Angular Kinematics and The Kinematic Chain During a Tennis Serve: The Body’s Summation of Speed

Within the science of Biomechanics, the branch of kinematics studies movement with reference to the amount of time taken to carry out the activity. Furthering this, angular kinematics denotes the analysis of angular motion which occurs when all parts of an object move through the same angle but do not undergo the same linear displacement. Here, the object or bodily segment will rotate around an axis of rotation that is a line perpendicular to the plane in which the rotation occurs. On the other hand, the kinematic chain represents how the body efficiently maximises the effect of joint angles and velocities to enhance maximal performance. This notion, along with angular kinematic analysis will be at the forefront of this article which focusses upon the performance of a tennis serve.

When performing the skill of a tennis serve the movement is first initiated with ground reaction force (GRF), the ball toss follows along with the drawing back of the racket. The legs flex at both the knee and ankle with a rapid drive from the lower limbs that follows through the hips. Leading onto rotation at the trunk which is then followed by extension at the shoulder and elbow, finishing with peak velocity at impact (ball and racket contact). The elbow and wrist do not fully extend until the final moments of the skill in order to maximise the effects of the kinematic chain i.e. the proximal to distal summation of speed. 

Perhaps the key consideration when performing a tennis serve is to attain maximum speed of the tennis ball. In order to achieve this, movements at the various joints and bodily segments mentioned above are used to gain maximum impact velocity of the racket with the ball. The timing of peak angular velocities must occur in order of proximal to distal (Elliot et al. 1995) and this is referred to as the kinematic chain. The proximal to distal concept is crucial to the timing of peak joint flexion, velocities and magnitudes in order to enhance technical performance. This aims to increase the rotation of each segment, giving it a large angular velocity, which in turn will make for an amplified tangential velocity. In the case of the tennis serve you could argue that two kinetic chains are present: Ankle – knee – hip and shoulder - elbow – wrist. The graph below displays the velocities observed during a maximal hit or throw (Hay, 1995).

Notice that the peak velocities of each joint occur one after the other, in relation to injury prevention, the timing of segmental movement can have a profound effect on overuse injury. When a segment is out of sync this can put a huge strain on the other links involved in the technique. Not only this but, it also results in a reduced accumulation of motion and therefore end point velocity. Furthering this, the observation of different serving styles by Elliot et al. (2003) suggests that variation in techniques load the shoulder differently and therefore have implications for injury.

With regard to the areas of interest, a kinematic analysis can provide information relevant to coaches for technique improvement and injury prevention. For example, Elliot et al. observed the contribution of each bodily segment to a serve, with the forearm being of primary importance. This would highlight to both coaches and athletes the aspects of the skill they should prioritise. Further to this, observing the timings of each segmental movement will indicate if the performer is maximizing their potential angular velocity. Proximal to distal timing of movements will allow for maximum velocity values to be attained due to enhanced accumulation of motion in the kinematic chain. Kinematic analysis does however have its inherent limitations, when using video observation for example, joint centres often rotate out of plane. Angle measurements are therefore inaccurate as it is assumed that in a two-dimensional image all the joints and segments line up, when in fact they do not. In this instance CODA motion tracking analysis would be beneficial as opposed to human, as it provides three-dimensional angles.

Overall kinematic analysis can provide meaningful evidence to support technique selection to both improve peak velocities within the tennis serve and reduce the likelihood of injury. All of which is fundamentally dependent on the kinematic chain, a principle which is of chief importance when considering movements that aim to achieve peak angular velocities such as the tennis serve.

"The depressing thing about tennis is that no matter how good I get, I'll never be as good as a wall." - Mitch Hedberg

VO₂ max: The Limiting Factors of Maximum Oxygen Uptake

VO₂ max, commonly known as maximum oxygen uptake, is defined as the highest rate that oxygen can be inspired and utilized in the body during severe exercise at sea level. Consequently, VO₂ max represents the maximal rate of aerobic respiration in the mitochondria and is a measure of an individual's maximal capacity to work aerobically. When exercising at work rates above VO₂ max the energy for this additional work is met entirely through anaerobic metabolism i.e. anaerobic glycolysis. Its current concept originated with the work of Hill et al. in 1923, hypothesising that¹:

•           An upper limit to oxygen uptake exists.
•           There are inter individual differences in VO₂ max.
•           A high VO₂ max is a prerequisite for success in middle- and long-distance running.
•           VO₂ max is limited by the ability of the cardiorespiratory system to transport O₂.

Although there are various inherent physiological limitations to VO₂ max, which will be discussed in turn later in this article, there are other mediums by which VO₂ is also influenced by. The first of which is the fitness level of the individual in question, typically the highest VO₂ max values are seen in athletes which participant in whole body endurance activities such cross-country skiing or long distance running. Another consideration is age, after the age of 25 VO₂ max tends to decline by 1% each year with muscle sarcopenia (the degenerative loss of skeletal muscle mass) accounting for much of the major decrease in values observed at old age. Lastly, gender contributes to a great deal of variation seen in VO₂ max values. Males possess greater amounts of muscle mass along with a larger heart and lungs, all of which allow for superior oxygen transportation. On the other hand, women vary in body composition by increased fat percentage, less muscle mass and smaller heart/lungs.

Perhaps the principal rule to consider when discussing the maximum oxygen uptake is the Fick equation, which is as follows:  

·         VO₂ = CO x a-v O₂ difference
So, VO₂ max = Maximal CO x max a-v O₂ difference.

In this equation, CO represents the cardiac output – in other words central oxygen delivery. On the other hand, a-v O₂ difference relates to the peripheral oxygen utilization - the difference in the oxygen content of the blood between the arterial blood and the venous blood.  Ultimately, maximal utilization of oxygen at the tissues requires an effective O₂ transport cascade and it is the limitations of this pathway which will determine VO₂ max:

Air    -    Alveolar    -    Arterial    -    Capillary    -    Myoglobin    -    Mitochondria.

The first of the limiting physiological factors to maximum oxygen uptake is the pulmonary system, this includes the lungs and the muscles of breathing and is responsible for the delivery of oxygen/removal of carbon dioxide from the blood. Surprisingly, with regards to this system it has been seen in highly trained athletes that arterial O₂ desaturation during maximal work occurs². Although trained individuals have a far superior maximal cardiac output than their sedentary counterparts, this leads to decreased transit time of the red blood cell in the pulmonary capillary. Consequently, there is not sufficient time to saturate the blood with oxygen before it exits the pulmonary capillary, thus significantly reducing the potential quantity of oxygen available to the working skeletal muscle.

In the field of sports science we know that the normal range of VO₂ max values among sedentary and untrained individuals is mainly due to variation in maximal stroke volume, since considerably less variation exists in maximum heart rate and systemic oxygen extraction. Throughout maximal exercise almost all of the available oxygen is extracted from the blood that circulates the active muscles³, the approximate oxygen content of arterial blood is 200mL O₂∙L⁻¹ and in venous blood draining maximally this falls to about 20-30mL O₂∙L⁻¹. Showing there is little oxygen remaining for extraction during severe exercise. As a result the principal method for increasing the VO₂ max with relevant training must be an increase in blood flow, it is estimated that 70-85% of maximum oxygen uptake is linked to maximal cardiac output.⁴
A variety of longitudinal studies have displayed the notion that a training induced VO₂ max increase results from a greater cardiac output, as opposed to a widening of the a-vO₂ difference.⁵  

Within the active skeletal muscle fibres, the mitochondria act as the site where oxygen is consumed in the final step of the electron transport chain during aerobic respiration. It would be reasonable to suggest that an increase in the number of mitochondria would result in a higher maximum oxygen uptake. However, one study observed a modest 20-40% increase in VO₂ max despite a 2.2 fold increase in mitochondrial enzymes⁶. This finding is constant with the view that maximal oxygen uptake during a bout of whole body exercise is limited by oxygen delivery, not it’s utilization at the skeletal muscle.  

1985 saw the definitive research experiment showing that maximal oxygen uptake is limited by oxygen delivery due to restricted blood flow. Saltin et al⁷ observed the effects of maximal exercise using only a small amount of muscle mass, allowing a great amount of cardiac output to be directed onto a concentrated area. Under such conditions the measure oxygen uptake at the quadriceps was 2-3 times than in the same area during a whole body maximal bout of activity. It was therefore concluded that skeletal muscle has a remarkable capacity for blood flow and thus VO₂, however this simply cannot be matched by maximal cardiac output of the heart during whole body exercise. Proving that VO₂ max is bound by the delivery of oxygen and not by the ability of the mitochondria to utilize oxygen.

From the wide range of studies and research discussed throughout this article, it is clear that each step in the pathway of oxygen transport contributes to the determination of VO₂ max. A reduction in this transportation network will predictably result in a lower maximal oxygen uptake. The evidence also demonstrates that it is primarily the ability of the cardiorespiratory system to transport oxygen to the skeletal muscle and not the muscle mitochondria’s ability to consume it that limits and athlete’s VO₂ max value.

References

1.  Hill, D.K. and Lupton, H. (1923) Muscular exercise, lactic acid and the supply and utilisation of oxygen. Quarterly Journal of Medicine. 16: 135-171.
2.    Dempsey, J.A., Hanson, P.G., and Henderson, K.S. (1984). Exercise-induced arterial hypoxaemia in healthy human subjects at sea level. Journal of Physiology. 355: 161-175
3.   Shephard, R. (1977) Endurance Fitness. Toronto and Buffalo: Univ. of Toronto Press. 2:64–103.
4.  Cerretelli P, Di Prampero PE. (1987). Gas exchange in exercise. Handbook of Physiology. The Respiratory System. 4: 297–339.
5.   Ekblom, B., Åstrand, P.O., Saltin, B., Stenburg, J., and Wallstrom, B. (1968) Effect of training on circulatory response to exercise. Journal of Applied Physiology. 24:518–528
6.  Saltin, B., Henriksson, J., Nygaard, E. and Andersen, P. (1977) Fiber types and metabolic potentials of skeletal muscles in sedentary man and endurance runners. Annals of the New York Academy of Sciences. 301:3–29.
7.  Saltin, B. (1985) Hemodynamic adaptations to exercise. American Journal of Cardiology. 55:42-47

Running the Risk of Injury: Achilles Tendon Strain Prevention

The Achilles tendon strain is a perhaps one of the most common injuries found in long distance runners with its primary cause predominantly due to overuse. However, other causes include:

·         Increasing one’s physical activity levels too rapidly.

·         Insufficient pre-exercise stretching.

·         Over pronation, otherwise known as fallen arches or flat feet. The impact of each step in this condition causes the arch of the foot to collapse, therefore excessively stretching the Achilles tendon.

Such activities lead to an inflammation and tenderness of the tendon which is localised 2-6cm proximal of its insertion, a notion which is only exacerbated due to the fact blood supply to this region is limited. If left untreated degeneration and rupture of the Achilles tendon may result.

In this article, the focal prevention strategy for this hindrance to performance is the insertion of heel lifts, placed to the rear of the shoe. The use of heel lifts has previously been associated with a reduction in Achilles tendon injury¹, through the suggestion that they reduce peak ankle dorsiflexion that occurs during the midstance of running². This therefore causes a reduction in the stretch and strain experienced by the tendon.

The triceps surae is a muscle tendon complex consisting of the gastrocnemius and soleus muscles (see figure below), which together have the common insertion of the Achilles tendon at the calcaneus. This muscle-tendon complex crosses both the knee and ankle joints, thus its overall length is determined by alterations in ankle plantar- and dorsi-flexion as well as knee flexion and extension. However, this is dependent upon the type of muscle contraction and sporting activity being performed³. Previous literature states that the Achilles tendon contributes predominantly to the increased total length of the triceps surae directly following ground contact during running⁴, with surrounding muscle fibres providing a negligible contribution to movement⁵. Through this period of ground contact an eccentric muscle contraction occurs in order to control movements that follow impact, this is the point where Achilles tendon strain can arise.   

In the most recent study of its kind a statistically significant reduction in peak ankle dorsiflexion has been observed for increased heel lift conditions⁶, therefore providing biomechanical support to clinicians and practitioners that an increased heel lift leads to a reduction in Achilles tendon strain. It was found that a somewhat small heel lift of 7.5mm produced this significant effect on ankle dorsi flexion and that further increases to the magnitude of the heel lift could result in rear foot instability. We can therefore conclude that a relatively modest heel lift could be of benefit the long distance runners that engage in high volumes of training. However, the future direction of research regarding this topic should focus upon the biological make-up of the Achilles tendon. This will provide a greater understanding of how the tendon reacts to repetitive strain and its requirements for an enhanced recovery time.

References

1.   Grisogono V, 1989. Physiotherapy Treatment for Achilles Tendon Injuries. The Journal of the Chartered Society of Physiotherapy. 75, p. 562-572.
2.  Clement DB, Taunton JE & Smart GW, 1984. Achilles tendinitis and peritendinitis: etiology and treatment. American Journal of Sports Medicine. 12, p. 179-184.
3.    Bobbert et al, 1986. A model of the human triceps surae muscle-tendon complex applied to jumping. Journal of Biomechanics. 19, p. 887–898.
4.  Caldwell G.E, 1995. Tendon elasticity and relative length: Effects on the Hill two-component model. Journal of Applied Biomechanics. 11, p. 1-24.
5.   Van Ingen Schenau G.J, 1984. An alternative view of the concept of utilisation of elastic energy in human movement. Human Movement Science. 3, p. 301-336.
6.  Dixon S.J & Kerwin D.G, 1999. The influence of heel lift manipulation on sagittal plane kinematics in running. Journal of Applied Biomechanics. 15, p. 139-151.