This informal CPD article ‘Biomechanical Analysis of the Lower Limb - Part 1: Vectorial Dominances of the Hip and Knee’, was provided by Dr. Mauro Lastrico, Physiotherapist at AIFiMM Formazione, an organisation recognised by the Italian Ministry of Health as an authorised CME provider. They offer organised training courses in the Mézières Method, a rehabilitative and postural approach.
This article applies to the lower limb the physical principles presented in previous contributions of this series: the model of muscle shortening as viscoelastic deformation of connective components, with the distinction between Resistant Force and Work Force [1,11]; the interpretation of body equilibrium as alignment between the weight force (G) and the ground reaction force (R) [2]; and vector analysis as a tool for identifying the muscular dominances responsible for alterations in physiological joint sequence [3,4]. Subsequent contributions have applied these principles to the vertebral column in the frontal [16,17] and sagittal [18] planes, to the hyoid bone [19], to the temporomandibular joint [20,21] and to the shoulder complex [22,23]. The present work demonstrates how a single skeletal segment — the femur — transmits mechanical resultants to both joints, and how loaded and unloaded conditions radically modify the vectorial dominances.
1. The Hip Joint
1.1 Functional Classification of Hip Muscles
The muscles of the hip can be distinguished into two functional categories according to the length of their line of force and their vectorial behaviour [5,6,13,30]. Stabiliser muscles are monoarticular muscles with a short line of force, whose vectors primarily favour joint stabilisation; their excessive tension manifests through compaction of the femoral head within the acetabulum [5,7,24]. Dynamic muscles are polyarticular and monoarticular muscles with a significant line of force — such as the adductors — whose vectors favour movement and positioning of the femur [5,6,29].
This distinction carries direct clinical implications: alterations in the joint axis are predominantly determined by the dynamic muscles, while the stabiliser muscles respond by increasing basal tone to contain the femoral head, acting as true active ligaments capable of adapting to intra-articular stresses [5,7,24].
1.2 Flexion–Extension Dominances: the Loaded–Unloaded Distinction
The flexion–extension dominances of the hip are expressed in radically different ways depending on whether the femur is the mobile point or the fixed point [5,6,8].
With the femur as mobile point (unloaded limb), the vectorial dominance is in hip flexion. The flexors — iliopsoas, rectus femoris, sartorius, femoral adductors, gracilis, tensor fasciae latae and pectineus — are numerically and vectorially superior to the extensors, represented essentially by the hamstrings and glutei [5,6,13].
With the femur as fixed point (foot in contact with the ground), these same muscles change the direction of their action: rather than approximating the femur to the pelvis, they approximate the pelvis to the femur [5,8,14]. The iliopsoas and rectus femoris, pulling through their pelvic insertions, produce pelvic anteversion which draws the lumbar vertebrae along, increasing the lordosis [5,8,15]. The hip extensors, whilst opposing this action, are subdominant when the axial load increases the demand for joint stabilisation [5,6]. Under load, therefore, the vectorial resultant favours pelvic anteversion and lumbar hyperlordosis.
1.3 Adduction–Abduction Dominances
The vectorial dominance in adduction–abduction is in favour of adduction [5,6,30]. The adductors — femoral adductors, gracilis, gluteus maximus with insertion on the gluteal tuberosity, pectineus, quadratus femoris and obturator externus — are numerically superior to the abductors, represented by tensor fasciae latae, gluteus medius and minimus, gluteus maximus with insertion on the fascia lata, piriformis and obturator internus [5,6].
The adduction dominance manifests primarily at the distal portion of the femur, projecting the femoral head towards dislocation [5,7]. The abductors, conversely, express their action predominantly at the proximal portion, acting as dynamic ligaments capable of adapting to intra-articular stresses [5,7,15].
1.4 Rotatory Dominances
The rotatory dominances of the hip present a specificity linked to the loaded condition [5,6]. When unloaded — for example in the supine position or during the swing phase of gait — the external rotators are numerically superior and dominant: adductors, biceps femoris, sartorius, gluteus maximus, gluteus medius and minimus with their dorsal fibres, iliopsoas, quadratus femoris, obturator internus and piriformis [5,6,14].
In the standing position with the foot in contact with the ground, this relationship is reversed. Considering the length of forces and the expressible power, the dominant vectors become the semitendinosus and semimembranosus, in co-agonism with the adductor magnus and gracilis [5,6,8,28]. The resulting vectorial dominance is thus expressed in the direction of internal rotation.
1.5 Joint Equilibrium and Compensations: the Piriformis Syndrome
The muscles with long vectors that, through modest intrinsic shortenings, alter the joint axis must be counterbalanced by the monoarticular muscles which, acting as active ligaments, raise their basal tone [5,7,24]. This increase in tone may produce local symptoms [12,26].
The piriformis syndrome constitutes a paradigmatic clinical example and may manifest in two opposing scenarios [5,7,9,26]. In the first scenario, the muscular dominance brings the femoral head into internal rotation and abduction — as occurs in knee valgus, where distal adduction of the femur produces proximal abduction — and the piriformis must activate at high intensity to contain the joint [5,7]. In the second scenario, in knee varus, the femoral head is driven into the acetabulum and the piriformis, with its insertions in approximation, must work with increased basal tone to remain effective in its role as an active ligament [5,7,25].
In both cases, in terms of the Resistant Force/Work Force ratio [1,11], the increase in Resistant Force reduces the available Work Force, producing mechanical inefficiency and overload that may compress the sciatic nerve [1,5,7,9].
Hamstrings maintaining their line of force
2. The Knee
2.1 The Mechanism of Hyperextension Under Load
In the standing position with the foot as fixed point in contact with the ground, the hamstrings and the triceps surae do not reverse their action, but the direction of their traction produces an opposite mechanical effect to that expected [5,6,10,15].
The hamstrings, maintaining their line of force between the ischium and the tibia, with the foot as fixed point pull the tibia posteriorly. Since the tibia cannot move backwards — being blocked by the foot in contact with the ground — the traction is translated into a thrust of the knee towards extension [5,10]. Similarly, the triceps surae, with its femoral insertion anterior to the heel as fixed point, pulls the femur posteriorly: this traction too, with the foot blocked, is converted into knee extension [5,10].
The rectus femoris, with the foot as fixed point, expresses its extensor component only in the portion between the patella and the tibial tuberosity — a minimal fraction of its total length. Its action is therefore one of participation in extension, not of primary mover [5,6]. The true motors of extension under load are the hamstring–triceps surae couple.
This dynamic is even more evident when rising from a chair, walking uphill or climbing stairs [5,14,28]. The knee extends through the action of the hamstring–triceps surae couple, whilst the rectus femoris is engaged primarily in pelvic stabilisation: it is the patella, functioning as a force multiplier, that enables it to counterbalance the hamstrings, which would otherwise produce pelvic retroversion and render dynamic action impossible [5,6,10].
Genu recurvatum also produces alterations at the hip and ankle joints. The overall G and R forces, unable to distribute along the entire femur in hyperextension, remain localised within the acetabular cavity, producing potential mechanical conflicts [2,5].
2.2 Internal Rotation and Flexion
Under load, the dominant vectors of femorotibial rotation are those of the semitendinosus and semimembranosus, in association with the femoral adductors with an internal rotation component [5,6]. Hyperextension and internal rotation frequently compose an associated pattern.
The hyperextending action of the hamstring–triceps surae couple is limited by the femorotibial joint [5]. Once the maximum limit is reached, if the shortening of these two muscle groups progresses, the final resulting line of force will produce knee flexion: the tibial insertions of the hamstrings will be found posterior to the PSIS, just as the femoral insertions of the triceps surae will be posterior to the heel [5,10,11].
In this condition, the two muscle groups once again become knee extensors, but their vertical vectorial components act at such intensity as to prevent extension itself [5]. The sum of horizontal and vertical vectorial components, in the standing position, cannot extend the knee but can, in collaboration with the quadriceps, oppose falling to the ground. This action requires great energy expenditure with consequent joint stiffening [5,10,15].
2.3 External Rotation and Progression of Patterns
If, once the articular limit of internal rotation is reached, the hamstrings shorten further, the external rotation component of the biceps femoris prevails, supported by those adductors with an external rotation action [5,6].
The four patterns — hyperextension, internal rotation, flexion and external rotation — represent a progression of worsening [5,6,29]. A knee that appears well positioned may truly be so, but it may equally have exhausted the first two directions of movement and flowed into the subsequent ones [5]. The two patterns have as their extremes internal rotation and genu recurvatum on one side, and external rotation and flexion on the other. During the transition, the components may produce intermediate patterns in various associations. This progression, as an expression of further muscular shortening, renders the knee joint progressively stiffer, increasing the intra-articular compressive components [5,6,12].
The tibialis posterior
2.4 Valgus and Varus
In the absence of congenital or acquired skeletal alterations, valgus is determined by shortening of the adductors — which, by adducting the distal portion of the femur, create a valgising force couple — and of the triceps surae which, as a strong heel supinator, with the foot in contact with the ground deviates the distal portion of the femur medially [5,6,10]. The tibialis posterior contributes similarly, deviating the proximal portion of the tibia medially [5,28].
Varus is vectorially determined by shortening of the muscles originating from the foot when the foot is the fixed point: tibialis anterior and peronei [5,6]. The hip abductor muscles, being monoarticular and acting at the proximal level of the femur, have little influence on the femorotibial relationship but are highly effective in stabilising the femoral head within the acetabulum [5,7].
To unmask the rotatory component that may disguise the true valgus–varus relationship, the derotation test is indicated: in the standing position, the patient is asked to derotate the femurs whilst maintaining the feet parallel and the knees extended. Elimination of the rotatory component reveals the actual valgus–varus relationship of the joint, guiding identification of the primary components of the alteration [5,6,12,13].
Conclusions
Analysis of the hip–knee complex reveals how the femur constitutes the mechanical element through which vectorial dominances propagate between the two joints [5,6,15]. The distinction between loaded and unloaded conditions radically modifies the direction of muscular resultants: when unloaded, hip flexion and external rotation prevail; under load, pelvic anteversion with lumbar hyperlordosis and internal rotation dominate [5,8,14].
The mechanism of hyperextension under load, in which the hamstring–triceps surae couple acts as the true motor of knee extension, demonstrates how the physics of force application points — not a change in muscular function — determines the resulting effect [5,10]. The progression of pathological knee patterns — from hyperextension and internal rotation to flexion and external rotation — confirms that observable alterations follow precise and predictable physical laws [5,6].
As with all the districts analysed, the coherent therapeutic sequence involves first the reduction of Resistant Force in shortened dominant muscles, followed by strengthening to consolidate the correction obtained [1,3,25,27]. The alterations of the knee and the foot mutually influence each other through the kinematic chain of the lower limb: the analysis of the vectorial dominances of the foot will be the subject of the next contribution.
We hope this article was helpful. For more information from AIFiMM Formazione, please visit their CPD Member Directory page. Alternatively, you can go to the CPD Industry Hubs for more articles, courses and events relevant to your Continuing Professional Development requirements.
References
1. Lastrico M. Clinical Assessment of Muscle Shortening. The CPD Certification Service; 2025.
2. Lastrico M. Body Equilibrium — A Physical-Clinical Interpretation of Human Upright Stability. The CPD Certification Service; 2025.
3. Lastrico M. Vector Analysis in Musculoskeletal Biomechanics — Part 1: Foundations and Clinical Principles. The CPD Certification Service; 2025.
4. Lastrico M. Vector Analysis in Musculoskeletal Biomechanics — Part 2: Clinical Applications and Case Interpretation. The CPD Certification Service; 2025.
5. Kapandji IA. The Physiology of the Joints. Vol. 2: The Lower Limb. 6th ed. Edinburgh: Churchill Livingstone; 2011.
6. Neumann DA. Kinesiology of the Musculoskeletal System: Foundations for Rehabilitation. 3rd ed. St. Louis: Elsevier; 2017.
7. Levangie PK, Norkin CC. Joint Structure and Function: A Comprehensive Analysis. 5th ed. Philadelphia: F.A. Davis; 2011.
8. Sahrmann SA. Diagnosis and Treatment of Movement Impairment Syndromes. St. Louis: Mosby; 2002.
9. Hopayian K, Danielyan A. Somatic dysfunction of the piriformis muscle and the sciatic nerve. J Back Musculoskelet Rehabil. 2018;31(3):395–401.
10. Winter DA. Biomechanics and Motor Control of Human Movement. 4th ed. Hoboken: Wiley; 2009.
11. Fung YC. Biomechanics: Mechanical Properties of Living Tissues. 2nd ed. New York: Springer-Verlag; 1993.
12. Magee DJ. Orthopedic Physical Assessment. 6th ed. St. Louis: Elsevier; 2014.
13. Kendall FP, McCreary EK, Provance PG, Rodgers MM, Romani WA. Muscles: Testing and Function with Posture and Pain. 5th ed. Baltimore: Lippincott Williams & Wilkins; 2005.
14. Perry J, Burnfield JM. Gait Analysis: Normal and Pathological Function. 2nd ed. Thorofare: Slack Incorporated; 2010.
15. Nordin M, Frankel VH. Basic Biomechanics of the Musculoskeletal System. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2012.
16. Lastrico M. Vector Analysis of the Vertebral Column in the Frontal Plane — Part 1. The CPD Certification Service; 2025.
17. Lastrico M. Vector Analysis of the Vertebral Column in the Frontal Plane — Part 2. The CPD Certification Service; 2025.
18. Lastrico M. Vector Analysis of the Vertebral Column in the Sagittal Plane. The CPD Certification Service; 2025.
19. Lastrico M. Hyoid Bone Biomechanical Analysis. The CPD Certification Service; 2025.
20. Lastrico M. TMJ Biomechanical Analysis — Part 1. The CPD Certification Service; 2025.
21. Lastrico M. TMJ Biomechanical Analysis — Part 2. The CPD Certification Service; 2025.
22. Lastrico M. Biomechanical Analysis of the Shoulder — Part 1. The CPD Certification Service; 2025.
23. Lastrico M. Biomechanical Analysis of the Shoulder — Part 2. The CPD Certification Service; 2025.
24. Panjabi MM. The stabilizing system of the spine. Part I. Function, dysfunction, adaptation, and enhancement. J Spinal Disord. 1992;5(4):383–389.
25. Boyling JD, Jull GA. Grieve’s Modern Musculoskeletal Physiotherapy. 4th ed. Edinburgh: Churchill Livingstone; 2004.
26. Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Vol. 2. Baltimore: Williams & Wilkins; 1992.
27. Kisner C, Colby LA, Borstad J. Therapeutic Exercise: Foundations and Techniques. 7th ed. Philadelphia: F.A. Davis; 2017.
28. Michaud TC. Human Locomotion: The Conservative Management of Gait-Related Disorders. Newton: Newton Biomechanics; 2011.
29. Page P, Frank CC, Lardner R. Assessment and Treatment of Muscle Imbalance: The Janda Approach. Champaign: Human Kinetics; 2010.
30. Netter FH. Atlas of Human Anatomy. 7th ed. Philadelphia: Elsevier; 2019.
