Repeated-Sprint Ability Part II: Recommendations for Training

Abstract

Short-duration sprints, interspersed with brief recoveries, are common during most team sports. The ability to produce the best possible average sprint performance over a series of sprints (≤10 seconds), separated by short (≤60 seconds) recovery periods has been termed repeated-sprint ability (RSA). RSA is therefore an important fitness requirement of team-sport athletes, and it is important to better understand training strategies that can improve this fitness component. Surprisingly, however, there has been little research about the best training methods to improve RSA. In the absence of strong scientific evidence, two principal training theories have emerged. One is based on the concept of training specificity and maintains that the best way to train RSA is to perform repeated sprints. The second proposes that training interventions that target the main factors limiting RSA may be a more effective approach. The aim of this review (Part II) is to critically analyse training strategies to improve both RSA and the underlying factors responsible for fatigue during repeated sprints (see Part I of the preceding companion article). This review has highlighted that there is not one type of training that can be recommended to best improve RSA and all of the factors believed to be responsible for performance decrements during repeated-sprint tasks. This is not surprising, as RSA is a complex fitness component that depends on both metabolic (e.g. oxidative capacity, phosphocreatine recovery and H+ buffering) and neural factors (e.g. muscle activation and recruitment strategies) among others. While different training strategies can be used in order to improve each of these potential limiting factors, and in turn RSA, two key recommendations emerge from this review; it is important to include (i) some training to improve single-sprint performance (e.g. 'traditional' sprint training and strength/power training); and (ii) some high-intensity (80-90% maximal oxygen consumption) interval training to best improve the ability to recover between sprints. Further research is required to establish whether it is best to develop these qualities separately, or whether they can be developed concurrently (without interference effects). While research has identified a correlation between RSA and total sprint distance during soccer, future studies need to address whether training-induced changes in RSA also produce changes in match physical performance.

Full text

Repeated-Sprint Ability –Part II
Recommendations for Training
David Bishop,
1
Olivier Girard
2
and Alberto Mendez-Villanueva
3
1 Institute of Sport, Exercise and Active Living (ISEAL), School of Sport and Exercise Science,
Victoria University, Melbourne, VIC, Australia
2 ASPETAR –Qatar Orthopaedic and Sports Medicine Hospital, Research and Education Centre,
Doha, Qatar
3 Physiology Unit, Sport Science Department, ASPIRE Academy for Sport Excellence, Doha, Qatar
Contents
Abstract................................................................................. 741
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 742
2. Training the Limiting Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 743
2.1 Energy Supply. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 743
2.1.1 Phosphocreatine Resynthesis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 743
2.1.2 Anaerobic Glycolysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 744
2.1.3 Aerobic Metabolism. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 745
2.2 H
+
Accumulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 745
2.3 Muscle Activation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 747
3. Specific Training Strategies and Repeated-Sprint Ability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 748
3.1 Repeated-Sprint Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 748
3.2 Sprint Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 750
3.3 Small-Sided Games . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 750
3.4 Resistance Training . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 751
4. Conclusions........................................................................... 752
Abstract Short-duration sprints, interspersed with brief recoveries, are common
during most team sports. The ability to produce the best possible average
sprint performance over a series of sprints (£10 seconds), separated by short
(£60 seconds) recovery periods has been termed repeated-sprint ability
(RSA). RSA is therefore an important fitness requirement of team-sport
athletes, and it is important to better understand training strategies that can
improve this fitness component. Surprisingly, however, there has been little
research about the best training methods to improve RSA. In the absence of
strong scientific evidence, two principal training theories have emerged. One
is based on the concept of training specificity and maintains that the best way
to train RSA is to perform repeated sprints. The second proposes that
training interventions that target the main factors limiting RSA may be a
more effective approach. The aim of this review (Part II) is to critically ana-
lyse training strategies to improve both RSA and the underlying factors
responsible for fatigue during repeated sprints (see Part I of the preceding
REVIEW ARTICLE Sports Med 2011; 41 (9): 741-756
0112-1642/11/0009-0741/$49.95/0
ª2011 Adis Data Information BV. All rights reserved.

companion article). This review has highlighted that there is not one type of
training that can be recommended to best improve RSA and all of the factors
believed to be responsible for performance decrements during repeated-sprint
tasks. This is not surprising, as RSA is a complex fitness component that
depends on both metabolic (e.g. oxidative capacity, phosphocreatine recovery
and H
+
buffering) and neural factors (e.g. muscle activation and recruitment
strategies) among others. While different training strategies can be used in
order to improve each of these potential limiting factors, and in turn RSA,
two key recommendations emerge from this review; it is important to include
(i) some training to improve single-sprint performance (e.g. ‘traditional’
sprint training and strength/power training); and (ii) some high-intensity
(80–90%maximal oxygen consumption) interval training to best improve the
ability to recover between sprints. Further research is required to establish
whether it is best to develop these qualities separately, or whether they can be
developed concurrently (without interference effects). While research has
identified a correlation between RSA and total sprint distance during soccer,
future studies need to address whether training-induced changes in RSA also
produce changes in match physical performance.
1. Introduction
Short-duration sprints (£10 seconds), inter-
spersed with brief recovery periods, are common
during most team sports.
[1]
The ability to produce
the best possible average sprint performance over a
series of sprints, separated by short (£60 seconds)
recovery periods, is therefore important for all
team-sport athletes and has been termed re-
peated-sprint ability (RSA). While RSA is often
equated with a low fatigue index (i.e. the de-
crease in performance from the first to the last
sprint), it is important to note that a good RSA
is better described by a high average sprint per-
formance, with or without a low fatigue index
(e.g. a marathon runner with a low average sprint
performance, but a very low fatigue index, would
not be classified as having good repeated-sprint
ability) [see also Part I of the preceding compa-
nion article
[2]
]. Mean time recorded during an
RSA test predicts the distance of high-intensity
running (>19.8 km/h), and the total sprint dis-
tance during a professional soccer match.
[3]
This suggests that improving RSA should result
in greater team-sport physical performance, and
that it is important to better understand train-
ing strategies that can enhance this fitness
component.
Recently, there has been an increase in scien-
tific research regarding the importance of RSA
for team- and racket-sport athletes.
[1,3-7]
Sur-
prisingly, however, there has been little research
about the best training methods to improve this
fitness component.
[8]
In the absence of strong
scientific evidence, one concept that has emerged
is that the best way to train RSA may be to per-
form repeated sprints.
[9]
While such a concept
appeals to the concept of training specificity, the
scientific evidence in support of this approach is
currently lacking. Indeed, many studies have re-
ported significant improvements in RSA with
more generic training (e.g. interval training).
[9-12]
The aim of this review is to critically analyse
training strategies to improve both RSA and the
underlying factors responsible for fatigue during
repeated sprints.
In order to obtain the necessary articles for this
review, several databases were searched includ-
ing SportDiscus

, PubMed, Web of Science,
MEDLINE and Google Scholar. Key search terms
used included ‘repeated-sprint ability’, ‘repeated-
sprint exercise’, ‘multiple sprints’, ‘team sports’,
‘training’, ‘rugby’, ‘soccer’, ‘football’, ‘basket-
ball’, ‘conditioning’, ‘endurance’ and ‘small-sided
games’. Manual searches were also made using
the reference lists from recovered articles. Due to
742 Bishop et al.
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

the small number of articles relating to training
and RSA, there was no limit to the search period.
2. Training the Limiting Factors
During repeated-sprint exercise (RSE), the
inability to reproduce performance across sprint
repetitions (fatigue) is manifested by a decline in
sprint speed (i.e. increased time to cover a fixed
distance) or peak/mean power output. Proposed
factors responsible for these performance decre-
ments have previously been reviewed
[13]
(see also
Part I of this review
[2]
) and include limitations to
energy supply (e.g. phosphocreatine resynthesis,
aerobic and anaerobic glycolysis) and metabolite
accumulation (e.g. inorganic phosphate [P
i
], H
+
).
Increasing evidence suggests that failure to fully
activate the contracting muscle may also limit
repeated-sprint performance.
[14,15]
Training inter-
ventions that are able to lessen the influence of
these limiting factors should improve RSA.
2.1 Energy Supply
2.1.1 Phosphocreatine Resynthesis
As the brief recovery times between repeated
sprints will lead to only a partial restoration of
phosphocreatine stores,
[16,17]
it has been proposed
that the ability to resynthesize phosphocreatine
may be an important determinant of the ability to
reproduce sprint performance.
[17,18]
In line with
this proposition, strong relationships have been
reported between phosphocreatine resynthesis
and the recovery of performance during both re-
peated, 30-second, all-out exercise bouts
[17,18]
and
repeated 6-second sprints (Mendez-Vallanueva A.
et al., unpublished data). These findings suggest
that the performance of repeated sprints may be
improved by training interventions that increase
the rate of phosphocreatine resynthesis.
The oxidative metabolism pathways are es-
sential for phosphocreatine resynthesis during
the recovery from high-intensity exercise.
[19]
This
suggests that individuals with an elevated aerobic
fitness (i.e. high maximal oxygen consumption
[.
VO
2max
] or lactate threshold) should be able to
more rapidly resynthesize phosphocreatine be-
tween repeated sprints. Indeed, cross-sectional re-
search
[17,20-23]
and one training study
[24]
support
the hypothesis that endurance training enhances
phosphocreatine resynthesis following low-intensity
exercise. Recently, it has also been reported that
high-intensity interval training (6–12 ·[2 minutes
at ~100%.
VO
2max
: 1 minute rest]), can signif-
icantly improve phosphocreatine resynthesis dur-
ing the first 60 seconds following high-intensity
exercise (figure 1).
[25]
In contrast, no changes in
the rate of phosphocreatine resynthesis have been
reported following interval (8 ·[30 seconds at
†
*†
†
†
Rest
45
50
55
PCr content (mmoL/kg dw)
60
65
70
75
80
85
90
Post-ex
Timepoint
Post-60 sec Post-180 sec
Post-train
Pre-train
Fig. 1. Changes in resting and post-exercise phosphocreatine (PCr) content following high-intensity interval training (
[25]
and Bishop D. et al.,
unpublished research). dw =dry weight;
*
indicates significantly different from pre train; -indicates significantly different from rest.
Training to Improve Repeated-Sprint Ability 743
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

~130%.
VO
2max
: 90 seconds rest]), or intermittent-
sprint training (15 ·[6-second sprint: 1-minute
jog recovery]),
[12]
or training involving repeated,
30-second, all-out efforts (4–7·[30 seconds ‘all-
out’: 3–4 minutes rest]).
[26]
These results can possibly
be attributed to the absence of significant changes
in aerobic fitness (as measured by .
VO
2max
) with
these types of training. Alternatively, these results
may be related to the fact that these studies all
measured phosphocreatine resynthesis 3-minutes
post-exercise, a timepoint when phosphocreatine
resynthesis is largely complete and therefore less
likely to be influenced by training. Nonetheless,
while the optimal training intensity has not yet
been established, the limited research to date
suggests that improvements in aerobic fitness
may be required to improve phosphocreatine re-
synthesis. As repeated-sprint training has been
reported to increase aerobic fitness,
[4,27]
further
research is required to investigate whether this
type of training can also increase the fast com-
ponent (e.g. first 60 seconds) of phosphocreatine
resynthesis, and whether such changes are su-
perior to those observed following aerobic train-
ing (e.g. interval training
[25]
).
2.1.2 Anaerobic Glycolysis
The large drop in intramuscular phospho-
creatine, along with the concomitant rise in P
i
and
adenosine monophosphate, stimulates the rapid
activation of anaerobic glycolysis at the start of a
sprint.
[28]
As a consequence, anaerobic glycolysis
is an important source of adenosine triphosphate
(ATP) during a single sprint.
[29]
During subsequent
sprints however, there is a dramatic decrease in
the ATP production, via anaerobic glycolysis,
during sprint efforts that has been attributed
to the acidosis resulting from the maximal anaero-
bic degradation of glycogen during the early
sprints.
[18,30]
It is therefore unclear whether in-
creasing the maximal anaerobic glycogenolytic
and glycolytic rate will lead to improvements in
RSA. On one hand, it could be argued that
training that increases the ability to supply
ATP from anaerobic glycolysis would be detri-
mental to RSA due to the negative correlation
between anaerobic ATP production during the
first sprint and sprint decrement during a
repeated-sprint test.
[29,31]
On the other hand, it
also needs to be considered that subjects with a
greater glycogenolytic rate have also been re-
ported to have a greater initial sprint perfor-
mance,
[29]
and that researchers have reported a
strong positive correlation between initial sprint
performance and both final sprint perfor-
mance
[29]
and total sprint performance
[32,33]
during tests of RSA. Thus, while these findings
highlight the difficulties associated with inter-
preting contrasting effects on the various RSA
test measures,
[34]
they suggest that increasing the
anaerobic contribution is likely to improve both
initial and mean sprint performance, and thus the
ability to perform repeated sprints. It should be
noted, however, that some researchers have re-
ported significant increases in glycolytic enzymes
following sprint training without a corresponding
increase in sprint performance.
[35,36]
Further re-
search is therefore required to investigate the re-
lationship between improvements in anaerobic
ATP production and RSA.
As training does not increase the amount of
phosphocreatine breakdown during high-intensity
exercise,
[12,25,37]
changes in the ability to produce
ATP via anaerobic glycolysis are likely to be well
reflected by training-induced changes in indirect
measures of anaerobic capacity, such as maximal
accumulated oxygen deficit (MAOD). A high
rate of anaerobic energy release during exercise
has been proposed to be an important stimulus to
increase MAOD.
[38]
This is supported by increases
in MAOD in response to high-intensity (20–
120-second intervals at 100–200%.
VO
2max
),
[38-40]
but not moderate-intensity (60 minutes at 70%
.
VO
2max
) endurance training.
[40]
Furthermore,
the greatest changes in MAOD have typically
been reported in response to interval training that
produces large changes in blood lactate con-
centration (>10 mmol/L).
[38,40]
These results are
consistent with the observation that training-
induced changes in enzymes important for anae-
robic glycolysis (e.g. phosphofructokinase and
phosphorylase) are greater following training that
involves repeated 30-second bouts than repeated
6-second bouts
[41]
or continuous training.
[42]
In
the only study to date, 6 weeks of repeated-sprint
training did not increase phosphofructokinase
744 Bishop et al.
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

activity.
[43]
Greater increases in glycolytic enzymes
have typically been reported when high-intensity
intervals are separated by long (10–15 min-
ute),
[36,44]
rather than by short (£4 minute),
[45-47]
rest periods. This is consistent with the larger
increases in peak blood or muscle lactate when
30-second all-out efforts are separated by 10-
to 15-minute rest periods,
[35,48]
compared with
3–4-minute rest periods.
[37]
From this research, it
is difficult to determine whether this is an effect of
recovery duration per se, or the better mainten-
ance of exercise intensity with longer recoveries.
The above research suggests that to increase the
anaerobic performance of team-sport athletes
one should utilize short (20–30 second), high-
intensity (all-out) intervals separated by relatively
long rest periods (~10 minutes).
2.1.3 Aerobic Metabolism
Several physiological adaptations related to an
increased reliance on aerobic metabolism to re-
synthesize ATP, such as greater mitochondrial
respiratory capacity,
[49]
faster oxygen uptake ki-
netics,
[50,51]
an accelerated post-sprint muscle re-
oxygenation rate,
[52]
a higher lactate threshold
[53]
and a higher .
VO
2max,[51,54-57]
have been associated
with an enhanced ability to resist fatigue dur-
ing repeated sprints. The most studied factor is
.
VO
2max
that has been reported to be moderately
correlated (0.62 <r<0.68; p <0.05) with RSA (both
mean sprint performance and sprint decre-
ment).
[51,54-56]
Research has also shown that
subjects with a greater .
VO
2max[58]
have a superior
ability to resist fatigue during RSE, especially
during the latter stages of a repeated-sprint test
when subjects may reach their .
VO
2max
.
[59]
This
suggests that improving .
VO
2max
may allow for a
greater aerobic contribution to repeated sprints,
potentially improving RSA. However, research
also indicates that there is not a linear relation-
ship between .
VO
2max
and various repeated-sprint
fatigue indices.
[32,60]
Thus, it may be more im-
portant to develop an ‘optimal’, rather than a
maximal, .
VO
2max
. Further research is required to
determine what an appropriate level of .
VO
2max
is,
above which further increases may not be ac-
companied by comparable improvements in RSA.
In addition, the possible links between other aerobic
fitness indices (e.g. lactate threshold, economy,
oxygen kinetics, the velocity associated with
.
VO
2max
), which are relatively independent of the
.
VO
2max
, should be the subject of further research.
Many physiologists believe that it is the re-
duced muscle oxygen levels during training that
provide the stimulus to increase .
VO
2max
.
[61]
As
the oxygen level in the muscle decreases with in-
creases in exercise intensity up to 100%.
VO
2max
,
but does not decrease further once the exercise
intensity exceeds this point,
[62]
this suggests that
interval training at intensities that approximate
.
VO
2max
may be most effective for improving
.
VO
2max
. This is supported by previous studies
that have reported greater improvements in
.
VO
2max
after interval training (at approximately
the .
VO
2max
intensity) when compared with con-
tinuous training matched for total work.
[61,63-65]
It should be noted, however, that most of these
studies performed their continuous training
at very low intensities (£56%of the power at
.
VO
2max
).
[61,63,64]
When compared with con-
tinuous training performed at intensities >60%
of the power at .
VO
2max
, interval training has
been reported to produce similar improvement in
.
VO
2max
.
[66-69]
These results therefore suggest that
if a minimum training intensity is exceeded (>60%
of the power output at .
VO
2max
), and total work is
equivalent, the choice of either interval or con-
tinuous training will result in similar improve-
ments in .
VO
2max
. However, one advantage of
interval training is that it may concurrently de-
velop other factors (e.g. the rate of phosphocreatine
resynthesis
[25]
and muscle buffer capacity
[69]
).
The above research suggests that to increase the
aerobic fitness of team-sport athletes, one should
utilize high-intensity interval training (80–90%
of .
VO
2max
) interspersed with rest periods (e.g.
1 minute) that are shorter than the work periods
(e.g. 2 minutes).
2.2 H
+
Accumulation
It has been argued that the considerable in-
creases in muscle
[58,69,70]
and blood
[32,71]
H
+
accu-
mulation observed following sprinting may impair
repeated-sprint performance.
[72]
In support of
this, correlations have been observed between
Training to Improve Repeated-Sprint Ability 745
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

sprint decrement, and both muscle buffer capa-
city (Xm) and changes in muscle and blood
pH.
[32,54,55,58,73]
This suggests that RSA may be
improved by interventions that can increase the
removal of H
+
from the muscle.
[12,54,73]
The re-
moval of intracellular H
+
during intense skeletal
muscle contractions (such as repeated sprints)
occurs via intracellular buffering (bm
in vitro
) and
a number of different membrane transport sys-
tems, especially the monocarboxylate transpor-
ters (MCTs) [figure 2].
[74]
The MCTs appear to be
the dominant regulator of muscle pH during and
after high-intensity exercise.
[74]
A large increase in muscle H
+
and/or lactate
during exercise has been proposed to be an im-
portant stimulus for adaptations of the muscle
pH regulating systems.
[75]
This is supported by
increases in bm
in vitro
in response to high-intensity
interval training (6–10 ·[2 minutes at 120–140%
of the lactate threshold] :1 minute rest), but not
moderate-intensity, continuous training (~30 min-
utes at 80–95%lactate threshold).
[69]
However,
greater accumulation of lactate and H
+
during
training has not always been associated with
greater increases in MCTs
[12,76]
or bm
in vitro
.
[25]
Furthermore, research suggests that too large an
accumulation of H
+
during training (e.g. interval
training performed at intensities >100%.
VO
2max
)
may have a detrimental effect on adaptations to
the pH regulatory systems within the muscle.
[25,77]
Thus, while further research is required, it ap-
pears that intramuscular accumulation of H
+
and/or lactate provides an important stimulus to
improve the muscle pH regulating systems; how-
ever, maximizing H
+
accumulation during train-
ing does not maximize these adaptations. It
should be noted, however, that most of this re-
search has been conducted on moderately-trained
subjects and further research is required to con-
firm these observations in well trained, team-
sport athletes.
The above considerations have important im-
plications for the design of training programmes
to improve the muscle pH regulating systems and
hence, RSA. To increase bm
in vitro
, it appears im-
portant to employ high-intensity interval training
(~80–90%.
VO
2max
), interspersed with rest periods
that are shorter than the work periods (e.g.
2 minutes of exercise followed by 1 minute of rest),
so that the muscle is required to contract while
experiencing a reduced pH.
[69,78]
Interval training
at intensities >.
VO
2max
does not appear to provide
additional benefits, and has the potential to ac-
tually decrease bm
in vitro
.
[25]
In addition, the use of
rest periods that are longer than the work periods
allows greater removal of lactate and H
+
prior to
NHE
MCT
NBC
Proteins
Dipeptides
(e.g.carnosine
and anserine)
Phosphates
CO2 + H2O → H+ + HCO3
−
La
CI−
Na+
Na+
H+H
+
+
HCO3
−
H2CO3
Fig. 2. Muscle (H
+
) regulation. MCT =monocarboxylate transporters; NBC =sodium-bicarbonate co-transporter; NHE =sodium-hydrogen
exchanger.
746 Bishop et al.
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

subsequent intervals
[79]
and typically does not
result in a significant increase in bm
in vitro
.
[37,48]
While an optimal training volume to improve
bm
in vitro
is yet to be established, it appears that
interval training at the above-mentioned inten-
sities, 2–3 times per week, for 3–5 weeks, can re-
sult in significant increases in bm
in vitro
.
[69,75,80]
In
the only study to date, repeated-sprint training
(5–8·[5 ·25–35 m sprints: 21 seconds of rest])
was reported to be less effective than high-
intensity interval training (5–8·[2 minutes at
~100%.
VO
2max
:1–3 minute of rest]) for improv-
ing bm
in vitro
in team-sport athletes, even when
matched for total training volume.
[27]
It is more difficult to recommend the ideal
training programme to increase the MCTs as
significant increases have been reported follow-
ing both moderate-
[81-83]
and high-
[76,84]
intensity
training. However, one factor that these train-
ing programmes tend to have in common is that
they are associated with only modest post-
training increases in blood lactate concentration
(~4–8 mmol/L). When high-intensity training has
been employed, the rest periods between high-
intensity intervals have ranged from 90 to 240
seconds (e.g. a work-to-rest ratio of £1:2),
[76,85]
allowing substantial removal of lactate and H
+
prior to subsequent intervals.
[79]
Thus, in contrast
to the high-intensity training required to increase
bm
in vitro
, it appears that both moderate- and
high-intensity training can increase the MCTs,
but that training should be structured so as to pro-
voke only a modest increase in blood lactate con-
centration (~4–8mmol/L). This might explain why,
in the only study to date that has recruited well
trained subjects, training at 60–70%.
VO
2max
(post-
exercise blood lactate concentration <1.5 mmol/L)
was insufficient to maintain MCT content.
[65]
Significant changes in MCT content appear
more likely when training is performed 2–3 times
per week for 6–8 weeks. While no studies to our
knowledge have investigated the influence of
repeated-sprint training on changes in MCT con-
tent, intermittent-sprint training (15 ·[6-second
sprint: 1-minute jogging recovery]) and inter-
val training (8 ·[30 seconds at 130%.
VO
2max
:
90-seconds rest]) have been reported to be equally
effective for increasing MCT1 content.
[12]
Further
research is therefore required to determine the
effects of repeated-sprint training on the muscle
lactate transporters.
2.3 Muscle Activation
Sprinting requires considerable levels of neural
activation.
[86]
Among the various potential neurally-
mediated mechanisms determining RSA (in par-
ticular, sprint decrement), the ability to voluntarily
fully activate the working musculature and to
maintain muscle recruitment and rapid firing
over sprint repetitions may critically affect fati-
gue resistance.
[14,15,31,87]
This suggests that under
conditions of considerable fatigue development
(e.g. sprint decrement score and fatigue index
>25%) the failure to fully activate the contracting
musculature may become an important factor
limiting performance during RSE. Other factors,
including disruption of optimal temporal sequenc-
ing of agonist and antagonist muscle activation
(i.e. muscle coordination patterns) and/or motor
unit recruitment strategies (e.g. decreased recruit-
ment of fibres with faster conduction velocities),
can also potentially limit RSA, as a multitude
of different muscles must be activated at the ap-
propriate times and intensities to maximize sprint-
ing efficiency.
[88,89]
A variety of training methods have been em-
ployed to successfully improve the degree of muscle
activation (e.g. electromyostimulation, eccentric
strength and plyometric training).
[90]
There is
also evidence that such neural adaptations could
enhance subsequent athletic performance.
[91,92]
While such research suggests that training which
improves muscle activation has the potential to
improve RSA, specific training studies are required
before scientifically-based training recommend-
ations can be given. This will not be easy as much
of the fatigue experienced during RSE appears to
be mediated by metabolic factors (see Part I of
the preceding companion review
[2]
), and such re-
search will need to demonstrate that training-
induced improvements in RSA can be attributed
to improvements in actual muscle activation, and
not concurrent improvement in metabolic factors.
It has also been postulated that the ability for
fast torque development depends, among other
Training to Improve Repeated-Sprint Ability 747
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

factors, on the specific ability for fast muscle ac-
tivation at contraction onset (i.e. earlier recruit-
ment of large motor units, increased synchrony,
elevated motor unit firing rate
[93]
). Training-based
studies that have reported corresponding in-
creases in the rate of force rise and EMG devel-
opment
[94,95]
support this viewpoint. Pending
confirmatory research, these adaptations have
the potential to improve rapid and forceful field/
on-court movements such as sprinting involving
muscle contraction times of less than 250 msec. It
is therefore recommended that measurement of
rate of force development and concomitant EMG
activity (0–200 msec time frame) should be em-
ployed in future training studies (during stan-
dardized tests on a dynamometer or by exploring
the early slope of vertical ground-reaction force-
time curves during running-based RSE) to shed
more light on neural adaptations to training tar-
geting an improvement in sprint performance.
Although it is tempting to propose that enhan-
cing performance during initial sprint efforts may
provide an effective strategy to improve mean
sprint performance (e.g. total mechanical work),
it also needs to be acknowledged that this is also
likely to lead to a higher sprint decrement score.
[31,32]
Thus, additional training regimens may also
need to be implemented to develop those fatigue-
resistance factors.
3. Specific Training Strategies and
Repeated-Sprint Ability
3.1 Repeated-Sprint Training
Anecdotally, repeated-sprint training is a pop-
ular training method used by team-sport athletes
to improve RSA. However, despite the belief that
such specific training will improve RSA more
than generic training (e.g. interval training), very
few studies have directly compared these two
forms of training. We are aware of seven studies
that have investigated adaptations to repeated-
sprint training (table I). Only five of these studies
incorporated a control training group, and only
four of these studies recruited team-sport ath-
letes. It is therefore difficult to make solid con-
clusions about the benefits of repeated-sprint
training in comparison to other types of training.
Nonetheless, despite the obvious need for further
research, some tentative conclusions can be made.
Repeated-sprint training is able to improve
.
VO
2max
. In the studies performed to date,
5–12 weeks of repeated-sprint training has been
reported to result in a 5.0–6.1%increase in
.
VO
2max
. Moreover, this increase is similar to that
reported in the two studies, which incorporated a
control group who performed interval training
(5.2–6.6%increase in .
VO
2max
).
[4,27]
However, as
other studies utilizing different types of interval
training have reported more than 10%increases
in .
VO
2max
,
[10,101]
further research, comparing re-
peated-sprint training and these other types of
training, is required to verify the best means to
improve .
VO
2max
in team-sport athletes. Further
research is also required to investigate additional
physiological adaptations to repeated-sprint train-
ing (e.g. changes in ion regulation, anaerobic
capacity, phosphocreatine resynthesis, etc). For
example, the limited evidence to date suggests
that, compared with repeated- or intermittent-sprint
training, interval training produces superior in-
creases in both bm
in vitro[27]
and Na
+
/K
+
pump
isoform content.
[12]
With respect to RSA, repeated-sprint training
has been reported to produce greater improve-
ments in best sprint time
[12,27,96]
and mean sprint
time,
[4,12,27,96]
compared with interval-based train-
ing. In contrast, interval training appears to be
superior to repeated-sprint training to decrease
(i.e. improve) the sprint decrement score (or the
fatigue index).
[12,27]
However, due to the prob-
lems associated with interpreting changes in the
sprint decrement score when there are concurrent
changes in best sprint time,
[102]
it is difficult to
make universal recommendations. For example,
Mohr et al.
[12,103]
have suggested that the greater
improvement in sprint decrement following in-
terval training (termed ‘speed-endurance’ train-
ing [SET] by the authors), when compared with
intermittent-sprint training (ST) [figure 3], is a sign
that interval training is superior for improving
RSA. However, this interpretation has been ques-
tioned
[34]
as a closer analysis of their data suggests
that the intermittent-sprint-training group had a
greater improvement in single-sprint performance
748 Bishop et al.
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

Table I. A summary of the characteristics and results of training studies that have investigated changes in repeated-sprint ability following running-based training
Study (y) Subjects Training programme Adaptations
type .
VO
2max
(mL/kg/min)
a
best sprint (%) mean sprint (%)DS(%).
VO
2max
(%)
Buchheit et al.
[9]
(2008)
9, MA, M, TS NR 2 ·([5–6·30–40 m shuttle sprints: 14–23 sec]: 2min rest);
2d/wk, 9 wk
›0.3 NS
›1.4
*
›1.0 NS
›1.5
*
›19 NS
›44 NS
NR
8, MA, M, TS 9–24 ·(15–20 sec at 105–115%.
VO
2max
:15–20 sec); 2 d/wk,
9wk
Buchheit et al.
[96]
(2010)
7, MA, M, TS NR 3–4·([4–6·accelerations/sprints (<5 sec): 30 sec]: 3 min rest);
2d/wk, 4 wk
›2.7 ›22 ›35 NR
7, MA, M, TS 3–5·(30 sec all-out shuttle sprints: 4 min rest), 2 d/wk, 4 wk
(both groups also performed two other team training sessions)
›0.7 ›0.8 ›39
Dawson et al.
[43]
(1998)
9, MA, M 57.0 –2.4 4–6·([5 ·30 to 80 m sprints: 30–90 sec rest]: 2–4 min rest);
3d/wk, 6 wk
›2.4
*
›2.2
*
›16 NS ›6.1
*
Bravo et al.
[4]
(2008)
21, MA, M, TS 55.7 –2.3 3 ·([6 ·40 m sprint: 20 sec rest]: 4 min rest); 2 d/wk, 12 wk NR ›2.1
*
NR ›5.0
*
21, MA, M, TS 52.8 –3.2 4 ·(4 min at 95%HR
max
:3minat75%HR
max
); 2 d/wk, 12 wk
(both groups also performed two other team training sessions)
›0.3 NS ›6.6
*
Mohr et al.
[12]
(2007)
6, MA, M 50.2 –3.7 15 ·(6 sec sprint:1 min jog recovery); 3–5d/wk, 8 wk ›4.0
*
›4.3
*
›13 NS NR
7, MA, M 49.0 –4.2 8 ·(30 sec at 130%max: 90 sec rest); 3–5d/wk, 8 wk ›0.7 NS ›2.4
*
›54
*
Schneiker and
Bishop
[27]
(2008)
7, MA, M TS 56.2 –6.8 5–8·(5 ·25 to 35 m sprints: 21 sec rest); 3 d/wk, 5 wk ›1.3
*
›1.6
*
›12 NS ›5.1
*
7, MA, M, TS 56.6 –5.3 5–8·(2 min at 110%.
VO
2max
: 2 min rest); 3 d/wk, 5 wk fl0.5 NS ›0.6 NS ›26
*
›5.2
*
Serpiello et al.
[97]
(2011)
10, M, M, F 53.7 –6.9 3 ·([5 ·4 sec sprint: 16 sec rest]: 4.5 min rest); 3 d/wk, 4 wk
(training/tests performed on a non-motorized treadmill)
›5.5
*
›8.8
*
NR ›2.0
Walklate et al.
[98]
(2009)
6, MA, M, TS NR Control (squad training) ›0.6 NS ›1.4 NS ›2NS NR
6, MA, M, TS Squad training +7–15 ·(20 sec sprint: 10 sec rest);2 d/wk, 4 wk fl0.2 NS ›5.0 NS ›8NS
Buchheit et al.
[99]
(2009)
15, MA, M, TS NR Small-sided games (2–4·2.5–4 min games) ›3.7
*
›4.6
*
›23 NS NR
17, MA, M, TS 12–24 ·(15 sec at 105–115%.
VO
2max
:15–20 sec); 2 d/wk,
10 wk
›3.5
*
›3.4
*
›3NS
Hill-Haas et al.
[100]
(2009)
10, MA, M, TS 59.3 –4.5 Small-sided games 2–6·(6–13 min games:1–3 min of rest) ›0.6 NS ›0.2 NS fl5NS fl0.7 NS
9, MA, M, TS 60.2 –4.6 Generic training (see review for more details) ›1.5 NS fl0.2 NS fl23 NS ›2.0 NS
a Data presented as mean –SD unless NR.
DS =decrement score (or fatigue index); F=Females; HR
max
=maximal heart rate; M=Males; MA =moderate aerobic fitness; max =maximum; NR =not reported; NS =not
significant; TS =team-sport athletes; .
VO
2max
=maximal oxygen consumption;
*
indicates significant difference between pre and post (p <0.05); ›indicates improved;
flindicates worsened.
Training to Improve Repeated-Sprint Ability 749
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

(including the final sprint; 4.5 vs 3.2%) and mean
sprint time (4.3%vs 2.4%) [figure 3]. Further-
more, the smaller improvement in the fatigue
index by the intermittent-sprint training group is
likely to be related to their much-improved first
sprint. Thus, it appears that while interval train-
ing may be superior at minimizing the decrement
during repeated sprints (possibly due to greater
physiological adaptations, as outlined in section 2),
intermittent- or repeated-sprint training is su-
perior at improving the performance of in-
dividual sprints. As a result, the combination of
the two (i.e. repeated-sprint training to improve
sprint performance plus interval training to im-
prove the recovery between sprints) may be the
best strategy to improve RSA. Further research
is required to investigate the optimal volume
and duration of a repeated-sprint training macro
cycle, as anecdotal evidence suggests that too much
repeated-sprint training is stressful and may lead
to decreases in RSA.
3.2 Sprint Training
Given the improvements in individual sprint
times following repeated- and intermittent-sprint
training (see table II), a logical question is whe-
ther or not similar (or greater) improvements in
individual and mean sprint times can be achieved
by traditional sprint training (i.e. short sprints
interspersed with complete recovery periods
[107]
).
To date, we are unaware of research that has in-
vestigated the influence of ‘traditional’ sprint
training on RSA. However, it is possible that
such training may produce even better improve-
ments in both best sprint time and mean sprint
time,
[86]
and further research is warranted. In
support of this, a targeted sprint/agility training
protocol (incorporating incomplete rest periods)
improved mean sprint time by 2.2%in a group of
young soccer players. These changes in mean
sprint time were associated with concurrent impro-
vements in single-sprint performance (approxi-
mately 2.7%reduction in 10 m sprint time), while
no changes in aerobic fitness were observed.
[96]
Despite the obvious need of more research in this
area, these results seem to confirm that in well
trained team-sport athletes, maximization of mean
repeated-sprint time is linked to improvements in
single-sprint performance.
[33]
3.3 Small-Sided Games
Recently, there has been an increased em-
phasis on the use of small-sided games to improve
both team-sport-related fitness (e.g. .
VO
2max
, in-
termittent exercise capacity) and technical
skills.
[108,109]
To date, however, only two studies
(table I) have investigated the effects of small-
sided-games training on RSA, and both have re-
ported only small, nonsignificant differences in
terms of RSE performance enhancement when
4.30
123 4
Sprint number Sprint number
5 Mean sprint
time
12345
SET
ST
Mean sprint
time
4.40
Times (sec)
Times (sec)
4.50
4.60
4.70
4.80
4.90
5.00
ab
4.30
4.40
4.50
4.60
4.70
4.80
4.90
5.00
Fig. 3. (a) Pre-training and (b) post-training individual and mean sprint times derived from a repeated-sprint test cons isting of five 30 m
sprints, separated by 25 sec periods of active recovery during which the subjects jogged back to the starting line. ST performed intermittent-
sprint training, while SET performed ‘speed-endurance’ training (a type of interval training). [See table II for more details of the training
performed]. Post-training there was a significant decrease in initial sprint time for ST only, but a significant decrease in mean sprint time for both
groups.
[12]
750 Bishop et al.
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

compared with generic training.
[99,100]
For example,
when training twice per week for 10 weeks, a
similar ~4%improvement in best and mean sprint
time has been reported following both small-
sided games (2–4·[2.5–4-minute ‘games’]) and
interval training (12–24 ·[15 seconds at ~105–115%
.
VO
2max
: 15 seconds of rest]).
[99]
As the small-sided
game protocols employed in these studies targeted
the development of aerobic fitness, it is likely that
the mechanisms responsible for the reported im-
provements in RSA are also related to improve-
ments in aerobic fitness. In addition, factors other
than aerobic fitness, such as neuromuscular fac-
tors (e.g. acceleration and turning) that can also
be developed with the use of small-sided games,
might also explain the observed improvements in
RSA.
[99,100]
However, given the limited research
to date, further research is obviously required,
especially research comparing the use of small-
sided games with other types of training that have
previously been demonstrated to improve RSA.
Additional research is also required to determine
whether small-sided games can be used to im-
prove other factors such as H
+
regulation and
phosphocreatine resynthesis.
3.4 Resistance Training
While there is good evidence to suggest that
resistance training could be beneficial for single-
sprint performance,
[110-112]
the impact of such
training on RSA is less clear (table III). To date,
three studies have reported that resistance train-
ing (2–5 sets of 10–15 maximal repetitions) pro-
duces similar increases in mean work during a
repeated-sprinttest(~12%)
[113-115]
compared with
high-intensity interval training (~13%)
[10]
or sprint
training (~12%).
[105]
Resistance training also im-
proved both first-sprint performance (8–9%) and
the sprint decrement score (~20%).
[113,114]
The
increases in RSA reported in these studies are
likely to be accounted for, at least in part, by
strength gains. However, factors other than im-
provements in maximal strength may also be in-
volved as we have observed greater improve-
ments in RSA when sets of resistance training
were separated by 20 seconds, compared with
80 seconds of rest, despite half the increase in
maximal leg strength (20 vs 46%).
[114]
This sug-
gests that resistance training that includes a high
metabolic load (e.g. blood lactate concentration
Table II. A summary of the characteristics and results of training studies that have investigated changes in cycle repeated-sprint ability (RSA)
following different types of training performed on a cycle ergometer
Study (y) Subjects Training programme Adaptations
type .
VO
2max
(mL/kg/min)
a
sprint 1
(%)[W]
total work
(%) [kJ]
DS (%).
VO
2max
(%)
Edge et al.
[10]
(2005)
10, MA, F 42.4 –6.3 6–10 ·(2 min at 120–140%LT: 1 min
rest); 3 d/wk, 5 wk
›6.2
*
›6.9
*
›13.0
*,-
›8.5
*
›10 NS
fl16 NS
›13.2
*
›10.4
*
10, MA, F 41.3 –7.3 20–30 min at 80–95%LT; 3 d/wk, 5 wk
Bishop and
Edge
[104]
(2005)
11, MA, F 39.0 –6.4 3–12 ·(2 min at 130–180%LT: 1 min
rest); 3 d/wk +RSA test (5 ·6 sec sprint
every 30 sec); 1 d /wk, 8 wk
›21.2
*
›28.3
*
fl14 NS ›14.6
*
Glaister
et al.
[11]
(2007)
12, MA, M, TS
9, MA, M, TS
46.6 –4.2
52.1 –3.6
20 min at 70%.
VO
2max
;3d/wk, 6 wk
Control (normal recreational activities)
›4.0
*
–
›9.4
*
›1.4 NS
›46
*
›10 NS
›9.9
*
–
Ortenblad
et al.
[105]
(2000)
9, MA, M 61.3 –1.7 20 ·(10 sec sprint: 50 sec rest); 3d/wk,
5wk
›6.6
*
–
›12
*
›1.0 NS
›27
*
–
–
–
6, MA, M 64.0 –0.5 Control (normal recreational activities)
a Data presented as mean –SD.
DS =decrement score (or fatigue index); F=females; LT =lactate threshold (as determined using the modified Dmax method
[106]
); M=males;
MA =moderate aerobic fitness; NR =not reported; NS =not significant; TS =team-sport athletes; .
VO
2max
=maximal oxygen consumption;
*
indicates significant difference between pre and post (p <0.05); -indicates significantly greater improvement than the alternate training
group; ›indicates improved; flindicates worsened; –indicates no change.
Training to Improve Repeated-Sprint Ability 751
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

‡10 mmol/L), rather than resistance training which
maximizes strength gains (e.g. using 1–4 maximal
repetitions), may best improve RSA (possibly
via greater improvements in H
+
regulation
[113]
).
Further research is required though as the sub-
jects involved in these studies were only moder-
ately trained. Given that success in repeated-sprint
activities is also likely to depend on an athlete’s
explosive power, further research is also required
to investigate the importance of explosive muscle
strength training on RSA.
4. Conclusions
RSA is an important fitness component of many
popular team sports. This review has highlighted
that there is not one type of training that can be
recommended to best improve RSA and all of the
factors believed to be responsible for perfor-
mance decrements during repeated-sprint tasks.
This is not surprising, as RSA is a complex fitness
component that depends on both metabolic (e.g.
oxidative capacity, phosphocreatine recovery
and H
+
buffering) and neural factors (e.g. muscle
activation and recruitment strategies) among
others (figure 4). While different training strate-
gies can be used in order to improve each of these
potential limiting factors, and in turn RSA, the
concurrent implementation of different forms of
training may be the best strategy to improve
RSA. However, the currently unknown synergies
and interferences resulting from the combination
of various training contents
[116]
on the metabolic,
neural and mechanical determinants of RSA
make guidelines on how training content should
be manipulated and periodized difficult. None-
theless, two key recommendations can be made
based on the existing literature as follows:
1. It is important to include some training to
improve single-sprint performance. This should
include (i) specific sprint training; (ii) strength/
power training; and (iii) occasional high-intensity
(>.
VO
2max
) training (e.g. repeated, 30-second, all-
out efforts separated by ~10 minutes of recovery)
to increase the anaerobic capacity.
2. It is also important to include some interval
training to best improve the ability to recover
between sprints (if the goal is to improve fatigue
resistance). High-intensity (80–90%.
VO
2max
) in-
terval training, interspersed with rest periods (e.g.
1 minute) that are shorter than the work periods
(e.g. 2 minutes) is efficient at improving the ability
to recover between sprints by increasing aerobic
fitness ( .
VO
2max
and the lactate threshold), the
rate of phosphocreatine resynthesis and bm
in vitro
.
In support of the above recommendation, to
date, the greatest improvements in both single
and mean sprint performance have been reported
Table III. A summary of the characteristics and results of training studies that have investigated changes in cycle repeated-sprint ability (RSA)
following different types of resistance training
Study (y) Subjects Training programme Adaptations
type .
VO
2max
(mL/kg/min)
a
sprint 1
(%) [kJ]
total work
(%) [kJ]
DS (%).
VO
2max
(%)
Edge et al.
[113]
(2006)
8, MA, F 42.4 –9.6 Control ›2.7 NS ›3.0 NS ›3NS –
8, MA, F 44.8 –5.5 6 leg exercises for 2–5sets·(15–20 RM:
20 sec rest); 3 d/wk, 5 wk
›8.0 NS ›12.0
*,-
›22
*,-
–
Hill-Haas et al.
[114]
(2007)
8, MA, F 42.4 –9.6 6 leg exercises for 2–5sets·(15–20 RM:
80 sec rest); 3 d/wk, 5 wk
›9.3
*
›8.4
*
›5.4
*
›12.5
*,-
›21
*
›23
*
–
–
8, MA, F 44.8 –5.5 6 leg exercises for 2–5sets·(15–20 RM:
20 sec rest); 3 d/wk, 5 wk
Robinson et al.
[115]
(1995)
8, MA, M –2 leg exercises for 5 sets ·(10 RM:
30–180 sec rest); 4 d/wk, 5 wk
›6.6
*
›8.5
*
––
a Data presented as mean –SD unless no change.
DS =decrement score (or fatigue index); F=females; M=males; MA =moderate aerobic fitness; NS =not significant; .
VO
2max
=maximal
oxygen consumption;
*
indicates significant difference between pre and post (p <0.05); -indicates significantly greater improvement than the
alternate training group; ›indicates improved; flindicates worsened; –indicates no change.
752 Bishop et al.
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

after training that included both high-intensity
interval training and repeated sprints.
[104]
For most athletes, it is probably impossible to
perform all of the above-described training con-
currently. It is therefore paramount that a peri-
odized training programme, designed to improve
RSA, is structured such that different aspects are
emphasized, at different times, in accordance
with the competitive demands of each particular
sport and the strengths and weaknesses of the
individual athlete. As RSA requires a unique blend
of power (sprint speed) and endurance (recovery
between sprints), it needs to be established whe-
ther it is best to develop these qualities separately,
or whether they can be developed concurrently
(without interference effects). Future studies also
need to address whether training-induced chan-
ges in RSA actually impact upon field performance.
More importantly, as many studies to date have
used untrained subjects and/or a cycle ergometer,
future research must recruit highly-trained team-
sport athletes and be expanded to sport-specific
test settings with, in parallel, a high level of stan-
dardization and reliability of the measures.
Acknowledgements
The authors have no conflicts of interest that are directly
relevant to the content of this review. No funding was used to
assist in the preparation of this review.
References
1. Spencer M, Bishop D, Dawson B, et al. Physiological and
metabolic responses of repeated-sprint activities: specific
to field-based team sports. Sports Med 2005; 35: 1025-44
2. Girard O, Mendez-Villanueva A, Bishop D. Repeated-
sprint ability –part I: factors contributing to fatigue.
Sports Med 2011; 41 (8): 673-94
3. Rampinini E, Bishop D, Marcora SM, et al. Validity of
simple field tests as indicators of match-related physical
performance in top-level professional soccer players. Int J
Sports Med 2007; 28: 228-35
4. Ferrari Bravo D, Impellizzeri FM, Rampinini E, et al.
Sprint vs. interval training in football. Int J Sports Med
2008; 29: 668-74
5. Spencer M, Bishop D, Lawrence S. Longitudinal assess-
ment of the effects of field-hockey training on repeated
sprint ability. J Sci Med Sport 2004; 7: 323-34
6. Perrey S, Racinais S, Saimouaa K, et al. Neural and
muscular adjustments following repeated running sprints.
Eur J Appl Physiol 2010; 109 (6): 1027-36
7. Impellizzeri FM, Rampinini E, Castagna C, et al. Validity
of a repeated-sprint test for football. Int J Sports Med
2008; 29: 899-905
8. Bishop D. Game sense or game nonsense? J Sci Med Sport
2009; 12: 426-7
9. Buchheit M, Millet GP, Parisy A, et al. Supramaximal
training and postexercise parasympathetic reactivation in
adolescents. Med Sci Sports Exerc 2008; 40: 362-71
10. Edge J, Bishop D, Goodman C. Effects of high- and mod-
erate-intensity training on metabolism and repeated
sprints. Med Sci Sports Exerc 2005; 37: 1975-82
11. Glaister M, Stone MH, Stewart AM, et al. The influence of
endurance training on multiple sprint cycling perfor-
mance. J Strength Cond Res 2007; 21: 606-12
12. Mohr M, Krustrup P, Nielsen JJ, et al. Effect of two dif-
ferent intense training regimens on skeletal muscle ion
Repeated-sprint
ability
Recovery
between sprints
Aerobic
fitness
PCr
resynthesis
Initial sprint
performance
Stride length
Power
Strength Elastic strength
ATP
supply Flexibility
Stride frequency
Neural
co-ordination
Muscle
buffering
Fig. 4. A summary of factors which should be targeted by training to improve repeated-sprint ability. ATP =adenosine triphosphate; PCr =
phosphocreatine.
Training to Improve Repeated-Sprint Ability 753
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

transport proteins and fatigue development. Am J Physiol
Regul Integr Comp Physiol 2007; 292: R1594-602
13. Glaister M. Multiple sprint work: physiological responses,
mechanisms of fatigue and the influence of aerobic fitness.
Sports Med 2005; 35: 757-77
14. Racinais S, Bishop D, Denis R, et al. Muscle deoxygena-
tion and neural drive to the muscle during repeated sprint
cycling. Med Sci Sports Exerc 2007; 39: 268-74
15. Mendez-Villanueva A, Hamer P, Bishop D. Fatigue re-
sponses during repeated sprints matched for initial me-
chanical output. Med Sci Sports Exerc 2007; 39: 2219-25
16. Dawson B, Goodman C, Lawrence S, et al. Muscle phos-
phocreatine repletion following single and repeated short
sprint efforts. Scand J Med Sci Sports 1997; 7: 206-13
17. Bogdanis GC, Nevill ME, Boobis LH, et al. Contribution
of phosphocreatine and aerobic metabolism to energy
supply during repeated sprint exercise. J Appl Physiol
1996; 80: 876-84
18. Bogdanis GC, Nevill ME, Boobis LH, et al. Recovery of power
output and muscle metabolites following 30 s of maximal
sprint cycling in man. J Physiol 1995; 482 (Pt 2): 467-80
19. Haseler LJ, Hogan MC, Richardson RS. Skeletal muscle
phosphocreatine recovery in exercise-trained humans is de-
pendent on O2 availability. J Appl Physiol 1999; 86: 2013-8
20. Yoshida T, Watari H. 31P-Nuclear magnetic resonance spec-
troscopy study of the time course of ener gy metabolism during
exercise and recovery. Eur J Appl Physiol 1993; 66: 494-9
21. McCully KK, Boden BP, Tuchler M, et al. Wrist flexor
muscles of elite rowers measured with magnetic resonance
spectroscopy. J Appl Physiol 1989; 67 (3): 926-32
22. McCully KK, Vandenborne K, DeMeirleir K, et al. Muscle
metabolism in track athletes, using 31P magnetic resonance
spectroscopy. Can J Physiol Pharmacol 1992; 70: 1353-9
23. Yoshida T, Watari H. Metabolic consequences of repeated
exercise in long distance runners. Eur J Appl Physiol 1993;
67: 261-5
24. McCully KK, Kakihira H, Vandenborne K, et al. Non-
invasive measurements of activity-induced changes in
muscle metabolism. J Biomech 1991; 21: 153-61
25. Bishop D, Edge J, Thomas C, et al. Effects of high-intensity
training on muscle lactate transporters and postexercise re-
covery of muscle lactate and hydrogen ions in women. Am
J Physiol Regul Integr Comp Physiol 2008; 295: R1991-8
26. Stathis CG, Febbraio MA, Carey MF, et al. Influence of
sprint training on human skeletal muscle purine nucleo-
tide metabolism. J Appl Physiol 1994; 76 (4): 1802-9
27. Schneiker K, Bishop D. The effects oh high-intensity in-
terval training vs intermittent sprint training on physio-
logical capacities important for team sport performance.
In: Burnett A, editor. Science and nutrition in exercise and
sport. Melbourne (VIC): Exerc Sport Sci Aust, 2008
28. Crowther GJ, Carey MF, Kemper WF, et al. Control of
glycolysis in contracting muscle. I: turning it on. Am J
Physiol 2002; 282: E67-73
29. Gaitanos GC, Williams C, Boobis LH, et al. Human
muscle metabolism during intermittent maximal exercise.
J Appl Physiol 1993; 75 (2): 712-9
30. Sahlin K, Ren JM. Relationship of contraction capacity to
metabolic changes during recovery from a fatiguing con-
traction. J Appl Physiol 1989; 67: 648-54
31. Mendez-Villanueva A, Hamer P, Bishop D. Fatigue in re-
peated-sprint exercise is related to muscle power factors
and reduced neuromuscular activity. Eur J Appl Physiol
2008; 103: 411-9
32. Bishop D, Lawrence S, Spencer M. Predictors of repeated-
sprint ability in elite female hockey players. J Sci Med
Sport 2003; 6: 199-209
33. Pyne DB, Saunders PU, Montgomery PG, et al. Relation-
ships between repeated sprint testing, speed, and en-
durance. J Strength Cond Res 2008; 22: 1633-7
34. Bishop D, Schneiker KT. Different interpretation of the
effect of two different intense training regimens on re-
peated sprint ability [letter]. Am J Physiol 2007; 293 (3):
R1459
35. Jacobs I, Esbjornsson M, Sylven C, et al. Sprint training
effects on muscle myoglobin, enzymes, fibre types, and
blood lactate. Med Sci Sports Exerc 1987; 19: 368-74
36. Parra J, Cadefau JA, Rodas G, et al. The distribution of
rest periods affects performance and adaptations of en-
ergy metabolism induced by high-intensity training in
human muscle. Acta Physiol Scand 2000; 169: 157-65
37. Harmer AR, McKenna MJ, Sutton JR, et al. Skeletal
muscle metabolic and ionic adaptations during intense
exercise following sprint training in humans. J Appl Phy-
siol 2000; 89: 1793-803
38. Medbo JI, Burgers S. Effect of training on the anaerobic
capacity. Med Sci Sports Exerc 1990; 22: 501-7
39. Weber CL, Schneider DA. Increases in maximal accumulated
oxygen deficit after high-intensity interval training are not
gender dependent. J Appl Physiol 2002; 92: 1795-801
40. Tabata I, Nishimura K, Kouzaki M, et al. Effects of
moderate-intensity endurance and high-intensity inter-
mittent training on anaerobic capacity and VO2max. Med
Sci Sports Exerc 1996; 28: 1327-30
41. Costill DL, Coyle EF, Fink WF, et al. Adaptations in
skeletal muscle following strength training. J Appl Physiol
1979; 46: 96-9
42. Phillips SM, Green HJ, Tarnopolsky MA, et al. Progressive
effect of endurance training on metabolic adaptations in
working skeletal muscle. Am J Physiol 1996; 270 (2 Pt 1):
E265-72
43. Dawson B, Fitzsimons M, Green S, et al. Changes in perfor-
mance, muscle metabolites, enzymes and fibre types after
short sprint training. Eur J Appl Physiol 1998; 78: 163-9
44. Rodas G, Ventura JL, Cadefau JA, et al. A short training
programme for the rapid improvement of both aerobic and
anaerobic metabolism. Eur J Appl Physiol 2000; 82: 480-6
45. Barnett C, Carey M, Proietto J, et al. Muscle metabolism
during sprint exercise in man: influence of sprint training.
J Sci Med Sport 2004; 7: 314-22
46. Linossier MT, Dormois D, Perier C, et al. Enzyme adap-
tations of human skeletal muscle during bicycle short-
sprint training and detraining. Acta Physiol Scand 1997;
161: 439-45
47. MacDougall JD, Hicks AL, MacDonald JR, et al. Muscle
performance and enzymatic adaptations to sprint interval
training. J Appl Physiol 1998; 84 (6): 2138-42
48. Nevill ME, Boobis LH, Brooks ST, et al. Effect of training
on muscle metabolism during treadmill sprinting. J Appl
Physiol 1989; 67: 2376-82
754 Bishop et al.
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

49. Thomas C, Sirvent P, Perrey S, et al. Relationships between
maximal muscle oxidative capacity and blood lactate re-
moval after supramaximal exercise and fatigue indexes in
humans. J Appl Physiol 2004; 97: 2132-8
50. Dupont G, Millet GP, Guinhouya C, et al. Relationship
between oxygen uptake kinetics and performance in re-
peated running sprints. Eur J Appl Physiol 2005; 95: 27-34
51. Rampinini E, Sassi A, Morelli A, et al. Repeated-sprint
ability in professional and amateur soccer players. Appl
Physiol Nutr Metab 2010; 34: 1048-54
52. Buchheit M, Ufland P. Effect of endurance training on per-
formance and muscle reoxygenation rate during repeated-
sprint running. Eur J Appl Physiol 2011; 111 (2): 293-301
53. Fernandes da Silva J, Guglielmo LGA, Bishop D. Re-
lationship between different measures of aerobic fitness
and repeated-sprint ability in elite soccer players. J
Strength Cond Res 2010; 24: 2115-21
54. Bishop D, Edge J, Goodman C. Muscle buffer capacity and
aerobic fitness are associated with repeated-sprint ability
in women. Eur J Appl Physiol 2004; 92: 540-7
55. Bishop D, Spencer M. Determinants of repeated-sprint
ability in well-trained team-sport athletes and endurance-
trained athletes. J Sports Med Phys Fitness 2004; 44: 1-7
56. McMahon S, Wenger HA. The relationship between aero-
bic fitness and both power output and subsequent re-
covery during maximal intermittent exercise. J Sci Med
Sport 1998; 1 (4): 219-27
57. Tomlin DL, Wenger HA. The relationship between aerobic
fitness, power maintenance and oxygen consumption
during intense intermittent exercise. J Sci Med Sport 2002;
5 (3): 194-203
58. Bishop D, Edge J. Determinants of repeated-sprint ability
in females matched for single-sprint performance. Eur J
Appl Physiol 2006; 97: 373-9
59. McGawley K, Bishop D. Anaerobic and aerobic con-
tribution to two, 5 ·6-s repeated-sprint bouts [abstract].
Coach Sport Sci J 2008; 3: 52
60. Hoffman JR. The relationship between aerobic fitness and
recovery from high-intensity exercise in infantry soldiers.
Mil Med 1997; 162: 484-8
61. Daussin FN, Zoll J, Dufour SP, et al. Effect of interval
versus continuous training on cardiorespiratory and mi-
tochondrial functions: relationship to aerobic perfor-
mance improvements in sedentary subjects. Am J Physiol
Regul Integr Comp Physiol 2008; 295: R264-72
62. MacDougall D, Sale D. Continuous vs. interval training: a
review for the athlete and the coach. Can J Appl Sport Sci
1981; 6: 93-7
63. Gorostiaga EM, Walter CB, Foster A, et al. Uniqueness of
interval and continuous training at the same maintained
exercise intensity. Eur J Appl Physiol 1991; 63: 101-7
64. Helgerud J, Hoydal K, Wang E, et al. Aerobic high-
intensity intervals improve VO2max more than moderate
training. Med Sci Sports Exerc 2007; 39: 665-71
65. Eversten F, Medbo JI, Bonen A. Effect of training intensity on
muscle lactate transporters and lactate threshold of cross-
country skiers. Acta Physiol Scand 2001; 173: 195-205
66. Cunningham DA, McCrimmon D, Vlach LF. Cardio-
vascular response to interval and continuous training in
women. Eur J Appl Physiol 1979; 41: 187-97
67. Eddy DO, Sparks KL, Adelizi DA. The effects of con-
tinuous and interval training in women and men. Eur J
Appl Physiol 1977; 37: 83-92
68. Poole DC, Gaesser GA. Response of ventilatory and lac-
tate thresholds to continuous and interval training. J Appl
Physiol 1985; 58: 1115-21
69. Edge J, Bishop D, Goodman C. The effects of training in-
tensity on muscle buffer capacity in females. Eur J Appl
Physiol 2006; 96: 97-105
70. Spencer M, Dawson B, Goodman C, et al. Performance
and metabolism in repeated sprint exercise: effect of re-
covery intensity. Eur J Appl Physiol 2008; 103: 545-52
71. Ratel S, Williams CA, Oliver J, et al. Effects of age and
recovery duration on performance during multiple tread-
mill sprints. Int J Sports Med 2005; 26: 1-8
72. Spriet LL, Lindinger MI, Mckelvie RS, et al. Muscle gly-
cogenolysis and H+concentration during maximal inter-
mittent cycling. J Appl Physiol 1989; 66 (1): 8-13
73. Bishop D, Edge J, Davis C, et al. Induced metabolic alka-
losis affects muscle metabolism and repeated-sprint abil-
ity. Med Sci Sports Exerc 2004; 36: 807-13
74. Juel C. Muscle pH regulation: role of training. Acta Physiol
Scand 1998; 162: 359-66
75. Weston AR, Myburgh KH, Lindsay FH, et al. Skeletal
muscle buffering capacity and endurance performance
after high-intensity interval training by well-trained cy-
clists. Eur J Appl Physiol 1997; 75: 7-13
76. Juel C, Klarskov C, Nielsen JJ, et al. Effect of high-
intensity intermittent training on lactate and H+release
from human skeletal muscle. Am J Physiol Endocrinol
Metab 2004; 286: E245-51
77. Thomas C, Bishop D, Moore-Morris T, et al. Effects of high-
intensity training on MCT1, MCT4, and NBC expressions in
rat skeletal muscles: influence of chronic metabolic alkalosis.
Am J Physiol Endocrinol Metab 2007; 293: E916-22
78. Edge J, Bishop D, Goodman C. Effects of chronic NaH-
CO3 ingestion during interval training on changes to
muscle buffer capacity, metabolism, and short-term en-
durance performance. J Appl Physiol 2006; 101: 918-25
79. Sahlin K, Harris RC, Nylind B, et al. Lactate content and
pH in muscle obtained after dynamic exercise. Pflugers
Archiv 1976; 367: 143-9
80. Gibala MJ, Little JP, van Essen M, et al. Short-term sprint
interval versus traditional endurance training: similar in-
itial adaptations in human skeletal muscle and exercise
performance. J Physiol 2006; 575: 901-11
81. Bonen A, McCullagh KJA, Putman CT, et al. Short-term
training increases human muscle MCT1 and femoral ve-
nous lactate in relation to muscle lactate. Am J Physiol
Endocrinol Metab 1998; 274: E102-7
82. Dubouchaud H, Butterfield GE, Wolfel EE, et al. En-
durance training, expression, and physiology of LDH,
MCT1, and MCT4 in human skeletal muscle. Am J Phy-
siol Endocrinol Metab 2000; 278: E571-9
83. Juel C, Holten MK, Dela F. Effects of strength training on
muscle lactate release and MCT1 and MCT4 content in
healthy and type 2 diabetic humans. J Physiol 2004; 556
(1): 297-304
84. Burgomaster KA, Cermak NM, Phillips SM, et al. Divergent
responseof metabolite transport proteins in human skeletal
Training to Improve Repeated-Sprint Ability 755
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)

muscle after sprint interval training and detraining. Am J
Physiol Regul Integr Comp Physiol 2007; 292: R1970-6
85. Pilegaard H, Domino K, Noland T, et al. Effect of high-
intensity exercise training on lactate/hydrogen ion trans-
port capacity in human skeletal muscle. Am J Physiol
1999; 276: E255-61
86. Ross A, Leveritt M, Riek S. Neural influences on sprint
running: training adaptations and acute responses. Sports
Med 2001; 31: 409-25
87. Matsuura R, Arimitsu T, Kimura T, et al. Effect of oral
administration of sodium bicarbonate on surface EMG
activity during repeated cycling sprints. 2007; 101: 409-17
88. Billaut F, Basset FA, Giacomoni M, et al. Effect of high-
intensity intermittent cycling sprints on neuromuscular
activity. Int J Sports Med 2006; 27: 25-30
89. Billaut F, Basset FA, Falgairette G. Muscle coordination
changes during intermittent cycling sprints. Neurosci Lett
2005; 380: 265-9
90. Gabriel DA, Kamen G, Frost G. Neural adaptations to
resistive exercise: mechanisms and recommendations for
training practices. Sports Med 2006; 36: 133-49
91. Mikkola J, Rusko H, Nummela A, et al. Concurrent en-
durance and explosive type strength training improves
neuromuscular and anaerobic characteristics in young
distance runners. Int J Sports Med 2007; 28: 602-11
92. Murray DP, Brown LE, Zinder SM, et al. Effects of velo-
city-specific training on rate of velocity development,
peak torque, and performance. J Strength Cond Res 2007;
21: 870-4
93. Van Cutsem M, Duchateau J, Hainaut K. Changes in sin-
gle motor unit behaviour contribute to the increase in
contraction speed after dynamic training in humans. J
Physiol 1998; 513 (Pt 1): 295-305
94. Aagaard P, Simonsen EB, Andersen JL, et al. Increased
rate of force development and neural drive of human
skeletal muscle following resistance training. J Appl Phy-
siol 2002; 93: 1318-26
95. Del Balso C, Cafarelli E. Adaptations in the activation of
human skeletal muscle induced by short-term isometric
resistance training. J Appl Physiol 2007; 103: 402-11
96. Buchheit M, Mendez-Villaneuva A, Quod M, et al. Improving
acceleration and repeated sprint ability in well-trained ado-
lescent handball players: speed vs sprint interval training. Int
J Sports Physiol Perform 2010; 5: 152: 64
97. Serpiello FR, McKenna MJ, Stepto NK, et al. Performance
and physiological responses to repeated-sprint exercise: a
novel multiple-set approach. Eur J Appl Physiol 2011; 111
(4): 669-78
98. Walklate BM, O’Brien BJ, Paton CD, et al. Supplementing
regular training with short-duration sprint-agility training
leads to a substantial increase in repeated sprint-agility
performance with national level badminton players. J
Strength Cond Res 2009; 23: 1477-81
99. Buchheit M, Laursen PB, Kuhnle J, et al. Game-based
training in young elite handball players. Int J Sports Med
2009; 30: 251-8
100. Hill-Haas SV, Coutts AJ, Rowsell GJ, et al. Generic versus
small-sided game training in soccer. Int J Sports Med
2009; 30: 636-42
101. Helgerud J, Engen LC, Wisloff U, et al. Aerobic endurance
training improves soccer performance. Med Sci Sports
Exerc 2001; 33 (11): 1925-31
102. Billaut F, Bishop D. Muscle fatigue in males and females
during multiple-sprint exercise. Sports Med 2008; 39: 257-78
103. Mohr M, Krustrup P, Nielsen JJ, et al. Reply to Bishop and
Schneiker [letter]. Am J Physiol Regul Integr Comp Phy-
siol 2007; 293: R1460
104. Bishop D, Edge J. The effects of a 10-day taper on re-
peated-sprint performance in females. J Sci Med Sport
2005; 8: 200-9
105. Ortenblad N, Lunde PK, Levin K, et al. Enhanced sarco-
plasmic reticulum calcium release following intermittent
sprint training. Am J Physiol 2000; 279: R152-60
106. Bishop D, Jenkins DG, Mackinnon LT. The relationship be-
tween plasma lactate parameters, Wpeak and 1-h cycling per-
formance in women. Med Sci Sports Exerc 1998; 30 (8): 1270-5
107. Ross A, Leveritt M. Long term metabolic and skeletal muscle
adaptations to short-sprint training: implications for sprint
training and taper. Sports Med 2001; 31 (15): 1063-82
108. Impellizzeri FM, Marcora SM, Castagna C, et al. Physio-
logical and performance effects of generic versus specific
aerobic training in soccer players. Int J Sports Med 2006;
27 (6): 483-92
109. Gabbett TJ. Performance changes following a field con-
ditioning program in junior and senior rugby league
players. J Strength Cond Res 2006; 20: 215-21
110. Delecluse C, Van Coppenolle H, Willems E, et al. Influence
of high-resistance and high-velocity training on sprint
performance. Med Sci Sports Exerc 1995; 27: 1203-9
111. Delecluse C. Influence of strength training on sprint run-
ning performance: current findings and implications for
training. Sports Med 1997; 24: 147-56
112. Newman MA, Tarpenning KM, Marino FE. Relationships
between isokinetic knee strength, single-sprint perfor-
mance, and repeated-sprint ability in football players. J
Strength Cond Res 2004; 18: 867-72
113. Edge J, Hill-Haas S, Goodman C, et al. Effects of resistance
training on H+regulation, buffer capacity, and repeated
sprints. Med Sci Sports Exerc 2006; 38: 2004-11
114. Hill-Haas S, Bishop D, Dawson B, et al. Effects of rest
interval during high-repetition resistance training on
strength, aerobic fitness, and repeated-sprint ability. J
Sports Sci 2007; 25 (6): 619-28
115. Robinson JM, Stone MH, Johnson RL, et al. Effects of
different weight training exercise/rest intervals on
strength, power and high intensity exercise endurance. J
Strength Cond Res 1995; 9 (4): 216-21
116. Coffey VG, Jemiolo B, Edge J, et al. Effect of consecutive
repeated sprint and resistance exercise bouts on acute
adaptive responses in human skeletal muscle. Am J Phy-
siol Regul Integr Comp Physiol 2009; 297: R1441-51
Correspondence: Prof. David Bishop, Institute of Sport,
Exercise and Active Living (ISEAL), School of Sport and
Exercise Science, Victoria University, PO Box 14428
Melbourne, VIC 8001, Australia.
E-mail: David.Bishop@vu.edu.au
756 Bishop et al.
ª2011 Adis Data Information BV. All rights reserved. Sports Med 2011; 41 (9)