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Acute Effects of Caffeine on Strength and Muscle Activation of the Elbow Flexors
Michael A. Trevino1, Jared W. Coburn2, Lee E. Brown2, Daniel A. Judelson2, Moh H. Malek3,
Department of Health, Sport, and Exercise Sciences, University of Kansas, Lawrence, KS
Department of Kinesiology, Exercise Physiology Lab and Center for Sport Performance,
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This manuscript is original and not previously published, nor is it being considered elsewhere
until a decision is made as to its acceptability by the JSCR Editorial Review Board.
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Conflict of Interest Disclosure: There were no conflicts of interests with any of the authors.
Corresponding Author:
Michael A. Trevino
The University of Kansas
1301 Sunnyside Ave Rm 101
Lawrence, KS 66045
714-724-8224
mtrevino@ku.edu
caffeine (0, 5, or 10 mgkg1 of body mass), and performed three maximal isometric muscle
actions of the elbow flexors sixty minutes after ingestion. Maximal strength and rate of torque
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peak torque, RTD, normalized EMG amplitude or frequency, normalized MMG amplitude, or
EMD and PMD. Normalized MMG frequency was significantly lower (P < 0.05) following
ingestion of five mgkg1of body mass of caffeine compared to the placebo trial. This was most
likely an isolated finding as MMG frequency was the only variable to have a significant
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difference across all trials. The results suggested that ingestion of either five or ten mgkg1 of
body mass of caffeine does not provide an ergogenic effect for the elbow flexors during
isometric muscle actions.
effects of caffeine include increased catecholamine secretion (7), enhanced calcium release from
the sarcoplasmic reticulum (13), adenosine receptor antagonism (7), improved neuromuscular
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transmission (20), and increased ability to attain maximal muscular activation (12). Traditionally,
researchers have tested the effects of caffeine during aerobic exercise such as cycle ergometry
(8) and submaximal running (5), suggesting caffeine supplementation may increase performance
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The findings on caffeine use during maximal anaerobic exercise have been equivocal. For
example, Bazzucchi et al. (3) reported a caffeine dose of 6 mgkg1 of bodymass improved
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isometric and isokinetic performance of moderately active men along the torque-velocity curve
during elbow flexion. In addition, Beck et al. (4) found an average caffeine dose of 2.4 mgkg1
of bodymass significantly increased bench press one repetition maximum (1RM) strength of
recreationally active males. Astorino et al. (2), however, reported a caffeine dose of 6 mgkg1 of
bodymass had no effect on 1RM strength of recreationally active males performing the same
exercise. Absolute caffeine doses of 200 mg (18), 300 mg (19), and 400 mg (10) as well as
relative doses of 2 mgkg1 of bodymass (6) have also failed to elicit significant effects in trained
and untrained males performing 1RM bench press. The discrepancies in these findings may
derive from the muscle being tested, the caffeine dosage, the activity performed, or the training
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researchers an avenue for examining motor control strategies and mechanical aspects of muscle
performance (14). EMG is a measure of muscle electrical activity, while MMG measures the
sound of muscle contractions due to lateral oscillations and dimensional changes in active
muscle fibers. MMG has been described as the mechanical counterpart to EMG. The amplitude
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of EMG and MMG signals are associated with motor unit recruitment while the MMG frequency
signal is associated with the firing rate of activated motor units (15). Thus, if caffeine
supplementation affects any of these aspects of neuromuscular function, EMG and MMG may
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between the onset of EMG and acceleration while PMD has been defined as the time lag between
the commencement of the MMG signal, reflecting cross-bridge cycling, and acceleration
(resulting from force/torque production) (16). As non-invasive tools, concurrent use of EMG
and MMG may contribute to understanding any alteration that occurs in motor control strategies
or the mechanical function of muscle following caffeine ingestion. For example, it has been
suggested that caffeine can alter sarcolemmal and t-tubule excitability and excitation/contraction
coupling via dihydropyridine-ryanodine receptor alterations (17). These physiological events
Even though some studies have found caffeine may be able to improve maximal upper
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body strength (3, 4), no known studies have investigated the acute effects of caffeine on upper
body strength while performing a single joint exercise with simultaneous use of EMG and
MMG. Therefore, the purpose of this study was to examine the acute effects of caffeine
ingestion on maximal isometric strength performance of the elbow flexors. It was hypothesized
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there would be acute increases in elbow flexor maximal isometric strength, RTD, and the
amplitude and frequency of the EMG and MMG signals following caffeine ingestion. It was
further hypothesized there would be decreases in both PMD and EMD after caffeine ingestion.
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Lastly, it was hypothesized there would be no difference in any of these variables between the
two caffeine conditions.
METHODS
the laboratory with at least 48 hours between visits. Visit one was a familiarization visit, while
visits two through four each tested for maximal voluntary isometric elbow flexion strength,
RTD, EMD, and PMD on a HUMAC NORM isokinetic dynamometer (CSMi, Inc., Stoughton,
MA). A single joint, isometric muscle action exercise task was utilized in order facilitate
electrical and mechanical aspects of muscle contractions, respectively. During the familiarization
visit, there was no placebo or caffeine ingestion. One hour before testing during visits two, three,
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and four, participants consumed a drink with caffeine (5 or 10 mgkg1 of body mass) or without.
The caffeinated drink was composed of U.S.P. grade anhydrous caffeine mixed into an
artificially flavored drink with no caloric value (Crystal Light). Two different caffeine levels
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were administered to test for a dose-response relationship. The non-caffeinated drink had the
same artificially flavored drink mix and was mixed to the same consistency. The non-caffeinated
drink was designed so there was no difference in color, odor, taste, or volume than the caffeine
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drinks. The order of drink administration for each subject (0, 5 or 10 mgkg1 of body mass) was
randomly determined. After ingesting the drink, participants rested quietly in the lab for 60
minutes before testing (8).
Subjects
Thirteen young males (mean SD, age: 21.38 1.26 years; body mass: 86.15 12.20 kg;
height: 173.35 6.91 cm) in good health were recruited to participate in this repeated measures,
crossover design study. Participants were required to have at least two years of current resistance
training experience. Resistance training experience was defined as a minimum of two sessions
per week. Subjects were precluded from participation in the study if it was determined from their
health history questionnaire that they were at a health risk due to cardiopulmonary, metabolic, or
supplements for the duration of the study. Participants were not allowed to use any medication
that significantly impacted the study. Finally, participants were asked to not change their diets
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Individuals who habitually consumed caffeine, as well as those who did not, were allowed
to participate in the study. Twelve of the thirteen subjects reported to be caffeine nave. All
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participants were asked to refrain from caffeine intake the day of testing. Participants were also
asked to limit physical activity 48 hours before testing. Each participant was asked to drink one
liter (L) of water the night prior to and one-half L the day of testing. This request was in addition
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to their normal water intake to assure ample hydration before testing. All sessions for a given
subject were standardized for time of day. The University Institutional Review Board approved
this study before testing began, and each subject signed a written informed consent document
before testing.
Procedures
A calibrated HUMAC NORM Testing and Rehabilitation system (CSMi, Stoughton, MA)
was used to measure the maximal isometric elbow flexion strength of the right limb of all
subjects. The subjects were positioned supine for testing according to the HUMAC NORM
Testing and Rehabilitation System Users Guide. Torque was determined with the lever arm of
up, three separate 6 s maximal voluntary isometric trials were performed, with the highest output
being selected as the maximal voluntary isometric strength. Participants were given a two-minute
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rest period between each isometric strength trial. EMG and MMG signals were recorded from
the biceps brachii during each strength testing session.
The S-gradient formula by Zatsiorsky and Kraemer [S-gradient = F.05/T.05, where F.05 is
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one-half of maximal torque (Fm) and T.05 is time to achieve that torque] was used to calculate
RTD (22). Custom programs written with LabVIEW software (version 7.1, National Instruments,
Austin, Texas) were used to analyze the data.
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A bipolar (4.1 cm center-to-center), disposable surface electrode arrangement (circular 4mm diameter Ag-AgCl, BIOPAC EL500, BIOPAC Systems Inc., Goleta, CA) was placed on the
right limb over the biceps brachii muscle, distal to the estimated location of the innervation zone,
with the reference electrode placed over the anterior distal end of the forearm between the styloid
processes of the radius and ulna. Shaving of the area, light abrasion, and rubbing the area with an
alcohol pad were used to reduce interelectrode impedance. The EMG signals were pre-amplified
(gain 1000) using a differential amplifier (EMG100C, BIOPAC Systems Inc., Goleta, CA;
bandwidth = 1-500 Hz). An accelerometer (Entran, EGAS-FT-10-/V05, Entran Devices Inc.,
Fairfield NJ, USA) was used to detect the MMG signals. The accelerometer was placed between
with custom programs written with LabVIEW software (version 7.1, National Instruments,
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Austin, Texas).The EMG and MMG signals were bandpass filtered (fourth-order Butterworth) at
10-500 Hz and 5-100 Hz respectively. The amplitude (root mean square) and mean power
frequency (MPF) values for EMG and MMG were calculated for the middle 2 s of the 6 s
isometric contraction. EMD was calculated as the time interval between the onset of the EMG
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signal and the onset of torque, while PMD was calculated as the time interval between the onset
of the MMG signal and the onset of torque. Both EMG and PMD were determined using custom
programs written with LabVIEW software, as previously cited. Previous research from our lab
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has reported reliability coefficients ranging from 0.84 to .98 for EMG, MMG, and torque data,
MPF, RTD, EMD, and PMD data. Post-hoc follow up tests included pair-wise comparisons with
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Bonferroni adjustments. An alpha of P <0.05 was considered significant for all comparisons.
RESULTS
The results of the study indicated the ingestion of 0 (placebo), 5 or 10 mgkg1 of body
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mass of caffeine did not significantly influence (P > 0.05) peak torque (figure 1) or RTD (figure
2). Likewise, normalized EMG (figure 3) and MMG amplitude (figure 4), and EMG frequency
(figure 5) were not affected. However, there was a significant difference (P < 0.05) among the
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placebo and the caffeine trials for normalized MMG MPF. Normalized MMG MPF following
ingestion of 5 mgkg1 of body mass of caffeine was significantly less than the placebo trial
(figure 6). EMD (figure 7) and PMD (figure 8) were not significantly affected by caffeine (P >
The purpose of this study was to investigate the effects of caffeine on maximal isometric
strength, RTD, EMG and MMG amplitude and frequency, and EMD and PMD of the elbow
flexors. To our knowledge, no studies have investigated the acute effects of caffeine on upper
body strength while performing a single joint exercise with simultaneous use of EMG and
MMG. Previous research has indicated that under certain conditions, caffeine may increase
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resulted from the type of muscle action and exercise performed, caffeine dose used, muscle
group tested, or training status of the subjects. Our protocol used a single joint isometric exercise
to test the effects of caffeine doses of 5 and 10 mgkg1 of body mass on maximal strength of the
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elbow flexors in resistance trained males (participating in at least 2 training sessions per week).
Beck et al. (6) reported that a 201 mg dose of caffeine significantly increased bench press one
repetition maximum (1RM) in resistance trained males (participating in at least 4 training
sessions per week). Since significant results were found with a caffeine dose less than ours
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(average absolute doses in the current study were 426.7 and 853.4 mg for the 0 and 5 mgkg1
body mass conditions, respectively), it seems that the exercise test and training status may have
led to different findings between the studies. The bench press is an exercise requiring dynamic
involvement of the pectoralis major, deltoid, and triceps. Our study required participants to
complete a single joint isometric exercise test using only the elbow flexors. In addition, the
subjects in the study by Beck et al. (6) had a greater training status as they were required to
participate in at least 4 training sessions per week as opposed to 2 in our study. Training status
may be of great importance as Beck et al. (7) again tested the effects of a 201 mg dose of
caffeine on bench press 1RM in untrained subjects and found no ergogenic effect from caffeine
ingestion. It is possible the subjects in our study and Beck et al. (7) were not trained enough to
maximal isometric strength with our caffeine doses of 5 and 10 mgkg1 of body mass, studies
testing the knee extensors have reported significant strength increases with lower caffeine doses
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of 7 mgkg1 of body mass (19), 6 mgkg1 of body mass (20), and 5 mgkg1 of body mass (3).
In addition to maximal strength levels, a high rate of torque development (RTD) is
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desirable for athletic performance in tasks which involve explosive movements. To our
knowledge, ours is the first study to test the effects of caffeine on RTD of an upper body muscle.
Jacobson et al. (19) found that a 7 mgkg1 of body mass dose of caffeine significantly increased
performance during the first 125 ms during a 300s1 knee extension. In contrast to their
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findings, we did not find a significant difference in RTD after caffeine ingestion. Training status
may again be a factor since the subjects in the study by Jacobson et al. (19) had a much greater
training status than ours as they were division one football players. It may also be that the knee
extensors are more sensitive to caffeine supplementation than the elbow flexors or that caffeine
affects isokinetic performance differently than isometric performance.
Insert figure 2 about here
We found caffeine did not have a significant effect on EMG amplitude or frequency and
therefore did not have a significant effect on the number or type of activated motor units. This
finding contradicts other research (4) which reported that a 6 mgkg1 of body mass dose of
research (20) which found that a 6 mgkg1 of body mass dose of caffeine was able to increase
maximal muscle activation and neuromuscular transmission of the vastus lateralis during
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isometric muscle actions of the knee extensors. Our findings do agree with Williams, Barnes,
and Gadberry (32), who found that a 7 mgkg1 of bodyweight dose of caffeine was not able to
significantly increase isometric MVC or EMG frequency of adult males performing a hand grip
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exercise. These findings suggest caffeine may affect isometric, as used in the present study, and
isokinetic performance differently and warrants more investigation on caffeine with these
different types of strength testing demands.
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Consistent with our findings for EMG amplitude and frequency, we found that caffeine did
not have an effect on MMG amplitude. While a plateau in the MMG amplitude at high torque
levels may result from muscle stiffness (27) or limited oscillations of muscle fibers caused by
high motor unit firing rates (23), the lack of increase in EMG amplitude and torque suggest that
the lack of increase in MMG amplitude reflects the fact that caffeine did not enhance
neuromuscular function.
an isolated finding as MMG frequency was the only variable to have a significant difference
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Simultaneous use of EMG and MMG also allowed examination of electromechanical delay
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(EMD) and phonomechanical (PMD) delay. The time delay between the onset of the EMG signal
and force or torque is EMD (26). It is of interest because it accounts for the time necessary to
create tension after activating the muscle. Cavanagh and Komi (9) stated this delay may be
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attributed to the action potential propagating along the excitable muscle membranes, calcium
release from the sarcoplasmic reticulum and binding to ensuing active sites, cross bridge
formation, and tension of the series elastic component (SEC). We tested EMD as caffeine is
regarded to possibly affect calcium release (21), and cross bridge formation (20). However, we
found no difference in mean EMD between trials, suggesting that caffeine did not affect these
processes. The results for EMD did approach statistical significance (P = 0.056), however, so
future researchers may wish to investigate this further. Decreasing the time delay between the
stimulus for muscle contraction (electrical) and force generation from cross-bridge formation
(mechanical) might positively affect performance, even in the absence of an increase in maximal
force production.
to our knowledge, the first study to test them in conjunction with caffeine.
PRACTICAL APPLICATIONS
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These findings suggest that caffeine does not have an ergogenic effect on 1RM strength
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trained individuals, and is less likely to affect single joint, small muscle mass exercises
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Williams JH, Barnes WS, and Gadberry WL. Influence of caffeine on force and EMG in
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FUNDING
There was no funding for this project.
CONFLICT OF INTEREST DISCLOSURE
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FIGURES
Figure 1. Isometric Maximal Voluntary Contraction (MVC) (Nm) SEM. The ingestion of 0, 5
or 10 mgkg1 of body mass of caffeine did not significantly influence mean isometric maximal
voluntary contractions (P > 0.05) between trials.
Figure 2. Rate of torque development (Nms-1) SEM. Mean rate of torque development was
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not significantly different (P > 0.05) between caffeine and placebo trials.
Figure 3. EMG Amplitude (V rms) SEM. Mean EMG amplitude was not significantly
different (P> 0.05) between caffeine and placebo trials.
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Figure 4. MMG amplitude (m/s2) SEM. Mean MMG amplitude was not significantly different
(P > 0.05) between caffeine and placebo trials.
Figure 5. EMG mean power frequency (Hz) SEM. Mean EMG frequency was not significantly
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Figure 6. MMG mean power frequency (Hz) SEM. * = MMG mean power frequency for 5
mgkg1 of body mass of caffeine was significantly less (P < 0.05) than the placebo trial.
Figure 7. Electromechanical delay (s) SEM. Mean electromechanical delay was not
significantly different (P > 0.05) between caffeine and placebo trials.
Figure 8. Phonomechanical delay (s) SEM. Mean phonomechanical delay was not
significantly different (P > 0.05) between caffeine and placebo trials.