Typical match movement characteristics

Movements in TS matches can be measured through Global Positioning System (GPS),4 or other systems2 and activity profile variables, expressed in metres per minute of match time (m/min), which typically include total distance, standing, walking, jogging, striding and sprinting.2 ,4 Striding and sprinting are categorised as ‘high-intensity activities’, while standing, walking and jogging, which occur in between high-intensity bouts to recover from these bouts, are described as ‘low-intensity activities’.7 ,18 ,19 Intensity, however, is dependent on an individual's perception of effort,20 ,21 and ‘activity’ can include movements such as accelerating or leaping for ball possession. As this review focuses on movement characteristics, walking and jogging will be referred to as low-velocity running (LVR, 0.01–4.16 m/s), and striding and sprinting as high-velocity running (HiVR, 4.17–10 m/s). In addition, the frequency of maximal accelerations per minute (≥2.78 m/s²) can be quantified.8 ,22

Soccer athletes, for example, regularly repeat short, high-intensity efforts, interspersed with longer intervals of rest or submaximal exercise over ≥30 min.2 The typical distance covered by top-class centre-midfielders is ∼9–13 km/match,1 ,2 which is comprised of 70% low-intensity activity and ∼150–250 brief intense actions (average sprint distances of ∼10–20 m).7 ,23 ,24 Australian footballers cover the highest distances in field sports,4 up to 15 km in finals matches,1 and undertake up to 30% of this distance as HiVR.1 ,23 In addition to these locomotive activities, athletes must perform other energy-demanding activities (eg, jumping, moving while controlling the ball and tackling) during matches that require them to accelerate.7 ,23 ,25 ,26 These high-intensity movements and accelerations often occur in response to cues such as ball movement or opponents’ actions. Such movements are typically short and, when started from a low velocity, have not been traditionally accounted for in match analysis research.8 In fact, analysis from elite soccer athletes reveals that 85% of accelerations (≥2.78 m/s²) do not exceed the determined HiVR threshold.8 Thus, in match analysis studies that only report movements occurring at high velocities, accelerations are often excluded. A recent study demonstrated a 13-fold increase in high-intensity actions over the course of a match when combining sprint bouts and accelerations in the analysis.8 It is imperative to consider these short actions, as they are energetically the most challenging during a match5 and thus contribute greatly to total energy expenditure in a match.5

Characteristics of elite team-sport athletes

Elite TS athletes must adapt to varied physical demands during the course of a match. Typically, athletes compete on average at 70% of their maximal aerobic O₂ uptake (VO_2max),27 and cover an average distance of ∼9–13 km/match.7 ,23 ,24 ,27 This suggests that, in addition to the intermittent high-intensity nature of TS, high aerobic power is important for success. In fact, while elite TS athletes do not exhibit the specific physical/physiological capacities of elite endurance and sprint athletes, they do possess high levels of ‘aerobic’ and ‘anaerobic’ potentials.14 ,17

Match activity profiles at altitude

Owing to the large distance covered in games and the numerous accelerations to be performed, competing at altitude is likely to exacerbate fatigue in TS athletes and influence the outcome of matches. In fact, field data demonstrate large inequalities in the probability to win for a sea-level team playing against a home team at moderate/high altitude.15

The first study, to the best of our knowledge, to report altitude-induced performance decrement analysed match data from the official game statistics of the 2010 FIFA World Cup held in South Africa, where 64 matches were played by 105 teams at sea level, 660, 1200–1400 and 1401–1753 m.35 The results show a 3.1% lower total distance covered by teams during matches played at 1200–1400 and 1401–1753 m, compared with those played at sea level. Interestingly, however, the players’ top-running speed was not different across altitudes, suggesting that at least single high-intensity work capacity is well maintained during matches. More recent data collected in preparation for the 2011 FIFA U20 World Cup corroborate these findings, reporting that the total running distance and LVR were reduced by 9% and 8%, respectively, during matches played 4 days after arrival in Denver, Colorado (1600 m), compared with sea-level matches.22 Interestingly, this study also indicates a 15% reduction in HiVR at altitude. Furthermore, a rolling 5 min sample period was used to identify the peak 5 min period of the match and the 5 min period occurring immediately after the peak 5 min period, which gives an indication of transiently lower output, possibly fatigue, during matches. With this technique, there was a 21% reduction in peak HiVR as well as HiVR in the subsequent 5 min stanza (−55%) at 1600 m than at sea level. While the frequency of accelerations performed during matches was not clearly affected at this low altitude, the acceleration frequency in the 5 min subsequent to the peak 5 min period dropped considerably (−51%) at 1600 m, suggesting transient neuromuscular fatigue.22 Other data consolidate the finding that altitude hinders TS athletes’ running performance during matches; the recent International Study on Soccer at Altitude 3600 m (ISA3600), in this supplement,36 also reports compelling negative effects of high altitude on soccer players, independent of whether they are high-altitude or sea-level natives.

It is also worth considering that findings from controlled lab studies do not translate directly to match performance of players at altitude. TS are complex and chaotic, whereas laboratory studies are well controlled, with known work and rest durations. Participants in those studies can plan their physical output with some certainty. TS athletes, however, may preserve their capacity to perform the hardest actions, such as CAC, in matches by modulating the amount of low-intensity activity undertaken, especially in the face of environmental challenges like altitude.36 Therefore, laboratory studies cannot accurately predict the changes in match activity that actually occur in TS situations. Keeping this in mind, it is therefore critical when considering the effects of, for example, altitude on match running that the running profile of players is measured during competition. Sporting regulatory bodies should allow these data to be collected in all matches to assist in our understanding.

Collectively, these first data collected on TS athletes competing at altitude are in good agreement with the scarce evidence available on simulated TS athlete performances at natural altitude. For example, compared with sea-level activity, the performance of rugby athletes during a 20 m shuttle run (−4%) and a rugby-specific repetitive power test (−16%) is decreased at 155037 and 1700 m, respectively.38

Laboratory studies

Owing to its high-energy demand, the skeletal muscle is sensitive to changes in partial pressure of O₂. Laboratory-based research indicates that a reduction in systemic O₂ delivery contributes to curtailment of CAC and repeated-sprint ability through varied metabolic and neuromuscular mechanisms. For example, total mechanical work during ten 10 s cycle sprints interspersed with 30 s of rest was reduced (−8%) in hypoxic (FiO₂ 0.13, ∼3600 m) versus normoxic conditions.13 In hypoxia, a ∼9-fold to 10-fold increase in deoxygenation of active muscles (assessed via near-infrared spectroscopy) occurs rapidly during the first repetition of a series of sprints.13 ,39 However, as this deoxygenation quickly plateaus, and is relatively similar in normoxia and hypoxia, the results have been interpreted to mean that the level of muscle deoxygenation per se, and presumably muscle O₂ extraction, is unlikely to limit CAC.13 ,39 On the other hand, the capacity of the muscle to get reoxygenated during recovery periods between efforts has been incriminated in the performance decline in hypoxia.40 For instance, impaired muscle O₂ supply has been associated with hindered PCr resynthesis.41 Interventions that reduce (eg, hypoxia) or prevent (eg, blood flow occlusion) O₂ supply to muscles reduce and prevent, respectively, PCr resynthesis.42 ,43 Furthermore, the reoxygenation rate of the skeletal muscle has similar recovery kinetics to PCr after exercise.44 ,45 Therefore, since PCr resynthesis is one of the main factors in performance during repeated efforts,46 ,47 the slower repletion of this critical substrate is a key mechanism by which hypoxia impairs TS athletes’ running performance at altitude.

Other studies have demonstrated greater anaerobic energy release and metabolic perturbations after single-sprint11 and repeated-sprint48 ,49 exercise in hypoxia. This suggests that sprinting in hypoxia leads to greater and/or earlier metabolic fatigue (and presumably muscle fatigue) than in normoxia. Another factor that could contribute to exacerbated fatigue and lower intermittent HiVR at altitude is the downregulation of the Na⁺, K⁺–ATPase in hypoxia.50 For instance, when Na⁺, K⁺–ATPase are inhibited, the Na⁺/K⁺ leak-to-pump ratio is increased, muscle tetanic force is depressed and muscle fatigue is accelerated.51 Furthermore, the influence of the build-up of energy metabolites such as inorganic phosphate and hydrogen ions on force development and calcium sensitivity, which is accelerated in hypoxia, has been well established during exercise.51 Although no data are available, particularly on sprint exercise, it is quite likely that these mechanisms are at play during TS matches at altitude and contribute to hinder HiVR.

The effects of hypoxia on the nervous system function have been well described,28 but once again, data collected from sprint exercise are very limited. A greater attenuation of the surface electromyographic activity (serving as a surrogate for the central motor drive to skeletal muscles) has been reported during repeated sprints in hypoxia.13 Motor neuron activity can be affected via two mechanisms in hypoxia. For example, an indirect inhibitory effect of the sensory afferent feedback (groups III/IV muscle afferents) originating from the fatiguing locomotor muscles occurs during endurance exercise.29 ,52 As mentioned above, the accelerated development of peripheral limb fatigue during sprints performed in hypoxia versus normoxia may strongly influence the regulation of central nervous system response and contribute to lower muscle recruitment.13 There is little doubt that these peripheral influences are increasingly important at altitude and would exert a detrimental effect on LVR and HiVR over an extended period of time, such as during TS matches. However, the consequences of arterial hypoxaemia on the complex relationship between peripheral perturbations, muscle fatigue development, neural adjustments and performance have yet to be examined during repeated sprints in TS athletes in an intervention trial. There is also the possibility of a direct effect of brain hypoxia on muscle recruitment. For instance, motor neuron activity is dramatically influenced by O₂ availability,53–55 and insufficient oxygenation of the cerebral cortex can impair neurotransmitter turnover and depress neuronal electrical activity,56 which has been incriminated in the occurrence of central fatigue.56 ,57 Of direct interest to TS athletes is that tests of repeated-sprint ability (10×10 s sprints with 30 s rest) in hypoxic conditions (FiO₂ 0.13) result in larger cerebral deoxygenation compared to normoxia,13 ,39 which leads to a larger decline in muscle recruitment in hypoxia.13 Changes in cerebral deoxyhaemoglobin concentration explained 83% of the variance in electromyographic activity in hypoxia.13 Therefore, it is possible that TS athletes playing at altitude exhibit such brain deoxygenation during high-intensity periods of a match that may contribute to curtailing their CAC.22

Maintaining CA capacity

Adaptations potentially favourable to high-intensity exercises and CAC may come from intermittent hypoxic training (IHT) in which athletes exercise in hypoxia.14 The resynthesis of PCr—known as a key metabolic pathway for CAC46 ,47 may be positively impacted by adding a hypoxic stimulus during training. In fact, IHT involving a single leg extension results in faster PCr resynthesis after high-intensity exercise than similar training in normoxia.58 The authors hypothesised that the faster PCr resynthesis observed after IHT was probably due to an enhanced muscle O2 delivery. Since hypoxia impairs the muscle reoxygenation capacity, which is directly linked to PCr resynthesis,44 ,45 it is possible that an IHT block that can accelerate the repletion of this substrate would benefit the recovery of power output and, therefore, CAC at altitude.

Compared with sea-level training, IHT induces additional metabolic stress59 and provoke specific molecular adaptations.60 ,61 The lower O₂ partial pressure in muscle tissue during IHT may induce a larger upregulation of the hypoxia-inducible factor 1á,58 ,60 ,61 which has in turn been shown to increase the fibre cross-sectional area, oxidative enzyme activity, mitochondrial density and capillary/fibre ratio.61–64 Recently, the idea was put forward that IHT involving sprint exercise would increase blood perfusion, thereby enhancing O₂ utilisation and improving the behaviour of fast-twitch fibres.65 Molecular adaptations in muscle tissue together with higher blood perfusion (presumably via nitric oxide-mediated vasodilatation mechanisms)66 ,67 after IHT could also positively influence sprint endurance in hypoxic environments and increase the chances of success for an ‘away’ team residing at sea level.

Reducing the general impact of altitude

Teams aiming at reducing the general impact of hypoxia when travelling at altitude for a match should seek acclimatisation to the altitude of the match.14 ,15 In this situation, the most effective strategy is likely to stage several days to weeks at the altitude of the match, particularly if travel across multiple time zones is also required.15 ,37 For example, it was recently reported that the negative impact of an altitude of 1600 m on total distance covered during a match (−9.1%) and HiVR (−15.2%) in youth TS athletes was progressively reversed after only 6 days of residence at this low altitude (total distance: 6.2%, HiVR: 18.3%).22 For moderate altitude (2000–3000 m), 1–2 weeks may be suitable to maximise physiological acclimatisation (eg, O₂ transport and acid–base balance),68 although such data are not available in a population of TS athletes. Competition at high altitude (>3000 m) poses other challenges. However, there is evidence of incomplete acclimatisation in TS athletes after more than 2 weeks at altitude.69 ,70