Caffeine and Anaerobic Performance Ergogenic.2

Caffeine and Anaerobic PerformanceErgogenic 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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8131. Ergogenic Effect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 814

1.1 Wingate/Sprint Cycling Power . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8141.2 Sprinting/Sport-Specific Testing . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8161.3 Agility . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8171.4 Speed Endurance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8171.5 Muscular Endurance/One-Repetition Maximum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8181.6 Isokinetic Peak Torque . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8191.7 Isometric Maximal Force and Endurance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8201.8 Interindividual Variability . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 820

2. Mechanisms of Action . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8212.1 Peripheral Mechanisms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8212.2 Catecholamines . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8212.3 Lactic Acid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8212.4 Blood Glucose. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8222.5 Potassium. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8222.6 Calcium/Phosphodiesterase Inhibition/Cyclic Adenosine Monophosphate Cascade. . . . . . . . . 823

3. Central Mechanism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8233.1 Adenosine Antagonism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8233.2 Pain Perception . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8233.3 Rating of Perceived Exertion. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8263.4 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 ergogenicpotential 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 trainedsubjects and paradigms specific to intermittent sports activity support thenotion that caffeine is ergogenic to an extent with anaerobic exercise. Caffeineseems highly ergogenic for speed endurance exercise ranging in duration from60 to 180 seconds. However, other traditional models examining power out-put (i.e. 30-second Wingate test) have shown minimal effect of caffeine onperformance. Conversely, studies employing sport-specific methodologies

REVIEW ARTICLESports Med 2009; 39 (10): 813-8320112-1642/09/0010-0813/$49.95/0

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(i.e. hockey, rugby, soccer) with shorter duration (i.e. 4–6 seconds) showcaffeine to be ergogenic during high-intensity intermittent exercise. Recentstudies show caffeine affects isometric maximal force and offers introductoryevidence for enhanced muscle endurance for lower body musculature. How-ever, isokinetic peak torque, one-repetition maximum and muscular en-durance for upper bodymusculature are less clear. Since relatively few studiesexist with resistance training, a definite conclusion cannot be reached on theextent caffeine affects performance.

It was previously thought that caffeine mechanisms were associated withadrenaline (epinephrine)-induced enhanced free-fatty acid oxidation and con-sequent glycogen sparing, which is the leading hypothesis for the ergogeniceffect. It would seem unlikely that the proposed theory would result in improvedanaerobic performance, since exercise is dominated by oxygen-independentmetabolic pathways. Other mechanisms for caffeine have been suggested, suchas enhanced calcium mobilization and phosphodiesterase inhibition. However,a normal physiological dose of caffeine in vivo does not indicate this mechanismplays a large role. Additionally, enhanced Na+/K+ pump activity has beenproposed 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 thenegative effects adenosine induces on neurotransmission, arousal and painperception. The hypoalgesic effects of caffeine have resulted in dampened painperception and blunted perceived exertion during exercise. This could poten-tially have favourable effects on negating decreased firing rates of motor unitsand possibly produce a more sustainable and forceful muscle contraction. Theexact 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 otherproducts. It is metabolized in the liver to di-methyxanthines (paraxanthine, theobromine,theophylline) and is proposed to affect varioustissues throughout the body, including peripheraland central tissues.[1] The popularity of caffeineas an ergogenic aide has increased dramaticallyover the last decade, and various forms of admin-istration (i.e. sports drinks, sports gels, energydrinks) have become more available in recentyears. Athletes commonly consume caffeine in anattempt to enhance performance. However, ethicalconsiderations have been raised regarding theeffect of caffeine on performance, leading theNational Collegiate Athletic Association (NCAA)to implement urinary caffeine restrictions. Nu-merous reviews[1-8] have examined the effects onperformance that caffeine elicits, but this has pri-marily been directed toward aerobic performance.

Few reviews have examined the effect of caffeinesolely on anaerobic performance. Rather, theyhave treated the effects on anaerobic perfor-mance merely as a subset of the review.[1-8] In thecurrent review we exclusively examine anaerobicperformance. More specifically, exercise bouts of4–180 seconds in duration are examined. The firstsection explores the influence of caffeine in variousanaerobic paradigms with particular attentiongiven 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 measureof power output and anaerobic capacity[9] andhas been commonly employed when assessing

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

ergogenic aids and anaerobic performance. Three30-second repeated Wingate tests have shown thehighest percentage of energy production fromanaerobic metabolism consisting of 60–84% ofoxygen-independent ATP production.[10-13] Stu-dies examining effects of caffeine onWingate per-formance have typically shown minimal ergogeniceffects.[14-22] Greer et al.[17] actually showed anergolytic effect of caffeine with a decrease inpower-output on the fourth Wingate bout com-pared with placebo. Only one study supports thenotion of that caffeine is ergogenic within thisparadigm.[23]

Testing untrained subjects presents problemsin interpreting the ergogenic potential of caffeinein trained individuals. Most studies failing toshow ergogenic potential have incorporated un-trained subjects (not specifically accustomed tointermittent-sprint exercise),[14,15,17,18,20-22] withonly 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 bethe best model to assess the ergogenic effect ofcaffeine within this exercise paradigm. The onlystudy to support an ergogenic effect with caffeineon 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 5.0mg/kgmass caffeine and placebo in counterbalancedorder. Caffeine significantly increased totalpower, mean power and peak power in bothgroups compared with placebo, with no differ-ence noted between caffeine doses. It is unclearwhy untrained subjects improved performancefor Kang et al.,[23] considering other studies uti-lizing untrained subjects have found no changein performance.[14,15,17,18] Beck et al.[16] hadresistance-trained subjects perform two Wingatetests, consuming 201mg 1 hour prior to the trial.There were no differences between caffeine andplacebo for peak power, mean power and per-centage decrease in performance. However, theseresults should be interpreted with caution con-sidering resistance-trained subjects were em-ployed. While likely accustomed to high-intensityanaerobic exercise, subjects participating in reg-

ular sprints, particularly cycling, might be betteradapted to perform repeat Wingate tests. Ad-ditionally, caffeine was not administered relativeto body mass, and when the mean mass for sub-jects is equated with dose administered (200mg)mean consumption per subject is 2.4mg/kg(2.1–3.0mg/kg), potentially negating an ergo-genic effect. However, other studies have foundimproved performance with similar doses of caf-feine.[23-25] Consequently, the dose may havebeen inadequate to enhance performance and thesubjects’ training background (resistance-trainedvs cyclist) could account for equivocal results.Future studies using the Wingate protocol withrepeated bouts should use highly anaerobic-trained subjects accustomed to intermittent boutsof cycling to ascertain whether caffeine is ergo-genic in this paradigm.

Although the Wingate test is typically used toexamine anaerobic capacity, it does not reflectthe performance requirements of sports involvingintermittent high-intensity efforts (e.g. ice hock-ey, soccer, field hockey, American football), andconsequently it is uncertain whether the results ofcaffeine on Wingate performance would be ob-served during sports-specific activities. Court orfield-base team sports often consist of short boutsof intermittent sprints (2–5 seconds), performedover short distances (10–20m), and with brief restperiods between bouts.[26] In order to mimicathletic competition more closely, Schneikeret al.[27] assessed the effects of caffeine on ama-teur level team sport athletes from local and stateclubs (e.g. football, soccer and hockey), con-suming 6mg/kg of caffeine. To simulate a sports-specific paradigm, subjects (n = 10) performed2 · 36-minute halves, with each half composed of18 · 4-second maximal exertion cycling boutswith 2 minutes recovery at 35%

.VO2max between

sprints. Compared with placebo, caffeine use re-sulted in a significant improvement for the firsthalf (8.5%) and second half (7.6%) for total work.Similarly, there was a significant improvementfor the first half (7.0%) and second half (6.6%) forpeak power. These results show that when thetesting protocol more closely mimics athleticcompetitions with trained subjects accustomed tointermittent-sprint bouts, caffeine does provide

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an ergogenic effect. Anselm et al.[28] found a 7%increase in maximal anaerobic power (Wmax)with untrained subjects during a single 6-secondsprint following consumption of 250mg of caf-feine. However, Williams et al.[19] found no benefitfrom caffeine (7mg/kg) during maximal exercise(15 seconds) for peak power, total power andfatigue index with untrained subjects. AlthoughWilliams et al.[19] failed to find improved perfor-mance during a 15-second Wingate test, resultsindicate that caffeine is beneficial for trained anduntrained subjects when bouts are 4–6 seconds’duration, which may more closely mimic the timeframe 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 · 20msprints with 10 seconds’ recovery between sprints.Bouts were completed following 6mg/kg caffeineconsumption and placebo. Caffeine resulted insignificantly slower mean sprint time (0.1%):compared with the first sprint, a 14.0% increase intime over 10 sprints was noted for placebo versus14.7% for caffeine. One potential problem dis-cussed in the article, possibly due to lack of space,is that at the end of the 20m sprint, subjects hadto decelerate. Anticipation of deceleration likelyimpaired sprint times and could have masked anyergogenic effects of caffeine. Stuart et al.[30] simu-lated a rugby game with Australian rugby playersperforming seven circuits in each 2 · 40-minutehalf, with 10 minutes’ half-time rest after con-suming 6mg/kg of caffeine. Skill tasks assessedincluded sprinting, agility, power generation andpassing accuracy. Eleven stations were performedper circuit with 30-second intervals between sta-tions, and two stations consisted of straight-linesprinting (20–30m sprints). Caffeine significantlyimproved sprint time by 0.5–2.9% for the entiretrial (all sprints combined); specifically, perfor-mance improved in the first half for 20–30m(0.5, 2.3%) and second half for 20–30m sprints(1.4, 3.4%). Reasons for equivocal results be-tween Stuart et al.[30] and Paton et al.[29] are un-

clear. Although distances were relatively the same,recovery duration between sprints was different(10 seconds[29] vs 30 seconds[30]). The rest :workratio used by Paton et al.[29] was between 2 : 1 and3 : 1, depending on how long it took the subject tocomplete the 20m sprint, where Stuart et al.[30]

employed a 4.5 : 1 ratio for rest to work. Therest :work ratio could have a dramatic effect onrecovery, and the short rest :work ratio employedby Paton et al.[29] could have prevented the au-thors from observing any ergogenic effect. Thus,the effect of rest :workmight play a crucial role inallowing caffeine to magnify its effect. Futurestudies should investigate to what extent rest ��work or total volume plays on allowing caffeineto elicit its effect on performance.

Only one study to date has examined the ef-fects of caffeine on anaerobic performance inswimmers.[31] Collomp et al.[31] used a within-subjects design in order to examine the effects ofcaffeine 250mg on a 2 · 100m maximal exertionfreestyle swim, with 20 minutes passive recoverybetween bouts, on trained and untrained swim-mers. Overall, trained swimmers significantly im-proved swimming velocity with caffeine (vs placebo)compared with untrained subjects, with greaterimprovement noted during the second 100m.Trained swimmers had been competitive for5 years and had been training 5–6 days a week for4 consecutive months at the time of the study.These results[31] seem promising; however, futurestudies are warranted. Considering the 2007NCAA 100m freestyle final for first and secondplace was separated by 0.73 seconds and first andtenth by 1.58 seconds, if caffeine could elicitsimilar results shown with trained subjects asStuart et al.[30] showed on sprint performance(0.5–2.9%), a competitive advantage is plausible.While worthy of further inquiry, it should also benoted that precise simulation of the competitiveenvironment in a controlled laboratory settingis difficult. It is possible that if caffeine actsvia CNS function (discussed in detail later in sec-tion 3), the level of arousal typically associatedwith competition may mask ergogenic propertiesthat might be observed during laboratory testing.However, it could still be an important trainingtool during practice.

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1.3 Agility

Athletic competitions involving brief periodsof high-intensity exercise consist of a combina-tion of sprints and agility-based performances.Studies on the ergogenic effect caffeine has onagility performance have shown equivocal re-sults.[20,30] Conflicting results could stem from themethodology employed between these studies.Stuart et al.[30] examined agility by having partici-pants perform three agility sprints (22, 33 and 31m)performed in a swerving (or zigzag) pattern. Caf-feine improved overall mean agility sprint perfor-mance for all three sprints by 2.2% compared withplacebo in the first half, with second half perfor-mance improved by 1.7%; however, whether thiswas 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 tofind a significant difference between caffeine andplacebo for the pro-agility test. The reasons forconflicting results could be due to exercise para-digm and the subject familiarity. Although bothstudies incorporated a double-blind, crossoverdesign, Stuart et al.[30] used trained subjects (rugbyplayers) where Lorino et al.[20] used untrainedsubjects who were unaccustomed to the pro-agilitytest. Thus, untrained subjects not commonlyperforming agility work on a regular basis couldhave negated a potential ergogenic effect. Futureinvestigations examining agility skills should in-corporate trained subjects commonly performingagility drills on a weekly basis in order to under-stand what impact caffeine has on this type ofperformance.

1.4 Speed Endurance

Several studies have evaluated high-intensityexercise lasting between 60 and 180 seconds.A method that has commonly been employed toassess speed endurance has involved protocolsusing maximal accumulated oxygen deficit(MAOD). The MAOD model is considered asuitable test for a non-invasive indirect measure-

ment of anaerobic ATPmetabolism,[32,33] althoughothers have argued its value.[34,35]MAOD involvesrunning at a supramaximal intensity (e.g. 125%.VO2max), with volitional fatigue typically occur-ring at 2–3 minutes,[15,32,36] depending upon aparticipant’s level of training. MAOD allowsfor a unique exercise paradigm, with duration oftime similar to short-term track events (800m).Doherty[32] was the first to examine the MAODparadigmwith caffeine. His group showed caffeine(vs placebo) improved run time to exhaustion by14% (29 – 6 seconds). In a similar study, Dohertyet al.[36] had subjects perform supramaximal125%

.VO2max to exhaustion, with subjects sup-

plementing with caffeine or placebo after a 7-dayloading phase with oral creatine (20 g/day). Timeto fatigue was significantly greater by 23.8 sec-onds with caffeine plus creatine compared withplacebo (creatine only), and 21.3 seconds com-pared with baseline measurements. The resultsindicated caffeine is ergogenic within this para-digm, highlighting the potential use of acute caf-feine ingestion after oral creatine loading. Thisbrings novel insight to stacking these ergogenicaids in this manner because when caffeine is takenthroughout the loading phase of creatine a sy-nergistic effect has not been shown.[37,38] Caffeineinhibits elevations in intramuscular phospho-creatine levels.[37] Bell et al.[15] employed theMAOD model using cycle ergometry instead of atreadmill.[32,36] Time to fatigue at 125%

.VO2max

significantly increased by 8.8 seconds with caffeinecompared with placebo. Time to fatigue for Bellet al.[15] was not as great compared with Dohertyet al.;[32,36] however, a possible explanation is the useof trained[32,36] compared with untrained subjects.[15]

Collectively, studies using the MAOD modelseem favourable regarding the ergogenic effectsof caffeine, with positive results shown regardlessof training status,[15,32,36] but seem to impact per-formance to a greater extent for trained subjects.

Several studies have examined speed enduranceusing various protocols other than the MAODmodel. Doherty et al.[39] had subjects cycle for2 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 sprintwas significantly higher with caffeine (794– 164W)



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compared with placebo (750 – 163W). Wileset al.[40] examined performance time, mean speedand peak power with trained cyclists across three1 km cycling bouts. Using caffeine resulted in sig-nificantly improved performance (2.3 seconds),and significantly greater mean power (18.1W) andpeak power (75.5W), and faster mean speed(1.6 km/h). Crowe et al.[41] showed an ergolytic ef-fect with caffeine 6mg/kg during two 60-secondmaximal cycling bouts (separated by 3 minutes’passive seated recovery) with recreationally trainedsubjects (i.e. soccer, rugby, basketball). Use ofcaffeine resulted in a significantly slower time toreach peak power in exercise bout two comparedwith placebo, and in a greater decrease in peakpower 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 boutslasting 60–180 seconds seems beneficial for trainedand untrained individuals.[15,32,36,39,40]

1.5 Muscular Endurance/One-RepetitionMaximum

Compared with other popular ergogenic aids,few studies have assessed the effects of caffeine onresistance training performance. However, withstudies showing ergogenic effects of caffeineduring anaerobic performance, it is plausible thatcaffeine may affect resistance training, which isalso dominated by oxygen-independent meta-bolic pathways.

Common methods for examining muscularfitness are to assess strength by determining aone-repetition maximum (1RM) or to assess mus-cular endurance using repetitions to failure. Re-petitions to failure involve performing an all-outeffort of repetitions to volitional fatigue, usuallyperformed at a percentage of 1RM or multiplerepetitions max test (i.e. 10–12 repetitions). Themajority of studies examining repetitions to fail-ure have used subjects with various resistancetraining histories (8 weeks,[42,43] 1 year,[16] 2 years,[44]

6 years[45]), performing resistance training bouts2–4 (times) per week.[16,42-45] Green et al.[42] tested17 subjects (13 males, 4 females) performing threesets of bench presses and leg presses to failure

at 80% of 1RM in a double-blind, placebo-controlled design, with a dosage of 6mg/kg ofcaffeine. No significant difference was shown forbench presses or sets one and two for the legpresses between caffeine and placebo. However,the third set for leg presses showed a signifi-cant improvement for the caffeine trial. Hudsonet al.[43] had 15 subjects perform four sets of armflexion and knee extension exercises to exhaus-tion, using a 12RM resistance model performedto volitional fatigue. Compared with placebo,caffeine use resulted in significantly greater totalrepetitions (knee extension) and repetitions in thefirst set (knee extension and arm flexion), andapproached significance for the fourth set (kneeextensions; p= 0.051). The effect size for kneeextension and arm flexion was ‡5 repetitions.Performance for 53% of subjects exceeded thisnumber for total repetitions (all combined) forknee extension and arm flexion, while 47% ofsubjects exceeded this number for the first setalone in both exercises. This study emphasizes theimportance of evaluating individual data versusgroup means only. That is, it is possible that inmany data sets half the subjects could be labelledas responders (benefitting from caffeine), whilethe other half are nonresponders (for unknownreasons, they do not benefit). This situation mayresult in non-significant differences when evalu-ating mean data. However, it would be inaccurateto conclude caffeine has no ergogenic propertiesfrom such a data set. Further work is needed toelucidate 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-blinddesign where participants in both caffeine andplacebo arms performed one set at 80% 1RM tofailure for bench press and leg extension. Themean increase in bench press for total volume ofweight lifted to failure was greater for caffeine(34.0 kg) versus placebo (24.0 kg), with the dif-ference approaching significance (p = 0.074). Nosignificant difference was observed for leg exten-sion between caffeine and placebo. Williamset al.[44] recently examined one set of repetitions tofailure for bench press and leg press at 80% 1RM

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with caffeine (300mg). No significant differencewas found with caffeine on muscular endurancefor bench press or leg press. A similar study byAstorino et al.[45] had subjects perform one set ofrepetitions to failure for bench press and leg pressat 60% 1RM with 6mg/kg of caffeine. No sig-nificant difference was found for bench press orleg press with caffeine compared with placebo;however, an 11% and 12% improvement wasnoted for bench press and leg press, respectively.Jacobs et al.[46] studied 13 male subjects who wereeither currently involved in a resistance trainingprogramme or had been involved within the pre-ceding year. The subjects consumed 4mg/kg ofcaffeine 90 minutes prior to performing supersetsof leg press (80% 1RM) immediately followed bybench press (70% 1RM) to failure. Subjectscompleted a total of three supersets with 2minutes’recovery between each superset. No significantdifference was noted for caffeine compared withplacebo during the three supersets or betweenexercises for bench press or leg press.

The effects of caffeine on 1RM have receivedvery little attention until recently, showing con-flicting results. Beck et al.[16] examined 1RM forbench press and leg extension. Caffeine use re-sulted in a significant improvement in 1RM forbench press (2.1 kg) but failed to show an effectfor leg extension. Williams et al.[44] and Astorinoet al.[45] both failed to find an effect for 1RMwithcaffeine for bench press and leg press. A reasonfor these discrepancies between studies is unclear.It appears caffeine has minimal effects of 1RM,and further studies are needed before a definiteconclusion can be reached.

Studies of caffeine and resistance training aresparse, with results being equivocal and implica-tions of the ergogenic potential of caffeine un-clear. Typically within the first set for muscularendurance involving leg musculature no differ-ence has been reported for caffeine comparedwith placebo.[16,42,44-46] However, in one study[43]

improvement was observed in early sets. Multiplesets offer evidence[42,43] that caffeine may elicit itseffects for the leg musculature later when fatiguemay play a more prominent role compared withearlier sets. Although this was not shown byJacobs et al.,[46] the subjects’ training background

may have potentially affected the results. Caf-feine effects on upper body musculature offeropposite results compared with lower body ex-ercises, showing greater improvements in the firstsets.[16,43] Overall, the majority of studies do notsupport an ergogenic effect with caffeine onmuscle endurance.[42,44-46] This raises the ques-tion whether the ergogenic properties of caf-feine are limited by the amount of muscle massrecruited and by the total number of sets per-formed. Potential limitations of these studies in-clude incorporating only one upper and lowerbody exercise, typically with a low number of setsbeing performed. Considering typical resistancetraining programmes use multiple exercises forupper and lower body, future investigationsshould seek to use multiple exercises, with agreater number of sets, in order to understandwhether caffeine is ergogenic within a more eco-logically valid paradigm. Although relatively fewstudies have been conducted in this area, it ap-pears caffeine has minimal effects with upperbody exercise for 1RM and muscle endurance.Multiple sets of resistance training with caffeineoffer 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 ergogenicpotential of caffeine administration on isokineticpeak torque, with studies showing equivocal re-sults. Bond et al.[47] gave 12 collegiate tracksprinters a 5mg/kg dose of caffeine (comparedwith placebo). They tested the sprinters for max-imal voluntary contraction (MVC) on kneeextension and flexion. MVC is defined as amuscle exerting a maximal amount of force dur-ing a static contraction against an immovableresistance.[48] Subjects performed six maximumrepetitions at three sequential ordered speeds(30�, 150� and 300�/second). Peak torque, peakpower and fatigue index were compared betweencaffeine and placebo trials. Results showed nodifference in peak torque, peak power and fatigueindex at any of the velocities with caffeine sup-plementation. Jacobson and Edwards[49] examined



isokinetic peak torque on the knee extensor andflexors (75�, 180� and 300�/second) of 36 untrainedsubjects (20 male, 16 female) with performancefor the first 125 msec and power recorded during300�/second. Subjects were assigned to one ofthree groups based on a caffeine dosage of 600mgor 300mg, or placebo. Caffeine use resulted in nosignificant performance difference for any doseamong velocities. Jacobson et al.[50] performed afollow-up study with trained (division one foot-ball players) male athletes (n = 20), who took a7mg/kg dose of caffeine (vs placebo). Peak tor-que of the knee extensor and flexors (30�, 150� and300�/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 torquefor the knee extensors at 30� and 300�/second ve-locities and flexors at all (30�, 150� and 300�/second)velocities. Performance improvements for thefirst 125 msec were only significant for kneeflexors, where power (W) was significant for kneeextensors only. This follow-up study[50] withtrained athletes offers introductory evidence thatcaffeine affects peak torque; however, with only asmall volume of research testing this paradigm,many questions still remain.

1.7 Isometric Maximal Force and Endurance

Studies evaluating the effect of caffeine onisometric contractions have typically examinedergogenic properties by assessing muscular en-durance (time to exhaustion or a predeterminedminimum force level) and maximal force-generating capacity by MVC. Earlier studies donot support an effect on either MVC or muscularendurance with caffeine on isometric contrac-tions.[51,52] Williams et al.[51] showed no differ-ence in endurance or MVC during voluntaryisometric handgrip exercise following ingestionof caffeine 7mg/kg. Lopes et al.[52] also noted nodifference with caffeine 500mg on MVC or en-durance time during sustained contractions ofthe 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

(n = 5,[52] n= 6[51]), which might have potentiallynegated results. However, Lopes et al.[52] did finda 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 sustainedendurance with caffeine during submaximalisometric knee extensions (50% MVC) with caf-feine 6mg/kg.[53-55] An increase of 17–25% inendurance capacity has been reported with sub-maximal contractions of the quadriceps,[53-55] butwith equivocal results for MVC. An increasedMVC force production of 4.4% has recently beenreported,[56] with Kalmar and Cafarelli[55] alsoreporting an increase in MVC. However, otherstudies have failed to show a difference withcaffeine on MVC.[53,57] The reasons for thesediscrepancies are unclear. It appears caffeine pro-longs muscle endurance within this paradigm, butthe impact on maximal force-generating capacitywhen assessed byMVC should be further explored.Although discussed later (section 3), these resultsmay indicate caffeine fails to alter the maximalforce-generating capacity of a muscle but mayfunction to extend time to fatigue by acting viaaltered pain perception. More detail is provided insection 3.

1.8 Interindividual Variability

The effect of caffeine on performance hascommonly been reported as a group mean amongsubjects, with relatively few studies examiningindividual response. Studies reporting individualdata do not show improved performance forevery individual.[32,36,39,40,43,53,56] Future studiesshould employ a test-retest study design and ex-amine the factors that may influence the effects ofcaffeine on performance. Studies should be de-signed to try to elucidate what factor(s) causes aperson to be a responder versus a nonresponder.Thus, individuals showing a positive response(responders) with specific supplementation shouldpossibly consider this for practice and competi-tion, while others showing minimal improvementsor potential ergolytic effects (nonresponders)should discontinue supplementation. The reasonwhy individuals may not respond to caffeine is

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unclear. Considering most studies assessing dif-ferences between habitual and non-habitual usershave found no difference in performance para-meters for anaerobic[15,32,36,39,57] and aerobic ex-ercise,[58-61] it seems other unknown mediatorsare 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 enhancedfree-fatty acid oxidation and glycogen sparingprimarily thought to occur by an amplifiedadrenaline (epinephrine) output;[62] however, thisnotion has been challenged and it seems likelycaffeine may operate via alternative mechanisms.[1]

It is unlikely a model based on enhanced oxida-tion of fatty acids would affect exercise dominatedby oxygen-independent metabolic pathways, suchas high-intensity exercise. Therefore, the follow-ing section examines mechanisms by which caf-feine may be ergogenic. Peripheral and centralpathways are explored.

2.2 Catecholamines

Studies examining catecholamine response tohigh-intensity exercise have shown an increasedadrenaline secretion with caffeine administrationcompared with placebo.[14,15,17,30,36] This is con-sistent with endurance exercise.[63-65] Only a fewstudies do not show an increase associated withcaffeine ingestion.[66,67] Increased adrenaline le-vels could potentially enhance performance viaan increased glycolytic flux, although studies thathave shown enhanced adrenaline levels and im-proved performance have not always showngreater glycolytic flux (e.g. assessed via lacticacid).[15,36] Also, elevated adrenaline output hasnot consistently translated to increased perfor-mance for all studies.[14,17] In some studies,[17,41]

increased adrenaline levels were not observedyet a subsequent increased glycolytic flux wasevident via greater production or declined re-moval. However, studies assessing glycolyticflux have not measured it directly but measureda mixed venous blood,[14,15,17,36] which is a crude

tool for studying glycolysis in the hopes of detect-ing differences in flux. Although adrenaline mightplay a permissive role in enhanced performance, itseems unlikely that it acts as the main mechanismresponsible for the ergogenic effects of caffeine.

2.3 Lactic Acid

Caffeine has been shown through various ex-ercise paradigms to result in greater lactic acidconcentration for endurance exercise.[64,65,68-72]

Lactic acid along with other variables (i.e. K+,glucose) has been shown to increase in restingconditions with caffeine consumption. This hasbeen attributed to hepatic and resting skeletaltissue.[73] However, the results from high-intensity exercise have been equivocal. Somestudies show increased lactate[14,15,27,28,39,41] andothers show no increase.[17,23,32,36] It is interestingto note that despite training status, the majorityof studies showing an increase in lactate have alsoshown an increase in performance.[14,15,27,28,39]

Some authors speculate that increased lactatemight have been detrimental to perfor-mance,[14,41] although a few studies failed to showan effect on performance with an increase inlactate concentration.[14,41] Conversely, studiesshowing no difference in lactate with caffeinehave reported an increase in performance.[23,32,36]

Only one study showed no effect on perfor-mance.[17] As previously mentioned, the effect ofcaffeine on increased lactate levels does not al-ways seem to be primarily mediated throughadrenaline. A possible explanation for an in-crease in glycolytic flux could lie with caffeinestimulating the CNS and consequently dampen-ing pain perception. While the role of the CNSand pain perception in fatigue is not well defined,it is plausible that blunting pain perception wouldmitigate fatigue by extending the timepoint atwhich a level of pain is experienced that wouldresult in exercise termination. Extended durationconsequent to blunted pain may result in greaterlactate accumulation. The two may be related bycoincidence rather than revealing a mechanisticfunction of caffeine at the level of the muscle.This is discussed in the following section ingreater detail.



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2.4 Blood Glucose

Hepatic output of glucose has been shown todramatically increase during high-intensity ex-ercise[74,75] as a result of a parallel rise in adrenalineand noradrenaline (norepinephrine).[76] As men-tioned earlier (section 2.2), caffeine has been shownto amplify adrenaline output from the adrenalmedulla. Therefore, it would seem plausible thatblood-borne glucose would subsequently increasemore with caffeine administration. The majority ofstudies support this notion,[14,28,32,77,78] with only afew studies showing no effect.[15,17,41] Althoughstudies not supporting this relationship have useduntrained subjects, this does not explain why anincrease in adrenaline for both studies did notmirror that of blood-borne glucose. Other studiesutilizing 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 ofenhanced glycolytic turnover. Previously men-tioned by Graham[1] on the aerobic paradigm,these mechanisms seem to offer sparse insightinto the influence of caffeine on anaerobic per-formance. Enhanced glycolytic output does notseem to be directly affected by caffeine but has anindirect effect, primarily acting through the CNS.

2.5 Potassium

The proposed model stating that caffeine couldenhance excitation-contraction coupling stemsfrom caffeine facilitating Na+/K+ ATPase activ-ity.[79] Several authors provide evidence for thisindirectly through attenuation of plasma K+ levelsduring rest[40] and exercise.[36,77,80] During mus-cular contractions, depolarization of a muscle cellresults in K+ efflux into the extracellular fluid,which then can diffuse into blood plasma.[81,82].Maintaining an electrochemical gradient ofNa+ and K+ is important if a forceful output ofmuscle contractions is to occur.[83] Thus, prevent-ing a rise in plasma K+ by enhanced Na+/K+

ATPase activity could create a more favourableenvironment for excitation-contraction, poten-tially delaying fatigue.[84] Caffeine metabolites

(paraxanthine) have been shown to stimulateresting skeletal muscle K+ transport by increasingNa+/K+ ATPase activity.[85] Caffeine has beenshown to attenuate the increase in plasma K+

during aerobic work.[77,80] However, compara-tively little work has been conducted within theanaerobic paradigm on attenuation of plasma [K+]with caffeine. It is nevertheless reasonable toassume this could be a contributing factor whencaffeine use results in enhanced performance. Con-sidering plasma K+ concentrations during exercisehave shown a parallel increase with exercise inten-sity,[86] it seems plausible that caffeine would elicitits effect to a greater extent during high-intensityexercise. However, this has not been the case.Greer et al.[17] showed no significant effect on at-tenuating plasmaK+ levels. Crowe et al.[41] showeda decrease in plasma K+ prior to exercise butfailed to show an effect during exercise. Dohertyet al.[36] showed a reduction in plasma K+ withcaffeine compared with placebo during exercise.Although Doherty et al.[36] showed attenuationof K+ during high-intensity exercise, it should beconsidered that caffeine was supplemented afterthe loading phase of creatine when interpretingtheir results. It is important to note with Lindingeret al.[80] that 9mg/kg of caffeine had a greaterimpact on attenuating plasma K+ compared withlower doses (3–6mg/kg). They also noted that theattenuated response of caffeine on K+ was moreconsistent at 78%

.VO2max compared with 85%.

VO2max. Furthermore, in Lindinger et al.,[80] somesubjects but not all showed attenuated levelsof plasma K+. Studies failing to show an impacton K+ during exercise do not seem to be hinderedby relative dose employed, with subjects consum-ing 5[17] or 6[41] mg/kg. Studies showing an effectused 3–9mg/kg.[36,76,79] Recreationally trained[41]

and untrained[17] subjects both failed to show animpact onK+ during exercise. Thus, it appears thatan intensity-dependent relationship may exist forcaffeine attenuation of plasma K+. It is impor-tant for future studies to assess what impactcaffeine has on attenuating plasma K+ levels anddetermine whether an intensity-related responsefor caffeine on K+ levels exists with trainedsubjects in an environment specific to the sportsparadigm.

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2.6 Calcium/PhosphodiesteraseInhibition/Cyclic Adenosine MonophosphateCascade

Calcium and phosphodiesterase inhibition havebeen proposed to play an intimate role in themechanisms for a caffeine ergogenic effect. Caf-feine has been shown to inhibit phosphodiester-ase enzymes in vitro,[87] allowing an increase inintracellular cyclic adenosine monophosphate(cAMP).[88] An increase in cAMP would lead to agreater lipolysis, due to the cAMP relationshipwith regulation of adipose tissue.[89,90] Thus, caf-feine potentially plays a mechanistic role for therationale of caffeine-enhanced free-fatty oxidation(and with a subsequent glycogen sparing) eventhough, as noted, this mechanism is unlikely toexplain any ergogenic value of caffeine duringhigher-intensity bouts. Caffeine has been shown tocause a greater increase in calcium mobilizationfrom the sarcoplasmic reticulum.[91-93] Addi-tionally, compared with fast twitch fibres, caffeinemay have a greater sensitivity for affecting slowtwitch muscle fibres[94-96] and slow twitch sarco-plasmic reticulum[97] in vitro. This could havefavourable effects on excitation-contraction cou-pling, potentially attenuating muscle fatigue.Although a strong argument can be made for theeffects of caffeine on inhibiting phosphodiesteraseand mobilizing calcium in vitro (specifically me-thylxanthines), in vivo it appears the physiologicaldose required to do this would be toxic. Thus, it isunlikely 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 stimulatesthe CNS – specifically, with the effects mediatedthrough adenosine receptor antagonism.[101-106]

Adenosine is a compound composed of adenineand ribose, and has been shown to be a powerfulvasodilator.[107] Adenosine metabolism is regu-lated primarily through adenine nucleotide(ATP, adenosine diphosphate, adenosine mono-phosphate) breakdown,[108] thus exercise canincrease adenosine concentration in skeletal

muscle,[107] smooth muscle, the circulatory systemand the brain.[109] Specifically, a physiologicalstimulus is thought to initiate adenosine releasefrom neurons, where degradation of nucleotidesoccurs later.[107] Adenosine is a molecule similarin structure to caffeine,[98] and has been shown toenhance 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 beenshown to counter these inhibitory effects of ade-nosine.[100,101,112,114,119] Various receptors foradenosine are located throughout the CNS andbrain, depending on receptor subtype.[120] Fourdifferent receptor subtypes exist for adenosine(A1, A2a, A2b and A3), with various receptorsproducing varying response with adenosine.[121]

Inhibitory effects of adenosine act throughA1 receptor activation, while excitatory responseoccurs with A2 receptors.[107,112] Caffeine is anonselective adenosine inhibitor and can easilycross the blood-brain barrier by simple diffusionand carrier-mediated transport due to its lipo-philic nature.[122] The effects are primarily elicitedthrough the A1 and A2a receptors due to theirhigher affinity for adenosine compared with A2b

and A3 receptors, which have a lower affinity foradenosine and seem to be stimulated underperiods of hypoxia or ischaemia.[100,107,123] Asdiscussed below (section 3.2), the hypotheses forcaffeine mechanisms are thought to occur frominhibitory effects on adenosine, thus leading tomodified pain perception while sustaining motorunit firing rates and neuro-excitability. This thenis the leading hypothesis for the ergogenic effectof caffeine on performance, particularly duringanaerobic performance.

3.2 Pain Perception

The pain adaptation model states that painreduces output of muscles when they act as ago-nists and increases the output when they becomeantagonists.[124] This leads to a reduction inMVCand velocity of movement.[124] Ultimately, the abil-ity for forceful muscle contraction is reduced.[124]

Experimentally, pain has been shown to influencemotor unit recruitment (i.e. decreased firing



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rate).[98,125,126] This has been correlated to theintensity of muscle pain[125] through sensorynerve transmission signalling.[102] Pain may beinduced intramuscularly by injecting capsai-cin[126] or hypertonic saline[127-130] in the massetermuscles or other muscles to try and replicateclinical muscle pain.[126,130] Adenosine has beenshown to induce muscle pain when infused in-travenously in both healthy subjects and patientswith angina.[110,111,131,132] This shows its ability toreduce the pain threshold.[133] Antinociceptive(pain suppression) effects occur from activationof A1 adenosine receptors, where stimulation ofA2 receptors elicits a hyperalgesic (pain en-hancement) response.[102,134-136] Clinically selec-tive blockade of A2A receptors could play a majorrole in the therapeutic development of painmedications[137] and may have implications forHuntington’s disease[138] and anti-Parkinsondrugs.[139] The majority of studies designed tostudy pain have used different methods to inducepain. However, naturally occurring pain throughexercise is not well understood.[140,141]

Caffeine is commonly used in over-the-countermediations for its pain-relieving effect[142] dueto its blockade of adenosine receptors.[104] Clini-cally it has been commonly used to help re-duce headaches.[143,144] Caffeine combined withother analgesic medications (e.g. paracetamol[acetaminophen]) has been shown to enhancepain-relieving ability better than with certainmedications alone.[142] Additionally, the analge-sic effects of caffeine have been shown to reduceexperimental muscle pain.[145] Thus, one of themain concepts behind the caffeine mechanismseems to be concerned with pain perception. Ifcaffeine can decrease naturally occurring pain ofexercise and sustain or increase firing rates ofmotor units, a greater force output should bemaintained. This hypothesis might explain theeffects of caffeine in studies showing positive ef-fects on anaerobic performance. However, it iscrucial to state, as mentioned by Kalmar,[98] thatno study data (to our knowledge) have examinedthe effect of caffeine on motor unit firing rateswith experimentally induced pain. Recently,Greer et al.[18] had subjects not accustomed to therigour of high-intensity exercise each perform a

traditional 30-second Wingate test. They foundthat caffeine had no effect on electromyogram(EMG) activity. Williams et al.[19] also failed tofind an effect with caffeine on EMG signallingduring maximal and submaximal isometric handgrip contraction. Meyers and Cafarelli[54] alsofound no difference during submaximal isometriccontractions on EMG activity for caffeine. Thesestudies imply that caffeine may not affect motorunit recruitment. Recently, more sophisticatedtechniques were used to examine motor unit fir-ing rates and recruitment with caffeine. No dif-ferences were found for either enhanced motorunit recruitment[53-55] or increased output ofmotor unit firing rates[54] with caffeine comparedwith placebo during submaximal (e.g. 50% MVC)isometric contractions.

Recent work has shown leg muscle pain to bereduced during 30 minutes of cycling at 60%.VO2max with caffeine.[146] The authors concludedthat the ergogenic effects of caffeine might bepartially explained by the hypoalgesic (pain-relieving) properties of caffeine,[146] postulatingA2a receptor blockade exceeded that of A1 re-ceptor antagonist effect of caffeine; i.e. caffeineblocked 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 with10mg/kg compared with 5mg/kg of caffeine inmales for 30minutes of cycling at 60%

.VO2max.

[147]

However, Motl et al.[148] did not show a dose-dependent response for pain perception withfemales but noted a lower overall muscle painperception for females compared with males be-tween these studies during 30 minutes of cyclingat 60%

.VO2max. Similar results for decreased leg

muscle pain during exercise for females have beenreported.[149] However, other studies inducingpain experimentally have shown females having ahigher muscle pain rating and lower pain thresh-old.[150,151] What difference in impact caffeinewould have on performance between males andfemales is unclear, considering relatively fewstudies have included female participants (table I)and no study (to our knowledge) has examinedperformance measures on sex differences withcaffeine.

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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

16 F

600 mg

300 mg

Recreationally active 2 peak torque

Bond et al.[47] (1986) 12 M 5 mg/kg Intercollegiate track

sprinters

2 peak torque

Dynamic training

Beck et al.[16] (2006) 13 M 201 mg Weight-trained subjects

(>1 year)› 1RM bench press, 2 1RM leg press,

2 reps to failure

Green et al.[42] (2007) 13 M

4 F

6 mg/kg Weight-trained subjects

(>8 weeks)

2 reps to failure: bench press, leg press

Hudson et al.[43] (2007) 15 M 6 mg/kg Weight-trained subjects

(>8 weeks)› reps to failure: leg extension;

2 arm curls

Jacobs et al.[46] (2003) 13 M 4 mg/kg Weight-trained, currently

or involved in past year

2 reps to failure: leg press, bench press

Astorino et al.[45] (2008) 22 M 6 mg/kg Weight-trained subjects

(>6 years)

2 reps to failure: leg press, bench press;

21RM

Williams et al.[44] (2008) 9 M 300 mg Weight-trained subjects

(>2 years)

2 reps to failure: bench press, latissimus

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) 6 M 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) 9 F 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) 9 F 5 mg/kg Untrained fl pain perception/attenuated DOMS,

› peak force

Sprint power cycling

Anselm et al.[28] (1992) 10 M

4 F

250 mg Recreationally active › power output

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) 9 M 6 mg/kg Recreationally active 2 power output

Kang et al.[23] (1998) 14 (N/S) 5 mg/kg

2.5 mg/kg

Trained cyclist and

recreationally active

subjects

› total power, mean power, peak power:

both populations

Beck et al.[16] (2006) 13 M 201 mg Weight trained 2 mean power, peak power

Hoffman et al.[21] (2007) 8 M

2 F

450 mg

(coffee)

Recreationally active 2 power output

Collomp et al.[14] (1991) 3 M

3 F

5 mg/kg Untrained 2 power output

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



Studies examining pain perception with caffeineduring 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 perceptionmay havebeen suppressed with caffeine.[43] Caffeine hasrecently been shown to attenuate delayed-onsetmuscle pain and force loss following eccentricexercise induced by electrical stimulation of thequadriceps.[56] A statistically significant hypo-algesic effect was shown during maximal volun-tary isometric contractions, with a decrease of12.7 raw visual analogue scale (VAS) units withcaffeine compared with 1.9 VAS for placebo.A smaller nonsignificant decrease was reportedfor caffeine (7.8 VAS) compared with placebo(1.9 VAS) during submaximal voluntary eccentriccontractions 1 hour after ingestion of caffeine5mg/kg in untrained female subjects. This studyshows novel insight of the hypoalgesic effect of

caffeine within this paradigm. However, whetherthese results apply to trained subjects using amore practical model assessing pain on eccentrictraining (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 caffeinemay act primarily via stimulating the CNS, the roleof peripheral tissue should not be diminished.Some studies show an effect with caffeine in whichthe CNS played a minimal role.[52,57,152] Futureinvestigations should be conducted in order toelucidate the exact mechanisms of caffeine.

3.3 Rating of Perceived Exertion

As previously mentioned, the effects of caffeineon pain perception are well documented in clinicalsettings. However, only recently have the analgesiceffects of caffeine been applied to naturally occur-ring pain of exercise. It would seem logical thatcaffeine could potentially decrease perceived

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) 5 M

5 F

450 mg

(coffee)

Recreationally active 2 mean power, peak power, time to peak

power

Speed endurance cycling/running

Wiles et al.[40] (2006) 8 F 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) 9 M 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

5 F

6 mg/kg Recreationally active fl time to peak power (significant), total

power, peak power between bouts 1 and 2

(not significant)

Sprints

Collomp et al.[31] (1992) 5 M,

9 F

250 mg Trained and untrained

swimmers› performance (trained), 2 performance

untrained

Stuart et al.[30] (2005) 9 M 6 mg/kg Australian rugby players › sprint, power, passing performance

Paton et al.[29] (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) 9 M 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.

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exertion, thus possibly allowing athletes to work ata greater intensity or prolong the duration of ex-ercise. In a recent meta-analysis, Doherty andSmith[8] reviewed the effects of caffeine on rating ofperceived exertion (RPE), showing that caffeinedampened perceived exertion by 5.6% comparedwith placebo. Regression analysis revealed that29% of the variance explained the ergogenic effectof caffeine on performance by decreased RPE. Theeffects of caffeine on RPE have been extensivelyexamined in the aerobic paradigm,[62,153,154] butresearch examining the effects of caffeine onanaerobic performance has been scarce. Only a fewstudies have examined RPE while performinghigh-intensity exercise, with the majority of studiesshowing no difference for RPE between caffeineand placebo,[27,42,43] and others showing a de-creased RPE,[36,39] or even an increased RPEcompared with placebo.[41] Doherty et al.[36] foundthat caffeine showed a clear trend for decreasedRPE at every 30-second timepoint (RPE taken for2 minutes); however, a significant difference wasonly noticed at 90 seconds for run time to fatigue at125%

.VO2max. Doherty et al.[39] also found a de-

creasedRPE 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 caffeinecompared with placebo between bouts 1 and 2during 60 seconds of high-intensity cycling.

The effects caffeine exerts on RPE duringresistance training have only recently beenexamined. Green et al.[42] and Hudson et al.[43]

both failed to show a difference in RPE withcaffeine compared with placebo during resistancetraining. However, both studies did find an in-crease in repetitions with caffeine at various setsthroughout their protocol, suggesting RPE wasblunted to an extent with caffeine. As mentionedpreviously (section 1.2), caffeine has been shownto enhance short duration high-intensity exercisewhen 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 notdecrease 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

to accomplish more work despite the same per-ceived exertion as placebo, offering introductoryevidence that caffeine blunts perceived exertionduring high-intensity exercise. The lack of dif-ferences between studies perhaps suggests theRPE scale is too gross to be used to detect chan-ges in perception at such high exercise intensities.Although these studies offer promising insight onthe mechanism of caffeine for improved perfor-mance, more research is clearly needed in thisarea before the extent of the effect of caffeine canbe fully understood.

3.4 Fatigue

The effects of fatigue have been associatedwith both peripheral and central mechanisms.However, it is beyond the scope of this review toevaluate whether fatigue is more a product ofperipheral or central fatigue – but merely to ex-amine what effects caffeine has on attenuatingfatigue during exercise. Caffeine has recentlybeen proposed as a tool to examine fatigue,[155]

considering it affects both peripheral and centralpathways in vivo and in vitro. When fatigue isevaluated via aerobic performance, caffeine hascommonly shown increased time to fatigue forhumans[64,65,71,78,152,156] and animals[157] com-pared with placebo. Recent work from our lab-oratory (unpublished observation) supports thenotion that caffeine attenuates fatigue duringsprint-type activity. Studies have attributed en-hanced anaerobic performance,[27,30] submaximalisometric contractions,[53-55] and speed enduranceprotocols[15,32,36,39] to attenuated fatigue. Thus, itappears caffeine not only delays fatigue in aero-bic exercise but also in protocols that rely heavilyon 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 forupper body musculature, and 1RM show equi-vocal results, with caffeine having minimalergogenic effect within these areas. Studies of



repetitions to failure for lower body musculatureoffer introductory evidence that caffeine has aneffect on resistance training. Recent work sup-ports the notion that caffeine affects isometricmuscle endurance. Considering a relatively largebody of research has not been conducted withinthese areas, more studies are clearly needed be-fore a definite conclusion can be reached onmuscular endurance and muscular force. Tradi-tional measures of power output observed duringthe 30-second Wingate protocol do not seemfavourably enhanced by caffeine administration.Yet this has been examinedmost often in untrainedathletes. Speed endurance (i.e. 60–180 secondsin 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 thatmimic sport activities (i.e. 4–6 seconds), whileagility performance remains unclear. Therefore,sports such as soccer, rugby, lacrosse and foot-ball would seem to be favourably affected bycaffeine.

Earlier research examining the effects of caf-feine on performance typically employed un-trained subjects with methodologies not specificto high-intensity intermittent sport activities.These designs and subject characteristics poten-tially contributed to the conclusion that caffeinemay not be beneficial in this paradigm. However,recent studies have started employing trainedsubjects accustomed to the rigour of the proto-cols tested. Therefore, caffeine seems to be themost beneficial for trained subjects, with themajority of studies showing little to no effect onuntrained subjects. The reason for such differ-ences in training status between subjects iscurrently unclear. Additionally, a subject’shabituation status with caffeine does not seem tohave an effect on either aerobic or anaerobicexercise.

Although an argument can be made regardingthe impact caffeine has on the peripheral me-chanisms, specifically regarding Na+/K+ pumps,it seems likely that caffeine mechanisms actprimarily by stimulating the CNS through ade-nosine antagonism, dampening pain perception,blunting perceived exertion, and delaying fatigue.

Caffeine has received tremendous attentionwithin exercise models dominating aerobic ATPpathways. It has received relatively less attentionwith respect to work bouts relying principally onanaerobic ATP pathways, thus leaving manyquestions unanswered. Future research shouldexamine the impact and the extent caffeine has onhigh-intensity performance, with individual andgroup data being assessed, and also whethersex differences exist. Studies are also needed tounderstand whether individuals respond similarlyduring repeated bouts of exercise (true responders)with caffeine consumption and elucidate theunderlying mechanisms between responders andnonresponders. Furthermore, the acute andchronic effects of caffeine on muscular enduranceperformance incorporating multiple exercisesand 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 interestthat are directly relevant to the content if this review.

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Correspondence: Dr J.K. Davis, Department of Healthand Human Performance, PO BOX 3011, Texas A&MUniversity-Commerce, Commerce, TX 75429, USA.E-mail: [email protected]

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