Effect of Caffeine Ingestion on Maximal Voluntary Contraction Strength in Upper- and Lower-Body Muscle Groups : The Journal of Strength & Conditioning Research

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Effect of Caffeine Ingestion on Maximal Voluntary Contraction Strength in Upper- and Lower-Body Muscle Groups

Timmins, Tomas D.; Saunders, David H.

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Journal of Strength and Conditioning Research 28(11):p 3239-3244, November 2014. | DOI: 10.1519/JSC.0000000000000447
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There is substantial evidence that acute caffeine supplementation may increase work output and time to exhaustion of endurance exercise (10,20). Caffeine has also been shown to enhance both short-term high-intensity exercise (16,43) and team sport performance (36,39). However, the effect of caffeine on muscle strength and explosive power output is less clear, with support both for (26,28) and against (31,40) an ergogenic effect.

Many studies that have examined the effect of caffeine on strength-power performance have compared that of upper- and lower-body musculature, but the results are inconsistent. A number of studies have demonstrated improvements for upper-body but not lower-body strength (9,43). For instance, Beck et al. (9) examined the effects of 201 mg (2.1–3.0 mg·kg−1) of caffeine on maximal voluntary contraction (MVC) strength and strength endurance in resistance-trained men. This low dose of caffeine was found to significantly improve bench press 1 repetition maximum (1RM), although significant increases were not reported for bilateral leg extension 1RM or for strength endurance. In contrast, some studies have reported improvements for lower-body but not upper-body strength (2,21). Astorino et al. (2) found that 6 mg·kg−1 of caffeine significantly (p > 0.05) improved leg press to fatigue at 70–80% 1RM, but not that of bench press, shoulder press, or bilateral row in resistance-trained men. Other studies have reported no change in upper- or lower-body strength (4,23). Astorino et al. (5) found no significant increase in either bench press or leg press 1RM when supplementing resistance-trained men with 6 mg·kg−1. Possible causes of this inconsistency include variation in training status, individual habituation, dose of caffeine, and mode of strength (i.e., isoinertial, isometric, or isokinetic) between studies (17).

Of note is the meta-analysis conducted by Warren et al. (42). They examined a total of 34 studies (n = 726 subjects), between 1939 and 2008, which tested the impact of caffeine ingestion on MVC strength (27 studies) and strength endurance (23 studies). The results show a large ergogenic effect (14%) on strength endurance (effect size[ES] = 0.28, p = 0.00005) and a small ergogenic effect (4%) on MVC strength (ES = 0.19, p = 0.0003). Interestingly, subgroup meta-analyses found that muscle group size and location were significant (p ≤ 0.01) factors within MVC strength, but not strength endurance, i.e., studies that examined large (ES = 0.31) or lower-body (ES = 0.29) muscle groups were shown to have greater overall effect sizes relative to those that examined small (ES = 0.05) or upper-body (ES = 0.07) muscles groups. According to Warren et al. (42), a possible reason for these findings relates to voluntary muscle activation. Using the twitch interpolation technique, previous research has found that muscle activation during MVC is less in larger muscle groups, such as the knee extensors (85–95%), than in smaller muscle groups, such as the ankle plantar flexors (90–99%) (37). Therefore, mechanistically, if caffeine operates mainly through the central nervous system (CNS) stimulation, then its capacity to increase motor unit (MU) recruitment or MU firing rates, and so enhance maximal force production, should be greater with larger muscle groups. This would also explain the effect of muscle group location, as lower-body muscle groups are typically larger than their upper body counterparts. Alternatively, if caffeine has a direct effect on muscle, its capacity to enhance maximal force production should be similar across muscle groups.

Although current research regarding the effect of caffeine on strength-power performance is equivocal, caffeine use among strength-power athletes is prevalent. For instance, measurement of more than 4600 samples across 56 sports in 2004 revealed a greater average urinary caffeine concentration and a larger percentage of higher urinary caffeine concentrations in strength-power sports relative to other sports (12). Hence, further investigation in strength-power performance is required, especially comparing that of the upper and lower body. Additionally, such studies not only provide information concerning the ergogenic potential of caffeine for strength-power athletes, but also produce evidence for possible mechanisms of caffeine action (19).

Although Warren et al. (42) have indirectly compared the effect of caffeine on the MVC strength of certain muscle groups depending on location and size, no published study to date has done so directly (i.e., using the same subjects). Consequently, as the 2 factors are somewhat related, it is difficult to verify whether the effect of caffeine effect is dependent on muscle group location, size, or both. Furthermore, the meta-analysis fails to account for a number of key variables within studies, including subject number, gender and training status, dose of caffeine, and MVC strength mode. This knowledge gap has been noted by a number of recent documents (23,42,43). Therefore, the primary aim of this investigation was to determine the effect of caffeine ingestion on the MVC strength of large and small muscle groups within upper- and lower-body locations. An additional goal was to provide further insight into caffeine's mechanistic action on strength-power performance.


Experimental Approach to the Problem

A randomized, subject-blind crossover design was used. Testing sessions were held on 2 separate occasions at the same time of day ± 1 hour per person. On each occasion, the subjects ingested 5 ml·kg−1 of a carbohydrate-free, fruit-flavored solution containing 6 mg·kg−1 of caffeine (CAF) or 5 ml·kg−1 of a caffeine-free placebo (PLA). Subjects consumed the opposite solution during the second testing session, which occurred at the same time of the day, 1 week later. A 6 mg·kg−1 dose was used, as this has been shown to maximize levels of caffeine in the blood (20). Moreover, there is no further benefit at higher doses of 9 mg·kg−1 or more, which may also cause adverse side effects (3). Maximal voluntary contraction strength was determined in 2 upper- and 2 lower-body muscle groups using a Biodex System 3 Pro (Biodex Medical Systems, Shirley, New York) isokinetic dynamometer. Isokinetic dynamometry, the preferred technique for the quantification of muscle strength (7), was used to better isolate each muscle group. Additionally, the Biodex System 3 Pro is considered mechanically reliable and valid (15). A low angular velocity (60°·s−1) was used because, according to the force-velocity relationship, the ability of muscle to develop force is greater at slower contraction velocities (14).


Sixteen resistance-trained men (age, 21.1 ± 0.8 years; body mass, 80.9 ± 7.5 kg; height, 182.7 ± 4.1 cm) were recruited for this study, which was approved by the University of Edinburgh Institute of Sport, Physical Education and Health Sciences. Each subject signed an informed consent document outlining the purpose, procedures, and risks of the protocol. They also completed a questionnaire addressing daily caffeine consumption. Former research has found no significant difference in performance between heavy users (≥300 mg·d−1) and low users (≤50 mg·d−1) (10). However, only subjects with intakes ≤300 mg·d−1 were selected, as heavy consumption may dampen the upregulation of adenosine receptors (44). All subjects were resistance trained; similar to Beck et al. (9), they had at least 1 year of resistance training, and were completing at least 2 resistance training sessions per week. Subjects were also required to be nonsmokers, as nicotine increases caffeine degradation (34). Women were deliberately excluded from the study, as caffeine clearance is attenuated during the luteal phase of the menstrual cycle (30) and oral contraceptive increases the half-life of caffeine (1).


All subjects attended a familiarization session 1 week before testing. They were instructed not to consume caffeine-containing products 24 hours before testing, to reduce the effect of any caffeine tolerance, and were asked to abstain from heavy exercise and alcohol consumption during this period.

During the first testing session, anthropometric measures were recorded, including height and body weight. Subjects were then randomly assigned to a treatment order using a random number grid. After consumption of the caffeine or placebo solutions, subjects performed a 15-minute warm-up, involving both static and dynamic stretches. They were also asked if they perceived they had ingested the caffeine solution, the placebo solution, or were unsure.

After 30 minutes, MVC strength testing began using the isokinetic dynamometer, which was calibrated before each testing session. Maximal voluntary contraction strength was determined in a large (elbow flexors) and a small (wrist flexors) upper-body muscle group, and a large (knee extensors) and a small (ankle plantar flexors) lower-body muscle group, for each subject in a random order. All subjects performed 3 consecutive maximal repetitions for each muscle group. The greatest isokinetic peak torque achieved over the 3 repetitions was automatically recorded in Newton meters (N·m) by the isokinetic dynamometer and presented on its monitor. During knee extension, the leg was moved from a 90° flexed position to full extension and then returned. During ankle plantar flexion, the ankle was moved from a neutral position to full plantar flexion and then returned. During elbow flexion, the arm was supinated and moved from an 180° extended position to full flexion and then returned. During wrist flexion, the wrist was pronated and moved from a neutral position to full flexion and then returned. Before each set was performed, the relevant joint axis was aligned with the load cell, during active conditions, and fixed using a cuff attached to the dynamometer. Furthermore, to prevent undesired motion, the subjects were stabilized using appropriate straps and instructed to grip the handles either side of the seat when possible. Finally, maximum range of motion was set to allow subjects to reach maximal voluntary activation. Five-minute rest was permitted between each exercise. During this period, the isokinetic dynamometer was prepared for the subsequent exercise. All subjects were consistently verbally encouraged to exert maximal effort. After completion of all 4 exercises, subjects performed a 5-minute cooldown.

The exact same protocol was followed during the second testing session, after subjects received the opposite treatment. Following the second testing session, subjects were debriefed and notified of the treatment order.

Statistical Analyses

Statistical analyses were performed using SPSS Statistics 19.0 (SPSS Inc., Chicago, IL). A Shapiro-Wilk test confirmed that the groups represent a normally distributed population. A 2 (treatment) × 4 (muscle group) repeated-measures analysis of variance (ANOVA) was then used to analyze the main effects of treatment and muscle group, and the interaction between treatment and muscle group on isokinetic peak torque. The Greenhouse-Geisser correction was used to account for unequal variances across groups as sphericity was compromised. Significance was established at p ≤ 0.05 for all statistical tests. Finally, effect sizes for each muscle group were calculated using Cohen's d (13).


Testing was completed and well tolerated by all subjects, with no reports of any adverse side effects. For both treatments, the majority of subjects were unsure whether they had received the caffeine or placebo solution. Of those that guessed, there was an even mix of correct and incorrect answers. Using a comprehensive list detailing the caffeine content of common products (12), analysis of the caffeine consumption questionnaire revealed a mean estimated intake of 95.4 ± 80.0 mg·d−1SD). No subjects were identified as heavy caffeine users (≥300 mg·d−1), 13 were identified as moderate users, and 3 were identified as low users (≤50 mg·d−1). All subjects claimed they had adhered to the instructions regarding restriction of exercise, alcohol consumption, and caffeine consumption.

Mean peak isokinetic torque values of the PLA and CAF treatments for each of the 4 muscle groups are presented in Table 1. The 2 (treatment) × 4 (muscle group) repeated-measures ANOVA showed that isokinetic peak torque was significantly higher after the CAF treatment (F1,15 = 8.52, p = 0.011) and that a significant difference in isokinetic peak torque existed between muscle groups (F1.26,18.9 = 206, p < 0.001). In addition, a treatment × muscle group interaction was revealed, which approaches significance (F1.26,18.4 = 3.91, p = 0.056), i.e., as muscle group size increased so too did the improvement in mean isokinetic peak torque from PLA to CAF. This is presented by the relative %differences and effect sizes (Cohen's d) in Table 1. According to Cohen (13), there was a moderate effect of caffeine on the knee extensors (d = 0.53) and a small to moderate effect of that on the ankle plantar flexors (d = 0.43), elbow flexors (d = 0.38) and wrist flexors (d = 0.36). This trend is further demonstrated by Figure 1.

Table 1:
Isokinetic peak torque values (N·m) of the 4 muscle groups for the PLA and CAF treatments at an angular velocity of 60°·s−1, in addition to %differences and effect sizes between the 2 treatments.*
Figure 1:
Mean isokinetic peak torque values (N·m) of the 4 muscle groups for the PLA and CAF treatments at an angular velocity of 60°·s−1. Error bars represent the SD. PLA = placebo; CAF = caffeine.


A major finding of the present study is that acute caffeine supplementation (6 mg·kg−1) appears to enhance MVC strength, as demonstrated by the significant (p = 0.011) increase in mean isokinetic peak torque in upper- and lower-body muscle groups. Research testing caffeine on isokinetic strength is limited, and the data are equivocal, with a number of studies suggesting there is (8,17,25) or is not (11,24) an ergogenic effect. For example, Bond et al. (11) found no effect of 5 mg·kg−1 of caffeine on peak torque of the knee extensors and flexors at 30, 150, and 300°·s−1 in collegiate sprinters. Conversely, Jacobson et al. (25) found that 7 mg·kg−1 of caffeine significantly (p ≤ 0.05) increased peak torque of the knee extensors at 30 and 300°·s−1, and the knee flexors at 30, 150, and 300°·s−1 in elite male athletes.

In comparison, research using other modes of MVC strength, i.e., maximal isoinertial (4,23) and maximal isometric (29,32), provides less support for caffeine's ergogenic potential. A potential explanation is the difference in reliability between the 3 strength modes. The test-retest reliability of isokinetic strength appears to be greater than that of isoinertial and isometric strength (15). This may reduce variability and increase statistical power, which may generate more significant results within isokinetic research.

Within each strength mode, the variation in study data may be a product of differences in training status, dose of caffeine, and individual habituation (17). As with the present investigation, the majority of studies that demonstrate an increase in MVC strength have used a moderate dose of caffeine (17,27,35). For instance, Astorino et al. (5) found that 5 mg·kg−1 of caffeine significantly (p ≤ 0.05) enhanced isokinetic peak torque of the knee flexors, whereas a 2 mg·kg−1 dose did not. Furthermore, those studies that have used trained athletes (25) or resistance-trained subjects (9,17) have found a beneficial effect of caffeine more commonly than those that have used untrained subjects (23,24). It is likely that trained athletes and resistance-trained subjects have greater motivation to perform, and may do so more consistently, which again, may reduce variability and increase statistical power (3). Alternatively, training may cause specific physiological adaptations, which in combination with caffeine may enhance performance (18). A number of studies that demonstrate improvements in MVC strength have employed subjects who were low caffeine users (8,25,27). This may potentiate caffeine's ergogenic effects relative to high caffeine users, who likely have greater tolerance (27). For instance, Bell and McLellan (10) found that performance was significantly (p ≤ 0.05) greater in low users (≤50 mg·d−1) than in heavy users (≥300 mg·d−1) after caffeine ingestion. Furthermore, as with many drugs, there may be individual responders and nonresponders to caffeine (3). Caffeine is metabolized by cytochrome P450 1A2 in the liver. Its production is dependent on genotype and is highly variable between individuals (22). Consequently, minor differences may influence the rate of caffeine metabolism (38) and the performance response to caffeine ingestion (3). However, no individual in the present study may be regarded as a certain nonresponder, as isokinetic peak torque improved with caffeine in at least 1 of the 4 muscle groups in each subject.

Another finding of the present study relates to muscle group size. The increase in isokinetic peak torque from the PLA treatment to the CAF treatment between muscle groups (i.e., the treatment × muscle group interaction) is not statistically significant (p = 0.056). However, it does approach the p ≤ 0.05 level. Moreover, the figures for mean isokinetic peak torque indicate that as muscle group size increased, so too did the %improvement in MVC strength (Table 1)—this trend is supported by the relative effect sizes, and is also presented in Figure 1. Furthermore, it is important to note that the %improvement in mean isokinetic peak torque of the larger muscle groups within each location (i.e., the knee extensors and elbow flexors) increased more with caffeine than that of the smaller muscle groups (i.e., the ankle plantar flexors and wrist flexors). Thus, muscle group size may account for the effect of muscle group location, identified by Warren et al. (42), as lower-body muscle groups are typically larger than their upper-body counterparts. This finding may also reinforce the central effects hypothesis. As formerly mentioned, muscle activation during MVC appears to be less in larger muscle groups, such as the knee extensors (85–95%) and ankle plantar flexors (90–99%), than in smaller muscle groups, such as the elbow flexors or wrist flexors (37). Therefore, the ability of caffeine, as an adenosine antagonist, to enhance maximal voluntary activation through CNS stimulation, and so improve maximal force production, may increase with muscle group size.

An effect of caffeine on maximal voluntary activation was initially presented by Kalmar and Cafarelli (27). Using 6 mg·kg−1, they reported a small (3.5%) but significant (p < 0.01) increase in maximal voluntary activation of the knee extensors. This was accompanied by a significant (p ≤ 0.05) increase in MVC knee extensor strength (∼5%). Similar results have been replicated by Plaskett and Cafarelli (35). Unlike the current investigation, both studies used isometric force to estimate MVC strength. However, research indicates that maximal voluntary activation of dynamic contractions may be less than that of isometric contractions. For instance, Babault et al. (6) recorded maximal voluntary activations of 95.2 and 89.7% for isometric and concentric dynamic contractions of the quadriceps femoris, respectively. This may explain the greater improvement in MVC knee extensor strength demonstrated by the current data (13.7%) relative to that of Kalmar and Cafarelli (27). Less research has been conducted using other muscle groups, but a similar pattern would be expected.

In contrast to the findings of Kalmar and Cafarelli (27) and Plaskett and Cafarelli (35), some studies have reported similar improvements in strength-power performance, but no effect on maximal voluntary activation (32,33,41). Therefore, peripheral mechanisms of caffeine action cannot be discounted. Hence, although most research, including the present study, appears to favor the central effects hypothesis, ultimately, the model for caffeine's potential ergogenic effect on strength-power performance may be multifactorial, and may extend beyond any single biological mechanism (38).

The present study contains certain limitations. For instance, the experimenter was not blinded to the treatment order, which increases the likelihood of bias during the investigation. Furthermore, as shown by the results, muscle group size may be a key determinant of caffeine's effect on MVC strength, but the cross-sectional area (CSA) of the muscle groups used were not recorded, i.e., the relative sizes of each muscle group were merely assumed. Finally, unlike previous researches (27,32,35,41), the present study did not assess maximal voluntary activation using the twitch interpolation technique. Consequently, while the increase in %improvement of MVC strength with muscle group size may suggest that caffeine enhances maximal voluntary activation, through CNS stimulation, a direct link cannot be made.

Practical Applications

The current results indicate that a moderate dose of caffeine (6 mg·kg−1), consumed approximately 30 minutes before performance, improves MVC strength in upper- and lower-body muscle groups, in resistance-trained men. This research may be useful for competitive and recreational athletes aiming to increase strength-power performance.

Further investigation is required to verify the effect of muscle group size. Therefore, future research should replicate the present study using specific muscle group CSAs. Supramaximal electrical stimulation and measurement of biochemical markers, such as dopamine and epinephrine, should also be used to provide further insight into the mechanistic action of caffeine.


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ergogenic; isokinetic; muscle group size; muscle group location; mechanism

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