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Repeat sprint ability


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Repeat sprint ability

  1. 1. Repeat Sprint Ability Anthony N. Turner, MSc, CSCS*D1 and Perry F. Stewart, MSc, CSCS2 1 London Sport Institute, Middlesex University, London, United Kingdom; and 2 Sport Science and Medicine department, Queens Park Rangers Football Club, London, United Kingdom S U M M A R Y SPRINT SPEED IS RELATED TO THE ABILITY TO DEPLETE LARGE AMOUNTS OF HIGH-ENERGY PHOSPHATES AT A FAST RATE. TO SPRINT REPEATEDLY, THE AEROBIC SYSTEM MUST RESYNTHESIZE POLYMERASE CHAIN REACTION, REMOVE ACCUMULATED INTRACELLULAR INORGANIC PHOSPHATE, AND OXIDIZE LACTATE DURING REST PERIODS. WHETHER THIS CAN BE APPRECIABLY IMPROVED VIA A HIGH V̇O2MAX REMAINS CONTROVERSIAL. HOWEVER, IT IS LIKELY IMPROVED VIA ANAEROBIC QUALITIES SUCH AS STRENGTH, POWER, AND SPEED, ALONG WITH THE ATHLETE’S VELOCITY AT ONSET OF BLOOD LACTATE ACCUMULATION. WHEN REPORTING REPEAT SPRINT ABILITY TEST RESULTS, TOTAL OR MEAN TIME SHOULD BE USED. INTRODUCTION R epeat sprint ability (RSA) describes the ability of an athlete to recover and maintain maxi- mal effort during subsequent sprints, an attribute considered important to team sports. It is often trained and mea- sured via high-intensity sprints, inter- spersed with brief recovery bouts (#30 seconds). Most strength and con- ditioning coaches agree that for val- idity and dynamic correspondence, the RSA training session or testing protocol should resemble the work to rest ratio (W:R) and movement mechanics of the sport in question. What is less clear, are the physiological variables most responsible for improving RSA. This, coupled with how to report results, will be the topic of this review. For the pur- poses of this article, the term sprint refers to efforts of #6 seconds, whereby peak power/velocity could be main- tained throughout the repetition. This sprint duration is considered valid as a recent review of RSA by Spencer et al. (35) found that field-based team sports are consistent in mean sprint time and distance, 2–3 seconds and 10–20 m, respectively. THE BIOCHEMISTRY OF REPEAT SPRINT ABILITY To appreciate RSA, we must first look at the biochemical production of power. From a metabolic perspective, power is dictated by the rate at which adenosine triphosphate (ATP) is used to fuel mus- cle contractions. For example, sprint speed is related to the ability to deplete large amounts of high-energy phos- phates at a fast rate (20). Thus, power is a reflection of the intensity of muscle contraction and the rate at which ATP is being used (37). The human muscle typically stores 20–25 mmol/kg dry muscle of ATP, at a peak ATP turnover rate of around 15 mmol/kg dry muscle per second, which is enough to fuel 1–2 seconds of maximal work (17). In fact, ATP is never depleted (as it is used for basic cellular functioning too), depleting by 45% in a 30-second sprint (11) and between 14 and 32% in a 10-second sprint (24). As ATP stores are broken down, various metabolic pathways (energy systems) collaborate to resyn- thesize ATP and maintain peak rates of turnover. The contribution of each energy system is determined by exercise intensity and duration of rest period (18). The energy systems are phosphocrea- tine (PCr), anaerobic glycolysis, and the aerobic/oxidative system; these are briefly discussed in turn. PHOSPHOCREATINE There are around 80 mmol/kg dry muscle of PCr stored in the muscle (17) and with a turnover rate of around 9 mmol ATP/kg dry muscle per sec- ond (23); stores are largely depleted within 10 seconds of sprinting (18). However, as with ATP, because of the contribution made by the other pathways, PCr is not normally depleted. For example, more than 30 seconds PCr is only depleted by 60–80% (11), 10 seconds 40–70% (24), 6 seconds 30–55% (11), and 2.5 seconds (of elec- trical muscle stimulation) 26% (23); these results suggest that the ATP for short sprints is also heavily subsidized by anaerobic glycolysis. PCr is resynthesized by the aerobic system, and thus, its contribution to subsequent sprints is governed by the length of rest period; it resynthesizes at around 1.3 mmol/kg dry muscle per second (17). Approximately 84% of PCr stored are restored in 2 minutes, 89% in 4 minutes, and 100% in 8 minutes (19,22). Because the recov- ery of power output maps the time course of PCr resynthesis (10,30,33) and is attenuated by creatine supple- mentation (25,40), PCr availability is likely to be a major factor governing the rate of fatigue (18). ANAEROBIC GLYCOLYSIS During brief maximal sprints, the rapid drop in PCr is offset by increased acti- vation of glycolysis. Glycolysis describes the breakdown of glycogen in the muscle or glucose in the blood to resynthesize ATP. The maximal turnover rate of ATP production via K E Y W O R D S : multiple sprints; energy systems; recovery Copyright Ó National Strength and Conditioning Association Strength and Conditioning Journal | 37
  2. 2. glycolysis is around 5–9 mmol/kg dry muscle per second (17,23,24,28). This system involves multiple enzy- matic reactions, so it is not as fast as the PCr system, but the 2 combine to maintain an ATP turnover rate of 11–14 mmol/kg dry muscle per second (11,17). The rapid onset of anaerobic glycolysis with maximal work can be noted by studies that report high values (.4 mmol) of lactate within 10 seconds (11,24). Surprisingly, values as high as 40 mmol/kg dry muscle (16) and 4 mmol/kg dry muscle (23) have been recorded after just 6-second sprint cycling and 1.28 seconds of electrical stimulation, respectively. With intramuscular stores of around 300 mmol/kg dry muscle (17), glycogen availability is not likely to majorly com- promise ATP provision during repeated sprints (using protocols similar to current investigations) (18). Instead, it may be the progressive changes in metabolic environment (as noted by the aforemen- tioned high lactate values, also see “Fatigue” section) that ultimately cause a reduction in ATP provision via this system. For example, Gaitanos et al. (17), using 10 3 6-second sprints with 30-second rest periods, found that the first sprint produced ATP using 50% PCr and 44% glycolysis, whereas the tenth used 80% PCr and 16% glycolysis; this was accompanied by a 27% loss in power output, an 11.3 mmol/L increase in lactate, and a significant drop in ATP production rate (Table 1). Of note, in field-based team sports, glycogen- loading strategies are important in minimizing performance decrements (35). For example, in soccer, players with the lowest glycogen concentra- tion at half time covered less distance in the second half than those with the highest concentrations (31). How- ever, the significance of such loading may only become apparent as sprint frequency increases and rest periods become long enough to again fully engage anaerobic glycolysis. CAUSES OF FATIGUE The anaerobic conversion of pyru- vate yields lactate and H+ , not always lactic acid (the lactic acid molecule cannot exist at the physiological pH of 7); thus, despite the high correla- tion, lactate is not the cause of fatigue (12). In fact, lactate can be used as an energy substrate via gluconeogenesis (formation of glucose from noncarbo- hydrate sources), where it is trans- ported in the blood to the liver, referred to as the Cori cycle, or con- verted within the muscle fiber itself. It is likely that H+ accumulation via lac- tate formation decreases intracellular pH and inhibits glycolytic enzymes (such as phosphofructokinase) and the binding of calcium to troponin and thus muscle excitation-contrac- tion coupling (26). Glaister (18) sum- marizes that fatigue may also be a consequence of a lack of ATP for actin-myosin coupling, NA+ /K+ pumping, and Ca2+ uptake by the sar- coplasmic reticulum (SR). Also, intra- cellular Pi accumulation may interfere with muscle function by inhibiting Ca2+ release from SR, control actin- myosin cross-bridge interactions, and thereby regulate force production. AEROBIC METABOLISM This system contributes to ATP provi- sion sooner than commonly believed. For example, during the first 6 seconds of a 30-second maximal sprint (28) or the first 5 seconds of a 3-minute intense bout (.120% V̇O2max) (7), an ATP turnover rate of 1.3 mmol ATP/kg dry muscle per second and 0.7 mmol ATP/kg/s, respectively, was hypothe- sized, both contributing around 10% of total energy produced. If sprints are repeated, the V̇O2 of successive sprints will increase (17,35) if recovery periods are not sufficient to resynthesize PCr, oxidize lactate, and remove accumu- lated intracellular Pi (via adenosine diphosphate phosphorylation). How- ever, although V̇O2 uptake may increase with successive sprints, the supply of ATP made by the aerobic system is sig- nificantly less than required for repeated sprints (17) and uses a lower ATP turn- over rate. As such, although this could guard against a buildup of fatiguing by-products (and sprint frequency/ duration can be increased), it would not be able to sustain power output (i.e., sprint performance). RSA tested under hyperoxic (hypobaric chamber) (14,21) conditions or those with enhanced oxygen availability (via erythropoietin injection) (3) reports superior results; the opposite is true for hypoxic conditions (4). The consen- sus is that a greater quantity of PCr at the start of each sprint would reduce the demand on anaerobic glycolysis (and concomitant fatiguing by-products, e.g., H+ and Pi) and enhance ATP turnover (18). Glaister (18) concludes that the key role of the aerobic system during repeated sprints is the return to homeo- stasis during rest. The natural assump- tion is that aerobic endurance training, by virtue of increasing V̇O2max, will increase recovery rates and thus improve RSA; this is discussed later. Table 1 Estimates of ATP by Gaitanos et al. (17) after 10 3 6-second cycle sprints, with 30-second rest periods ATP production (mmol/kg dry muscle) ATP production rate (mmol/kg dry muscle/s) Sprint 1 Sprint 10 Sprint 1 Sprint 10 Total 89.3 6 13.4 31.6 6 14.7 14.9 6 2.2 5.3 6 2.5 PCr 44.3 6 4.7 25.3 6 9.7 7.4 6 0.8 4.2 6 1.6 Glycolysis 39.4 6 9.5 5.1 6 8.9 6.6 6 1.6 0.9 6 1.5 Repeat Sprint Ability VOLUME 35 | NUMBER 1 | FEBRUARY 201338
  3. 3. SPRINT DURATION, RECOVERY TIME, AND REPEAT SPRINT ABILITY In summary, maximal effort sprints rely on a fast and constant turnover of ATP, powered by the PCr system and anaer- obic glycolysis (17). As such, sprint speed is related to the ability to deplete large amounts of high-energy phos- phates at a fast rate. If performance is to be maintained across successive sprints, rest periods must be sufficient enough to allow the aerobic system to resynthesize PCr, remove accumulated intracellular inorganic phosphate (Pi), and oxidize lactate. It is clear that sprint duration, recovery time, and their inter- action affect RSA and energy system contribution. For example, sprints of around 5 seconds performed every 120 seconds show no significant de- creases in performance after 15 sprints. Only when recovery is reduced to 90 seconds does fatigue significantly affect sprint time, but this is only after the 11th sprint (5). Also, Balsom et al. (6) found that 40 3 15-m sprints (around 2.6 seconds), with 30-second rest, could be completed without any reduction in performance. However, 30-m (4.5 sec- onds) and 40-m (6 seconds) sprint times increased significantly, and after only the third 40-m sprint, times were already significantly longer. TRAINING REPEAT SPRINT ABILITY Having discussed the biochemical fac- tors governing RSA, the aim of the fol- lowing sections is to briefly outline how we can train to improve RSA: whether increasing aerobic power (V̇O2max), anaerobic power (speed/strength/ power), or lactate threshold is beneficial. This will be followed by suggestions for reporting results from RSA testing pro- tocols and the requirements for future research within this area. V̇O2MAX Because rest periods are often too short, the assumption is that a higher aerobic capacity (V̇O2max) will lead to quicker recovery and thus improved RSA. However, there are conflicting findings regarding this relationship, which appear largely attributable to the RSA test used. For example, a mod- erate correlation (r 5 20.35) between V̇O2max and RSA was found when using 8 3 40-m sprints with 30 seconds of active recovery between sprints (1) but not 6 3 20-m sprints with 20 sec- onds of recovery between sprints (2). The discrepancy is likely attributable to the length of the sprints used, as this may alter the contribution of the aero- bic system (5). In essence, V̇O2max has not been reported to relate to RSA when sprints of less than 40 m (or 6 sec- onds) have been used (15). Also, in protocols using W:R $ 1:5, there may be sufficient recovery provided for the aerobic system to resynthesize ATP and PCr despite fitness levels. Although the issue of whether RSA is affected by a high V̇O2max seems dependent on the protocol used, one must consider the validity of the tests to the sport in question (discussed later: see “Ecological Validity and Future Research” section). LACTATE THRESHOLD Most studies use V̇O2max as the major indicator of aerobic fitness. However, because V̇O2max is largely determined by central factors (8), RSA may more strongly correlate with peripheral fac- tors (35). For example, Da Silva et al. (15) showed that an RSA test consist- ing of 7 3 35-m sprints (involving a change of direction), and a between- sprint recovery period of 25 seconds, produced high values of lactate (15.4 6 2.2 mmol/L), thus demonstrating the large contribution of anaerobic glycoly- sis. Logically, Da Silva et al. (15) found that the velocity at onset of blood lac- tate accumulation (vOBLA) better cor- related with RSA performance (r 5 20.49); vOBLA reflects peripheral aer- obic training adaptations and is associ- ated with an increased capillary density and capacity to transport lactate and H+ ions (9,39). Therefore, to improve RSA, it appears prudent to target the devel- opment of vOBLA. ANAEROBIC POWER Da Silva et al. (15) (protocol aforemen- tioned) and Pyne et al. (29) (using 6 3 30-m sprints with 20-second rest) found that the strongest predictor of RSA was anaerobic power, that is, the fastest individual sprint time, and this explained 78% of the variance and had a relationship (r) of 0.66, respectively. Results suggest that in addition to training targeting the improvement of vOBLA, it should also focus on improving sprint speed, strength, and power. Also, type II mus- cle fibers contain higher amounts of PCr than type I (32), suggesting that individuals with a greater percentage of fast-twitch fibers (either through genetics or through high-intensity training) may be able to replenish ATP faster via the PCr system when working anaerobically. ECOLOGICAL VALIDITY AND FUTURE RESEARCH Although mean values for W:R are available, they do not suggest the typ- ical movement patterns. This is likely to have a significant effect, as changes in direction, especially those involving large eccentric contractions and the need to stop, will affect energy expen- diture. Also, most studies investigating RSA use passive rest during recovery periods (35) despite active recovery, showing more promise in reducing the drop in performance. For example, an active recovery (versus passive) con- sisting of cycling at submaximal inten- sities significantly increased peak power using 8 3 6-second cycle sprints with 30-second rest (34). The active recovery may have reduced muscle aci- dosis by speeding up the removal of lactate from the working muscles, and this would also increase its use as a fuel source (34). Because the majority of field-based team sports involve active recovery, its athletes may indi- rectly be employing this method (35). Another significant issue with the val- idity of RSA testing is the fact that the players from most sports are expected to maintain RSA over many more sprints than the number used in many of the current protocols. Also, sprints are not done with a unique and constant W:R. Therefore, the significance of a high V̇O2max may be more important only after a certain number of sprints (38). Strength and Conditioning Journal | 39
  4. 4. Logically, researchers are skeptical to conclude that V̇O2max is not an impor- tant variable to RSA until protocols of match duration are performed (13). REPORTING RESULTS The method of data analysis for RSA testing is largely a question of 2 alter- natives: reporting total (or mean) sprint time for all sprints or the rate of fatigue (or performance drop-off). The latter can be reported by 1 of 2 methods: sprint decrement (Sdec) or the fatigue index (FI). The formula (Equations 1 and 2) for each, according to Spencer et al. (35), is listed below. Unlike the FI, the Sdec takes into account all sprints and is less influenced by a good or bad start or finish (35). Sdec ð%Þ 5 ð½S1 þ S2 þ S3 þ . þ SfinalŠ=S1 3 number of sprints Á 2 1 3 100 ð1Þ FI ð%Þ 5 ð½Sslowest 2 SfastestŠ=Sfastest Á 3 100: (2) To improve reliability, Spencer et al. (35) advise that 5 minutes before test- ing, athletes complete a single criterion sprint. During the first sprint, athletes must achieve at least 95% of this score. Should they fail, the test is terminated and restarted after another 5-minute break. Although total (or mean) sprint time demonstrates good reliability (CV, , 3%), indices of fatigue are much less reliable (CVs, 11–50%); therefore, the former should be used (27,36). CONCLUSIONS Sprint speed is related to the ability to deplete large amounts of high-energy phosphates at a fast rate. This is fueled by the PCr system and anaerobic glycolysis. Significant involvement (.10%) from the aerobic system would reduce ATP production rate and thus sprint speed. However, the ability to sprint repeatedly in quick succession is determined by the aerobic system’s ability to resynthesize PCr, remove accumulated intracellular Pi, and oxidize lactate during rest periods. Whether this ability can be appreciably improved via a high V̇O2max still remains controver- sial. It is likely that sports that require repeated high-intensity efforts over a prolonged period, in which athletes are required to cover .40 meters per interval and regularly produce efforts in excess of 6 seconds, would indeed benefit from training targeting its devel- opment. Based on the above, RSA (as tested by the studies presented) can be improved via anaerobic qualities such as strength, power, and speed, along with the athlete’s vOBLA; this is regardless of the between-sport variabil- ity in RSA demands. When reporting RSA test results, total or mean time should be used. Conflicts of Interest and Source of Funding: The authors report no conflicts of interest and no source of funding. REFERENCES 1. Aziz AR, Chia M, and Teh KC. The relationship between maximal oxygen uptake and repeated sprint performance indices in field hockey and soccer players. J Sports Med Phys Fitness 40: 195–200, 2000. 2. Aziz AR, Mukherjee S, Chia M, and Teh KC. Relationship between measured maximal oxygen uptake and aerobic endurance performance with running repeated sprint ability in young elite soccer players. J Sports Med Phys Fitness 7: 401–407, 2007. 3. Balsom P, Ekblom B, and Sjo¨din B. Enhanced oxygen availability during high intensity intermittent exercise decreases anaerobic metabolite concentrations in blood. Acta Physiol Scand 150: 455–456, 1994. 4. Balsom P, Gaitanos D, Ekblom B, and Sjo¨din B. Reduced oxygen availability during high intensity intermittent exercise impairs performance. Acta Physiol Scand 152: 279–285, 1994. 5. Balsom P, Seger J, Sjo¨din B, and Ekblom B. Maximal-intensity intermittent exercise: Effect of recovery duration. Int J Sports Med 13: 528–533, 1992. 6. Balsom PD, Seger YJ, Sjo¨din B, and Ekblom B. Physiological responses to maximal intensity intermittent exercise. Eur J Appl Physiol Occup Physiol 65: 144–149, 1992. 7. Bangsbo J, Krustrup P, Gonza´lez-Alonso J, and Saltin B. ATP production and efficiency of human skeletal muscle during intense exercise: Effect of previous exercise. Am J Physiol Endocrinol Metab 280: E956–E964, 2001. 8. Basset DR and Howley ET. Limiting factors for maximum oxygen uptake and determinants of endurance performance. Med Sci Sports Exerc 32: 70–84, 2000. 9. Billat VL, Sirvent P, Py G, Koralsztein JP, and Mercier J. The concept of maximal lactate steady state. Sport Med 33: 406–426, 2003. 10. Bogdanis GC, Nevill ME, Boobis LH, Lakomy HK, and Nevill AM. Recovery of power output and muscle metabolites following 30 s of maximal sprint cycling in man. J Physiol 482: 467–480, 1995. 11. Boobis LH, Williams C, and Wooton SA. Human muscle metabolism during brief maximal exercise in man. J Physiol 338: 21–22, 1982 12. Brooks GA, Fahey TD, and Baldwin KM. Exercise Physiology: Human Bioenergetics and Its Applications (4th ed). New York, NY: McGraw-Hill Higher Education, 2005. 13. Castagna C, Manzi V, D’Ottavio S, Annino G, Padua E, and Bishop D. Relation between maximal aerobic power and the ability to repeat sprints in young basketball players. J Strength Cond Res 21: 1172–1176, 2007. 14. Fulco CS, Lewis SF, Frykman PN, Boushel R, Smith S, Harman EA, Cymerman A, and Pandolf KB. Muscle fatigue and exhaustion during dynamic leg exercise in normoxia and hypobaric hypoxia. J Appl Physiol 81: 1891–1900, 1996. 15. Da Silva JF, Guglielmo LGA, and Bishop D. Relationship between different measures of aerobic fitness and repeated sprint ability in elite soccer players. J Strength Cond Res 24: 2115–2121, 2010. 16. Dawson B, Goodman C, Lawrence S, Preen D, Polglaze T, Fitzsimons M, and Fournier P. Muscle phosphocreatine repletion following single and repeated short sprint efforts. Scand J Med Sci Sports 7: 206–213, 1997. 17. Gaitanos GC, Williams C, Boobis LH, and Brooks S. Human muscle metabolism during intermittent maximal exercise. J Appl Physiol 75: 712–719, 1993. 18. Glaister M. Multiple sprint work: Physiological responses, mechanisms of fatigue and the influence of aerobic fitness. Sports Med 35: 757–777, 2005. Repeat Sprint Ability VOLUME 35 | NUMBER 1 | FEBRUARY 201340
  5. 5. 19. Harris RC, Edward RH, Hultman E, Nordesjo LO, Nylind B, and Sahlin K. The time course of phosphorylcreatine resynthesis during recovery of the quadriceps muscle in man. Pflu¨gers Arch 367: 137–142, 1976. 20. Hirvonen J, Rehunen S, Rusko H, and Ha¨rko¨nen M. Breakdown of high-energy phosphate compounds and lactate accumulation during short supramaximal exercise. Eur J Appl Physiol Occup Physiol 56: 253–259, 1987. 21. Hogan MC, Kohin S, Stary CMT, and Hepple RT. Rapid force recovery in contracting skeletal muscle after brief ischemia is dependent on O2 availability. J Appl Physiol 87: 2225–2229, 1999. 22. Hultman E, Bergstrom J, and Anderson NM. Breakdown and resynthesis of phosphorylcreatine and adenosine triphosphate in connection with muscular work in man. Scand J Clin Lab Invest 19: 56–66, 1967. 23. Hultman E and Sjo¨holm H. Energy metabolism and contraction force of human skeletal muscle in situ during electrical stimulation. J Physiol 345: 525–532, 1983. 24. Jones NL, McCartney N, Graham T, Spriet LL, Kowalchuk JM, Heigenhauser GJ, and Sutton JR. Muscle performance and metabolism in maximal isokinetic cycling at slow and fast speeds. J Appl Physiol 59: 132–136, 1985. 25. Mujika I, Padilla S, Adilla S, Ibanez J, Izquierdo I, and Gorostiaga E. Creatine supplementation and sprint performance in soccer players. Med Sci Sports Exerc 32: 518–525, 2000. 26. Nakamaru Y and Schwartz A. The influence of hydrogen ion concentration on calcium binding and release by skeletal muscle sarcoplasmic reticulum. J Gen Physiol 59: 22–32, 1972. 27. Oliver JL. Is a fatigue index a worthwhile measure of repeated sprint ability? J Sci Med Sport 12: 20–23, 2009. 28. Parolin ML, Chesley A, Matsos MP, Spriet LL, Jones NL, and Heigenhauser GJF. Regulation of skeletal muscle glycogen phosphorylase and PDH during maximal intermittent exercise. Am J Physiol Endocrinol Metab 277: E890–E900, 1999. 29. Pyne DB, Saunders PU, Montgomery PG, Hewitt AJ, and Sheehan K. Relationships between repeated sprint testing, speed, and endurance. J Strength Cond Res 22: 1633–1637, 2008. 30. Sahlin K and Ren JM. Relationship of contraction capacity to metabolic changes during recovery from a fatiguing contraction. J Appl Physiol 67: 648–654, 1989. 31. Saltin B. Metabolic fundamentals in exercise. Med Sci Sports 5: 137–146, 1973. 32. Sant’Ana Pereira JA, Sargeant AJ, Rademaker AC, de Haan A, and van Mechelen W. Myosin heavy chain isoform expression and high energy phosphate content in human muscle fibres at rest and post-exercise. J Physiol 496: 583–588, 1996. 33. Sargeant AJ and Dolan P. Effect of prior exercise on maximal short-term power output in humans. J Appl Physiol 63: 1475–1480, 1987. 34. Signorile JF, Tremblay LM, and Ingalls C. The effects of active and passive recovery on short-term, high intensity power output. Can J Appl Physiol 18: 31–42, 1993. 35. Spencer M, Bishop D, Dawson B, and Goodman C. Physiological and metabolic responses of repeated-sprint activities: Specific to field-based team sports. Sports Med 35: 1025–1044, 2005. 36. Spencer M, Fitzsimons M, and Dawson B. Reliability of a repeated sprint test for field- hockey. J Sci Med Sport 9: 181–184, 2006. 37. Stone MH, Stone M, and Sands W. Principles and Practice of Resistance Training. Champaign, IL: Human Kinetics, 2009. 38. Thebault N, Leger LA, and Passelergue P. Repeated-sprint ability and aerobic fitness. J Strength Cond Res 25: 2857–2865, 2011. 39. Thomas C, Sirvent P, Perrey S, Raynaud E, and Mercier J. Relationships between maximal muscle oxidative capacity and blood lactate removal after supramaximal exercise and fatigue indexes in humans. J Appl Physiol 97: 2132–2138, 2004. 40. Yquel RJ, Arsac LM, Thiaudiere E, Canioni P, and Manier G. Effect of creatine supplementation on phosphocreatine resynthesis, inorganic phosphate accumulation and pH during intermittent maximal exercise. J Sports Sci 20: 427–437, 2002. Strength and Conditioning Journal | 41