Repeat sprint ability (RSA) describes the ability of an athlete to recover and maintain maximal effort during subsequent sprints, an attribute considered important to team sports. It is often trained and measured via high-intensity sprints, interspersed with brief recovery bouts (≤30 seconds). Most strength and conditioning coaches agree that for validity 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 purposes of this article, the term sprint refers to efforts of ≤6 seconds, whereby peak power/velocity could be maintained 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 muscle contractions. For example, sprint speed is related to the ability to deplete large amounts of high-energy phosphates 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 resynthesize 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 phosphocreatine (PCr), anaerobic glycolysis, and the aerobic/oxidative system; these are briefly discussed in turn.
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 second (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 electrical 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 recovery of power output maps the time course of PCr resynthesis (10,30,33) and is attenuated by creatine supplementation (25,40), PCr availability is likely to be a major factor governing the rate of fatigue (18).
During brief maximal sprints, the rapid drop in PCr is offset by increased activation 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 glycolysis is around 5–9 mmol/kg dry muscle per second (17,23,24,28). This system involves multiple enzymatic 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 compromise 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 aforementioned 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 × 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 concentration at half time covered less distance in the second half than those with the highest concentrations (31). However, 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 pyruvate yields lactate and H+, not always lactic acid (the lactic acid molecule cannot exist at the physiological pH of 7); thus, despite the high correlation, lactate is not the cause of fatigue (12). In fact, lactate can be used as an energy substrate via gluconeogenesis (formation of glucose from noncarbohydrate sources), where it is transported in the blood to the liver, referred to as the Cori cycle, or converted within the muscle fiber itself. It is likely that H+ accumulation via lactate formation decreases intracellular pH and inhibits glycolytic enzymes (such as phosphofructokinase) and the binding of calcium to troponin and thus muscle excitation-contraction coupling (26). Glaister (18) summarizes that fatigue may also be a consequence of a lack of ATP for actin-myosin coupling, NA+/K+ pumping, and Ca2+ uptake by the sarcoplasmic reticulum (SR). Also, intracellular Pi accumulation may interfere with muscle function by inhibiting Ca2+ release from SR, control actin-myosin cross-bridge interactions, and thereby regulate force production.
This system contributes to ATP provision 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% V[Combining Dot Above]O2max) (7), an ATP turnover rate of 1.3 mmol ATP/kg dry muscle per second and 0.7 mmol ATP/kg/s, respectively, was hypothesized, both contributing around 10% of total energy produced. If sprints are repeated, the V[Combining Dot Above]O2 of successive sprints will increase (17,35) if recovery periods are not sufficient to resynthesize PCr, oxidize lactate, and remove accumulated intracellular Pi (via adenosine diphosphate phosphorylation). However, although V[Combining Dot Above]O2 uptake may increase with successive sprints, the supply of ATP made by the aerobic system is significantly less than required for repeated sprints (17) and uses a lower ATP turnover 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 consensus 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 homeostasis during rest. The natural assumption is that aerobic endurance training, by virtue of increasing V[Combining Dot Above]O2max, will increase recovery rates and thus improve RSA; this is discussed later.
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 anaerobic glycolysis (17). As such, sprint speed is related to the ability to deplete large amounts of high-energy phosphates 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 interaction affect RSA and energy system contribution. For example, sprints of around 5 seconds performed every 120 seconds show no significant decreases 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 × 15-m sprints (around 2.6 seconds), with 30-second rest, could be completed without any reduction in performance. However, 30-m (4.5 seconds) 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 factors governing RSA, the aim of the following sections is to briefly outline how we can train to improve RSA: whether increasing aerobic power (V[Combining Dot Above]O2max), anaerobic power (speed/strength/power), or lactate threshold is beneficial. This will be followed by suggestions for reporting results from RSA testing protocols and the requirements for future research within this area.
V[Combining Dot Above]O2MAX
Because rest periods are often too short, the assumption is that a higher aerobic capacity (V[Combining Dot Above]O2max) 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 moderate correlation (r = −0.35) between V[Combining Dot Above]O2max and RSA was found when using 8 × 40-m sprints with 30 seconds of active recovery between sprints (1) but not 6 × 20-m sprints with 20 seconds 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 aerobic system (5). In essence, V[Combining Dot Above]O2max has not been reported to relate to RSA when sprints of less than 40 m (or 6 seconds) 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 V[Combining Dot Above]O2max 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).
Most studies use V[Combining Dot Above]O2max as the major indicator of aerobic fitness. However, because V[Combining Dot Above]O2max is largely determined by central factors (8), RSA may more strongly correlate with peripheral factors (35). For example, Da Silva et al. (15) showed that an RSA test consisting of 7 × 35-m sprints (involving a change of direction), and a between-sprint recovery period of 25 seconds, produced high values of lactate (15.4 ± 2.2 mmol/L), thus demonstrating the large contribution of anaerobic glycolysis. Logically, Da Silva et al. (15) found that the velocity at onset of blood lactate accumulation (vOBLA) better correlated with RSA performance (r = −0.49); vOBLA reflects peripheral aerobic training adaptations and is associated 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 development of vOBLA.
Da Silva et al. (15) (protocol aforementioned) and Pyne et al. (29) (using 6 × 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 muscle 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 typical 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 expenditure. 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) consisting of cycling at submaximal intensities significantly increased peak power using 8 × 6-second cycle sprints with 30-second rest (34). The active recovery may have reduced muscle acidosis 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 indirectly be employing this method (35).
Another significant issue with the validity 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 V[Combining Dot Above]O2max may be more important only after a certain number of sprints (38). Logically, researchers are skeptical to conclude that V[Combining Dot Above]O2max is not an important variable to RSA until protocols of match duration are performed (13).
The method of data analysis for RSA testing is largely a question of 2 alternatives: 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).
To improve reliability, Spencer et al. (35) advise that 5 minutes before testing, 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).
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 V[Combining Dot Above]O2max still remains controversial. 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 development. 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 variability in RSA demands. When reporting RSA test results, total or mean time should be used.
1. Aziz AR, Chia M, 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, 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, Sjödin 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, Sjödin B. Reduced oxygen availability during high intensity intermittent exercise impairs performance. Acta Physiol Scand 152: 279–285, 1994.
5. Balsom P, Seger J, Sjödin B, Ekblom B. Maximal-intensity intermittent exercise: Effect of recovery
duration. Int J Sports Med 13: 528–533, 1992.
6. Balsom PD, Seger YJ, Sjödin B, Ekblom B. Physiological responses to maximal intensity intermittent exercise. Eur J Appl Physiol Occup Physiol 65: 144–149, 1992.
7. Bangsbo J, Krustrup P, González-Alonso J, 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, 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, Mercier J. The concept of maximal lactate steady state. Sport Med 33: 406–426, 2003.
10. Bogdanis GC, Nevill ME, Boobis LH, Lakomy HK, 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, Wooton SA. Human muscle metabolism during brief maximal exercise in man. J Physiol 338: 21–22, 1982
12. Brooks GA, Fahey TD, 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, 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, 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, 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, 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, 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.
19. Harris RC, Edward RH, Hultman E, Nordesjo LO, Nylind B, Sahlin K. The time course of phosphorylcreatine resynthesis during recovery
of the quadriceps muscle in man. Pflügers Arch 367: 137–142, 1976.
20. Hirvonen J, Rehunen S, Rusko H, Härkönen 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, 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, 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, Sjöholm 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, 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, Gorostiaga E. Creatine supplementation and sprint performance in soccer players. Med Sci Sports Exerc 32: 518–525, 2000.
26. Nakamaru Y, 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, 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, Sheehan K. Relationships between repeated sprint testing, speed, and endurance. J Strength Cond Res 22: 1633–1637, 2008.
30. Sahlin K, 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, 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, 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, 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, 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, Dawson B. Reliability of a repeated sprint test for field-hockey. J Sci Med Sport 9: 181–184, 2006.
37. Stone MH, Stone M, Sands W. Principles and Practice of Resistance Training. Champaign, IL: Human Kinetics, 2009.
38. Thebault N, Leger LA, 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, 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, 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.