How may a maximal velocity shot in soccer lead Essay Example
How may a maximal velocity shot in soccer lead Essay Example

How may a maximal velocity shot in soccer lead Essay Example

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  • Pages: 10 (2641 words)
  • Published: January 4, 2018
  • Type: Research Paper
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Soccer is a widely popular sport worldwide, renowned for its high intensity and physical demands. However, it also has a significant occurrence of injuries, especially in the lower extremities.

According to Barile et al (1998), ankle impingement syndrome is a common soccer injury characterized by joint tissue friction and causing pain. The exact cause of this injury is unknown. However, Massada (1991) found that up to 60% of soccer players have osteophytes or bony spurs. These osteophytes were initially called "athlete's ankle" or "footballer's ankle" by Morris (1943) and later by McMurray (1950). The origin and presence of these osteophytes are still not fully understood.

Ankle impingement syndrome can be better understood by having knowledge of the ankle joint. The ankle joint is a complex joint that consists of two separate joints: the true ankle joint and the subtalar joint. The true ank

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le joint, consisting of the tibia, fibula, and talus bones, allows for vertical movements of the ankle. Below the true ankle joint is the subtalar joint, which includes the talus and calcaneus bones and permits lateral foot movement.

The ankle consists of multiple ligaments, such as the anterior tibiofibula ligament which connects the tibia and fibula, lateral collateral ligaments that join the fibula and calcaneus, and deltoid ligaments that link the tibia, calcaneus, and talus.

According to Hall (1991), velocity is the change in position or displacement that happens over a specific time period. The concept of velocity holds significance.

There are two theories explaining the cause and development of taliotibial osteophytes. One theory suggests that traction spurs occur due to recurrent traction on the joint capsule when the foot undergoes maximal plantar flexion movements, such as kickin

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actions in soccer. This theory was proposed and cited by Biedert (1991), Cutsuries et al (1994), Massada (1991), and McMurray (1950).

Multiple studies have indicated that osteophyte formation in the ankle is the result of both direct damage to the anterior ankle cartilage rim and repetitive micro trauma. The primary cause of this damage is believed to be the impact of a soccer ball on the front part of the ankle. Several researchers, including Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997), have proposed and referenced this theory.

Although several studies have suggested theories, there remains a dearth of experimental evidence supporting these claims, leading to uncertainty in comprehending the formation of osteophytes and the occurrence of ankle impingement syndrome.

According to Beraud and Gahery (1997), the kicking action can be divided into two phases. The first stage, known as early postural adjustment (EPA), involves minimal movement and occurs between the initial movement of the knee and the first muscle event. The second phase comprises the back lift and follow through of the kick.

The study conducted by Tol et al. (2002) is the most important previous study that examines the association between a maximal velocity shot in soccer and ankle impingement syndrome. Tol et al. (2002) analyzed 150 kicking actions performed by 15 professional soccer players. The researchers observed the point of contact between the ball and the foot, as well as the presence of osteophytes in the participants.

In order to achieve this, Tol et al utilized high speed video equipment and joint markers. The findings of their study supported the theory proposed

by Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997), which concluded that ankle impingement syndrome is caused by "recurrent ball impact" (Tol et al, 2002).

The experiment will use 2D video analysis to study a soccer kick. To achieve this, the subject will need to strike a soccer ball with maximum velocity using the instep of their foot, as this generates the fastest ball speed (Asai et al, 2002). The 2D video analysis will then be used to determine if the ankle moves into hyper-plantarfelxion and to draw conclusions about the occurrence of osteophytes from the repeated maximal velocity soccer kick.

Previous research has focused on studying the biomechanics of a soccer kick (Tol et al, 2002) and the causes of ankle impingement syndrome (Biedert, 1991). However, there remains a gap in understanding the connection between these two factors. As a result, this study seeks to investigate and record the association between reaching peak velocity in a soccer kick and developing ankle impingement syndrome.

Methodology

The study utilized a 25-year-old male subject who was 183cm tall and weighed 83kg. The subject did not have any current injuries or past injuries that would limit their ability to perform a maximum velocity soccer kick. Additionally, the subject had prior training experience as a semi-professional soccer player.

The University of Teesside's Biomechanics laboratory used a black and white high-speed camera (Privo CTM, AOS Technologies, AG) to record a maximum soccer kick. The camera had a shutter speed of 50% and a sampling frequency of 500 Hz. It was positioned at a distance of 5 metres from the performance

plane, at a height of 0.3 metres.

Once the camera was accurately positioned, joint markers were placed on three points of the subject's lower leg. These points included the fifth metatarsal of the foot, the base of the calcaneus, and the midpoint between the posterior convexities of the femoral condyles of the knee.

The participant's maximal static plantarflexion was measured by placing markers on his lower leg. The measurement involved seating the participant on a wheeled chair with both feet parallel and flat on the floor. The participant moved as far back as possible while keeping his feet flat on the ground. Three trials were conducted, and the average maximal static angle recorded was -49.0. Figure 1 shows the joint markers and angle to be measured.

Figure 1 displays the subject's joint markers and their static maximal plantarflexion.

The subject was instructed to 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 a maximum of three times. The target was placed 5 meters ahead and the subject was asked to kick the football straight towards it. Prior to recording the performance trials, the subject was given time to practice.

The video trials depicting the maximal velocity kick were converted into Bitmap images after filming was finished. These images were then transferred onto a CD and prepared for digitization using a program called digiTEESer, developed by the University of Teesside. In the digitization process, a software called Privo 1.0.0 (AOS Technologies, AG) was utilized to calculate linear and angular velocity, as well as hyper-plantarflexion of the ankle. This analysis involved studying individual frames from the

2D-video.

Following the completion of the digitalization process, further analysis of the data involved "smoothing" it. This entailed examining the subject's ankle position in the initial three frames, as smoothing was essential for rectifying any errors that may have occurred during the digitalization phase of data analysis.

Results

Figure 2
Figure 2 demonstrates that during the maximal velocity kick 1, the foot made contact with the ball for a duration of 0.01 seconds (s) from the initiation of the kick. It also compares the subject's ankle plantarflexion during a maximal velocity soccer kick to their maximum static ankle plantarflexion. It is clear that there was no hyper-plantarflexion of the ankle in maximal velocity kick 1 as its angle did not exceed -49, which was previously identified as the maximum static ankle plantarflexion.

Figure 2 shows 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, indicating hyper-plantarflexion in both kicks.

Figure 2 compares the ankle plantarflexion during maximal velocity kicks 1, 2, and 3 with the maximum static ankle plantarflexion.

Figure 3 depicts the relationship between ankle plantarflexion and angular velocity in the maximal kick 1. The graph demonstrates that as the backswing stage of the kick progresses and angular velocity declines, the ankle experiences plantarflexion. As a result, when the ankle's angular velocity rises again, there is a reduction in the extent of plantarflexion just before contact with the ball occurs.

Figure 3 demonstrates that the

ankle does not experience hyper-plantarflexion as its angle does not surpass the maximum static plantarflexion angle.

Figure 3 depicts the correlation between ankle plantarflexion in maximal kick 1 and its corresponding angular velocity.

Figure 4 depicts the ankle's plantarflexion during the maximal kick 2 in relation to its angular velocity. Similar to Figure 3, the backswing phase leads to a decrease in angular velocity and subsequent ankle plantarflexion. Subsequently, as the angular velocity rises, there is a reduction in the amount of plantarflexion before contacting the ball. However, Figure 4 also demonstrates that alongside regular plantarflexion, the ankle undergoes hyper-plantarflexion. This can be observed by comparing the ankle angle with that of average maximal static plantarflexion.

Figure 3 depicts a demonstration of hyper-plantarflexion that endures for a duration of 0.018 seconds.

Figure 4 shows the correlation between ankle plantarflexion and angular velocity in maximal kick 2.

Figure 5 illustrates that, during the maximum kick 3, there is a decline in angular velocity, leading to ankle plantarflexion. This trend is similar to what can be observed in Figure 3 and Figure 4, where ankle plantarflexion occurs during the backswing phase of the kick due to a decrease in angular velocity. As the angular velocity rises, the ankle continues to undergo plantarflexion; however, the extent of plantarflexion decreases before the foot comes into contact with the ball. Moreover, not only does the ankle move into plantarflexion but it also surpasses average maximum static plantarflexion and reaches hyper-plantarflexion.

Figure 5 demonstrates hyper-plantarflexion for a duration of 0.018s.

Figure 5 demonstrates the relationship between ankle plantarflexion in maximal kick 3 and angular velocity.

Based on the provided data, it is clear that hyper-plantarflexion occurs during a maximum

speed kick. Furthermore, there is a direct correlation between plantarflexion level and angular velocity. This relationship is evident as angular velocity decreases during the backswing of the kick but then increases again, resulting in decreased ankle plantarflexion. As a result, hyper-plantarflexion happens just before making contact with the ball.

The data demonstrates that kick 1 differs from kicks 2 and 3. Kick 1 lacked hyper-plantarflexion, whereas kicks 2 and 3 displayed hyper-plantarflexion. Additionally, kicks 2 and 3 yielded similar results, with kick 2 exhibiting a slightly lower degree of hyper-plantarflexion.

When the soccer ball is touched, the ankle joint encounters resistance in accordance with Newton's third law. According to this law, every force applied has an equal and opposite force. As a result, this resistance causes a reduction in ankle velocity and leads to hyper-plantarflexion, as illustrated in Figures 4 and 5.

Discussion: The findings of this study indicate that the results obtained from all three maximal velocity kicks exhibit comparable patterns. These patterns suggest that the angular velocity has a direct impact on whether the foot experiences hyper-plantarflexion during a maximal velocity kick. More specifically, an increase in angular velocity results in hyper-plantarflexion.

The findings reveal that in kick 1, the angle of the ankle in plantarflexion did not exceed the mean maximal static plantarflexion of -49. This finding is unusual when compared to kicks 2 and 3 where hyper-plantarflexion was observed. However, kick 1 followed the same patterns and trends as kicks 2 and 3, but had only a slight deviation from hyper-plantarflexion. One possible explanation for the absence of hyper-plantarflexion in kick 1 could be that the subject held back and did not perform a maximal

velocity kick, possibly due to muscle tension involved in producing the kicking motion.

Figures 4 and 5 reveal that during kicks 2 and 3 performed at maximum speed, the ankle experienced hyper-plantarflexion, surpassing the average static plantarflexion. These findings demonstrate excessive flexion upon contact with the ball, which is consistent with the theory proposed by Biedert (1991), Cutsuries et al (1994), Massada (1991), and McMurray (1950). According to this theory, repeated strain on the joint capsule during intense plantar flexion movements such as soccer kicks leads to traction spurs. Our results also partially support another theory put forth by Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997). This theory suggests that direct damage to the rim of the anterior ankle cartilage combined with recurring micro-trauma triggers osteophyte formation. In our study, we observed both hyper-plantarflexion during the impact phase of maximum velocity kicks and the ball striking against the front of the ankle where osteophytes form and ankle impingement syndrome develops. However, since our study did not specifically examine the anterior region of the ankle, we are unable to fully confirm or refute this theory based on our findings. Therefore, we cannot definitively validate or dismiss this theory.

If the accuracy of the theory presented and referenced by Lees et al (1991), Levendusky et al (1988), McCrudden et al (1991), van Dijk et al (1996), and van Dijk et al (1997) is proven, it may explain why osteophytes have been observed in up to 60% of soccer players (Massada, 1991). This is because the repetitive striking of the ball against the anterior

rim of the ankle can cause osteophyte development if the impact force is significant enough to result in micro trauma.

On the other hand, the theory presented by Biedert (1991), Cutsuries et al (1994), Massada (1991), and McMurray (1950) can also be applied. This is because during soccer games and training, the foot makes repeated maximal impacts with the ball, causing the ankle to experience maximal plantarflexion and hyper-plantarflexion movements. As a result, traction spurs and ankle impingement syndrome can occur.

The study had several methodological limitations, with the main one being the use of 2D video analysis to record the maximum velocity kick. This limitation was significant because it only captured the kick in one direction and did not consider rotation in the joints being studied. An improved filming method would have been 3D filming, which accounts for joint rotation and movement in various body planes.

Another limitation of the study is the use of a data analysis programme that was subjective. The process involved clicking on joint markers placed on the subject for each frame of each kick, which introduced individual error. Additionally, this process was time consuming and tedious, leading to a potential loss of concentration for the experimenter.

As a result, the data collected was less reliable, potentially impacting the angular velocity and consequently affecting the intended mean maximal static plantarflexion value.

The study had limitations because it was conducted in a Biomechanics laboratory instead of a soccer environment. The subject's footwear was also not soccer specific, which may have limited ankle plantarflexion. However, the footwear could have also allowed for more ankle plantarflexion compared to soccer specific footwear. To address this, the subject should have

worn soccer specific footwear to accurately replicate a maximal velocity kick on a soccer pitch with the correct equipment.

Although the study only had one subject, it is crucial to acknowledge that the findings might not accurately reflect the entire population. To overcome this limitation, it would have been advantageous to involve more subjects, as Tol et al (2002) did by utilizing 15 subjects. Increasing the number of subjects can also improve the ecological validity of the results. Additionally, it is recommended to analyze a greater number of kicks to obtain a more comprehensive understanding of the kicking action being investigated and establish a more reliable average.

The study confirms that hyper-plantarflexion occurs when a soccer ball is kicked at maximum velocity, as seen in Figures 4 and 5. These findings support the hypothesis suggested by Biedert (1991), Cutsuries et al (1994), Massada (1991), and McMurray (1950), who argue that recurrent traction on the joint capsule during maximal plantar flexion movements of the foot, such as kicking in soccer, causes traction spurs. Although kick 1 did not display hyper-plantarflexion, it follows the trends shown in Figures 4 and 5 before and after this occurrence.

Further research is needed to investigate 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 could not definitively confirm the accuracy of the theory because the location of the ball on the anterior ankle was recorded.

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