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Introduction

Patellofemoral pain syndrome (PFPS) is thesecond most common musculoskeletalcomplaint presented to physiotherapists(Witvrouw et al , 1996; Hilyard, 1990).Clinical features of PFPS include theinsidious onset of diffuse retropatellar pain,aggravated by squatting, kneeling, stairs,slopes, prolonged flexed knee sitting, andrising after prolonged sitting (Arroll et al ,1997; Hilyard, 1990). Many factors areinvolved in complex interactions that influence the patellofemoral joint, and the

exact aetiology of PFPS is often enigmatic(Fulkerson and Hungerford, 1990;Finestone et al , 1993). However, there isconsensus that malalignment andmaltracking of the patella are major features

of PFPS (Maclntyre and Robertson, 1992;Gerrard, 1989). While accepting that many factors and structures influence PFPS, thisstudy focuses on the role of the quadriceps

femoris muscle group, with particularemphasis on vastus lateralis (VL) and vastusmedialis obliquus (VMO).

The force generated by and withinthe quadriceps is recognised as a majorinfluence on patellar tracking (Roberts,1989; Knight, 1985), and interplay withinthis group is vital to efficient functioning of the patellofemoral joint (Herrington andPayton, 1997; Witvrouw et al , 1996).Disruption of the tension characteristicsof component quadriceps can induce

imbalance in the transverse forces acting onthe patella (Karst and Jewett, 1993). Relative we akne ss in one of th e qu ad ri ce ps wi lldisrupt the normal synergy of the groupand induce imbalance. Although thereis disagreement whether quadricepsdysfunction is a primary or secondary occurrence in PFPS, it is accepted as aninherent part of the vicious cycle that isfrequently identified. A model for thepathogenesis of PFPS is presented in figure 1overleaf.

There is a well-established link between VMO insufficiency and PFPS (Kowall et al ,1996; McConnell, 1987b). Boucher et al (1992) found that increased severity of PFPSsymptoms correlated with decreasing VMOactivity. Ahmed et al (1988) found that a50% reduction in VMO activity produced a5 mm lateral shift of the patella, whichrepresents a considerable disruption topatellar tracking.

Traditionally, the cornerstone of physiotherapeutic intervention in PFPS hasinvolved general quadriceps strengthening

(Antich and Brewster, 1986; Karst and Jewett, 1993), with many protocols beinghighlighted in literature from more than 50

years ago (Nicoll, 1943; DeLorme, 1945).That they are still used today, despite later

The Effect of McConnell'sVastus Lateralis InhibitionTaping Technique on VastusLateralis and Vastus MedialisObliquus Activity

Summary This study was conducted to investigate the effects ofJenny McConnell’s vastus lateralis (VL) inhibition taping techniqueon VL and vastus medialis obliquus (VMO) muscle activity, and itspossible application in quadriceps rehabilitation, particularly in

patellofemoral pain syndrome.Eighteen asymptomatic subjects (11 female and 7 male)participated, and completed a functional task (stair descent) underthree test conditions: no tape, placebo tape and active tape.

Surface electrodes were used to determine theelectromyographic activity of VL and VMO during the tests.

High variance and abnormal distribution meant that the datarequired non-parametric analysis, which was completed withFriedman and Wilcoxon tests for each muscle. Results of theFriedman test for VL revealed a significant difference in activityacross the conditions (p < 0.05). Further investigation with theWilcoxon tests revealed that the application of the active tape wasresponsible for significantly decreasing VL activity. The Friedmantest on VMO activity revealed no significant difference betweenexperimental conditions (p > 0.05), although a Wilcoxon testbetween the placebo tape and active tape conditions wassignificant.

These findings suggest that McConnell’s VL inhibition tapingtechnique does inhibit VL, but the effects of this inhibition onVMO require further investigation.

Key WordsPatellofemoral pain syndrome,

VL:VMO activity,quadriceps imbalance,EMG, McConnell taping.

by Sue TobinGill Robinson

Tobin, S and Robinson, G(2000) . ‘The effect of McConnell’s vastuslateralis inhibition tapingtechnique on vastuslateralis and vastusmedialis obliquusactivity’, Physiotherapy , 86,4, 173-183.



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advances in biomechanics, pathophysiology and knowledge of specificity of musclefunction, gives cause for concern. AsRichardson wrote in 1985: ‘For too long, allmuscles have been exercised on the sameprinciples without accounting for thedifferent muscle types and their behaviourpatterns.’

The use of quadriceps programmes that do not address muscle specificity and thecrucial interplay between the components of this muscle group may help to explain why many treatment protocols have the poor

long-term success rates identified by Devereaux and Lachman (1984) andFitzgerald and McClure (1995), and why PFPS frequently becomes a chronic disorder.The onus is on physiotherapists to establishmechanisms to isolate or disproportionately stimulate the activity of one muscle withrespect to the others, ie to manipulate the

components of a muscle group to restoreoptimal synergy. That VMO and VL havedifferent specificity of function ishighlighted by their respective physiologicalfeatures, which are presented in table 1.

Table 1: Physiological features of VL and VMO

Feature VL VMO Reference

Muscle type Mobility Stability Richardson (1985)

Muscle fibre 15° to 18° to 46° to 52° to Lieb and Perry (1968)alignment femoral axis femoral axis

Muscle fibre Predominantly Predominantly type I Herrington and Payton (1997)type type II fast twitch slow twitch

Muscle activity Phasic power Tonic, endurance McConnell (1995)

Action Leg extension Dynamic patellar Speakman andstabilisation Weisberg (1977)

Active range Throughout knee Throughout knee Speakman andflexion/extension flexion/extension Weisberg (1977)

Functional Maximal when Maximal in work Richardson (1985)activity distal segment associated with

is free joint compression,eg weightbearing

Interrelationship Agonist Antagonist Hodges andRichardson (1993)

Adaptive To become short To become long Norris (1996)tendencies and tight and weak

VMO function

Inhibition of musclefunction

Dynamic patellarstabilisation

Articular cartilagestress

Quadriceps imbalance

Overpull by VL

Pain Effusion

Joint damage

Lateral displacement ofpatella

Fig 1: Pathogenesis of patellofemoral pain syndrome (adapted from Stokes and Young (1994), Richardson (1985) and Pevsner et al (1979)



175Professional articles

The advent of the McConnell patello-femoral treatment plan (1985) provideda development in physiotherapeuticintervention in PFPS. McConnell’s plan

works on the premise that if a patien t’ssymptoms are due to poor patellaralignment, then correcting this alignment should reduce the symptoms, allowingthe undertaking of a functional rehabi-litation programme designed to stim-ulate VMO activity preferentially, thereby addressing the accompanying quad-riceps imbalance. By using tape toaddress patellar position, the VMO isassisted in its efforts to resist the pull of the

VL and stabi lise the patella (McConnell,1995). Facilitating the VMO away from a

lengthened position also optimises itspotential for cross-bridge formation (Harms-Ringdahl, 1993), and allows it to work froma position of increasing mechanicaladvantage, which should facilitate theincreased muscle activity required forhypertrophy.

Research findings into McConnell’spatellar taping techniques are numerousand somewhat contradictory (Brockrath et al , 1993; Cerny, 1995; Crome et al , 1987;Gerrard, 1989; Shelton, 1992). However, all

these studies, as well as McConnell’s own work, have focused on directly increasing VMO activity to establish optimal VMO:VLbalance. None has addressed the possibility of restoring this balance through thereduction of VL activity. Although Witvrouw et al (1996) briefly refer to retarding VLactivity, and McConnell herself has devised ataping technique designed to do this,literature searches revealed no studies inthis area.

McConnell proposes in her course hand-book that her VL inhibition technique works

via the type IV nociceptors, but does not elaborate. Given the dearth of relevant literature, it is appropriate to proposemechanisms by which application of thistechnique could inhibit VL activity, and alsofacilitate VMO activity.

Type IV nociceptors respond to deepmechanical stimuli, and have small diameterC-fibre afferents which bifurcate uponentering lamina I and lamina II (substantiagelatinosa) of the dorsal horn in the spinalcord (Kandel et al , 1991, page 386).

It is therefore conceivable that, via thelocal inhibitory interneurones, alpha motorneurones of VL are inhibited by thestimulation of nociceptors. This wouldreduce the electrical activity within

VL , whi ch sh ould be de tectab le by electromyography (EMG). Whether thehigher centres, stimulated by projectionneurones, would exert any influence isunclear.

For the proposed influence on VMOmuscle activity there are at least two possiblemechanisms. The first is biomechanical/physiological and involves the previously mentioned facilitation of VMO into aposition of increasing mechanical advantageand cross-bridge formation. This mechanismrequires adaptive shortening and would takeseveral days for any effect to becomeapparent. The second possibility isneurological and counters the VLmechanism. Nociceptive afferents from

VL cou ld inf luenc e loc al exc itat ory interneurones supplying the alpha motorneurones of the antagonist muscle, ie VMO.Similar types of neural circuits are already established, eg the flexor withdrawal reflex(Kandel et al , 1991, page 588). If this neuralcircuit were used, the electrical activity in

VM O wo uld inc re as e wh ich sh oul d bedetectable by EMG.

DesignEighteen asymptomatic volunteers took part

in a same subject test-retest study, thereby ensuring optimal group matching (Robson,1996, page 94). Counterbalancing was usedto overcome inherent dangers of order,fatigue and carry-over effects (Hicks, 1995,page 72).

The activity chosen for analysis was stairdescent, partly for its functional relevanceto daily activities, and partly because it formspart of McConnell’s VMO trainingprogramme (McConnell, 1995).

The experiment involved three test conditions: no tape (control); placebo tape;and active tape.

Each subject was tested three times undereach of the experimental conditions, withEMG being used as an appropriate measureof muscle activity (Kumar and Mital, 1996).

Apparatus and MaterialsFixomull ® stretch tapeLeukotape ® P tapeEMG with MIE MT8-MBM base unit andtelemetry belt

2 x 4 k pre-amplifiersSelf-adhesive silver-silver chloride electrodesMyodat 5.0 software packageSPSS software package

Authors

Sue Tobin BHSc MCSP isa physiotherapist at theRoyal LiverpoolUniversity Hospital. Thisis an abridged version of her dissertation, which

was submitted in parialfulfilment of the BHScphysiotherapy course at the University of Leeds.

Gill Robinson MCSPDipTP is a seniorlecturer, Division of Physiotherapy, School of Human and HealthSciences, University of

Huddersfield HD1 3DH.She was the project supervisor.

This article was receivedon February 22, 1999,and accepted onDecember 2, 1999.

Address forCorrespondence

Miss S Tobin BHSc MCSP.Physiotherapy Department, RoyalLiverpool University Hospital. Prescot Street,Liverpool L7 8XP.



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Procedure Areas required for electrode placement wereshaved, lightly abraded with sandpaper andcleaned with acetone to reduce impedance(Kumar and Mital, 1996).

Active electrodes for VL and VMO wereplaced parallel to each other with an inter-electrode distance of 1 cm (Herrington andPayton, 1997), and orientated according toLieb and Perry (1968) ie 15˚-18˚ to thefemoral axis for VL and 46˚-52˚ for VMO.For VL, the distal edge of the distalelectrode was placed four fingerbreadthsfrom the superolateral edge of the patella(Delagi et al , 1975; page 192). Correct

electrode position was confirmed by palpation during quadriceps contraction with and without hip flexion to exclude therectus femoris (Cerny, 1995). For the VMO,the distal edge of the distal electrode was

placed 2 cm from the superomedial borderof the patella. Correct electrode position wasconfirmed by palpation during quadricepscontraction with and without hip adductionto distinguish between the VMO and the

vastus medial is longus (Bose et al , 1980).Ground electrodes for both muscles were

placed over convenient, electrically independent bony landmarks (Worrell et al ,1995). For the VL, the head of fibula wasdeemed appropriate, and for the VMO it wasthe anterior tibial shaft.

EMG ProcedureEach set of electrodes was connected to a 4 kpre-amplifier, and following the advice of Ortengren (1996) were taped to the skin to

reduce movement-related artefacts. The gainfor each channel was x 1, and the signal (viathe telemetry belt) was calibrated on theoscilloscope of the base unit before every test. The sampling frequency was 400 Hz.

StandardisationTwo lines were drawn on each subject’s leg,one between the anterior superior iliacspine (ASIS) and the tibial tubercle toapproximate the line of rectus femoris, andthe other between the greater trochanter

and the fibular head to approximate the lineof the iliotibial tract. These lines served tooutline VL. Finally, the halfway point of the

ASIS-tibial tubercle line was marked (fig 2). All tape was applied with the subject in non-dominant side lying with a pillow betweenthe knees.

Fixomull ApplicationThe same procedure was used for both theplacebo and active tape conditions. Threepieces of tape were cut to a length that overlapped the outlined VL transversely by about 2 cm. All strips were applied across VL

without tension or wrinkles. The distal edgeof the first piece was aligned with thehalfway mark on the ASIS-tibial tubercle line(fig 2).

The second and third pieces were thenapplied proximal to their predecessors,overlapping them by half the width (fig 3).

Active Leukotape ApplicationThree pieces of tape were cut to a lengththat failed to span the VL markings by about

2 cm. The following procedure is from theinstructions McConnell gives on page 40 of her 1995 course handbook: ‘Apply a piece of tape to the anterior thigh. Firmly pull thetape laterally and posteriorly while collecting

Fig 2: Tape standardisation lines

Fig 3: Application of three pieces of Fixomull ®




the lateral thigh tissues with the other hand. Attach the tape to the posterolateral thigh ina horizontal direction.’

The first piece was applied proximal to thedistal edge of the underlay to ensure there

was no direct skin contact (fig 4) The secondand third pieces were applied in the same

way, each overlapping its predecessor by half the width (fig 5). The desired effect was afurrow running down the VL.

Placebo Leukotape ApplicationThis procedure mirrored that of the activetape with the exception that the placebotape was applied without tension and

without movement of the tissues.

Testing ProtocolFollowing the application of the appropriatecondition, each subject was asked to stand at the top of the designated stairs, the samestairs being used throughout testing.Instructions given to each subject beforeeach descent were standardised as follows:

Descend the stairs normally.Do not use the handrails.Step first with the non-dominant leg.Stand still on reaching the bottom of the

stairs. A ‘3 – 2 – 1 – Go’ cue to start.

No further communication occurred untilthe descent was completed to avoiduncontrolled extraneous variables.

Each subject completed three descents foreach condition, after which any tape wasimmediately removed. Subjects rested for aminimum of five minutes before beingprepared for their next condition.Electrodes remained in place throughout the session.

Treatment of Raw EMG TracesMYODAT 5 0 software was used to full-waverectify and envelope the raw EMG traces,rendering the data less susceptible to errorand more reliable than the raw traces(Boucher et al , 1992). The start and finish of each descent was identified and theintervening portion of data was used foranalysis.

Results

SPSS was used to calculate the mean elec-trical activity for each muscle, per subject,per test, for each of the experimental con-ditions. By averaging three mean values persubject, per condition, one figure was

obtained to represent the activity of eachmuscle. The modified data were used forthe descriptive and inferential analysis.

Descriptive StatisticsTable 2 and figure 6 (overleaf) reveal a cleartrend in VL activity under each test condition. Taking the no tape condition asthe baseline, there was an increase in activity after application of the placebo tape, 421.89mv to 489.15 mv (an increase of 16%). Afterapplication of the active tape, VL activity fellfrom 42l.89 mv to 239.l8 mv (a decrease of 43%). Possible implications are highlightedin the discussion.

Table 3 and figure 6 indicate that the

trend in VMO activity mirrors that of VL.There was an increase in activity after theapplication of the placebo tape, 502.56 mv to 528.50 mv (an increase of 5%). Afterapplication of the active tape, VMO activity

Fig 4: Application of first piece of Leukotape ®

Fig 5: Application of three pieces of Leukotape ®



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fell from 502.56 mv to 415.20 mv (adecrease of 19%). Although this trend wasunexpected, possible explanations areproposed in the discussion.

Although trends in VL and VMO activity are similar, figure 6 illustrates that activetape disrupted VL:VMO balance. Under notape and placebo tape conditions, the height of the bars reveals that the ratio wasapproximately 1:1. However, under theactive tape condition, decrease in VL activity

was considerably greater than that of VMO.This indicates that VL:VMO balance wasinfluenced in favour of VMO. Possibleimplications are again addressed in thediscussion.

Ranges for VL and VMO activity are

surprisingly large, even allowing forindividual variability and it is possible that some extremely high scores unduly influenced inter-subject ranges. Thispossibility is given further credence by thepercentile values. The differences betweenthe 25th and 50th percentiles for both VLand VMO are considerably smaller thanthose between the 50th and 75th percentiles.

As the percentiles reflect the distance fromthe median with respect to a distributioncurve (Polgar and Thomas, 1995, page 214),

it can be seen that the data are ‘top-heavy' whi ch cou ld be an ind icat ion of theinfluence of extreme scores.

There are large differences between meanand median values for both VL and VMOunder each condition (tables 2 and 3). Thisindicates that the data are abnormally distributed (Polgar and Thomas, 1995,page 226).

Var iance be tw ee n the co nd it io ns an dabnormal distribution of the data renderedparametric analysis inappropriate.

Table 2: Descriptive statistics for VL and VMO

Subject No tape Placebo tape Active tape

Vastus lateralis

1 272.23 210.10 160.66

2 428.96 445.20 727.93

3 1119.97 976.94 558.54

4 21.716 254.97 177.30

5 636.82 808.97 314.65

6 249.35 223.30 160.50

7 1213.17 1934.10 213.12

8 254.08 378.28 157.88

9 630.32 558.35 179.89

10 102.63 123.08 90.78

11 211.64 222.24 196.68

12 188.91 361.98 200.22

13 401.01 391.42 234.15

14 296.89 350.06 232.45

15 234.27 268.74 151.68

16 366.10 408.46 172.26

17 468.70 704.32 275.46

18 111.77 184.22 101.11

Vastus medialis obliquus

1 322.543 266.85 251.90

2 453.39 435.72 403.03

3 504.67 338.55 492.17

4 385.98 422.96 386.86

5 728.31 831.18 790.01

6 318.01 356.75 340.01

7 1858.97 1876.12 230.508 335.09 350.37 362.63

9 617.39 694.75 661.04

10 139.71 170.74 136.36

11 198.58 233.31 202.72

12 330.40 377.28 363.64

13 381.42 362.43 378.72

14 954.01 858.66 899.90

15 297.66 685.59 444.23

16 373.91 363.03 305.88

17 658.51 677.86 627.63

18 176.51 211.87 195.41

100

VL VMONo tape Active tapePlacebo tape

VL VMO VL VMO

200

300

400

500502.56

489.15

528.50

239.18

415.20421.89

E l e r c t r i c a

l a c t i v i t y

( m i l l i o n s )

Fig 6: Overall mean values for VL and VMO




Inferential StatisticsThe data were subjected to a Friedman test,

and as no post hoc test is associated with theFriedman, the data were subjected to furtherinvestigation with Wilcoxon tests (table 4).

Descriptive statistics revealed that VL and VMO acti vi ty fo llowed simila r tr ends of difference between the conditions. With theaccepted probability level of α = 0.05, theFriedman test on VL indicated that one of the differences was significant. Wilcoxontests then established that the active tapecondition was responsible. It can beconcluded that application of McConnell's

VL inh ibi tion taping tec hn iqu e didinhibit VL. Wi th re sp ect to VM O ac tivity, the

Friedman test was insignificant, but there was a significant difference found by one of the Wilcoxon tests. However, if it is acceptedthat the no tape condition represented thebaseline activity level, the significant difference was uncovered only after VMOactivity had been elevated under theinfluence of the placebo tape condition.Consequently, relevance of this result isquestionable.

DiscussionThis study was conducted to investigate theeffects of McConnell's VL taping techniqueon VL and VMO activity. Results can besummarised thus:

Activity of the VL and VMO increasedunder the placebo tape condition.Neither of these increases was statistically significant.

Activity of the VL and VMO decreasedunder the active tape condition. Thedecrease in VL activity was statistically significant, but the decrease in VMOactivity was not.

In view of the dearth of relevant literature,these results cannot be related to otherstudies.

Increased VL activity under the placebotape condition is unsurprising given thecutaneous stimulation provided by the tape.Kandel et al (1991, page 586) confirm that cutaneous stimulation can elicit reflexcontraction of the muscle underlying thearea of stimulation. Kandel et al (1991, page587) also identify an indirect effect. They report that cutaneous stimulation reducesthe threshold of the motor neurones in theunderlying muscle, thereby making themeasier to excite and motor units easier torecruit. Both these mechanisms wouldmanifest themselves as increased electricalactivity within the muscle, hence theelevated EMG.

Explanation for increased VMO activity under the placebo tape is less apparent. Thelack of cutaneous stimulation renders theabove mechanisms irrelevant. It could bethat increased VMO activity represents areaction to increased activity of the VL. Thisis suggestive of an inherent capacity tocounter the creation of muscle imbalance

wi th in the quad riceps , wh ich ra ises the

intriguing question of why this mechanismthen fails, as it appears to in PFPS. Thedebate regarding quadriceps imbalancebeing a primary or secondary occurrence inPFPS was identified in the introduction. The

Table 3: Ranges of activity for VL and VMO

Condition Mean Median SD Variance Range Percentile 25th 50th 75th

Vastus lateralis

No tape 421.89 331.50 311.28 96894.11 1110.54 215.78 331.50- 508.23Placebo tape 419.15 370.13 426.70 182070.10 1811.02 223.04 370.13 594.84Active tape 239.18 188.29 159.32 25381.39 637.15 158.85 188.29 244.48

Vastus medialis obliquusNo tape 502.56 377.67 396.47 157184.62 1719.26 312.92 377.67 627.67Placebo tape 528.50 370.16 396.29 157043.52 1705.38 320.63 370.16 687.13Active tape 415.20 371.18 209.45 43870.42 763.62 246.55 371.18 526.04

Table 4: Inferential analysis

Muscle Condition Friedman test Wilcoxon test

VL No tape vs placebo tape vs active tape P < 0.05 Not applicableVMO No tape vs placebo tape vs active tape P > 0.05 Not applicableVL No tape vs placebo tape Not applicable P > 0.05VL No tape vs active tape Not applicable P < 0.05

VL Placebo tape vs active tape Not applicable P < 0.05

VMO No tape vs placebo tape Not applicable P > 0.05VMO No tape vs active tape Not applicable P < 0.05VMO Placebo tape vs active tape Not applicable P < 0.05



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apparent ability of the VMO to respond toan increase in VL activity in asymptomaticindividuals could indicate that quadricepsimbalance requires some factor(s) toprecede it, thereby supporting the secondary feature theory.

It was proposed that stimulation of thetype IV nociceptors could have a direct inhibitory effect on the VL. Following theapplication of the active tape, there wasimmediate decrease in VL activity asdetected by the EMG. This suggests that theproposed mechanism may well have beenemployed, ie the inhibition of the alphamotor neurones for the VL via the C-fibreafferents and local inhibitory interneurones.

Although this circui t appears feasible, as

involvement of higher centres or othermechanisms is unknown, its influencecannot be assumed.

The explanation for the VMO response isagain less clear. It can be approached fromtwo ways: why VMO activity did not increase,and why it actually decreased. Twomechanisms, which could increase VMOactivity, were proposed in the introduction:

The biomechanical/physiological mech-anism involved adaptive tissue changes. Assubjects in this study were asymptomatic,their VMOs were unlikely to be elongatedand therefore had little potential toshorten and increase cross-bridgeformation. Such tissue changes would alsorequire several days to become apparent.Thus, the possible involvement of thismechanism was not addressed by thisstudy, and cannot therefore be dismissed.The neurological mechanism wasaddressed and it can be concluded that it is unlikely to feature in increasing VMOactivity, certainly in asymptomaticsubjects. If the C-fibre afferents from the

VL had formed an excitatory circuit withthe alpha motor neurones of the VMO,EMG would have reflected increasedelectrical activity in the VMO, which didnot happen.

The VMO response is indicative of aninherent capacity to react to the activity level of VL. Boucher et al (1992) foundthat the VMO:VL ratio was disrupted inPFPS, but in asymptomatic individuals,

although activity levels of both muscleschanged during knee movement, theratio stayed constant. Therefore, assubjects in this study were asymptomatic,it is possible that the fall in VMO activity

represented an attempt to keep the VMO:VL balance in equilibrium. It canalso be explained as a reaction to thereduced load placed on the VMO. By inhibiting the VL, the VMO had lesslateral force to resist which would requirefewer motor units to be recruited. This

wou ld ma nifest itse lf as decr eas edelectrical activity, which reflects theEMG recordings from this study.

Limitations and RecommendationsThe design of this study did have some

weaknesses, such as failing to control thespeed of each stair descent. Although suchcontrol would have reduced the normality of the activity, speed is a variable that can

influence muscle activity (MacIntyre andRobertson, 1992). This lack of control may have influenced results. There was a lack of standardisation of the resting intervalsbetween individual tests and betweenexperimental conditions. Nevertheless,the minimum resting interval betweenconditions and the counterbalancing of thetesting order may have ensured that these

weaknesses were not materially detrimentalto this study.

The size and nature of the sample have

implications for what can be inferred fromthe findings of this study. The sample beingsmall and convenient limits the populationto which the results can be confidently applied.

This taping technique is designed toaddress the problem of quadricepsimbalance. Voight and Weider (1991) foundthat VL contractions were faster andstronger in PFPS, implying that something

withi n or con tro lling the mus cl e hadchanged. As the aetiology of this muscleimbalance is not understood, it cannot beassumed that the quadriceps of asymptomatic subjects will respond in thesame way as those of symptomaticindividuals. Consequently these experimentsneed to be carried out on people with PFPSto increase their clinical relevance.

EMG measurements are accepted as anappropriate assessment of muscle activity (Kumar and Mital, 1996). However, there issome debate about the sensitivity of surfaceelectrodes and their potential forcontamination by cross talk. The author

believes that as the activity level changesfor VMO and VL differed, the surfaceelectrodes used in this study were sensitiveenough to distinguish between the twomuscles. Whether they were able to




differentiate between VMO and vastusmedialis longus is uncertain. Although the

VMO electrodes could have been detectingthe activity of vastus medialis as a whole, thedocumented placement of these electrodesmay have ensured that VMO provided themajor contribution to the EMG recordings.

Accordingly, it is appropriate to accept theserecordings as reflective of VMO activity.

It is possible that there was inconsistency in application of the tape, especially as thetension and pressure were not standardised.This inconsistency may explain why somesubjects did not show VL inhibition afterapplication of the active tape. Although theoverall decrease in VL activity was highly significant, influence of this variable cannot

be determined.Sample size and poor external validity mean that extreme caution must be used

when making recommendations from thisstudy. However, the results do suggest that this taping technique has the potential to bebeneficial in correction or prevention of quadriceps imbalance. Irrespective of

whether th is technique faci li ta te s VMOactivity, it may have a role in intervention forquadriceps imbalance. Provided VL activity is reduced more than any decrease in the

VMO, the imbalance is still being redressed.In order to evaluate the adaptive shorteningtheory proposed as a mechanism by which

VL inhibition could in fact facilitate VMO,future studies should be of sufficient duration for such changes to occur.

If this technique had a similar effect on VLactivity in a patient population, it may bethat a case can be made for using it in most quadriceps rehabilitation, either as aprophylactic or a correctional measure formuscle imbalance. If so, this technique has ahuge advantage over McConnell's patellartaping techniques. Cerny (1995), and

Fitzgerald and McClure (1995) are amongthose who have identified poor inter-raterand intra-rater reliability in the assessment of patellar position, which has implicationsfor selection of the appropriate realignment technique. As the VL technique requiresonly the identification of VMO insufficiency,it appears reasonable to expect that it wouldbe associated with higher inter-rater andintra-rater reliability, thereby increasing theappropriateness of selection technique andthe chances of a successful outcome.

A major recommendation resulting fromthis study is that a comprehensive review of quadriceps rehabilitation is needed. Asdiscussed previously, the principle behindmost quadriceps programmes is general re-

strengthening. However, as Harms-Ringdahl(1993) acknowledges, muscle imbalancemay pose a more potent threat to joint function and protection than simplemuscle weakness. Traditional quadricepsprogrammes do not account for thedifferent functions and training needs of thecomponents, so how they can restoreoptimal quadriceps interaction is unclear.

ConclusionIt seems that McConnell's VL inhibition

taping technique has the potential to be of considerable clinical value. This study foundthat application of this technique didsignificantly decrease VL activity. VMOactivity also fell but not by a statistically significant amount. This suggests that activity levels of the component quadricepscan be manipulated with respect to eachother, which has implications for lower limbrehabilitation, especially where quadricepsimbalance is present or may develop. Toapply these results safely to a clinicalcontext, research involving symptomaticindividuals is needed.

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Key Points

There is a need for physiotherapists tore-examine their approach to quadricepsrehabilitation and muscle specificity.

It is possible to inhibit the activity of the

vastus lateralis.

Vastus medius obliquus and vastuslateralis imbalance may be addressedmore effectively by inhibition of the VLbefore VMO rehabilitation.

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19, 2, 131-137. Witvrouw, E, Sneyers, C, Lysens, R, Victor, J andBellemans, J (1996) . ‘Reflex response times of

vastus medialis obliquus and vastus lateralis innormal subjects and subjects with patellofemoralpain syndrome’, Journal of Orthopaedic and Sports Physical Therapy , 24, 3, 160-165.

Worrell, T W, Connelly, S, and Hilvert, J (1995) .‘VMO: VL ratios and torque comparisons at fourangles of knee flexion’, Journal of Sport Rehabilitation , 4, 4, 264-271.

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