Single Leg Squat Task
The subjects then completed the same procedure for the SLS task as they did during the screening session. The subject was instructed as to what constituted a successful trial, specifically, the subject: (a) maintained proper testing position throughout the entire motion, (b) squatted until the gluteals came in contact with the mechanical block, (c) completed the task at the appropriate rate, (d) did not touch down with the nondominant foot, (e) did not touch the legs together, (f) maintained the heel in contact with the ground, and (g) the task was completed in a fluid motion. The subjects were given as many practice trials as needed to perform the task successfully. No additional feedback, coaching, or other instructions were provided to the subject concerning technique because capturing the subject's true movement patterns was vital to this study. EMG and kinematic data were collected simultaneously for 5 successful SLS trials with 1-minute rest given between trials.
A Motion Star (Ascension Technologies, Inc., Burlington, VT, USA) electromagnetic motion tracking system was used to track 3D LE kinematics. These data were used to identify the start position, the point of greatest knee flexion, and the end position of the SLS. Electromagnetic sensors were placed over the sacrum, lateral aspect of the thigh, and the anteromedial aspect of the proximal tibia and were secured with double-sided tape, prewrap, and athletic tape. A segment-linkage model of the pelvis and dominant LE was generated by digitizing the left and right anterior-superior iliac spines, medial and lateral femoral epicondyles, and medial and lateral malleoli. The location of the hip joint center was approximated using the Bell method (2). Joint centers for the knee and hip were defined as the midpoints of the medial and lateral femoral epicondyles and malleoli, respectively. Three-dimensional coordinate data were collected at a sampling rate of 100 Hz.
A surface EMG system (Bagnoli-8; Delsys, Inc., Boston, MA, USA) was used to record LE muscle activity of the gluteus maximus, gluteus medius, hip adductors, medial hamstrings, biceps femoris, vastus medialis, vastus lateralis, and medial gastrocnemius. Before electrode application, the same researcher identified and marked each electrode site with a felt-tip marker. Electrode sites were shaved, abraded, and cleaned with isopropyl alcohol to reduce skin impedance. Electrode placement was confirmed with manual muscle testing and observation of the muscle activity on an oscilloscope. A maximal voluntary isometric contraction (MVIC) was then performed for each muscle group (hip extensors, hip abductors, hip adductors, hamstrings, quadriceps, and plantar flexors) as previously described in the literature (1,34) to provide EMG normalization criteria. A handheld dynamometer (CSD300; Chatillon, Largo, FL, USA) was used to quantify the peak force for each trial, recorded in Newtons. Three 5-second MVICs were performed for each muscle with 1-minute rest between trials. All EMG data were collected at 1,000 Hz.
Data Processing and Reduction
Kinematic data were filtered using a fourth-order low-pass Butterworth filter at a cutoff frequency of 14.5 Hz. EMG data were passively demeaned, bandpass (10–350 Hz), and notch (59.5–60.5 Hz) filtered, and smoothed using a 25-ms root-mean-square sliding window function.
EMG and kinematic data were evaluated during the descent phase of the SLS, as defined as the time from the initiation of movement to peak knee flexion. Three-dimensional joint angles were identified at the start of the trial when the subject was in the initial position, at the point when the subject reached peak knee flexion, and once the subject returned to the initial position. Mean EMG amplitude during the descent phase of the SLS was normalized to MVIC activation averaged over the largest 1-second mean interval during each MVIC trial averaged across the 3 trials. All MVIC trials were normalized to each subject's weight, by dividing the subject's MVIC value by his/her weight. Muscle coactivation ratios were calculated for gluteus medius activation and hip adductor muscle activation by dividing the mean gluteus medius activity by the mean hip adductor activity (GMed:Hip Add). In addition, coactivation ratios were calculated for gluteus maximus activity and hip adductor muscle activation by dividing the mean gluteus maximus activity by the mean hip adductor activation (GMax:Hip Add). A ratio resulting in 1.0 would indicate completely balanced muscular activation; ratios resulting in values greater than 1.0 indicate greater activation of the muscle in the numerator (GMed and GMax) compared with the muscle in the denominator (Hip Add).
EMG and kinematic data were averaged over the 5 trials of the SLS, and PROM and MVIC data were averaged from the 3 trials of each measurement for use in statistical analyses. Three separate multivariate analysis of variance (MANOVAs) were used to compare peak EMG amplitude, EMG coactivation ratios, and PROM between the MKD and control groups. One-way ANOVA was used to evaluate significant MANOVAs post hoc. Six separate independent-samples t-tests were run to compare the normalized MVIC means for each muscle group between study groups. Additionally, 4 separate independent-samples t-tests were used to compare the means for the averaged height, weight, age, and amount of time participating in physical activity per week measures between the control and MKD groups. Statistical significance was set a priori at α < 0.05.
All MANOVA statistical analyses examining group differences for EMG amplitude, EMG coactivation ratios, and PROM measurements met the assumptions for Homogeneity of Covariance. For statistically significant MANOVAs, follow-up one-way ANOVA analyses were run to examine the main effect for group for the EMG coactivation ratios and PROM measurements; all follow-up ANOVAs met the assumptions for Homogeneity of Variance.
Subject Descriptive Statistics
No significant differences were observed between height (T38 = −0.250, p = 0.804), weight (T38 = −0.184, p = 0.855), age (T38 = 0.000, p = 1.00), or minutes of physical activity per week (T38 = 0.486, p = 0.630), between the control and MKD groups.
Maximal Voluntary Isometric Contraction
Means, SDs, and 95% confidence intervals for all normalized MVIC values are presented in Table 3. No significant differences were observed between groups for any of the normalized values for the 6 muscle groups tested with MVIC trials: hip extensors (T38 = −0.840, p = 0.460), hip abductors (T38 = −0.897, p = 0.376), hip adductors (T38 = −0.885, p = 0.382), hamstring group (T38 = 0.172, p = 0.865), quadriceps group (T38 = 0.733, p = 0.468), and plantar flexors (T38 = −0.718, p = 0.477).
Means, SDs, and 95% confidence intervals for all EMG amplitude measures are presented in Table 4. No significant differences were observed between the normalized EMG activation of the 2 groups (Wilk Lambda = 0.742, F10,29 = 1.301, p = 0.280, η2 = 0.49). While not significant, it is worth noting that the group difference in hip adductor muscle activation trended toward significance (F1,38 = 3.059, p = 0.089). Specifically, individuals in the MKD group tended to display greater hip adductor EMG activation (MKD = 20.1 ± 14.0, control = 13.3±9.8). One MKD subject's hamstring EMG value was identified as a statistical outlier, thus this subject was excluded from statistical analyses.
EMG Coactivation Ratios
Means, SDs, and 95% confidence intervals for calculated coactivation ratios are presented in Table 5. A significant multivariate main effect for group was observed for the coactivation ratios (Wilks' Lambda = 0.822, F10,29 = 4.003, p = 0.027, η2 = 0.68). Follow-up one-way ANOVAs revealed significant differences for the gluteus medius:hip adductor ratio (F1,38 = 5.187, p = 0.028) and the gluteus maximus:hip adductor ratio (F1,38 = 8.201, p = 0.007). Specifically, individuals in the MKD group displayed significantly lower gluteus medius:hip adductor (2.4 ± 1.1 vs. 4.5 ± 3.9) and gluteus maximus:hip adductor (1.1 ± 0.62 vs. 2.4 ± 1.8) ratios compared with the control group, indicating greater hip adductor EMG activation compared with gluteal EMG activation in the MKD group when compared with the control group.
Means, SDs, and 95% confidence intervals for all PROM measures are presented in Table 6. A significant multivariate main effect for group was observed for PROM measurements (Wilks' Lambda = 0.555, F10,29 = 2.321, p = 0.038, η2 = 0.83). Follow up one-way ANOVAs revealed significant group differences in dorsiflexion range of motion with the knee extended (F1,38 = 4.203, p = 0.047), dorsiflexion range of motion with the knee flexed (F1,38 = 4.857, p = 0.034), and posterior talar glide (F1,38 = 7.040, p = 0.012). Specifically, the MKD group displayed significantly less dorsiflexion PROM with the knee extended (5.5 ± 5.4 vs. 8.8 ± 4.7) and flexed (9.5 ± 6.2 vs. 14.2 ± 7.3), and greater posterior talar glide (29.8 ± 4.8 vs. 25.7 ± 5.0) in comparison to the control group. No other significant differences were observed.
Power and Effect Size
Observed power (range, 0.050–0.797) and effect size (range, 0.01–1.07) for each PROM and EMG measure were calculated and are presented in Table 7. This information will be discussed to describe the clinical significance of these findings.
To the authors' knowledge, this is the first study to identify differences in LE muscle activation and PROM between individuals presenting with MKD and those who do not during a SLS. In summary, the findings of this study revealed that the MKD group had lesser coactivation ratios compared with the control group, indicating that these individuals use a more hip adductor dominant activation strategy compared with control subjects. This study also found the MKD group displayed less dorsiflexion PROM and greater posterior movement of the talus compared with the control group. However, no other PROM measurements or any isometric strength measures were different between groups. These combined results suggest the combination of altered hip adductor and gluteal musculature coactivation and less ankle dorsiflexion ROM may contribute to dynamic knee valgus during a SLS.
No statistically significant differences in LE EMG activation were observed between groups. Previous research comparing muscle activation between sexes during SLS has identified greater activation of the rectus femoris (51) and lesser activation of the gluteus medius (25) in females, both of which are believed to contribute to increased risk of noncontact ACL injury. Padua et al. (41) reported 34% greater hip adductor activity in individuals displaying MKD during a double leg squat task compared with a control group that did not. Similar to this finding, the MKD group in the present investigation demonstrated 34% greater hip adductor activity during the SLS (not statistically significant; p = 0.089). In addition, there were no differences found between groups for the activation of the gluteus medius and gluteus maximus muscles, also similar to Padua et al. (41,47).
The relative coactivation between the gluteus medius and gluteus maximus with the hip adductors may contribute to MKD. Greater hip adductor activity that is not balanced by gluteal activity may permit greater hip adduction and internal rotation (41). This notion is supported by our finding that the GMed:Hip Add and GMax:Hip Add coactivation ratios in the MKD group were smaller than those in the control group. The coactivation ratio of GMed:Hip Add for the MKD group was 2.4 while the control group's ratio was 4.5 (effect size = 0.84); similarly, the ratios for the MKD and control groups for the GMax:Hip Add coactivation ratio were 1.1 and 2.4, respectively (effect size = 1.07). Larger coactivation ratios indicate that the GMed or GMax were more active relative to the Hip Add. Conversely, smaller coactivation ratios indicate greater reliance on the Hip Add muscles. The findings of this study indicate the MKD group placed greater reliance on their Hip Add musculature compared with the control group. It is generally thought that MKD may be caused by insufficient gluteal muscle strength (6) or activation (25). The current findings may help refine this theory and suggest that MKD may be caused by greater reliance on the Hip Add muscles rather than inadequate strength or activation of the gluteal musculature. The authors of this study believe that increased Hip Add muscles relative to GMed and GMax activation played a role in facilitating visual MKD during the SLS.
Lesser ankle dorsiflexion ROM in the MKD group supports our hypotheses. Based on these findings the authors believe decreased dorsiflexion ROM may be a large contributor to MKD during functional tasks. The MKD group was observed to have 37.5% and 33.1% less dorsiflexion ROM with the knee extended (effect size = 0.65) and flexed (effect size = 0.70), respectively. Similar differences in PROM have been observed between groups displaying MKD and a neutral knee position during a double leg squat (3,47). Limited dorsiflexion has been proposed to contribute to excessive rearfoot pronation and, in turn, result in compensatory increases in LE internal rotation (14), which may contribute to dynamic knee valgus (32). Similarly, Cortes et al. (8) reported that subjects had significantly greater knee valgus angle at initial contact and decreased dorsiflexion motion after landing when they performed rear-foot landings compared with self-preferred landing styles (8). Based on these combined findings it seems that restricted ankle dorsiflexion ROM may be an important factor contributing to MKD across a variety of functional tasks.
Decreased dorsiflexion PROM may be because of decreased extensibility of the gastrocnemius/soleus complex and/or restricted posterior talar glide on the tibia (11). Posterior glide of the talus within the talocrural joint is a necessary accessory motion to permit full ankle dorsiflexion PROM. The authors originally hypothesized decreased ankle dorsiflexion PROM in the MKD group may be because of restricted posterior talar glide motion. However, this hypothesis was not supported as MKD subjects demonstrated greater posterior talar glide compared with the control subjects (effect size = 0.84). This finding suggests that decreased ankle dorsiflexion ROM in the MKD group was most likely because of decreased extensibility of the gastrocnemius/soleus complex and not restricted posterior talar glide. However, the sensitivity of the posterior talar glide test has been questioned based on research demonstrating weak associations between the posterior talar glide test with open and closed kinetic chain measures of ankle dorsiflexion ROM (9). Thus, future research is needed to better understand the underlying mechanism contributing to decreased dorsiflexion PROM in the MKD group.
Each subject stood so that the foot was fixed on the ground with the toes pointing forward, and we assured the heel remained in contact with the ground throughout each trial. As the subject lowered the body to the required 60° angle of knee flexion, the ankle was required to move through dorsiflexion. Limited dorsiflexion ROM would inhibit the tibia from moving forward over the foot and may have caused MKD subjects to compensate for this lack of motion. The authors speculate that MKD subjects compensated for a lack of sagittal plane ankle motion by increasing frontal and/or transverse plane motion at the foot and up through the kinetic chain. Individuals may have compensated by going into more pronation of the foot, eversion of the talus, and internal rotation of the tibia (14) thus creating the visual appearance of MKD. Future research investigating the 3D kinematics of the foot and lower leg is needed to better understand if these compensatory motions actually do occur in those individuals displaying MKD.
There were no group differences observed in hip or knee PROM measurements, but the MKD group displayed limited ankle dorsiflexion ROM. The authors, therefore, propose that the imbalance that was observed in Hip Add to gluteal activation stems from a neuromuscular compensation as a result of the limited dorsiflexion ROM. Limited dorsiflexion PROM creates an abnormal axis of rotation of the tibia on the talus, resulting from altered arthokinematics which limit roll and glide between the joint surfaces. This abnormal rotation applies abnormal stresses on the tissues that have been suggested to produce altered proprioceptive input, which in turn causes the motor control system to adapt (12). The authors propose one such altered motor control response is using more frontal and transverse plane motion when sagittal plane motion is restricted, resulting in the leg being pulled actively inward. One possible neuromuscular mechanism used to achieve this is altering the adductor and gluteal coactivation ratios.
In conclusion, the findings of this study indicate that dorsiflexion range of motion measurements are lesser in subjects displaying MKD compared with those who do not. The authors believe this limited dorsiflexion may result in compensatory movements in the ankle and lower leg, resulting in foot pronation and tibial internal rotation. Greater levels of hip adductor activity without an associated increase in gluteus medius and/or gluteus maximus activity may increase femoral adduction and internal rotation; potentially increasing MKD during dynamic tasks (41). MKD is suggested to be a biomechanical factor associated with ACL injury, MCL injury, and PFPS. Rehabilitation and injury prevention programs that increase dorsiflexion range of motion, decrease hip adductor activity, and increase hip abductor and external rotator activity may decrease the incidence of these injuries.
The following limitations should be considered when interpreting the findings of this study. First, these findings are limited to a single-leg squatting task. Future research should look at whether findings carry over to when individuals perform more challenging dynamic tasks (i.e., jump-landing or cutting maneuvers). Also, these findings are limited to healthy physically active individuals who display visual MKD during an SLS and those who did not, thus they may not be applicable to injured populations or the population(s) at the greatest risk of LE injury. However, our population was similar to other populations in the literature (3,16,41,47). The subjects self-reported that they were healthy and physically active; the researchers had no means of checking the validity of these statements. Also, the researchers did not control for what physical activity, if any, was completed by the subject immediately preceding screening and testing sessions. Similarly, the time of day, the nutrition, and the hydration levels of the subjects were not controlled for during data collection sessions. These variables are important when assessing muscle function and could be additional limitations to this study.
Inherent limitations exist with the use of surface EMG. The assumption was made based on previous literature that EMG signal amplitudes represent levels of muscle activity. Cross talk may occur with the placement of the EMG surface electrodes on the skin and may not give a true reading of the underlying muscle activity. However, the researchers minimized the potential for error by using standard methods of applying the electrodes, sufficiently securing the electrodes to prevent movement, and checking the output of the electrodes before data collection to ensure proper placement. Finally, interpretation of the results was based on EMG signals normalized to maximal isometric voluntary activity (MVIC). Another assumption was made that all participants gave their maximal effort during the MVIC measurements and during the SLS; this would affect the normalized percentages used during the statistical analyses. In addition, other LE muscles not investigated in this study could be involved in dynamic control during a SLS.
Another potential limitation of this study is that the researcher who completed the measures of PROM was not blinded to the subject's group assignment. Also these measurements required the researcher to subjectively identify the point of first resistance felt in the muscle as the limb was moved through its PROM. Similarly, the measure of posterior talar glide was dependent on the researcher's ability to subjectively determine subtalar neutral position and the end feel/restriction in motion as the knee was moved into flexion. However, the researcher responsible for all PROM measurements established himself to have good reliability and precision with this measure (ICC = 0.93, SEM = 1.2° angle). Therefore, the authors do not believe these limitations were meaningful sources of error in the data. Future research should look at a more sensitive measure of quantifying restricted posterior talar glide as a possible factor limiting dorsiflexion ROM. Use of an ankle arthrometer to quantify posterior talar displacement and stiffness has been described in previous literature and may be a good tool for future research investigating factors associated with MKD (9).
Clinical screenings may be used by clinicians to help identify athletes at increased risk for LE injuries. These screening tools may also help identify which underlying factors contribute to the faulty movement patterns exhibited during the screening. The information gained from clinical screenings should then be used by the clinician to aid in the development of conditioning, rehabilitation, and injury prevention programs.
Specifically, the findings of this study suggest smaller Gluteal:Hip Add coactivation ratios and lesser dorsiflexion PROM in individuals displaying MKD may have important implications for knee injury prevention and rehabilitation programs. Individuals displaying smaller Gluteal:Hip Add coactivation ratios may benefit from rehabilitation exercises focused on increasing gluteus medius and gluteus maximus activation. These individuals may also benefit from inhibiting the hip adductors through stretching and inhibition techniques, such as self-myofascial release, which allow the muscle to relax to enhance stretching (31). Similar treatments could be used to increase gastrocnemius and soleus PROM and allow for greater ankle dorsiflexion. Ultimately, clinical screenings may aid in the development of better individualized prevention and treatment plans and decrease the incidence of noncontact knee injuries.
1. Anderson MK, Hall SJ, Martin M. Foundations of Athletic Training: Prevention, Assessment, and Management. Philadelphia, PA: Lippincott Williams & Wilkins, 2005.
2. Bell AL, Pedersen DR, Brand RA. A comparison of the accuracy of several hip center location prediction methods. J Biomech 23: 617–621, 1990.
3. Bell DR, Padua DA, Clark MA. Muscle strength and flexibility characteristics of people displaying excessive medial knee displacement. Arch Phys Med Rehabil 89: 1323–1328, 2008.
4. Boden BP, Griffin LY, Garrett WE Jr. Etiology and prevention of noncontact ACL injury. Phys Sportsmed 28: 53–60, 2000.
5. Bonci CM. Assessment and evaluation of predisposing factors to anterior cruciate ligament injury. J Athl Train 34: 155–164, 1999.
6. Claiborne TL, Armstrong CW, Gandhi V, Pincivero DM. Relationship between hip and knee strength and knee valgus
during a single leg squat. J Appl Biomech 22: 41–50, 2006.
7. Clark M, Lucett S. Optimum Performance Training for the Health and Fitness Professional (2nd ed.). Calabasas, CA: National Academy of Sports Medicine, 2004.
8. Cortes N, Onate J, Abrantes J, Gagen L, Dowling E, Van Lunen B. Effects of gender and foot-landing techniques on lower extremity kinematics during drop-jump landings. J Appl Biomech 23: 289–299, 2007.
9. Cosby NL, Hertel J. Relationships between measures of posterior talar glide and ankle dorsiflexion range of motion. Athl Train Sports Health Care 3, 2011.
10. Crill MT, Kolba CP, Chelboun GS. Using lunge measurements for baseline fitness testing. J Sport Rehabil 13: 33–53, 2004.
11. Denegar CR, Hertel J, Fonesca J. The effect of lateral ankle sprain on dorsiflexion range of motion, posterior talar glide, and joint laxity. J Orthop Sports Phys Ther 32: 166–173, 2002.
12. Denegar CR, Miller SJ III. Can chronic ankle instability be prevented? Rethinking management of lateral ankle sprains. J Athl Train 37: 430–435, 2002.
13. Devereaux MD, Lachmann S. Patello-femoral arthralgia in athletes attending a sports injury clinic. Br J Sports Med 18: 18–21, 1984.
14. DiGiovanni CW, Langer P. The role of isolated gastrocnemius and combined Achilles contractures in the flatfoot. Foot Ankle Clin 12: 363–379, viii, 2007.
15. DiMattia MA, Livengood AL, Uhl TL, Mattacola CG, Malone TR. What are the validity of the single-leg squat test and its relationship to hip-abduction strength? J Sport Rehabil 14: 108–123, 2005.
16. Distefano LJ, Blackburn JT, Marshall SW, Padua DA. Gluteal muscle activation during common therapeutic exercises. J Orthop Sports Phys Ther 39: 532–540, 2009.
17. Ekegren CL, Miller WC, Celebrini RG, Eng JJ, Macintyre DL. Reliability and validity of observational risk screening in evaluating dynamic knee valgus
. J Orthop Sports Phys Ther 39: 665–674, 2009.
18. Ferber R, Kendall KD, McElroy L. Normative and critical criteria for iliotibial band and iliopsoas muscle flexibility. J Athl Train 45: 344–348, 2010.
19. Fetto JF, Marshall JL. Medial collateral ligament injuries of the knee: A rationale for treatment. Clin Orthop Relat Res: 206–218, 1978.
20. Ford KR, Myer GD, Hewett TE. Valgus knee motion during landing in high school female and male basketball players. Med Sci Sports Exerc 35: 1745–1750, 2003.
21. Griffin LY, Agel J, Albohm MJ, Arendt EA, Dick RW, Garrett WE, Garrick JG, Hewett TE, Huston L, Ireland ML, Johnson RJ, Kibler WB, Lephart S, Lewis JL, Lindenfeld TN, Mandelbaum BR, Marchak P, Teitz CC, Wojtys EM. Noncontact anterior cruciate ligament injuries: Risk factors and prevention strategies. J Am Acad Orthop Surg 8: 141–150, 2000.
22. Griffin LY, Albohm MJ, Arendt EA, Bahr R, Beynnon BD, Demaio M, Dick RW, Engebretsen L, Garrett WE Jr, Hannafin JA, Hewett TE, Huston LJ, Ireland ML, Johnson RJ, Lephart S, Mandelbaum BR, Mann BJ, Marks PH, Marshall SW, Myklebust G, Noyes FR, Powers C, Shields C Jr, Shultz SJ, Silvers H, Slauterbeck J, Taylor DC, Teitz CC, Wojtys EM, Yu B. Understanding and preventing noncontact anterior cruciate ligament injuries: A review of the Hunt Valley II meeting, January 2005. Am J Sports Med 34: 1512–1532, 2006.
23. Griffith CJ, LaPrade RF, Johansen S, Armitage B, Wijdicks C, Engebretsen L. Medial knee injury: Part 1, static function of the individual components of the main medial knee structures. Am J Sports Med 37: 1762–1770, 2009.
24. Grindstaff TL, Beazell JR, Magrum EM, Hertel J. Assessment of ankle dorsiflexion range of motion restriction. Athl Train Sports Health Care 1: 7–8, 2009.
25. Hart JM, Garrison JC, Kerrigan DC, Palmieri-Smith R, Ingersoll CD. Gender differences in gluteus medius
muscle activity exist in soccer players performing a forward jump. Res Sports Med 15: 147–155, 2007.
26. Hewett TE, Ford KR, Myer GD. Anterior cruciate ligament injuries in female athletes: Part 2, a meta-analysis of neuromuscular interventions aimed at injury prevention. Am J Sports Med 34: 490–498, 2006.
27. Hewett TE, Lindenfeld TN, Riccobene JV, Noyes FR. The effect of neuromuscular training on the incidence of knee injury in female athletes. A prospective study. Am J Sports Med 27: 699–706, 1999.
28. Hewett TE, Myer GD, Ford KR. Prevention of anterior cruciate ligament injuries. Curr Womens Health Rep 1: 218–224, 2001.
29. Hewett TE, Myer GD, Ford KR, Heidt RS Jr, Colosimo AJ, McLean SG, van den Bogert AJ, Paterno MV, Succop P. Biomechanical measures of neuromuscular control and valgus loading of the knee predict anterior cruciate ligament injury risk in female athletes: A prospective study. Am J Sports Med 33: 492–501, 2005.
30. Hewett TE, Stroupe AL, Nance TA, Noyes FR. Plyometric training in female athletes. Decreased impact forces and increased hamstring torques. Am J Sports Med 24: 765–773, 1996.
31. Hirth CJ. Clinical movement analysis to identify muscle imbalances and guide exercise. ATT 12: 10–14, 2007.
32. Hollis JM, Takai S, Adams DJ, Horibe S, Woo SL. The effects of knee motion and external loading on the length of the anterior cruciate ligament (ACL): A kinematic study. J Biomech Eng 113: 208–214, 1991.
33. Hughston JC, Andrews JR, Cross MJ, Moschi A. Classification of knee ligament instabilities. Part I. The medial compartment and cruciate ligaments. J Bone Joint Surg Am 58: 159–172, 1976.
34. Kendall FP, McCreary EK, Provance PG. Muscles, Testing, and Function. Baltimore, MD: Williams & Wilkins, 1993.
35. Lloyd DG, Buchanan TS. Strategies of muscular support of varus and valgus isometric loads at the human knee. J Biomech 34: 1257–1267, 2001.
36. Magee DJ. Orthopedic Physical Assessment. Philadelphia, PA: Elsevier Sciences (USA), 2006.
37. McLean SG, Walker K, Ford KR, Myer GD, Hewett TE, van den Bogert AJ. Evaluation of a two dimensional analysis method as a screening and evaluation tool for anterior cruciate ligament injury. Br J Sports Med 39: 355–362, 2005.
38. Newton RU, Gerber A, Nimphius S, Shim JK, Doan BK, Robertson M, Pearson DR, Craig BW, Hakkinen K, Kraemer WJ. Determination of functional strength imbalance of the lower extremities. J Strength Cond Res 20: 971–977, 2006.
39. Nguyen A, Shultz SJ. Sex differences in clinical measurements of lower extremity alignment. J Orthop Sports Phys Ther 37: 389–398, 2007.
40. Noyes FR, Mooar PA, Matthews DS, Butler DL. The symptomatic anterior cruciate-deficient knee. Part I: The long-term functional disability in athletically active individuals. J Bone Joint Surg Am 65: 154–162, 1983.
41. Padua DA, Bell DR, Clark MA. Neuromuscular characteristics of individuals displaying excessive medial knee displacement. J Athl Train 47: 525–536, 2012.
42. Padua DA, Marshall SW, Boling MC, Thigpen CA, Garrett WE Jr, Beutler AI. The Landing Error Scoring System (LESS) is a valid and reliable clinical assessment tool of jump-landing biomechanics: The JUMP-ACL study. Am J Sports Med 37: 1996–2002, 2009.
43. Palmieri-Smith RM, Wojtys EM, Ashton-Miller JA. Association between preparatory muscle activation and peak valgus knee angle. J Electromyogr Kinesiol 18: 973–979, 2008.
44. Starkey C, Ryan J. Evaluation of Orthopedic and Athletic Injuries. Philadelphia, PA: F. A. Davis Company, 2002.
45. Stathopulu E, Baildam E. Anterior knee pain: A long-term follow-up. Rheumatology (Oxford) 42: 380–382, 2003.
46. Tyler TF, Nicholas SJ, Mullaney MJ, McHugh MP. The role of hip muscle function in the treatment of patellofemoral pain syndrome. Am J Sports Med 34: 630–636, 2006.
47. Vesci BJ, Padua DA, Bell DR, Strickland LJ, Guskiewicz KM. Influence of hip muscle strength, flexibility of the hip and ankle musculature, and hip muscle activation on dynamic knee valgus
during a double-legged squat. J Athl Train 42: S-83, 2007.
48. Wijdicks CA, Griffith CJ, LaPrade RF, Spiridonov SI, Johansen S, Armitage BM, Engebretsen L. Medial knee injury: Part 2, load sharing between the posterior oblique ligament and superficial medial collateral ligament. Am J Sports Med 37: 1771–1776, 2009.
49. Willson JD, Davis IS. Utility of the frontal plane projection angle in females with patellofemoral pain. J Orthop Sports Phys Ther 38: 606–615, 2008.
50. Willson JD, Ireland ML, Davis I. Core strength and extremity alignment during single leg squats. Med Sci Sports Exerc 38: 945–952, 2006.
51. Zeller BL, McCrory JL, Kibler WB, Uhl TL. Differences in kinematics and electromyographic activity between men and women during the single-legged squat. Am J Sports Med 31: 449–456, 2003.
Keywords:Copyright © 2013 by the National Strength & Conditioning Association.
knee valgus; dorsi flexion; hip adductor; gluteus medius; gluteus maximus