Why do we get tired playing football?

Written by Peter Joffe

It is the first of two articles that are devoted to the problem of fatigue during the football match.

Here I will discuss the possible reasons of exhaustion and their complex interaction. In the second article, I will consider the possible ways to improve endurance in football.

Introduction.

Every one of us, who is playing football, knows that we have become fatigued. The reason for this is very simple: because we run, jump, and making tackles.

However, if we look at the problem from a scientific and coaching perspective, this answer won’t be satisfactory. It is essential to know the exact cause of exhaustion, thus making training intervention more precise.  To achieve this, we need to understand physiological demands in the game, and, determine what prevents us from matching these demands. 

Yet,  due to its complexity of the football, this task presents a big challenge . Indeed, compared, for example, with track-and-field sport, where the workload is predictable and specific,  football demands complex abilities from the player. He/she covers distances comparable with a middle-distance runner and can accelerate like a sprinter. Players perform various actions in random patterns, and also, the workload may vary between player’s positions and different matches. All of these make finding the answer to the question which is put in the title quite difficult. Nevertheless, let’s try.

 Activity patterns during a game.

Interestingly, most of the time, players perform low-intensity activities like walking, jogging, and standing throughout the match. Nevertheless, various forms of high-intensity actions, including short and long sprints, sprints with the change of direction, jumps, and tackles, though occupy much less time, are crucial for the victory. Scientists try to quantify locomotion in the game to understand better physical demands in football.

Distance covered by footballers varies from 9 to 12 kilometres. That depends on many things such as opposition level, tactical guidance, player’s role, etc. This distance is covered in different intensities. Bradley et al. found that players stand for 5.6% of the total time during English Premier League matches. The low-intensity activity represented 85.4% of the total time, which consisted of 59.3% walking and 26.1% jogging.

High-intensity locomotion represented 9.0% of the whole time. It consisted of 6.4% speed running, 2.0% high-speed running, and 0.6% sprinting (Paul S. Bradley et al., 2009).

Yet, this type of analysis doesn’t provide a full picture of the game’s actions. For instance, most maximal accelerations do not result in speeds associated with high-intensity running. Still, they are metabolically taxing (P. S. Bradley et al., 2013). The same is true for tackles, dribbles, and jumps. Thus the comprehensive quantification of the  match workload yet remains a challenge.

 How do we know that players are tired.

Scientists are strange people. They are not taking on trust that footballers get tired during the game; they need proof.

Firstly, they compare distances covered by players in the second half and the first (table 1). Usually, but not always, players run less in the second half.

Secondly, they make the same comparison for high-intensity running. Again, on average, second half is less intense.

Also, they match the number of intense runs made by substitutes with the team’s average.

To assess temporally fatigue during a game, scientists may compare high-intensity running immediately after the most intense 5 min periods of the game with the match average (usually there are less intense runs).

And finally, they can conduct different physical tests before and after the game and inside the different periods of the match, searching for the fatigue manifestations.

Though these data are sometimes controversial, all these methods generally confirm that all players and coaches know anyway: we get tired when playing football.

Table 1: Difference in the distance covered in the first and second half of the match.

Adapted from: (Alghannam, 2012).

Usual suspects.

There are three major groups of reasons which may influence the ability to maintain intensity in the game. Here they are: fuel availability, accumulation of metabolic by-products, and exercise-induced muscle damage.

Fuel availability.

There are four primary sources of fuel that contribute to energy production during a football match.

1. ATP-is universal molecule of energy. Mostly it is produced from the different compounds (creatine phosphate, glucose, fat, and proteins ), but some small amount, which can support initiation of the work for 1-2 sec, is stored in the muscles.

2. Creatine phosphate (PCr) is the second most immediate energy source after muscle’s ATP . It can rapidly produce ATP during high-intensity work. PCr doesn’t need oxygen for utilisation. However, it demands oxygen for restoration.

PCr reserves are very limited in the muscles. Theoretically, they can be depleted in 10-12 sec. In reality, different sources of energy are used together; thus, PCr is never depleted completely (it can be 50% after 10 sec of maximal work). If oxygen is available, PCr can be rapidly restored (during 1-st min of the rest, half of the spent may be replaced, whereas 2-5 min are needed for full restoration after non-exhaustive exercise.

3. Glycogen is a form of glucose storage in the body (mostly in the muscles and liver). Stores inside the muscle cells are more immediate source of energy than the other sites, probably because they don’t need transporters through the cell’s membrane. Nevertheless, ATP production from glucose is slower than from PCr (reaction peaks not earlier than 6-10 sec after onset).

The liver’s reserves of glycogen are generally mobilised when the glucose level in the blood drops. Glycogen can produce ATP without oxygen (higher intensities) and with oxygen. The latter is around fifteen times more efficient in terms of ATP from one molecule of glucose.

Stores of glycogen in muscles are significant but limited. Its expenditure depends on work intensity, training status, nutrition, temperature, etc. During moderate, continuous work, it can be enough for two hours.  In high-intensity work with insufficient oxygen supply and/ or in a hot environment, glycogen depletes very rapidly(Svedenhag, 1994). Glycogen restores slowly after endurance events. It may take more than 48 hours, depends on nutrition, muscle damage, etc.)

4. Fat (lipids) is an infinite source of energy in muscles and body tissues. Its limitation is that it cannot be mobilised quickly and needs oxygen for utilisation. Fat is much more efficient than glycogen in terms of ATP per molecule but less efficient in terms of the amount of ATP per molecule of oxygen.

That makes fat usage more challenging during high-intensity work when the supply of oxygen is limited. Better endurance-trained athletes can better use fat, especially at high intensities. Sufficient fat utilisation helps to spare glycogen during exercise.

Due to ATP stores in muscles are extremely limited and fat deposits, in the opposite, are infinite but not readily available, probably, PCr and glycogen play a central role in fatigue development when we are considering fuel availability during the game. I will discuss that later.

Metabolites from anaerobic pathways (PCr and Glycolysis).

Metabolites from the anaerobic energy production are, probably, the main reason for fatigue when exercise intensity exceeds aerobic capacities. During high-intensity efforts, ATP utilisation is dramatically accelerates in attempt to satisfy the energy requirements.

With intense activity, aerobic ATP production  is unable to match ATP utilisation, and  anaerobic production occurs accompanied by accumulation of a range of metabolic by-products. These products change the ionic environment and disturb normal muscle cell functions resulting in fatigue. This type of fatigue is often referred to as metabolic (Green, 1997)

Some metabolites enter the bloodstream and start to change whole-body homeostasis, eventually leading to the brain’s command to stop the exercise. This is called central fatigue.

Exercise induced muscle damage (EIMD).

During exercise, muscles can be damaged. The reasons may be high mechanical forces, chemical reactions inside the muscles, and interactions of both. Especially EIMD is evident when eccentric contractions (tension applied to muscle while it is lengthening) are present. Many football actions such as sprints, braking actions, change of direction, and jumping provoke EIMD.

Fatigue in the game.

There are two kinds of fatigue during the match, which can be analysed separately: temporally and general.

Temporary fatigue.

During maximal intensity work, humans  become fatigued very quickly. For example, even throughout one hundred meters sprint, which lasts less than ten seconds, athletes start to decelerate in the last 20 meters.

In a football match, the short repeated bouts of high-intensity activities usually cause temporary fatigue, which can be overcome in the game throughout relatively quiet periods.

These repeated bouts may be quite variable which makes their quantification and qualification difficult. For instance, full-back could make series of long sprints (40-50 meters) during his/her intense periods of the game, participating in the attack and covering back, whereas forward usually makes short (less than 10 meters) sprints with the change of directions, dribbles and tackles.

Scientists frequently take for analysis 5-min periods of the game with the more intense activity than in the match average. Superiority in these short periods is the key aspect of success in the whole game; thus, understanding temporary fatigue would be useful.

Some authors suggest that muscle’s PCr reserve can be the primary determinant of fatigue during repeated high-intensity bouts. This idea is based on findings that after a bout of intense/maximal work, the recovery of force or power output follows a time-course similar to that of PCr resynthesis (Glaister, 2005).

However, it might be that the course of PCr  resynthesis just coincides with the course of metabolites clearance and Pcr availability probably, is not the direct cause of temporal fatigue.

For example, though muscle PCr can fall to 55% even after a single 6 seconds sprint and as low as 27% after five 6 seconds sprints with 30 seconds rest between (Dawson et al., 1997) , athletes could continue to sprint even with such a low level of PCr in muscles (Bangsbo, Mohr, & Krustrup, 2006). Besides, as it was already mentioned, the restoration of PCr is reasonably fast. In the same study, after 30 seconds rest, it was up from 55 to 69 % after one sprint and from 27 to 45% after series of five (Dawson, et al., 1997).

If we are looking at high-intensity bouts performed by a previously non-fatigued footballer,   metabolites from anaerobic pathways probably, will be the main reason for short-term fatigue. Low muscle PH (Iaia, et al., 2010), elevated inorganic phosphate, disturbance in ionic balance and ionic pumps, ROS (reactive oxygen species) are among the possible explanations but the exact mechanism is still unclear. There is most likely no sole cause for fatigue, and interaction between different metabolites plays a central role.

Rest intervals between separate bouts inside the maximal intensity period are essential determinants for fatigue. Most likely, they influence metabolite’s clearance and PCr restoration. For instance, participants in Balsom et al.’s study performed 15×40 m sprints with three different rest intervals (30;60 and 120 sec) between sprints (P. Balsom, Seger, Sj?din, & Ekblom, 1992). Generally, the performance was impaired in all conditions, not surprisingly, more quickly (already after 3-d sprint) with shortest – 30 sec rest.

However, inside the individual 40 m sprint, 10 m acceleration was decreased only in 30-sec rest conditions and remained unchanged with 60 sec and 120 sec rest. It is clear that the latter’s intervals were sufficient for restoration abilities to accelerate on initial 10 m but not enough to maintain efforts for the remaining 30 m.

Why was it the case? Perhaps, anaerobic metabolites could be cleared from the muscles below some threshold during longer rest intervals and that allows to start running without impairment. Nevertheless, because these metabolites’ concentration was still near the threshold, it rapidly exceeded the critical level and impaired the remaining 30 m run. When rest intervals were short (30 sec), there was not sufficient time for metabolite’s concentration to go below the critical level, and even an initial 10 m acceleration was impaired.

To conclude this section:

Fatigue inside short, intense periods of the game is most likely caused by the accumulation of metabolites from anaerobic energy production. However, it is important to note that this is true if we assume that previous activities do not influence initial conditions. Inside these intense periods, type of activities, duration, and rest between individual bouts are essential determinants of fatigue.

 General fatigue to the end of the match.

The general fatigue manifests in a reduction in distance covered and, more importantly, decreased high-intensity work towards the match’s end. That cannot be recovered during the game.

The availability of muscle glycogen can play a major role in general fatigue (P. D. Balsom, Gaitanos, S?derlund, & Ekblom, 1999) though the exact reason for that is not clear.

Actually, there is still enough glycogen in muscles when fatigue occurs; however, its consumption is not equal between different muscle fibres; thus, some can be short of glycogen or even completely empty, whereas others are still full (Bangsbo, et al., 2006). Another argument favouring glycogen importance is that players with glycogen shortage before the game were significantly more vulnerable to fatigue in the second half than players whose muscles were full (Bangsbo, et al., 2006) .

Now scientists are trying to understand how exactly glycogen shortage influenced fatigue. Williams et al. suggested a central mechanism. In his experiment, rats stopped to exercise when short of glycogen, but their muscles can continue to work without the brain’s participation when they were directly electrically stimulated (Williams, Batts, & Lees, 2013). Researchers found low glucose level in the rat’s blood and suggested that glycogen shortage leads to the low blood’s glucose level, and this initiate brain’s command to stop the exercise. It sounds plausible.

However, during the football game, in most cases, the player’s blood glucose level remains normal through the whole match due to increasing glycogen depletion in the liver and gluconeogenesis (glucose production from lactate, fat, and proteins). It looks like if there is a central mechanism, it is not due to a low blood glucose level.

Another explanation of how low glycogen level induces fatigue may be its influence of Ca ions release in muscles, which is crucial for contraction. When glycogen stores are depleted, Ca release and, consequently, muscle contractions are impaired (?rtenblad, Nielsen, Saltin, & Holmberg, 2011). The same study looked in more detail how the distribution of glycogen in muscle sites can influence fatigue. They suggested that a relatively small amount of muscle glycogen (10-15% of muscle reserves) stored in myofibrils can be crucial for Ca release. Its reduction through negative feedback can lead to central fatigue development even if there is still enough glycogen in the other sites.

These findings can explain contradictions in results about glycogen influence on fatigue when researchers take muscle as a whole without pay attention to where exactly glycogen stores are depleted. Can we somehow to control the sites of glycogen storage? To my knowledge, we cannot yet.

Exercise-induced muscle damage can significantly influence fatigue to the end of the game, especially if we are talking about performing intense exercise. It may be due to direct mechanical damage of the muscle’s fibres, particularly fast-twitch fibres, which are important during rapid maximal efforts (sprints, jumps, etc.).

Eccentric contraction, when a muscle is under tension while lengthening  is the main cause of EIMD. Many studies found that fast-twitch fibres are the most vulnerable during eccentric contractions (Byrne, Twist, & Eston, 2004). However, the influence of EIMD may be significantly more complicated than just “exclusion” some fibres from work. Our brain does not want to continue the exercise, causing damage; thus, the central component, acting through the pain feeling, may be involved (Twist & Eston, 2009). Another possible mechanism of central fatigue may be ions and enzymes flux to the blood through the damaged cell membranes that eventually influence whole-body homeostasis.

Even this maybe not the full picture. Komi discussed disturbance in the stretch-shortening cycle (SSC) in muscles due to EIMD (Komi, 2000). Our muscles are lengthening and shortening in sequence during real-life activities, and the delay between these two actions is very short. That allows the release of elastic energy stored during stretching in the shortening part of SSC, making muscle action much more efficient. This mechanism is actively involved in running. EIMD can negatively influence muscle’s stretch reflex and stiffness regulation that, in turn, disturbs SSC and, eventually, dramatically increases the energy cost of running.

Additional consideration about EIMD, is impairments in the function of glucose transporters, particular, GLUT4 (Asp, Daugaard, & Richter, 1995). These transporters deliver glucose from the blood into the muscle cells, and if they are not working correctly, muscles glycogen is depleted more rapidly and is restored slowly.

Eston, with colleagues, found another interesting aspect of possible EIMD involvement in fatigue development. That may be damage of the capillary bed, which can alter the muscle’s oxygenation process (Davies et al., 2008). That negatively influences aerobic energy production during exercise.

The damage resulting from eccentric exercise also compromises the awareness of joint position and subjective estimation of muscle force output. (Eston, Byrne, & Twist, 2003). It may impair a player’s agility and technique as well as the running economy. There are a few more possible mechanisms of how EIMD may influence fatigue (for review, see (Byrne, et al., 2004). This phenomenon has been intensively studying now. However, surprisingly, it is not often mentioned among fatigue’s main reasons during the football game.

Complex interaction.

All discussed above, causes and types of fatigue don’t act and happen in isolation during the game. They interact with each other, and this adds complexity to the picture. For instance, EIMD can alter energy status and the ionic environment in the muscles, whereas low energy levels and disturbance in ionic balance can distract the coordinated work of the fibres, thus accelerate muscle damage.

If we are talking about temporal fatigue during/after high-intensity periods of the game, it, to a great extent, depends on initial muscle’s conditions before this period.

Iaia et al. conducted an interesting study about how different kinds of previous exercises may influence high-intensity exhaustive (130 % VO2 max) cycle sprint performance.

So, this sprint was performed 2 min after:
1. Long low-intensity work (2 hours, 60% of VO2 max).
2. High-intensity work ( 3 min, 118% of VO2 max).
3. Very high intensity work (30sec, 196%of VO2max) (Iaia, Perez-Gomez, Nordsborg, & Bangsbo, 2010) .

Compare with controls (who performed sprint without previous exercise), time to exhaustion reduced in all three conditions but more markedly after the low-intensity and high-intensity exercise.

The authors tried to analyse how the different muscle conditions before sprint can influence the result. Their main interest was muscle acidosis (PH) and muscle glycogen. Not surprisingly, the lowest muscle glycogen was after prolonged, low-intensity exercise. That might influence consequent performance in the sprint and supported the importance of glycogen stores for performance. The lowest muscle PH (highest acidosis) was after high-intensity work, which might influence fatigue.

However, the authors concluded that neither glycogen concentration nor PH level alone was the STOP factor in the all-out sprint because participants could start the exercise and perform it at least 30 sec with pre-low glycogen or pre-low PH. It looks like there is no sole factor responsible for fatigue development. Instead, a complex interaction between multiple factors eventually makes us tired when we are playing football.

Summary of the reasons for fatigue in the game.

Two main types of fatigue occur during the game. The temporary impairments in performance happen in short periods of high-intensity work in the game, and athletes can recover during relatively lower intensity periods. Accretion of by-products from anaerobic energy production most likely is the main reason behind temporary fatigue. The general fatigue accumulates towards the end of the match, and players cannot recover during the game. Perhaps the main reasons for that are glycogen stores depletion in some muscle’s fibres and fibre’s sites and EIMD.

There is a very complex interaction between these two types of fatigue. Temporary fatigue is influenced by accumulated previous workload and depends on initial conditions. Thus, it may be different at the beginning and end of the game. In turn, general fatigue gets quicker when more intense bouts are performing, and more temporally fatigues occur during the game. Types of activities, length, and rest intervals inside and between high-intensity periods are essential in fatigue development.

Keep that in mind, sports scientists and coaches should answer the following questions:

1. How to train better metabolite’s clearance and tolerance?

2. How to increase fuel reserves and achieve more effective fuel utilisation?

3. How to deal with the EIMD?

My next article will be devoted to these questions.

References.

Alghannam, A. F. (2012). Metabolic limitations of performance and fatigue in football. Asian journal of sports medicine, 3(2), 65.

Asp, S., Daugaard, J. R., & Richter, E. A. (1995). Eccentric exercise decreases glucose transporter GLUT4 protein in human skeletal muscle. The Journal of Physiology, 482(3), 705-712.

Balsom, P., Seger, J., Sj?din, B., & Ekblom, B. (1992). Maximal-intensity intermittent exercise: effect of recovery duration. International journal of sports medicine, 13(7), 528-533.

Balsom, P. D., Gaitanos, G., S?derlund, K., & Ekblom, B. (1999). High-intensity exercise and muscle glycogen availability in humans. Acta Physiologica Scandinavica, 165, 337-346.

Bangsbo, J., Mohr, M., & Krustrup, P. (2006). Physical and metabolic demands of training and match-play in the elite football player. Journal of Sports Sciences, 24(07), 665-674.

Bradley, P. S., Carling, C., Gomez Diaz, A., Hood, P., Barnes, C., Ade, J., . . . Mohr, M. (2013). Match performance and physical capacity of players in the top three competitive standards of English professional soccer. Hum Mov Sci, 32(4), 808-821.

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Byrne, C., Twist, C., & Eston, R. (2004). Neuromuscular function after exercise-induced muscle damage. Sports Medicine, 34(1), 49-69.

Davies, R. C., Eston, R. G., Poole, D. C., Rowlands, A. V., DiMenna, F., Wilkerson, D. P., . . . Jones, A. M. (2008). Effect of eccentric exercise-induced muscle damage on the dynamics of muscle oxygenation and pulmonary oxygen uptake. Journal of Applied Physiology, 105(5), 1413-1421.

Dawson, B., Goodman, C., Lawrence, S., Preen, D., Polglaze, T., Fitzsimons, M., & Fournier, P. (1997). Muscle phosphocreatine repletion following single and repeated short sprint efforts. Scandinavian Journal of Medicine & Science in Sports, 7(4), 206-213.

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Glaister, M. (2005). Multiple sprint work. Sports Medicine, 35(9), 757-777.

Green, H. (1997). Mechanisms of muscle fatigue in intense exercise. Journal of Sports Sciences, 15(3), 247-256.

Iaia, F. M., Perez-Gomez, J., Nordsborg, N., & Bangsbo, J. (2010). Effect of previous exhaustive exercise on metabolism and fatigue development during intense exercise in humans. Scand J Med Sci Sports, 20(4), 619-629.

Komi, P. V. (2000). Stretch-shortening cycle: a powerful model to study normal and fatigued muscle. Journal of Biomechanics, 33(10), 1197-1206.

?rtenblad, N., Nielsen, J., Saltin, B., & Holmberg, H. C. (2011). Role of glycogen availability in sarcoplasmic reticulum Ca2+ kinetics in human skeletal muscle. The Journal of Physiology, 589(3), 711-725.

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Twist, C., & Eston, R. G. (2009). The effect of exercise-induced muscle damage on perceived exertion and cycling endurance performance. European Journal of Applied Physiology, 105(4), 559-567.

Williams, J. H., Batts, T. W., & Lees, S. (2013). Reduced Muscle Glycogen Differentially Affects Exercise Performance and Muscle Fatigue. ISRN Physiology, 2013, 8. doi: 10.1155/2013/371235