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CLINICAL SCIENCES: Clinical Investigations

Multiaxis muscle strength in ACL deficient and reconstructed knees: compensatory mechanism

ZHANG, LI-QUN; NUBER, GORDON W.; BOWEN, MARK K.; KOH, JASON L.; BUTLER, JESSE P.

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Medicine & Science in Sports & Exercise: January 2002 - Volume 34 - Issue 1 - p 2-8
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Abstract

It is well known that quadriceps atrophy and strength reduction in knee extension occur after anterior cruciate ligament (ACL) reconstruction using the central third of the patellar tendon, and the strength deficit persists long after the reconstructive surgery (24,26,30,35). To a lesser degree, the hamstring muscles may also undergo strength loss following ACL reconstruction (19,30,34). For the ACL deficient and unrepaired knees, it was reported that there existed considerable strength deficit in the knee extensor and flexor muscles, especially in extension (3,8,11,15,20). Relatively weak quadriceps activities were also observed in the ACL deficient population during functional tasks such as locomotion (2,27). The reduction in quadriceps strength could be attributable to disuse, disruption of the patellar tendon, joint effusion, nonoptimal activation, or reflex inhibition (15,18,26,31,32). It may also reflect a compensatory mechanism adopted by the patients after ACL injury (2,4).

In contrast to the well-known strength reduction in knee extension and flexion following ACL injury and reconstruction, it is not clear how the injury and reconstruction affect muscle strength in tibial rotation and abduction-adduction. Few studies have been performed to study muscle strength in tibial rotation and abduction even in the normal population (13,28,38). Considering the orientation of the ACL inside the knee (connecting obliquely between the anteromedial portion of the tibial eminence and the posteromedial aspect of the lateral femoral condyle) and the considerable load exerted on the ACL by tibial internal rotation and adduction (1,12,16), muscle strength about the tibial internal-external rotation and abduction-adduction axes may be affected by ACL injury and surgical reconstruction considerably.

Shoemaker and Markolf studied knee internal-external rotation strength as a function of knee flexion, tibial rotation, and hip flexion angles in 20 normal subjects, and reported that subjects generally had stronger internal rotation strength than external rotation strength (28). Noyes et al. analyzed dynamic joint loading of the ACL deficient knee with varus alignment during level walking, and they reported abnormally high (external) adduction moment associated with high medial tibiofemoral compartment loads and high lateral soft tissue forces at the affected knee (21). It was also reported that contraction of thigh muscles reduced knee varus-valgus laxity drastically (17,22). In addition, a number of studies have been performed to determine hip rotation muscle strength (5,13) that often contributes to knee abduction-adduction strength. However, there is a lack of information on the lower limb muscle strength about the knee internal-external rotation and abduction-adduction axes following ACL injury and reconstruction. Strength changes about these axes may reflect mechanisms adopted by patients to compensate for ACL injury and reconstruction, and rehabilitation can be designed to improve multiaxis muscle strength to better compensate for ACL injury/reconstruction.

The purposes of this study were to evaluate isometric muscle strength about the knee internal-external rotation, abduction-adduction, and flexion-extension axes in chronic ACL deficient, acute ACL deficient, ACL reconstructed, and normal populations, and to gain insights into the associated compensatory mechanisms adopted by the patients. The hypothesis was that ACL deficient patients develop relatively more strength in tibial external rotation and in abduction, which would help unload/protect the ACL and avoid unstable knee positions. Furthermore, ACL reconstruction reduces such a need for compensation. A better understanding of the changes in multiaxis muscle strength following ACL injury and reconstruction will help us develop more effective treatment modalities.

METHODS

Subjects.

Eighty-one subjects (age, 32.0 ± 7.7 yr) from four populations participated in the study (Table 1). Nineteen patients had chronic ACL injury (age, 33.4 ± 7.2 yr) and were evaluated more than 7 months after injury with mean ± standard deviation postinjury duration of 69.7 ± 75.4 months. Eighteen patients had acute ACL injury (age, 31.4 ± 8.5 yr) and were studied less than 3 months after ACL injury (1.6 ± 0.6 months). Patients whose ACL was injured between 3 and 7 months before the testing were excluded from the study to have a clear separation between the acute and chronic ACL deficient populations. All the injured patients were diagnosed as having complete ACL rupture. ACL rupture in all the acute injured patients and 17 of the 19 chronic injured patients was confirmed through arthroscopy and/or magnetic resonance imaging (MRI). The remaining two chronic injured patients were judged as having ACL rupture through physical examination, and their Lachman and pivot shift scores were both 2+. Twenty-one ACL reconstructed patients (age, 31.5 ± 6.8 yr) were studied long after arthroscopically assisted intra-articular reconstruction using the central third of the patellar tendon (19.3 ± 10.2 months after surgery). To evaluate postsurgery strength recovery about the multiple knee axes, 10 of the 21 ACL reconstructed patients also had additional strength evaluations at other times, ranging from shortly before the surgery to 1 yr after surgery. Twenty-three healthy subjects (age, 31.6 ± 8.6 yr) with no prior history of injury on either knee were used as normal controls. All four groups of subjects were physically active and were working/studying full-time, except during the period shortly after ACL reconstruction or injury. The study was approved by the Institutional Review Board, and the subjects gave written informed consent before the experiment.

T1-2
Table 1:
Subject data.

Experimental setup.

The subject was seated upright on a custom-designed joint driving device with the thigh fixed to the seat by a strap and clamps and the trunk strapped to the backrest (Fig. 1). To form a tight coupling between the leg and the force-measuring device and measure muscle strength reliably, the distal leg, ankle, and foot were cast with fiberglass tape and fixed to one end of an aluminum beam located on the lateral side of the leg through two half-rings. The other end of the beam was mounted onto a motor shaft through a six-axis force sensor (JR3 Inc., Woodland, CA). The motor shaft was locked at a selected knee flexion angle, allowing isometric torque and force measurement. The seat could be adjusted in four degrees of freedom so that knee flexion axis was aligned with the Z-axis of the force sensor. The seat was then locked tightly to form a solid base. The relative position between the cast and the aluminum beam was adjusted in four degrees of freedom so that the leg was aligned with the beam without undesired excessive loading onto the knee joint caused by the mounting. The femoral condyles were supported from both medial and lateral sides with cushioned clamps. The knee and hip were flexed at 60° and 85°, respectively.

F1-2
FIGURE 1:
Experimental setup of knee muscle strength testing. The seat was adjusted in four degrees of freedom to align the knee flexion axis with the motor shaft. The short-leg cast was fixed to the aluminum beam through the two half-rings, and it could be adjusted and locked in four degrees of freedom to achieve appropriate alignment. The other end of the beam was mounted on the motor shaft through a six-axis force sensor. The motor was locked at the selected knee flexion angle of 60° flexion, restricting the strength test at an isometric condition. Hip movement was blocked from both left and right sides. The thigh was strapped and clamped to the seat, and the trunk was strapped to the backrest at 85° hip flexion.

Protocol.

With the device locked at the selected knee position, the strength evaluation was conducted under isometric conditions. During each trial, the subjects were asked to generate an isometric maximum voluntary contraction in one of the following six directions: knee flexion, extension, internal rotation, external rotation, abduction, and adduction. They were instructed to do it with maximum effort using muscles around the knee but avoid moving the trunk and hips. Complete six-axis forces and moments generated during the isometric maximum voluntary contraction were measured by the six-axis force sensor. The measured forces/moments were transformed from the force sensor coordinate system to the knee joint coordinate system and displayed on a computer monitor in real time. The subjects used the displayed torque signals to learn to generate the desired maximum voluntary contraction in each direction. The maximal torque over multiple trials in each of the six directions was taken as the strength in the corresponding direction. EMG signals from the vastus medialis, vastus lateralis, semitendinosus, and biceps femoris muscles were recorded during the multiaxis maximal voluntary contractions (23). A pair of silver and silver-chloride electrodes were used to record the EMG signal for each muscle after cleaning the skin with alcohol pads. The input impedance and common mode rejection ratio of the amplifier were 109 Ω and 130 dB, respectively. All signals were low-pass filtered using eighth-order Butterworth filters (230-Hz cutoff frequency) and sampled at 500 Hz by a computer.

Additional MVC tests were performed on 10 of the 21 ACL reconstructed patients. Multiaxis muscle strength was measured several days before the surgery, and about 1 month, 3 months, and 1 yr after surgery. Their muscle strength at the above four points before and after surgery were used to investigate multiaxis strength recovery following surgery. Their last muscle strength evaluation (at least 1 yr after surgery) was used together with data from the remaining reconstructed patients to characterize multiaxis knee muscle strength for the reconstructed population (long after surgery).

Data analysis.

The recorded force and moment signals were low-pass filtered, decoupled between the different components, scaled to the appropriate physical units, and transformed from the force sensor coordinate system to the knee joint coordinate system. All six force and moment components were used in the decoupling and transformation. Only the three moment components (internal-external rotation, abduction-adduction, and flexion-extension) were analyzed in this study.

To normalize muscle strength across subjects, the torque ratios of internal rotation strength over external rotation strength, abduction strength over adduction strength, and flexion strength over extension strength were determined for each subject (strength at the contralateral knee was not used to normalize muscle strength because injury of one knee may affect strength of the other knee). The analysis of variance (ANOVA) procedure with Dunnett multiple comparisons was used to compare statistically the strength ratios between different populations (7,25). For each of the four populations, paired t-test was used to compare the internal rotation strength versus external rotation strength, and the abduction versus adduction strength. To evaluate the gradual strength changes after ACL reconstruction, postsurgery multiaxis muscle strength in any of the six directions (flexion, extension, abduction, adduction, internal rotation, and external rotation) was normalized to the presurgery strength in the corresponding direction. Paired t-tests were used to compare strength change between the different directions.

RESULTS

Internal/external rotation strength ratio.

The internal/external rotation strength ratio of the chronic ACL deficient population was significantly lower than that of the normal and acute deficient populations with P = 0.02 (Fig. 2). The chronic ACL deficient patients had stronger external rotation strength than internal rotation strength (P < 0.001). In contrast, the normal, acutely deficient, and reconstructed subjects all had stronger internal rotation strength than external rotation strength. However, the difference was statistically significant only in the normal controls (significantly stronger internal rotation than the external rotation strength with P = 0.008). The internal/external rotation strength ratio of the surgically reconstructed group was higher than that of the chronic ACL deficient population (P = 0.078) and was not statistically different from that of the normal control group.

F2-2
FIGURE 2:
Knee internal/external rotation strength ratio of the four populations: the normal, acute injured, chronic injured, and surgically reconstructed subjects, and the numbers of subjects in the four groups were 23, 18, 19, and 21, respectively. The vertical lines give the standard deviation across subjects in each population.

Abduction/adduction strength ratio.

On average, all the groups had stronger abduction than adduction strength. Paired t-tests showed that the difference was significant for the chronic and acute ACL deficient groups with P = 0.015 and P = 0.038, respectively. Similar to the internal/external rotation strength ratio, the mean abduction/adduction strength ratio of the surgically reconstructed patients was higher than that of the normal controls but lower than that of the chronic ACL deficient population (Fig. 3). However, the differences were not statistically significant.

F3-2
FIGURE 3:
Knee abduction/adduction strength ratio of the four populations: the normal, acute injured, chronic injured, and surgically reconstructed subjects, and the numbers of subjects in the four groups were 23, 18, 19, and 21, respectively. The vertical lines give the standard deviation across subjects in each population.

Flexion/extension strength ratio.

There was significant difference in the flexion/extension strength ratio among the different groups of subjects (P = 0.004) (Fig. 4). Specifically, the flexion/extension strength ratio of the ACL reconstructed group was significantly higher than that of the normal controls and the acute ACL deficient groups.

F4-2
FIGURE 4:
Knee flexion/extension strength ratio of the four populations: the normal, acute injured, chronic injured, and surgically reconstructed subjects, and the numbers of subjects in the four groups were 23, 18, 19, and 21, respectively. The vertical lines give the standard deviation across subjects in each population.

Gradual improvement of multiaxis muscle strength after ACL reconstruction.

In contrast to the substantial reduction in knee extension strength and its slow recovery after the ACL reconstruction, muscle strength reductions in the other directions were less after the reconstruction (Fig. 5). At 1 month after surgery, strength reduction relative to the presurgery level was least in internal-external rotation, followed by the knee abduction-adduction. Knee flexion-extension strength, especially the extension strength, was reduced the most. Relative muscle strength loss in knee extension (normalized to presurgery strength) was significantly more than the strength loss in all the other five directions (P < 0.03 for all cases). At 3 months after surgery, normalized strength (to corresponding presurgery level) in abduction was significantly higher than that of knee extension with P = 0.04. At 1 yr after surgery, normalized strength in knee extension was still the lowest among the normalized strength in all the six directions. However, the difference was no longer statistically significant, given the number of subjects available. From 1 month to 1 yr after surgery, muscle strength in all six directions increased gradually (Fig. 5).

F5-2
FIGURE 5:
Lower limb muscle strength in knee flexion, extension, abduction, adduction, internal rotation (IR), and external rotation (ER) of ACL reconstructed patients measured at 1 month, 3 months, and 1 yr after the reconstructive surgery. The strength in each direction was normalized to its corresponding strength before the surgery. The vertical lines represent the standard deviation.

Coupling between different torque components.

When the subject generated a maximum voluntary contraction about one of the three orthogonal axes (flexion-extension, abduction-adduction, and internal-external rotation), he or she also generated considerable moments about the other two axes. The unintended torque components were quite strong, especially when the intended maximum voluntary contraction was not in flexion or extension. Sometimes, the unintended moment was even stronger than the intended one. When a subject intended to generate a maximum tibial internal or external rotation moment, for example, he or she also generated substantial moments in abduction-adduction and flexion-extension (Fig. 6). The amplitude and direction (positive or negative) of the two unintended torque components varied from trial to trial and from subject to subject. There was cocontraction between agonist-antagonist muscles, as was seen in the case of tibial external rotation with the biceps femoris and semitendinosus as the agonist and antagonist, respectively (Fig. 6). The quadriceps components were not very active during the tibial rotation tasks, compared with the knee extension task.

F6-2
FIGURE 6:
Representative internal-external rotation, abduction-adduction, and flexion-extension moments (in N·m), and semitendinosus (ST) and biceps femoris (BF) EMG signals generated during isometric maximum tibial rotation tasks. Results from two similar trials (represented by the thick and thin lines) of maximum tibial internal rotation are plotted in the left column. The EMG signal of each muscle was normalized to its corresponding maximum value during maximum voluntary contraction tasks in all the six directions (flexion, extension, abduction, adduction, internal rotation, and external rotation). Similar results during two maximum tibial external rotation trials are plotted in the right column. Notice cocontraction of the biceps femoris and semitendinosus during maximal external rotation contraction.

DISCUSSION

The present study showed considerable changes in lower limb muscle strength in knee axial rotation and flexion-extension after ACL injury and reconstruction. Reduction in the internal/external rotation strength ratio indicated a compensatory mechanism developed by the chronic ACL deficient patients over time. Furthermore, the diminished changes in multiaxis strength in the ACL reconstructed patients as compared with the chronic deficient ones presumably reflected a reduced need for compensation after ACL reconstruction. A better understanding of the postinjury and postsurgery strength changes among the multiple axes and the associated compensatory mechanisms may help us develop more effective treatment modalities and evaluate treatment outcome more accurately.

Adaptations in tibial internal rotation.

As shown above, normal subjects generally had stronger tibial internal rotation strength than external rotation strength, which was consistent with a previous study (28). In contrast, the chronic ACL deficient patients had a significantly lower ratio of tibial internal-external rotation strength, indicating that the patients developed stronger external rotation strength (or weaker internal rotation strength) over a long period of adaptation process. Since internal rotation of the tibia relative to the femur loaded the ACL strongly (12,16), the significantly lower internal/external rotation strength ratio would help the chronic deficient patients unload a partially torn ACL and/or avoid getting into knee positions that were unstable because of the loss of ACL. On the other hand, the internal/external rotation strength ratio of the acute deficient patients was not significantly different from that of normal subjects, with the numbers available indicating the acute deficient subjects had not yet established such a compensatory mechanism in a short period of time. Furthermore, the internal/external rotation strength ratio of the ACL reconstructed patients was higher than that of chronic deficient patients but lower than that of the normal controls, indicating reduced need for such compensation with the ACL repaired.

The lower ratio of internal/external rotation strength associated with chronic ACL deficient patients is consistent with a related study on kinematic changes associated with chronic ACL deficient knees during locomotion. It was found in that study that chronic ACL deficient patients tended to walk with the tibia externally rotated (and abducted slightly) relative to the femur, compared with normal subjects (37). Similarly, it was observed in clinics that ACL deficient patients tended to walk with their foot externally rotated (see Warren’s comments in (33)). In another study on ACL deficiency through roentgen stereophotogrammetric examinations, it was observed that ACL deficient patients extended their knee with reduced internal rotation and adduction (10).

Furthermore, the lower ratio of internal/external rotation strength associated with chronic ACL deficient patients is also consistent with previous studies on lower limb muscle EMG activities of chronic ACL deficient patients in which the biceps femoris was found to be more active (6,14,29), the semitendinosus activity was delayed and less active around the heel contact (27), and the medial gastrocnemius muscle was more active (29) compared with normal controls. These changes in muscle activities seem to be consistent with roles of the individual muscles in loading/unloading the ACL and compensating for ACL deficiency (see further discussion below).

By electrically stimulating an individual muscle crossing the knee selectively and measuring the resulting flexion-extension, abduction-adduction, and internal-external rotation moments at the knee joint, it was found that the biceps femoris (and the medial gastrocnemius) generated considerable tibial external rotation moment, whereas the semitendinosus (and the lateral gastrocnemius) produced marked tibial internal rotation moment (36). Therefore, weaker medial hamstring activity and/or stronger lateral hamstring and medial gastrocnemius contractions would apply a net external rotation moment on the tibia, which would tend to unload and/or protect the ACL.

Multiaxis muscle strength following ACL reconstruction.

The higher flexion/extension strength ratio shown by the ACL reconstructed patients as compared with the normal controls and the acute ACL deficient groups was probably attributable to the quadriceps atrophy following the ACL reconstruction using the central third patellar tendon. In addition, discomfort and tentativeness after ACL reconstruction might also affect the subject’s ability of producing maximum voluntary knee extension.

That the amplitude of the internal/external rotation strength ratio of ACL reconstructed patients was between that of normal controls and chronic ACL deficient subjects indicated a reduced need for the compensation after ACL reconstruction. Furthermore, the measured lower limb muscle strength in internal-external rotation (and in abduction-adduction) was not affected by ACL reconstructive surgery as much as the knee extension strength, indicating the tibial rotation (and abduction-adduction) strength tends to be more easily recovered after ACL reconstruction. The less severe strength loss in tibial rotation and abduction following ACL reconstruction compared with that in knee extension indicates that the patients may better tolerate movement/exercise about these off-axes after ACL reconstruction. It prompts us to take advantage of such a better tolerance and strengthen especially those muscles that unload and protect the ACL to help the patients recover more easily.

Hip contributions.

Although lower limb muscle strength was measured about the three orthogonal axes at the knee joint, the abduction-adduction and internal-external rotation moments measured were determined by muscles crossing the hip as well as muscles crossing the knee joint. Considering that the knee was at a flexed position (60° of flexion with 0° of flexion, corresponding to full knee extension), the hip muscle contribution to the tibial internal-external rotation was relatively minor, whereas the hip muscle contribution to the measured abduction-adduction strength was more significant (38). Therefore, muscle strength measured about the knee abduction-adduction axis reflected strength at both the knee and hip (9,11). If needed, more strict and isolated evaluation of knee abduction-adduction strength can be performed by positioning the knee at full extension, to minimize the contribution from muscles crossing the hip (38).

On the one hand, muscle strength evaluated about the knee axes may be affected by muscles crossing the hip as well as muscles crossing the knee. On the other hand, hip muscle strength as well as knee muscle strength may be affected by ACL injury/reconstruction. For example, in a study on 27 patients who had undergone unilateral knee surgery including six ACL reconstruction and two ACL diagnostic arthroscope cases, it was reported that hip strength in the surgical lower extremities was reduced following knee surgery when compared with the nonsurgical extremities, especially in hip extension (9).

In summary, the lower ratio of tibial internal/external rotation strength in chronic ACL injury indicates a compensatory mechanism developed by ACL deficient patients (maybe subconsciously) over a period of time to unload a partially torn ACL and/or to avoid unstable knee positions because of the loss of the ACL. Such adaptations prompt us to develop new treatment modalities to strengthen muscles that help protect and unload the ACL. A lower ratio of tibial internal/external rotation strength can be achieved by either strengthening external rotator muscles or weakening internal rotator muscles. In general, it is desirable to treat patients through strengthening agonist muscles instead of weakening antagonist ones. Furthermore, although muscles like the medial hamstrings rotate the tibia internally, they also pull the tibia posteriorly, which helps unload the ACL. Therefore, selectively and differentially strengthening lower limb muscles that externally rotate the tibia may help protect and unload the ACL. For the hamstring muscles, for example, both medial and lateral hamstrings should be strengthened. However, differential strengthening with the lateral hamstrings strengthened more than the medial hamstrings may be helpful in protecting/unloading the ACL. For patients who do not adapt well after ACL injury, such selective and differential strengthening may help them better cope with the injury. For patients after ACL reconstruction, such selective and differential strengthening may help them protect the reconstructed ACL and reduce the likelihood of reinjury. Overall, stronger tibial external rotation strength and a higher ratio of external rotation strength over internal rotation strength may keep the knee strength on the safer side within the normal range and reduce the likelihood of potential ACL injury. Treatment outcome can also be evaluated more accurately with consideration of multiaxis muscle strength. Finally, future research is needed to correlate the multiaxis strength adaptation with other functional and stability measures.

The authors gratefully acknowledge the support of the Whitaker Foundation, the National Institutes of Health (grant no. AR45634), and the Falk Medical Research Trust.

Address for correspondence: Li-Qun Zhang, Rehabilitation Institute of Chicago, Room 1406, 345 E. Superior Street, Chicago, IL 60611; E-mail: [email protected]edu.

REFERENCES

1. Ahmed, A. M., D. L. Burke, N. A. Duncan, and K. H. Chan. Ligament tension pattern in the flexed knee in combined anterior translation and axial rotation. J. Orthop. Res. 10: 854–867, 1992.
2. Andriacchi, T. P., and D. Birac. Functional testing in the anterior cruciate ligament-deficient knee. Clin. Orthop. 288: 40–47, 1993.
3. Baugher, W. H., R. F. Warren, J. L. Marshall, and A. Joseph. Quadriceps atrophy in the anterior cruciate insufficient knee. Am. J. Sports Med. 12: 192–195, 1984.
4. Berchuck, M., T. P. Andriacchi, B. R. Bach, and B. Reider. Gait adaptations by patients who have a deficient anterior cruciate ligament. J. Bone Joint Surg. Am. 72: 871–877, 1990.
5. Cahalan, T. D., M. E. Johnson, S. Liu, and E. Y. S. Chao. Quantitative measurements of hip strength in different age groups. Clin. Orthop. 246: 136–145, 1989.
6. Ciccotti, M. G., R. K. Kerlan, J. Perry, and M. Pink. An electromyographic analysis of the knee during functional activities: II. The anterior cruciate ligament-deficient and -reconstructed profiles. Am. J. Sports Med. 22: 651–658, 1994.
7. Glass, G. V., and K. D. Hopkins. Statistical Methods in Education and Psychology, 3rd Ed. Boston: Allyn & Bacon, 1996, pp. 444–481.
8. Itoh, H., N. Ichihashi, T. Maruyama, M. Kurosaka, and K. Hirohata. Weakness of thigh muscles in individuals sustaining anterior cruciate ligament injury. Kobe J. Med. Sci. 38: 93–107, 1992.
9. Jaramillo, J., T. W. Worrell, and C. D. Ingersoll. Hip isometric strength following knee surgery. J. Orthop. Sports Phys. Ther. 20: 160–165, 1994.
10. Jonsson, H., J. Kärrholm, and L.-G. Elmqvist. Kinematics of active knee extension after tear of the anterior cruciate ligament. Am. J. Sports Med. 17: 796–802, 1989.
11. Kannus, P., K. Latvala, and M. Järvinen. Thigh muscle strength in the anterior cruciate ligament deficient knee: isokinetic and isometric long-term results. J. Orthop. Sports Phys. Ther. 9: 223–227, 1987.
12. Kennedy, J. C., R. J. Hawkins, and R. B. Willis. Strain gauge analysis of knee ligaments. Clin. Orthop. 129: 225–229, 1977.
13. Kulig, K., J. G. Andrews, and J. G. Hay. Human strength curves. Exerc. Sport Sci. Rev. 12: 417–466, 1984.
14. Limbird, T. J., R. G. Shiavi, M. Frazer, and H. Borra. EMG profiles of knee joint musculature during walking: changes induced by anterior cruciate ligament deficiency. J. Orthop. Res. 6: 630–638, 1988.
15. Lorentzon, R., L.-G. Elmqvist, M. Sjöström, M. Fagerlund, and A. R. Fugulmeyer. Thigh musculature in relation to chronic anterior cruciate ligament tear: muscle size, morphology, and mechanical output before reconstruction. Am. J. Sports Med. 17: 423–429, 1989.
16. Markolf, K. L., D. M. Byrchfield, M. M. Shapiro, M. F. Shepard, G. A. Finerman, and J. L. Slauterbeck. Combined knee loading states that generate high anterior cruciate ligament forces. J. Orthop. Res. 13: 930–935, 1995.
17. Markolf, K. L., A. Graff-Radford, and H. C. Amstutz. In vivo knee stability: a quantitative assessment using an instrumented clinical testing apparatus. J. Bone Joint Surg. Am. 60: 664–674, 1978.
18. Morrisey, M. C. Reflex inhibition of thigh muscles in knee injury: causes and treatment. Sports Med. 7: 263–276, 1989.
19. Morrisey, M. C., and C. E. Brewster. Hamstring weakness after surgery for anterior cruciate injury. J. Orthop. Sports Phys. Ther. 7: 310–313, 1986.
20. Murray, S. M., R. F. Warren, J. C. Otis, M. Kroll, and T. L. Wickiewicz. Torque-velocity relationships of the knee extensor and flexor muscles in individuals sustaining injuries of the anterior cruciate ligament. Am. J. Sports Med. 12: 436–440, 1984.
21. Noyes, F. R., O. D. Schipplein, T. P. Andriacchi, S. R. Saddemi, and M. Weise. The anterior cruciate ligament-deficient knee with varus alignment. Am. J. Sports Med. 20: 707–716, 1992.
22. Olmstead, T. G., H. W. Wevers, J. T. Bryant, and G. J. Gouw. Effect of muscular activity on valgus/varus laxity and stiffness of the knee. J. Biomech. 19: 565–577, 1986.
23. Perotto, A. O. Anatomic Guide for the Electromyographer: The Limbs and Trunk, 3rd Ed. Springfield, IL: Charles C Thomas Publisher, 1994, pp. 181–207.
24. Rosenberg, T. D., J. L. Franklin, G. N. Baldwin, and K. A. Nelson. Extensor mechanism function after patellar tendon graft harvest for anterior cruciate ligament reconstruction. Am. J. Sports Med. 20: 519–526, 1992.
25. SAS Institute, Inc. SAS/STAT User’s Guide. Cary, NC: SAS Institute, Inc., 1990, pp. 209–244.
26. Shelbourne, K. D., and D. A. Foulk. Timing of surgery in acute anterior cruciate ligament tears on the return of quadriceps muscle strength after reconstruction using an autogenous patellar tendon graft. Am. J. Sports Med. 23: 686–689, 1995.
27. Shiavi, R. G., L.-Q. Zhang, T. J. Limbird, and M. A. Edmondstone. Pattern analysis of electromyographic linear envelopes exhibited by subjects with uninjured and injured knees during free and fast speed walking. J. Orthop. Res. 10: 226–236, 1992.
28. Shoemaker, S. C., and K. L. Markolf. In vivo rotatory knee stability. J. Bone Joint Surg. Am. 64: 208–216, 1982.
29. Sinkjær, T., and L. Arendt-Nielsen. Knee stability and muscle coordination in patients with anterior cruciate ligament injuries: an electromyographic approach. J. Electromyogr. Kinesiol. 1: 209–217, 1991.
30. Snyder-Mackler, L., Z. Ladin, A. A. Schepsis, and J. C. Young. Electrical stimulation of the thigh muscles after reconstruction of the anterior cruciate ligament. J. Bone Joint Surg. Am. 73: 1025–1036, 1991.
31. Snyder-Mackler, L., P. F. D. Luca, P. R. Williams, M. E. Eastlack, and A. R. Bartolozzi. Reflex inhibition of the quadriceps femoris muscle after injury or reconstruction of the anterior cruciate ligament. J. Bone Joint Surg. Am. 76: 555–560, 1994.
32. Solomonow, M., R. Baratta, B. H. Zhou, et al. The synergistic action of the anterior cruciate ligament and thigh muscles in maintaining joint stability. Am. J. Sports Med. 15: 207–213, 1987.
33. Tibone, J. E., T. J. Antich, G. S. Fanton, D. R. Moynes, and J. Perry. Functional analysis of anterior cruciate ligament instability. Am. J. Sports Med. 14: 276–284, 1986.
34. Vegso, J. J., S. E. Genuario, and J. S. Torg. Maintenance of hamstring strength following knee surgery. Med. Sci. Sports Exerc. 17: 376–379, 1985.
35. Wilk, K. E., and J. R. Andrews. Current concepts in the treatment of anterior cruciate ligament disruption. J. Orthop. Sports Phys. Ther. 15: 279–294, 1992.
36. Zhang, L.-Q., J. P. Butler, G. Wang, G. W. Nuber, K. Zeng, and W. Z. Rymer. Mechanical actions of individual muscles at the human knee joint. Presented at the 21st Annual Meeting of the American Society of Biomechanics, Clemson, SC, September 24–27, 1997, pp. 290–291.
37. Zhang, L.-Q., S. Dobson, R. G. Shiavi, S. Peterson, and T. J. Limbird. Changes in knee kinematics caused by ACL deficiency during fast walking. Gait Posture 7:156, 1998. Abstract.
38. Zhang, L.-Q., D. Xu, G. Wang, and R. W. Hendrix. Muscle strength in knee varus and valgus. Med. Sci. Sports Exerc. 33: 1194–1199, 2001.
Keywords:

COMPENSATION; TIBIAL ROTATION; ABDUCTION; INJURY

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