J Appl Physiol 105: 800-804, 2008.
First published June 12, 2008; doi:10.1152/japplphysiol.00961.2007
8750-7587/08 $8.00
Quadriceps cross-sectional area changes in young healthy men with different magnitude of Q angle
Aikaterini E. Tsakoniti,1
Christoforos A. Stoupis,2 and
Spyros I. Athanasopoulos1
1Sports Physical Therapy Laboratory, Department of Sports Medicine and Biology of Exercise, Faculty of Physical Education and Sports Science, National and Kapodestrian University of Athens, Greece; and 2Department of Radiology, University of Berne and Spital Maennedorf, Berne, Switzerland
Submitted 12 September 2007
; accepted in final form 10 June 2008
 |
ABSTRACT
|
|---|
Knee pain and dysfunction have been often associated with an ineffective pull of the patella by the vastus medialis (VM) relative to the vastus lateralis (VL), particularly in individuals with knee joint malalignment. Such changes in muscular behavior may be attributed to muscle inhibition and/or atrophy that precedes the onset of symptoms. The aim of this study was to investigate possible effects of knee joint malalignment, indicated by a high quadriceps (Q) angle (HQ angle >15°), on the anatomic cross-sectional area (aCSA) of the entire quadriceps and its individual parts, in a group of 17 young asymptomatic men compared with a group of 19 asymptomatic individuals with low Q angle (LQ angle <15°). The aCSA of the entire quadriceps (TQ), VM, VL, vastus intermedius (VI), rectus femoris (RF), and patellar tendon (PT) were measured during static and dynamic magnetic resonance imaging (MRI) with the quadriceps relaxed and under contraction, respectively. A statistically significant lower aCSA was obtained in the HQ angle group, compared with the LQ angle group, for the TQ, VL, and VI in both static (TQ = 9.9%, VL = 12.9%, and VI = 9.1%; P < 0.05) and dynamic imaging (TQ = 10.7%, P < 0.001; VL = 13.4%, P < 0.01; and VI = 9.8%, P < 0.05) and the aCSA of the VM in dynamic MRI (11.9%; P < 0.01). The muscle atrophy obtained in the HQ angle group may be the result of a protective mechanism that inhibits and progressively adapts muscle behavior to reduce abnormal loading and wear of joint structures.
magnetic resonance imaging; knee; muscle inhibition; malalignment
KNEE JOINT MALALIGNMENT HAs been considered to be one of the factors that may contribute to musculoskeletal pathology of the knee joint itself, as well as the hip and the foot. Hungerford and Barry (18) using the quadriceps angle (Q angle), the angle that is formed between the line of action of the quadriceps muscle and the direction of the patellar tendon (Fig. 1), as an indicator of knee joint malalignment, stressed that when the knee joint is not properly aligned, such as in the case of a valgus knee, the quadriceps pulls the patella more outward and laterally than normal. Other authors have shown that Q angles higher than 15° for men and 20° for women are related more to patellofemoral pain and dysfunction of the extensor mechanism of the knee (1, 21). The coexisting changes in the contact surface of the patellofemoral joint in these individuals may predispose to chondromalacia (17, 23) and patellar subluxation or dislocation (18). The mechanism that may underlie the abnormal drive of the patella into the trochlea notch of the femur leading to knee pain and dysfunction may be related to a less effective pull of the vastus medialis (VM) relative to the vastus lateralis (VL), probably due to pain inhibition and/or muscle atrophy.

View larger version (25K):
[in this window]
[in a new window]
|
Fig. 1. Quadriceps femoris angle (Q angle) as formed by the line that connects the anterior superior iliac spine (ASIS) with the center of the patella (CP) and the line that connects the center of the patella with the tibial tubercle (TT).
|
|
To date, the majority of research studies focusing on the effectiveness of the quadriceps muscle have been performed on symptomatic individuals, regardless of knee joint malalignment (7, 25, 34, 41, 45). The results of these studies revealed a reduced EMG activity of the VM oblique (VMO) relative to VL, as it was shown by the alteration of VMO-to-VL ratio activation patterns (7, 41). A reversal in the firing sequence of these muscles has been also reported in patients with patellofemoral pain syndrome, compared with the control group (45). Based on this evidence, research suggests that the neuromuscular imbalance may have its origin in an abnormal mechanical alignment (7, 30, 41, 45). Furthermore, it remains unclear whether the lower EMG activity of the VM relative to VL was due to pain inhibition and/or muscle atrophy that preceded the onset of pain symptoms.The development of computed tomography has enabled researchers to determine the force-generating capacity of a muscle, based on the widely accepted concept that the maximum force that can be produced by a muscle is directly proportional to its cross-sectional area (CSA) (3, 22, 26). Strength changes of a muscle based on changes of its CSA have been monitored in several previous studies to determine whether that particular muscle was affected by aging (11, 27), training, or detraining (15, 16, 32) and disuse (e.g., bed rest, immobilization) of a body part (4, 35). To our knowledge, there is no information concerning the possible effect of knee joint malalignment on the CSA of the quadriceps muscle, neither in healthy individuals nor in individuals with knee joint pain and dysfunction. The purpose of the present study was to determine whether the CSA of the individual parts, as well as the entire quadriceps muscle, was altered in individuals with knee joint malalignment. To establish whether such possible changes preceded, or followed the onset of pain symptoms, measurements of the CSA of the quadriceps were performed on a sample of nonsymptomatic individuals. Such information would be of clinical importance, because it can improve both prevention and rehabilitation programs in patients with knee joint pain and dysfunction.
 |
METHODS
|
|---|
Subjects
Thirty-six healthy men were selected for this study, based on the magnitude of the Q angle, from a population of 265 first-year healthy male students of the Department of Physical Education and Sports Sciences. Setting a cutoff Q angle of 15°, subjects were divided into two groups. The first group was consisted of 17 subjects with Q angles lower than 15°, and the second group included 19 subjects with Q angles higher than 15°. Before selection, each subject underwent a thorough clinical assessment and was questioned about past medical history and the level of habitual physical activity. The physical activity level was quantified, using the kinetic activity assessment questionnaire (2). Subjects with postural deviations, such as leg length discrepancy, recurvatum knees, muscle shortening, kyphosis and/or scoliosis, past surgery, injury of the lower limbs or patellofemoral pain syndrome, thyroid dysfunction or rheumatic conditions, obesity, use of anabolic drugs and/or participation in organized athletic activities, or increased level of kinetic activity (>8 h/wk), were excluded from the experimental procedure. All subjects participated voluntarily, after being informed of the purpose of the study, signing a written consent. The experimental procedure was approved by the ethics committee of the University of Athens.
Procedures
Q angle determination.
The Q angle was measured in the dominant lower leg of the subjects, using a simple full-circle goniometer with a lengthened arm. Leg dominance was determined based on their individual preference when asked to kick a ball. Each subject was required to lie in supine position with the knees fully extended and the quadriceps relaxed. The foot was in a standardized position, so that the line connecting the middle of the heel with the second metatarsus was perpendicular to the ground (12), because the positioning of the foot in terms of inward-outward rotation influences the magnitude of the Q angle (33). Three landmarks were placed (8 mm in diameter), after palpation of the anterior superior iliac spine, at the center of the patella and the tibial tubercle. The patellar center was located at the intersection of a mediolateral line extending through the widest area of the patella and a superoinferior line connecting the base and the tip of the patella. The long arm of the goniometer was placed along the line connecting the anterior superior iliac spine with the center of the patella and the short arm along the line, connecting the center of the patella with the tibial tubercle. To determine interexaminer reliability, the landmarks were detached after each measurement, and the whole procedure was repeated a few minutes later by a second examiner who was not aware of the Q angle measured by the first examiner. A few days later, the whole procedure was repeated by the first examiner, to determine intraexaminer reliability.
Magnetic resonance imaging.
A CSA of the quadriceps muscle of the dominant side was measured via magnetic resonance imaging (MRI) using a 1.0-T imager (Impact, Siemens, Erlangen, Germany). The MRI was used because it provides maximum accuracy of a muscle's cross section in vivo measurements (31) and is radiation free. Each subject was placed in supine position. The knee of the dominant lower leg was placed in the commercial knee coil provided by the magnet manufacturer (quadrature-knee coil, a transmit-receive single-channel coil). The knee was supported and fixed in the coil using MRI-compatible cushions, also commercially available. The lower leg was also fixed, and the plantar surface of the foot was attached to a vertical MRI-compatible Plexiglas device to keep the foot fixed in this position. The hip was placed in a middle position in terms of rotation, while the knee was in a 10° flexion. The special knee coil was used for the static imaging (with the quadriceps relaxed at
10° flexion) and dynamic imaging (with isometric quadriceps contraction) of the knee at 0° extension. Images were obtained using longitudinal relaxation time- and transverse relaxation time-weighted spin echo standard techniques. Additional three-dimensional volume images were obtained with 1.6-mm-thick slices. All measurements were performed using the Numaris MRI computer software and were performed by an experienced radiologist who was not aware of the Q angle group classification of each subject.
Axial images were obtained and the anatomic CSA (aCSA) of the following muscles were measured, in relaxation and contraction: VM, VL, vastus intermedius (VI), rectus femoris (RF), and the total quadriceps muscle (TQ; total CSA of the quadriceps). The measurements were carried out in the middle area of the distal third of the distance between the femoral head and the femoral condyles. Additionally, the CSA of the patellar tendon (PT) was calculated based on its length and width, which were measured at the height of the intra-articular space.
Statistical analysis.
Statistical analysis was performed using the SPSS 14 software (SPSS, Chicago, IL). Comparisons between low Q (LQ) and high Q (HQ) angle groups, regarding the aCSA of the TQ, VL, VM, VI, RF, and PT measured under static and dynamic MRI, were performed using the nonparametric Mann-Whitney test because data were nonnormally distributed. Data are presented as means ± SD and median values. Inter- and intraobserver reliability for Q angle measurements was assessed using intraclass correlation coefficient (ICC) (37, 38). The level of statistical significance was set at 0.05.
 |
RESULTS
|
|---|
The magnitude of the Q angle in the LQ and HQ angle group was 10.1 ± 1.9 and 18.5 ± 2.6°, respectively. Differences in the anthropometric characteristics and activity levels of the subjects between the groups were not statistically significant (Table 1). The intraobserver reliability (ICC) for Q angle measurements was 0.90 ± 0.03, and the interobserver was 0.90 ± 0.04.
Descriptive data of aCSA for each muscle and of the CSA of the PT in LQ angle and HQ angle group for static and dynamic imaging are presented in Table 2. The aCSA of the TQ, VM, VL, and VI, measured under dynamic imaging, were statistically significant different between the LQ and HQ angle group (see Table 2 for individual P values). Static imaging revealed also a statistically significant difference regarding aCSA of the TQ, VL, and VI between the groups (see Table 2 for individual P values). VM aCSA on the LQ angle group was also greater compared with the HQ angle group; however, the differences were not statistically significant. Not statistically significant were also the differences between the two groups, regarding the VL-to-VM aCSA ratio for both static and dynamic imaging. The differences between LQ angle and HQ angle group regarding aCSA of RF and PT were not statistically significant in both static and dynamic conditions.
View this table:
[in this window]
[in a new window]
|
Table 2. Differences in each anatomic cross-sectional area of muscles and patellar tendon between the HQ angle and LQ angle group in static and dynamic imaging
|
|
 |
DISCUSSION
|
|---|
The findings of the present study revealed a 9.1–13.4% lower aCSA (muscle atrophy) of the entire quadriceps muscle, as well as the VM, VL, and VI in individuals with HQ angle compared with LQ angle. The muscle atrophy that was found in the HQ angle may be attributed to a neural mechanism by which length-tension changes in the capsuloligamentous and musculotendinous structures result in proprioceptive deficits, alterations in the afferent information to the central nervous system (CNS) and modifications in the efferent information. The role of capsuloligamentous mechanoreceptors is very important because they provide afferent information to the CNS via specific reflex arcs (10, 36) and thus contribute to the dynamic stability of a joint by facilitating and adjusting muscle kinetic response. In individuals with HQ angle, contraction of the quadriceps will tend to produce a "valgus vector" because of the patella's tendency to move laterally (18). This lateralization is resisted by the VMO, the passive medial soft tissue restraints, and the prominence of the lateral facet of the trochlea (8, 9, 14). In the face of chronic malalignment, the capsuloligamentous structures of the medial knee surface may become stretched (23) or loose due to accumulated creep (40), whereas those of the lateral surface become shortened and tight (23). These alterations have a direct effect on the receptors threshold, resulting in a degradation of kinesthesia and proprioceptive perception (40). Abnormal afferent information may in turn decrease
-motoneuron excitability, inhibiting muscle kinetic response (19, 20) and leading to muscle atrophy. Williams et al. (43) have shown, in a previous study, that proprioceptive deficits may be one of the factors that can cause impairment of voluntary contraction, muscle weakness, and nonuniform atrophy among the parts of the quadriceps in individuals who do not compensate well after anterior cruciate ligament injury (noncopers). These authors showed significantly lower volume and peak aCSA of the quadriceps with the VL and VI disproportionately atrophied compared with the uninjured side.
Alterations in the musculotendinous receptors threshold and differentiation in afferent and efferent neural signals may also contribute to the VM and VL muscle atrophy, in the individuals with HQ angle. These alterations may attribute to the different tensile loads applied along the myofibrils and the musculotendinous junction as joint angulation forces VL to function from a shortened position, whereas VM functions from a stretched position. Animal studies have shown that muscles immobilized in a shortened position developed a higher degree of atrophy than those immobilized in a stretched position (6). The muscle atrophy that is found is also accompanied by length-dependent changes in the cell shape. When a muscle is immobilized in a lengthened position, the number of the sarcomeres is increased and the length is reduced; the opposite occurs when a muscle is immobilized in a shortened position (44, 46). These findings also supported our observations regarding greater atrophy in the VL compared with VM.
Muscle atrophy of the entire quadriceps as well as the VL compared with VM may also be explained by the alterations in the efferent neural information originated from higher neural centers. Such changes have been reported in situations such as in joint immobilization (29, 48) and ligamentous injury (24), which have caused sensory deprivation and led to brain reorganization. Prolonged abnormal joint loading due to side-to-side differences in the length of the capsuloligamentous structures, as in individuals with HQ angle, may induce similar changes in the CNS, because the human body has the ability to ensure optimal joint function whenever this joint is dysfunctioned (39). In our study, quadriceps muscle activation may be lowered, and, therefore, atrophied through the years, to protect the joint structures from wear.
Another possible explanation for the differences in the cross sections of the quadriceps between the two groups is the different pennation angle of the quadriceps muscle fibers. The CSA of the quadriceps in the present study was measured based on axial images (aCSA) therefore the pennation angles of the individual parts of the quadriceps were not taken into account. The physiological CSA, on the other hand, is a method which has been used to calculate indirectly the perpendicular CSA of a muscle based on the muscle volume and length. This method has been used mainly in the assessment the of a muscle's capacity to generate force assuming that the muscle fiber pennation angle and the fiber-to-length ratios remain consistent (47). These conditions, however, do not apply to muscles with a complex architecture, such as the RF and VI, because their muscle fibers do not contract at the same rate (5). Therefore, the aCSA was favored over the physiological, taking into consideration that both the anatomical and physiological CSAs are highly correlated to the maximum voluntary strength produced by a muscle (3).
Based on our findings, the aCSA of the RF remained unaffected, compared with the other parts of the quadriceps in the HQ angle group. This may be explained by the fact that the biarticular RF is stronger as a hip flexor, rather than as a knee extensor, because the produced active force is determined by the fiber length of its proximal part (13). On the other hand, the VM and VL function to control the tracking of the patella in the trochlea groove (28) and may be more susceptible to muscle atrophy, as has been shown in previous studies (43).
The method used for the MRI of the quadriceps was one of the limitations in the present study. The aCSA of the quadriceps in our study was measured from images obtained in the middle of the distal third of the femur on both HQ and LQ angle groups. Other researchers (42), who, measuring the peak aCSA using a trapezoidal integration algorithm in young athletes, have reported a greater CSA of the quadriceps, compared with our findings. It is possible that performing the MRI on a different location of the quadriceps may result in a different aCSA between an HQ and an LQ angle group.
Our findings are also limited in the present study due to subjects positioning for Q angle and MRI measurements. Q angle in our study was measured in the supine position to be consistent with the supine position that each subject assumed during the MRI measurements. It should also be noted that, despite the fact that the lower extremity was fixed in the supine position, muscle contraction during a dynamic MRI could produce slight outward or inward movements, affecting our results. Q angle measurements performed in the standing position could reveal different values, because they can be influenced by the alignment of the adjacent joints (e.g., hip, ankle). Although such measurements would be more appropriate from a functional point of view, they would be inconsistent with the MRI, because such measurements are not possible in the standing position.
In conclusion, the results of this study revealed a lower aCSA in individuals with HQ angle. It is hypothesized that these changes may be attributed to neural alterations in the peripheral and CNS, which leads to muscle atrophy and possibly lowers muscle activation, to protect the joint from excessive loading and wear.
Further research is needed to determine the possible effect of knee joint malalignment on the strength, the activation patterns, the electromechanical efficiency, or fiber microstructure of the quadriceps muscle.
 |
GRANTS
|
|---|
This study was supported by the Secretariat General of Research and Technology and the European Union.
 |
ACKNOWLEDGMENTS
|
|---|
The authors gratefully acknowledge Dr. D. Mandalidis for his help in revising the manuscript, as well as all the participants for the effort devoted to this study.
 |
FOOTNOTES
|
|---|
Address for reprint requests and other correspondence: A. E. Tsakoniti, Sports Physical Therapy Laboratory, Dept. of Sports Medicine and Biology of Exercise, Faculty of Physical Education and Sports Science, National and Kapodestrian Univ. of Athens, 8 Isminis St., 172 37, Daphne, Greece (e-mail: ktsakon{at}phed.uoa.gr)
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
 |
REFERENCES
|
|---|
- Aglietti P, Insall JN, Cerulli G. Patellar pain and incongruence. I: measurements of incongruence. Clin Orthop Relat Res 217–224, 1983.
- Baecke JA, Burema J, Frijters JE. A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr 36: 936–942, 1982.[Abstract/Free Full Text]
- Bamman MM, Newcomer BR, Larson-Meyer DE, Weinsier RL, Hunter GR. Evaluation of the strength-size relationship in vivo using various muscle size indices. Med Sci Sports Exerc 32: 1307–1313, 2000.[Web of Science][Medline]
- Berg HE, Larsson L, Tesch PA. Lower limb skeletal muscle function after 6 wk of bed rest. J Appl Physiol 82: 182–188, 1997.[Abstract/Free Full Text]
- Blemker SS, Delp SL. Rectus femoris and vastus intermedius fiber excursions predicted by three-dimensional muscle models. J Biomech 39: 1383–1391, 2006.[CrossRef][Web of Science][Medline]
- Booth FW. Time course of muscular atrophy during immobilization of hindlimbs in rats. J Appl Physiol 43: 656–661, 1977.[Abstract/Free Full Text]
- Boucher JP, King MA, Lefebvre R, Pepin A. Quadriceps femoris muscle activity in patellofemoral pain syndrome. Am J Sports Med 20: 527–532, 1992.[Abstract/Free Full Text]
- Conlan T, Garth WP Jr, Lemons JE. Evaluation of the medial soft-tissue restraints of the extensor mechanism of the knee. J Bone Joint Surg Am 75: 682–693, 1993.[Abstract/Free Full Text]
- Desio SM, Burks RT, Bachus KN. Soft tissue restraints to lateral patellar translation in the human knee. Am J Sports Med 26: 59–65, 1998.[Abstract/Free Full Text]
- Dyhre-Poulsen P, Simonsen EB, Voigt M. Dynamic control of muscle stiffness and H reflex modulation during hopping and jumping in man. J Physiol 437: 287–304, 1991.[Abstract/Free Full Text]
- Frontera WR, Hughes VA, Fielding RA, Fiatarone MA, Evans WJ, Roubenoff R. Aging of skeletal muscle: a 12-yr longitudinal study. J Appl Physiol 88: 1321–1326, 2000.[Abstract/Free Full Text]
- Guerra JP, Arnold MJ, Gajdosik RL. Q angle: effects of isometric quadriceps contraction and body position. J Orthop Sports Phys Ther 19: 200–204, 1994.[Web of Science][Medline]
- Herzog W, Abrahamse SK, ter Keurs HE. Theoretical determination of force-length relations of intact human skeletal muscles using the cross-bridge model. Pflügers Arch 416: 113–119, 1990.[CrossRef][Web of Science][Medline]
- Hirokawa S. Effects of variation on extensor elements and operative procedures in patellofemoral disorders. J Biomech 25: 1393–1401, 1992.[CrossRef][Web of Science][Medline]
- Houston ME, Froese EA, Valeriote S, Green HJ, Ranney DA. Muscle performance, morphology and metabolic capacity during strength training and detraining: a one leg model. Eur J Appl Physiol 51: 25–35, 1983.[CrossRef][Web of Science]
- Hubal MJ, Gordish-Dressman H, Thompson PD, Price TB, Hoffman EP, Angelopoulos TJ, Gordon PM, Moyna NM, Pescatello LS, Visich PS, Zoeller RF, Seip RL, Clarkson PM. Variability in muscle size and strength gain after unilateral resistance training. Med Sci Sports Exerc 37: 964–972, 2005.[Web of Science][Medline]
- Huberti HH, Hayes WC. Patellofemoral contact pressures. The influence of Q angle and tendofemoral contact. J Bone Joint Surg Am 66: 715–724, 1984.[Abstract/Free Full Text]
- Hungerford DS, Barry M. Biomechanics of the patellofemoral joint. Clin Orthop Relat Res 144: 9–15, 1979.[Medline]
- Hurley MV. The effects of joint damage on muscle function, proprioception and rehabilitation. Man Ther 2: 11–17, 1997.[CrossRef][Medline]
- Hurley MV, Newham DJ. The influence of arthrogenous muscle inhibition on quadriceps rehabilitation of patients with early, unilateral osteoarthritic knees. Br J Rheumatol 32: 127–131, 1993.[Abstract/Free Full Text]
- Hvid I, Andersen LI, Schmidt H. Chondromalacia patellae. The relation to abnormal patellofemoral joint mechanics. Acta Orthop Scand 52: 661–666, 1981.[Web of Science][Medline]
- Ikai M, Fukunaga T. Calculation of muscle strength per unit cross-sectional area of human muscle by means of ultrasonic measurement. Eur J Appl Physiol 26: 26–32, 1968.[CrossRef]
- Insall J. Current concepts review: patellar pain. J Bone Joint Surg Am 64: 147–152, 1982.[Free Full Text]
- Kapreli E, Athanasopoulos S. The anterior cruciate ligament deficiency as a model of brain plasticity. Med Hypotheses 67: 645–650, 2006.[CrossRef][Web of Science][Medline]
- Karst GM, Willett GM. Onset timing of electromyographic activity in the vastus medialis oblique and vastus lateralis muscles in subjects with and without patellofemoral pain syndrome. Phys Ther 75: 813–823, 1995.[Abstract/Free Full Text]
- Knuttgen HG. Development of muscular strength and endurance. In: Neuromuscular Mechanisms for Therapeutic and Conditioning Exercise. Baltimore, MD: University Park Press, 1976, p. 97–118.
- Lexell J, Taylor CC, Sjostrom M. What is the cause of the ageing atrophy?: total number, size and proportion of different fiber types studied in whole vastus lateralis muscle from 15- to 83-year-old men. J Neurol Sci 84: 275–294, 1988.[CrossRef][Web of Science][Medline]
- Lieb FJ, Perry J. Quadriceps function. An anatomical and mechanical study using amputated limbs. J Bone Joint Surg Am 50: 1535–1548, 1968.[Abstract/Free Full Text]
- Liepert J, Tegenthoff M, Malin JP. Changes of cortical motor area size during immobilization. Electroencephalogr Clin Neurophysiol 97: 382–386, 1995.[CrossRef][Medline]
- Mariani PP, Caruso I. An electromyographic investigation of subluxation of the patella. J Bone Joint Surg Br 61-B: 169–171, 1979.[Web of Science][Medline]
- Mitsiopoulos N, Baumgartner RN, Heymsfield SB, Lyons W, Gallagher D, Ross R. Cadaver validation of skeletal muscle measurement by magnetic resonance imaging and computerized tomography. J Appl Physiol 85: 115–122, 1998.[Abstract/Free Full Text]
- Narici MV, Roi GS, Landoni L, Minetti AE, Cerretelli P. Changes in force, cross-sectional area and neural activation during strength training and detraining of the human quadriceps. Eur J Appl Physiol Occup Physiol 59: 310–319, 1989.[CrossRef][Web of Science][Medline]
- Olerud C, Berg P. The variation of the Q angle with different positions of the foot. Clin Orthop Relat Res 162–165, 1984.
- Powers CM. Patellar kinematics, part I: the influence of vastus muscle activity in subjects with and without patellofemoral pain. Phys Ther 80: 956–964, 2000.[Abstract/Free Full Text]
- Sargeant AJ, Davies CT, Edwards RH, Maunder C, Young A. Functional and structural changes after disuse of human muscle. Clin Sci Mol Med 52: 337–342, 1977.[Web of Science][Medline]
- Schultz RA, Miller DC, Kerr CS, Micheli L. Mechanoreceptors in human cruciate ligaments. A histological study. J Bone Joint Surg Am 66: 1072–1076, 1984.[Abstract/Free Full Text]
- Shoukri MM. Measures of Interobserver Agreement. London: Chapman & Hall, 2003.
- Shrout PE, Fleiss JL. Intraclass correlations: uses in assessing rater reliability. Psychol Bull 86: 420–428, 1979.[CrossRef][Web of Science][Medline]
- Simons DG, Travell JG, Simons LS. Myofascial Pain and Dysfunction: The Trigger Point Manual. Baltimore, MD: Williams & Wilkins, 1999.
- Solomonow M. Ligaments: a source of work-related musculoskeletal disorders. J Electromyogr Kinesiol 14: 49–60, 2004.[CrossRef][Web of Science][Medline]
- Souza DR, Gross MT. Comparison of vastus medialis obliquus: vastus lateralis muscle integrated electromyographic ratios between healthy subjects and patients with patellofemoral pain. Phys Ther 71: 310–316, 1991.[Abstract/Free Full Text]
- Tate CM, Williams GN, Barrance PJ, Buchanan TS. Lower extremity muscle morphology in young athletes: an MRI-based analysis. Med Sci Sports Exerc 38: 122–128, 2006.[CrossRef][Web of Science][Medline]
- Williams GN, Buchanan TS, Barrance PJ, Axe MJ, Snyder-Mackler L. Quadriceps weakness, atrophy, and activation failure in predicted noncopers after anterior cruciate ligament injury. Am J Sports Med 33: 402–407, 2005.[Abstract/Free Full Text]
- Williams PE, Goldspink G. Changes in sarcomere length and physiological properties in immobilized muscle. J Anat 127: 459–468, 1978.[Web of Science][Medline]
- Witvrouw E, Sneyers C, Lysens R, Victor J, Bellemans J. Reflex response times of vastus medialis oblique and vastus lateralis in normal subjects and in subjects with patellofemoral pain syndrome. J Orthop Sports Phys Ther 24: 160–165, 1996.[Web of Science][Medline]
- Witzmann FA, Kim DH, Fitts RH. Hindlimb immobilization: length-tension and contractile properties of skeletal muscle. J Appl Physiol 53: 335–345, 1982.[Abstract/Free Full Text]
- Zajac FE. Muscle and tendon: properties, models, scaling, and application to biomechanics and motor control. Crit Rev Biomed Eng 17: 359–411, 1989.[Web of Science][Medline]
- Zanette G, Tinazzi M, Bonato C, di Summa A, Manganotti P, Polo A, Fiaschi A. Reversible changes of motor cortical outputs following immobilization of the upper limb. Electroencephalogr Clin Neurophysiol 105: 269–279, 1997.[CrossRef][Medline]
Copyright © 2008 by the American Physiological Society.