The plasticity of skeletal muscle tissue means it can change its characteristics and structural composition to adapt to various functional demands, neuromuscular activity and hormonal signals (12, 18, 25). Football conditioning over the preparation period and throughout the season, is a structured process, consisting of a series of physiological stresses/responses that allow the player to maintain or enhance specific physiological components, in the hope it will subsequently increase the ability to tolerate the demands of training and competition. Conversely, training reversibility or detraining, is a concept in which physiological adaptations are partially or completely reversed when training is reduced or stopped completely. Measuring the reductions or losses from training-induced adaptations very much depends on the time frame of training reduction or cessation.

An average season will finish in early May, with pre-season return dates varying between clubs. Some teams might have play-off commitments which means their season can continue for another 3 weeks. Similarly, on a bi-yearly basis, international teams will compete in tournaments during the summer, requiring players to further their season again, potentially for an additional 3 weeks. Managing the different commitments of players over the summer period is pivotal, not only to allow regeneration from a strenuous season, but find a balance between rest, regeneration, maintenance and adaptation. It should also be considered that detraining characteristics will not be identical from team to team or even player to player within the same team (5, 15, 32, 40). Notable reductions in the physical conditioning of professional footballers can be detrimental to performance (5, 33), so when teams break for the off-season and training is drastically reduced, players must ensure that stimuli are maintained, so that the return to pre-season is not as laborious.

Football is an intermittent, high intensity sport, requiring both aerobic and anaerobic processes for energy release, as well as relying on technical, tactical and psychological input. Aerobic capacity is known to be highly important and a major contributor (~70-80%) of maximal capacity (10, 15). However, the observation of blood lactate levels during matches also highlights the importance of energy yielded from anaerobic contribution.

Within days of training cessation, aerobic capabilities can drop from 5-12%. This is largely in part to a reduced blood and plasma volume, meaning during exercise, ventricular filling is limited (6). Evidence is also available that has reported swimmers, cyclists and endurance trained runners showed signs of elevated blood lactate levels during standardised sub-maximal efforts after only days of training cessation (3, 4, 7, 35). Furthermore, lactate threshold occurs at a lower percentage of VO2Max (7, 27), which is indicative of a reduction in the oxidative capacity of muscles, which may fall by as much as 50% in one week (4). It should be considered that any detraining-induced reduction in absolute VO2 at which lactate threshold occurs, will reduce performance. Similarly, training done at the same absolute intensity after detraining, will result in a higher lactate accumulation and an increase in muscle glycogen utilisation and carbohydrate oxidation, subsequently reducing the time to fatigue (5, 6, 32). This is related to the decrease in muscle capillary diameter, leading to a reduced mean transportation time of blood flow through the active muscle, as proposed by Saltin et al. (1986). This can further limit the exchange of substrates and metabolites, requiring an increase in glycogenolysis to support the energy demands of the exercising muscle.

Enzyme activity is greatly affected with short term training cessation as skeletal muscle cytrate synthase activity decreases between 25-45% (2, 7, 20, 30, 32). Decreases in muscle oxidative capacity are further reflected by 12-27% reductions in β hydroxyacil-CoA dehydrogenase, malate dehydrogenase and succinate dehydrogenase respectively (2, 7, 23, 28). Additionally, lipoprotein lipase activity within skeletal muscle has been found to be reduced by 45-75%. Controversially, this enzyme’s activity increases by 86% at the adipose tissue level, favouring the storage of adipose (fat) tissue (37). Alterations in the regulation of protein synthesis rates are said to be the primary reason for this (22).

Short term training cessation has also been reported to induce small non-systematic changes in glycolytic enzyme activities, including phosphorylase, phosphofructokinase and hexokinase (4, 7). Glycogen synthase activity has also been shown to decrease by 42% after only 5 days without training (31), along with mitochondrial enzyme activity which has been shown to reverse back to pre-training levels after short term training reductions (26, 32, 39).

The body’s ability to use oxygen drops by 10% after just a week of detraining. Respiratory exchange ratio (RER), which is the ratio between the amount of CO2 produced in metabolism and the amount of oxygen used, is known to increase both at submaximal (8, 28, 32) and maximal (20) exercise intensities, which is indicative of a greater dependence on carbohydrate as a substrate for exercising muscles at the expense of lipid metabolism. This is due to the rapid decrease in sensitivity for insulin-mediated whole-body glucose uptake (1, 14, 21, 38). Research has also reported reductions in muscle GLUT-4 transporter protein content, as early as 6-10 days without training, which has been shown to decrease by 17-33% (30, 38). Energy storage in the form of glycogen also becomes compromised. Reductions in muscle glycogen stores have been identified in as little as one week after training cessation, with ~20% reductions being reported in competitive swimmers (4), triathletes, cyclists and runners after 4 weeks of detraining (23). This reduction is due to a rapid decline in the conversion of glucose to glycogen as well as glycogen synthase activity (31).

After a little under two weeks, heart rate is increased at both submaximal (28) and maximal levels (9) by roughly 5-10%. Early signs of reduced blood volume negatively affect stroke volume with reductions of 10-17% being reported after 12-21 days of training cessation (6, 8, 11, 29). Left ventricular wall thickness has been shown to reduce, with a 25% decrease suggested by Martin et al. (1986), along with a 19.5% reduction in left ventricular mass and a 12% reduction in the left ventricular end diastolic dimension (29) after 3 weeks of deconditioning.

Research has shown that mitochondrial activity (energy production) in cells begins to decrease rapidly after roughly two weeks of training cessation. In a similar period, Bangsbo and Mizuno (1987) reported decreases of 7%, in mean fibre cross-sectional area of samples of gastrocnemius muscle taken from footballers after training cessation. This change, however, was primarily due to a 12.4% decline in fast twitch fibre area. Losses in strength have showed to be slight but non-significant in exercises such as bench press, squat, vertical jump and both isometric and isokinetic concentric knee extension force. However, electromyogram (EMG) activity of the vastus lateralis muscle and isokinetic eccentric knee extension forces have shown significant decreases by 8.4-12.7% and 12% respectively (19, 33). These are of course important musculature involved in many football related actions. Squatting ability levels of Olympic weightlifters have also shown rapid decreases in muscle strength after training ceased (13). It is important to note that if a brief period of detraining or tapering has begun immediately after a high volume or high intensity training phase, then increases in strength adaptations may occur (11).

With regard to muscular strength, the performance of eccentric muscle actions has been shown not only to be essential in promoting greater and more prolonged neural adaptations but has an influential effect on an untrained limb when performing unilateral leg training. Research has shown that strength gains achieved through an 8-week period of unilateral, eccentric-only resistance training, have been shown to be retained not only in the trained limb but also in the contralateral untrained limb during a consecutive 8-week training cessation period (24). Interestingly, the maintenance of such characteristics is also dependent on the training modalities used during the previous training period. For example, Hodikin (1982) found that levels of speed-strength were better maintained during training cessation, when the previous training method focused on developing explosive strength.

Houston et al. (1979) reported a 6.3% reduction in capillary density after only 15 days without training in well-trained endurance runners. Bangsbo & Mizuno (1988) also found that the number of capillaries around slow twitch (ST) muscle fibres, decreased significantly from 6.0 to 5.8 after 3 weeks of training cessation in semi-professional footballers. From roughly 20-21 days, VO2Max (i.e. the efficiency of utilising oxygen during exercise) drops anywhere from 4-14% (29, 32). Coyle et al. (1984) also suggested that the greater the aerobic capacity (VO2Max) of the individual, the greater the decline during reduced training periods. It is also worth noting that the increase in maximum heart rate, mentioned earlier, is not enough to counterbalance the reduction in stroke volume. Cardiac output has been shown to be 8% lower after 21 days without training (8), with submaximal cardiac output increasing from 84-89% of the maximal at the same absolute exercise intensity (7). Coyle et al. (1986) estimated that ~30g of haemoglobin is lost in as little as 2 to 4 weeks of detraining. This corresponds to ~3.5% loss in total haemoglobin and may account for a portion of the reported decrease in VO2Max.

With more readily available research and greater evidence to highlight the importance of the effects of detraining, both players and conditioning staff are better equipped to structure off-season programmes that allow for appropriate rest, regeneration, maintenance and adaptation of certain physical components. Although long term alterations after detraining have more severe effects on performance, this review has only considered the short-term alterations due to the typical 4-6 week off-season period.


  1. Arciero PJ, Smith DL, Calles-Escandon J. 1998. Effects of short-term inactivity on glucose tolerance, energy expenditure, and blood flow in trained subjects. J Appl Physiol, 84(4), 1365-73
  2. Bangsbo J, Mizuno M. 1987. Morphological and metabolic alterations in soccer players with detraining and retraining and their relation to performance. In: Science and Football: Proceedings of Muscular Detraining. Medicine & Science in Sports & Exercise, First World Congress of Science and Football, Liverpool, England, T. Reilly, et al. (Eds.). New York: E. & F.N. Spon, 114-124
  3. Claude AB, Sharp RL. 1991. The effectiveness of cycle ergometer training in maintaining aerobic fitness during detraining from competitive swimming. J Swimming Res, 7(3), 17-20
  4. Costill DL, King DS, Thomas R, et al. 1985. Effects of reduced training on muscular power in swimmers. Physician Sports Med, 13(2), 94-101
  5. Coyle EF. 1988. Detraining and retention of training-induced adaptations. In: Resource Manual for Guidelines for Exercise Testing and Prescription, S. N. Blair, et al. (Eds.). Philadelphia: Lea & Febiger, 83-89
  6. Coyle EF, Hemmert MK, Coggan AR. 1986. Effects of detraining on cardiovascular responses to exercise: role of blood volume. J Appl Physiol, 60(1), 95-99
  7. Coyle EF, Martin III WH, Bloomfield SA, et al. 1985. Effects of detraining on responses to submaximal exercise. J Appl Physiol, 59(3), 853-859
  8. Coyle EF, Martin III WH, Sinacore DR, et al. 1984. Time course of loss of adaptations after stopping prolonged intense endurance training. J Appl Physiol, 57(6), 1857-1864
  9. Cullinane EM, Sady SP, Vadeboncoeur L, et al. 1986. Cardiac size and VO2max do not decrease after short-term exercise cessation. Med Sci Sports Exerc, 18(4), 420-424
  10. Ekblom, B. 1986. Applied physiology of soccer. Sports medicine, 3(1), 50-60
  11. Fleck SJ. 1994. Detraining: its effects on endurance and strength. J Strength Cond, 16(1), 22-28
  12. Gordon T, Pattullo MC. 1993. Plasticity of muscle fiber and motor unit types. Exerc. Sports Sci. Rev, 21, 331-362
  13. Hakkinen, K. Komi, PV. 1985. Changes in electrical and mechanical behaviour of leg extensor muscles during heavy resistance strength training. Scand J Sports Sci, 125, 573-585
  14. Hardman AE, Lawrence JEM, Herd SL. 1998. Postprandial lipemia in endurance-trained people during a short interruption to training. J Appl Physiol, 84(6), 1895-901
  15. Hawley JA. 1987. Physiological responses to detraining in endurance trained subjects. Aust J Sci Med Sport, 19(4), 17-20
  16. Helgerud, J. Engen, LC. Wisloff, U. Hoff, J. 2001. Aerobic endurance training improves soccer performance. Med Sci Sports Ex, 33(11), 1925-1931.
  17. Hodikin AV. 1982. Maintaining the training effect during work stoppage. Teoriya i Praktika Fiziocheskoi Kultury. 3, 45-48
  18. Hoppeler H. 1986. Exercise-induced ultrastructural changes in skeletal muscle. Int J Sports Med, 7, 187-204
  19. Hortobágyi T, Houmard JA, Stevenson JR et al. 1993. The effects of detraining on power athletes. Med Sci Sports Exerc, 25(8), 929-935
  20. Houmard JA, Hortobágyi T, Johns RA, et al. 1992. Effect of short term training cessation on performance measures in distance runners. Int J Sports Med, 13(8), 572-576
  21. Houmard JA, Hortobágyi T, Neufer PD, et al. 1993. Training cessation does not alter GLUT-4 protein levels in human skeletal muscle. J Appl Physiol, 74(2), 776-781
  22. Houston ME. 1986. Adaptations in skeletal muscle to training and detraining: the role of protein synthesis and degradation. In: Saltin B, editor. Biochemistry of exercise VI. Champaign (IL): Human Kinetics, 63-74
  23. Houston ME, Bentzen H, Larsen H. 1979. Interrelationships between skeletal muscle adaptations and performance as studied by detraining and retraining. Acta Physiol. Scand, 105, 163-170
  24. Housh TJ, Housh DJ, Weir JP, Weir LL. 1996. Effects of eccentric-only resistance training and detraining. Int J Sports Med, 17, 145-148
  25. Kannus P, Josza L, Renstrӧm P, Järvinen M, Kvist M, Lehto M, Oja P, Vuori I. 1992. The effects of training, immobilization and remobilization on musculoskeletal tissue. 1. Training and immobilization. Scand J Med Sci Sports, 2, 100-118
  26. Klausen K, Andersen LB, Pelle I. 1981. Adaptive changes in work capacity, skeletal muscle capillarization and enzyme levels during training and detraining. Acta Physiol Scand, 113, 9-16
  27. Londeree BR. 1997. Effect of training on lactate/ventilatory thresholds: a meta-analysis. Med Sci Sports Exerc, 29(6), 837-843
  28. Madsen K, Pedersen PK, Djurhuus MS, et al. 1993. Effects of detraining on endurance capacity and metabolic changes during prolonged exhaustive exercise. J Appl Physiol, 75(4), 1444-1451
  29. Martin III WH, Coyle EF, Bloomfield SA, et al. 1986. Effects of physical deconditioning after intense endurance training on left ventricular dimensions and stroke volume. J Am Coll Cardiol, 7(5), 982-989
  30. McCoy M, Proietto J, Hargreaves M. 1994. Effect of detraining on GLUT-4 protein in human skeletal muscle. J Appl Physiol, 77(3), 1532-1536
  31. Mikines KJ, Sonne B, Tronier B, et al. 1989. Effects of acute exercise and detraining on insulin action in trained men. J Appl Physiol, 66(2), 704-711
  32. Moore RL, Thacker EM, Kelley GA, et al. 1987. Effect of training/detraining on submaximal exercise responses in humans. J Appl Physiol, 63(5), 1719-1724
  33. Mujika, I, Padilla S. 2000. Detraining: loss of training-induced physiological and performance adaptations. Part I. Short-term insufficient training stimulus. Sports Med, 30, 79-87
  34. Mujika I, Padilla S. 2001. Muscular characteristics of detraining in humans. Med Sci Sports Exerc, 33(8), 1297-1303
  35. Neufer PD, Costill DL, Fielding RA, et al. 1987. Effect of reduced training on muscular strength and endurance in competitive swimmers. Med Sci Sports Exerc, 19(5), 486-490
  36. Saltin , Kiens B, Savard G, Pedersen PK. 1986. Role of haemoglobin and capillarization for oxygen delivery and extraction in muscular exercise. Acta Physiologica Scandinavica, 128(Suppl. 556), 21-32
  37. Simsolo RB, Ong JM, Kern PA. 1993. The regulation of adipose tissue and muscle lipoprotein lipase in runners by detraining. J Clin Invest, 92, 2124-2130
  38. Vukovich MD, Arciero PJ, Kohrt WM et al. 1996. Changes in insulin action and GLUT-4 with 6 days of inactivity in endurance runners. J Appl Physiol, 80(1), 240-244
  39. Wibom R, Hultman E, Johansson M, et al. 1992. Adaptation of mitochondrial ATP production in human skeletal muscle to endurance training and detraining. J Appl Physiol, 73(5), 2004-2110
  40. Wilber RL, Moffatt RJ. 1994. Physiological and biochemical consequences of detraining in aerobically trained individuals. J Strength Cond Res, 8(2), 110-124