Acute Effects of Caffeine on Strength and Muscle Activation of the Elbow Flexors. 2014 AHoP

8/10/2019 Acute Effects of Caffeine on Strength and Muscle Activation of the Elbow Flexors. 2014 AHoP

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Journal of Strength and Conditioning Research Publish Ahead of Print

DOI: 10.1519/JSC.0000000000000625

Effects of Caffeine on Torque1

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,

1Department of Health, Sport, and Exercise Sciences, University of Kansas, Lawrence, KS

2Department of Kinesiology, Exercise Physiology Lab and Center for Sport Performance,

California State University, Fullerton, Fullerton, CA

3

College

of Pharmacy and Health Sciences, Wayne State University, Detroit, MI

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.

Funding: There was no funding for this project.

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

[email protected]

Copyright Lippincott Williams & Wilkins. All rights reserved.


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ABSTRACT

The purpose of this study was to examine the effects of caffeine on strength and muscle

activation of the elbow flexors. Thirteen recreationally active male volunteers (mean SD, age:

21.38 1.26 years) came to the laboratory four times. Visit one served as a familiarization visit.

During visits two through four, subjects ingested a randomly assigned drink, with or without

caffeine (0, 5, or 10 mgkg1of body mass), and performed three maximal isometric muscle

actions of the elbow flexors sixty minutes after ingestion. Maximal strength and rate of torque

development (RTD) were recorded. Electromyographic (EMG) and mechanomyographic

(MMG) amplitude and frequency, and electromechanical delay (EMD) and phonomechanical

delay (PMD) were measured from the biceps brachii. The results indicated that the ingestion of 0

(placebo), 5 or 10 mgkg1of body mass of caffeine did not significantly influence (P> 0.05)

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

difference across all trials. The results suggested that ingestion of either five or ten mgkg

1

of

body mass of caffeine does not provide an ergogenic effect for the elbow flexors during

isometric muscle actions.

Key Words: biceps brachii, electromyography, ergogenic aid, mechanomyography, torque



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INTRODUCTION

The ability of caffeine to arouse the central nervous system has made it popular in

everyday life (21). Caffeine is quite ubiquitous as it can be found in sodas, coffee, alcoholic and

nonalcoholic drinks, energy drinks, and supplements. During the last few decades, caffeine

supplementation has gained popularity among athletes (11). Some proposed exercise-related

effects of caffeine include increased catecholamine secretion (7), enhanced calcium release from

the sarcoplasmic reticulum (13), adenosine receptor antagonism (7), improved neuromuscular

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

during endurance exercise.

The findings on caffeine use during maximal anaerobic exercise have been equivocal. For

example, Bazzucchi et al. (3) reported a caffeine dose of 6 mgkg1of bodymass improved

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 mgkg1of

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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status of the subjects. In any case, an athlete, strength and conditioning coach, or personal trainer

is left with many questions regarding the efficacy and physiological mechanisms of caffeine use.

The ability of a muscle to produce maximal force is largely regulated by two mechanisms:

motor unit recruitment and rate-coding (9). If strength and power performance are increased

after caffeine ingestion, it is likely that one or both of these mechanisms were positively affected.

Simultaneous use of electromyography (EMG) and mechanomyography (MMG) may provide

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

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

help to determine the specific physiological processes involved.

Simultaneous measurement of EMG and MMG can also allow examination of

electromechanical delay (EMD) and phonomechanical delay (PMD). EMD is the time measured

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



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might be detected via examination of the EMG and MMG signals, respectively. In addition,

enhanced release of calcium may increase the rate at which force (torque) is produced, even in

the absence of an increase in maximal force or torque. A measure of the time it takes for force

production is known as rate of force development (RFD), or in the case of rotational movement,

rate of torque development (RTD).

Even though some studies have found caffeine may be able to improve maximal upper

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

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.

Lastly, it was hypothesized there would be no difference in any of these variables between the

two caffeine conditions.

METHODS

Experimental Approach to the Problem

This study used a double-blind, randomized, cross-over design. Subjects made four visits to

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



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collection of the EMG, and especially the MMG signals. While these types of strength

movements are less commonly used during training, we feel it's important for practitioners to

understand the "why" and not just the "how" of caffeine's potential mechanisms of altering

neuromuscular function. During strength testing, EMG and MMG sensors were placed over the

biceps brachii muscle of the right limb. The EMG and MMG sensors were used to monitor the

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,

and four, participants consumed a drink with caffeine (5 or 10 mgkg1of 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

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

drinks. The order of drink administration for each subject (0, 5 or 10 mgkg1of 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



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orthopedic/musculoskeletal problems. Symptoms of these diseases included chest pain, heart

murmurs, severe dizziness, diabetes, hypertension, a family history of the diseases, arthritis, etc.

Women were not recruited for this study because oral contraception use has been shown to

increase the half-life of caffeine and slow the removal of caffeine during the luteal phase of the

menstrual cycle (1). Participants were asked to abstain from the use of any nutritional

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

for the length of the study.

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

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

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



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the dynamometer at an angle of 1.134 rad (65) above the horizontal plane. Prior to maximal

isometric strength testing, the subjects completed a 5-minute warm-up on the cycle ergometer

(Monark 839E, Varburg, Sweden). Subjects were instructed to pedal 60 repetitions per minute

against 50 watts of resistance. Each subject then performed five, 6-second voluntary isometric

actions at approximately 50% of their maximum on the HUMAC NORM. Following this warm-

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

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.05is

one-half of maximal torque (Fm) and T.05is 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.

A bipolar (4.1 cm center-to-center), disposable surface electrode arrangement (circular 4-

mm 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



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the two EMG leads (over the belly of the biceps brachii). Double-sided foam tape was used to

affix the accelerometer to the muscle.

A personal computer and commercially available software (AcqKnowledge v. 3.8.1,

BIOPAC Systems Inc., Goleta, CA) were used to store and display the EMG and MMG signals.

The signals were collected at a 1,000 Hz sampling frequency. Signal processing was performed

with custom programs written with LabVIEW software (version 7.1, National Instruments,

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

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

has reported reliability coefficients ranging from 0.84 to .98 for EMG, MMG, and torque data,

with and without caffeine ingestion.



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Statistical Analyses

Before the statistical analyses, all EMG and MMG amplitude and MPF data were

normalized to their highest recorded values during isometric MVC testing. Eight separate 1 3

(0, 5 or 10 mgkg1of body mass caffeine) repeated measures ANOVAs were used to analyze

maximal isometric elbow flexion strength, EMG amplitude, EMG MPF, MMG amplitude, MMG

MPF, RTD, EMD, and PMD data. Post-hoc follow up tests included pair-wise comparisons with

Bonferroni adjustments. An alpha of 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

placebo and the caffeine trials for normalized MMG MPF. Normalized MMG MPF following

ingestion of 5 mgkg1of 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>

0.05) during maximal voluntary isometric contractions of the elbow flexors.

DISCUSSION

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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muscle force production during anaerobic activities (4, 6, 19, 20). These studies were the basis

for the hypothesis caffeine would increase maximal voluntary isometric strength of the elbow

flexors. The results of our study revealed that caffeine did not significantly affect peak torque

during the maximal isometric contractions. This finding may be due to a variety of factors.

Insert figure 1 about here

Past equivocal findings with caffeine ingestion and anaerobic performance may have

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 mgkg1of body mass on maximal strength of the

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

(average absolute doses in the current study were 426.7 and 853.4 mg for the 0 and 5 mgkg

1

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



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experience a significant improvement with caffeine supplementation. The lack of familiarity with

performing maximal muscle actions may hide any potential benefits to be derived from caffeine

ingestion.

It is also possible that larger lower body muscles are more sensitive to the effects of

caffeine than smaller upper body muscles. While we did not find significant increases in

maximal isometric strength with our caffeine doses of 5 and 10 mgkg1of body mass, studies

testing the knee extensors have reported significant strength increases with lower caffeine doses

of 7 mgkg1of body mass (19), 6 mgkg

1of body mass (20), and 5 mgkg

1of body mass (3).

In addition to maximal strength levels, a high rate of torque development (RTD) is

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 mgkg1of body mass dose of caffeine significantly increased

performance during the first 125 ms during a 300s1knee extension. In contrast to their

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.


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 mgkg1of body mass dose of



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caffeine significantly increased maximal isokinetic elbow flexion at 250s1and was associated

with significant increases in EMG conduction velocity during the 60, 120, 180, and 250s1

isokinetic trials. However, it was also reported that significant increases in torque did not occur

at 0, 30, 60, 120, and 180s1and conduction velocity was not significantly improved at 0 and

30s1. These latter findings are in agreement with ours. Our results also disagree with other

research (20) which found that a 6 mgkg1of body mass dose of caffeine was able to increase

maximal muscle activation and neuromuscular transmission of the vastus lateralis during

isometric muscle actions of the knee extensors. Our findings do agree with Williams, Barnes,

and Gadberry (32), who found that a 7 mgkg

1

of bodyweight dose of caffeine was not able to

significantly increase isometric MVC or EMG frequency of adult males performing a hand grip

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.

Insert figures 3 and 4 about here

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.



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Our study found no significant increases in torque after caffeine ingestion so no change in

MMG frequency should also have been expected. However, it appears caffeine had an effect on

the firing rates of the activated motor units as MMG frequency was significantly less following

ingestion of 5 mgkg1of body mass of caffeine compared to the placebo trial. This is most likely

an isolated finding as MMG frequency was the only variable to have a significant difference

across all trials.


Simultaneous use of EMG and MMG also allowed examination of electromechanical delay

(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

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.



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The time lag between the commencement of the MMG signal and muscle acceleration has

been defined as PMD (26). For the isometric biceps brachii muscle in our study, PMD was

recorded from the onset of the MMG signal to the beginning of torque production. We found no

difference in mean PMD between trials. Research on EMD and PMD is scarce and this study is

to our knowledge, the first study to test them in conjunction with caffeine.


PRACTICAL APPLICATIONS

These findings suggest that caffeine does not have an ergogenic effect on 1RM strength

or neuromuscular function of the elbow flexors in recreationally resistance trained men.

Practitioners such as strength and conditioning coaches should consider that caffeines ergogenic

effects may be evident only with large muscle mass exercises performed by highly resistance

trained individuals, and is less likely to affect single joint, small muscle mass exercises

commonly used by athletes for hypertrophy or rehabilitation.



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FUNDING

There was no funding for this project.

CONFLICT OF INTEREST DISCLOSURE

The authors have no conflicts of interest.



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FIGURES

Figure 1. Isometric Maximal Voluntary Contraction (MVC) (Nm) SEM. The ingestion of 0, 5

or 10 mgkg1of 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

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.

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

different (P > 0.05) between caffeine and placebo trials.

Figure 6.MMG mean power frequency (Hz) SEM. * = MMG mean power frequency for 5

mgkg1of 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.

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Acute Effects of Caffeine on Strength and Muscle Activation of the Elbow Flexors. 2014 AHoP