Why do we get tired playing football?

This is the first from two articles which 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.


Every one of us, who are playing football, knows that, we have gradually become fatigued. The reason forFuballspielerin this is very simple: because we run, jump and making tackles. However if we look at the problem from scientific and coaching perspective this answer won’t be satisfactory. It is essential to know what exact cause of exhaustion is, thus to make training intervention more precise. Usually, to achieve this, we need to quantify the workload in particular activity, then to calculate its physiological demands and, eventually, to understand what is preventing us from matching these demands. Yet, in football this presents a big challenge due to its complexity. Indeed, in comparison with track-and-field sport, where workload is predictable and activity’s types are clearly separated between different events, football demands different abilities from the same player who covers distances comparable with a middle-distance runner and can accelerate like a sprinter. Players perform various actions in random patterns and, in addition, the workload may vary between player’s positions and different matches. All of these make the search for answer on the question which is put in the title very difficult. Nevertheless, let’s try.

Football activity patterns during a game.

Through the course of the match, most of the time, players perform low intensity activities like walking, jogging and standing. Nevertheless, various forms of high-intensity actions which include short and long sprints, sprints with the change of direction, jumps and tackles, though occupy much less time, are defining the victory. Scientists are trying to quantify locomotion in the game with the aim to understand better physical demands in football. In the game footballers on average cover from 9 to 12 kilometres which is dependent on many things such as: opposition level, tactical guidance, player’s role, weather and etc. This distance is covered in different intensities. Bradley et al. found that during English Premier League matches, players stood for 5.6% of the total time. Low-intensity activity represented 85.4% of total time, which consisted of 59.3% walking and 26.1% jogging. High-intensity runs represented 9.0% of total time, which consisted of 6.4% running, 2.0% high-speed running, and 0.6% sprinting (Paul S. Bradley et al., 2009).

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

3. How 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 proofs. Firstly, they are comparing distances covered by players in the second half and in the first (table 1).

Secondly, they make the same comparison for high-speed runs and sprints. In addition, they match amount of intense runs made by substitutes with the team’s average.

To assess a 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, as well as inside the different periods of the match, searching for the fatigue manifestations.

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

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

Reference League Distance Significant decrements in performance?
13 Swedish 3% greater distance in the first half yes
14 Brazilian 8% greater distance in the first half yes
15 Danish 5% greater distance in the first half yes
2 Italian 3% greater distance in the first half yes
16 Euro Cup 1% greater distance in the first half yes
17 English 2% greater distance in the first half yes
18 South American+English 4% greater distance in the first half yes

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, metabolic by-products and exercise-induced muscle damage.

Fuel availability.

There are four main sources of fuel which 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, glycose, 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 source of energy after muscle’s ATP . It can produce ATP rapidly 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 relatively quick restored (during 1-st min of the rest- half of the spent, 2-5 min- full restoration after non exhaustive exercise).

3. Glycogen is a form of glycose 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. However glycogenosis (ATP production from glycose) is slower than PCr reaction (peaked not earlier than 6-10 sec after onset) . Liver’s reserves of glycogen are generally mobilized when glycose level in blood drops. Glycogen can produce ATP without oxygen (higher intensities) and with oxygen. The latter is around nineteen times more efficient in terms of amount of ATP from one molecule of glycose. Stores of glycogen in muscles are significant but limited. During moderate, continuous work, with a sufficient oxygen supply, it can be enough for two hours. However this depends on work intensity, training status, nutrition, temperature and etc. In high intensity work with insufficient oxygen supply and/ or in hot environment glycogen depletes very rapidly(Svedenhag, 1994) . Glycogen restores slowly after endurance events (may be more than 48 hours, depends on nutrition, muscle damage and etc.)

4. Fat (lipids) is actually infinite source of energy in muscles and body tissues. Its limitation is, however, that it cannot be mobilized quickly and needs oxygen for utilisation. It is much more efficient compare to glycogen/glucose in terms of amount of ATP per molecule but less efficient in terms of amount of ATP per molecule of oxygen. This makes fat utilisation more difficult during high-intensity work, when supply of oxygen is limited. Lipids utilisation depends on training status and oxygen availability. Better endurance trained athletes can better use fat, especially at high intensities. Better fat utilisation helps to spare glycogen during exercise.

Due to ATP stores in muscles are extremely limited and fat deposits, in 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 Glycolisis)

Metabolites from the anaerobic energy production are, probably, the main reason for the fatigue when exercise intensity exceeds aerobic capacities. During high-intensity exercise, ATP utilisation is dramatically accelerated inside muscles in an attempt to satisfy the energy requirements. With intense activity, ATP production rates with oxygen are unable to match ATP utilisation rates, and ATP anaerobic production occurs accompanied by accumulation of a range of metabolic by-products. These products change ionic environment and disturb normal muscle cell functions resulting in fatigue. This type of fatigue is often referred to as metabolic (Green, 1997)

Some of metabolites enter the blood stream and start to change whole-body homeostasis which can, eventually, lead to brain’s command to stop the exercise. This is called a 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 actions in football 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.

Temporally fatigue

During maximal intensity work humans (included athletes) become fatigued very quickly. For example, even throughout one hundred meters sprint, which lasts less than ten seconds, athletes start to decelerate on the last 20 meters due to fatigue. In football match, usually, the short repeated bouts of high intensity activities cause temporally fatigue, which can be overcome in the game throughout relatively quiet periods. These repeated bouts may be different itself that 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 attack and covering back, whereas forward usually makes short (less than 10 meters) sprints with the change of directions 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 to understand the reason of fatigue would be useful.

Some authors suggest that muscle’s PCr reserve can be the main 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 coincides with the course of metabolites clearance. Though muscle PCr can fall to 55% even after single 6 seconds sprint and as low as 27% after five 6 seconds sprints with 30 seconds rest between (Dawson et al., 1997) , availability of Pcr, probably, is not the direct cause of temporally fatigue . During different tests athletes could continue to sprint even with relatively low level of PCr in muscles (Bangsbo, Mohr, & Krustrup, 2006). Besides, as it was already mentioned, restoration of PCr is reasonably quick. In the same study, after 30 seconds of 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 separate block of short, repetitive and high-intense bouts, performed by previously non-fatigued footballer, then metabolites from anaerobic passways (ATP-PCr depletion and anaerobic glycogenosis) probably, will be the main reason for short-term fatigue. Low muscle PH (Iaia, et al., 2010) elevated inorganic P, disturbance in ionic balance and ionic pumps, ROS (reactive oxygen species) are among possible explanations but exact mechanism is still unclear. Most likely there is no sole cause for fatigue and interaction between different metabolites is playing a central role.

Rest intervals between separate bouts inside maximal intensity period are important determinants for fatigue. Most likely they influence metabolite’s clearance and PCr restoration. Participants in Balsom et al. 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 performance was impaired in all conditions, not surprisingly, more quickly (already after 3-d sprint) with shortest – 30 sec rest. However, inside individual 40 m sprint, 10 m acceleration was decreased only in 30 sec rest condition and remained unchanged with 60 sec and 120 sec rest. It is clear that latter’s intervals were sufficient for restoration abilities to accelerate on initial 10 m but not enough to maintain efforts for remaining 30 m. Why it was the case? Possibly anaerobic metabolites could be cleared from the muscles below some threshold during longer rest intervals that allowed to start running without impairment. Nevertheless, because the concentration of these metabolites was still near the threshold, it rapidly went above critical level and impaired remaining 30 m run. When rest intervals were short (30 sec), there was not sufficient time for metabolite’s concentration to go below critical level and even initial 10 m acceleration was impaired.

To conclude this section it can be said that fatigue inside short intense periods of the game is most likely caused by accumulation of metabolites from anaerobic energy production. It important to note, however, that this is true if we assume that initial conditions are not influenced by previous activities. Inside these intense periods, type of activities, there duration and rest between individual bouts are important determinants of fatigue.

General fatigue to the end of the match

The general fatigue manifests in reduction in distance covered and, more importantly, decreased high intensity work towards the end of the match. This cannot be recovered during the game.

Availability of muscle glycogen can play a major role in general fatigue(P. D. Balsom, Gaitanos, S?derlund, & Ekblom, 1999) though exact reason for that is not clear. Actually, there is still enough glycogen in muscles, when fatigue occurs, however its consumption is not the equal between different muscle’s fibres, thus some of them can be short of glycogen or even completely empty whereas others are still full (Bangsbo, et al., 2006). Another argument in favour of glycogen importance is that players with glycogen shortage before the game were significantly more vulnerable to fatigue in the second half than players who’s muscles were full (Bangsbo, et al., 2006) . Now scientists are trying to understand how exactly glycogen shortage influenced fatigue. Williams et al. suggested central mechanism. In his experiment rats stopped to exercise when they were short of glycogen but their muscles can continue to work without 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 shortage of glycogen 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, player’s blood glycose level remains normal through the whole match due to increasing glycogen depletion in liver and gluconeogenesis (glucose production from lactate, fat and proteins). It looks like, if there is central mechanism, it is not due to low blood glycose level . Another explanation how low glycogen level induces fatigue may be its influence on Ca ions release in muscles which is crucial for contraction. When glycogen stores are depleted, Ca release and consequently muscles contractions are impaired (?rtenblad, Nielsen, Saltin, & Holmberg, 2011). The same study looked in more details how distribution of glycogen in muscle’s sites can influence fatigue. They suggested idea that relatively small amount of muscle glycogen (10-15% of muscle reserves) which is stored in myofibrils can be crucial for Ca release. Its reduction through the negative feedback can lead to the central fatigue development even if there is still enough glycogen in the other sites. These findings possibly can explain contradictions in results about glycogen influence on fatigue, when researchers take muscle at whole, without pay attention 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 ability to perform intense exercise. It may be due to direct mechanical damage of the muscle’s fibres, particular fast-twitch fibres which are important during rapid maximal efforts (sprints, jumps and etc.). Eccentric contractions, when muscle is under tension while it is lengthening, are 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 complex than just “exclusion” some fibres from work. Our brain does not want to continue the exercise which is 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’s membranes that, eventually, influences whole body homeostasis. Even this may be not the full picture. Komi discussed disturbance in stretch-shortening cycle (SSC) in muscles due to EIMD (Komi, 2000). During real-life activities our muscles are lengthening and shortening in sequence, where delay between these two actions is very short. That allows elastic energy, which is stored during stretching, to be used in shortening part of SSC thus to make muscles 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 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 glycose from the blood into the muscle cells and if they not working properly muscles glycogen is depleted more rapidly and is restored slowly. Eston with colleagues found another interesting aspect of possible EIMD involvement in fatigue’s development. That may be a damage in capillary bed due to EIMD which can altered muscle’s oxygenation process (Davies et al., 2008) . This 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 player’s agility and technique as well as running economy. There are a few more possible mechanisms of EIMD influence on fatigue (for review see (Byrne, et al., 2004) . This phenomenon has been intensively studying now. However, surprisingly, it is not often mentioned among the main reasons for fatigue 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 ionic environment in the muscles, whereas low energy level and disturbance in ionic balance can distract coordinated work of the fibres thus accelerate muscle damage.

If we are talking about temporally fatigue during/after high intensity periods of the game, it to the great extant depends on initial muscle’s conditions prior to this period. Iaia et al. conducted interesting study about how different kinds of previous exercises may influence performance in high-intensity exhaustive (130 % VO2 max) cycle sprint. This sprint was performed 2 min after: a) long low intensity work (2 hours, 60% of VO2 max) ; b) high intensity work ( 3 min, 118% of VO2 max); c) 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 low intensity and high intensity exercise. The authors tried to analyse how the different muscles conditions prior to sprint can influence the result. Their main interest was muscle acidosis (PH) and muscle glycogen. Not surprisingly, the lowest muscle glycogen was after long, low intensity exercise. This might influenced consequent performance in sprint and supported the notion of the importance the glycogen stores for performance. The lowest muscle PH (highest acidosis) was after high intensity work and that might influence the fatigue as well. However authors concluded that neither glycogen concentration nor PH level alone were the STOP factor in the following exhaustive sprint because participants could start exercise and perform it at least 30 sec with pre-low glycogen or pre-low PH. It looks like there is no a sole factor responsible for fatigue development. Rather, a complex interaction between multiple factors, eventually, makes us tired when we are playing football.

Summary about the reasons for fatigue during a football game

There are two main types of fatigue which occur during the game. The temporary impairments in performance happens in a 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. Probably the main reasons for that are glycogen stores depletion in some muscle’s fibres and/or fibre’s sites and EIMD.

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

Keep these in mind following questions should be answered by sport scientists and coaches:

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.


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.

Bradley, P. S., Sheldon, W., Wooster, B., Olsen, P., Boanas, P., & Krustrup, P. (2009). High-intensity running in English FA Premier League soccer matches. Journal of Sports Sciences, 27(2), 159-168. doi: 10.1080/02640410802512775

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.

Eston, R., Byrne, C., & Twist, C. (2003). Muscle function after exercise-induced muscle damage: Considerations for athletic performance in children and adults. Journal of Exercise Science and Fitness, 1(2), 85-96.

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.

Svedenhag, B. S. J. (1994). Assessment of endurance capacity. In C. W. Mark Harries, William D. Stanish, Lyle J. Micheli (Ed.), Oxford Textbook of Sports Medicine. Oxford: Oxford University Press.

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