Running Shoe Characteristics and Injury

The growing popularity of recreational running has resulted in an increase in associated injuries to lower extremities (Latter, 1981) and according to most reports 60% of these runners will experience injuries that limit their activity levels (Brody, 1982). Statistics have revealed that injury rate is higher in novice runners than their elite counter parts (Cook et al. 1990), this may be due to both biomechanical and physiological variables.

The impact period of the running stance phase is often called the heel strike, most runners make ground contact with the lateral aspect of the shoe sole at the heel. During the mid-support component, the foot rolls into a pronated position with both forefoot and rearfoot in contact with the ground. Control of this motion is affected by three muscle, tibialis posterior, flexor digitorium longus and flexor hallucius longus. Upon repetitive use, these muscle can become inflamed and produce conditions such as shin splits (Clement et al. 1981). The final component of the stance phase is  the push off, when the shoe should control the position of the foot with respect to the leg in order to maintain stability (Nigg et al., 1987).

Over pronation is not desirable; various running injuries have been reported to be associated with excessive foot pronation (Cook et al., 1990). However, the combined movement of eversion, abduction and dorsiflexion allows for surface adaptation and shock absorption and so is a necessary aspect to running gait (Perry & Lafortune, 1995). Nevertheless over pronation during the midstance phase results in a hyper flexible and unstable foot (Cheug et al., 2006). ‘Motion control’ training shoes attempt to negate these effects, either by realigning the foot or by a direct cushioning effect. Right leg foot positions and rear foot angles.

In order for a shoe to resist excessive or unwanted motion of the foot and ankle shoes can employ various characteristics such as a heel flare, medial posting and dual high density cushioning materials. Each intended to lessen the amount of rear foot movement experienced by an athlete. An increased medial heel flare has been shown to decrease rear foot movement (Clarke et al, 1983; Nigg & Morlock, 1987). Whilst a reduction in lateral heel flare reduces ankle leverage, therefore reducing rear foot movement (Nigg and Morlock, 1987).
The use of medial posting and dual high-density materials has also been found to reduce rear foot movement (Cheung & Nigg, 2007). Such motion control shoes have been shown to reduce rear foot angle by 4°. Although it has been found that pronation is of particular importance in the first 10% of stance (Duffey et al., 2000), as a reduction in rear foot movement at this time makes for a more rigid landing. Thereby increasing the impact shock to the lower extremity and contributing to overuse injury.

Alternatively, it has been suggested by Lieberman et al. (2010) that running shoes cause heel striking and that barefoot running would make for a flat/forefoot strike. It was thought that this forefoot strike would negate the impact peak of the heel strike that was linked to injury and thus this style of running would not subject athletes to the same types of impact loading. Ultimately, leading to the conclusion that running shoes cause an impact shock and accommodate higher injury susceptibility. Perhaps a key result of this study was the introduction of minimalist training shoes such as Nike Free and Vibram Five Fingers, such training shoes seek to emulate barefoot running since it was postulated that running shoe cushioning and heel lift were not beneficial. However, both running barefoot and with minimalist training shoes result in higher impact force magnitude and loading rates compared to traditional shod running (Squadrone & Gallozi, 2009). Both variables arguably possess a similar risk of injury as impact shock, thus highlighting flaws in the ‘safe’ and ‘gentle’ natural of running barefoot.

However, it has been shown that the impact force acts as an external input to our system, allowing us to detect the nature of the surface and adjust our muscle activation accordingly (Nigg + Wakeling, 2001). Contradicting the notion that impact peak is associated with injury (Zadpoort +Nikoofan, 2011) and instead providing a means for runners to efficiently adapt to different terrains. As opposed to examining ground reaction force data it has been suggested that the study of pressure variable would be more appropriate. This would allow for the identification of the area of the foot that first comes into contact with the ground, providing more detail of what foot contact style is being adopted for different conditions (Nunns et al., 2012).

Barefoot running is therefore not the miracle practice frequently speculated in the media, making athletes more efficient and injury free. Instead, it causes individuals to load the associated joints in a different manner through an alteration in stride type, the effects of which can be equally as injury inducing as traditional shod running. The notion that barefoot running also results in greater running economy can also be seen as a myth, although it rids the exerciser of the added mass from trainers (which increase oxygen consumption by 1% per 100g), it does not account for the need of greater proprioception. Overall leading to gait alterations that would have already been of optimal measures.

Overall, literature evidence is equivocal as to whether different footwear types truly can negate injury for runners. Although variations in heel flare may reduce rearfoot movement it is important to maintain a certain level of pronation (8-10°) for shock absorption and terrain adaptation.  This pronation is of particular significance during the first 10% of stance and so should not be eliminated. Whilst barefoot running/minimalist shoes have been shown to alter stride types, distributing impact forces differently and not necessarily preventing injury. It is important that coaches adopt a holistic assessment of their athlete when screening for injury risk. Taking into account training and physiological variables that may provide a clearer picture of injury, this may include strength of the surrounding skeletal muscles and the variance of the training programme.

Altitude Training Uncovered

There are many myths and misconceptions that surround the concept of altitude training within the disciplines of exercise physiology and sports training physiology. Such errors can lead to the misuse of training at altitude, which may lead to disappointment in subsequent performance. This article explores the subject of altitude training, defining what it is, acknowledging potential problems and its ultimate impact upon athletic performance.

Altitude training can be defined as training at heights greater than 2,500m above sea level. At such heights, it is commonly thought that there is a decreased percentage of atmospheric oxygen. However, the percentage of gases in the air we breathe remains unchanged from sea level to high altitude. Instead it is the partial pressure (PO₂) of each gas that is reduced as a drop in atmospheric pressure is seen at altitude. Therefore the air is less dense, consisting of less O₂, CO₂ and N₂ per litre, but the percentage of each gas forming this litre does not change. The fall in PO₂ reduces the driving pressure for gas exchange at the lungs, accordingly arterial O₂ saturations declines and so there is a rapid decline in O₂ availability to the working muscles. From near sea level, to a moderate altitude VO₂ max observes a linear reduction (Wehrlin and Hallen, 2006), on average this equates to -7.7% per 1000m of altitude despite a compensatory cardiorespiratory response.

It is this reduction in air density that can pose problems to training at altitude if an athlete is not fully prepared, one such consequence is a 1°C fall in temperature for each 100m ascent. The combination of a decreased temperature and pressure results in a reduced atmospheric water vapour content, which leads to increased respiration due to a decreased oxygen availability. This lends itself to greater water evaporation from the lungs, thus increasing the likelihood of severe dehydration that will inevitably cause a deterioration in athletic performance. As a result of these factors and a reduced cerebral O₂ saturation, many athletes suffer acute mountain sickness (AMS), the upshot of which leads to a lack of appetite, nausea, excessive weakness, vomiting and increased heart rate. Such symptoms dramatically impact upon the wellbeing of an athlete and in severe cases pulmonary or cerebral oedema can ensue. In order to prevent AMS a gradual introduction to altitude is needed, allowing for acclimation to occur which can take up to two weeks for heights of 2300m. This can be achieved through artificial means such as a hypoxic sleeping chamber or nitrogen generator to lower the atmospheric O₂ content.

An example of a hypoxic sleeping chamber. 

Within the realm of sport and exercise science there has been much debate as to whether the practice of altitude training can improve aerobic performance. It has been hypothesized that the compensatory physiological responses at altitude will result in adaptations that transfer to improved sea-level performance. However, this has been seen to be untrue. 

Altitude training has only been seen to cause performance improvements at altitude, with the majority of studies confirming that altitude endurance training fails to enhance sea-level performance. This outcome relates to the inability to perform at a sufficiently high intensity at altitude, at a height of 4000m exhaustion occurs at just 40% of sea level VO₂ max, thus failing to elicit the relevant aerobic physiological adaptations. However, the live high-train low rationale (Stray-Gundersen and Levine, 2008) provides hope for the significance of the inclusion of altitude for athletes. This theory states that the combined haematological adaptations from altitude and the maintenance of training intensity at sea level results in an improved endurance performance at sea level, giving leave to a 7.8% increase in O₂ carrying capacity. An adaptation such as this is achieved by increases in red blood cell mass, haemoglobin and erythropoietin, therefore increasing the delivery of oxygen to the working muscles.

Overall it has been shown that the combination of living high and training low can enhance sea level performance. This allows for a high training intensity to be maintained whilst also attaining the important haematological alterations that are associated with a high altitude.

References

Stray-Gundersen J., Levine B. D. (2008) Live high, train low at natural altitude. Scandinavian Journal of Medicine & Science in Sports. (1) pp. 21-28.

Wehrlin, J. P. and Hallen, J. (2006) Linear decrease in VO₂ max and performance with increasing altitude in endurance athletes. European Journal of Applied Physiology (96) pp. 404-412

Barefoot running: Factors affecting performance and the implications for injury

Barefoot running and minimalist training shoes have been a hot topic for debate among both amateur and professional runners in recent years. With the emergence of headlines such as ‘Runners without shoes land more gently on the ground, avoiding impact injuries’ (Independent, 2010) there is little wonder as to why the craze has continued to grow. This article looks to explore the practice of barefoot running, deconstructing the myths that surround it whilst also giving some practical advice for performance and injury prevention.

The paper to spark this debate of the benefits to barefoot running was by Lieberman et al. (2010) suggesting that running shoes cause heel striking and that running barefoot would make for a flat/forefoot strike. It was thought that this forefoot strike would negate the impact peak of the heel strike that was frequently linked to running injuries and thus running with this style will not subject the body to the same impact loading. Ultimately, leading to the conclusion that running shoes cause impact shock and accommodate higher injury susceptibility. Perhaps a key result of this study was the introduction of minimalist training shoes such as Nike Free and Vibram Five Fingers, such trainers seek to emulate barefoot running since it was suggested that running shoe cushioning and heel lift were not beneficial. However, running both barefoot and whilst wearing minimalist training shoes result in higher impact force magnitudes and loading rates compared with traditional shod running (Squadrone and Gallozi, 2009). Both variables arguably possess a similar risk of injury as impact shock, thus highlighting flaws in the ‘safe’ and ‘gentle’ nature of running barefoot.

However it has been shown that the impact force acts as an external input to our system, allowing us to detect the nature of the surface and adjust our muscle activation accordingly (Nigg & Wakeling, 2001). Contradicting the notion that impact peak is associated with injury (Zadpoor & Nikooyan, 2011) and instead providing a means for runners to become more efficient in adjusting to different terrains. As opposed to examining ground reaction force data it has been suggested that the study of pressure variables would be more appropriate. This would allow for the identification of the area of the foot that first comes in contact with the ground providing more detail of what foot contact style is being adopted for different conditions (Nunns et al., 2012).

Current empirical evidence is equivocal regarding the potential benefits to barefoot running and running economy. Nevertheless there are a number of factors to consider that may affect oxygen consumption whilst running. The first of which being the affect of added mass, with each 100g shoe mass resulting in a 1% increase in oxygen consumption and with the average training shoe possessing a mass of 300g this could mean an O₂ uptake increase of up to 6%. On the other hand, due to the absence of footwear there is a metabolic cost associated with active cushioning. This takes places via changes in muscular activity in the supporting muscles, all of which is likely to result in a less efficient running performance. Lastly, during barefoot running there is a need for greater sensory feedback. Since the runners feet are coming into direct contact with the ground heightened proprioception is necessary and this may lead to gait alterations making for less efficient strides.
Although barefoot running may allow for the effective use of elastic energy in foot through a forefoot strike one’s strike pattern has not been proven to affect an individual’s running economy. So, forefoot striking offers no economical advantage over heel striking and given that runners naturally adopt their optimal stride type this could reduce their running economy.

 To conclude, barefoot running is not the miracle running practice that sporting professionals originally thought, making athletes more efficient and injury free. Instead it just causes individuals to load the associated joints in a different manner and changing their stride type, the effects of which can be equally as injury inducing. The notion that barefoot running also resulting in greater running economy can also be seen to be a myth as although it rids the exerciser of the added mass effect from trainers it does not account for the need of greater proprioception. Overall leading to gait alterations that would have already been at the optimal measures. 

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. 

Lactic Acid and Exercise Performance: Friend or Foe?

Among athletes and exercisers alike there is a distinct belief that lactic acid is the cause of fatigue within working skeletal muscle. However, this is simply a convenient explanation for a complicated sequence of biochemical processes. Blood lactate is not the cause of fatigue, in fact it can be used as a highly efficient and useful energy source¹ – and this is why.

In order to understand blood lactate and how it behaves, a basic understanding of exercise metabolism is firstly required. The body utilizes three metabolic pathways to serve energy to the active muscles during exercise, each pathway converts a certain chemical or macronutrient substrate into ATP. ATP is regarded as a high-energy phosphagen that enables the contraction of skeletal muscle fibres.

Immediate energy, as soon as any physical activity commences, is provided by the ATP-PCr (phosphocreatine) system. It has the ability to provide immediate energy since very few reactions and enzymes are involved in the pathway, this is of great advantage to high intensity, explosive sports such as weight lifting and shot put. However, the body only stores 15 mmol of the pathway’s substrate (phosphocreatine) within each kilogram of skeletal muscle. As a consequence, during intense exercise intramuscular stored glycogen must provide the means to resynthesize ATP in the second of the metabolic pathways, anaerobic glycolysis. This pathway also has the ability to rapidly produce ATP due to only a few short steps being necessary. Yet, it is this anaerobic production of ATP via glycolysis (glucose breakdown) that leads to the formation of lactate and hydrogen ions. Although these two products result from the same reaction to give lactic acid, they dissociate very quickly and so it is highly unlikely any lactic acid will be found in the blood.

It is in the last of our metabolic systems that lactate realises its full potential. Lactate has the ability to circulate from the fast twitch muscle fibres where it is produced, to the slow switch muscle fibres where it undergoes conversion into the compound pyruvate during aerobic energy metabolism. Pyruvate then undergoes conversion into acetylCoA and enters the Krebs cycle, a cyclical chain of reactions whereby aerobic ATP production takes place. Skeletal muscles oxidize much of the lactate they produce before it is even released into the blood, meaning that a capacity to generate increased lactate levels enhances maximal power output.

Alternatively, the liver possesses the ability to accept skeletal muscle born lactate for synthesis into glucose via the Cori Cycle. This lactate derived glucose can either return to the blood for energy metabolism within active skeletal muscle or it can be synthesized into glycogen for storage and future energy use by the liver. These uses of lactate make it a valuable source of energy for skeletal and cardiac muscle, whilst also being a fundamental contributor to the making of glucose within the liver². The picture below illustrates the relationship between lactate and energy production. 

Since lactic acid is in fact a myth in the domain of sport and exercise and since lactate can be used as an energy substrate, it is the presence of hydrogen ions (H⁺) that are responsible for muscle fatigue during intense bouts of physical activity.  H⁺ ions that result from anaerobic glycolysis lower the intracellular pH within the muscle, increasing acidity and interfering with muscle contractions. This increased acidity denatures various metabolic enzymes that are key to energy transfer and reduces skeletal muscles contractility due to the progressive loss of intracellular potassium³.

While the notion of lactic acid is easily relatable to athletes and exercisers, its presence has hindered the knowledge we now have regarding skeletal muscle fatigue for the last two decades. So to summarise, appreciable amounts of lactic acid are not found in the blood and so is not the direct cause of skeletal muscle fatigue. It is in fact a valued and necessary source of energy, whilst also being fundamental in the biochemical process of gluconeogenesis⁴.

References

1.  Brooks G. A, 1986. The lactate shuttle during exercise and recovery. Medicine and Science in Sports and Exercise. 18, p. 360-368.
2. Consoli et al, 1990. Contribution of liver and skeletal muscle to alanine and lactate metabolism in humans. American Journal of Physiology. 259, p. 677-684.
3. Nielsen et al, 2004. Effects of high-intensity intermittent training on potassium kinetics and performance in human skeletal muscle. Journal of Physiology. 554, p. 857-870. 
4. Miller et al, 2002. Metabolic and cardiorespiratory responses to "the lactate clamp". American Journal of Physiology – Endocrinology and Metabolism. 283, p. 889-898.