- Published: October 18, 2022
- Updated: October 18, 2022
- Language: English
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Soccer is a high energy, high contact sport played by millions worldwide with a prominent injury rate. As soccer is a high intensity and due to the nature of the sport, most of the injuries occur within the lower extremity of the leg.
Ankle impingement syndrome is a frequent injury which occurs in soccer, and Barile et al (1998) classified joint impingement syndrome as “ a painful syndrome caused by friction of the joint tissues.” Yet there is no definite hypothesis for why this injury occurs. It is known, however, that osteophytes, which are bony spurs, have been reported in as many as 60% of soccer players, Massada (1991), this condition was first named “ athlete’s ankle” or “ footballers ankle” by Morris (1943) and later by McMurray (1950). Although it is clear that these osteophytes are present, it is not fully understood how they occur and why they are present.
In order for ankle impingement syndrome to be fully understood the ankle joint needs to be explained. The ankle is a complex joint, and is actually made up of two joints: the true ankle joint and also the subtalar joint. The true ankle joint consists of the tibia, fibula and the talus, and is responsible for the up and down movements of the ankle. The subtalar joint lies beneath the true ankle joint and consists of the talus and the calcaneus, and is responsible for side to side movement of the foot.
Ligaments are also present in the ankle and the major ligaments are: the anterior tibiofibula ligament, which connects the tibia to the fibula, the lateral collateral ligaments, which connect the fibula to the calcaneus, and also the deltoid ligaments, which connect the tibia to the talus and calcaneus.
It is also important to understand what the term velocity means, and Hall (1991) classified velocity as “ the change in position, or displacement which occurs during a given period of time.”
Two theories currently exists to try and explain the exact cause and formation of taliotibial osteophytes, and one such theory is that, “ recurrent traction on the joint capsule during maximal plantar flexion movements of the foot, as is assumed to occur during kicking actions in soccer, is the essential cause, resulting in traction spurs.” This theory was proposed and cited by Biedert (1991), Cutsuries et al (1994), Massada (1991), and McMurray (1950).
More recent studies have concluded another theory for osteophyte formation is “ direct damage to the rim of the anterior ankle cartilage in combination with recurrent micro trauma” this could be caused by the direct impact of the soccer ball on the anterior of the ankle. This theory was proposed and cited by Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997).
Although these theories are suggested in many other studies there is relatively little experimental support for any of the theories, and therefore results in the formation of osteophytes and ankle impingement syndrome remaining ambiguous.
There have been two phases identified in a kicking action, and these phases were proposed by Beraud and Gahery, (1997). They identified the first stage of the kick as the early postural adjustment (EPA), and stated that little movement was present during this stage, and that it occurred between the “ first movement of the postural knee and the first muscle event” Beraud and Gahery, (1997). The second phase of the kick was identified as the back lift and follow through of the kicking action.
The most relevant previous study to examine when observing how a maximal velocity shot in soccer may lead to ankle impingement syndrome is that conducted by Tol et al (2002). The study examined 150 kicking actions performed by 15 professional soccer players, and observed where the ball made contact with the foot, and the location of osteophytes in the participating players.
In order for this to be achieved Tol et al used high speed video equipment and joint markers. The results from this study supported the theory proposed and cited by Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997), as the study concluded that ankle impingement syndrome is caused by “…recurrent ball impact” Tol et al (2002).
The experiment being conducted for this experiment will involve using 2D video analysis of a soccer kick. In order for this to be achieved, the subject will have to strike a soccer ball with maximal velocity using the instep of their foot, as this type of kick generates the fastest ball speed. (Asai et al, 2002). The 2D video analysis will then be used to examine whether the ankle moves into hyper-plantarfelxion, and enable a conclusion to be drawn on whether osteophytes are prone to occur due to the repeated nature of the maximal velocity soccer kick.
Although research has been carried out investigating the biomechanical aspects of a soccer kick, Tol et al (2002), and also the origins of ankle impingement syndrome, Biedert (1991), there is a lack of studies exploring the relationship between the two. Therefore the aim of this study is to observe and record the association between a maximal velocity soccer kick and ankle impingement syndrome.
The subject used for the study was a 25 year old male, 183cm in height, 83kg in weight. The subject suffered from no current injuries or had experienced any previous injuries which would restrict a maximal velocity soccer kick. The subject had previous experience of training as a semi-professional soccer player.
The subject was filmed performing a maximal soccer kick in the Biomechanics laboratory at the University of Teesside. A high speed camcorder: black and white high speed camera (Privo CTM, AOS Technologies, AG) was used for the filming of the kick, and the camera had a shutter speed of 50% and a sampling frequency of 500 Hz. The camera was positioned 5 metres away from the performance plane at a height of 0. 3 metres.
After the camera had been positioned correctly and accurately, joint markers were placed at three points on the subject’s lower leg. The first marker was placed on the fifth metatarsal of the foot, the second on the base of the calcaneus, and the third marker was placed at the mid point of the line through the centres of the posterior convexities of the femoral condyles of the knee.
Once all the markers had been placed on the lower leg of the participant his maximal static plantarflexion was measured. This measurement was established by seating the participant on the edge of a wheeled chair with both feet flat on the floor parallel to each other. With their feet still flat on the ground the participant was asked to move as far back as possible while their feet remained flat. Three trails were performed and the mean maximal static angle was -49. 0. The joint markers and angle to be measured can be seen in Figure 1.
Figure 1. Joint markers and static maximal plantarflexion of the subject.
The subject was then instructed to maximally kick a static football (Adidas Terrestra ms, size 5, 0. 6-0. 8 BAR, adidas-Salomon AG Adi-Dassler-Strasse 1-2, 91074 Herzogenaurach Germany) with the instep of the foot 3 times. The subject was asked to kick the football straight ahead at a target placed 5 metres away. Before the performance trails were recorded the subject was given time to practice.
After the filming of the maximal velocity kick had been completed, the video recorded trials were converted into Bitmap images and transferred onto CD ready for Digitising on a University of Teesside developed programme named digiTEESer using Privo 1. 0. 0 (AOS Technologies, AG), which involved the calculation of linear and angular velocity, along with hyper-plantarflexion of the ankle. This was done by examining individual frames of the 2D-video analysis.
Once all the digitising had been completed, the data was then “ smoothed”, and this was a process of analysing the position of the subject’s ankle over the first three frames. It was essential for the data to be “ smoothed” as this combated errors made during the digitising aspect of the data analysis.
Figure 2 illustrates that in maximal velocity kick 1 the foot contacted the ball at for a time of 0. 01 seconds (s) from the beginning of the kick; Figure 2 also displays the subject’s ankle plantarflexion during a maximal velocity soccer kick compared against maximal static ankle plantarflexion. As is clearly shown, during maximal velocity kick 1 the ankle did not experience hyper-plantarflexion as the angle of the ankle did not exceed -49, which as previously mentioned was the maximal static ankle plantarflexion.
Maximal velocity kicks 2 and 3 are also displayed in Figure 2, and it is apparent that the foot impacted with the ball for a time of 0. 012s in maximal velocity kick 2 and for a time of 0. 008s in kick 3. The subject’s ankle plantarflexion for maximal velocity kicks 2 and 3 are also displayed in Figure 2, and the data shows that in both kicks the ankle encountered hyper-plantarflexion.
Figure 2. Ankle plantarflexion during maximal velocity kicks 1, 2 and 3 vs. Maximal static ankle plantarflexion.
Figure 3 displays the ankle plantarflexion during maximal kick 1 in relationship with angular velocity. As is seen in Figure 3, angular velocity decreases in the backswing stage of the kick and causes the ankle to experience plantarflexion, before the ankle then increases in angular velocity, which in turn decreases the degrees of plantarflexion, preceding contact between the foot and ball.
Figure 3 portrays that the ankle does not experience hyper-plantarflexion, as the angle of the ankle does not exceed that of the maximal static plantarflexion.
Figure 3. Ankle plantarflexion in maximal kick 1 vs. Angular velocity.
Figure 4 illustrates the ankle plantarflexion during maximal kick 2 in relationship with angular velocity. As with Figure 3, angular velocity again decreases in the backswing stage of the kick and causes plantarflexion of the ankle, before angular velocity increases and the degrees of plantarflexion decrease before contact is made with the ball. However, Figure 4 also displays the fact that not only does the ankle experience plantarflexion, it also continues into hyper-plantarflexion. This is evident as the ankle angle moves beyond that of the mean maximal static plantarflexion.
Hyper-plantarflexion is experienced for a time of 0. 018s in Figure 3.
Figure 4. Ankle plantarflexion in maximal kick 2 vs. Angular velocity.
Figure 5 exhibits ankle plantarflexion in maximal kick 3 against angular velocity. Again, as with Figure 3 and Figure 4, angular velocity decreases in the backswing stage of the kick and causes plantarflexion of the ankle, before angular velocity increases and the degrees of plantarflexion decrease before the foot impacts with the ball. Again the ankle does not only move into plantarflexion, but continues through the degrees of plantarflexion and surpasses the mean maximal static plantarflexion and experiences hyper-plantarflexion.
Hyper-plantarflexion again occurs for a time period of 0. 018s in Figure 5.
Figure 5. Ankle plantarflexion in maximal kick 3 vs. Angular velocity.
The above figures clearly display that hyper-plantarflexion occurs during a maximal velocity kick and also that angular velocity and degrees of plantarflexion are directly related. This is evident as angular velocity decreases in the backswing of the kick, before increasing and thus decreasing the degrees of plantarflexion in the ankle, causing hyper-plantarflexion, before contact with the ball in made.
The figures also illustrate that kick 1 is anomalous when compared with kicks 2 and 3. This is because kick 1 did not experience hyper-plantarflexion, whilst kicks 2 and 3 did experience hyper-plantarflexion. Along with this, kicks 2 and 3 portray nearly identical results with kick 2 experiencing a smaller degree of hyper-plantarflexion.
It should also be noted that it is apparent that resistance is being applied to the ankle joint when the foot come into contact with the soccer ball, this is due to Newton’s third law, which states that “ each force has an equal and opposite force acting upon it”. This in turn causes the velocity of the ankle to decrease and move the ankle in hyper-plantarflexion, as can been seen in Figures 4 and 5.
As is seen and mentioned in the results section of this study, the results obtained are all very similar in regards of the trends that are present during all three of the maximal velocity kicks. The trends display that angular velocity has a direct influence of whether the foot experienced hyper-plantarflexion during a maximal velocity kick, as when angular velocity increases hyper-plantarflexion occurs.
The results, however, display that in maximal velocity kick 1 the angle of the ankle whilst in plantarflexion did not surpass that of the mean maximal static plantarflexion of -49. This result is anomalous when compared to kicks 2 and 3 as they both encountered hyper-plantarflexion; nevertheless, kick 1 followed the same patterns and trends as kicks 2 and 3 and failed to encounter hyper-plantarflexion by the smallest of degrees. An explanation for the subject not experiencing hyper-plantarflexion could be that as it was the first recorded trial he held back and did not produce a maximal velocity kick, this could be due to tension in the muscles used to produce the kicking action.
Maximal velocity kicks 2 and 3 (Figures 4 and 5) produced results which displayed that the ankle did encounter hyper-plantarflexion as they exceeded the mean maximal static plantarflexion. Hyper-flexion occurred in these results during contact with the ball, and as a result these results support the theory proposed and cited by Biedert (1991), Cutsuries et al (1994), Massada (1991), and McMurray (1950), who proposed that “ recurrent traction on the joint capsule during maximal plantar flexion movements of the foot, as is assumed to occur during kicking actions in soccer, is the essential cause, resulting in traction spurs.”
However, the results obtained from this study also support, in part, the theory proposed and cited by Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997), who stated that “ direct damage to the rim of the anterior ankle cartilage in combination with recurrent micro trauma” was the cause of osteophyte formation. Our results support both of these theories, as during the impact phase of the maximal velocity kick the foot is hyper-plantarflexing, and also the ball is striking the anterior of the ankle, where osteophytes are formed and where ankle impingement syndrome is found. Nevertheless, in this study we have not examined the anterior region of the ankle, and therefore it is impossible for this theory to be supported fully by the results of our study, and thus we are unable to corroborate or reject this theory.
If the theory proposed and cited by Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997) was proved to be correct, then it would explain why osteophytes have been reported in as many as 60% of soccer players (Massada, 1991), as the ball would be repeatedly striking the anterior rim of the ankle, and if the impact force of the ball was large enough to cause micro trauma, then osteophyte formation would occur.
Conversely, the same could be applied to the theory composed and cited by Biedert (1991), Cutsuries et al (1994), Massada (1991), and McMurray (1950), as during soccer games and training the ball has a maximal impact with the foot numerous times, and therefore would cause the ankle to encounter maximal plantarflexion and hyper-plantarflexion movements, resulting in traction spurs and ankle impingement syndrome.
The study conducted did possess a number of methodological limitations, with the greatest limitation being the 2D video analysis that was used to record the maximal velocity kick. This was the greatest limitation to the study as it only allowed the kick to be filmed in one plane of movement, and was unable to take into account rotation in the joints being examined. A superior method of filming would have been 3D filming, as this is able to take into consideration both joint rotation and also movement in different planes of the body.
A further limitation of the study is the data analysis programme used. The digitising of the Bitmap images was a very subjective process, as the individual was required to click on joint markers placed on the subject, for each individual frame of each kick. Therefore the whole process was open to individual error, as the experimenter had to ensure they clicked in the same place on the joint marker each time. The process was also very time consuming and tedious, which could have caused the experimenter to have lost concentration on the task.
Due to this, the validity of the data collected was reduced and therefore the angular velocity and in turn the supposed mean maximal static plantarflexion value could have been compromised.
Another limitation of the study conducted, was the fact that it was conducted in the Biomechanics laboratory, and not actually in a soccer environment. The footwear the subject wore could also be a limitation as it was not soccer specific footwear, and therefore could have restricted the ankle plantarflexion of the subject. Conversely the footwear could have allowed more ankle plantarflexion than soccer specific footwear. To combat this, the subject should have worn soccer specific footwear in order to replicate a maximal velocity kick on a soccer pitch in the correct kit.
An additional limitation is that only 1 subject was used in the study and therefore the results are not representational to the population as a whole. To prevent against this, more subjects should have been used, such as the numbers used by Tol et al (2002) who used 15 subjects, yet more could be used for greater ecological validity. Along with this recommendation is the fact that more kicks should be analysed to give a greater overall view of the kicking action to be examined, and also to achieve a more reliable average.
The overall conclusion of the study conducted is that hyper-plantarflexion does occur when a maximal velocity kick contacts with a soccer ball, and this is verified in Figures 4 and 5. These results support the hypothesis proposed and cited by Biedert (1991), Cutsuries et al (1994), Massada (1991), and McMurray (1950), who specified that , “ recurrent traction on the joint capsule during maximal plantar flexion movements of the foot, as is assumed to occur during kicking actions in soccer, is the essential cause, resulting in traction spurs.” Although kick 1 did not achieve hyper-plantarflexion it does follow both Figure 4 and 5 in terms of the trends up to and after hyper-plantarflexion.
A further conclusion of the study is that more research needs to be carried out into the theory proposed and cited by Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997), as this study was unable to categorically state whether the theory was correct due to the location of the ball on the anterior ankle being recorded.
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