affect VMO (Kennedy et al., 1982; Spencer et al.,1984; Torry et al., 2000). Therefore there is a now a needfor the intensity of VMO and VL EMG activity to beinvestigated in OA knee patients, as it is possible thatthis is where any preferential inhibitory effect on VMOmay be exhibited. The need for more research intomuscle function in OA knee is clear. Subsequent tostudies reporting muscle inhibition in OA knee patients(Hurley and Newham, 1993; Hurley et al., 1997), a studyhas found that not all OA knee patients exhibit muscleinhibition but some asymptomatic participants do(Lewek et al., 2004). Quadriceps strength and muscleinhibition do not show the expected correlation withseverity of cartilage damage (Pap et al., 2004). Similarly,the findings that quadriceps strengthening may actuallynot benefit patients with malaligned knees (Sharma etal., 2003) shows that further research is urgentlyrequired. This seems particularly important with regardto the heterogeneity and variability within the OA kneepopulation, if treatments are to be efficacious.

5. Conclusion

Our acceptance of the null hypothesis agrees with theonly other studies into the activation timing of VMOand VL in OA knee (Hinman et al., 2002; Dixon et al.,2004). This evidence of this exploratory study for thelack of a preferential delay in VMO activation in OAknee patients contrasts with findings of a preferentialeffect in PFPS. Rehabilitation programmes for OA kneepatients should not therefore be aimed at altering thetiming of VMO activation relative to VL, as a growingbody of evidence seems to indicate that no temporaldelay exists.

Acknowledgements

The authors wish to thank Vicki Whittaker for statisticaladvice and assistance, and all the participants who tookpart. This work was supported by a University of TeessideSchool of Health and Social Care Ph.D. Studentship.

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