Update 29/03/13 : This was originally posted in September 2012 but John has kindly updated and expanded it.

It is generally accepted that endurance exercise performance is related to the level of aerobic metabolism that can be maintained over a prolonged period of time (Coyle, 2007; Jones, 2006). In order to facilitate the aerobic resynthesis of adenosine triphosphate (ATP) the body must be able to deliver sufficient oxygen from the atmosphere to the mitochondria (the aerobic powerhouse within the muscle cell) in the skeletal muscle and supply adequate fuel in the form of carbohydrate and fats. As such, there are several key physiological factors that are thought to influence endurance exercise performance and it is suggested that training should be structured to take the following into account (Coyle, 2007; Jones, 2006; Midgley, McNaughton & Jones, 2007):

Maximal oxygen uptake (V̇O2max) Sustainable percentage of V̇O2max that an individual is able to utilise (linked to lactate threshold) Running economy

These three physiological factors are closely linked together. The highest average oxygen uptake required to maintain performance during endurance exercise is known as performance V̇O2 and is the product of V̇O2max and the sustainable percentage of V̇O2max that an individual is able to utilise. Running economy is a measure of how efficient an athlete is at converting the aerobic resynthesis of ATP into running speed and performance (Bassett & Howley, 2000; Jones, 2006).

Maximal oxygen uptake – aerobic interval training (‘intervals’)

What is V̇O2max?

The maximal rate at which aerobic resynthesis of ATP takes place is an important determinant of endurance exercise performance (Jones, 2007). Maximum oxygen uptake has been defined as the highest rate of oxygen that can be utilised by a given individual during exercise at sea level and for a significant muscle mass (Bassett & Howley, 2000). The V̇O2max is a product of the volume of blood pumped by the heart in one minute (maximal cardiac output) and the oxygen requirement of the skeletal muscles which exceeds the oxygen being delivered by the blood (maximal arterio-venous oxygen difference).

Factors Limiting V̇O2max

There are a number of physiological processes that take place before oxygen from the atmosphere can be used by the exercising skeletal muscles. These processes include:

The ability of the lungs to saturate arterial blood with oxygen (pulmonary diffusing capacity) The maximum volume of blood pumped by the heart in one minute (maximal cardiac output) The oxygen carrying capacity of the blood The ability of the skeletal muscles to extract oxygen from the blood

Each of these processes has the potential to limit the body’s ability to maximally utilise oxygen (Bassett & Howley, 2000). However, for endurance athletes, it is generally accepted that, at sea level, V̇O2max is limited by the ability of the cardiorespiratory system to deliver oxygen to the skeletal muscle rather than the muscle’s ability to extract oxygen from the blood (Bassett & Howley, 2000).

The delivery of oxygen in the blood is determined by the amount of blood pumped by the heart (maximal cardiac output) each minute. Cardiac output is, in turn, influenced by:

Heart rate

Maximal stroke volume (the volume of blood pumped from one ventricle with each heart beat).

As maximal heart rate remains the same or decreases with age, it has been concluded that an increase in stroke volume is necessary in order to increase maximal cardiac output (Midgley, McNaughton & Wilkinson, 2007).

The increase in stroke volume is due to adaptations associated with the mechanical overload of the heart during sustained exercise. The sustained increase in ventricular diastolic stretch and increased resistance to ventricular emptying results in adaptations which include thickening of the left ventricular wall (increases the force of each contraction and the percentage of blood pumped out with each contraction) and increases in the left ventricle chamber size (allows more blood to fill the ventricle and be pumped out with each contraction).

Other adaptations will include increased plasma volume (total blood volume is increased resulting in greater stroke volume), increased haemoglobin content (oxygen carrying capacity of the blood is improved), increased skeletal mitochondrial density and oxidative enzyme concentrations which facilitate the muscle’s extraction of oxygen from the blood (Kubukeli, Noakes & Dennis, 2002).

Training suggestions to improve maximum oxygen uptake

For less experienced endurance runners, the adaptations mentioned above are likely to be obtained through long sub-maximal training runs at a moderate intensity – i.e. 60-75% of your maximum heart rate.

However, for those athletes who have some degree of endurance training, increasing the volume of long slow distance running over and above normal training may not be sufficient to stimulate the heart adaptations needed to enhance maximal oxygen uptake (Laursen & Jenkins, 2002).

It was initially suggested that training at approximately 75% V̇O2max would be sufficient to evoke these adaptations. However, a more recent study using moderately trained athletes demonstrated that high intensity interval training (HIT) was significantly more effective in improving V̇O2max than performing the same training sessions at sub-maximal (at lactate threshold or 70% HRmax) intensities (Helgerud et al, 2007). The improvements in relative V̇O2max (6.4% & 8.8%) reported by in this study were similar to the 9.6% increase observed in cyclists by Bayati et al (2011) and the 6.2% and 9.1% increases in the relative V̇O2max of moderately trained runners observed by Esfarjani & Laursen (2007).

Franch, Madsen, Djurhus & Pedersen (1998) found significant increases in V̇O2max after just 6 weeks of intensive distance running (5.9%), long interval running (6%) or short interval training (3.6%). The sessions took place 3 days a week over a six week period with the speed and number of repetitions chosen so that the athletes would reach exhaustion within the training session.

Ideally, sessions should last three to five minutes with recovery periods equal to or slightly less than the work periods and the work rate should be at an intensity close to your maximum heart rate – i.e. 95-100% of your maximum heart rate.

e.g. 4 x 4 minutes (at 95-100% maximum heart rate) with 3 minutes recovery jog

It is important to monitor signs of overtraining if an athlete decides to progressively increase training at V̇O2max intensity. There is a danger that if the training stress becomes too demanding then the athlete’s ability to recover is reduced and the physiological adaptations may be restricted (Midgley, McNaughton & Wilkinson, 2006).

Percentage of VO2max – lactate training (can also be steady state runs)

What are the lactate thresholds?

Although V̇O2max is often used for assessing endurance capability (Jones, 2006) the lactate thresholds are seen as a good predictor of performance particularly amongst a group of athletes with similar V̇O2max values. They may also be more sensitive as indicators to changes in an athlete’s training status and be less disruptive during a competitive season (Burnley & Jones, 2007; Edwards, Clark & Macfadyen, 2003).

There are two apparent thresholds in the blood lactate response to incremental exercise (BASES, 2007):

The point during increasing exercise where blood lactate production exceeds lactate clearance and results in an accumulation above resting levels (Jung, 2003; Wilmore & Costill, 2004).

It occurs around 2.0 mmol.L-1 and is generally referred to as the lactate threshold (LT).

LT is closely associated with underlying shifts in the exchange of oxygen and carbon dioxide (Oshima et al, 1997) but it does not necessarily indicate that exercise has become partly anaerobic.

As exercise intensity increases, bicarbonate is used by the body to ‘buffer’ the increasing level of hydrogen ions in the blood. This buffering process produces carbonic acid which immediately dissociates to form carbon dioxide (CO2) and water. This non-metabolic increase in CO2 stimulates central and peripheral chemoreceptors to increase ventilation in proportion to the increasing CO2 levels (Beaver, Wasserman & Whipp, 1986)

This gas exchange threshold is known as the ventilatory threshold (VT).

LT and VT generally occur at 50 – 60% V̇O2peak (Jones, 2006).

The point at which there is a very rapid rise in blood lactate is known as the lactate turnpoint (LTP) and represents the upper limit of lactate production and clearance.

Usually occurs around 2.5 – 4.0 mmol.L-1 (Jones, 2006).

The LTP is often determined using the fixed lactate concentration of 4.0 mmol.L-1 (Onset of Blood Lactate Accumulation).

If exercise intensity continues to increase beyond the LTP blood lactate levels will continue to accumulate and the second gas exchange threshold, known as the respiratory compensation point (RCP), will occur.

This is due to the diminished buffering capacity of bicarbonate (Meyer, Faude, Scharhag, Urhausen & Kindermann, 2004) resulting in a build up of hydrogen ions and a reduction in blood pH.

Ventilation continues to increase but continued stimulation of the central and peripheral chemoreceptors, increases ventilation out of proportion to the increase in CO2 causing hyperventilation (Meyer, Faude, Scharhag, Urhausen & Kindermann, 2004).

If exercise continues at an increasing intensity beyond this point, hyperventilation will occur resulting in the onset of exercise acidosis and fatigue.

The LTP provides an approximation of another lactate determination point called the ‘maximal lactate steady state’ (Jones, 2006).

What causes the lactate threshold?

First of all, it’s important to clear up a few myths:

Lactate is being produced by our bodies at all times.

Lactate allows the regeneration of a substance called NAD which, in turn, enables glycolysis to continue to make a meaningful contribution to energy production. So rather than cause fatigue, lactate does its best to prevent fatigue.

Contrary to popular belief, lactic acid does not exist in the body for any length of time.

For exercise lasting more than a few seconds, energy (ATP) is derived from the anaerobic metabolism of glycogen – this process is known as glycolysis. During glycolysis, carbohydrate (blood glucose or muscle glycogen) is broken down in a series of chemical reactions to form pyruvate.

For the chemical reactions in glycolysis to continue, pyruvate must be removed. During low intensity exercise pyruvate can be broken down via the aerobic pathway to produce carbon dioxide and water rather than lactate. As exercise intensity increases, there is an increased recruitment of Type IIa and IIb (fast twitch) muscles fibres resulting in an acceleration of glycolysis. The aerobic pathway is unable to accept the increasing number of hydrogen ions. Some are directed towards pyruvate which accepts them and is subsequently reduced to lactic acid. The lactic acid immediately dissociates to form sodium and lactate.

Lactate or ‘lactic acid’ is often considered to be bad for the body by increasing the acidity of the blood causing fatigue. However, this is just a myth and lactate is actually has a very important role in prolonging endurance performance by ‘consuming’ the hydrogen ions which are the real culprit for acidifying the blood. The problem occurs when exercise intensity continues to increase and the increasing amount of hydrogen in the blood is unable to be removed by lactate.

What type of training will enhance the lactate threshold?

Training at, or near to the lactate threshold has been shown to significantly improve running speed (Carter, Jones & Doust, 1999). However, it should be noted that the subjects in this study were not well trained endurance athletes.

A more relevant study by Denadai et al. (2006) reported significant improvements in running velocities at OBLA in well trained runners over a 4 week training period. They suggested 2 high intensity sessions a week at velocities close to V̇O2max (95 and 100%) together with 4 sub-maximal sessions (1 session at OBLA velocity and 3 continuous sessions at 60-70 V̇O2max).

Lactate threshold workouts include:

Continuous runs at lactate threshold pace – may also be steady state runs

Intervals run at lactate threshold pace with short rest periods; and

Shorter intervals run at slightly faster than lactate threshold pace with very short rest periods

Without having the benefit of being able to test blood lactate levels in a lab, the lactate threshold is likely to occur about:

10km race pace for recreational runners; and

About 15 seconds per mile slower than 10km race pace for highly trained runners

The pace has been described as being ‘comfortably hard’

For lactate threshold runs, training should be at approximately 85-90% of your maximum heart rate.

For those wishing to train at a higher intensity nearer the second threshold, the intensity should be around 90-95% of your maximum heart rate.

Some example sessions may include:

Low end lactate threshold training – training at or just below the first threshold point

Continuous run of 40 – 90 mins

Include a warm up pace and warm down pace

Marathon race pace or slightly faster for 20 – 45 mins in the middle of the run

Middle zone lactate threshold training – training above the first threshold point but below the second threshold point

Continuous run of 40 – 90 mins

Include a warm up pace and warm down pace

10km race pace for recreational runners or 15 seconds per mile slower than 10km race pace for highly trained runners

Higher end lactate threshold training – training near the second threshold point

Aimed more towards highly trained runners

Aim for a pace which equates to 90% of your maximum heart rate

2 x 25 mins with 5 mins recovery

6 x 15 mins with 2 mins recovery

5 x 10 mins with 2 mins recovery

4-6 miles with 1 min recovery; or

Shorter intervals run at 5 – 10 seconds per mile faster than your lactate threshold pace such as 2 sets of 4 x 1km with 45 seconds rest between reps and 2 mins rest between sets.

These sessions should be started at a lower number of repetitions and increased as you become more experienced.

Running economy – long runs/steady state

What is running economy?

Running economy (RE) relates to the metabolic cost of running at a steady state sub-maximal speed and is closely related to an athlete’s lactate threshold, the ability to metabolise lipids at a higher work rate and being able to run at race pace with low energy expenditure. RE is an important factor because it is often seen as the best indication of performance amongst an elite class of athletes (Saunders, Pyne, Telford & Hawley, 2004).

Athletes with good RE (a lower V̇O2 for a given running speed) will perform at a lower percentage of their V̇O2max and benefit from glycogen sparing and delayed fatigued (Jones, 2006).

It is important to note that RE can be pace specific and some individuals may be more economical running at slower speeds (i.e. marathon runners) or higher speeds (i.e. 3,000 m runner).

What determines running economy?

RE has been associated with a number of different physiological, anthropometric, metabolic and biomechanical variables:

Endurance athletes tend to have a high proportion of Type I (slow twitch) muscle fibres which has been associated with improved RE. This suggests that the metabolic activity within the muscle or the contractile speed by have an impact on RE during prolonged exercise (Saunders et al, 2004).

Exposure to endurance training results in an increase in the density of mitochondria within muscle cells and an increase in the muscle capillary network. Both of these changes enable the muscle to become more efficient at processing and diffusing oxygen from the blood. In addition, there chemical changes which take place as a result of endurance training that enable the body is able to increase the use of its fat stores and spare muscle glycogen at the same given work rate (Midgley et al, 2007).

The long training runs result in repetitions of complex movement patterns which utilise the majority of major muscles and joints within the body (Saunders et al, 2004). Endurance training may improve biomechanics and more efficient techniques (reduced arm movement, low vertical movement of centre of mass) resulting in less energy wasted on braking forces (Jones, 2006; Saunders et al, 2004).

Strength and power training along with plyometric type exercises have been shown to increase the stiffness of muscles which in turn increases the energy stored by the tendons resulting in more energy returned on each step (Saunders et al, 2004).

Body height, limb dimensions and body mass all have the potential to affect RE (Saunders et al, 2004). A recent study by Lucia et al (2006) found a negative correlation between lower leg circumference (calf muscle) and oxygen uptake in Eritrean runners at a set running speed of 21.0 km.h-1 when compared to Spanish runners. This suggests that the Eritrean athletes were more economical than the Spanish athletes despite having similar V̇O2max values.

What type of training will enhance the running economy?

It is suggested that RE is associated with training over a prolonged period of years rather than by training volume. A study of an elite marathon runner between 1992 and 2003 demonstrated a 15% improvement in RE (Jones, 2006).

Carter, Jones & Doust (1999) demonstrated improvements in RE over a shorter period of time (6 weeks) in recreationally active students. Similar results were also reported by Franch, Madsen, Djurhus & Pedersen (1998). The authors found significant improvements in RE after 6 weeks of either intensive distance running or long interval running. Interestingly, they found no significant difference in RE in the short interval training group.

It has been suggested that RE may be more difficult to improve in well trained athletes and that alternative interventions such as plyometrics and strength training may provide a greater stimulus (Jung, 2003; Saunders et al, 2004).

Heavy-strength training was found to have significant influence on running economy in well trained athletes after a 14 week concurrent strength and endurance training programme (Millet, Jaouen, Borrani & Candau, 2002). Similar results were found with female endurance athletes who took part in a 3 day/week strength training component in addition to their normal training (Johnston, Quinn, Kertzer & Vroman, 1997). These results are promising because even small improvements in RE may be beneficial to an athlete performing over a prolonged period of time (i.e. marathon).

It should be noted that whilst strength training may have a positive influence on RE, it could result in changes in body composition which may negate the intervention.

In order to overcome the potential for increases in body composition and to make the training more sport specific, plyometric training may be considered. Paavolainen, Hakkinen, Hamalainen, Nummela & Rusko (1999) found that plyometric training over a 9 week period (in addition to endurance and sprint training) improved RE by 8.1% and reduced 5,000 m running times by 3.1%. The authors suggested that the improvements were due suggested to improved neuromuscular characteristics which were transferred into improved muscle power and RE.

There is limited evidence to suggest that altitude training may have a positive effect on RE. Saunders et al. (2004, p. 933) reported that 20 nights sleeping at simulated altitude (2,000-3,100 m) and training at 600 m altitude reduced whole body V̇O2 uptake (i.e. improved RE) in elite distance runners compared with a control group who lived and trained near sea level. They found that RE improved over a range of running speeds (14, 16, and 18 km.h-1).

Training distribution and intensity

Training zones supported by easily identifiable physiological markers can be meaningfully applied to training and are shown in the below. A ratio of 80:20 low to high intensity training provides the optimal stimulus for endurance adaptations (Seiler & Tonnessen, 2009). Higher intensity training (zones 2 & 3) should be split on a ratio of 12:8 (Esteve-Lanao, Foster, Seiler & Lucia, 2007) as shown in the table below:

Table 1: Three-zone scale defined by the measurement of the athlete’s blood lactate and heart rate during the sub-maximal treadmill tests and the physiological determination of the lactate thresholds

Sourced from: Seiler & Tonnessen (2009) and Esteve-Lanao, Foster, Seiler & Lucia (2007)

Low intensity training in Zone 1 is effective for endurance athletes provided it is supplemented by high-intensity training (Esteve-Lanao, Foster, Seiler & Lucia, 2007).

If experienced athletes accumulate more time in Zones 2 and 3 they will not necessarily convert the training into faster running times (Esteve-Lanao, Foster, Seiler & Lucia, 2007). It is therefore important for them to ensure that their training prescription is varied and includes training at different intensities.

Long runs should be built up very slowly and you should only lengthen the run by 1 to 1 ½ miles a week for three to four weeks and then reduce the mileage for a recovery week.

Your body tends to have a better concept of time rather than distance and so time on your feet is often more important than the distance. The physiological adaptations mentioned above will start to occur immediately but will develop more rapidly as your body becomes ‘stressed’ as the mileage or running period increases.

Finally……

For all the sessions mentioned above, it’s important to remember that your training philosophy should never compromise quality for quantity. If you feel too tired to undertake a session at the appropriate intensity, take a rest rather than complete the session sub-optimally.

References:

Bassett, D. R., & Howley, E. T. (2000). Limiting factors for maximum oxygen uptake and determinants of endurance performance. Medicine & Science in Sports & Exercise, 32(1), 70-84.

Bayati, M., Farzad, B., Gharakhanlou, R. & Agha-Alinejad, H. (2011). A practical model of low-volume high-intensity interval training induces performance and metabolic adaptations that resemble ‘all-out’ sprint interval training. Journal of Sports Science and Medicine, 10, 571-576

Beaver, W. L., Wasserman, K., & Whipp, B. J. (1986). Bicarbonate buffering of lactic acid generatd during exercise. Journal of Applied Physiology, 60(2), 472-478.

Burnley, M., & Jones, A. M. (2007). Oxygen uptake kinetics as a determinant of sports performance. European Journal of Sports Science, 7(2), 63-79.

Carter, H., Jones, A. M., Barstow, T. J., Burnley, M., Williams, C., & Doust, J. H. (2000). Effect of endurance training on oxygen uptake kinetics during treadmill running. Journal of Applied Physiology, 89, 1744-1752.

Carter, H., Jones, A. M. & Doust, J. H. (1999). Effect of 6 weeks endurance training on the lactate minimum speed. Journal of Sports Sciences, 17, 957-967

Coyle, E. (2007). Physiological regulation of marathon performance. Sports Medicine, 37(4-5), 306-311

Davis, J. A., Frank, M. H., Whipp, B. J., & Wasserman, K. (1979). Anaerobic threshold alterations caused by endurance training in middle-aged men. Journal of Applied Physiology: Respiratory, Environmental & Exercise Physiology, 46, 1039-1046.

Denadai, B. S., Ortiz, M. J., Greco, C. C. & De Mello, M. T. (2006). Interval training at 95% and 100% of the velocity at V̇O2max: Effects on aerobic physiological indexes and running performance. Applied Physiology, Nutrition and Metabolism, 31, 1-7

Edwards, A. M., Clark, N., & Macfadyen, A. M. (2003). Lactate and ventilatory thresholds reflect the training status of professional soccer players where maximum aerobic power is unchanged. Journal of Sports Science & Medicine, 2, 23-29.

Esfarjani, F. & Laursen, P. B. (2007). Manipulating high-intensity interval training: Effects on V̇O2max, the lactate threshold and 3000 m running performance in moderately trained males. Journal of Science and Medicine in Sport, 10, 27-35.

Esteve-Lanao, J., Foster, C., Seiler, S. & Lucia, A. (2007). Impact of training intensity distribution on performance in endurance athletes. Journal of Strength and Conditioning Research, 21(3), 943-949

Franch, J., Madsen, K., Djurhuus, M. S. & Pedersen, P. K. (1998). Improved running economy following intensified training correlates with reduced ventilatory demands. Medicine & Science in Sports & Exercise, 30, 1250-1256

Helgerud, J., Hoydal, K., Wang, E., Karlsen, T., Berg, P., Bjerkaas, M., Simonsen, T., Helgesen, C., Hjorth, N., Bach, R. & Hoff J. (2007). Aerobic high-intensity intervals improve V̇O2max more than moderate training. Medicine and Science in Sports and Exercise, 39(4), 665-671.

Johnston, R. E., Quinn, T. J., Kertzer, R. & Vroman, N. B. (1997). Strength training in female distance runners: Impact on running economy. Journal of Strength and Conditioning Research, 11(4), 224-229

Jones, A. M. (1998). A ﬁve year physiological case study of an Olympic runner. British Journal of Sports Medicine, 32, 39-43

Jones, A. M. (2006). The physiology of the world record holder for the women’s marathon. International Journal of Sports Science & Coaching, 1(2), 101-116.

Kubukeli, Z. N., Noakes, T. D. & Dennis, S. C. (2002). Training techniques to improve endurance exercise performances. Sports Medicine, 32(8), 489-509

Laursen, P. B. & Jenkins, D. G. (2002). The scientific basis for high-intensity interval training: Optimising training programmes and maximising performance in highly trained endurance athletes. Sports Medicine, 32(1), 53-73

Lucia, A., Esteve-Lanao, J., Olivan, J., Gomes-Gallego, F., San Juan, A. F., Santiago, C., Perez, M., Chamorro, C. & Foster, C. (2006). Physiological characteristics of the best Eritrean runners – exceptional running economy. Applied Physiology, Nutrition and Metabolism, 31, 1-11

Midgley, A. W., LcNaughton, L. R. & Jones, A. M. (2007). Training to enhance the physiological determinants of long-distance running performance: Can valid recommendations be given to runners and coaches based on current scientific knowledge? Sports Medicine, 37(10), 857-880

Midgley, A. W., LcNaughton, L. R. & Wilkinson, M. (2006). Is there an optimal training intensity for enhancing the maximal oxygen uptake of distance runners? Empirical research findings, current opinions, physiological rationale and practical recommendations. Sports Medicine, 36(2), 117-132

Millet, G. P., Jaouen, B. Borrani, F. & Candau, R. (2002). Effects of concurrent endurance and strength training on running economy and V̇O2 kinetics. Medicine & Science in Sports & Exercise, 34(8), 1351-1359

Meyer, T., Faude, O., Scharhag, J., Urhausen, A., & Kindermann, W. (2004). Is lactic acidosis a cause of exercise induced hyperventilation at the respiratory compensation point? British Journal of Sports Medicine, 38, 622-625.

Oshima, Y., Miyamoto, T., Tanaka, S., Wadazmi, T., Kurihara, N., & Fujimoto, S. (1997). Relationship between isocapnic buffering and maximal aerobic capacity in athletes. European Journal of Applied Physiology, 76, 409-414.

Paavolainen, L., Hakkinen, K., Hamalainen, I., Nummela, A. & Rusko, H. (1999). Explosive-strength training improves 5-km running time by improving running economy and muscle power. Journal of Applied Physiology, 86(5), 1527-1533

Saunders, P. U., Pyne, D. B., Telford, R. D. & Hawley, J. A. (2004). Factors affecting running economy in trained distance runners. Sports Medicine, 34(7), 465-485

Saunders, P. U., Telford, R. D., Pyne, D. B., Cunningham, R. B., Gore, C. J., Hahn, A. G. & Hawley, J. A. (2004). Improved running economy in elite runners after 20 days of simulated moderate-altitude exposure. Journal of Applied Physiology, 96, 937-937

Seiler, S. & Tonnessen, E. (2009). Intervals, thresholds and long slow distance: The role of intensity and duration in endurance training. Sports Science, 13, 32-53

The British Association of Sport and Exercise Sciences. (2007). Sport and exercise physiology testing guidelines: the British Association of Sport and Exercise Sciences guide, Volume 1, Sport testing. London, UK: Routledge

Wilmore, J. H., & Costill, D. L. (2004). Physiology of Sport and Exercise Science (3rd ed.). USA: Human Kinetics.