This document discusses factors that influence an athlete's ability to perform repeated sprint efforts, known as repeat sprint ability (RSA). It covers the biochemical pathways and energy systems involved in sprinting and recovery between sprints. Phosphocreatine (PCr) and anaerobic glycolysis provide energy for initial sprints, while the aerobic system is important for recovery. The duration of sprints and recovery periods impact which energy systems can replenish between efforts. While a high aerobic capacity (VO2max) may aid recovery to some degree, RSA seems more closely tied to anaerobic qualities like speed, power, and the velocity at lactate threshold. Reporting total or mean sprint times is recommended when assessing RSA test

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 | www.nsca-scj.com 37

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. 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 | www.nsca-scj.com 39

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. 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 | www.nsca-scj.com 41