Quadriceps Weakness, Atrophy, and

Activation Failure in Predicted Noncopers

After Anterior Cruciate Ligament Injury
Glenn N. Williams,* PT, PhD, Thomas S. Buchanan,* PhD, Peter J. Barrance,* PhD,
†‡ †§
Michael J. Axe,* MD, and Lynn Snyder-Mackler,* PT, ScD
From the *Center for Biomedical Engineering Research, University of Delaware, Newark,
†
Delaware, the Department of Physical Therapy, University of Delaware, Newark, Delaware,
‡
and First State Orthopaedics, Newark, Delaware

Background: Quadriceps weakness is common after anterior cruciate ligament injury, especially in those who do not compen-
sate well for the injury (“noncopers”). Both atrophy and activation failure have been demonstrated in this population but have
not been directly related to quadriceps weakness.
Hypotheses: (1) Quadriceps strength, volumes, and cross-sectional areas of the noncopers would be smaller than those of the
contralateral muscles, whereas other muscles would not demonstrate atrophy. (2) Quadriceps muscle activation deficits would
be observed. (3) Atrophy and activation failure would account for the quadriceps weakness in these patients.
Study Design: Cross-sectional study, Level of evidence, 3.
Methods: Seventeen noncopers with isolated anterior cruciate ligament injury underwent burst-superimposition strength and
activation testing of the quadriceps and magnetic resonance imaging of 12 muscles an average of 2 months after injury.
Morphological characteristics was described by digitally reconstructing each muscle from the axial images and calculating mus-
cle volume and peak cross-sectional area.
Results: The quadriceps muscles of the anterior cruciate ligament–deficient limb were significantly weaker (average 25%) than
those of the uninjured side; activation failure (8%-10%) was observed for the quadriceps muscles of both limbs. The total
quadriceps, vastus lateralis, and vastus intermedius volume and cross-sectional area were significantly smaller in the anterior
cruciate ligament–deficient limb. There was no significant atrophy of any other muscle or muscle group. Atrophy and activation
failure explained more than 60% of the variance in quadriceps weakness (P = .004).
Conclusion: The quadriceps femoris weakens soon after acute anterior cruciate ligament injury. Activation deficits and atrophy
occur and affect quadriceps strength. Rehabilitation techniques that address activation deficits as well as atrophy may be nec-
essary to restore quadriceps strength.
Keywords: knee; morphology; inhibition; athletes

Quadriceps femoris muscle weakness is common after
ACL rupture in people who do not compensate well for the
injury (“noncopers”).3 Evidence suggests that there may be
an important neurosensory connection between the ACL and
the quadriceps muscles that is disrupted when the ACL is
§
Address correspondence to Lynn Snyder-Mackler, PT, ScD, Center
for Biomedical Engineering Research, Department of Physical Therapy,
301 McKinly Lab, University of Delaware, Newark, DE 19716 (e-mail:
smack@udel.edu).
No potential conflict of interest declared. See Acknowledgment for
funding information.
The American Journal of Sports Medicine, Vol. 33, No. 3
DOI: 10.1177/0363546504268042
© 2005 American Orthopaedic Society for Sports Medicine
ruptured.10,12,13 Loss of feedback from mechanoreceptors in
the ACL may result in chronic suppression of recruitment
of high-threshold motor units during voluntary contrac-
tion of the quadriceps, presumably via elimination of feed-
back from the ACL to gamma motor neurons.12 There is
indirect evidence in support of these findings in studies of
quadriceps atrophy and failure of voluntary activation
after ACL injury.11 Atrophy alone may not account for the
loss of muscle strength (eg, peak torque or force measure-
ments) demonstrated after ACL rupture. Most studies
have shown a lack of correlation between quadriceps
femoris muscle cross-sectional area (CSA), morphological
measures, and muscle strength in ACL-deficient
patients,4,9,17 although there have been no recent studies of
the morphological characteristics of the quadriceps after

402
Vol. 33, No. 3, 2005 Quadriceps Weakness, Atrophy, and Activation Failure in Noncopers
ACL rupture. Even though muscle force and CSA are
strongly and directly related in studies of healthy muscle,
muscle volume appears to be better related to muscle
torque, the measured strength variable in most studies
and in the clinic.7 Perhaps the calculation of muscle vol-
ume would allow for a more accurate prediction of the con-
tribution of atrophy to muscle weakness.
Studies of quadriceps activation after ACL rupture have
demonstrated significant impairment of voluntary activa-
tion (inhibition), suggesting that a major consequence of
ACL rupture is altered motor unit utilization, which pre-
sumably results in atrophy.1,23 Konishi et al14 have demon-
strated abnormal gamma loop function in the involved and
uninvolved quadriceps femoris muscle of patients with
ACL rupture. Recent reports have demonstrated bilateral
activation deficits after ACL injury.1,14 Adjusting con-
tralateral knee strength for activation and considering the
activation of the involved quadriceps may allow for a more
accurate assessment of the relative contribution of atro-
phy and activation failure to the quadriceps weakness that
occurs after ACL rupture.
The purpose of this study was to characterize the mus-
cle weakness, atrophy, and failure of voluntary activation
after acute, isolated, complete ACL rupture in active non-
copers after range of motion is restored and impairments
are resolved. We hypothesized that the quadriceps
strength measures, volumes, and CSAs would be smaller
than those of the contralateral muscles and that the other
muscles would not demonstrate atrophy. We also hypothe-
sized that there would be activation deficits in the quadri-
ceps and that atrophy and activation failure would
account for a significant portion of the quadriceps weak-
ness in these patients.
MATERIALS AND METHODS
Subjects
Seventeen subjects with ACL deficiency who were classi-
fied as noncopers volunteered to participate in this study.
All had been regular participants in activities that chal-
lenge the stability of the knee joint, such as basketball,
volleyball, and skiing, before sustaining their ACL
injuries. The group included 13 male and 4 female partici-
pants ranging in age from 15 to 45 years (mean = 24.3 ±
10.8 years). All ACL tears were diagnosed by a sports fel-
lowship–trained orthopaedic surgeon and had been con-
firmed by MRI, knee arthrometry, and, subsequently,
direct visualization during ACL reconstructive surgery.
The noncopers were identified using an established
screening examination that differentiates people who may
be able to cope with an ACL injury from those who will not
be able to cope by using hop testing and self-report ques-
tionnaires.5 This examination differentiates potential cop-
ers from noncopers with a high degree of accuracy.5
Prerequisites for this screening examination included (1)
the resolution of physical and functional impairments
such as joint effusions, gait abnormalities, and range of
motion deficits; and (2) the ability to hop on 1 leg without
403
pain.22 (All of the subjects had been enrolled in a preoper-
ative rehabilitation program designed to control impair-
ments in preparation for surgery.6) Enrollment exclusion
criteria included a previous ACL injury, concomitant liga-
ment abnormality, fractures, knee joint effusion, an abnor-
mal gait pattern, and the presence of hip or ankle abnor-
mality. All predicted noncopers were required to have
recent ACL injuries to prevent confounding effects from
chronic knee instability (mean ± SD duration = 3.2 ± 2.0
months; range, 0.5-6.0 months). The mean scores on the
screening examination (timed hop scores: 89% ± 11%;
Knee Outcome Survey–Activities of Daily Living Scale
score: 81.5% ± 11%; global rating of knee function: 61% ±
15%; and episodes of giving way: 4 ± 2) demonstrate that
the noncopers were indeed suffering from repetitive knee
instability and poor function. This study was approved by
the University of Delaware Human Subjects Review
Committee, and all subjects provided signed informed con-
sent forms for participation.
Evaluation of Muscle Strength and Activation
Injured- and uninjured-side quadriceps strength and acti-
vation were assessed by maximal voluntary isometric con-
traction (MVIC) using the burst-superimposition
method.22 Subjects were seated on a KIN-COM
dynamometer (Chattanooga Corporation, Hixson, Tenn)
with their hips and knees positioned in 90° of flexion.
Velcro® straps were used to secure the distal shank to the
dynamometer force arm and the thigh and pelvis to the
device’s chair. After the area was cleansed with sterile
alcohol, 6 cm × 8 cm self-adhesive electrodes used to deliv-
er the electrical stimulus during testing were placed over
the vastus lateralis and vastus medialis muscle bellies.
After a 5-minute rest, quadriceps strength testing
began. The subjects performed a 5-second maximum effort
contraction during which a supramaximal, 10-pulse (600
µs, 130 V), 100 pulses per second train of electrical stimu-
lation was delivered to the muscle to assess muscle activa-
tion level (ie, burst-superimposition technique). With a
maximal contraction, no increase in force is elicited by the
burst. If a subject was unable to activate the quadriceps
muscle fully (ie, the burst augmented the force by more
than 5%), MVIC testing was repeated up to 2 additional
times. The maximal voluntary force recorded during the 3
tests was used in the analysis. Each attempt at achieving
an MVIC was separated by at least 5 minutes to minimize
the effects of muscle fatigue on test performance. Custom
software programmed in LabView (National Instruments,
Austin, Tex) was used to identify the maximal force during
the volitional effort contraction and the force attributable
to the electrical burst.
A quadriceps index was calculated using the following
formula: (injured-side force/uninjured-side force) × 100.
Volitional activation was estimated using the central acti-
vation ratio (CAR) defined by Kent-Braun and Le Blanc.11
The CAR is calculated by dividing the maximum voluntary
force by the total force (including any force augmentation
from the burst). A CAR of 1.0 signifies complete activation.
404 Williams et al
Evaluation of Muscle Morphological Characteristics
Axial spin-echo T1-weighted MRI images were acquired
from the level of the ankle mortise to the iliac crest while
subjects lay supine in a 1.5-T SignaLX scanner (General
Electric Medical Systems, Milwaukee, Wis). The images
were acquired in 4 sequences: lower leg, knee, thigh, and
pelvis. Both limbs were imaged simultaneously using the
scanner’s body coil. The imaging protocol was as follows:
repetition time (TR) = 350 milliseconds, echo time (TE) = 9
milliseconds, slice thickness = 10 mm (except in the knee
section where it was 5 mm to acquire more detailed tendon
data), gap between slices = 1.5 mm (except in the knee sec-
tion where it was 1.0 mm), with a 256 × 160 matrix and a
field of view that varied with subject size.
The muscle volume and peak CSA of 12 muscles were
evaluated by digitally reconstructing each muscle from the
MRI images. The muscles studied included the hamstring
muscle group (semitendinosus, semimembranosus, biceps
femoris–long head, and biceps femoris–short head),
quadriceps muscle group (vastus lateralis, vastus medi-
alis, rectus femoris, and vastus intermedius), sartorius,
gracilis, and the medial and lateral gastrocnemius mus-
cles. In addition to evaluating the 12 individual muscles,
we assessed the characteristics of the total quadriceps and
total hamstrings muscle groups. Muscle shape was digital-
ly reconstructed by tracing the outer margin of each mus-
cle in each axial image in which it was present using a dig-
itization tablet (Intuos2, Wacom Technology Corp,
Vancouver, Wash) and IMOD software (University of
Colorado, Boulder, Colo).15 The contours of each muscle
were then grouped and used to build patient-specific triangle-
based mesh surface models using Nuages software
(INRIA, Sophia-Antipolis, France).8 All digitization was
performed by a single rater who demonstrated a high
degree of reproducibility in a preliminary test-retest relia-
bility study including ACL-deficient and uninjured sub-
jects (n = 8; intraclass correlation coefficients ranged from
0.951 to 0.998 for the 12 muscles studied). Muscle volumes
were calculated using subroutines from the Visualization
Toolkit (Kitware Inc, Clifton Park, NY).21 The proximal
and distal tendons of the muscles were excluded from the
analyses of muscle volume to obtain measurements that
more precisely described the volume of contractile tissue
present. The peak CSA of each muscle was calculated by
first transforming the contours of each muscle from pixel
coordinates to physical coordinates (millimeters) using
parameters from the MRI header and then running a
trapezoidal integration algorithm that calculated the area
encompassed within each contour (plane). The contour of
each muscle with the greatest plane area defined its peak
CSA.
Data Management and Analysis
Uninvolved quadriceps MVIC was adjusted for activation
level to create a valid quadriceps index.1,23 The values of
the uninvolved limb were compared to ACL-deficient limb
muscle strength, activation, CSAs, and volumes using
paired t tests with Bonferroni correction; the adjusted sig-
The American Journal of Sports Medicine
nificance level (α) was .0084. Multiple linear regression
was used to assess the effect atrophy (volume and CSA)
and activation of the quadriceps on quadriceps weakness.
A priori statistical power to detect a difference of 5% in
volume and CSA given the variances of our pilot subjects
using paired samples tests gives a power of >0.9 for our
sample size (17) and the adjusted P value of .0084. The
suggested sample size from the a priori tests for a power of
0.8 was between 9 and 15 subjects depending on the muscle.
RESULTS
There was no significant difference (P = .039) between the
CARs of the ACL-deficient limb (.90 ± .09) and uninjured-
limb (.92 ± .06) quadriceps muscles. The quadriceps mus-
cles of the ACL-deficient limbs (mean = 1096.85 ± 279.76 N)
were significantly weaker (P < .001) than those of the
uninjured limbs (mean = 1482.06 ± 346.65 N). The average
quadriceps index was 75% ± 12%. The vastus lateralis, vas-
tus intermedius, and total quadriceps volumes (P < .001,
P = .007, P < .001, respectively) and CSAs (P = .001, P =
.001, P < .001, respectively) from the ACL-deficient limbs
were significantly smaller than the respective values from
the quadriceps muscles of the uninjured limbs (Table 1,
Figures 1 and 2). There was no difference in the CSAs or
volumes of any other muscle (Table 1).
The variance in quadriceps weakness was significantly
accounted for by activation deficit and atrophy measured
by total quadriceps CSA (R2 = 0.623, P = .005). The vari-
ance in quadriceps weakness was also significantly
accounted for by activation deficit and atrophy measured
by total quadriceps volume (adjusted R2 = 0.650, P = .004)
(Figure 3).
DISCUSSION
Our hypotheses that the involved-side quadriceps volume
and CSA would be smaller than in the uninvolved knee
were partially supported by the results. Total quadriceps
volume and CSA were indeed smaller, but the atrophy was
not uniform across the heads of the quadriceps. The vastus
lateralis and vastus intermedius were disproportionately
affected. The vastus medialis and rectus femoris were not
significantly atrophied compared to the uninvolved side.
Both the involved and uninvolved quadriceps demonstrated
lower activation levels than reported in the literature for
young, active subjects without knee injury. There was no
difference in activation between the 2 sides. Atrophy (as
measured by CSA or volume) and activation accounted for
more than 60% of the variance in quadriceps weakness.
This relationship was significant.
Despite conventional clinical wisdom that the vastus
medialis is the quickest of the heads of the quadriceps to
atrophy, the medialis was not significantly affected.
Rather, the vastus lateralis and intermedius were pro-
foundly atrophied. The vastus lateralis and intermedius
are the largest of the quadriceps muscles, which may make
them more vulnerable to the results of neural disruption
that occurs when the ACL is ruptured. There is recent evi-
Vol. 33, No. 3, 2005 Quadriceps Weakness, Atrophy, and Activation Failure in Noncopers 405

TABLE 1
Muscle Volumes and Peak Cross-Sectional Areasa (N = 17)

Uninjured ACL Deficient P

Peak Peak Peak
Muscle(s) Volume CSA Volume CSA Volume CSA

Total quadriceps group 1673.64 ± 345.60 87.34 ± 12.95 1526.94 ± 354.63 79.57 ± 12.90 <.001 <.001
Vastus lateralis 592.81 ± 137.03 29.66 ± 5.68 516.06 ± 146.32 26.23 ± 5.98 .007 .001
Vastus intermedius 465.40 ± 93.26 23.41 ± 3.50 431.73 ± 99.74 21.42 ± 3.79 <.001 .001
Vastus medialis 386.68 ± 94.90 22.08 ± 3.65 358.98 ± 83.58 20.02 ± 3.51 NS NS
Rectus femoris 228.75 ± 56.05 12.19 ± 2.37 220.17 ± 56.99 11.90 ± 2.42 NS NS
Total hamstring group 606.26 ± 133.89 40.51 ± 6.58 608.43 ± 125.87 40.21 ± 5.91 NS NS
Semimembranosus 203.48 ± 55.89 12.26 ± 2.86 203.99 ± 56.45 11.97 ± 2.56 NS NS
Semitendinosus 160.04 ± 51.89 9.59 ± 2.92 159.37 ± 43.27 9.60 ± 2.59 NS NS
Biceps femoris–long 177.29 ± 36.85 12.96 ± 2.29 174.04 ± 31.12 12.71 ± 2.04 NS NS
Biceps femoris–short 65.46 ± 22.62 5.69 ± 1.50 71.03 ± 26.82 5.94 ± 1.37 NS NS
Gracilis 63.41 ± 13.62 3.51 ± 0.66 67.34 ± 20.89 3.71 ± 1.01 NS NS
Sartorius 87.81 ± 26.57 2.84 ± 0.69 91.03 ± 25.34 2.95 ± 0.68 NS NS
Medial gastrocnemius 207.55 ± 40.30 13.62 ± 2.64 209.41 ± 46.59 13.96 ± 3.00 NS NS
Lateral gastrocnemius 132.77 ± 27.75 12.15 ± 2.51 121.35 ± 25.59 10.45 ± 2.71 NS NS

Data are presented as mean ± SD. Units = muscle volume, cm3; peak CSA, cm2. CSA, cross-sectional area; NS, no significant difference
a

at the Bonferroni adjusted significance level, which was set at .0084.

rogate for the subject’s normal quadriceps strength, acti-

Figure 1. MRI cross sections of the thigh showing quadri-
ceps atrophy. The cross-sectional areas of the vastus later-
alis and vastus intermedius were significantly smaller in the
ACL-deficient legs (11.6% and 8.5%, respectively). RF, rec-
tus femoris; VM, vastus medialis; VL, vastus lateralis; VI, vas-
tus intermedius.
dence in animal models of a differential effect of ACL
injury on the various quadriceps muscles.18 Okuyama et al
have demonstrated increased oxidative stress and disrupted
antioxidant capacity by depression of heat shock pro-
teins—stress proteins that have protective antioxidant
properties—in the vastus lateralis and vastus medialis
but not the rectus femoris of rats after ACL resection.18
The implications for rehabilitation are large because the
focus on the vastus medialis may be misplaced.
There were small but significant alterations in volun-
tary activation in the quadriceps of the involved and unin-
volved knees; this is consistent with recent reports in the
literature and necessitates consideration when calculating
quadriceps indices.1,23 To use the uninvolved side as a sur-
vation level must be used to adjust the strength measures.
The unadjusted mean quadriceps index was 82%. When
calculated compared to the MVIC of the uninjured quadri-
ceps corrected for activation, the quadriceps index was
75%. Past research has failed to demonstrate a relation-
ship between atrophy and weakness of the quadriceps
after ACL rupture. Perhaps this has been both a direct and
indirect effect of failing to account for the effect of activa-
tion failure. Neither the direct effect of activation failure
on the involved quadriceps strength nor the indirect effect
of activation failure on the validity of the quadriceps index
has been estimated. Consequently, the present study was
able to demonstrate that atrophy as measured by either
peak CSA or volume combined with activation failure
accounted for more than 60% of the variance in the loss of
strength. Muscle volume and peak CSA appear to provide
similar, accurate information about atrophy.
Quadriceps weakness was profound in this population of
ACL-deficient noncopers. An average of 3 months after
incident injury, the average quadriceps strength was 75%
of that of the uninvolved quadriceps. All of the subjects
had been enrolled in a preoperative rehabilitation pro-
gram designed to control impairments in preparation for
surgery.6 Despite strengthening exercises, the subjects
were quite weak. Quadriceps weakness is a hallmark of
noncopers.3,19,20 Noncopers demonstrate aberrant gait pat-
terns that are strongly related to their quadriceps weak-
ness, which can persist after reconstruction.2,16
The results of this study have important implications for
rehabilitation and surgical planning. Because both atro-
phy and activation affect quadriceps strength, rehabilita-
tion specialists should employ techniques that address
activation deficits as well as atrophy in their efforts to
restore quadriceps strength. The extent of the quadriceps
406 Williams et al
Figure 2. Vastus lateralis of a noncoper. The solid muscle is
the involved side (left), but it is flipped left-to-right to look like
a right-side muscle and moved within the “mesh” model,
which is the right (uninjured side), to demonstrate muscle
volume change.
weakness and the rapidity with which it occurs should be
considered in planning surgical reconstruction in noncop-
ers after range of motion is restored and effusion is
resolved.
ACKNOWLEDGMENT
The authors acknowledge Terese Chmielewski, PT, PhD,
for her assistance in data collection, as well as Brandi
Dilks and Christine Tate for their help in acquiring and
digitally reconstructing the MRI images. This study was
funded by National Institutes of Health grants R01-
HD37985 (principal investigator, Lynn Snyder-Mackler)
and R01-AR46386 (principal investigator, Thomas S
Buchanan) and the Foundation for Physical Therapy
(Promotion of Doctoral Studies funding, Glenn N
Williams).
The American Journal of Sports Medicine
0.6
Actual Strength Deficit
0.5
0.4
0.3
0.2
0.1
0
0 0.1 0.2 0.3 0.4 0.5 0.6
Predicted Strength Deficit (activation and volume)
Figure 3. Predicted quadriceps strength loss plotted against
actual strength loss. The predicted strength deficit was cal-
culated from a regression of the quadriceps activation and
volume. The actual strength deficit was measured on a KIN-
COM dynamometer (Chattanooga Corporation, Hixson,
Tenn) during maximal voluntary isometric contractions using
the burst-superimposition method.
REFERENCES
1. Chmielewski TL, Stackhouse S, Axe MJ, et al. A prospective analysis
of incidence and severity of quadriceps inhibition in a consecutive
sample of 100 patients with complete acute anterior cruciate liga-
ment rupture. J Orthop Res. 2004:25;925-930.
2. DeVita P, Hortobagyi T, Barrier J. Gait biomechanics are not normal
after anterior cruciate ligament reconstruction and accelerated reha-
bilitation. Med Sci Sports Exerc. 1998;30:1481-1488.
3. Eastlack ME, Axe MJ, Snyder-Mackler L. Laxity, instability, and func-
tional outcome after ACL injury: copers versus noncopers. Med Sci
Sports Exerc. 1999;31:210-215.
4. Elmqvist LG, Lorentzon R, Johansson C, et al. Does a torn anterior
cruciate ligament lead to change in the central nervous drive of the
knee extensors? Eur J Appl Physiol Occup Physiol. 1988;58:203-207.
5. Fitzgerald GK, Axe MJ, Snyder-Mackler L. A decision-making
scheme for returning patients to high-level activity with nonoperative
treatment after anterior cruciate ligament rupture. Knee Surg Sports
Traumatol Arthrosc. 2000;8:76-82.
6. Fitzgerald GK, Axe MJ, Snyder-Mackler L. Proposed practice guide-
lines for nonoperative anterior cruciate ligament rehabilitation of
physically active individuals. J Orthop Sports Phys Ther.
2000;30:194-203.
7. Fukunaga T, Miyatani M, Tachi M, et al. Muscle volume is a major
determinant of joint torque in humans. Acta Physiol Scand.
2001;172:249-255.
8. Geiger B. Three-Dimensional Modeling of Human Organs and Its
Application to Diagnosis and Surgical Planning [PhD thesis].
Rocquencourt, France: Institut National de Recherche en
Informatique et Automatique; 1993.
9. Gerber C, Hoppeler H, Claassen H, et al. The lower-extremity mus-
culature in chronic symptomatic instability of the anterior cruciate lig-
ament. J Bone Joint Surg Am. 1985;67:1034-1043.
10. Johansson H, Sjolander P, Sojka P. Activity in receptor afferents from
the anterior cruciate ligament evokes reflex effects on fusimotor neu-
rones. Neurosci Res. 1990;8:54-59.
11. Kent-Braun JA, Le Blanc R. Quantitation of central activation failure
during maximal voluntary contractions in humans. Muscle Nerve.
1996;19:861-869.
Vol. 33, No. 3, 2005 Quadriceps Weakness, Atrophy, and Activation Failure in Noncopers
12. Konishi Y, Fukubayashi T, Takeshita D. Mechanism of quadriceps
femoris muscle weakness in patients with anterior cruciate ligament
reconstruction. Scand J Med Sci Sports. 2002;12:371-375.
13. Konishi Y, Fukubayashi T, Takeshita D. Possible mechanism of
quadriceps femoris weakness in patients with ruptured anterior cru-
ciate ligament. Med Sci Sports Exerc. 2002;34:1414-1418.
14. Konishi Y, Konishi H, Fukubayashi T. Gamma loop dysfunction in
quadriceps on the contralateral side in patients with ruptured ACL.
Med Sci Sports Exerc. 2003;35:897-900.
15. Kremer JR, Mastronarde DN, McIntosh JR. Computer visualization of
three-dimensional image data using IMOD. J Struct Biol.
1996;116:71-76.
16. Lewek M, Rudolph K, Axe M, et al. The effect of insufficient quadri-
ceps strength on gait after anterior cruciate ligament reconstruction.
Clin Biomech (Bristol, Avon). 2002;17:56-63.
17. Lorentzon R, Elmqvist LG, Sjostrom M, et al. Thigh musculature in
relation to chronic anterior cruciate ligament tear: muscle size, mor-
phology, and mechanical output before reconstruction. Am J Sports
Med. 1989;17:423-429.
407
18. Okuyama R, Honda M, Fujiya H, et al. Expression of heat shock pro-
tein 72 in rat quadriceps muscles following anterior cruciate ligament
resection. J Orthop Sci. 2003;8:213-217.
19. Rudolph KS, Axe MJ, Buchanan TS, et al. Dynamic stability in the
anterior cruciate ligament deficient knee. Knee Surg Sports Traumatol
Arthrosc. 2001;9:62-71.
20. Rudolph KS, Eastlack ME, Axe MJ, et al. Movement patterns after
anterior cruciate ligament injury: a comparison of patients who com-
pensate well for the injury and those who require operative stabiliza-
tion. J Electromyogr Kinesiol. 1998;8:349-362.
21. Schroeder W, Martin K, Lorensen B. The Visualization Toolkit. 2nd ed.
Upper Saddle River, NJ: Prentice Hall, Inc; 1997.
22. Snyder-Mackler L, De Luca PF, Williams PR, et al. Reflex inhibition of
the quadriceps femoris muscle after injury or reconstruction of the
anterior cruciate ligament. J Bone Joint Surg Am. 1994;76:555-560.
23. Urbach D, Awiszus F. Impaired ability of voluntary quadriceps activa-
tion bilaterally interferes with function testing after knee injuries: a
twitch interpolation study. Int J Sports Med. 2002;23:231-236.