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.

Dietary Supplements: Potential Benefits and Risks to Athletic Performance

In the world of professional and recreational sport today the prevalence of supplementation in a bid to enhance performance is widespread and estimated to be at between 57-94% of athletes (Ronsen et al. 1999). In one study (Lazie et al. 2009), 75% of the 912 athletes analysed used at least one dietary supplementation product. The most common of those used were multivitamins, taken by over half of the subjects. However, in an eight month study conducted some time before that of Lazie’s it was found that although vitamin and mineral supplementation increased blood vitamin levels, no specific performance benefits were evident (Telford et al. 1992). Many claim their reasoning behind taking multivitamins is as a ‘safety net’ to ensure adequate levels of each micronutrient in the body, however research has shown that if one has a healthy and balanced diet they will already receive plenty of these nutrients (Rodriguez at al. 2009). It should also be stated that in the case of a poor diet with little fresh fruit or vegetables, multivitamin supplements should not replace the role of food, this may give an athlete a false sense of security and lead to detrimental health effects.

Unpublished research from Depiesse revealed the reasons given by athletes for their ingestion of dietary supplements:

•          To aid recovery from training
•          Prevent or treat illness
•          For general health
•          Performance improvement
•          Compensate for poor diet

Of course many dietary supplements on the commercial market today do have their evident ergogenic benefits, the first of which can be seen in the various forms of protein supplements such as shakes, bars and snacks. These products are easily accessible for the professional and recreational market alike and provide a convenient means of ensuring that adequate protein is ingested following a bout of exercise. Skeletal muscle synthesis is stimulated through exercise (Biolo et al. 1995) and protein feeding (Rennie et al. 1982), this effect can be enhanced by the consumption of protein following activity to promote a positive net protein balance within the skeletal muscle (Moore et al. 2009). Muscle protein synthesis is specifically maximised by the intake of 20g of high quality protein (Moore et al. 2009), intake below 20g results in sub optimal rates of muscle protein synthesis whereas intake above leads to irreversible amino acid oxidation. However, this is often the case, with many individuals overcompensating their protein intake which only requires the excretion of its nitrogen component. For the active elderly population a higher dose of post exercise protein is beneficial as they are more receptive to protein than younger exercisers. Although there is no metabolic window for this enhancement of muscle protein synthesis, it may be of benefit to eat within half an hour of a workout in order to replenish other physiological stores such as glycogen.

Another popular supplement, especially among strength and power athletes is creatine. Having been proven to improve power, strength and intermittent sprint performance through the stimulation of muscle anabolism following resistance exercise. The net result of which is muscle hypertrophy alongside increases in free creatine and phosphorylcreatine content. With regards to endurance exercise, nitrate supplementation has provided promising and significant results in reducing oxygen consumption during submaximal exercise and the ATP cost of muscular contraction.

Supplementation may also be of benefit to particular populations, especially female athletes involved in endurance sports or on a reduced calorie diet due to participation in aesthetic sports such as gymnastics. Poor nutrition alongside intense training, low body fat and weight loss can blunt oestrogen synthesis by peripheral fat. It is the effect of this, coupled with hormonal alterations that results in exercise related amenorrhea.

Many of these supplements can however result in the unintentional ingestion of banned substances (Geyer et al. 2004) as a result of contamination or poor labelling (Baylis et al). Not only can such an event lead to lifetime ban from sport but also potentially life threatening adverse effects to health.
It has also been observed that herbal supplements such as ginseng, guarna and non-herbal products including zinc and chromium can lead to detrimental health effects.

It is fair to state that the use of dietary supplements is extensive among the sporting population, this is at both a professional and recreational level. However, these individuals should be made aware that few supplements can match there extravagant ergogenic claims and should also never be used to compensate for a poor diet. This also highlights the need for the education of coaches and instructors as it has been found they pose the most influence on an athlete’s dietary habits. Lastly, the risk of obtaining a positive doping test as a result of poor supplement labelling or contamination is very much real and so these risks should be balanced against the potentials benefits before ingestion. 

Recovery Strategies: Be your best

Carrying out an intense and heavy training load will inevitably provoke muscle damage that gives way to exercise induced muscle soreness, having a detrimental effect on exercise performance. In between training sessions the primary goal is to bring the athlete into the supercompensation zone (see figure below), once this is achieved the previous regime may be completed with ease. Alternatively, training intensity and volume can be increased to ensure a steady progression of positive adaptation. In order to reach this desired state within the supercompensation theory optimal recovery is key and strategies to obtain this may come in a variety of ways, ranging from supplementation, active recovery, hydrotherapy, cryotherapy and massage. The present article aims to discuss each of these strategies in turn, highlighting their possible benefits to performance and any evident flaws they possess.

 

Firstly, it is integral to discuss how exercise induced muscle damage (EIMD) occurs and the symptoms it can generate. EIMD is typically characterised as muscular soreness 24-48 hours following a bout of exercise, resulting in reduced muscle functioning and swelling. This damage occurs due to carrying out an unaccustomed amount of exercise with a particularly high eccentric contraction component. As there is little myofilament overlap (see top picture in figure below), muscle sarcomeres become overstretched and damaged. It is this process that causes the membrane damage that allows an intracellular influx of calcium ions and t-tubule disruption. Ca²⁺ entry results in an inflammatory response and so swelling in major muscle groups results, whereas t-tubule disruption leads to a loss of muscular strength as a result of excitation-coupling dysfunction.

 

Arguably the most common strategy employed by coaches and athletes is the completion of an active recovery. The theory behind this low intensity exercise following training is that it will allow a gradual decrease in core body temperature, whilst also clearing metabolic waste products such as the hydrogen ions associated with lactic acid. One particular study carried out wrist flexion until an intramuscular pH of 6.4 was reached, there after the active recovery group continued flexion at a 5% decrease every minute. Compared with those in the resting control protocol, the intracellular pH of subjects taking part in an active recovery decreased far more rapidly. It can therefore be concluded that an active recovery is an effective strategy to promote recovery from metabolic acidosis and enhances the body’s natural ability to return to a pre exercise state. It is also fundamental that each week to ten days the athlete dedicates one day solely to an active recovery, this can be achieved through a light jog or cross training in a low impact activity such as swimming or cycling. Not only will this prevent overtraining but also break up to monotony of a religious training schedule, therefore sustaining interest and motivation.

With regards to supplementation cherry juice consumption has produced promising results for endurance athletes. Due to its antioxidant properties it can help negate the cellular damaging free radicals that are produced during exercise. Marathon runners consumed either a cherry juice or placebo drink five days before and for 48 hours following a marathon race. Those that ingested cherry juice displayed reduced inflammation/muscular swelling and recovered isometric strength significantly faster than those in the placebo group (Connolly et al. 2006). Branched chain amino acid (BCAA) consumption has also proved to elicit beneficial results, such as no increase in blood markers of muscle damage that can cause inflammatory responses and a lower perceived soreness level (Jackman et al 2010).

The resultant effects of massages are equivocal and their full benefits are not yet fully understood. However, it is through that sports massages can promote circulation, release muscular tension and reduce inflammatory responses. In a group of healthy untrained participants a ten minute massage followed 10X6 bout of maximal isokinetic eccentric actions at the elbow joint. The employment of this massage led to a decrease in the severity of the soreness experienced by subjects compared with no post exercise massage (Zainaddin et al 2005). If you don’t have the time or money for a professional massage self-administered techniques such as foam rolling may also prove effective in alleviating pain and reducing inflammation induced by exercise.

The use of hydrotherapy and cryotherapy has seen substantial increases in recent years, particularly with reference to ice baths. Everyone from tennis players, weight lifters and marathon runners include ice baths within their recovery programme following a heavy training session or competition. The theory behind cold water immersion is that it will promote vasoconstriction in those blood vessels that are beneath the icy water. Blood rich in metabolic waste products is then drained from the legs, allowing fresh oxygenated blood to flush through the limbs once the athlete is removed from the bath. Studies have confirmed that cold water immersion (CWI) and contrast water therapy (CWT) prove effective in reducing the detrimental physiological effects brought about by exercise induced muscle damage. It was found that squat jump performance recovered more rapidly to baseline measures and increases in mid-thigh circumference were reduced following CWI and CWT (Vaile et al. 2008). It is unclear as to the practical recommendations of hot water immersion. Although no significant scientific evidence can confirm its benefits anecdotal reports suggest that added warmth can treat muscular soreness and prepare the muscle for masses/physical activity. However it is important to note that heat should not be added to inflamed muscles as this will only promote further unwanted swelling.

Lastly, sleep is an essential component for optimal recovery. Those athletes who fail to have an adequate amount of sleep will compromise their reaction time, neuromuscular patterns and ability to store muscle and liver glycogen.

Recovery itself is extremely individualistic, no two athletes will recover optimally in identical ways due to training differentiation and personal preferences. The key is finding a recovery tool that works for you as an athlete, whether this reduces the effect of muscular swelling or simply refreshes the major muscle groups in time for the subsequent training bout. However, adequate nutrition, hydration and sleep are vital, regardless of your athletic discipline. The correct recovery strategies can require the same amount of effort and discipline as training itself but by getting its key principles correct injury and illness risks are significantly decreased.

“Recovery is where the gains in your training actually occur, and valuing your recovery is the key to both short-term and long-term success” – Sage Rountree, Team USA Triathlon World Championship team member and ultrarunning coach.

Exercise Euphoria: The runner’s high

Many avid runners will already know what I mean by the “Runner’s High” and the feelings that it provokes, often it is completely unanticipated yet feels as though it’s the most natural feeling in the world. Frequently when on longer training runs that are up to six to ten miles in length, I have slipped into the running high, finding myself in another world for between one and two miles. The run seems effortless, I’m almost gliding with every pace and a sense of fulfilment encapsulates me. One definition from Sach and Berger states the runner’s high is a “euphoric sensation experienced during running, usually unexpected, in which the runner feels a heightened sense of wellbeing, enhanced appreciation of nature and a transcendence of time and space”.

It has been reported that among runners who have previously experienced the high up to 30% of those encounter it on their daily runs, claiming to feel a sense of mental awareness, liberation, exhilaration and pain suppression. Additionally, in an interview of 60 runners it was revealed that the high brought about by running cannot be reliably predicted but can be facilitated by the absence of distraction and cool weather conditions. Runs should be ≥6 miles in length at a comfortable pace and it is also vital there is no concern with regards to timing or pacing.

Several theories exist regarding how the running high is brought about with perhaps the most famous being that of endorphin release, the body’s natural painkiller. However this theory has several problems, fundamentally endorphins are simply too large to pass over the blood-brain barrier. Consequently, although endorphin concentrations do increase within the circulation during exercise, without reaching the brain they cannot be held accountable for the high exercisers experience. Another key hypothesis is that of the opioid system, opioids are psychoactive chemicals that resemble morphine in their pharmaceutical effects. Research has revealed that release of endogenous opioids occurs following prolonged exercise and that this release is closely correlated with perceived euphoria among runners. However, it is also known that the opioid system is accountable for responses such as respiratory depression and other effects that are detrimental to running performance.

Perhaps the most feasible alternative to the endorphin theory is the ‘endocannabinoid hypothesis’’. Cannabinoids, an active ingredient found in marijuana binds with the nervous system to reduce pain and aniexty, producing a profound sense of wellbeing. Our body has the ability to create its own cannabinoids (endocannabinoids), these are composed of lipid molecules small enough to pass over the blood-brain barrier to provoke an affect in the brain. Research findings have shown that exercise increases the concentrations of these endocannabinoids, producing psychological effects closely resembling those associated with the runner’s high. The endocannabinoid systems activation is also thought to elicit a reduction in attentional span, time estimation difficulties, memory impairment and a sense of wellbeing. All of which characteristics are often included in the reported psychological profiles of long distance runners. These findings may be as a consequence of decreased metabolism in the prefrontal regions of the brain with increased endocannabinoid concentrations, whilst also demonstrating disadvantageous affects to cognitive functioning.

As yet there is no reference to a cyclist’s or swimmer’s high, it is likely this is due to endocannabinoid receptors residing in the skin and so as runner’s make contact with ground endocannabinoid release is stimulated. Another key point worth noting is that low level skills such as running are highly controlled by the basal ganglia which are responsible for cognition and habitual behaviours. The net result of this is that they more readily activate the endocannabinoid system than high skilled activities such as hockey or basketball.

Furthermore, endocannabinoids interaction with the neurotransmitter dopamine suggest that they play a role in the brain’s rewarding system, possibly contributing to exercise/running addiction. This many result in detrimental health affects among athletes who continue to train despite a chronic overuse injury. Lastly, it has be observed that the endocannabinoid system also attributes peripheral effects including bronchodilation and vasodilation. Such physiological changes can facilitate endurance performance by allowing for more efficient oxygen transportation, thereby promoting feelings of ease and effortlessness.

This article intended to provide an overview of the “Runner’s High” phenomenon, there is still much room for further research however it is clear that endurance runners frequently encounter many of the mood components mentioned whilst training. The most promising theory is that of endocannabinoids, providing both a physiological and psychological explanation for the exercise high. Although these feelings are subject to great individual variation and it is still unclear how age, sex and exercise intensity can affect the feeling of exercise euphoria.

"I always loved running... it was something you could do by yourself, and under your own power. You could go in any direction, fast or slow as you wanted, fighting the wind if you felt like it, seeking out new sights just on the strength of your feet and the courage of your lungs." - Paula Radcliffe

The myths and mysteries of optimal dietary protein intake

It has been a long posed question as to whether elite and recreation athletes alike require an increase amount of protein within their diets in order to optimise training gains. This article will discuss the need for protein within an athletic diet, its optimal dosage, and overall guidelines that can be applied to an individualized nutritional programme.

We know that the average individual contains approximately 12kg protein, much of this is contractile skeletal muscle and the remainder resides as free amino acids found either in the circulation or intracellularly within muscle fibres. A continual bodily protein turnover shows that humans require a regular and adequate level of protein intake in order to carry out basic biological functioning and that this level of intake is somewhat increased for active individuals. Such a consensus was reached due to an observed increased in leucine oxidation during exercise, as well as multiple studies showing greater protein intake results in an improved muscle mass and muscular strength.

It is also clear that exercise causes increases in muscle protein synthesis alongside muscle protein breakdown, however exercise alone does not result in a positive net muscle protein balance. It is essential exercise is coupled with amino acid ingestion, as this will stimulate muscle protein synthesis and inhibit exercise induced protein down. This way muscle mass will gradually increase (hypertrophy). At the other end of the spectrum, inactivity will lead to an inhibition of protein synthesis and actually stimulate the breakdown of proteins, resulting in a net loss of muscle mass (atrophy) and decreased muscular strength. Although it has been shown that just a minimal amount of resistance training can prevent the inhibition of protein synthesis, this is of greater importance during periods of recovery or injury when muscle wastage is most likely to occur.

Now to perhaps the key question; how much protein do athletes  actually need to consume? Firstly, it should be noted that specific recommendations are extremely difficult to determine due to the variation in parameters such as age, sex, sport, playing position and the individuals training status. However, ingesting 20 grams of egg or whey protein can be said to be the general guideline of consumption to maximise the anabolic response of the muscles to exercise. There is little need to consume more than 20 grams of protein following a bout of physical activity, since the body is unable to utilise further amounts and so it will be either oxidised or excreted. No metabolic window exists for this consumption, as muscle protein synthesis experiences no change whether intake occurs immediately following training or three hours later. Although eating immediately after exercise is necessary to optimise recovery with regards to other substances such as glycogen.

Depending on the nature of one's nutritional goals some individuals may benefit from excess protein intake.  This is true of those with a primary aim of gaining lean mass and muscular strength where carbohydrate intake is not an concern. It may also be of benefit to those on a hypocaloric diet for weight loss, as a high protein diet will prevent the loss of lean tissue. The main concern here resides with the notion that excessive protein consumption may compromise the intake of other macronutrients such as carbohydrate.

Another key argument with regards to protein is whether there is a real need for its supplementation. It has been shown that training actually increases protein balance, which allows for enhanced reutilization of amino acids and thus reduces intake requirements. Therefore more ample amounts of protein are consumed in the diet and so there is little need for supplements. Despite this many do still seek further means of protein intake, with whey being a very popular choice. Compared to other supplements such as casein or soy, whey protein stimulates a superior anabolic response of muscle protein synthesis. This is because it contains greater amounts of leucine, an important essential amino acid.

With reference to the possible dangers of a high protein intake, evidence is at best equivocal that it will lead to negative health effects. Kidney problems and bone loss in healthy individuals are almost uncertain, let alone those who are physically active. It is however important that an increased amino acids intake does not override that of other essential nutrients.

When applying the contents of this article to your own nutritional programme the following guidelines may be followed; although it is probably not necessary whey protein is the best supplement option. 20 grams of protein is sufficient to stimulate optimal muscle protein synthesis following exercise and can increase strength by 40-50%. However this should only be used as a general figure and individually tailored with regards to age, sex, sport and training status.

Overtraining and Performance Deterioration: Knowing when to take a rest day

It is universally agreed by sport and fitness professionals that overtraining is a necessary requirement in order to achieve the relevant physiological adaptations for peak performance. However, when prescribed in inappropriate quantities a deterioration in performance can be provoked. This article considers the impact of overtraining on the psychological and athletic state of an individual, highlighting the importance of various themes presented in my previous blogs.

Overtraining can be defined as a cycle of training whereby the athlete is exposed to excessive maximal capacity training loads. If this training cycle proceeds without adequate rest, a reduction in workload or in conjunction with psychological/physical stressors then overtraining syndrome (OTS) results and subsequently a deteriorated performance is seen.

At present there is no single test that can be utilized to diagnose overtraining, its recognition requires the identification of a number of stress markers which remain elevated despite a period of recovery. Stressors that may be observed include:

•          Diminished skeletal muscle glycogen stores
•          Aerobic efficiency deterioration
•          Suppressed immune system
•          Depression
•          Distorted sleeping pattern

These parameters should be regularly screened for alteration by sport professionals, this will ensure that the short term fatigue related with overload is not confused with the chronic fatigue generated by overtraining.

Numerous studies have taken place to review the effects of overtraining on physiological and psychological functioning, one of which observed that mood state disturbances increase in a dose-response fashion to the training stimulus. These fail to return back to baseline levels even after a significant reduction in training load. It has also been reported that 80% of ‘stale’/overtrained athletes are clinically depressed, substantially affecting other aspects of an individual’s life and overall wellbeing. Alternative research has also shown that 60% of female and 64% of male elite long distance runners have experienced at least one bout of staleness within their running careers, whereas this fell to 30% in highly trained sub elite runners (Morgan, O Connor, Ellickson and Bradley 1988). It is also thought that once staleness is experienced subsequent episodes are more probable, thus emphasising the need for the observation of stress markers in athletic populations. Failure to identify key characteristics may lead to premature retirement from sport, increased injury risk or greater susceptibility to illness.   

It has been argued that a high training volume coupled with insufficient rest will produce muscle, skeletal and/or joint trauma. Such trauma will result in the activation of circulating monocytes by injury related cytokines that produce systemic inflammation, this inflammatory response can trigger the symptoms of diseases such as stroke, heart attack and arthritis. The elevation of cytokines within the circulation also directs a response known as ‘sickness behaviour’, which by means of the central nervous system stimulates negative mood and behavioural changes. In addition, liver function is adjusted to support greater gluconeogenesis (the generation of glucose) alongside de novo synthesis of various proteins and it is this hypercatabolic state that results in muscle wastage. Theoretically meaning that the body’s primary focus is upon survival/recovery, as oppose to the adaptation that training aims to elicit. With regard to immune function, a decrease in glutamine concentration contributes to immunosuppression as it acts as a key fuel for immune system cells.  

As a result of these biological responses it is common for overtrained athletes to present a deteriorated mood state, typically complaining of sleeping disorders, lack of motivation and ‘heavy legs’. An impaired anaerobic performance and lactic acid threshold has also been observed, causing a reduction in the time to exhaustion during high intensity endurance exercise.  

For the prevention of this decline in performance it is essential that training is periodised and tailored to match the Profile of Mood States (stress levels) of the athlete, as well as tapering training prior to competition. These practices should be coupled with adequate carbohydrate ingestion to fuel and recover from physical activity, ensuring the maximum amount of energy is available for exercise. It is also vital the training is abstained from following periods of illness, high stress and extreme environmental conditions for the maintenance of motivation. 

With professional and amateur sporting calendars now including events all year round it is fundamental that athletes of all abilities allow for adequate rest within their regimes. Research clearly documents profound affects to physical and psychological health if individuals fail to do so, these may ultimately lead to severe injury, depression or performance decline. 

The Taper: Physiological Peaking and Optimal Athletic Performance

It is common practice for elite and recreational athletes to spend months, perhaps even years training in preparation for a specific sporting event. However, the physiological and arguably the psychological gains achieved by an intense training regime are useless if the exerciser does not conduct an effective taper.

The first article of this month discussed the importance of a long term training programme, the current article will serve well to complement the previous issues raised and ensure even more refined physiological peaks are achieved. The taper is a fundamental element to sporting preparation and can be characterised as a mesocycle, within which the training stimulus sees a significant reduction. This may be achieved in a linear or nonlinear fashion. The aim of this practice is to minimise any fatigue accumulated during prior training, whilst preventing the loss of relevant biological adaptations. Therefore highlighting the need to maintain training but at a reduced level.

The taper should be exclusively tailored to an individual’s preferences, as any reduction in training will also cause profound psychological effects to occur. Such psychological stressors are due to the absence of a structured lifestyle and increased time to over think performance, both of which account for a greater pre-competition anxiety level that can be detrimental to performance.

There are distinct patterns to tapering, these include a step taper, linear taper or exponential taper which involves a fast or slow decay of the training stimulus. During a step taper a sudden, standardised reduction in training can be observed and lasts for the full taper length. Alternatively, a more gradual decline in the training load can be seen in a progressive linear taper. Lastly, an exponential taper may be implemented, whereby a fast constant of decay elicits a rapid reduction in training load. On the other hand, a slow decay allows for a gradual training load reduction. The graph below displays these taper variations and the training load reduction one can expect to observe throughout its duration.

Current research indicates that a fast decay taper may enhance athletic performance better than a slow decay, as this provides the athlete with more time to overcome accumulated fatigue from the final weeks of an intensive training regime. It is also thought that an advanced reduction to training followed by a subsequent increase could further optimise performance. The reasoning behind this practice is that the athlete would be able to take advantage of a reduction in fatigue, effectively responding to training carried out during the taper.

The effects one can expect from an effective taper include –

•         Hypervolemia, this is an increase in blood plasma albumin content which provides the mechanism to metabolise greater amounts of fat.
•         An increase in red blood cell production, meaning oxygen carrying capacity is greater and improvements to VO₂ max can be expected.
•         Restoration of skeletal muscle and liver glycogen reserves, this is particularly prominent when coupled with appropriate nutritional techniques such as carbohydrate loading.
•         A decrease in total mood disturbance.
•         Increased muscular strength due to a greater maximum shortening velocity.

As a result of the physiological benefits brought about by an effective taper, the mean expected improvement to performance time is approximately 3% (Mujika and Padilla, 2003). This may seem like a fairly modest enhancement, however it could reduce one’s half marathon time from 1:30 to 1:27, decreasing the average running pace per mile from 6:52 down to 6:38.

Finally, in order to achieve an effective taper a reduction in training volume should be seen for a duration of two weeks, the intensity and frequency of this training should be maintained to at least 80% of the pre-taper levels. This ensures the quality of training is not compromised but sufficient recovery time can still occur. A fast decay, nonlinear taper design will also mean no negative psychological responses occur that have often been associated with step designs.  

A Sports Training Phenomenon: The Relevance and Versatility of High Intensity Interval Training (HIIT)

 It is well known in the world of sport and exercise that regular participation in endurance training causes improvements to performance in activities that rely mainly on aerobic metabolism. This is largely due to adaptations that allow for greater oxygen transportation and the subsequent utilization of the more efficient energy fuel, fat. On the other hand, high intensity anaerobic training is generally perceived to have less of an impact upon aerobic capacity and oxidative energy metabolism. However, various publications have shown that regular involvement in high intensity interval training (HIIT) for at least 6 weeks can increase VO₂ max and endurance capacity. Much of the recently published evidence also suggests that these biological adaptations associated with aerobic performance enhancement can be obtained more rapidly via HIIT. The current article will present the recent findings regarding speed endurance/high intensity interval training and discuss its relevance for aerobic performance enhancement.

High intensity interval training can be defined as repeated bouts of high intensity exercise (≥90% VO₂ max) lasting between a few seconds and a few minutes, interspersed with relatively longer periods of rest or low intensity active recovery. The length and nature of this recovery period is very much dependant on the athletes training aims.

Several studies have been carried out to investigate the effects of a HIIT regime; one remarkable finding by Burgomaster et al. (2005) was that despite a dramatic reduction in training volume, vast improvements to aerobic performance were seen when eliciting a high intensity protocol. They found subjects could maintain a fixed submaximal work rate for double the length of time (from 26 to 51 minutes, cycling at 80% of pretraining VO₂ max). These results were achieved after just six HIIT workouts, whilst the control group displayed no alteration in performance.
In another study, conducted by Gibala (2006) the experimental subjects performed a generic HIIT protocol whilst the control group carried out six continuous cycling sessions (65% VO₂ max, 90-120 minutes∙d⁻¹). The total training time completed by each group was 2.5 and 10.5 hours respectively, meaning that the HIIT training group saw a 90% reduction in training volume. Although significantly different in almost every sense of the FITT principles(frequency, intensity, time and type), the two protocols attained virtually identical physiological alterations.

Such a markedly improved aerobic performance can be accounted for by the following biological and metabolic changes:

•       Increased resting glycogen content in the skeletal muscle and liver which can be utilized as an energy fuel.
•          A greater total number of muscle glucose transporters, enabling more metabolic fuel to enter the blood and reach active muscles.
•          Increased density of muscle capillarization, providing the network to transport oxygen and nutrients such as liver glycogen to the working muscles. This also allows for the removal of the fatiguing waste product H⁺ ions, associated with lactic acid and a lowered intramuscular pH that leads to a decline in muscle contraction strength.
•          Speed endurance not only increases the presence of glycolytic enzymes involved in anaerobic metabolism, but also causes greater concentrations of beta oxidation enzymes (citrate synthase and cytochrome oxidase). These are responsible for the metabolization  of fat , thus sparing the body's limited glycogen stores and reducing lactate production.
•          There is an increase in the amount of potassium ions pumped back into the cell, limiting its accumulation in the interstitial fluid and therefore delaying progressive membrane depolarisation. This serves to maintain action potential amplitude - consequently delaying the onset of fatigue.
•          Increased  VO₂ max, enabling a greater aerobic endurance performance.
•          Finally, a greater  buffering capacity of lactate has been observed due to HIIT. More H⁺ transporters means that vast amounts of lactic acid's associated H⁺ ions are able to leave the muscle and move into the blood. Here they combine with bicarbonate to give carbonic acid. When carbonic acid dissociates its products of carbon dioxide and water can simply be exhaled, causing no negative effects to athletic performance.

These adaptations have significant implications in enhancing endurance performance. Firstly, running economy has been seen to gain considerable improvement, this means less energy is required to run at the same velocity. Furthering this point, a decreased energy requirement will allow for the already increased glycogen reserves to be maintained even longer. In addition, faster VO₂ kinetics at the onset of physical activity enables oxygen to be utilized faster for aerobic metabolism. As a result there is less break down of the body's anaerobic reserves and a reduction in metabolite (lactate) accumulation.

To conclude, it is the practical applications of HIIT that are of primary concern to elite athletes and recreational exercisers. It is known that highly endurance trained athletes find it increasingly difficult to achieve further biological adaptations through continuous endurance training alone. However, it has been observed that HIIT can improve endurance performance in already trained aerobic performers by increasing  their VO₂ max and running economy. Furthermore, implementation of this efficient training method will allow for more time to be spent on technical/tactical skills training.

On the level of recreational exercise participation and exercise prescription the most common barrier to physical activity is a lack of time, with many adults even failing to meet the minimum exercise guidelines. The innovations of HIIT could significantly contribute to combating this problem as identical adaptations from prolonged endurance training are obtained in a third of the time.

"I do it as a therapy. I do it as something to keep me alive. We all need a little discipline. Exercise is my discipline" - Jack LaLanne

Long Term Training Plans: Traditional vs Block Periodisation

The periodisation of training can be explained as a division of the entire season or year into smaller, more manageable periods of training blocks. The traditional approach to this training organisation was propose five decades ago, originating in Eastern Europe until spreading West and achieving a virtual monopoly over the way in which sporting professionals devised annual training regimes. However, gradually contradicting training concepts came to light which began to modify the way in which coaches approached  competition preparation, this is known as block periodisation. Today, the vast majority of sporting populations now implement this training structure with considerable athletic benefits being produced that are supported by a variety of journal and professional publications.

Within a traditional periodisation design the following hierarchy of training elements exists:

•             Macrocycle - May range from four years (Olympic preparation), to an annual cycle or several months.
•            Mesocycle - Consists of multiple microcycles, lasting several weeks.
•            Microcycle - Often a week long and is formed of multiple workouts.
•            Workout - Can last up to several hours, any break longer than 40 minutes separates one workout from another.

Ultimately, all macrocycles will focus upon a clear goal, whether this is attaining a personal best or winning an Olympic gold medal.  In a more recreational sense, the aim of an individuals macrocycle may be to reach their goal weight or complete a sub four hour marathon for charity. The macrocycle is then divided into three distinct phases, the first being the preparatory phase; whereby the focus is more generalized in order to improve the athletes basic components of fitness such as aerobic capacity. Secondly, the competition phase, is far more event specific and training would be tailored towards the athletes sport or position with a team. It is possible that this phase will also be interspersed with qualifying rounds or warm up running events for a prospective charity marathon runner. The third and final distinct phase is the transition phase, here an active recovery is completed following the major athletic event. It is vital that training volume is significantly reduced but does not cease completely, this will ensure that the athlete does not enter a state of detraining or experience burnout. Meso and microcycles fall next in the training hierarchy, often the aims of these are to perfect a sport specific technique or develop an aspect of fitness such as speed endurance. Lastly, workouts are the primary building block of any macrocycle, where performance is practically developed and the aims are fulfilled.    

There are aspects of the traditional periodisation model that are still applicable to sport training today, such as the use of relevant terminology and distinction between generalised and sport specific preparations. However, due to a virtually year long athletic seasons and severe time pressures many aspects of this method are unrealistic.

The first of four key drawbacks to traditional periodisation is its inability to give way to multiple physiological peaks that are vital to elite level sport. Numerous peaks in biological adaptations require a radical remodelling of long term training plans, the following three factors will explain why this is so. The traditional design of periodisation involves prolonged mixed training which research suggests results in several negative consequences; specifically the increased secretion of creatine phosphokinase alongside various stress hormones. Thus indicating excessive fatigue,  which may lead to staleness, burnout and ultimately a chronic overuse injury or dropout. It is also apparent that mixed training produces significant performance enhancement during its initial phases, especially among beginners. However, this soon plateaus often with a stagnation or decline in performance following. Furthermore, if this exhaustive mixed training is to last between three and five weeks a profound stress response is caused, this will significantly increase the athletes risk of overtraining or an overuse injury.  

Additionally, multi targeted  training that traditional periodisation encompasses is highly incompatible, often producing conflicting biological responses. These potentially eliminate gains made by one training aim through carrying out exercise aimed at other targets, this time could be better spent training  for a single physiological adaptation. Finally, with regards to high level elite athletes mixed targeted training often does not provide a sufficient stimulus in order to promote any physiological adjustment. In such high performance athletes the required adaptations are so specific that a highly concentrated workload is required to provide an adequate stimuli for their progression. Something that is simply unobtainable with intensive mixed training and may even bring about a decline in performance.

Within the last 30 years the world of sport has seen dramatic changes that account for the radical remodelling of traditional periodisation. Due to the formation of global sporting governing bodies there is now greater opportunity for competition and leagues than ever before. As a consequence multi physiological peaks are necessary, a requirement the new approach of block periodisation can accommodate. Because of this many of the previously seen training periods have been replaced by competition performance, this considerably reduces the training volume and so only focuses on a single key aim during performance preparation. Not only will this be of benefit to the individual physically by allowing appropriate recovery time for maximal energy levels, but also psychologically by decreasing the risk of overtraining that often leads to chronic stress and a lack of motivation.

A further consideration for coaches and exercise leaders is that sporting performance within any club or organisation manifests a wide variety of abilities. In the case of intense mixed training only a minute number of athletes will be developed simultaneously, highly concentrated training on an individual basis can only be developed consecutively - not concurrently.

The general foundations of block periodisation consist of all mesocycle training block and compared with traditional methods are greater in concentration, specificity and manageability. These mesocycle blocks can be further divided into three types, the first of which is the accumulation block. Accumulation targets the masses, intending to enhance basic performance components such as muscular strength and aerobic endurance. It is the longest of mesocycles, lasting two to six weeks. Next transmutation, which typically lasts two to four weeks, targets sport specific techniques, muscular endurance and tactical elements. Finally, realisation sets to model perfect competitive performance whilst reducing the training load prior to competition. This phase also allows for an active recovery alongside controlling emotional stress pending competition, its typical duration lasts 8 to 15 days. 

It is known that the accumulation mesocycle produces the longest training residuals, followed by the transmutation and realisation mesocycle blocks. This provides the basis for the optimal relationship between training effects in order to facilitate athletic performance significantly for varying sporting abilities. Therefore activating general adaptations which amplify the body's hormonal, metabolic and protein synthesis responses.
Conversely, during mixed training stress reactions are more prevalent, suppressing the regulation of hormonal and metabolic homeostasis. Subsequently leading to a dramatic deterioration in the fitness of sub elite and elite athletes, primarily a reduction in VO₂ max, the anaerobic threshold and maximal muscular strength. Whereas the modified periodisation ensures the correct interaction between training loads to exploit maximal physiological adaptations.

"If you train hard, you'll not only be hard, you'll be hard to beat" - Herschel Walker