International Journal of Sport Nutrition and Exercise Metabolism, 2008, 18, 412-429 2008 Human Kinetics, Inc. The Effect of Caffeine as an Ergogenic Aid in Anaerobic Exercise Kathleen Woolf, Wendy K. Bidwell, and Amanda G. Carlson
The study examined caffeine (5 mg/kg body weight) vs. placebo during anaerobic exercise. Eighteen male athletes (24.1 ± 5.8 yr; BMI 26.4 ± 2.2 kg/m2) completed a leg press, chest press, and Wingate test. During the caffeine trial, more total weight was lifted with the chest press, and a greater peak power was obtained during the Wingate test. No differences were observed between treatments for the leg press and average power, minimum power, and power drop (Wingate test). There was a significant treatment main effect found for postexercise glucose and insulin concentrations; higher concentrations were found in the caffeine trial. A significant interaction effect (treatment and time) was found for cortisol and glucose concentrations; both increased with caffeine and decreased with placebo. Postexercise systolic blood pressure was significantly higher during the caffeine trial. No differences were found between treatments for serum free-fatty-acid concentrations, plasma lactate concentrations, serum cortisol concentrations, heart rate, and rating of perceived exertion. Thus, a moderate dose of caffeine resulted in more total weight lifted for the chest press and a greater peak power attained during the Wingate test in competitive athletes. Keywords: hormonal responses, exercise metabolites, physiological responses, RPE
Caffeine, one of the most widespread and socially acceptable drugs consumed
around the world, is commonly ingested by people who participate in sports in an
attempt to enhance performance (Desbrow & Leveritt, 2006; Ellender & Linder,
2005; Graham, 2001; Juhn, 2003; Keisler & Armsey, 2006; Maughan, King, &
Lea, 2004). Caffeine is found in a variety of foods and beverages including coffee,
chocolate, tea, cola drinks, and energy drinks. It is also present in some widely
consumed over-the-counter medications such as analgesics and diuretics. Caffeine
is most commonly consumed in the form of coffee, tea, and soda. Energy drinks,
a relatively new category of beverages, contain caffeine in amounts that exceed
those in soft drinks and are similar to the concentrations found in coffee (Mandel,
In high doses, caffeine is a monitored or restricted drug for competitive ath-
letes. The World Anti-Doping Agency (WADA) recently removed caffeine from its
prohibited list and added it to its monitoring program during competition (WADA,
Woolf and Bidwell are with the Dept. of Nutrition, Arizona State University, Mesa, AZ 85212. Carlson is with Athletes’ Performance, 650 S. Athletes’ Place, Tempe, AZ 85281.
Caffeine and Anaerobic Exercise 413
2007b). WADA monitors substances like caffeine during competition to detect
patterns of misuse in sport (WADA, 2007a). The National Collegiate Athletic
Association still considers a urinary level of >15 µg/ml after competition illegal
(National Collegiate Athletic Association, 2007). The WADA antidoping code has
been accepted by many sport organizations including the International Olympic
Committee. It takes about 13 mg per kilogram body weight (BW) of caffeine (about
700 mg caffeine, or 8 cups of brewed coffee) to reach the maximum allowable
urinary concentration (Ellender & Linder, 2005; Graham, 2001).
Research has suggested that exercise performance might be improved by
ingesting as little as 150–250 mg of caffeine (~1–2 cups of coffee; Anselme, Col-
lomp, Mercier, Ahmaidi, & Prefaut, 1992; Collomp, Ahmaidi, Chatard, Audran,
& Prefaut, 1992; Graham & Spriet, 1995; Wiles, Bird, Hopkins, & Riley, 1992).
Many athletes use caffeine as an ergogenic aid in hopes of enhancing performance
(Ellender & Linder, 2005; Graham, 2001; Juhn, 2003; Keisler & Armsey, 2006;
Maughan et al., 2004). Evidence from the research literature suggests that caffeine
enhances endurance and improves performance over a wide range of exercise
protocols, particularly prolonged and exhaustive exercises (Bell & McClellan,
2003; Bell & McClellan, 2002; Graham & Spriet; Pasman, vanBaak, Jeukendrup,
& deHaan, 1995; Trice & Haymes, 1995). It has also been suggested that caffeine
reduces fatigue, improves concentration, and enhances mental alertness (Lieber-
man, Tharion, Shukitt-Hale, Speckman, & Tulley, 2002; Magill et al., 2003; van
Duinen, Lorist, & Zijdewind, 2005).
The evidence for caffeine as an ergogenic aid for short-term, high-intensity
athletic performance, however, is mixed (Anselme et al., 1992; Bell, Jacobs, & Eller-
ington, 2001; Bell, Jacobs, & Zamecnik, 1998; Bruce et al., 2000; Collomp et al.,
2002; Collomp, Ahmaidi, Audran, Chanal, & Prefaut, 1991; Collomp et al., 1992;
Denadai & Denadai, 1998; Doherty, Smith, Davison, & Hughes, 2002; Doherty,
Smith, Hughes, & Davison, 2004; Greer, McLean, & Graham, 1998; Jackman,
Wendling, Friars, & Graham, 1996; Jacobs, Pasternak, & Bell, 2003; Jacobson,
Weber, Claypool, & Hunt, 1992; Paton, Hopkins, & Vollebregt, 2001; Wiles et
al., 1992). For example, caffeine ingestion (2–9 mg/kg BW) during short-term,
high-intensity protocols (Bruce et al.; Doherty et al., 2002, 2004; Jackman et al.;
Wiles et al.), sprint protocols (Anselme et al.; Collomp et al., 1992), and strength
and power exercise (Jacobson, 1992) significantly improved exercise performance.
In other studies, caffeine ingestion (~3.6–7 mg/kg BW) during short-term, high-
intensity cycling protocols (Bell et al., 1998; Collomp et al., 2002), Wingate tests
(Bell et al., 2001; Collomp et al., 1991; Greer et al.), sprint protocols (Collomp et
al., 1992; Paton et al.; Williams, Signorile, Barnes, & Henrich, 1988), and strength
and power exercise (Jacobs et al.) did not improve performance. The mixed results
might be a result of training status of research participants, habitual use of caffeine
by research participants, dose of caffeine used in the studies, and performance
Because of the widespread use of caffeine by athletes who engage in both
aerobic and anaerobic activities, further research is needed to determine its efficacy
as an ergogenic aid. Athletes who regularly consumer caffeine might respond dif-
ferently to caffeine in a research study than nonusers of caffeine. Unfortunately,
most previous studies have not examined typical caffeine intake of the research
participants. Few studies have examined the impact of caffeine on biochemical
414 Woolf, Bidwell, and Carlson
markers during high-intensity exercise such as the Wingate test. This information
might help us understand the mechanisms by which caffeine exerts an ergogenic
action on anaerobic exercise performance. Heart rate (HR) and blood pressure (BP)
should be monitored for the safety of the participants and to help determine any
negative side effects. In addition, few studies have examined the effect of caffeine
on short-term, high-intensity exercise or athletic performance in highly trained
athletes. Thus, studies are needed that take a comprehensive approach including
biochemical and physiological factors, fitness, and diet.
The primary purpose of this study was to examine the effects of a moderate dose
of caffeine (5 mg/kg BW) on anaerobic exercise performance, hormonal responses
(serum insulin and serum cortisol), exercise metabolites (serum free fatty acids
[FFA], plasma lactate, and plasma glucose), physiological responses (BP and HR),
and rating of perceived exertion (RPE) in highly trained male athletes. Our primary
null hypothesis was that ingesting a shake with a 5.0-mg/kg BW dose of caffeine
would not alter exercise performance (leg press, chest press, and 30-s Wingate
test), hormonal responses, exercise metabolites, physiological responses, and RPE
compared with a placebo in male athletes during anaerobic exercise. Methodology
This randomized, double-blind, crossover study examined the impact of a moder-
ate dose of caffeine (5 mg/kg BW) during anaerobic exercise in 19 highly trained
competitive male athletes, 18–40 years of age.
Recruitment flyers were posted at Athletes’ Performance, a facility that trains
elite and professional athletes. This study was approved by the Human Subjects
Institutional Review Board at Arizona State University, and the procedures were
conducted in accordance with their guidelines. Participants Participants were eligible if they were male, 18–40 years of age, and participated
in ≥12 hr/week of programmed physical activity. They were currently participating
in a comprehensive training program including strength, movement, and endurance
Participants reported to Athletes’ Performance on two occasions separated by
1 week for exercise testing. They fasted for 8–12 hr and abstained from caffeinated
products for 48 hr. So that we could assess their historical caffeine intake, partici-
pants completed the Arizona Food Frequency Questionnaire (AFFQ; University
of Arizona, Tucson, AZ; Martinez et al., 1999). Each provided a urine sample at
baseline to detect caffeine. HR and BP were also monitored. An 8-hr fasting blood
sample was taken by venipuncture to assess serum cortisol, serum insulin, serum
FFA, plasma lactate, and plasma glucose concentrations.
Immediately after the blood draw, participants consumed a commercial shake
either with caffeine (caffeine, 5.0 mg/kg BW; carbohydrate [CHO], 0.125 g/kg
BW) or without caffeine (placebo; CHO, 0.125 g/kg BW). Other ingredients in the
shake included sucrose, natural and artificial flavors, pectin, mannitol, citric acid,
sucralose, malic acid, Food and Drug and Cosmetics (FD&C) yellow #5, silicon
Caffeine and Anaerobic Exercise 415
dioxide, and FD&C blue #1. Fifteen minutes after ingesting the shake, participants
ate a breakfast consisting of 8 fluid oz of orange juice, 2 cups of Cheerios, 8 fluid
oz of 1% milk, two pieces of toast, 2 tablespoons of peanut butter, and one banana
(~917 kcal; 14% protein, 62% CHO, 24% fat). Researchers noted the amount of
food and drink consumed by each participant. A midpoint HR and BP were mea-
sured 30 min after the participants drank the shake. Sixty minutes after consuming
the shake, participants performed three exercise tests with 60 s of rest between
tests. This scenario is similar to how an athlete would use caffeine in competition
Before the exercise tests, the participants completed a 10-min warm-up
consisting of both dynamic and static stretches. The exercise tests consisted of a
leg press, chest press, and 30-s Wingate test. The order of the leg press and chest
press was determined at random; the Wingate test was always the final test. Par-
ticipants completed the leg and chest press on Keiser exercise equipment (model
A420, Fresno, CA), which uses pneumatic resistance during the extension phase.
Participants were asked to push maximally with each repetition until they could
no longer perform a full extension. The number of repetitions completed and total
weight lifted (pounds × number of repetitions) were recorded after each test. The
Wingate test was completed on a Peak Bike by Monark (Ergomedic model 894E,
Vansbro, Sweden). Participants cycled with no resistance until they reached their
perceived maximal speed. At this time, the predetermined load (7.5% BW) was
dropped and the test continued at maximal effort for 30 s. The peak power, average
power, minimum power, and power drop were calculated during the Wingate test
using Monark’s anaerobic test software (version 1.0). Peak power was the highest
power output achieved during any 5-s interval. Average power was the average
power output over the 30-s test. Minimum power was the lowest power output
achieved during any 5-s interval. Power drop was the difference between the peak
Participants estimated perceived effort after each exercise test using Borg’s
RPE (scale from 6 to 20). Researchers measured HR and BP immediately after
participants completed the Wingate test, and then a postexercise blood sample was
drawn to assess for serum cortisol, serum insulin, serum FFA, plasma lactate, and
plasma glucose concentrations. Participants also provided a postexercise urine
sample to detect the presence of caffeine. Anthropometric Measures Height was measured (without shoes) to the nearest centimeter using a stadiom-
eter with each participant’s back against the wall. Each participant’s weight was
measured to the nearest kilogram using a digital platform scale (Avadia model
Blood Analysis A sample of approximately 20 ml of blood was taken twice by venipuncture by a
trained phlebotomist at each visit. The first blood draw (fasting) was collected at
arrival, and participants performed three exercise tests 60 min later. The second
blood draw was collected immediately after the final exercise test (postexercise).
416 Woolf, Bidwell, and Carlson
After the blood samples were collected, they were immediately placed on ice and
centrifuged within 30 min at 4 °C. The blood was separated and samples stored at
–45 °C until analysis. Concentrations of serum cortisol, serum insulin, serum FFA,
plasma lactate, and plasma glucose were determined for each participant during
each treatment (caffeine, placebo) and time (fasting, postexercise).
Plasma glucose concentrations were run in duplicate at Arizona State University
using an enzymatic kit from Sigma Diagnostics (St. Louis, MO). The intra-assay
variation was 2.2%, and the interassay variation was 4.4%. Serum insulin concen-
trations were run in duplicate at Arizona State University by radioimmunoassay
using the ImmuChem insulin 125I RIA assay kit. The intra-assay variation was 3.7%,
and the interassay variation was 10.8%. Serum cortisol was determined by radio-
immunoassay using the ImmuChem cortisol 125I RIA assay kit (MP Biomedicals
Diagnostics Division, Orangeburg, NY). The intra-assay variation was 3.0%, and
the interassay variation was 12.5%. Serum FFA and plasma lactate were analyzed
by Sonora Quest Laboratories (Phoenix, AZ). Serum FFA concentrations were
determined by an enzymatic assay using spectrophotometry, and plasma lactate
concentrations were determined using a photometric assay. Urine Analysis Participants provided approximately 100 ml of urine twice (fasting and postexercise)
at each study visit. Urine was analyzed for the presence or absence of caffeine by
Sonora Quest Laboratories (Phoenix, AZ) using thin-layer chromatography. Dietary Intake Participants completed the AFFQ so we could determine their usual eating pat-
terns over the past few months. The AFFQs were analyzed by the NCS OpScan
5 (Al-Bassam International, Al-Khobar, Saudi Arabia). Usual caffeine intake was
assessed for each research participant. Power Calculations Power calculations were completed to determine the participant sample size. Based
on postexercise plasma glucose concentrations (Doherty et al., 2002; Greer et al.,
1998), blood lactate concentrations (Collomp et al., 1992; MacIntosh & Wright,
1995), serum FFA concentrations (Trice & Haymes, 1995), and plasma insulin
concentrations (Graham, Helge, MacLean, Kiens, & Richter, 2000), we determined
that 20 participants would be recruited. Only 19 research participants completed
Statistical Analysis We assessed the data for normality by examining histograms depicting the distribu-
tions, normal probability plots, and the Kolmogorov–Smirnov statistic (Altman &
Bland, 1995). Tests for normality were met for all variables except serum insulin,
plasma lactate, leg press (total weight), RPE, and blood pressure. Serum insulin
and plasma lactate values were transformed using the inverse, and leg-press data
were transformed using the inverse square root (Bland & Altman, 1996). Means
and standard deviations presented in the result tables are the untransformed values;
Caffeine and Anaerobic Exercise 417
the p values reflect the results using the transformed data. A nonparametric test
was used to analyze RPE, systolic blood pressure (SBP), and diastolic blood pres-
Descriptive statistics (age, height, weight, and body-mass index) were
expressed as M ± SD. Paired t tests determined the independent effects of caffeine
versus no caffeine on exercise performance during the bench press, leg press, and
Wingate test. A repeated-measures analysis of variance (ANOVA) determined the
independent effects of caffeine versus no caffeine on plasma glucose, serum insulin,
serum FFA, plasma lactate, serum cortisol concentrations, and HR. Bonferroni’s
post hoc test was used to determine differences between the preexercise, midpoint,
and postexercise HR values. Wilcoxon’s signed rank test determined the indepen-
dent effects of the treatment on RPE, as well as treatment and time effects on BP.
All values were expressed as M ± SD, and results were considered significant at
the .05 level. Statistical analyses were completed using the Statistical Package for
Social Sciences (SPSS; version 14.0, 2005, Chicago, IL).
Nineteen participants completed this study; one participant was excluded from
the analysis because his blood markers (elevated glucose and insulin) suggested
that he was not in a fasted state at baseline during the caffeine trial. Therefore, 18
participants were included in the final analysis (Table 1). Most participants were
not regular caffeine users; typical dietary caffeine intake was 40.8 ± 51.0 mg/day
according to the AFFQ. Thirteen participants consumed ≤50 mg/day (caffeine
Table 1 Characteristics of Study Participants (N = 18) Variable
Body-mass index (kg/m2) , M ± SD
Typical dietary caffeine intakea (mg), M ± SD
aData obtained from Arizona Food Frequency Questionnaire. 418 Woolf, Bidwell, and Carlson
naive), and 5 participants were low to moderate users, consuming >50 mg/day
(68–179 mg/day). All participants consumed less than the average daily amount of
caffeine in the U.S. population (193 mg/day; Frary, Johnson, & Wang, 2005). Urinary Caffeine All participants’ urine tested negative for the presence of caffeine at study entry.
They also tested negative for caffeine postexercise during the placebo trial. During
the caffeine trial, participants tested positive for caffeine postexercise. Exercise Performance Performance on the exercise tests was analyzed using paired t tests. Total weight
lifted in the chest press was significantly greater for the caffeine trial than for the
placebo trial (p < .05; Table 2), with 67% of the participants showing improvement
in the caffeine trial. Although total weight lifted in the leg press was not signifi-
cantly higher in the caffeine trial than in the placebo trial (p = .09; Table 2), 78%
of the participants showed improvement in the caffeine trial. During the Wingate
test, peak power was significantly greater during the caffeine trial than during the
placebo trial (p < .05; Table 2), with 78% of the participants showing improvement
in the caffeine trial. Although mean scores for average power and minimum power
were greater during the caffeine trial, the results were not statistically significant
(Table 2). Power drop was less during the caffeine trial than during the placebo
trial; however, the results were not statistically significant (Table 2). Furthermore,
only 50% of the participants had a higher minimum power and less of a power drop
in the caffeine trial than in the placebo trial, but 72% obtained a greater average
power in the caffeine trial than in the placebo trial. Hormonal Responses and Exercise Metabolites Fasting and postexercise blood samples were obtained from each participant and
analyzed for concentrations of serum cortisol, serum insulin, serum FFA, plasma
lactate, and plasma glucose. All fasting blood samples for each participant were
Table 2 Exercise Performance of Study Participants (N = 18), M ± SD Variable Caffeine p
Chest press, total weight lifted (lb × reps.)
Leg press, total weight lifted (lb × reps.)a
Note. Data were analyzed using a paired t test. aData were transformed using the inverse square root (1 over the square root of the variable) before statistical analysis; M ± SD data are presented untransformed. *Significantly different between treatments (p < .05).
Caffeine and Anaerobic Exercise 419
within normal limits. Using paired t tests, no differences in fasting concentrations
of the blood markers were observed between the caffeine and placebo treatments.
Using paired t tests, postexercise plasma lactate, serum cortisol, plasma glucose, and
serum insulin concentrations were all significantly higher during the caffeine than
the placebo treatment (lactate: caffeine = 14.4 ± 4.0, placebo = 12.1 ± 2.9 mmol/L;
cortisol: caffeine = 635 ± 166, placebo = 524 ± 138 nmol/L; glucose: caffeine =
5.6 ± 0.9, placebo = 4.9 ± 0.7 mmol/L; insulin: caffeine = 264 ± 111, placebo =
208 ± 97 pmol/L; p < .05). Postexercise serum FFA were not significantly different
between treatments (caffeine = 0.17 ± 0.07, placebo = 0.15 ± 0.05 mmol/L).
Using two-way repeated-measures ANOVA, blood markers were analyzed to
test for differences in time, treatment, and their interaction. The time main effect
was significant for serum insulin, plasma lactate, and serum FFA. Postexercise
blood concentrations significantly increased for serum insulin (p < .05) and plasma
lactate (p < .05; Table 3). They significantly decreased for serum FFA with both
treatments (p < .05; Table 3).
The treatment main effect was significant for serum insulin and plasma glu-
cose. Concentrations for serum insulin and plasma glucose concentrations were
significantly higher during the caffeine treatment than the placebo treatment (p <
.05; Table 3). In addition, a significant interaction (treatment by time) was observed
for serum cortisol and plasma glucose concentrations (p < .05), with an increase in
the postexercise caffeine trial but a decrease in the postexercise placebo trial (Table
3). There were no significant treatment main effects for serum cortisol, serum FFA,
and plasma lactate (Table 3). There were no significant interaction effects (treatment
by time) for plasma lactate, serum insulin, and serum FFA (Table 3). Table 3 Effect of Caffeine on Fasting and Postexercise Blood Concentrations Between Two Treatments (N = 18), M ± SD Caffeine Variable Postexercise Postexercise Note. Data were analyzed using repeated-measures analysis of variance and Bonferroni’s post hoc test. aNormal values from Pagana and Pagana (2002). bLactate was not run for 1 participant (N = 17) because of a laboratory error. cData were transformed using the inverse (1/variable) before statistical analysis; M ± SD data are presented untransformed. *Significant time difference within the same treatment (time effect; p < .01). †Significant treatment difference for given time period (treatment effect; p < .05). ‡Significant difference for the interaction (treatment and time; p < .05). 420 Woolf, Bidwell, and Carlson Heart Rate and Blood Pressure A two-way repeated-measures ANOVA and Bonferroni’s post hoc test were used
to examine differences in HR by time and treatment and their interaction. Postex-
ercise values for HR were significantly higher than both the fasting and midpoint
measurements (p < .05; Table 4). No differences in HR were seen for the treatment
main effect or the interaction of treatment and time.
Because the SBP and DBP data were not normally distributed, we used Wil-
coxon’s signed rank test to test for differences. Postexercise values for SBP were
significantly higher than both the fasting and midpoint measurements (p < .05;
Table 4). Postexercise values for DBP were significantly lower than both the fasting
and midpoint measurements (p < .05; Table 4). Midpoint DBP was significantly
higher than the fasting DBP measurement in the caffeine treatment (p < .05; Table
4). Postexercise SBP was significantly higher with the caffeine treatment than with
the placebo treatment (p < .05; Table 4). Midpoint DBP was significantly higher
with the caffeine treatment than with the placebo treatment (p < .05; Table 4). No
significant differences in blood pressure were seen for the interaction of treatment
We separated our research participants into two different groups: responders
and nonresponders. The responders (n = 5) had a >10% increase in SBP at the mid-
point reading during the caffeine trial. The increase in SBP at the midpoint reading
was ≤10% for the nonresponders (n = 13). Four of the five responders reported
daily caffeine intakes <50 mg/day. Forty percent of the responders and 77% of the
nonresponders lifted more total weight on the chest press during the caffeine trial.
One hundred percent of the responders and 69% of the nonresponders obtained
a greater peak power and lifted more total weight on the leg press during the caf-
feine trial. One hundred percent of the responders and 61% of the nonresponders
obtained a greater average power during the caffeine trial. RPE Because RPE data were not normally distributed, we used Wilcoxon’s signed rank
test for the analysis. No differences were observed for RPE between treatments in
Table 4 Caffeine’s Effect on Heart Rate and Blood Pressure Between Time and Two Treatments, M ± SD Caffeine Variable
176 ± 18*‡ 118 ± 10 120 ± 8 168 ± 22*
Note. Blood-pressure data were analyzed using Wilcoxon’s signed rank test. Heart-rate data were analyzed using repeated-measures analysis of variance and Bonferroni’s post hoc test. No significant difference was observed for the interaction (treatment and time). Pre = fasting; Mid = 30 min posttreat-ment; Post = postexercise; SBP = systolic blood pressure; DBP = diastolic blood pressure. *Significant difference from Pre and Mid by time (time effect; p < .05). †Significant difference from Pre by time (time effect; p < .05). ‡Significant difference between treatments at the same time (treat-ment effect; p < .05).
Caffeine and Anaerobic Exercise 421
any of the exercises (chest press: caffeine = 19 ± 1, placebo = 20 ± 1; leg press:
caffeine = 19 ± 1, placebo = 19 ± 1; Wingate test: caffeine = 19 ± 2, placebo =
This study examined the effect of a moderate dose of caffeine (5 mg/kg BW)
on anaerobic exercise performance, hormonal responses (serum cortisol, serum
insulin), exercise metabolites (serum FFA, plasma lactate, and plasma glucose),
physiological responses (HR and BP), and RPE in highly trained competitive male
athletes. In our study, all the participants consumed less than the U.S. population’s
average intake of caffeine of 193 mg/day (Frary et al., 2005). Thus, the participants
were caffeine naive or very low caffeine consumers. Exercise Performance Performing a chest press and leg press to fatigue is a measure of muscle endurance
used primarily with the anaerobic system. In our study, caffeine ingestion signifi-
cantly improved performance for the chest press but not the leg press. The leg press
uses larger muscle groups than the chest press. Thus, if caffeine acts directly on the
skeletal muscle or increases muscle-fiber recruitment, one would expect a greater
effect of caffeine in the leg press. The chest press and leg press were administered
in a random order to control for fatigue.
In our study, the participants were caffeine naive or very low caffeine con-
sumers. Some participants reported feeling shaky or jittery, and 1 participant
vomited at the end of the testing. These feelings might have negatively affected
Unfortunately, our statistical tests were also underpowered (leg press, .161).
Thus, if more participants were included, significant results might have been
obtained. Nonetheless, 67% of the participants lifted more total weight during the
caffeine trial for the leg press and chest press.
Jacobs et al. (2003) also examined the impact of caffeine on exercise perfor-
mance during the leg press and bench press. In this study, no significant differ-
ences were observed with the caffeine trial compared with the placebo trial. The
participants lifted slightly more weight, however, in the leg press and bench press
during the first set of three supersets after caffeine ingestion. Jacobs et al. included
recreational athletes instead of highly trained athletes, which we used in our study.
In addition, Jacobs et al. administered a lower dose of caffeine (4 mg/kg BW) 90
min before testing instead of the 5-mg/kg BW dose 60 min before testing in our
study. The dose of caffeine used, the timing of the dose, and the fitness level of
the participants might explain the differences in the results. Elite athletes gener-
ally have more muscle mass than recreational athletes. If caffeine acts directly on
muscle fibers, the effect of caffeine would be greater in individuals with a larger
muscle mass. It could be, however, that a larger dose of caffeine is needed to get
an ergogenic effect for short-term, high-intensity exercise.
Collomp et al. (1992) compared the effects of caffeine in trained and untrained
swimmers and found a significantly greater swimming velocity using 4.3 mg/kg
BW of caffeine during 100-m swimming sprints in the trained participants only.
422 Woolf, Bidwell, and Carlson
Using a 7-mg/kg BW dose of caffeine with elite football athletes, Jacobson et al.
(1992) observed a significantly greater peak torque during leg-extension and -flexion
exercises after caffeine ingestion. Anselme et al. (1992) found a significantly greater
maximal anaerobic power using 3.5 mg/kg BW of caffeine during high-intensity
cycling with recreational athletes. Other studies, however, found no significant
differences in performance with recreational athletes using 3.5–4 mg/kg BW
during a 10-km run (Bell & McClellan, 2002), cycle-ergometer graded exercise
test (Dodd, Brooks, Powers, & Tulley, 1991), and high-intensity cycling (Collomp
et al., 2002). The potential to improve might be small and difficult to measure in
short-term, high-intensity exercise performance. In addition, studies have used a
variety of exercise protocols, caffeine doses, and research participants, thus making
A Wingate test was used to measure anaerobic power output. Our results
indicate that caffeine ingestion resulted in a significantly greater peak power. An
increase in peak power is important for competitions involving sprints or power
lifting. Average power, minimum power, and power drop were not significantly
different between treatments, but 72% of the participants obtained a greater aver-
age power during the caffeine trial than during the placebo trial. Bell et al. (2001),
Collomp et al. (1991), and Greer et al. (1998) found no significant differences in
exercise performance on the Wingate test with caffeine ingestion, but Bell et al.
and Collomp et al. observed nonsignificant improvements. Greer et al. also found
nonsignificant improvements in the first three of four Wingate tests. The dose
of caffeine was 5 mg/kg BW in two of studies (Bell et al., 2001; Collomp et al.,
1991) and 6 mg/kg BW in the other (Greer et al.). Greer et al. found a significant
negative effect of caffeine on peak power in the last of four repeated Wingate tests.
Conflicting results might be related to the training level of the participants. In the
current study, highly trained athletes were evaluated, whereas in the other three
Wingate studies, untrained or recreational participants were examined. Thus, caf-
feine might be ineffective for improving anaerobic performance during the Wingate
test in recreational trained or untrained participants.
The participants in our study were all relatively low users of caffeine, consum-
ing less than the average daily intake in the United States. Attwood, Higgs, and
Terry (2007) found that the sensitivity of caffeine consumers to the performance-
enhancing effects of caffeine is related to habitual intake. They found that higher
caffeine consumers performed better on cognitive tests after a dose of caffeine than
moderate consumers of caffeine. Thirteen of our participants consumed less than 50
mg/day of caffeine, and 5 consumed 68–179 mg/day. We might have found different
results in exercise performance if they had been high caffeine users. Hormonal Responses In our study, postexercise insulin concentrations were significantly increased,
which would be expected after eating a meal. There was also a treatment main
effect during the caffeine trial, with higher insulin concentrations than in the pla-
cebo trial. These results agree with those of Collomp et al. (2002). In our study,
similar to Collomp et al., the research participants ate a preexercise meal before
testing. During competition or practice, an athlete would use caffeine in addition
Caffeine and Anaerobic Exercise 423
Keijzers, De Galan, Tack, and Smits (2002) observed that an acute caffeine
infusion decreased insulin sensitivity (~15%) in healthy humans. The decrease,
however, might have resulted from elevated plasma epinephrine concentrations.
Petrie et al. (2004) also showed that acute caffeine ingestion significantly reduced
insulin sensitivity in obese, nondiabetic males. The protocol used in those studies,
however, did not include measuring the impact of caffeine on insulin sensitivity
during exercise. The additional increase in insulin concentrations observed after
caffeine ingestion in our study is most likely a result of increased blood glucose
In the current study, a significant interaction (treatment by time) effect of caf-
feine was observed in serum cortisol concentrations after caffeine ingestion. Cortisol
concentrations increased during the caffeine trial and decreased during the placebo
trial. These results agree with those of Laurent et al. (2000) and MacIntosh and
Wright (1995). Cortisol is known to elevate blood glucose and FAA to ensure an
adequate fuel supply. In our study, we saw an increase in cortisol concentrations
after caffeine ingestion, which might be responsible for the increase seen in glucose
concentrations. There was a significant decrease in postexercise FFA concentra-
tions in both treatments, however, possibly because of an increase in postexercise
insulin concentrations. Availability of glucose and FFA is not the limiting factor
in short-term, high-intensity exercise protocols. Exercise Metabolites In our study, the participants ate a meal 45 min before testing. In addition, the shake
contained CHO. Glucose is needed for anaerobic glycolysis during short-term,
high-intensity exercise bouts. Other studies have reported an increase in blood
glucose with caffeine ingestion (Graham et al., 2000; Graham & Spriet, 1995; Trice
& Haymes, 1995). In the current study, postexercise glucose concentrations were
significantly higher in the caffeine trial than in the placebo trial. There was also a
treatment main effect, with higher plasma glucose concentrations during the caf-
feine trial than during the placebo trial. Bell et al. (2001) also observed significantly
higher postexercise glucose concentrations with caffeine ingestion than in a placebo
trial, but postexercise concentrations were higher than preexercise concentrations
with both treatments. Denadai and Denadai (1998) also observed a slight increase
in postexercise glucose concentrations with caffeine ingestion and a slight decrease
in postexercise glucose concentrations with a placebo trial, but no significant differ-
ences were observed between trials. Bell et al. (1998), Collomp et al. (2002), and
Greer et al. (1998) observed slight increases in postexercise glucose concentrations,
with the caffeine trial tending to be higher than the placebo trial. Caffeine ingestion
might lead to a reduction in glucose uptake (via a caffeine-induced reduction in
insulin sensitivity) or an increase in gluconeogenesis, resulting in elevated blood
During anaerobic exercise, lactate is formed during the metabolism of glu-
cose instead of proceeding to the Kreb’s cycle or aerobic metabolism (Balady et
al., 2000). Caffeine might inhibit lactate clearance. In the current study, plasma
lactate concentrations were significantly higher postexercise in both trials than
fasting concentrations. These results are consistent with the literature (Bell et al.,
2001, 1998; Collomp et al., 2002, 1991, 1992; Denadai & Denadai, 1998; Greer et
424 Woolf, Bidwell, and Carlson
al., 1998). No significant treatment main effect was observed with plasma lactate
concentrations. Some studies report no differences with caffeine in postexercise
plasma lactate concentrations during high-intensity cycling protocols (Denadai &
Denadai; Jackman et al., 1996) or the Wingate test (Greer et al.). Others, however,
have observed that postexercise lactate concentrations are significantly increased
with caffeine compared with a placebo trial during high-intensity cycling protocols
(Anselme et al., 1992; Bell et al., 2001, 1998; Collomp et al., 2002) and the Wingate
test (Bell et al., 2001; Collomp et al., 1991).
Fat oxidation does not play as big a role in short-term, high-intensity exercise
protocols. In our study, postexercise FFA concentrations were significantly reduced
during both treatments. These results are similar to other short-term, high-intensity-
exercise studies (Bell et al., 1998; Denadai & Denadai, 1998). Bell et al. showed
a significant decrease in FFA concentrations after exercise with both treatments.
In that study, the postexercise FFA concentrations were significantly higher with
caffeine ingestion. Denadai and Denadai also reported no significant differences in
postexercise FFA concentrations between treatments during cycling above anaero-
bic threshold. These results do not support the theory that caffeine increases FFA
oxidation, thereby sparing glucose concentrations in these conditions. An increase
in FFA oxidation and glucose sparing is not as important, however, in anaerobic
Previous studies have examined physiological responses to caffeine. Most research-
ers found no effect of acute caffeine ingestion on resting HR (Arciero, Gardner,
Benowitz, & Poehlman, 1998; Bond et al., 1987; Bruce et al., 2000; Denadai &
Denadai, 1998). One study, however, reported an increase in resting HR with acute
caffeine ingestion (Robertson et al., 1978). Most researchers have also reported
that caffeine might increase postexercise HR, but not significantly when compared
with placebo (Bell et al., 2001; Bond et al.; Denadai & Denadai; O’Connor, Molt,
Broglio, & Ely, 2004). Our data are in agreement with most of the research. Our
results showed that resting HR was not significantly different between trials. In
addition, HR was significantly increased after exercise in both trials, but no sig-
nificant differences were seen in HR between trials.
Fewer studies have examined the impact of caffeine on BP response to exer-
cise. In our study, resting DBP (midpoint) and postexercise SBP were significantly
increased during the caffeine trial compared with the placebo trial. The research
literature has documented that regular caffeine intake increases BP (Hartley, Lovallo,
& Whitsett, 2004; Noordzij et al., 2005). Other research has reported no significant
differences in resting (Arciero et al., 1998; Karatzis et al., 2005) or postexercise
(O’Connor et al., 2004) SBP and DBP after caffeine ingestion. Furthermore, we
did not see any trends in sympathetic-nervous-system response to caffeine and
Caffeine and Anaerobic Exercise 425 Potential Mechanisms Caffeine might exert an effect on the central nervous system (CNS) by acting as
a potent adenosine antagonist, thus blocking adenosine receptors or interacting
with dopamine receptors (Ribeiro, Sebastiao, & de Mendonca, 2003). Adenosine
inhibits the release of most excitatory neurotransmitters in the brain, particularly
dopamine, and might reduce dopamine synthesis (Ribeiro et al.). Because adenosine
receptors are abundant in many areas of the brain, caffeine might inhibit adenosine
from blocking neuronal transmission and thus alter perception of pain, sympathetic
activity, motor recruitment, and fatigue. In this capacity, caffeine might also increase
time to exhaustion. Because caffeine is a dopamine agonist, it could possibly reduce
RPE. In our study, however, we did not see a reduction in RPE with caffeine.
Adenosine receptors are abundant in skeletal muscles. In anaerobic activity,
the ergogenic effect of caffeine might result from the antagonism of adenosine
receptors. Svenningsson, Nomikos, Ongini, and Fredholm (1997) found that caf-
feine doses as low as 7.5 mg/kg BW might cause an increase in motor activity
in rats primarily through the antagonism of adenosine receptors. Highly trained
athletes might have more muscle mass than recreational athletes and might respond
to the ergogenic effect of caffeine differently (via the adenosine receptors) than
recreational athletes. Thus, caffeine might have a direct effect on muscle that is
independent of substrate metabolism. Future studies should examine the impact
of caffeine using different muscle groups.
Performance enhancement in anaerobic exercise might also be associated
with CNS stimulation (increased motor recruitment or masking of fatigue). In
tests using maximal voluntary contraction, the level of muscle activation increases
after caffeine ingestion (Kalmar & Cafarelli, 1999; Meyers & Cafarelli, 2005;
O’Connor et al., 2004; Williams, Barns, & Gadberry, 1987), suggesting that caf-
feine might influence sarcoplasmic handling of calcium. These results have only
been significant, however, using low frequencies, which would primarily affect
Limitations In our study, factors such as rest, prior exercise, and over-the-counter medications
might have affected the participants’ responses to the caffeine. The training that the
participants undertook during the weeks before the study might have been quite
different. A crossover design was used to help control for this variability, however.
Furthermore, at the time of study recruitment, the participants were training at the
same facility. Thus, a similar training protocol was performed during the 2 days
before each testing day. Caffeine might have produced a sympathetic-nervous-
system response exhibited by an increase in HR or BP in some participants and no
effect in other participants. We did not ask the participants which treatment they
thought they received or how they felt after each treatment. Unfortunately, we did
not take a blood sample after the meal just before the start of exercise. Information
426 Woolf, Bidwell, and Carlson
on the effects of caffeine before exercise would have been useful to include in the
study design. In addition, we did not measure plasma caffeine concentrations. In
our study, 13 of the participants were caffeine naïve. We might have found dif-
ferent results in exercise performance if our research participants had been high
Caffeine ingestion combined with a meal significantly increased upper body muscle
endurance during the chest press and increased peak power during the Wingate test.
Caffeine and a meal increased postexercise concentrations of plasma glucose, serum
insulin, and serum cortisol during high-intensity exercise. Multiple mechanisms
might be responsible for performance enhancement in different types of exercise
(aerobic vs. anaerobic). In anaerobic exercise, the mechanisms for improvement
are likely to be independent of any effect of caffeine on fat mobilization. During
anaerobic exercise, caffeine might influence the CNS. The participants did not
report any differences in RPE, however, between the caffeine and placebo trials.
The participants in our study were caffeine naive or very low caffeine consumers,
which might have contributed to the results. Regular consumers of higher doses of
caffeine might exhibit more benefits of caffeine as an ergogenic aid. Thus, research
is needed that compares the effect of caffeine in caffeine-naive versus habituated
caffeine consumers in anaerobic exercise performance. Future studies should include
different muscle groups, trained versus untrained participants, and habituated caf-
feine consumers versus caffeine-naive participants. Because of the widespread use
of caffeine by athletes, more research is needed examining the impact and safety
of this ergogenic aid on exercise performance. Acknowledgments
This research was supported by a grant from Experimental and Applied Science, Inc. References
Altman, D.G., & Bland, J.M. (1995). The normal distribution. British Medical Journal,
Anselme, F., Collomp, K., Mercier, B., Ahmaidi, S., & Prefaut, C. (1992). Caffeine increases
maximal anaerobic power and blood lactate concentration. European Journal of Applied Physiology,65, 188–191.
Arciero, P.J., Gardner, A.W., Benowitz, N.L., & Poehlman, E.T. (1998). Relationship of
blood pressure, heart rate and behavioral mood state to norepinephrine kinetics in
younger and older men following caffeine ingestion. European Journal of Clinical Nutrition,52, 805–812.
Attwood, A.S., Higgs, S., & Terry, P. (2007). Differential responsiveness to caffeine and
perceived effects of caffeine in moderate and high regular caffeine consumers. Psy-chopharmacology,190, 469–477.
Balady, G.J., Berra, K.A., Golding, L.A., Gordon, N.F., Mahler, D.A., Myers, J.N., et al.
(2000). Guidelines for exercise testing and prescription (6th ed.). Philadelphia: Lip-
Caffeine and Anaerobic Exercise 427
Bell, D.G., Jacobs, I., & Ellerington, K. (2001). Effect of caffeine and ephedrine ingestion
on anaerobic exercise performance. Medicine and Science in Sports and Exercise,33(8), 1399–1403.
Bell, D.G., Jacobs, I., & Zamecnik, J. (1998). Effects of caffeine, ephedrine and their com-
bination on time to exhaustion during high-intensity exercise. European Journal of Applied Physiology,77, 427–433.
Bell, D.G., & McClellan, T.M. (2002). Exercise endurance 1, 3, and 6 h after caffeine inges-
tion in caffeine users and nonusers. Journal of Applied Physiology,93, 1227–1234.
Bell, D.G., & McClellan, T.M. (2003). Effect of repeated caffeine ingestion on repeated
exhaustive exercise endurance. Medicine and Science in Sports and Exercise,35(8),
Bland, J.M., & Altman, D.G. (1996). Transforming data. British Medical Journal,312, 770.
Bond, V., Adams, R., Balkissoon, B., McRae, J., Knight, E., Robbins, S., et al. (1987).
Effects of caffeine on cardiorespiratory function and glucose metabolism during rest
and graded exercise. The Journal of Sports Medicine,27, 47–52.
Bruce, C.R., Anderson, M.E., Fraser, S.F., Stepto, N.K., Klein, R., Hopkins, W.G., et al.
(2000). Enhancement of 2000-m rowing performance after caffeine ingestion. Medicine and Science in Sports and Exercise,32(11), 1958–1963.
Collomp, K., Ahmaidi, S., Audran, M., Chanal, J.L., & Prefaut, C.H. (1991). Effects of
caffeine ingestion on performance and anaerobic metabolism during the Wingate test. International Journal of Sports Medicine,12, 439–443.
Collomp, K., Ahmaidi, S., Chatard, J.C., Audran, M., & Prefaut, C.H. (1992). Benefits of
caffeine ingestion on sprint performance in trained and untrained swimmers. European Journal of Applied Physiology,64, 377–380.
Collomp, K., Candau, R., Millet, G., Mucci, P., Borrani, F., Prefaut, C., et al. (2002). Effects
of salbutamol and caffeine ingestion on exercise metabolism and performance. Inter-national Journal of Sports Medicine,23, 549–554.
Denadai, B.S., & Denadai, M.L.D.R. (1998). Effects of caffeine on time to exhaustion in
exercise performed below and above the anaerobic threshold. Brazilian Journal of Medical and Biological Research,31(4), 581–585.
Desbrow, B., & Leveritt, M. (2006). Awareness and use of caffeine by athletes competing
at the 2005 Ironman Triathlon World Championships. International Journal of Sport Nutrition and Exercise Metabolism,16, 545–558.
Dodd, S.L., Brooks, E., Powers, S.K., & Tulley, R. (1991). The effects of caffeine on graded
exercise performance in caffeine naive versus habituated subjects. European Journal of Applied Physiology,62, 424–429.
Doherty, M., Smith, P.M., Davison, R.C.R., & Hughes, M.G. (2002). Caffeine is ergogenic
after supplementation of oral creatine monohydrate. Medicine and Science in Sports and Exercise,34(11), 1785–1792.
Doherty, M., Smith, P.M., Hughes, M.G., & Davison, R.C.R. (2004). Caffeine lowers per-
ceptual response and increases power output during high-intensity cycling. Journal of Sports Sciences,22, 637–643.
Ellender, L., & Linder, M.M. (2005). Sports pharmacology and ergogenic aids. Primary Care:Clinics in Office Practice,32, 277–292.
Frary, C.D., Johnson, R.K., & Wang, M.Q. (2005). Food sources and intakes of caffeine in
the diet of persons in the United States. Journal of the American Dietetic Association,105(1), 110–113.
Graham, T.E. (2001). Caffeine and exercise. Metabolism, endurance and performance. Sports Medicine (Auckland, N.Z.),31(11), 785–807.
Graham, T.E., Helge, J.W., MacLean, D.A., Kiens, B., & Richter, E.A. (2000). Caffeine
ingestion does not alter carbohydrate or fat metabolism in human skeletal muscle during
exercise. The Journal of Physiology,529(3), 837–847. 428 Woolf, Bidwell, and Carlson
Graham, T.E., & Spriet, L.L. (1995). Metabolic, catecholamine, and exercise perfor-
mance responses to various doses of caffeine. Journal of Applied Physiology,78(3),
Greer, F., McLean, C., & Graham, T.E. (1998). Caffeine, performance, and metabolism during
repeated Wingate exercise tests. Journal of Applied Physiology,85(4), 1502–1508.
Hartley, T.R., Lovallo, W.R., & Whitsett, T.L. (2004). Cardiovascular effects of caffeine in
men and women. The American Journal of Cardiology,93, 1022–1026.
Jackman, M., Wendling, P., Friars, D., & Graham, T.E. (1996). Metabolic, catecholamine,
and endurance responses to caffeine during intense exercise. Journal of Applied Physi-ology,81(4), 1658–1663.
Jacobs, I., Pasternak, H., & Bell, D.G. (2003). Effects of ephedrine, caffeine, and their
combination on muscular endurance. Medicine and Science in Sports and Exercise,35(6), 987–994.
Jacobson, B.H., Weber, M.D., Claypool, L., & Hunt, L.E. (1992). Effect of caffeine on
maximal strength and power in elite male athletes. British Journal of Sports Medicine,26(4), 276–280.
Juhn, M.S. (2003). Popular supplements and ergogenic aids. Sports Medicine (Auckland, N.Z.),33(12), 921–939.
Kalmar, J.M., & Cafarelli, E. (1999). Effects of caffeine on neuromuscular function. Journal of Applied Physiology,87(2), 801–808.
Karatzis, E., Papaioannou, T.G., Aznaouridis, K., Karatzi, K., Stamatelopoulos, K., Zampelas,
A., et al. (2005). Acute effects of caffeine on blood pressure and wave reflections in
healthy subjects: Should we consider monitoring central blood pressure? International Journal of Cardiology,98, 425–430.
Keijzers, G.B., De Galan, B.E., Tack, C.J., & Smits, P. (2002). Caffeine can decrease insulin
sensitivity in humans. Diabetes Care,25(2), 364–369.
Keisler, B.D., & Armsey, T.D. (2006). Caffeine as an ergogenic aid. Current Sports Medicine Reports,5, 215–219.
Laurent, D., Schneider, K.E., Prusaczyk, W.K., Franklin, C., Vogel, S.M., Krssak, M., et
al. (2000). Effects of caffeine on muscle glycogen utilization and the neuroendocrine
axis during exercise. The Journal of Clinical Endocrinology and Metabolism,85(6),
Lieberman, H.R., Tharion, W.J., Shukitt-Hale, B.S., Speckman, K.L., & Tulley, R. (2002).
Effects of caffeine, sleep loss, and stress on cognitive performance and mood during
U.S. Navy SEAL training. Sea-Air-Land. Psychopharmacology,164, 250–261.
MacIntosh, B.R., & Wright, B.M. (1995). Caffeine ingestion and performance of a
1,500-metre swim. Canadian Journal of Applied Physiology,20(2), 168–177.
Magill, R.A., Waters, W.F., Bray, G.A., Volaufova, J., Smith, S.R., Lieberman, H.R., et al.
(2003). Effects of tyrosine, phentermine, caffeine D-amphetamine, and placebo on
cognitive and motor performance deficits during sleep deprivation. Nutritional Neu-roscience,6(4), 237–246.
Mandel, H.G. (2002). Update on caffeine consumption, disposition and action. Food and Chemical Toxicology,40, 1231–1234.
Martinez, M.E., Marshall, J.R., Graver, E., Whitacre, R.C., Woolf, K., Ritenbaugh, C., et
al. (1999). Reliability and validity of a self-administered food frequency questionnaire
in a chemoprevention trial of adenoma recurrence. Cancer Epidemiology, Biomarkers & Prevention,8, 941–946.
Maughan, R.J., King, D.S., & Lea, T. (2004). Dietary supplements. Journal of Sports Sci-
Meyers, B.M., & Cafarelli, E. (2005). Caffeine increases time to fatigue by maintaining force
and not by altering firing rates during submaximal isometric contractions. Journal of Applied Physiology,99, 1056–1063.
Caffeine and Anaerobic Exercise 429
National Collegiate Athletic Association. NCAA banned-drug classes 2007–08. Retrieved
Noordzij, M., Uiterwaal, C.S.P.M., Arends, L.R., Kok, F.J., Grobbee, D.E., & Geleijnse,
J.M. (2005). Blood pressure response to chronic intake of coffee and caffeine: A meta-
analysis of randomized controlled trials. Journal of Hypertension,23, 921–928.
O’Connor, P.J., Motl, R.W., Broglio, S.P., & Ely, M.R. (2004). Dose-dependent effect of
caffeine on reducing leg muscle pain during cycling exercise is unrelated to systolic
blood pressure. Pain,109, 291–298.
Pagana, K.D., & Pagana, T.J. (2002). Mosby’s manual of diagnostic and laboratory tests
Pasman, W.J., vanBaak, M.A., Jeukendrup, A.E., & deHaan, A. (1995). The effect of differ-
ent dosages of caffeine on endurance time. International Journal of Sports Medicine,16(4), 225–230.
Paton, C.D., Hopkins, W.G., & Vollebregt, L. (2001). Little effect of caffeine ingestion on
repeated sprints in team-sport athletes. Medicine and Science in Sports and Exercise,33(5), 822–825.
Petrie, H.J., Chown, S.E., Belfie, L.M., Duncan, A.M., McLaren, D.H., Conquer, J.A., et al.
(2004). Caffeine ingestion increases the insulin response to an oral-glucose-tolerance
test in obese men before and after weight loss. The American Journal of Clinical Nutrition,80, 22–28.
Ribeiro, J.A., Sebastiao, A.M., & de Mendonca, A. (2003). Adenosine receptors in the nervous
system: Pathophysiological implications. Progress in Neurobiology,68, 377–392.
Robertson, D., Froelich, J.C., Carr, R.K., Watson, J.T., Hollifield, J.W., Shand, D.G., et al.
(1978). Effects of caffeine on plasma renin activity, catecholamines and blood pressure. The New England Journal of Medicine,298, 181–186.
Svenningsson, P., Nomikos, G.G., Ongini, E., & Fredholm, B.B. (1997). Antagonism of
adenosine A2A receptors underlies the behavioral activating effect of caffeine and is
associated with reduced expression of messenger RNA for NGFI-A and NGFI-B in
caudate-putamen and nucleus accumbens. Neuroscience,79(3), 753–764.
Trice, I., & Haymes, E.M. (1995). Effects of caffeine ingestion on exercise-induced changes
during high-intensity, intermittent exercise. International Journal of Sport Nutrition,5, 37–44.
van Duinen, H., Lorist, M.M., & Zijdewind, I. (2005). The effect of caffeine on cognitive
task performance and motor fatigue. Psychopharmacology,180, 539–547.
Wiles, J.D., Bird, S.R., Hopkins, J., & Riley, M. (1992). Effect of caffeinated coffee on
running speed, respiratory factors, blood lactate and perceived exertion during 1500-m
treadmill running. British Journal of Sports Medicine,26(2), 116–120.
Williams, J.H., Barns, W.S., & Gadberry, W.L. (1987). Influence of caffeine on force and
EMG in rested and fatigued muscle. American Journal of Physical Medicine,66(4),
Williams, J.H., Signorile, J.F., Barnes, W.S., & Henrich, T.W. (1988). Caffeine, maximal
power output and fatigue. British Journal of Sports Medicine,22(4), 132–134.
World Anti-Doping Agency. (2007a). The World Anti-Doping Code. The 2007 monitoring program. Retrieved July 27, 2007, from www.wada-ama.org
World Anti-Doping Agency. (2007b). The World Anti-Doping Code. The 2007 prohibited list international standard. Retrieved July 27, 2007, from www.wada-ama.org
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