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

Trevino, Michael A.1; Coburn, Jared W.2; Brown, Lee E.2; Judelson, Daniel A.2; Malek, Moh H.3

Journal of Strength and Conditioning Research: February 2015 - Volume 29 - Issue 2 - p 513–520
doi: 10.1519/JSC.0000000000000625
Original Research
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Trevino, MA, Coburn, JW, Brown, LE, Judelson, DA, and Malek, MH. Acute effects of caffeine on strength and muscle activation of the elbow flexors. J Strength Cond Res 29(2): 513–520, 2015—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 4 times. Visit 1 served as a familiarization visit. During visits 2 through 4, subjects ingested a randomly assigned drink, with or without caffeine (0, 5, or 10 mg·kg−1 of body mass), and performed 3 maximal isometric muscle actions of the elbow flexors 60 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 mg·kg−1 of 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 5 mg·kg−1 of body mass of caffeine compared with the placebo trial. This was most likely an isolated finding because MMG frequency was the only variable to have a significant difference across all trials. The results suggested that ingestion of either 5 or 10 mg·kg−1 of body mass of caffeine does not provide an ergogenic effect for the elbow flexors during isometric muscle actions.

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

2Exercise Physiology Lab and Center for Sport Performance, Department of Kinesiology, California State University, Fullerton, Fullerton, California; and

3Department of Health Care Sciences, College of Pharmacy and Health Sciences, Wayne State University, Detroit, Michigan

Address correspondence to Michael A. Trevino, mtrevino@ku.edu.

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Introduction

The ability of caffeine to arouse the central nervous system has made it popular in everyday life (16). Caffeine is quite ubiquitous because 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 (14). Some proposed exercise-related effects of caffeine include increased catecholamine secretion (10), enhanced calcium release from the sarcoplasmic reticulum (18), adenosine receptor antagonism (10), improved neuromuscular transmission (27), and increased ability to attain maximal muscular activation (17). Traditionally, researchers have tested the effects of caffeine during aerobic exercise such as cycle ergometry (11) and submaximal running (7), 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. (4) reported that a caffeine dose of 6 mg·kg−1 of body mass improved isometric and isokinetic performance of moderately active men along the torque-velocity curve during elbow flexion. In addition, Beck et al. (6) found that an average caffeine dose of 2.4 mg·kg−1 of body mass significantly increased bench press 1 repetition maximum (1RM) strength of recreationally active males. Astorino et al. (2), however, reported that a caffeine dose of 6 mg·kg−1 of body mass had no effect on 1RM strength of recreationally active males performing the same exercise. Absolute caffeine doses of 200 mg (25), 300 mg (26), and 400 mg (13) and relative doses of 2 mg·kg−1 of body mass (9) 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 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 2 mechanisms: motor unit recruitment and rate coding (12). 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 (19). Electromyography is a measure of muscle electrical activity, whereas MMG measures the sound of muscle contractions resulting from lateral oscillations and dimensional changes in active muscle fibers. Mechanomyography has been described as the mechanical counterpart to EMG. The amplitude of EMG and MMG signals is associated with motor unit recruitment, whereas the MMG frequency signal is associated with the firing rate of activated motor units (21). 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). Electromechanical delay is the time measured between the onset of EMG and acceleration, whereas PMD has been defined as the time lag between the commencement of the MMG signal, reflecting cross-bridge cycling, and acceleration (resulting from force or torque production) (22). As noninvasive 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 by dihydropyridine-ryanodine receptor alterations (24). These physiological events might be detected by 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 or, in the case of rotational movement, rate of torque development (RTD).

Even though some studies have found that caffeine may be able to improve maximal upper-body strength (4,6), 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 that 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 that there would be decreases in both PMD and EMD after caffeine ingestion. Finally, it was hypothesized that there would be no difference in any of these variables between the 2 caffeine conditions.

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Methods

Experimental Approach to the Problem

This study used a double-blind, randomized cross-over design. Subjects made 4 visits to the laboratory with at least 48 hours between visits. Visit 1 was a familiarization visit, whereas visits 2 through 4 each tested for maximal voluntary isometric elbow flexion strength, RTD, EMD, and PMD on a HUMAC NORM isokinetic dynamometer (CSMi, Inc., Stoughton, MA, USA). A single-joint, isometric muscle action exercise task was used to facilitate collection of the EMG, and especially the MMG signals. Although these types of strength movements are less commonly used during training, we feel that it is 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 2, 3, and 4, participants consumed a drink with caffeine (5 or 10 mg·kg−1 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 were administered to test for a dose-response relationship. The noncaffeinated drink had the same artificially flavored drink mix and was mixed to the same consistency. The noncaffeinated 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 mg·kg−1 of body mass) was randomly determined. After ingesting the drink, participants rested quietly in the laboratory for 60 minutes before testing (11).

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Subjects

Thirteen young men (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-measure, crossover design study. The age range of the subjects was 19 to 28 years old. Participants were required to have at least 2 years of current resistance training experience. Resistance training experience was defined as a minimum of 2 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 because of cardiopulmonary, metabolic, or 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, and those who did not, were allowed to participate in the study. Twelve of the 13 subjects reported to be caffeine naive. All participants were asked to refrain from caffeine intake on the day of testing. Participants were also asked to limit physical activity 48 hours before testing. Each participant was asked to drink 1 L of water the night before testing and 1.5 L on 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.

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Procedures

A calibrated HUMAC NORM Testing and Rehabilitation system (CSMi) 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 User's Guide. Torque was determined with the lever arm of the dynamometer at an angle of 1.134 rad (65°) above the horizontal plane. Before maximal isometric strength testing, the subjects completed a 5-minute warm-up on the cycle ergometer (Monark 839E, Varberg, Sweden). Subjects were instructed to pedal 60 repetitions per minute against 50 W 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, 3 separate 6-second maximal voluntary isometric trials were performed, with the highest output being selected as the maximal voluntary isometric strength. Participants were given a 2-minute rest period between each isometric strength trial. Electromyographic and MMG signals were recorded from the biceps brachii during each strength testing session.

The S-gradient formula by Zatsiorsky and Kraemer (S-gradient = F0.05/T0.05, where F0.05 is one-half of maximal torque [Fm] and T0.05 is time to achieve that torque) was used to calculate RTD (29). Custom programs written with LabVIEW software (version 7.1; National Instruments, Austin, TX, USA) 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, USA) 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., 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 the 2 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.,) 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). The EMG and MMG signals were bandpass filtered (fourth-order Butterworth) at 10–500 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 seconds of the 6-second isometric contraction. Electromechanical delay was calculated as the time interval between the onset of the EMG signal and the onset of torque, whereas 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 laboratory has reported reliability coefficients ranging from 0.84 to 0.98 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 mg·kg−1 of body mass of caffeine) repeated-measure analyses of variance 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 pairwise comparisons with Bonferroni adjustments. An alpha of p ≤ 0.05 was considered significant for all comparisons.

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Results

The results of the study indicated that the ingestion of 0 (placebo), 5, or 10 mg·kg−1 of body 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 placebo and the caffeine trials for normalized MMG MPF. Normalized MMG MPF following ingestion of 5 mg·kg−1 of body mass of caffeine was significantly less than the placebo trial (Figure 6). Electromechanical delay (Figure 7) and PMD (Figure 8) were not significantly affected by caffeine (p > 0.05) during maximal voluntary isometric contractions of the elbow flexors.

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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 muscle force production during anaerobic activities (3,6,15,17). These studies were the basis for the hypothesis that 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 result from a variety of factors.

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 mg·kg−1 of 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 1RM in resistance trained males (participating in at least 4 training sessions per week). Because 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 mg·kg−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 because 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. (5) 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 that the subjects in our study and in the study by Beck et al. (5) were not trained enough to 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. Although we did not find significant increases in maximal isometric strength with our caffeine doses of 5 and 10 mg·kg−1 of body mass, studies testing the knee extensors have reported significant strength increases with lower caffeine doses of 7 mg·kg−1 of body mass (15), 6 mg·kg−1 of body mass (17), and 5 mg·kg−1 of body mass (3).

In addition to maximal strength levels, a high RTD is desirable for athletic performance in tasks that 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. (15) found that a caffeine dose of 7 mg·kg−1 of body mass significantly increased performance during the first 125 milliseconds during a 300°·s−1 knee 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 because the subjects in the study by Jacobson et al. (15) had a much greater training status than ours as they were Division I 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 that 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 caffeine dose of 6 mg·kg−1 of body mass significantly increased maximal isokinetic elbow flexion at 250°·s−1 and was associated with significant increases in EMG conduction velocity during the 60, 120, 180, and 250°·s−1 isokinetic trials. However, it was also reported that significant increases in torque did not occur at 0, 30, 60, 120, and 180°·s−1 and conduction velocity was not significantly improved at 0 and 30·s−1. These latter findings are in agreement with ours. Our results also disagree with other research (17), which found that a caffeine dose of 6 mg·kg−1 of body mass 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 et al. (28), who found that a caffeine dose of 7 mg·kg−1 of body mass was not able to significantly increase isometric MVC or EMG frequency of adult males performing a hand grip exercise. These findings suggest that 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.

Consistent with our findings for EMG amplitude and frequency, we found that caffeine did not have an effect on MMG amplitude. Although a plateau in the MMG amplitude at high torque levels may result from muscle stiffness (23) or limited oscillations of muscle fibers caused by high motor unit firing rates (20), 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.

Our study found no significant increases in torque after caffeine ingestion so no change in MMG frequency should also have been expected. However, it seems that caffeine had an effect on the firing rates of the activated motor units as MMG frequency was significantly less following ingestion of 5 mg·kg−1 of body mass of caffeine compared with the placebo trial. This is most likely an isolated finding because MMG frequency was the only variable to have a significant difference across all trials.

Simultaneous use of EMG and MMG also allowed examination of EMD and PMD. The time delay between the onset of the EMG signal and force or torque is EMD (22). It is of interest because it accounts for the time necessary to create tension after activating the muscle. Cavanagh and Komi (8) stated that 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. We tested EMD as caffeine is regarded to possibly affect calcium release (18) and cross bridge formation (17). 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.

The time lag between the commencement of the MMG signal and muscle acceleration has been defined as PMD (22). 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.

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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 caffeine's 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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Keywords:

biceps brachii; electromyography; ergogenic aid; mechanomyography; torque

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