scienza e sport

locandina Sezioni Tematiche
  Prima Pagina
Traumatologia sportiva
Medicina dello Sport 54(4): 295-304, 2001

Electromyographic analysis in the reconstruction of anterior cruciate ligament: a new control and prevention method.

Gian Nicola Bisciotti(1)
Rossano Bertocco
Pier Paolo Ribolla
Jean Marcel Sagnol (1)

  1. Facoltà di Scienze dello Sport, Università Claude Bernard, Lione (F).



In this study ten subjects, whose age, weight and height were respectively 25 + 3 years (mean + standard deviation), 71.1 + 6.5 kg and 179.7 + 4.2 cm were taken into account after they had been fully informed about the purposes of the research. They were all accustomed to sporting activity and had reported an isolated or associated breakage of anterior cruciate ligament (ACL), surgically treated through arthroscopy.

Each subject was asked to perform a series of 6 maximal isometric leg contractions at the height of the thigh with an articular angle standardized at 90°, both with the injured limb as well as with the sane counterpart, during which we recorded the value of the maximal isometric force as well as the electromyographic superficial signal (EMG) of the Vastus Medialis Obliquus (VMO) and of the Vastus Lateralis (VL). The deficiency of the force in the injured limb was equal to 30.27 + 21.655 (p< 0.005), the EMG VMO/VL Ratio of the sane limb and of the injured limb were equal to, respectively, 1.12 + 0.08 and 0.95 + 0.04, the difference proved to be statistically significant (p<0.006). The results show that following an operation to reconstruct the ACL, there is a greater contractile deficiency in the VMO compared to that of the VL, which shows up in a modification of the EMG Ratio, which in turn is a sign of an alteration in the patterns of the neuromuscular activation.

Key words: Electromyography , Anterior Cruciate Ligament, Vastus Medialis, Vastus Lateralis, Functional Deficiency.


An important aspect within the diagnosis of articular injury is a careful evaluation of the changes in the functional response of the muscles directly involved in the main movements of the joints.

In the context of a functional evaluation following an injury, the muscular dysfunction can show up as an altered pattern of muscular recruitment in the injured limb in regards to that of its sane counterpart1. This alteration within the strategy of the neuromuscular response, which can be seen in the injured limb, proofs a change in the neural input of the muscles involved in the specific movement. The surface electromyography (EMG) can represent a method of clinic investigation to underline a possible alteration in the muscular recruitment strategy or a "compensatory" recruitment pattern in the injured limb in comparison to health one1 15. The changes in the pattern of the neuromuscular activation and the following physiological mechanisms of adjustment of the muscular response, which can be seen by means of EMG, can be used successfully (in our opinion) for diagnostic purposes, especially if we consider the good reproducibility of this kind of study 3 66 47. The aim of this study is in fact to set out an EMG research protocol to be used for diagnostic purposes within articular injuries based on the alteration of the neuromuscular activation, which can be monitored in the injured limb in contrast to the sane counterpart in the specific case of the reconstruction of anterior cruciate ligament (ACL), following an isolated or an associated injury of the ligament and evaluating the available data concerning the rehabilitation therapy carried out and the possible risk of traumatic relapse (giving way)

For a better understanding of this matter, we believe it to be important to briefly clarify certain aspects directly related to the field of study in question.

The possible causes of damage to muscular tissue.

Damage to the muscular fibre can be caused by a single muscular contraction or as the culminating effect of a series of contractions 2. However the mechanism which appears to be a main correlating factor in the possible damaging of muscular fibre seems to be an eccentric type of contraction 1 14 26 52. The reason that there is higher incidence of traumas on a muscular level registered during situations of eccentric contractions is probably due to the fact that more force is produced in such a contraction than in a concentric or isometric activation 57 26. In fact in an eccentric contraction carried out at a velocity 90° s-1 the muscular region registers a force three times greater than the one registered at the same velocity during a concentric contraction 43. Moreover, during an eccentric contraction, the passive elements of the connective tissues of the muscle undergoing extension produce a greater force 18. Referring mainly to this datum, we must stressed that even the purely mechanical phenomenon of elongation can play an important role in bringing on an injury, since this can take place in a muscle which is active during the stretching phase or in a muscular region which is passive during the extension phase 27. During an eccentric contraction, in fact, the muscle undergoes a ‘overstretching’ phenomenon which, as such, can cause damage at the insertion of the tendon, at the muscle-tendon joint, or on a muscular region made more fragile by a vascular deficiency 43. It is interesting to note that the bi-articular muscles are the ones mainly exposed to traumatic injuries because, through their eccentric contraction, they have to control the articular range of more articulations7.

The different typology of the muscular fibres also gives a different incidence of traumatic injuries. Compared to the ST fibres, the FT fibres are in fact more exposed to structural damage probably due to their greater contractile capacity, which is turned into a greater production of force and contraction velocity 24 22. Moreover, the muscles which show a high percentage of FT are generally more superficial 41 and usually affect two or more articulations. Both these factors create a predisposition towards structural damage7 26. It is also interesting to note that a traumatic injury is mainly localized in the muscular-tendon joint, which proofs that there is a greater mechanical stress in the final portion of the muscular fibre 26 27 42 53 58 59.

Finally, we must underline the particular metabolic conditions connected to an eccentric contraction. Since in an eccentric contraction the muscular vascularisation is interrupted, the work carried out is anaerobic and creates an increase of the local temperature and an acidosis state, as well as an evident cellular anoxia. These metabolic situations create an increase in muscular fragility and a possible cellular necrosis on a muscular level and of the connective support43.

The alteration in the cellular functioning of the muscular tissue following a traumatic injury.

In consequence of an injury it is possible to register a series of effects on a muscular level that can be fundamentally connected to a degeneration of the muscular fibres, characterized by myofibrillar destruction together with damage, both on a mitochondrial level and of the sarcoplasmatic reticulum9. Moreover, in this condition of ultra structural muscular alteration there can be a sarcolema discontinuity10. Its loss of sarcolemma integrity with the damage to the sarcoplasmatic reticulum can cause a rise of the intracellular concentration of Ca++. The resulting alteration in the capacity to pump Ca++ from the sarcoplasm causes a parallel Ca++ homeostasis alteration, which would result in an uncontrolled contraction of the sarcomeres2 This uncontrolled contraction of the muscular fibres can persist even in the absence of a potential action able to depolarises the fibres, until the intracellular concentration of Ca++ remains high and the availability of ATP is sufficiently adequate 2 60. The mechanical forces, caused by this chain of events and persisting on a myofibrillar level after a traumatic injury, can cause an expansion of the affected myofibrillar region 2. If the damage suffered by the muscular tissue is severe, the clinical symptoms are manifested by a more or less painful symptomatology, both in passive extension and in active contraction26, swelling, inflammation or oedema in the muscular tissue itself 25, a reduction in the force capacity of the muscular region in question and an alteration of the proprioceptive schemes.26 32 42 44 53 58

Nevertheless is important to note that in many cases, after an appropriate period of rehabilitation, the duration of which depending obviously on the severity of the trauma suffered, the contractile characteristics and thus the capacity of the muscular region in question to generate force, can return within normal limit26. Moreover during the period of rehabilitation and after the muscle could be at a greater risk of suffering further injuries than it would in a situation of complete physiological normality17.

The alteration of the neuromuscular activation pattern following a traumatic injury.

The surface electromyography (EMG) is usually used in clinical and functional examinations as an instrumental methodology apt for giving information regarding the patterns of neuromuscular activation in the muscular regions in question6 33 36 37. The electromyographic signals obtainable by using the surface electromyography depends every instant on the number of active motor units (MU), on their discharge frequency, on their degree of synchronisation and on their action potential6. A traumatic injury suffered on a muscular level can cause an alteration of the EMG signal and in particular of the Force/EMG Ratio (F/EMG Ratio) of the injured limb in contrast to that registered in its healthy counterpart during a muscular contraction17 . This alteration of the EMG signal can be caused mainly by two types of mechanisms, the first is connected to the sensation of pain felt during the contraction itself. The nociceptive reaction can in fact be responsible for an alteration of the responses of the multiple motoneurons pool, whose activation is conditioned by the anatomical location of the muscular injury suffered and by the intensity of the pain felt17 31 55. The second mechanism which can cause an alteration of the F/EMG Ratio is not necessary linked to the sensation of pain felt by the patient. In fact, in certain cases the severity of the injury and the consequent functional limitation linked to this do not necessarily bring about a sensation of pain of the same severity17. In the field of this particular clinical condition the alteration of the F/EMG Ratio of the injured limb compared to its healthy counterpart can be attributed to an increased number of motor neurons being recruited to compensate the force deficiency of the injured muscular region17. This particular kind of compensatory mechanism can affect the MU belonging to a region of the same muscular group not directly affected by the traumatic injury or it can involve the MU belonging to the other synergic muscular groups, which are able to carry out the same kind of biomechanical activity17 23 51.

Muscular pain concomitant with an isolated or associate ACL injury

An isolated or associate ACL injury, which has to be surgically reconstructed by means of arthroscopyc technique using patellar tendon or semitendinous or gracilis tendon, can cause an evident amyotrophia of the thigh muscles29. Muscular hypotrophy involves both the flexor muscles and the extensor ones even of the muscular damage suffered by extensor muscles seems much greater46 . The associated injury of the internal meniscus seems to worsen the dynamic function deficiency in flexion while injuries of the external meniscus worsen the overall dynamic function in extension46. The loss of muscle tone, observable above all in the femoral quadriceps causes a loss of the contractile capacity during a muscular contraction carried out following isokinetic and isometric methods46 68. The loss of force in the extensor muscles in patients that have undergone surgery to reconstruct the ACL, seems to be linked to the velocity of contraction called for and it becomes particularly evident when muscles contraction takes place at a low velocity28. The hypotrophy and the consequent loss of force affects above all the Vastus Medialis Obliquus (VMO)65 and could cause an alteration of the EMG Ratio Vastus Medialis Obliquus / Vastus Lateralis (VMO/VL Ratio) thus weakening the dynamic neuromuscular activation pattern17.



In this study ten subjects were taken into account whose age, weight and height were respectively 25 ± 3 years (average ± standard deviation), 71.1 ± 6.5 kg and 179.7 ± 4.2 cm. All the subjects took part in some kind of sports activity (table 1) and had suffered an isolated or associated injury of the ACL treated surgically by means of an arthroscopyc reconstruction (table 2). All the subjects, during the test period continued their normal physiotherapy rehabilitation activities. None of the subjects showed symptoms of muscular or neuromuscular problems apart from the one described above. When the test was carried out the subjects were in their 60° ± 7° post- operative day and had completely recuperated the articular mobility of the injured limb. Moreover all the subjects had been informed of the aim of the study and of the possible risks involved.


Determination test for the EMG registration on a maximal isometric contraction.

Each subject asked to carry out 6 maximal isometric contractions for limb of the leg extensor muscles at the height of the thigh in open kinetic chain. The contractions lasted 5’’ with a standardized articular angle of the knee of 90°17 64. The value of maximal isometric force (MIF) was registered by means of a strain gauge (Globusitalia, Treviso, Italy, Mod. Ergometer, sample rate 100 Hz, non linearity hysteresis and repeatability 0.02% of R.O, temperature compensated 0° to 50°, charge scale 0-300 kg). At the same time as the MIF was being registered a surface electromyography was carried out on the Vastus Medialis Oblique (VMO) and the Vastus lateralis (VL) of each limb. The electrodes (Neuro Line Disposable Neurology Elecrodes, Type 720-00-S Qty/Menge 25) were placed on both limbs in conformity with the positions indicated by Perotto and coll.45. The registration of the EMG (IEMG) was carried out with a pair of bipolar electrodes positioned on the abdominal muscles 20 mm apart. The signal given by the electromyography apparatus (Ergo system EMG by Globusitalia, Treviso, Italy, 2000 Hz sample ratebandWith 25-500 Hz, sensibility 0,48 microV.) and by the strain gauge were synchronised and analysed using a programme designed specifically for this purpose (Ergometer Total Rehabilitation, Globus Italia).

The following values were thus calculated:

1. the maximal isometric force (MIF) given by the highest value of force reached on the force reached on the force —time scale after 900 ms of isometric contraction39 54. This value was calculated for both limbs.

2. the difference of percentage of the MIF registered for each limb (D%F).

3. the integral of electromyography activity relative to the VMO and the VL (ò VMO, ò VL) both of the injured limb and the healthy one.

4. the electromyographic Ratio between VMO and VL (VMO/VL Ratio) obtained by using the relation between VMO and VL integrals of electromyographic activity. This value was calculated on both limbs.

4. the Ratio between the isometric force value and the total electromyographic activity (F/EMG Ratio) calculated by using the relation between the force integral with the sum of the integral of electromyographic activity of the VMO and the VL. This value was calculated on both limbs.

5. the difference of percentage between the sum of electromyographic surface of the VMO and VL registered for the healthy limb and the injured limb (D%ò VMO+ò VL).

6. the percentage difference between the electromyographic surface of the VMO of the healthy limb and the injured limb (D%ò VMO).

7. the percentage difference between the electromyographic surface of the VL of the healthy limb and the injured one (D%ò VL).


Ordinary statistical indexes such as average, standard deviation and variance were calculated for each single variable and situation.

With Wilkoxon’s non parametric test the injured and the healthy limbs were compared and the the differences between the average values of the MIF, ò VMO, ò VL, VMO/VL Ratio and the F/EMG Ratio were recorded.

The percentage difference between the sum of the ò VMO and the ò VL of the healthy and of the injured limb (D% ò VMO+ò VL) was correlated with the percentage difference of the force recorded in the two limbs (D% F) using the Spearman’s rank order correlation coefficient.

Moreover, using again the Spearman’s rank order correlation coefficient the following values were correlated whether D%F with the difference between the values of the ò VMO (D% ò VMO) and the ò VL (D% ò VL) of both the healthy and the injured limb, or the values of the D% ò VMO and of the D% ò VL.

The level of statistical significance was fixed at p<00.5.


The MIF values recorded on the healthy and on the injured limb were equal to, respectively 681.90 ± 49.17 and 704.41 ± 174.83 N. The difference between the two values (D% F), equal to 30.27 ± 21.65%, resulted statistically significant (p<0.005).

The ò VMO values of the healthy and of the injured limb were respectively 1.82 ± 0.66 and 0.92 ± 0.39 mV· s. The difference equal to the 43.86 ± 27.93% resulted statistically significant (p<0.005).

The ò VL values of the healthy and of the injured limb were respectively 1.60 ± 0.42 and 0.98 ± 0.43 mV · s. The difference equal to 34.04 ± 12.25% resulted statistically significant (p<0.01).

The difference between the ò VMO and the ò VL values of the healthy limb, equal to 10.69 ± 6.58%, was statistically significant (p<0.01).

The difference between the ò VL and the ò VMO values of the injured limb, equal to 5.01 ± 3.65%, resulted statistically significant (p<0.05).

The VMO/VL Ratio between the healthy and the injured limb, equal respectively to 1.12 ± 0.08 and 0.95 ± 0.04, resulted statistically significant (p<0.006).

The F/EMG Ratio of the healthy and the injured limb equal respectively to 1071.30 ± 346.43 and 1308.80 + 310.54 [ N · s] · [ mV ·s] -1, is not resulted statistically significant.

The D % ò VMO + ò VL resulted positively correlated to the D%F (r = 0.80, p<0.004).

The D% ò VMO resulted positively correlated to the D%F (r = 0.97, p<0.001).

The D%ò VL resulted positively correlated to the D% F (r = 0.80, p<0.004).

The relation between the D%ò VMO and D% ò VL resulted statistically significant (r = 0.84, p<0.002).


After a surgical reconstruction of an isolated or associated injury of the ACL, the main causes of the knee’s instability are hypo-tonus and hypo-trophy of the femoral quadriceps, in particular of the VMO, which has suffered hypo-functioning consequent to the operation and is the most damaged

muscular region.8 48 It is also important to remember that VMO is the muscular district chiefly injured when the knee ligament apparatus is damaged35. The VMO plays an important mechanical role in many sporting motions. In most movements directly connected with sports activities that involve running, the VMO carries out an important mechanical function, being particularly active when the athlete touches the ground after jumping11 12, walks or runs laterally67. It is the most important power generator during the push-off phases in speed-skating4 and also it is the most important force generator during isokinetic leg extensions at the height of the thigh34. Finally during eccentric contractions the VMO is also much more active than the VL19. In addition to these considerations, in the functional ambit it is important to note that the VMO is the muscular region of the thigh that shows the greater signs of fatigue during the various movements carried out in sports activity that require an intense and prolonged muscular activity, both to healthy38 and to injured subjects61 (suffering patellar pathology). Due to the fatigue phenomenon of the leg extensor muscles, the VMO presents a more important reflex response time in comparison to the VL, on the contrary in consequence to fatigue phenomenon the VL presents a quicker reflex response time63. Given the importance of the VMO in the stability of the knee articulation, one of the main causes of distortion traumas, particularly in team sport activities (football, basketball, rugby) may be its fatigue.

In healthy subjects the physiological value of the EGM VMO/VL Ratio is usually considered equal to 130 40 67. Nevertheless, some studies record VMO/VL Ratio values between 1e 1.213 66, while others underline that the VMO/VL Ratio value is always extremely individualised62and dependent on the articular angle20. This study has collected data in line with the latest bibliography. The VMO/VL Ratio values recorded were, in fact, 1.12 ± 0.08 in the healthy limb and 0.95 ± 0.04 in the injured counterpart. The alteration in the VMO/VL Ratio value in the injured limb was related to a diminution of the surface IEMG both of the VMO (-43.86 ± 27.93%, p<0.005) and of the VL (-34.04 ± 12.25%, p<0.01), and to a parallel diminution of the MIF value (-30.27 ± 26.3%, p<0.005). Moreover, our results are in the line with the studies carried out on the force reduction16 and on the EMG signal 61 in subjects who showed the results of knee articular injuries.

The EMG signal is better recorded during an isometric contraction than during a dynamic movement. It is important to note that the absence of movement (or reduced movement and however only to onset phase of movement) of the muscles recorded in comparison to the surface electrodes , as in this study, eliminates a condition which would seriously compromise the reliability of the EMG signal49 50. Moreover, in an isometric contraction, the EMG signal gives a linear relationship with the intensity of the force produced, whereas in a dynamic contraction the Force/EMG Ratio is curvilinear and is given by the sum of two indexes: the first corresponding to the spatial recruitment of MU and the second to the MU temporal recruitment6.

In this study the linearity between the EMG signal and the production of isometric force is evident and the relationship between DF% and ò VMO + ò VL shows a strong positive correlation (r = 0.80, p<0.004). It is very important to note that, since the relationships between DF% and ò VMO and between DF% and ò VL gives respectively a correlation index equal to 0.97 (p<0.001) and 0.80 (p<0.004), the loss of force in the injured limb is probably caused more by the diminution of the contractile capacity of the VMO in comparison to the VL. This datum is further confirmed by the significant statistical change in the VMO/VL Ratio of the healthy limb in comparison to the injured limb (1.12 ± 0.08 versus 0.95 ± 0.04, p<0.006). However, as the relation between D% ò VMO and D% ò VL is statistically significant (r 0 0.84, p<0.002), the reconstruction of the ACL, VL and VMO is always followed by functional suffering of VL and VMO but more intense in the VMO. Moreover, as the F/EMG Ratio of both limbs does not show variations statistically significant, we hypothesis that the diminution in force in the injured limb is caused not by a deficit within the expression of the contractile force produced, but just by the deficit within the UM spatial recruitment.

Literature has extensively reported the EMG Ratio variations between VMO and VL in the various knee articulation pathologies, giving particular attention to the subjects affected by patellar syndrome5 16 56.Nevertheless, there are no studies backed by electromyographic researches which link muscular injuries mainly to the VMO after ACL reconstruction. In this particular context, the EMG research supplies the information needed to quantify, in an objective way, the muscular deficit caused by the hypo-functional period following the operation8 46 48 68. For diagnostic and preventive purposes the comparison of the VMO/VL Ratio of the healthy and of the injured limb is very important too. The alteration of this latter causes a simultaneous alteration of the neuromuscular activation patterns which, in final analysis, may expose the neo- ligament to the risk of relapsing traumas, especially at the end of the rehabilitation period when the subject starts again to perform a sporting activity17 21.

The simple reacquisition of force in the injured limb, tested through isometric, isotonic or isokinetic methodologies, does not ensure a parallel restoration of the neuromuscular activation patterns as these may be substantially different, since the forces recorded result equal just thanks to the compensating mechanisms of the muscles17. In an arthro-muscular context, a simultaneous dynamometric and electromyographic evaluation allows us to work with data much more complete and reliable.


Sport practiced









Total 10

Table 1: Subjects distribution in function of the practiced sport

Type of suffered injury


ACL isolated breakage


ACL breakage associated to MCL second degree injury


ACL breakage associated to a medial and lateral meniscus injury


ACL breakage associated to a lateral meniscus injury



Total 10

Table 2: Subjects distribution in function to the suffered injury.


Nel presente studio sono stati considerati 10 soggetti la cui età, peso ed altezza erano rispettivamente 25 ± 3 anni (media ± deviazione standard), 71.1 ± 6.5 kg, 179.7 ± 4.2 cm, tutti praticanti attività sportiva ed aventi subito una rottura isolata od associata del legamento crociato anteriore (LCA), trattata chirurgicamente tramite ricostruzione artroscopia

Ad ogni soggetto è stato richiesto di effettuare una serie di 6 contrazioni isometriche massimali della gamba sulla coscia con angolo articolare standardizzato a 90°, sia con l’arto leso che con il controlaterale sano, durante le quali è stato registrato, sia il valore di massima forza isometrica, sia il segnale elettromiografico di superficie del Vasto Mediale Obliquo (VMO), che dal Vasto Laterale (VL). Il deficit di forza a carico dell’arto leso è stato pari a al 30.27 ± 21.65% (p<0.005), la Ratio EMG VMO/VL dell’arto sano e dell’arto leso è stata pari rispettivamente a 1.12 ± 0.08 e 0.95 ± 0.04, la differenza è risultata statisticamente significativa (p< 0.006). I risultati mostrano come in seguito ad intervento ricostruttivo del LCA, si verifichi un deficit contrattile maggiore a carico del VMO rispetto al VL, che si traduce in una modificazione della Ratio EMG che è a sua volta indice di un’alterazione dei pattern di attivazione neuromuscolare.

A questo proposito è importante ricordare che una delle principali cause d’instabilità del ginocchio conseguente all’intervento ricostruttivo del LCA, in seguito ad una sua rottura isolata od associata, è costituita dall’ ipotonia e dall’ipotrofia del quadricipite femorale, ed in particolar modo del VMO, conseguente al periodo di ipofunzionalità successivo all’atto operatorio

Poter quindi comparare la Ratio VMO/VL dell’arto sano nei confronti del controlaterale leso appare soprattutto interessante a fini diagnostici e preventivi, un’alterazione di quest’ultima comporta infatti una contemporanea alterazione dei patterns di attivazione neuromuscolare che potrebbe, in ultima analisi, esporre il neo-legamento al rischio di recidiva traumatica, soprattutto nella fase in cui il soggetto praticante un’attività sportiva, alla fine del periodo riabilitativo, si riavvicini attivamente a quest’ultima. La semplice riacquisizione di forza dell’arto leso nei confronti del controlaterale sano, testabile attraverso modalità isometriche, isotoniche od isocinetiche, infatti non garantisce, a nostro parere, un parallelo ripristino dei patterns di attivazione neuromuscolare, che potrebbero essere comunque sostanzialmente diversi, anche in presenza di un’eguale espressione di forza, grazie a dei meccanismi muscolari di compenso. Una contemporanea valutazione dinamometria ed elettromiografia, permetterebbe invece di poter disporre di un quadro valutativo della situazione artro-muscolare sicuramente più completo ed attendibile.

Parole chiave: Elettromiografia , Legamento Crociato Anteriore, Vasto Mediale, Vasto laterale, Deficit Funzionale.


  1. Armstrong RB. Initial events in exercise induced muscular injury. Med Sci Sports Exerc 1990; 22: 429-437.
  2. Armstrong RB, Warren GL, Warren A. Mechanism of exercise induced fiber injury. Sports Med 1991; 12: 184-207.
  3. Bamman MM, Ingram S, Caruso G, Greenisen MC. Evaluation of surface electromyography during maximal voluntary contraction. Journal of strength and conditioning research (Champaign, Ill.) 1997; 11(2): 68-72.
  4. Boer RW, Cabri J, Vaes W, Clarijs JP, Hollander AP, De Groot G, Van Ingen Schenau GJ. Moments of force, power and muscle coordination in speed-skating. International Journal of Sport Medicine 1987; 8(6): 371-378.
  5. Boucher JP, King M, Lefebre R, Pepin A. Quadriceps femoris muscle activity in patellofemoral pain syndrome. American Journal of Sports Medicine 1992; 20(5): 527-532.
  6. Bouisset S, Maton B. Muscles, posture et mouvement. Bases et applications de la méthode électromyographique. Paris : Hermann Editeurs, 1995 : 295.
  7. Brewer BJ. Instructional Lecture American Academy of Orthopaedic Surgeons 17: 354-358, 1960.
  8. Brunet-Guedj E, Genéty J. Le genou du sportif en pratique courante (2e Edition). Paris : Editions Vigot, 1987 : 120
  9. Byrd S. Alterations in the sarcoplasmatic reticulum: a possible link to exercise-induced muscle damage. Med Sci Sports Exerc 1992; 24: 531-536.
  10. Carlson BM, Faulkner JA. The regeneration of skeletal muscle fibers following injury: a review. Med Sci Sports Exerc 1983 ; 15: 187-198.
  11. Carpentier A, Duchateau J. Etude biomecanique du saut en longeur : comparaison d’impulsion effectuées à partir de hauteurs differentes. Science et Motricité 1990 ; 10 : 21-26.
  12. Caster BL, Bates BT. The assessment of mechanical and neuromuscular response strategies during landing. Medicine and Science in Sports and Exercise 1995; 27(5): 736-744.
  13. Cerny K. Vastus medialis oblique/vastus lateralis muscle activity ratios for selected exercises in persons whith and without patellofemoral pain syndrome. Physical Therapy 1995; 75(8): 672-683.
  14. Cuillo JV, Zarins B. Biomechanics of the musculotendinous unit: relation to athletic performance and injury. Clin Sports Med 1983; 2: 71-86.
  15. De Luca CJ. Use of the surface EMG signal for performance evaluation of back muscles. Muscle Nerve 1993; 16: 210-216.
  16. Della Villa S, Zanobbi M, Nanni G. La riabilitazione dopo ricostruzione chirurgica del legamento crociato anteriore. In: Aggiornamenti in riabilitazione Sportiva. Milano: Edi Ermes Editions, 1997: 61-74.
  17. Edgerton VR, Wolf SL, Levendowsky DL, Roy RR. Theoretical basis for patterning EMG amplitudes to assess muscle dysfunction. Medecine and Science in Sports and Exercise 1996; 28 (6)744-751.
  18. Elftman H. Biomechanics of muscle. J Bone Joint Surg 1966; 48A : 363.
  19. Fiebert I, Hardy CJ, Werner KL. Electromyographyc analysis of the quadriceps femoris during isokinetic eccentric activation. Isokinetic and Exercise Science 1992; 2(1): 18-23.
  20. Fiebert IM, Le Blanc W, Mc Guane SA, Schnoes CD, Strickland KM. The relationship of electromyographic activity and force af tehe vastus medialis oblique and vastus lateralis muscle during maximal isometric knee extension contractions. Isokinetic and Exercise Science 1992; 2(3): 116-123.
  21. Freiwald J, Starischka S, Engelhardt M. Rehabilitatives Krafttraining. Deutsche Zeitschrift für Sportmedizin 1993; 44 (9): 376
  22. Friden J, Lieber RL. Structural and mechanical basis of the exercise-induced muscle injury. Med Sci Sports Exerc 1992; 24: 521-530.
  23. Gardiner P, Michel R, Bowman C, Noble E. Increased EMG of rat plantaris during locomotion following surgical removal of sinergist. Brain Res 1986; 380: 114-121.
  24. Garret WE Jr, Califf JC, Basset FH. Histochemical correlates of hamstring injuries. Am. J. Sports Med 1984; 12: 98-103.
  25. Garret WE Jr, Rich FR, Nikolaou PK, Vogler JB. Computed tomography of hamstring muscle strains. Med Sci Sports Exerc 1989; 21: 506-514.
  26. Garret WE. Muscle strain injury: clinical and basic aspects. Med Sci Sports Exerc 1990; 22: 439-443.
  27. Garrett WE, Safran MR, Seaber AV. Biomechanical comparison of stimulated and non stimulated skeletal muscle pulled to failure. Am J Sports Med 1987 ; 15: 448-454.
  28. Gobelet C, Monnier B, Leyvraz PF. Force isometrique et sport. Medecine du Sport 1984 ; 58 (1) : 51-56.
  29. Gremion G, Fourticq G, Lacraz A, Meunier C, Chantraine A. Traitement des amyotrophies par elecrostimulation. Annales de kinesitherapie Paris 1992 ; 19 (2) : 61-65.
  30. Gryzlo SM, Patek RM, Pink M, Perry J. Electromyographic analysis of knee rehabilitation exercises. The Journal of Orthopaedic and Sports Physical Therapy. 1994; 20(1): 36-42.
  31. Henneman E, Somjen G, Carpenter DO. Functional significance of cell size in spinal motoneurons. J Neurophysiol 1965; 28: 555-560.
  32. Herring SA. Rehabilitation of muscle injuries. Med Sci Sports Exerc 1990; 22: 453-456.
  33. Hodgson JA. The relationship between soleus and gastrocnemius muscle activity in conscious cat — a model for motor unit recruitement. J Physiol 1983; 337: 553-562.
  34. Housh DJ, Donlin P, Housh TJ, Weir JP, Weir LL, Stout JR, Johnson GO. Isokinetic peak torque and cross-sectional area of the quadriceps. Isokinetics and Exercise Science 1994; 4(1): 3-7.
  35. Hunter SC, Marascalco R, Hughston JC. Disruption of the vastus medialis obliquus with medial knee ligament injuries. American Journal of Sport Medicine 1983; 11(6): 427-431.
  36. Hutchison DL, Roy RR, Hodgson JA, Edgerton VR. EMG amplitude relationship between rat soleus and medial gastrocnemius during various motor task. Brain Res 1989; 502: 233-244.
  37. Hutton RS, Atwater SW. Acute and chronic adaptations of muscle propriocetors in response to increased use. Sports Med 1992; 14: 406-421.
  38. James CR. Effects of fatigue on mechanical and muscular component of performance during drop landing. Thesis (M.S.) University of Oregon, 1993.
  39. Komi PV, Virmavirta M. Ski jumping take-off performance: determining factors and methodological advance. In: Science and Skiing. Edited by H. Müller, H. Schwameder, E. Kornexl, C. Rashner, University of Salzburg, 1997.
  40. Laprade J, Culham E, Brouwer B. Comparison of five isometric exercises in the recruitement of the vastus medialis oblique in persons with and without patellofemoral pain syndrome. Journal of Orthopaedic and Sports Physical Therapy 1998; 27(3): 197-204, 1998.
  41. Lexell J, Henriksson-Larsen K, Sjostrom M. Distribution of different fibre types in human skeletal muscles. A study of cross-sections of whole m. vastus lateralis. Acta Physiol Scand 1983; 117: 115-122.
  42. Lieber RL., Woodburn TM., Friden J. Muscle damage induced by eccentric contractions of 25% strain. J Appl Physiol 1991; 70: 2498-2507.
  43. Middleton P, Trouve P, Puig P. Etude critique des rapports agonistes/antagonistes concentriques chez le sportif. Actualités en réeducation fonctionelle. 19° serie, Paris : Masson Ed., 1994: 18-21.
  44. Nikolaou PK, MacDonald BL, Glisson RR. Biomechanical and histological evaluation of muscle after controlled strain injury. Am J Sports Med 1987; 15: 9-14.
  45. Perrotto A, Delagi EF, Iazzetti J, Morrison D. Anatomical guide for the elecromyographer. Third Edition, Springfield (Illinois) USA: Charles C Thomas Publisher, 1994: 204-207.
  46. Poty P, Padilla S, Castells J. Influence des ruptures du ligament croisé anterieur isolées ou associées sur les couples de force musculaire de la cuisse. Mèsure par dynamomètrie isokinetique. Medecine du sport. 1985 ; 59 (2) : 32-38.
  47. Poyhonen T, Keskinen K, Hautala A, Savolainen J, Malkia E. Human isometric force production and electromyogram activity of knee extensor muscle in water and on dry land. European Journal of Applied Physiology and Occupational Physiology 1999; 80(1): 52-56.
  48. Poyhonen T, Laurinen O, Rahko L, Vanharanta H, Savoilanen J. Surface EMG spectral changes of vastus medialis after ACL surgery and immobilisation. In : 11th International Congress of World Confederation for Physical Therapy proceedings. London, World Confederation for Physical Therapy: Chartered Society of Physiotherapy, 1991: 1505-1507.
  49. Rainoldi A, Galardi G, Maderna L, Comi G, Lo Conte L, Merletti R., Repeatability of surface EMG variables durino voluntary isometric contractions of the biceps brachii muscle. Journal of Elecromiography and Kinesiology 1999; 9: 105-119.
  50. Rainoldi A, Nazzaro M, Merletti R, Farina D, Caruso I, Gaudenti S. Geometrical factors in dynamic surface EMG of the vastus medialis and lateralis. Journal of Elecromiography and Kinesiology 2000; Vol 10, 5: 327-336.
  51. Roy RR, Hodgson JA, Chalmers GR, Buxton W, Edgerton VR. Responsiveness of the cat plantaris to functional overload. In: Medicine and Sports Sciences: Integration of Medical and Sport Sciences. Vol 37. Y. Sato , J Poortmans, J Hashimoto and Y. Basel, Switzerland: Oshida (Eds.). Basel, Switzerland: Karger Press, 1992: 43-51.
  52. Roy RR, Hutchinson DJ, Pierotti JA, Hodgson JA, Edgerton VR. EMG patterns of rat ankle extensor and flexors during treadmill locomotion and swimming. J Appl Physiol 1991; 70: 2522-2529.
  53. Russell B, Dix DJ, Haller DL. Repair of injured skeletal muscle: a molecular approach. Med Sci Sports Exerc 1992; 24: 189-196.
  54. Schimdtbleicher D. Adattamenti neuronali e metodi allenamento della forza. SdS, rivista di cultura sportiva. 1983; 2: 15-21.
  55. Schouenborg J., Weno HR., Holmberg H. Modular organisation of spinal nociceptive reflexes: a new hypotesis. N.I.P.S. 1994; 9: 261-265.
  56. Souza DR, Gross MT. Comparison of vastus medialis obliquus : vastus lateralis muscle integrated electromyographic ratios between healty subjects and patients with patellofemoral pain. Physical Therapy 1991; 71(4): 310-320.
  57. Stauber WT. Eccentric action of muscles: physiology, injury and adaptation. Exerc. Sport Sci Rev 1989; 17: 157-185.
  58. Taylor DC, Dalton JD. Experimental muscle strain injury. Am J Sports Med 1993; 21: 190-194.
  59. Tidball JG. Myotendinous junction injury in relation to junction structure and molecular composition. Exerc Sports Sci Rev 1991 ; 19 : 419-445.
  60. Travell JG, Simons DG. Myofascial Pain and Dysfunction: The trigger Point Manual. Baltimore: Williams & Wilkins Ed, 1983: 35.
  61. Vaatainen U, Nurmi H, Airaksinen O. Muscle Spectral analysis in anterior knee pain. Sportorvosi szemle — Hungarian Review of Sports Medicine 1991; 32(4): 281-286.
  62. Ventura A, Boschetti GF, Gaultieri D. A surface electromyographic study of vastus medialis and vastus lateralis dominance in knee extension. Journal of Sport Traumatology and Related Research 1994; 16(4): 152-160.
  63. Voight ML, Wieder DL. Comparative reflex response times of vastus medialis obliquus and vastus lateralis in normal subjects and subjects with extensor mechanism dysfunction. An electromyographic study. American Journal of Sports Medicine 1991; 19(2): 131-137.
  64. Wilson GJ, Lyttle D, Ostrowski KJ, Murphy AJ. (1995).Assessing dynamic performance: A comparison of rate of force development tests. J of Strength and Conditioning Association 1995; 9: 176-181.
  65. Wirhed R. Abilità atletica ed anatomia del movimento. Milano: Edi Ermes Ed., 1986: 46.
  66. Worrel TW, Crisp E, La Rosa C. Electromyographic reliability and analysis of selected lower extremity muscles during lateral step-up conditions. Journal of Athletic Training 1998; 33(2): 156-162.
  67. Worrell TW, Connelly S, Hilvert J. VMO:VLO ratios and torque at four angles of knee flexion. Journal of sport rehabilitation (Champaign, Ill.) 1995; 4 (4): 264-272.
  68. Zaccherotti G, Aglietti P, Bandinelli I. Long-term isokinetic evaluation of quadriceps and hamstring strength following ACL reconstruction. A case-control study. Journal of Sports Traumatology and Related Research 1997; 19 (3): 141-158.
Sezioni tematiche
Kinemove Center

  Sezioni tematiche
Fisiologia e biomeccanica
Metodologia dell'allenamento
Traumatologia sportiva
Curriculum vitae (italiano)
Curriculum vitae (english)

Il Ginocchio
Il Corpo in Movimento
Teoria e Metodologia del Movimento Umano


Kinemove Center

Sezioni tematiche
Kinemove Center

© 2004 - 2012 Created by CDM Maurizio Bardi