Soccer is the most popular sport in the world and is performed by men and women, children and adults with different levels of expertise. Soccer performance depends upon a myriad of factors such as technical/biomechanical, tactical, mental and physiological areas. One of the reasons that soccer is so popular worldwide is that players may not need to have an extraordinary capacity within any of these performance areas, but possess a reasonable level within all areas. However, there are trends towards more systematic training and selection influencing the anthropometric profiles of players who compete at the highest level. As with other activities, soccer is not a science, but science may help improve performance. Efforts to improve soccer performance often focus on technique and tactics at the expense of physical fitness. During a 90-minute game, elite-level players run about 10 km at an average intensity close to the anaerobic threshold (80-90% of maximal heart rate). Within this endurance context, numerous explosive bursts of activity are required, including jumping, kicking, tackling, turning, sprinting, changing pace, and sustaining forceful contractions to maintain balance and control of the ball against defensive pressure. The best teams continue to increase their physical capacities, whilst the less well ranked have similar values as reported 30 years ago. Whether this is a result of fewer assessments and training resources, selling the best players, and/or knowledge of how to perform effective exercise training regimens in less well ranked teams, is not known. As there do exist teams from lower divisions with as high aerobic capacity as professional teams, the latter factor probably plays an important role. This article provides an update on the physiology of soccer players and referees, and relevant physiological tests. It also gives examples of effective strength- and endurance-training programmes to improve on-field performance. The cited literature has been accumulated by computer searching of relevant databases and a review of the authors' extensive files. From a total of 9893 papers covering topics discussed in this article, 843 were selected for closer scrutiny, excluding studies where information was redundant, insufficient or the experimental design was inadequate. In this article, 181 were selected and discussed. The information may have important implications for the safety and success of soccer players and hopefully it should be understood and acted upon by coaches and individual soccer players.

http://carlocapelli.it/ftp/didattica/master calcio/bibliografia_essenziale/stolen_et_al_2005.pdf

Physiology of Soccer: An Update

Regularly performed endurance exercise induces major adaptations in skeletal muscle. These include increases in the mitochondrial content and respiratory capacity of the muscle fibers. As a consequence of the increase in mitochondria, exercise of the same intensity results in a disturbance in homeostasis that is smaller in trained than in untrained muscles. The major metabolic consequences of the adaptations of muscle to endurance exercise are a slower utilization of muscle glycogen and blood glucose, a greater reliance on fat oxidation, and less lactate production during exercise of a given intensity. These adaptations play an important role in the large increase in the ability to perform prolonged strenuous exercise that occurs in response to endurance exercise training.

Adaptations of skeletal muscle to endurance exercise and their metabolic consequences

Fatigue, defined as the failure to maintain the required or expected power output, is a complex problem, since multiple factors are clearly involved, with the relative importance of each dependent on the fiber type composition of the contracting muscles(s), and the intensity, type, and duration of the contractile activity. The primary sites of fatigue appear to be within the muscle cell itself and for the most part do not involve the central nervous system or the neuromuscular junction. The major hypotheses of fatigue center on disturbances in the surface membrane, E-C coupling, or metabolic events. The cell sites most frequently linked to the etiology of skeletal muscle fatigue are shown in Figure 1. Skeletal muscles are composed of at least four distinct fiber types (3 fast twitch and 1 slow twitch), with the slow type I and fast type IIa fibers containing the highest mitochondrial content and fatigue resistance. Despite fiber type differences in the degree of fatigability, the contractile properties undergo characteristic changes with the development of fatigue that can be observed in whole muscles, single motor units, and single fibers. The Po declines, and the contraction and relaxation times are prolonged. Additionally, there is a decrease in the peak rate of tension development and decline and a reduced Vo. Changes in Vo are more resistant to fatigue than Po and are not observed until Po has declined by at least 10% of its initial prefatigued value. However, the reduced peak power by which fatigue is defined results from both a reduction in Vo and Po. In the absence of muscle fiber damage, the prolonged relaxation time associated with fatigue causes the force-frequency curve to shift to the left, such that peak tensions are obtained at lower frequencies of stimulation. In a mechanism not clearly understood, the central nervous system senses this condition and reduces the alpha-motor nerve activation frequency as fatigue develops. In some cases, selective LFF develops that displaces the force-frequency curve to the right. Although not proven, it appears likely that this condition is associated with and likely caused by muscle injury, such that the SR releases less Ca2+ at low frequencies of activation. Alternatively, LFF could result from a reduced membrane excitability, such that the sarcolemma action potential frequency is considerably less than the stimulation frequency.(ABSTRACT TRUNCATED AT 400 WORDS)

Cellular mechanisms of muscle fatigue

HELGERUD, J., K. HKYDAL, E. WANG, T. KARLSEN, P. BERG, M. BJERKAAS, T. SIMONSEN, C. HELGESEN, N. HJORTH, R. BACH, and J. HOFF. Aerobic High-Intensity Intervals Improve VO2max More Than Moderate Training. Med. Sci. Sports Exerc., Vol. 39, No. 4, pp. 665-671, 2007. Purpose: The present study compared the effects of aerobic endurance training at different intensities and with different methods matched for total work and frequency. Responses in maximal oxygen uptake (VO2max), stroke volume of the heart (SV), blood volume, lactate threshold (LT), and running economy (CR) were examined. Methods: Forty healthy, nonsmoking, moderately trained male subjects were randomly assigned to one of four groups:1) long slow distance (70% maximal heart rate; HRmax); 2) lactate threshold (85% HRmax); 3) 15/15 interval running (15 s of running at 90-95% HRmax followed by 15 s of active resting at 70% HRmax); and 4) 4 4 min of interval running (4 min of running at 90-95% HRmax followed by 3 min of active restingat 70% HRmax). All four training protocols resulted in similar total oxygen consumption and were performed 3 dIwk j1 for 8 wk. Results: High-intensity aerobic interval training resulted in significantly increased VO2max compared with long slow distanceandlactate-thresholdtrainingintensities(P G 0.01). The percentage increases for the 15/15 and 4 4 min groups were 5.5 and 7.2%, respectively, reflecting increases in VO2max from 60.5 to 64.4 mLIkg j1 Imin j1 and 55.5 to 60.4 mLIkg j1 Imin j1 . SV increased significantly by approximately 10% after interval training (P G 0.05). Conclusions: High-aerobic intensity endurance interval training is significantly more effective than performing the same total work at either lactate threshold or at 70% HRmax, in improving VO2max. The changes in VO2max correspond with changes in SV, indicating a close link between the two. Key Words: LACTATE THRESHOLD, AEROBIC POWER, 4 4-MIN INTERVALS, 15/15 TRAINING, STROKE VOLUME, BLOOD VOLUME

Aerobic high-intensity intervals improve VO2max more than moderate training.

Background: A high level of strength is inherent in elite soccer play, but the relation between maximal strength and sprint and jumping performance has not been studied thoroughly. Objective: To determine whether maximal strength correlates with sprint and vertical jump height in elite male soccer players. Methods: Seventeen international male soccer players (mean (SD) age 25.8 (2.9) years, height 177.3 (4.1) cm, weight 76.5 (7.6) kg, and maximal oxygen uptake 65.7 (4.3) ml/kg/min) were tested for maximal strength in half squats and sprinting ability (0–30 m and 10 m shuttle run sprint) and vertical jumping height. Result: There was a strong correlation between maximal strength in half squats and sprint performance and jumping height. Conclusions: Maximal strength in half squats determines sprint performance and jumping height in high level soccer players. High squat strength did not imply reduced maximal oxygen consumption. Elite soccer players should focus on maximal strength training, with emphasis on maximal mobilisation of concentric movements, which may improve their sprinting and jumping performance.

https://bjsm.bmj.com/content/bjsports/38/3/285.full.pdf

Strong correlation of maximal squat strength with sprint performance and vertical jump height in elite soccer players

UNLABELLED Stroke volume (SV) responses during graded treadmill exercise were studied in 1) elite male distance runners (N = 5), 2) male university distance runners (N = 10), and 3) male untrained university students (N = 10). METHODS Cardiac output (Q) and SV were determined by a modified acetylene rebreathing procedure. RESULTS There were no differences in SV responses among the three groups during the transition from rest to light exercise (P > 0.05). However, the rates of change of SV during light to maximal exercise in untrained subjects (slope = -0.1544 mL x beat(-1)) and university distance runners (slope = 0.1041) did not change, whereas it dramatically increased (P < 0.001) in elite distant runners (slope = 0.6734). Moreover, the elite distance runners showed a further slope increase in SV when heart rate was above 160 bpm, which resulted in an average maximal SV of 187 +/- 14 mL x beat(-1) compared with 145 +/- 8 and 128 +/- 14 mL x beat(-1) in the university runners and untrained students, respectively (P < 0.001). Similarly, max Q reached 33.8 +/- 2.3, 26.3 +/- 1.7, and 21.3 +/- 1.5 L x min(-1) in the three groups, respectively (P < 0.001). On the other hand, there was a nonsignificant tendency for maximal arteriovenous oxygen content difference to be lower in the elite athletes compared with the other groups. CONCLUSION Results from university distance runners and untrained university students support the classic observation that SV plateaus at about 40% of maximal oxygen consumption despite increasing intensity of exercise. In contrast, stroke volume in the elite athletes does not plateau but increases continuously with increasing intensity of exercise over the full range of the incremental exercise test.

Stroke volume does not plateau during graded exercise in elite male distance runners.

Ten competitive cyclists were exercised to exhaustion to test the potential of a 24-h fast for increasing endurance. One group (n = 4) was tested at an initial intensity of 86% maximum O2 uptake (VO2max) (HI) and a second group (n = 6) at 79% VO2max (MI). Both groups repeated test rides in fasted and normal-diet conditions. Time to fatigue was designated at two points: fatigue 1 occurred when pedal frequency could not be maintained at the initial percent VO2max; fatigue 2 occurred when pedal frequency could not be maintained at a workload of approximately 65% VO2max. In both HI and MI the 24-h fast had no effect on resting muscle glycogen stores but significantly increased plasma free fatty acid (FFA) levels. Despite the increased FFA availability, time to fatigue was reduced in the fasted groups. Fatigue 1 and 2 times (mean +/- SE) for HI-fasted were 42.0 +/- 6.2 and 170.0 +/- 20.4 min, respectively, compared with those of the HI-normal diet of 115.3 +/- 25.6 and 201.0 +/- 14.8 min. Fatigue 1 and 2 times for MI-fasted were 142.0 +/- 19.6 and 167.5 +/- 10.5 min compared with those of the MI-normal diet of 191.3 +/- 25.0 and 214.3 +/- 18.9 min. The cause of fatigue at fatigue 1 was not readily apparent. Fatigue 2 in all groups seemed to be related to hypoglycemia as well as muscle glycogen depletion.

Effects of 24-hour fast on cycling endurance time at two different intensities.

To test the effects of tyrosine ingestion with or without carbohydrate supplementation on endurance performance, nine competitive cyclists cycled at 70% peak oxygen uptake for 90 min under four dif...

https://secure.footprint.net/gatorade/prd/gssiweb/pdf/200818646890.pdf

Effects of l-tyrosine and carbohydrate ingestion on endurance exercise performance

It is well accepted that exercise endurance is directly related to the amount of carbohydrate stored in muscle and that a low carbohydrate diet reduces glycogen storage and exercise performance. However, more recent evidence has shown that when the organism adapts to a high fat diet endurance is not hindered. The present study was designed to test that claim and to further determine if animals adapted to a high fat diet could recover from exhausting exercise and exercise again in spite of carbohydrate deprivation. Fat-adapted (3 to 4 weeks, 78% fat, 1% carbohydrates) rats (FAT) ran (28 m/min, 10% grade) as long as carbohydrate-fed (69% carbohydrates) animals (CHO) (115 v 109 minutes, respectively) in spite of lower pre-exercise glycogen levels in red vastus muscle (36 v 54 mumols/g) and liver (164 v 313 mumols/g) in the FAT group. Following 72 hours of recovery on the FAT diet, glycogen in muscle had replenished to 42 mumols/g (v 52 for CHO) and liver glycogen to 238 mumols/g (v 335 for CHO). The animals were run to exhaustion a second time and run times were again similar (122 v 132 minutes FAT v CHO). When diets were switched after run 1, FAT-adapted animals, which received carbohydrates for 72 hours, restored muscle and liver glycogen (48 and 343 mumols/g, respectively) and then ran longer (144 minutes) than CHO-adapted animals (104 minutes) that ate fat for 72 hours and that had reduced glycogen repletion. We conclude that, in contrast to the classic CHO loading studies in humans that involved acute (72 hours) fat feedings and subsequently reduced endurance, rats adapted to a high fat diet do not have a decrease in endurance capacity even after recovery from previous exhausting work bouts. Part of this adaptation may involve the increased storage and utilization of intramuscular triglycerides (TG) as observed in the present experiment.

Glycogen repletion and exercise endurance in rats adapted to a high fat diet

In brief: Thirty trained men carrying either nothing, 1-lb weights, or 5-lb weights in each hand were tested on a motorized treadmill. The purpose was to determine whether using hand-held weights elicits a pressor reflex, in which heart rate and BP rise disproportionately to oxygen consumption (VO2). VO2 was measured during walking and running to see if it changed in proportion to heart rate response. Both walking and running while carrying 5-lb weights produced significant increases in V2, but only walking produced significant differences in heart rate. The oxygen pulse (the amount of oxygen used per heart beat) was not different for any of the three treatments. The authors concluded that carrying weights in the hands can help increase the training intensity for walkers or joggers who cannot or do not wish to jog or run at a higher speed.

Physiological Responses to Hand-Carried Weights.

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