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Caffeine and anaerobic performance: ergogenic value and mechanisms of action

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ª 2009 Adis Data Information BV. All rights reserved.

Caffeine and Anaerobic Performance

Ergogenic Value and Mechanisms of Action
J.K. Davis1 and J. Matt Green2
1 Department of Health and Human Performance, Texas A&M University-Commerce, Commerce, Texas, USA
2 Department of Health, Physical Education and Recreation, University of North Alabama, Florence,
Alabama, USA

Contents
Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 813
1. Ergogenic Effect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 814
1.1 Wingate/Sprint Cycling Power . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 814
1.2 Sprinting/Sport-Specific Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 816
1.3 Agility . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 817
1.4 Speed Endurance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 817
1.5 Muscular Endurance/One-Repetition Maximum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 818
1.6 Isokinetic Peak Torque . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 819
1.7 Isometric Maximal Force and Endurance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 820
1.8 Interindividual Variability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 820
2. Mechanisms of Action . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 821
2.1 Peripheral Mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 821
2.2 Catecholamines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 821
2.3 Lactic Acid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 821
2.4 Blood Glucose. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 822
2.5 Potassium. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 822
2.6 Calcium/Phosphodiesterase Inhibition/Cyclic Adenosine Monophosphate Cascade. . . . . . . . . 823
3. Central Mechanism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 823
3.1 Adenosine Antagonism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 823
3.2 Pain Perception . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 823
3.3 Rating of Perceived Exertion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 826
3.4 Fatigue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 827
4. Conclusion and Future Directions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 827

Abstract The effect caffeine elicits on endurance performance is well founded.

However, comparatively less research has been conducted on the ergogenic
potential of anaerobic performance. Some studies showing no effect of caf-
feine on performance used untrained subjects and designs often not con-
ducive to observing an ergogenic effect. Recent studies incorporating trained
subjects and paradigms specific to intermittent sports activity support the
notion that caffeine is ergogenic to an extent with anaerobic exercise. Caffeine
seems highly ergogenic for speed endurance exercise ranging in duration from
60 to 180 seconds. However, other traditional models examining power out-
put (i.e. 30-second Wingate test) have shown minimal effect of caffeine on
performance. Conversely, studies employing sport-specific methodologies
814 Davis & Green

(i.e. hockey, rugby, soccer) with shorter duration (i.e. 4–6 seconds) show
caffeine to be ergogenic during high-intensity intermittent exercise. Recent
studies show caffeine affects isometric maximal force and offers introductory
evidence for enhanced muscle endurance for lower body musculature. How-
ever, isokinetic peak torque, one-repetition maximum and muscular en-
durance for upper body musculature are less clear. Since relatively few studies
exist with resistance training, a definite conclusion cannot be reached on the
extent caffeine affects performance.
It was previously thought that caffeine mechanisms were associated with
adrenaline (epinephrine)-induced enhanced free-fatty acid oxidation and con-
sequent glycogen sparing, which is the leading hypothesis for the ergogenic
effect. It would seem unlikely that the proposed theory would result in improved
anaerobic performance, since exercise is dominated by oxygen-independent
metabolic pathways. Other mechanisms for caffeine have been suggested, such
as enhanced calcium mobilization and phosphodiesterase inhibition. However,
a normal physiological dose of caffeine in vivo does not indicate this mechanism
plays a large role. Additionally, enhanced Na+/K+ pump activity has been
proposed to potentially enhance excitation contraction coupling with caffeine.
A more favourable hypothesis seems to be that caffeine stimulates the CNS.
Caffeine acts antagonistically on adenosine receptors, thereby inhibiting the
negative effects adenosine induces on neurotransmission, arousal and pain
perception. The hypoalgesic effects of caffeine have resulted in dampened pain
perception and blunted perceived exertion during exercise. This could poten-
tially have favourable effects on negating decreased firing rates of motor units
and possibly produce a more sustainable and forceful muscle contraction. The
exact mechanisms behind caffeine’s action remain to be elucidated.

Caffeine – a 1,3,7 trimethylxanthine – is com-
monly found in over-the-counter medications,
coffee, tea, cola, chocolate and in various other
products. It is metabolized in the liver to di-
methyxanthines (paraxanthine, theobromine,
theophylline) and is proposed to affect various
tissues throughout the body, including peripheral
and central tissues.[1] The popularity of caffeine
as an ergogenic aide has increased dramatically
over the last decade, and various forms of admin-
istration (i.e. sports drinks, sports gels, energy
drinks) have become more available in recent
years. Athletes commonly consume caffeine in an
attempt to enhance performance. However, ethical
considerations have been raised regarding the
effect of caffeine on performance, leading the
National Collegiate Athletic Association (NCAA)
to implement urinary caffeine restrictions. Nu-
merous reviews[1-8] have examined the effects on
performance that caffeine elicits, but this has pri-
marily been directed toward aerobic performance.
Few reviews have examined the effect of caffeine
solely on anaerobic performance. Rather, they
have treated the effects on anaerobic perfor-
mance merely as a subset of the review.[1-8] In the
current review we exclusively examine anaerobic
performance. More specifically, exercise bouts of
4–180 seconds in duration are examined. The first
section explores the influence of caffeine in various
anaerobic paradigms with particular attention
given to the impact on performance variables.
The second section focuses on various mechan-
isms, both peripheral and central, that may con-
tribute to the ergogenic effect of caffeine.
1. Ergogenic Effect
1.1 Wingate/Sprint Cycling Power
The Wingate test is a widely accepted measure
of power output and anaerobic capacity[9] and
has been commonly employed when assessing

ª 2009 Adis Data Information BV. All rights reserved. Sports Med 2009; 39 (10)
Caffeine and Anaerobic Performance
ergogenic aids and anaerobic performance. Three
30-second repeated Wingate tests have shown the
highest percentage of energy production from
anaerobic metabolism consisting of 60–84% of
oxygen-independent ATP production.[10-13] Stu-
dies examining effects of caffeine on Wingate per-
formance have typically shown minimal ergogenic
effects.[14-22] Greer et al.[17] actually showed an
ergolytic effect of caffeine with a decrease in
power-output on the fourth Wingate bout com-
pared with placebo. Only one study supports the
notion of that caffeine is ergogenic within this
paradigm.[23]
Testing untrained subjects presents problems
in interpreting the ergogenic potential of caffeine
in trained individuals. Most studies failing to
show ergogenic potential have incorporated un-
trained subjects (not specifically accustomed to
intermittent-sprint exercise),[14,15,17,18,20-22] with
only one study incorporating trained subjects[16]
for single[15,18-20,22] and repeated[14,16,17,21] Win-
gate tests. Using untrained subjects may not be
the best model to assess the ergogenic effect of
caffeine within this exercise paradigm. The only
study to support an ergogenic effect with caffeine
on Wingate performance was by Kang et al.,[23]
who tested both trained (professional cyclists)
and untrained subjects. Kang et al.[23] had sub-
jects perform a single traditional 30-second Win-
gate test. Subjects consumed 2.5 and 5.0 mg/kg
mass caffeine and placebo in counterbalanced
order. Caffeine significantly increased total
power, mean power and peak power in both
groups compared with placebo, with no differ-
ence noted between caffeine doses. It is unclear
why untrained subjects improved performance
for Kang et al.,[23] considering other studies uti-
lizing untrained subjects have found no change
in performance.[14,15,17,18] Beck et al.[16] had
resistance-trained subjects perform two Wingate
tests, consuming 201 mg 1 hour prior to the trial.
There were no differences between caffeine and
placebo for peak power, mean power and per-
centage decrease in performance. However, these
results should be interpreted with caution con-
sidering resistance-trained subjects were em-
ployed. While likely accustomed to high-intensity
anaerobic exercise, subjects participating in reg-
ª 2009 Adis Data Information BV. All rights reserved.
815
ular sprints, particularly cycling, might be better
adapted to perform repeat Wingate tests. Ad-
ditionally, caffeine was not administered relative
to body mass, and when the mean mass for sub-
jects is equated with dose administered (200 mg)
mean consumption per subject is 2.4 mg/kg
(2.1–3.0 mg/kg), potentially negating an ergo-
genic effect. However, other studies have found
improved performance with similar doses of caf-
feine.[23-25] Consequently, the dose may have
been inadequate to enhance performance and the
subjects’ training background (resistance-trained
vs cyclist) could account for equivocal results.
Future studies using the Wingate protocol with
repeated bouts should use highly anaerobic-
trained subjects accustomed to intermittent bouts
of cycling to ascertain whether caffeine is ergo-
genic in this paradigm.
Although the Wingate test is typically used to
examine anaerobic capacity, it does not reflect
the performance requirements of sports involving
intermittent high-intensity efforts (e.g. ice hock-
ey, soccer, field hockey, American football), and
consequently it is uncertain whether the results of
caffeine on Wingate performance would be ob-
served during sports-specific activities. Court or
field-base team sports often consist of short bouts
of intermittent sprints (2–5 seconds), performed
over short distances (10–20 m), and with brief rest
periods between bouts.[26] In order to mimic
athletic competition more closely, Schneiker
et al.[27] assessed the effects of caffeine on ama-
teur level team sport athletes from local and state
clubs (e.g. football, soccer and hockey), con-
suming 6 mg/kg of caffeine. To simulate a sports-
specific paradigm, subjects (n = 10) performed
2 · 36-minute halves, with each half composed of
18 · 4-second maximal exertion. cycling bouts
with 2 minutes recovery at 35% VO2 max between
sprints. Compared with placebo, caffeine use re-
sulted in a significant improvement for the first
half (8.5%) and second half (7.6%) for total work.
Similarly, there was a significant improvement
for the first half (7.0%) and second half (6.6%) for
peak power. These results show that when the
testing protocol more closely mimics athletic
competitions with trained subjects accustomed to
intermittent-sprint bouts, caffeine does provide
Sports Med 2009; 39 (10)
816
an ergogenic effect. Anselm et al.[28] found a 7%
increase in maximal anaerobic power (Wmax)
with untrained subjects during a single 6-second
sprint following consumption of 250 mg of caf-
feine. However, Williams et al.[19] found no benefit
from caffeine (7 mg/kg) during maximal exercise
(15 seconds) for peak power, total power and
fatigue index with untrained subjects. Although
Williams et al.[19] failed to find improved perfor-
mance during a 15-second Wingate test, results
indicate that caffeine is beneficial for trained and
untrained subjects when bouts are 4–6 seconds’
duration, which may more closely mimic the time
frame associated with high-intensity sports.[27,28]
1.2 Sprinting/Sport-Specific Testing
Few studies have examined the effects of caf-
feine on sprinting performance and agility.[29-31]
Paton et al.[29] had 16 team sport athletes (e.g.
basketball, hockey, rugby) perform 10 · 20 m
sprints with 10 seconds’ recovery between sprints.
Bouts were completed following 6 mg/kg caffeine
consumption and placebo. Caffeine resulted in
significantly slower mean sprint time (0.1%):
compared with the first sprint, a 14.0% increase in
time over 10 sprints was noted for placebo versus
14.7% for caffeine. One potential problem dis-
cussed in the article, possibly due to lack of space,
is that at the end of the 20 m sprint, subjects had
to decelerate. Anticipation of deceleration likely
impaired sprint times and could have masked any
ergogenic effects of caffeine. Stuart et al.[30] simu-
lated a rugby game with Australian rugby players
performing seven circuits in each 2 · 40-minute
half, with 10 minutes’ half-time rest after con-
suming 6 mg/kg of caffeine. Skill tasks assessed
included sprinting, agility, power generation and
passing accuracy. Eleven stations were performed
per circuit with 30-second intervals between sta-
tions, and two stations consisted of straight-line
sprinting (20–30 m sprints). Caffeine significantly
improved sprint time by 0.5–2.9% for the entire
trial (all sprints combined); specifically, perfor-
mance improved in the first half for 20–30 m
(0.5, 2.3%) and second half for 20–30 m sprints
(1.4, 3.4%). Reasons for equivocal results be-
tween Stuart et al.[30] and Paton et al.[29] are un-
ª 2009 Adis Data Information BV. All rights reserved.
Davis & Green
clear. Although distances were relatively the same,
recovery duration between sprints was different
(10 seconds[29] vs 30 seconds[30]). The rest : work
ratio used by Paton et al.[29] was between 2 : 1 and
3 : 1, depending on how long it took the subject to
complete the 20 m sprint, where Stuart et al.[30]
employed a 4.5 : 1 ratio for rest to work. The
rest : work ratio could have a dramatic effect on
recovery, and the short rest : work ratio employed
by Paton et al.[29] could have prevented the au-
thors from observing any ergogenic effect. Thus,
the effect of rest : work might play a crucial role in
allowing caffeine to magnify its effect. Future
studies should investigate to what extent rest 
work or total volume plays on allowing caffeine
to elicit its effect on performance.
Only one study to date has examined the ef-
fects of caffeine on anaerobic performance in
swimmers.[31] Collomp et al.[31] used a within-
subjects design in order to examine the effects of
caffeine 250 mg on a 2 · 100 m maximal exertion
freestyle swim, with 20 minutes passive recovery
between bouts, on trained and untrained swim-
mers. Overall, trained swimmers significantly im-
proved swimming velocity with caffeine (vs placebo)
compared with untrained subjects, with greater
improvement noted during the second 100 m.
Trained swimmers had been competitive for
5 years and had been training 5–6 days a week for
4 consecutive months at the time of the study.
These results[31] seem promising; however, future
studies are warranted. Considering the 2007
NCAA 100 m freestyle final for first and second
place was separated by 0.73 seconds and first and
tenth by 1.58 seconds, if caffeine could elicit
similar results shown with trained subjects as
Stuart et al.[30] showed on sprint performance
(0.5–2.9%), a competitive advantage is plausible.
While worthy of further inquiry, it should also be
noted that precise simulation of the competitive
environment in a controlled laboratory setting
is difficult. It is possible that if caffeine acts
via CNS function (discussed in detail later in sec-
tion 3), the level of arousal typically associated
with competition may mask ergogenic properties
that might be observed during laboratory testing.
However, it could still be an important training
tool during practice.
Sports Med 2009; 39 (10)
Caffeine and Anaerobic Performance
1.3 Agility
Athletic competitions involving brief periods
of high-intensity exercise consist of a combina-
tion of sprints and agility-based performances.
Studies on the ergogenic effect caffeine has on
agility performance have shown equivocal re-
sults.[20,30] Conflicting results could stem from the
methodology employed between these studies.
Stuart et al.[30] examined agility by having partici-
pants perform three agility sprints (22, 33 and 31 m)
performed in a swerving (or zigzag) pattern. Caf-
feine improved overall mean agility sprint perfor-
mance for all three sprints by 2.2% compared with
placebo in the first half, with second half perfor-
mance improved by 1.7%; however, whether this
was significant was not reported. Lorino et al.[20]
had 16 subjects perform three pro-agility tests:
this test is commonly known as the 20-yard shut-
tle run and is used as an indicator of athletic per-
formance in American football at the high school,
collegiate and professional level. They failed to
find a significant difference between caffeine and
placebo for the pro-agility test. The reasons for
conflicting results could be due to exercise para-
digm and the subject familiarity. Although both
studies incorporated a double-blind, crossover
design, Stuart et al.[30] used trained subjects (rugby
players) where Lorino et al.[20] used untrained
subjects who were unaccustomed to the pro-agility
test. Thus, untrained subjects not commonly
performing agility work on a regular basis could
have negated a potential ergogenic effect. Future
investigations examining agility skills should in-
corporate trained subjects commonly performing
agility drills on a weekly basis in order to under-
stand what impact caffeine has on this type of
performance.
1.4 Speed Endurance
Several studies have evaluated high-intensity
exercise lasting between 60 and 180 seconds.
A method that has commonly been employed to
assess speed endurance has involved protocols
using maximal accumulated oxygen deficit
(MAOD). The MAOD model is considered a
suitable test for a non-invasive indirect measure-
ª 2009 Adis Data Information BV. All rights reserved.
817
ment of anaerobic ATP metabolism,[32,33] although
others have argued its value.[34,35] MAOD involves
running at a supramaximal intensity (e.g. 125%
.
VO2 max ), with volitional fatigue typically occur-
ring at 2–3 minutes,[15,32,36] depending upon a
participant’s level of training. MAOD allows
for a unique exercise paradigm, with duration of
time similar to short-term track events (800 m).
Doherty[32] was the first to examine the MAOD
paradigm with caffeine. His group showed caffeine
(vs placebo) improved run time to exhaustion by
14% (29 – 6 seconds). In a similar study, Doherty
et al.[36]
. had subjects perform supramaximal
125% VO2 max to exhaustion, with subjects sup-
plementing with caffeine or placebo after a 7-day
loading phase with oral creatine (20 g/day). Time
to fatigue was significantly greater by 23.8 sec-
onds with caffeine plus creatine compared with
placebo (creatine only), and 21.3 seconds com-
pared with baseline measurements. The results
indicated caffeine is ergogenic within this para-
digm, highlighting the potential use of acute caf-
feine ingestion after oral creatine loading. This
brings novel insight to stacking these ergogenic
aids in this manner because when caffeine is taken
throughout the loading phase of creatine a sy-
nergistic effect has not been shown.[37,38] Caffeine
inhibits elevations in intramuscular phospho-
creatine levels.[37] Bell et al.[15] employed the
MAOD model using cycle ergometry instead
. of a
treadmill.[32,36] Time to fatigue at 125% VO2 max
significantly increased by 8.8 seconds with caffeine
compared with placebo. Time to fatigue for Bell
et al.[15] was not as great compared with Doherty
et al.;[32,36] however, a possible explanation is the use
of trained[32,36] compared with untrained subjects.[15]
Collectively, studies using the MAOD model
seem favourable regarding the ergogenic effects
of caffeine, with positive results shown regardless
of training status,[15,32,36] but seem to impact per-
formance to a greater extent for trained subjects.
Several studies have examined speed endurance
using various protocols other than the MAOD
model. Doherty et al.[39] had subjects cycle for
2 minutes at 100% maximal power output, imme-
diately followed by a 1-minute all-out sprint.
Mean power output for the 1-minute all-out sprint
was significantly higher with caffeine (794 – 164 W)
Sports Med 2009; 39 (10)
818
compared with placebo (750 – 163 W). Wiles
et al.[40] examined performance time, mean speed
and peak power with trained cyclists across three
1 km cycling bouts. Using caffeine resulted in sig-
nificantly improved performance (2.3 seconds),
and significantly greater mean power (18.1 W) and
peak power (75.5 W), and faster mean speed
(1.6 km/h). Crowe et al.[41] showed an ergolytic ef-
fect with caffeine 6 mg/kg during two 60-second
maximal cycling bouts (separated by 3 minutes’
passive seated recovery) with recreationally trained
subjects (i.e. soccer, rugby, basketball). Use of
caffeine resulted in a significantly slower time to
reach peak power in exercise bout two compared
with placebo, and in a greater decrease in peak
power and total work from bout one to two,
although this was not statistically significant.
While there are inconsistencies, collectively caf-
feine supplementation for maximal exertion bouts
lasting 60–180 seconds seems beneficial for trained
and untrained individuals.[15,32,36,39,40]
1.5 Muscular Endurance/One-Repetition
Maximum
Compared with other popular ergogenic aids,
few studies have assessed the effects of caffeine on
resistance training performance. However, with
studies showing ergogenic effects of caffeine
during anaerobic performance, it is plausible that
caffeine may affect resistance training, which is
also dominated by oxygen-independent meta-
bolic pathways.
Common methods for examining muscular
fitness are to assess strength by determining a
one-repetition maximum (1RM) or to assess mus-
cular endurance using repetitions to failure. Re-
petitions to failure involve performing an all-out
effort of repetitions to volitional fatigue, usually
performed at a percentage of 1RM or multiple
repetitions max test (i.e. 10–12 repetitions). The
majority of studies examining repetitions to fail-
ure have used subjects with various resistance
training histories (8 weeks,[42,43] 1 year,[16] 2 years,[44]
6 years[45]), performing resistance training bouts
2–4 (times) per week.[16,42-45] Green et al.[42] tested
17 subjects (13 males, 4 females) performing three
sets of bench presses and leg presses to failure
ª 2009 Adis Data Information BV. All rights reserved.
Davis & Green
at 80% of 1RM in a double-blind, placebo-
controlled design, with a dosage of 6 mg/kg of
caffeine. No significant difference was shown for
bench presses or sets one and two for the leg
presses between caffeine and placebo. However,
the third set for leg presses showed a signifi-
cant improvement for the caffeine trial. Hudson
et al.[43] had 15 subjects perform four sets of arm
flexion and knee extension exercises to exhaus-
tion, using a 12RM resistance model performed
to volitional fatigue. Compared with placebo,
caffeine use resulted in significantly greater total
repetitions (knee extension) and repetitions in the
first set (knee extension and arm flexion), and
approached significance for the fourth set (knee
extensions; p = 0.051). The effect size for knee
extension and arm flexion was ‡5 repetitions.
Performance for 53% of subjects exceeded this
number for total repetitions (all combined) for
knee extension and arm flexion, while 47% of
subjects exceeded this number for the first set
alone in both exercises. This study emphasizes the
importance of evaluating individual data versus
group means only. That is, it is possible that in
many data sets half the subjects could be labelled
as responders (benefitting from caffeine), while
the other half are nonresponders (for unknown
reasons, they do not benefit). This situation may
result in non-significant differences when evalu-
ating mean data. However, it would be inaccurate
to conclude caffeine has no ergogenic properties
from such a data set. Further work is needed to
elucidate interindividual responses to caffeine.
Also, it is advisable for future studies to also ex-
amine data in a manner that permits close eval-
uation of individual responses.
Beck et al.[16] used a randomized, double-blind
design where participants in both caffeine and
placebo arms performed one set at 80% 1RM to
failure for bench press and leg extension. The
mean increase in bench press for total volume of
weight lifted to failure was greater for caffeine
(34.0 kg) versus placebo (24.0 kg), with the dif-
ference approaching significance (p = 0.074). No
significant difference was observed for leg exten-
sion between caffeine and placebo. Williams
et al.[44] recently examined one set of repetitions to
failure for bench press and leg press at 80% 1RM
Sports Med 2009; 39 (10)
Caffeine and Anaerobic Performance
with caffeine (300 mg). No significant difference
was found with caffeine on muscular endurance
for bench press or leg press. A similar study by
Astorino et al.[45] had subjects perform one set of
repetitions to failure for bench press and leg press
at 60% 1RM with 6 mg/kg of caffeine. No sig-
nificant difference was found for bench press or
leg press with caffeine compared with placebo;
however, an 11% and 12% improvement was
noted for bench press and leg press, respectively.
Jacobs et al.[46] studied 13 male subjects who were
either currently involved in a resistance training
programme or had been involved within the pre-
ceding year. The subjects consumed 4 mg/kg of
caffeine 90 minutes prior to performing supersets
of leg press (80% 1RM) immediately followed by
bench press (70% 1RM) to failure. Subjects
completed a total of three supersets with 2 minutes’
recovery between each superset. No significant
difference was noted for caffeine compared with
placebo during the three supersets or between
exercises for bench press or leg press.
The effects of caffeine on 1RM have received
very little attention until recently, showing con-
flicting results. Beck et al.[16] examined 1RM for
bench press and leg extension. Caffeine use re-
sulted in a significant improvement in 1RM for
bench press (2.1 kg) but failed to show an effect
for leg extension. Williams et al.[44] and Astorino
et al.[45] both failed to find an effect for 1RM with
caffeine for bench press and leg press. A reason
for these discrepancies between studies is unclear.
It appears caffeine has minimal effects of 1RM,
and further studies are needed before a definite
conclusion can be reached.
Studies of caffeine and resistance training are
sparse, with results being equivocal and implica-
tions of the ergogenic potential of caffeine un-
clear. Typically within the first set for muscular
endurance involving leg musculature no differ-
ence has been reported for caffeine compared
with placebo.[16,42,44-46] However, in one study[43]
improvement was observed in early sets. Multiple
sets offer evidence[42,43] that caffeine may elicit its
effects for the leg musculature later when fatigue
may play a more prominent role compared with
earlier sets. Although this was not shown by
Jacobs et al.,[46] the subjects’ training background
ª 2009 Adis Data Information BV. All rights reserved.
819
may have potentially affected the results. Caf-
feine effects on upper body musculature offer
opposite results compared with lower body ex-
ercises, showing greater improvements in the first
sets.[16,43] Overall, the majority of studies do not
support an ergogenic effect with caffeine on
muscle endurance.[42,44-46] This raises the ques-
tion whether the ergogenic properties of caf-
feine are limited by the amount of muscle mass
recruited and by the total number of sets per-
formed. Potential limitations of these studies in-
clude incorporating only one upper and lower
body exercise, typically with a low number of sets
being performed. Considering typical resistance
training programmes use multiple exercises for
upper and lower body, future investigations
should seek to use multiple exercises, with a
greater number of sets, in order to understand
whether caffeine is ergogenic within a more eco-
logically valid paradigm. Although relatively few
studies have been conducted in this area, it ap-
pears caffeine has minimal effects with upper
body exercise for 1RM and muscle endurance.
Multiple sets of resistance training with caffeine
offer introductory evidence for enhanced perfor-
mance on lower body musculature. However,
1RM does not appear to be affected.
1.6 Isokinetic Peak Torque
Very little work has examined the ergogenic
potential of caffeine administration on isokinetic
peak torque, with studies showing equivocal re-
sults. Bond et al.[47] gave 12 collegiate track
sprinters a 5 mg/kg dose of caffeine (compared
with placebo). They tested the sprinters for max-
imal voluntary contraction (MVC) on knee
extension and flexion. MVC is defined as a
muscle exerting a maximal amount of force dur-
ing a static contraction against an immovable
resistance.[48] Subjects performed six maximum
repetitions at three sequential ordered speeds
(30, 150 and 300/second). Peak torque, peak
power and fatigue index were compared between
caffeine and placebo trials. Results showed no
difference in peak torque, peak power and fatigue
index at any of the velocities with caffeine sup-
plementation. Jacobson and Edwards[49] examined
Sports Med 2009; 39 (10)
820
isokinetic peak torque on the knee extensor and
flexors (75, 180 and 300/second) of 36 untrained
subjects (20 male, 16 female) with performance
for the first 125 msec and power recorded during
300/second. Subjects were assigned to one of
three groups based on a caffeine dosage of 600 mg
or 300 mg, or placebo. Caffeine use resulted in no
significant performance difference for any dose
among velocities. Jacobson et al.[50] performed a
follow-up study with trained (division one foot-
ball players) male athletes (n = 20), who took a
7 mg/kg dose of caffeine (vs placebo). Peak tor-
que of the knee extensor and flexors (30, 150 and
300/second) was examined. Additionally, per-
formance for the first 125 msec and power (W)
were recorded at 300/second. Caffeine consump-
tion resulted in significantly greater peak torque
for the knee extensors at 30 and 300/second ve-
locities and flexors at all (30, 150 and 300/second)
velocities. Performance improvements for the
first 125 msec were only significant for knee
flexors, where power (W) was significant for knee
extensors only. This follow-up study[50] with
trained athletes offers introductory evidence that
caffeine affects peak torque; however, with only a
small volume of research testing this paradigm,
many questions still remain.
1.7 Isometric Maximal Force and Endurance
Studies evaluating the effect of caffeine on
isometric contractions have typically examined
ergogenic properties by assessing muscular en-
durance (time to exhaustion or a predetermined
minimum force level) and maximal force-
generating capacity by MVC. Earlier studies do
not support an effect on either MVC or muscular
endurance with caffeine on isometric contrac-
tions.[51,52] Williams et al.[51] showed no differ-
ence in endurance or MVC during voluntary
isometric handgrip exercise following ingestion
of caffeine 7 mg/kg. Lopes et al.[52] also noted no
difference with caffeine 500 mg on MVC or en-
durance time during sustained contractions of
the adductor pollicis muscle, although a 12% in-
crease in endurance was shown following caffeine
(vs placebo) supplementation. These studies fail-
ing to find an effect have used small sample sizes
ª 2009 Adis Data Information BV. All rights reserved.
Davis & Green
(n = 5,[52] n = 6[51]), which might have potentially
negated results. However, Lopes et al.[52] did find
a significant effect for other variables with caf-
feine (i.e. tension developed at lower frequencies).
Recent studies using larger sample sizes (n = 10–15)
have reported an ergogenic effect on sustained
endurance with caffeine during submaximal
isometric knee extensions (50% MVC) with caf-
feine 6 mg/kg.[53-55] An increase of 17–25% in
endurance capacity has been reported with sub-
maximal contractions of the quadriceps,[53-55] but
with equivocal results for MVC. An increased
MVC force production of 4.4% has recently been
reported,[56] with Kalmar and Cafarelli[55] also
reporting an increase in MVC. However, other
studies have failed to show a difference with
caffeine on MVC.[53,57] The reasons for these
discrepancies are unclear. It appears caffeine pro-
longs muscle endurance within this paradigm, but
the impact on maximal force-generating capacity
when assessed by MVC should be further explored.
Although discussed later (section 3), these results
may indicate caffeine fails to alter the maximal
force-generating capacity of a muscle but may
function to extend time to fatigue by acting via
altered pain perception. More detail is provided in
section 3.
1.8 Interindividual Variability
The effect of caffeine on performance has
commonly been reported as a group mean among
subjects, with relatively few studies examining
individual response. Studies reporting individual
data do not show improved performance for
every individual.[32,36,39,40,43,53,56] Future studies
should employ a test-retest study design and ex-
amine the factors that may influence the effects of
caffeine on performance. Studies should be de-
signed to try to elucidate what factor(s) causes a
person to be a responder versus a nonresponder.
Thus, individuals showing a positive response
(responders) with specific supplementation should
possibly consider this for practice and competi-
tion, while others showing minimal improvements
or potential ergolytic effects (nonresponders)
should discontinue supplementation. The reason
why individuals may not respond to caffeine is
Sports Med 2009; 39 (10)
Caffeine and Anaerobic Performance
unclear. Considering most studies assessing dif-
ferences between habitual and non-habitual users
have found no difference in performance para-
meters for anaerobic[15,32,36,39,57] and aerobic ex-
ercise,[58-61] it seems other unknown mediators
are involved other than habituation.
2. Mechanisms of Action
2.1 Peripheral Mechanisms
Early mechanisms for a caffeine ergogenic ef-
fect with aerobic performance stem from enhanced
free-fatty acid oxidation and glycogen sparing
primarily thought to occur by an amplified
adrenaline (epinephrine) output;[62] however, this
notion has been challenged and it seems likely
caffeine may operate via alternative mechanisms.[1]
It is unlikely a model based on enhanced oxida-
tion of fatty acids would affect exercise dominated
by oxygen-independent metabolic pathways, such
as high-intensity exercise. Therefore, the follow-
ing section examines mechanisms by which caf-
feine may be ergogenic. Peripheral and central
pathways are explored.
2.2 Catecholamines
Studies examining catecholamine response to
high-intensity exercise have shown an increased
adrenaline secretion with caffeine administration
compared with placebo.[14,15,17,30,36] This is con-
sistent with endurance exercise.[63-65] Only a few
studies do not show an increase associated with
caffeine ingestion.[66,67] Increased adrenaline le-
vels could potentially enhance performance via
an increased glycolytic flux, although studies that
have shown enhanced adrenaline levels and im-
proved performance have not always shown
greater glycolytic flux (e.g. assessed via lactic
acid).[15,36] Also, elevated adrenaline output has
not consistently translated to increased perfor-
mance for all studies.[14,17] In some studies,[17,41]
increased adrenaline levels were not observed
yet a subsequent increased glycolytic flux was
evident via greater production or declined re-
moval. However, studies assessing glycolytic
flux have not measured it directly but measured
a mixed venous blood,[14,15,17,36] which is a crude
ª 2009 Adis Data Information BV. All rights reserved.
821
tool for studying glycolysis in the hopes of detect-
ing differences in flux. Although adrenaline might
play a permissive role in enhanced performance, it
seems unlikely that it acts as the main mechanism
responsible for the ergogenic effects of caffeine.
2.3 Lactic Acid
Caffeine has been shown through various ex-
ercise paradigms to result in greater lactic acid
concentration for endurance exercise.[64,65,68-72]
Lactic acid along with other variables (i.e. K+,
glucose) has been shown to increase in resting
conditions with caffeine consumption. This has
been attributed to hepatic and resting skeletal
tissue.[73] However, the results from high-
intensity exercise have been equivocal. Some
studies show increased lactate[14,15,27,28,39,41] and
others show no increase.[17,23,32,36] It is interesting
to note that despite training status, the majority
of studies showing an increase in lactate have also
shown an increase in performance.[14,15,27,28,39]
Some authors speculate that increased lactate
might have been detrimental to perfor-
mance,[14,41] although a few studies failed to show
an effect on performance with an increase in
lactate concentration.[14,41] Conversely, studies
showing no difference in lactate with caffeine
have reported an increase in performance.[23,32,36]
Only one study showed no effect on perfor-
mance.[17] As previously mentioned, the effect of
caffeine on increased lactate levels does not al-
ways seem to be primarily mediated through
adrenaline. A possible explanation for an in-
crease in glycolytic flux could lie with caffeine
stimulating the CNS and consequently dampen-
ing pain perception. While the role of the CNS
and pain perception in fatigue is not well defined,
it is plausible that blunting pain perception would
mitigate fatigue by extending the timepoint at
which a level of pain is experienced that would
result in exercise termination. Extended duration
consequent to blunted pain may result in greater
lactate accumulation. The two may be related by
coincidence rather than revealing a mechanistic
function of caffeine at the level of the muscle.
This is discussed in the following section in
greater detail.
Sports Med 2009; 39 (10)
822
2.4 Blood Glucose
Hepatic output of glucose has been shown to
dramatically increase during high-intensity ex-
ercise[74,75] as a result of a parallel rise in adrenaline
and noradrenaline (norepinephrine).[76] As men-
tioned earlier (section 2.2), caffeine has been shown
to amplify adrenaline output from the adrenal
medulla. Therefore, it would seem plausible that
blood-borne glucose would subsequently increase
more with caffeine administration. The majority of
studies support this notion,[14,28,32,77,78] with only a
few studies showing no effect.[15,17,41] Although
studies not supporting this relationship have used
untrained subjects, this does not explain why an
increase in adrenaline for both studies did not
mirror that of blood-borne glucose. Other studies
utilizing untrained subjects have shown a re-
lationship.[14,28] The results of these studies com-
bined with previously mentioned mechanisms (i.e.
adrenaline, lactate) do not support any glycogen-
sparing effect, and in fact support the idea of
enhanced glycolytic turnover. Previously men-
tioned by Graham[1] on the aerobic paradigm,
these mechanisms seem to offer sparse insight
into the influence of caffeine on anaerobic per-
formance. Enhanced glycolytic output does not
seem to be directly affected by caffeine but has an
indirect effect, primarily acting through the CNS.
2.5 Potassium
The proposed model stating that caffeine could
enhance excitation-contraction coupling stems
from caffeine facilitating Na+/K+ ATPase activ-
ity.[79] Several authors provide evidence for this
indirectly through attenuation of plasma K+ levels
during rest[40] and exercise.[36,77,80] During mus-
cular contractions, depolarization of a muscle cell
results in K+ efflux into the extracellular fluid,
which then can diffuse into blood plasma.[81,82].
Maintaining an electrochemical gradient of
Na+ and K+ is important if a forceful output of
muscle contractions is to occur.[83] Thus, prevent-
ing a rise in plasma K+ by enhanced Na+/K+
ATPase activity could create a more favourable
environment for excitation-contraction, poten-
tially delaying fatigue.[84] Caffeine metabolites
ª 2009 Adis Data Information BV. All rights reserved.
Davis & Green
(paraxanthine) have been shown to stimulate
resting skeletal muscle K+ transport by increasing
Na+/K+ ATPase activity.[85] Caffeine has been
shown to attenuate the increase in plasma K+
during aerobic work.[77,80] However, compara-
tively little work has been conducted within the
anaerobic paradigm on attenuation of plasma [K+]
with caffeine. It is nevertheless reasonable to
assume this could be a contributing factor when
caffeine use results in enhanced performance. Con-
sidering plasma K+ concentrations during exercise
have shown a parallel increase with exercise inten-
sity,[86] it seems plausible that caffeine would elicit
its effect to a greater extent during high-intensity
exercise. However, this has not been the case.
Greer et al.[17] showed no significant effect on at-
tenuating plasma K+ levels. Crowe et al.[41] showed
a decrease in plasma K+ prior to exercise but
failed to show an effect during exercise. Doherty
et al.[36] showed a reduction in plasma K+ with
caffeine compared with placebo during exercise.
Although Doherty et al.[36] showed attenuation
of K+ during high-intensity exercise, it should be
considered that caffeine was supplemented after
the loading phase of creatine when interpreting
their results. It is important to note with Lindinger
et al.[80] that 9 mg/kg of caffeine had a greater
impact on attenuating plasma K+ compared with
lower doses (3–6 mg/kg). They also noted that the
attenuated response .of caffeine on K+ was more
consistent
. at 78% VO2 max compared with 85%
VO2 max . Furthermore, in Lindinger et al.,[80] some
subjects but not all showed attenuated levels
of plasma K+. Studies failing to show an impact
on K+ during exercise do not seem to be hindered
by relative dose employed, with subjects consum-
ing 5[17] or 6[41] mg/kg. Studies showing an effect
used 3–9 mg/kg.[36,76,79] Recreationally trained[41]
and untrained[17] subjects both failed to show an
impact on K+ during exercise. Thus, it appears that
an intensity-dependent relationship may exist for
caffeine attenuation of plasma K+. It is impor-
tant for future studies to assess what impact
caffeine has on attenuating plasma K+ levels and
determine whether an intensity-related response
for caffeine on K+ levels exists with trained
subjects in an environment specific to the sports
paradigm.
Sports Med 2009; 39 (10)
Caffeine and Anaerobic Performance
2.6 Calcium/Phosphodiesterase
Inhibition/Cyclic Adenosine Monophosphate
Cascade
Calcium and phosphodiesterase inhibition have
been proposed to play an intimate role in the
mechanisms for a caffeine ergogenic effect. Caf-
feine has been shown to inhibit phosphodiester-
ase enzymes in vitro,[87] allowing an increase in
intracellular cyclic adenosine monophosphate
(cAMP).[88] An increase in cAMP would lead to a
greater lipolysis, due to the cAMP relationship
with regulation of adipose tissue.[89,90] Thus, caf-
feine potentially plays a mechanistic role for the
rationale of caffeine-enhanced free-fatty oxidation
(and with a subsequent glycogen sparing) even
though, as noted, this mechanism is unlikely to
explain any ergogenic value of caffeine during
higher-intensity bouts. Caffeine has been shown to
cause a greater increase in calcium mobilization
from the sarcoplasmic reticulum.[91-93] Addi-
tionally, compared with fast twitch fibres, caffeine
may have a greater sensitivity for affecting slow
twitch muscle fibres[94-96] and slow twitch sarco-
plasmic reticulum[97] in vitro. This could have
favourable effects on excitation-contraction cou-
pling, potentially attenuating muscle fatigue.
Although a strong argument can be made for the
effects of caffeine on inhibiting phosphodiesterase
and mobilizing calcium in vitro (specifically me-
thylxanthines), in vivo it appears the physiological
dose required to do this would be toxic. Thus, it is
unlikely that the effects of caffeine would be eli-
cited through these proposed mechanisms.[88,98-100]
3. Central Mechanism
3.1 Adenosine Antagonism
It is commonly known that caffeine stimulates
the CNS – specifically, with the effects mediated
through adenosine receptor antagonism.[101-106]
Adenosine is a compound composed of adenine
and ribose, and has been shown to be a powerful
vasodilator.[107] Adenosine metabolism is regu-
lated primarily through adenine nucleotide
(ATP, adenosine diphosphate, adenosine mono-
phosphate) breakdown,[108] thus exercise can
increase adenosine concentration in skeletal
ª 2009 Adis Data Information BV. All rights reserved.
823
muscle,[107] smooth muscle, the circulatory system
and the brain.[109] Specifically, a physiological
stimulus is thought to initiate adenosine release
from neurons, where degradation of nucleotides
occurs later.[107] Adenosine is a molecule similar
in structure to caffeine,[98] and has been shown to
enhance pain perception,[110,111] induce sleep,[112]
reduce arousal,[113] depress spontaneous loco-
motor activity[114] and act as a neuromodu-
lator.[100,101,115-118] However, caffeine has been
shown to counter these inhibitory effects of ade-
nosine.[100,101,112,114,119] Various receptors for
adenosine are located throughout the CNS and
brain, depending on receptor subtype.[120] Four
different receptor subtypes exist for adenosine
(A1, A2a, A2b and A3), with various receptors
producing varying response with adenosine.[121]
Inhibitory effects of adenosine act through
A1 receptor activation, while excitatory response
occurs with A2 receptors.[107,112] Caffeine is a
nonselective adenosine inhibitor and can easily
cross the blood-brain barrier by simple diffusion
and carrier-mediated transport due to its lipo-
philic nature.[122] The effects are primarily elicited
through the A1 and A2a receptors due to their
higher affinity for adenosine compared with A2b
and A3 receptors, which have a lower affinity for
adenosine and seem to be stimulated under
periods of hypoxia or ischaemia.[100,107,123] As
discussed below (section 3.2), the hypotheses for
caffeine mechanisms are thought to occur from
inhibitory effects on adenosine, thus leading to
modified pain perception while sustaining motor
unit firing rates and neuro-excitability. This then
is the leading hypothesis for the ergogenic effect
of caffeine on performance, particularly during
anaerobic performance.
3.2 Pain Perception
The pain adaptation model states that pain
reduces output of muscles when they act as ago-
nists and increases the output when they become
antagonists.[124] This leads to a reduction in MVC
and velocity of movement.[124] Ultimately, the abil-
ity for forceful muscle contraction is reduced.[124]
Experimentally, pain has been shown to influence
motor unit recruitment (i.e. decreased firing
Sports Med 2009; 39 (10)
824
rate).[98,125,126] This has been correlated to the
intensity of muscle pain[125] through sensory
nerve transmission signalling.[102] Pain may be
induced intramuscularly by injecting capsai-
cin[126] or hypertonic saline[127-130] in the masseter
muscles or other muscles to try and replicate
clinical muscle pain.[126,130] Adenosine has been
shown to induce muscle pain when infused in-
travenously in both healthy subjects and patients
with angina.[110,111,131,132] This shows its ability to
reduce the pain threshold.[133] Antinociceptive
(pain suppression) effects occur from activation
of A1 adenosine receptors, where stimulation of
A2 receptors elicits a hyperalgesic (pain en-
hancement) response.[102,134-136] Clinically selec-
tive blockade of A2A receptors could play a major
role in the therapeutic development of pain
medications[137] and may have implications for
Huntington’s disease[138] and anti-Parkinson
drugs.[139] The majority of studies designed to
study pain have used different methods to induce
pain. However, naturally occurring pain through
exercise is not well understood.[140,141]
Caffeine is commonly used in over-the-counter
mediations for its pain-relieving effect[142] due
to its blockade of adenosine receptors.[104] Clini-
cally it has been commonly used to help re-
duce headaches.[143,144] Caffeine combined with
other analgesic medications (e.g. paracetamol
[acetaminophen]) has been shown to enhance
pain-relieving ability better than with certain
medications alone.[142] Additionally, the analge-
sic effects of caffeine have been shown to reduce
experimental muscle pain.[145] Thus, one of the
main concepts behind the caffeine mechanism
seems to be concerned with pain perception. If
caffeine can decrease naturally occurring pain of
exercise and sustain or increase firing rates of
motor units, a greater force output should be
maintained. This hypothesis might explain the
effects of caffeine in studies showing positive ef-
fects on anaerobic performance. However, it is
crucial to state, as mentioned by Kalmar,[98] that
no study data (to our knowledge) have examined
the effect of caffeine on motor unit firing rates
with experimentally induced pain. Recently,
Greer et al.[18] had subjects not accustomed to the
rigour of high-intensity exercise each perform a
ª 2009 Adis Data Information BV. All rights reserved.
Davis & Green
traditional 30-second Wingate test. They found
that caffeine had no effect on electromyogram
(EMG) activity. Williams et al.[19] also failed to
find an effect with caffeine on EMG signalling
during maximal and submaximal isometric hand
grip contraction. Meyers and Cafarelli[54] also
found no difference during submaximal isometric
contractions on EMG activity for caffeine. These
studies imply that caffeine may not affect motor
unit recruitment. Recently, more sophisticated
techniques were used to examine motor unit fir-
ing rates and recruitment with caffeine. No dif-
ferences were found for either enhanced motor
unit recruitment[53-55] or increased output of
motor unit firing rates[54] with caffeine compared
with placebo during submaximal (e.g. 50% MVC)
isometric contractions.
Recent work has shown leg muscle pain to be
reduced
. during 30 minutes of cycling at 60%
VO2 max with caffeine.[146] The authors concluded
that the ergogenic effects of caffeine might be
partially explained by the hypoalgesic (pain-
relieving) properties of caffeine,[146] postulating
A2a receptor blockade exceeded that of A1 re-
ceptor antagonist effect of caffeine; i.e. caffeine
blocked A2A receptors more compared with A1
receptors, thus producing a hypoalgesic effect.
Additionally, a dose-dependent response on re-
duced pain perception has been shown with
10 mg/kg compared with 5 mg/kg of .caffeine in
males for 30 minutes of cycling at 60% VO2 max .[147]
However, Motl et al.[148] did not show a dose-
dependent response for pain perception with
females but noted a lower overall muscle pain
perception for females compared with males be-
tween these
. studies during 30 minutes of cycling
at 60% VO2 max . Similar results for decreased leg
muscle pain during exercise for females have been
reported.[149] However, other studies inducing
pain experimentally have shown females having a
higher muscle pain rating and lower pain thresh-
old.[150,151] What difference in impact caffeine
would have on performance between males and
females is unclear, considering relatively few
studies have included female participants (table I)
and no study (to our knowledge) has examined
performance measures on sex differences with
caffeine.
Sports Med 2009; 39 (10)
Caffeine and Anaerobic Performance 825

Table I. Summary of literature pertaining to caffeine and anaerobic performance

Study (year) No. and sex Dosage Population Findings
Isokinetic peak torque
Jacobson et al.[50] (1992) 20 M 7 mg/kg Elite male athletes › peak torque, › power output
Jacobson et al.[49] (1991) 20 M 600 mg Recreationally active 2 peak torque
16 F 300 mg
Bond et al.[47] (1986) 12 M 5 mg/kg Intercollegiate track 2 peak torque
sprinters
Dynamic training
Beck et al.[16] (2006) 13 M 201 mg Weight-trained subjects › 1RM bench press, 2 1RM leg press,
(>1 year) 2 reps to failure
Green et al.[42] (2007) 13 M 6 mg/kg Weight-trained subjects 2 reps to failure: bench press, leg press
4F (>8 weeks)
Hudson et al.[43] (2007) 15 M 6 mg/kg Weight-trained subjects › reps to failure: leg extension;
(>8 weeks) 2 arm curls
Jacobs et al.[46] (2003) 13 M 4 mg/kg Weight-trained, currently 2 reps to failure: leg press, bench press
or involved in past year
Astorino et al.[45] (2008) 22 M 6 mg/kg Weight-trained subjects 2 reps to failure: leg press, bench press;
(>6 years) 21RM
Williams et al.[44] (2008) 9M 300 mg Weight-trained subjects 2 reps to failure: bench press, latissimus
(>2 years) dorsi pulldown; 2 1RM
Isometric force production and endurance
Kalmar and Cafarelli[55] (1999) 11 M 6 mg/kg N/S › peak force, muscle endurance
Williams[117] (1987) 6M 7 mg/kg N/S 2 peak force, muscle endurance
Lopes et al.[52] (1983) 5 (N/S) 500 mg N/S 2 peak force, muscle endurance
Plaskett and Cafarelli[53] (2001) 15 M 6 mg/kg N/S 2 peak force, › muscle endurance
Maridakis et al.[56] (2007) 9F 5 mg/kg Untrained › peak force
Meyers and Cafarelli[54] (2005) 10 M 6 mg/kg N/S › muscle endurance
Tarnopolsky and Cupido[57] (2000) 12 M 6 mg/kg N/S 2 peak force
Muscle soreness and damage
Maridakis et al.[56] (2007) 9F 5 mg/kg Untrained fl pain perception/attenuated DOMS,
› peak force
Sprint power cycling
Anselm et al.[28] (1992) 10 M 250 mg Recreationally active › power output
4F
Greer et al.[18] (2006) 18 M 5 mg/kg Recreationally active 2 peak power, mean power, percentage
decline in power
Greer et al.[17] (1998) 9M 6 mg/kg Recreationally active 2 power output
Kang et al.[23] (1998) 14 (N/S) 5 mg/kg Trained cyclist and › total power, mean power, peak power:
2.5 mg/kg recreationally active both populations
subjects
Beck et al.[16] (2006) 13 M 201 mg Weight trained 2 mean power, peak power
Hoffman et al.[21] (2007) 8M 450 mg Recreationally active 2 power output
2F (coffee)
Collomp et al.[14] (1991) 3M 5 mg/kg Untrained 2 power output
3F
Lorino et al.[20] (2006) 16 M 6 mg/kg Recreationally active 2 power output
Bell et al.[15] (2001) 16 M 5 mg/kg Untrained 2 power output

Continued next page

ª 2009 Adis Data Information BV. All rights reserved. Sports Med 2009; 39 (10)
826 Davis & Green

Table I. Contd
Study (year) No. and sex Dosage Population Findings
Schneiker et al.[27] (2006) 10 M 6 mg/kg Team sport athletes › total work, mean power
Roberts et al.[22] (2007) 5M 450 mg Recreationally active 2 mean power, peak power, time to peak
5F (coffee) power
Speed endurance cycling/running
Wiles et al.[40] (2006) 8F 5 mg/kg Trained cyclist › mean speed, mean power, peak power,
performance
Doherty and Smith[7] (2004) 11 M 5 mg/kg Trained cyclist › mean power
Doherty et al.[36] (2002) 14 M 5 mg/kg Trained › run time to exhaustion
Doherty[32] (1998) 9M 5 mg/kg Trained › run time to exhaustion
Bell et al.[15] (2001) 16 M 5 mg/kg Untrained › cycling time to exhaustion
Crowe et al.[41] (2006) 12 M 6 mg/kg Recreationally active fl time to peak power (significant), total
5F power, peak power between bouts 1 and 2
(not significant)
Sprints
Collomp et al.[31] (1992) 5 M, 250 mg Trained and untrained › performance (trained), 2 performance
9F swimmers untrained
Stuart et al.[30] (2005) 9M 6 mg/kg Australian rugby players › sprint, power, passing performance
[29]
Paton et al. (2001) 16 M 6 mg/kg Team sport athletes fl performance
Agility
Lorino et al.[20] (2006) 16 M 6 mg/kg Recreationally active 2 pro-agility
Stuart et al.[30] (2005) 9M 6 mg/kg Australian rugby players › agility
1RM = one-repetition maximum; DOMS = delayed-onset muscle soreness; F = female subjects; M = male subjects; N/S = not specified;
reps = repetitions; fl indicates decrease; › indicates increase; 2 indicates no difference.

Studies examining pain perception with caffeine
during an anaerobic paradigm have been sparse.
Pain perception index during repetitions to fail-
ure for resistance training has shown no differ-
ence between caffeine and placebo. However,
repetitions were greater at various sets through-
out the trial, suggesting pain perception may have
been suppressed with caffeine.[43] Caffeine has
recently been shown to attenuate delayed-onset
muscle pain and force loss following eccentric
exercise induced by electrical stimulation of the
quadriceps.[56] A statistically significant hypo-
algesic effect was shown during maximal volun-
tary isometric contractions, with a decrease of
12.7 raw visual analogue scale (VAS) units with
caffeine compared with 1.9 VAS for placebo.
A smaller nonsignificant decrease was reported
for caffeine (7.8 VAS) compared with placebo
(1.9 VAS) during submaximal voluntary eccentric
contractions 1 hour after ingestion of caffeine
5 mg/kg in untrained female subjects. This study
shows novel insight of the hypoalgesic effect of
caffeine within this paradigm. However, whether
these results apply to trained subjects using a
more practical model assessing pain on eccentric
training (i.e. free weights) remains unknown.
The effects of caffeine on altering pain percep-
tion and affecting the CNS are well documented.
Although the mechanisms of the effects of caffeine
may act primarily via stimulating the CNS, the role
of peripheral tissue should not be diminished.
Some studies show an effect with caffeine in which
the CNS played a minimal role.[52,57,152] Future
investigations should be conducted in order to
elucidate the exact mechanisms of caffeine.
3.3 Rating of Perceived Exertion
As previously mentioned, the effects of caffeine
on pain perception are well documented in clinical
settings. However, only recently have the analgesic
effects of caffeine been applied to naturally occur-
ring pain of exercise. It would seem logical that
caffeine could potentially decrease perceived

ª 2009 Adis Data Information BV. All rights reserved. Sports Med 2009; 39 (10)
Caffeine and Anaerobic Performance
exertion, thus possibly allowing athletes to work at
a greater intensity or prolong the duration of ex-
ercise. In a recent meta-analysis, Doherty and
Smith[8] reviewed the effects of caffeine on rating of
perceived exertion (RPE), showing that caffeine
dampened perceived exertion by 5.6% compared
with placebo. Regression analysis revealed that
29% of the variance explained the ergogenic effect
of caffeine on performance by decreased RPE. The
effects of caffeine on RPE have been extensively
examined in the aerobic paradigm,[62,153,154] but
research examining the effects of caffeine on
anaerobic performance has been scarce. Only a few
studies have examined RPE while performing
high-intensity exercise, with the majority of studies
showing no difference for RPE between caffeine
and placebo,[27,42,43] and others showing a de-
creased RPE,[36,39] or even an increased RPE
compared with placebo.[41] Doherty et al.[36] found
that caffeine showed a clear trend for decreased
RPE at every 30-second timepoint (RPE taken for
2 minutes); however, a significant difference was
only noticed
. at 90 seconds for run time to fatigue at
125% VO2 max . Doherty et al.[39] also found a de-
creased RPE of approximately 1 point (Borg Scale)
during high-intensity cycling for 3 minutes. How-
ever, Crowe et al.[41] found an increased RPE ap-
proaching significance (p = 0.055) for caffeine
compared with placebo between bouts 1 and 2
during 60 seconds of high-intensity cycling.
The effects caffeine exerts on RPE during
resistance training have only recently been
examined. Green et al.[42] and Hudson et al.[43]
both failed to show a difference in RPE with
caffeine compared with placebo during resistance
training. However, both studies did find an in-
crease in repetitions with caffeine at various sets
throughout their protocol, suggesting RPE was
blunted to an extent with caffeine. As mentioned
previously (section 1.2), caffeine has been shown
to enhance short duration high-intensity exercise
when the methodology has been matched to mi-
mic athletic competitions (i.e. 4–6 seconds).[27,30]
Schneiker et al.[27] found that caffeine did not
decrease RPE compared with placebo; however,
total sprint work and peak power were greater.
Therefore, participants for Green et al.,[42]
Hudson et al.[43] and Schneiker et al.[27] were able
ª 2009 Adis Data Information BV. All rights reserved.
827
to accomplish more work despite the same per-
ceived exertion as placebo, offering introductory
evidence that caffeine blunts perceived exertion
during high-intensity exercise. The lack of dif-
ferences between studies perhaps suggests the
RPE scale is too gross to be used to detect chan-
ges in perception at such high exercise intensities.
Although these studies offer promising insight on
the mechanism of caffeine for improved perfor-
mance, more research is clearly needed in this
area before the extent of the effect of caffeine can
be fully understood.
3.4 Fatigue
The effects of fatigue have been associated
with both peripheral and central mechanisms.
However, it is beyond the scope of this review to
evaluate whether fatigue is more a product of
peripheral or central fatigue – but merely to ex-
amine what effects caffeine has on attenuating
fatigue during exercise. Caffeine has recently
been proposed as a tool to examine fatigue,[155]
considering it affects both peripheral and central
pathways in vivo and in vitro. When fatigue is
evaluated via aerobic performance, caffeine has
commonly shown increased time to fatigue for
humans[64,65,71,78,152,156] and animals[157] com-
pared with placebo. Recent work from our lab-
oratory (unpublished observation) supports the
notion that caffeine attenuates fatigue during
sprint-type activity. Studies have attributed en-
hanced anaerobic performance,[27,30] submaximal
isometric contractions,[53-55] and speed endurance
protocols[15,32,36,39] to attenuated fatigue. Thus, it
appears caffeine not only delays fatigue in aero-
bic exercise but also in protocols that rely heavily
on oxygen-independent metabolic pathways.
4. Conclusion and Future Directions
Caffeine seems to be ergogenic during high-
intensity exercise, depending on the paradigm.
Exercises examining isokinetic peak torque,
isometric maximal force, muscular endurance for
upper body musculature, and 1RM show equi-
vocal results, with caffeine having minimal
ergogenic effect within these areas. Studies of
Sports Med 2009; 39 (10)
828
repetitions to failure for lower body musculature
offer introductory evidence that caffeine has an
effect on resistance training. Recent work sup-
ports the notion that caffeine affects isometric
muscle endurance. Considering a relatively large
body of research has not been conducted within
these areas, more studies are clearly needed be-
fore a definite conclusion can be reached on
muscular endurance and muscular force. Tradi-
tional measures of power output observed during
the 30-second Wingate protocol do not seem
favourably enhanced by caffeine administration.
Yet this has been examined most often in untrained
athletes. Speed endurance (i.e. 60–180 seconds
in duration) seems to be highly affected by caf-
feine. High-intensity exercise seems to be favour-
ably affected (i.e. sprinting, sprint cycling power)
with methodologies employing protocols that
mimic sport activities (i.e. 4–6 seconds), while
agility performance remains unclear. Therefore,
sports such as soccer, rugby, lacrosse and foot-
ball would seem to be favourably affected by
caffeine.
Earlier research examining the effects of caf-
feine on performance typically employed un-
trained subjects with methodologies not specific
to high-intensity intermittent sport activities.
These designs and subject characteristics poten-
tially contributed to the conclusion that caffeine
may not be beneficial in this paradigm. However,
recent studies have started employing trained
subjects accustomed to the rigour of the proto-
cols tested. Therefore, caffeine seems to be the
most beneficial for trained subjects, with the
majority of studies showing little to no effect on
untrained subjects. The reason for such differ-
ences in training status between subjects is
currently unclear. Additionally, a subject’s
habituation status with caffeine does not seem to
have an effect on either aerobic or anaerobic
exercise.
Although an argument can be made regarding
the impact caffeine has on the peripheral me-
chanisms, specifically regarding Na+/K+ pumps,
it seems likely that caffeine mechanisms act
primarily by stimulating the CNS through ade-
nosine antagonism, dampening pain perception,
blunting perceived exertion, and delaying fatigue.
ª 2009 Adis Data Information BV. All rights reserved.
Davis & Green
Caffeine has received tremendous attention
within exercise models dominating aerobic ATP
pathways. It has received relatively less attention
with respect to work bouts relying principally on
anaerobic ATP pathways, thus leaving many
questions unanswered. Future research should
examine the impact and the extent caffeine has on
high-intensity performance, with individual and
group data being assessed, and also whether
sex differences exist. Studies are also needed to
understand whether individuals respond similarly
during repeated bouts of exercise (true responders)
with caffeine consumption and elucidate the
underlying mechanisms between responders and
nonresponders. Furthermore, the acute and
chronic effects of caffeine on muscular endurance
performance incorporating multiple exercises
and sets should be examined further. Finally,
work is necessary to isolate the precise mechan-
isms by which caffeine acts as an ergogenic aid.
Acknowledgements
No sources of funding were used to assist in the prepara-
tion of this review. The authors have no conflicts of interest
that are directly relevant to the content if this review.
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Correspondence: Dr J.K. Davis, Department of Health
and Human Performance, PO BOX 3011, Texas A&M
University-Commerce, Commerce, TX 75429, USA.
E-mail: JonKyle_Davis@tamu-commerce.edu
Sports Med 2009; 39 (10)