There is a growing body of research that has observed the effects of caffeine on short-term, high-intensity exercise (ST; i.e., an exercise intensity requiring > 100% V̇O2max) lasting from a few seconds up to ∼ 6 min. The mode of ST has included Wingate tests (both single (3,6) and repeated (15)), constant load tests to exhaustion (3,10), and performance tests (4,7). Although some researchers claim that caffeine exerts no effect on ST (27), a large number of studies have shown significant improvements in power output (1,3), “anaerobic” capacity (3,10), and other anaerobic-based performance measures (4,7,30). In a recent review, Graham (13) concluded that with ST lasting at least 60 s, caffeine can be ergogenic. However, as yet, there is no clear explanation of how caffeine exerts its effect during ST. Earlier reports noted an elevated rise in plasma epinephrine with a concomitant increase in blood lactate (1,6,7). It was hypothesized that the raised epinephrine levels enhanced muscle glycogenolysis, which in turn drove anaerobic metabolism and muscle power output (1,6,7). More recent studies have dismissed this metabolic hypothesis and speculated that caffeine exerts its effect during ST by direct action on muscle and/or the nervous system (3,4,10). One suggestion is that caffeine may attenuate fatigue caused by loss of potassium (K+) from skeletal muscle and its accumulation in the extracellular space (13,18,19). This could be achieved by an accelerated Na2+/K+ ATPase activity of inactive skeletal muscle leading to increased rates of K+ uptake (13,18,24). This may indirectly result in enhanced motor unit activation and/or enhanced force generated per motor unit (13,18,24).
One aspect of caffeine’s ergogenic effects is a lower rating of perceived exertion (RPE) at the same submaximal exercise intensity in comparison with placebo (8,19,25). In addition, other studies have shown that a greater amount of work can be accomplished when RPE is held constant (5,30). Finally, a hypoalgesic effect of caffeine has also been observed using a visual analog scale during ischemic muscle contractions (21). Because fatigue has been defined as an acute impairment of exercise performance that includes both an increase in the perceived effort necessary to produce a power output and the eventual inability to maintain that power output (9), measuring perceptual response during exercise performance can be beneficial (12). In comparison with endurance-based studies, there have been no systematic attempts to investigate the perceptual response of caffeine during ST. This possibly reflects the belief that subjective estimates of exertion during ST are not viable (12). However, Doherty et al. (12) have recently shown that RPE (Borg scale, 6–20) displays a reliable linear response during the first 2 min of constant-load, ST treadmill running. The authors concluded that the inclusion of RPE might add a new dimension to ST investigations and could contribute to an improved understanding of the perceptual response to extremely high-intensity exercise.
Another popular ergogenic aid that has been much used by power-based athletes is creatine monohydrate (2,17,26,27). Not surprisingly, applied sport scientists have begun to investigate the possible synergistic effects of caffeine and creatine on anaerobic exercise (26,27). A frequently referred to study in this regard is by Vandenberghe et al. (27), who investigated the effects of combining creatine monohydrate supplementation with caffeine ingestion and hypothesized that caffeine, a potent sympathomimetic agent, might facilitate the uptake of exogenous creatine by muscle tissue. Before and after 6 d of placebo, creatine monohydrate or a combination treatment of caffeine and creatine monohydrate loading, a maximal intermittent exercise fatigue test of the knee extensors was performed. The results showed that creatine loading improved dynamic torque production but that the ergogenic effect was completely eliminated when caffeine was taken with the creatine monohydrate. This suggests that caffeine, when ingested with creatine monohydrate during 6 d of creatine loading, interfered with the ergogenic effects of creatine. An alternative strategy to optimize the independent effects of creatine and caffeine and to minimize the interference of combining these nutritional interventions would be to supplement with creatine while abstaining from caffeine for the duration of the loading period. Ingestion of a single dose of caffeine would then be taken before exercise (i.e., as is the case in most caffeine studies). Thus, the purpose of the present study was for subjects to complete 6 d of creatine loading and caffeine abstinence and to follow this with: 1) a single dose of caffeine taken 1 h before ST (i.e., treadmill running at 125% V̇O2 max to exhaustion) and 2) a placebo ST trial. It was hypothesized that the caffeine trial would increase both maximal accumulated oxygen deficit and run time to exhaustion, and lower the RPE during the first 2 min of the run.
From recent reliability studies conducted in our laboratory (11,12), we estimated that the smallest worthwhile effects (16) for the maximal accumulated oxygen deficit (MAOD), run time to exhaustion (Tlim), and rating of perceived exertion scores (Borg scale, 6–20) at a running speed equivalent to 125% V̇O2max were 0.5 L O2 Eq, 13 s, and 1.0 RPE point, respectively. These effects, together with their respective standard error of measurements were used to estimate sample size (Eq. 1 (16)):
where SEM = standard error of measurement and d = the smallest worthwhile effect.
All sample size estimates were less than 10; however, 14 male volunteers, who had all been involved in two recent MAOD reliability studies (11,12), were recruited on the basis of their familiarity and habituation to the procedures; for this reason, no female subjects were recruited. The mean (± SD) age, height, body mass, and V̇O2max of the subjects were 22.7 ± 3.5 yr, 1.76 ± 0.06 m, 70.6 ± 8.8 kg, and, 58.1 ± 2.0 mL·kg−1·min−1, respectively. The procedures used were approved by a departmental committee for ethics in research, and all participants provided written informed consent. The subjects were recruited on the basis of their fitness, i.e., a moderately high V̇O2max, rather than for uniformity in their caffeine habits. Caffeine consumption was estimated from a checklist of common foods and beverages to be 920 ± 370 mg·wk−1 (mean ± SD). Although the subjects continued to train over the duration of the study, they were instructed to refrain from physical activity for 24 h before the tests and to present themselves at the laboratory in a 2-h postabsorptive state. Subjects were asked to avoid caffeine-containing foods and beverages, 24 h before the first pretreatment MAOD. In addition, because a previous study (27) suggested there was an ergolytic interaction between creatine loading and caffeine supplementation, the subjects were also asked to avoid caffeine-containing foods and beverages during the entire investigation.
All subjects were tested on four separate occasions:
1) Preliminary test session: measurement of V̇O2max and estimation of the treadmill speed equivalent to 125% V̇O2max.
2) A pretreatment (i.e., creatine supplementation) MAOD (baseline).
3) A posttreatment MAOD (12–24 h after the end of creatine supplementation).
4) A second posttreatment MAOD, 3–5 d after the first posttreatment MAOD.
Both posttreatment MAODs were preceded by either caffeine or placebo ingestion, 1 h before the start of the test, in a cross-over, double-blind, randomized manner. After their final trial, subjects completed a questionnaire that asked whether they had abstained from caffeine for the duration of their participation in the study and whether they had experienced any withdrawal symptoms. They were also asked whether they could identify the caffeine trial. An assumption made in this study was that muscle creatine levels were fully saturated after the supplementation period and that they remained so up to 5 d after supplementation.
All subjects undertook a creatine monohydrate loading program. This involved self-administration of creatine over a 6-d period. Subjects ingested a total of 0.3 g·kg−1 of creatine monohydrate (Isostar Creatine Direct, Westcott and Westcott Ltd., Clevedon, UK) for each of 6 consecutive days. The daily dose was divided into four sachets, each containing ∼5 g of creatine monohydrate. The subjects were instructed to consume their treatment at four regular intervals throughout the day by dissolving the contents of a single sachet in a supplied sweetened drink.
Caffeine and placebo ingestion.
One hour before the posttreatment MAODs, subjects consumed one of two beverages, either 1) 5 mg·kg−1 of caffeine (Roche, Welwyn Garden City, UK) in 200 mL of an artificially sweetened water drink (caffeine), or 2) 200 mL of artificially sweetened water drink (placebo). Subjects drank the assigned beverage immediately and then relaxed in preparation for the MAOD test.
The calculated oxygen demand of supramaximal intensity exercise was determined using an extrapolation method adapted from procedure 3 of the methods described by Medbø et al. (20). To relate V̇O2 to running velocity, each subject performed three, 6-min discontinuous treadmill (Powerjog, Cranlea & Co., Birmingham, UK) runs of increasing exercise intensity approximating 80%, 85%, and 90% V̇O2max with 5-min recovery between runs. All tests were conducted on a 10.5% incline. On the basis of the preliminary treadmill test and the relation between V̇O2 and running velocity, an individual linear regression equation was derived for each subject. This was used to calculate the running velocity required to elicit an exercise intensity equivalent to 125% V̇O2max for the subsequent MAOD test.
Subjects were informed that RPE was to be measured throughout the test but remained uninformed that the RPE measurements were to be taken every 30 s for the first 2 min of the test. RPE was only taken for the first 2 min of the test because a previous study (12) revealed that the excessive and disorientating fatigue associated with high-intensity exercise ruled-out collection of RPE during the latter part (i.e., approximately the last minute) of the test. Before testing, subjects were reminded of the instructions on the use of the RPE scale (22; pp. 77–81).
Subjects had to:
1) Understand the definition of RPE and receive an explanation of the nature and use of the scale.
2) “Anchor” the top and bottom perceptual ratings to previously experienced sensations of the easiest and most difficult exercise encountered.
3) Ensure they gave an “all-over,” integrated rating, which included both muscular and cardiorespiratory sensations.
4) Understand the subjective nature of the RPE scale; that there are no “right” or “wrong” responses.
The treadmill belt was adjusted to the predetermined velocity, and, when the subjects were ready, they lowered themselves onto the moving treadmill belt. A digital stop clock was started to indicate the start of exercise and the commencement of the collection of expired air. To ensure accurate recording of RPE, a printed scale was presented immediately in front of the subject on a large (0.91 × 0.61 m) board. Subjects then pointed to the number or verbal descriptor that adequately represented their RPE. In practice, this took no longer than 1–2 s and thus did not interfere with the exercise test. The treadmill velocity, i.e., range, 3.0–4.0 m·s−1 at 10.5% incline, was sufficiently slow to allow subjects to indicate RPE during the exercise without risk of injury. Subjects breathed through a Hans Rudolph no. 2700 valve (Hans Rudolph, Kansas City, MO) and were connected to either a series of 200-L Douglas bags (i.e., preliminary assessment) or one 1000-L Douglas bag (MAOD test) by means of short, lightweight wide-bore tubing. The MAOD test was terminated, together with the collection of expired air, when the subject could no longer maintain the required running velocity. The time to exhaustion (Tlim) for the MAOD test was recorded to the nearest 0.1 s. One liter of air from each Douglas bag was drawn off for the determination of the fractions of oxygen and carbon dioxide by using a paramagnetic oxygen analyzer (Servomex 570A, Crowborough, UK) and an infrared carbon dioxide analyzer (Servomex PA404), both of which had previously been calibrated against gases of known concentration (15.1% O2 and 5% CO2; British Oxygen Co., Wembley, UK). The remaining volume of each sample was then measured with a Harvard dry-gas meter (Harvard Apparatus Ltd., Kent, UK). Total V̇O2 (L) was estimated by multiplying the mean V̇O2 (L·min−1) obtained during the MAOD test with Tlim. The contribution of energy supply (anaerobic: aerobic) to the total energy demand was determined by calculating the proportion of MAOD and total V̇O2.
Eight milliliters was taken from an antecubital forearm vein via a Monovette® blood collection system (Sarstedt, Numbrecht, Germany), immediately before and as soon as possible after each of the three MAOD tests. As soon as the subjects stopped exercising, they were led to a chair at the side of the treadmill and remained seated for the duration of the blood sampling. The venepuncture and blood withdrawal then took between 30 and 60 s to perform (NB: an indwelling catheter was not used because of the risk of not maintaining catheter patency during the treadmill run). The blood sample was immediately transferred to ice-cold lithium-heparin tubes and centrifuged with the plasma being stored at −70°C. The plasma was later assayed for glucose and lactate (Analox GLM Instruments, Hammersmith, UK), potassium (Beckman Synchron CX® system, Beckman Instruments, Inc., La Brea, CA), and epinephrine and norepinephrine (HPLC with electrochemical detection). Pre-MAOD plasma caffeine was assayed by an enhanced turbidimetric inhibition immunoassay with a minimum detection of 5 μmol·L−1 (Dade Behring Dimension Analyzer, Marburg, Germany, using Syva® Emit Caffeine Assay, Milton Keynes, UK). Final plasma data were not corrected for changes in plasma volume.
Data were tested with one-way repeated ANOVAs (plasma caffeine, body mass, MAOD, Tlim, and total V̇O2), and two-way repeated ANOVAs for all other dependent variables (Bonferroni, post hoc). The sphericity assumption was checked by Mauchly’s test of sphericity. A paired t-test was used to determine whether there was an effect between the order in which the placebo and caffeine trials were performed. Pearson product moment correlation coefficients were used to determine the relationships between measured variables. Ninety-five percent confidence intervals were computed for all relevant statistics. An alpha level of ≤ 0.05 was chosen to indicate significance. All statistical procedures were performed using SPSS for Windows, Version 9.0 (SPSS, Inc., Chicago, IL).
Plasma caffeine concentrations were not detectable before the baseline or placebo trials. However, a mean caffeine concentration of 35 (± 8.8) μmol·L−1 was recorded before the caffeine trial. It should be noted that this moderate caffeine concentration is unlikely to have resulted in the IOC banned level of 12 μmol·L−1 of urinary caffeine being attained (13). After the investigation, it was revealed that 7 of the 14 subjects correctly identified the caffeine trial. All subjects maintained that they had abstained from caffeine consumption for the duration of their participation in the study, and two subjects claimed they had suffered from “headaches” as a result of the caffeine abstention. There was no relationship between reported caffeine consumption and any of the other variables, including Tlim (r = 0.04, P = 0.90).
Body mass was increased in 11 of the 14 subjects after creatine loading. In addition, the increase in body mass was maintained for both posttreatment trials, i.e., up to 5 d after supplementation (Table 1). There was no relationship between changes in body mass and changes in any of the other dependent variables, including MAOD (r = −0.22, P = 0.45) and Tlim (r = −0.28, P = 0.32).
MAOD, Tlim, total V̇O2, and contribution of energy supply to total energy demands.
There was no statistical difference between the order in which the placebo and caffeine trials were performed for either MAOD (5.56 ± 1.74 L O2 Eq vs 5.23 ± 1.55 L O2 Eq, mean ± SD) or Tlim (213.0 ± 50.2 s vs 207.4 ± 47.2 s, mean ± SD) for first trial versus second trial, respectively. Caffeine MAOD increased by 0.50 (0.0–1.1) L O2 Eq and 0.49 (−0.1–1.1) L O2 Eq (mean difference and lower and upper bound 95% confidence interval difference) in comparison with the baseline and placebo conditions, respectively (Table 1). However, these differences did not reach statistical significance. By contrast, Tlim was increased by 21.3 s (1.1–41.4 s) and 23.8 s (9.5–38.1 s) (mean difference and lower and upper bound 95% confidence interval difference) in the caffeine condition compared with baseline and placebo conditions, respectively (Table 1). In addition, there was marked individual variation in the Tlim response to caffeine. Although 9 of the 14 subjects improved Tlim from 13 to 58 s, five subjects failed to show any substantial change from the baseline and placebo conditions (range −8 s to 3 s, Fig. 1). Total V̇O2 was significantly increased in the caffeine trial in comparison with the placebo trial (Table 1). However, there were no statistically significant differences in the contribution of energy supply to the total energy demands (Table 1).
Rating of perceived exertion.
The RPE data at all four time points measured (i.e., 30 s, 60 s, 90 s, and 120 s) and in all trials revealed a linear response to exercise duration. There was a clear trend for RPE to be lower during the caffeine trials at all time points; however, RPE only attained statistical significance at 90 s (Fig. 2).
There was a significant main effects “time” increase in all variables from pre- to post-exercise in all trials (Table 2). Plasma epinephrine and plasma glucose concentrations were higher in the postexercise caffeine treatment in comparison with the baseline and placebo trials (Table 2). In contrast, plasma potassium did not increase after caffeine ingestion compared with the baseline and placebo trials (Table 2). There was no difference in blood lactate in any of the trials (Table 2).
The main finding from this study was that acute caffeine ingestion (5 mg·kg−1) before a treadmill run to voluntary exhaustion at 125% V̇O2max increased Tlim by over 10% (0.5–20.7%; 95% confidence interval) in comparison with baseline and placebo trials (Table 1). Because the caffeine trial was performed within 5-d of a program of creatine supplementation, the results suggest that the ergogenic effects of caffeine during ST (1,3,4,7,10,30) were not altered by either creatine loading or by the accompanying increase in body mass typically found with creatine loading (2,17). The ∼ 20 s improvement in Tlim was of a similar magnitude to a previous study that observed an enhanced ST performance after caffeine ingestion (10). In addition, having recently evaluated the reliability (from 3 trials) of Tlim at 125% V̇O2max in a group of similarly trained subjects (11), we are confident the improvement seen after the caffeine trial is worthwhile; the upper-bound 95% confidence interval for the standard error of measurement in the reliability assessment was 13.0 s. Although it is usual to have subjects whose performance is not enhanced after caffeine ingestion (i.e., so-called, “nonresponders” (13)), it may well be that for some of the nonresponders in the present study (N = 5;Fig. 1), there was some interference caused by the creatine supplementation. On the other hand, it is unlikely that the increase in body mass accompanying creatine supplementation (Table 1) contributed to the nonresponders performance as there was no association between improvement in Tlim and the change in body mass (r = −0.28, P = 0.32). It is possible that the effects of acute caffeine ingestion in the present study were influenced by the period of caffeine abstinence that accompanied the creatine supplementation. This would be of most relevance to those subjects who have a high caffeine consumption (>300 mg·d−1). However, there was no relationship between reported caffeine consumption and Tlim (r = 0.04, P = 0.90). Wiles et al. (30) found no relationship between caffeine habits and the degree of performance response in 1500-m runners (completing the exercise in approximately the same time as our subjects). Our data also support recent work where 0-, 2-, and 4-d withdrawal from caffeine showed no difference in Tlim at 80% V̇O2max (29). It is of interest to note Tlim was not improved after creatine supplementation, i.e., in the placebo trial (Table 1). Although most studies have generally concluded that creatine supplementation is ergogenic during repeated ST (2,27), there is limited support for (17) and against (2) creatine enhancing a single bout of high-intensity exercise lasting ∼3–5-min. Because there is also likely to be variability in subject muscle creatine uptake after creatine supplementation (14) (i.e., in addition to the variable response to caffeine), future studies should investigate creatine uptake by direct muscle measurements to better quantify any interaction between caffeine, creatine, and exercise performance. The wide individual variation of Tlim responses (Fig. 1) reinforces statements alerting sportsmen and women to perform individual assessments of specific ergogenic aids before use and not to rely solely on generalisations from the scientific literature.
Unlike previous studies, MAOD was not improved after either acute caffeine ingestion (10) or creatine loading (17). The reason for the nonsignificant MAOD in comparison with Tlim is possibly related to the MAOD being a less reliable measure. The reduced reliability may be because of the many single measurements associated with respiratory gas analysis used during MAOD in comparison with the one simple time measurement of Tlim (11). Doherty et al. (11) found that, although traditional measures of reliability (including coefficient of variation and intraclass correlation coefficient) were favorable, the 95% limits of agreement (95 LoA) revealed the MAOD to have relatively poor reliability. Based on the 95 LoA, it was estimated that a sample size of 20 was required to detect a 10% change in MAOD (11). The sample size estimation of the present study may therefore have underestimated the number of subjects required to determine a change in MAOD. Hopkins (16) concluded that, from a measurement sensitivity perspective, the use of constant distance, constant work, and constant duration tests are more reliable than, and recommended over, constant exercise intensity tests to exhaustion (i.e., as used in this study). Where repeated trials use the same supramaximal exercise intensity, one would expect that the contribution of energy sources to the total energy demand would follow the same trend in all trials (20). Thus, it is somewhat surprising to find that total V̇O2 was significantly increased in the caffeine trial in comparison with the placebo trial. This is despite the fact that there were no changes in the contribution of energy supply to the total energy demands (Table 1; possibly because MAOD also increased along with total V̇O2 but just failed to reach statistical significance). It may be that subjects either achieved a higher V̇O2max or attained V̇O2max at a faster rate in the caffeine trial. Unfortunately, we are only able to speculate on this because the protocol used in this study did not facilitate measurement of V̇O2 kinetics or serial collections of V̇O2. The elevated total V̇O2 may have been caused by stimulation of the sympathetic nervous system (13), including an increased secretion of epinephrine, after the caffeine trial (Table 2). Interestingly, Wiles et al. (30) also found that ingestion of 3 g of caffeinated coffee in 1500-m runners (N = 6) elevated V̇O2 in a 1500-m run at a velocity that was 0.5 km·h−1 slower than the athlete’s fastest 1500-m pace.
It is self-evident that a run to exhaustion at 125% V̇O2max requires a very high degree of motivation. Given that V̇O2max is likely to have been achieved within the first 2 min of the MAOD test (20), the issue becomes one of how the subjects in the caffeine trial were able to maintain such a high exercise intensity for a further 20 s. It may well be that the improvement in exercise performance after caffeine was not due to alterations in energetics per se but to the well-known stimulatory effects of caffeine on the central nervous system (CNS;5,13,21,23,25,28–30). Rating of perceived exertion, with its strong relation to factors indicating fatigue, is an important index in the evaluation of CNS drive and the extent of fatigue (22; pp. 93–104). The RPE data (Fig. 2), although not fully conclusive, are suggestive of a dampened perceptual response during ST after caffeine ingestion. In comparison with the many endurance-based caffeine studies that have observed a reduction in RPE at the same standardized exercise intensity after caffeine ingestion (5,8,19,25), this study provides additional evidence that caffeine’s ergogenic effect during ST may also manifest itself via a dampened perceptual response (30), i.e., during the first 2 min of ST. Furthermore, it may be that the difference in perceptual response with caffeine to maximal exercise lasting between 3 and 5 min becomes even greater during the last third of the exercise, that is, the part of the exercise test where RPE was not monitored. The reason why only the 90-s time point showed a significant reduction may be the rather crude category RPE measure that was used. Future studies investigating the connection between caffeine ingestion and perceived exertion may wish to use alternative, more sensitive visual analog scales.
There are a number of theories relating caffeine to a reduction in RPE in endurance-based studies. In a review of this area, Spriet and Howlett (25) speculated that the lowered RPE with caffeine could be due to a decrease in the neuronal activation threshold of motoneurons and/or alterations in muscle contraction force. These mechanisms would result in lowered sensory feedback from the exercising muscle, and thus a reduced RPE, the first mechanism because more motor units would be recruited for a given task and the second because force for a given stimulus would be greater (25). Of the measurements reported in this study, the reduction in postexercise plasma [K+] after the caffeine treatment may be a possible link to improved muscle contractility. It has been suggested that K+ efflux from skeletal muscle cells plays a role in the development of muscle fatigue (24). Loss of K+ decreases the intracellular [K+], which in turn reduces the muscle action potential and excitability (13,18,24). These changes are likely to interfere with excitation-contraction coupling (13,18,24) and would result in less motor unit activation and/or less force production per motor unit (13,18,24). Other in vivo studies have also shown less of an increase in plasma [K+] after caffeine ingestion (18,19). It is speculated that caffeine, and/or the associated increase in epinephrine (as reported in the present study), affects the washout of K+ from the active muscle and/or the clearance of K+ by stimulating resting muscle Na2+/K+ ATPase to take up more K+ (13).
Caffeine exerts a hypoalgesic effect during ischemic muscle contractions and acts as an analgesic adjuvant in combination with other compounds (21). There is evidence that caffeine directly affects the release of β-endorphins and other hormones and neurotransmitters that influence feelings of pain associated with some forms of exercise (25). However, some authors believe that CNS changes are not important and cite the caffeine-induced increases in muscle endurance reported in tetraplegic patients (28). In a recent study that used a constant-sensation technique to determine whether caffeine (6 mg·kg−1) influenced force sensation during 100 s of an isometric contraction of the quadriceps at 50% maximum voluntary contraction, Plaskett and Cafarelli (23) found that caffeine reduced force sensation during the first 10–20 s of the contraction. In a separate experiment, Plaskett and Cafarelli (23) also observed a caffeine-induced increase in Tlim. They concluded that caffeine increases Tlim because subjects may have been more willing to maintain near-maximal activation longer due to alterations in muscle sensory processing (23). This may have been caused by feedback from mechanoreceptors sensitive to tension or pressure, alterations in feedforward information, and/or alterations in the central processing of either feedforward or feedback information (23).
The increases in plasma epinephrine and plasma glucose in the caffeine trial have been observed repeatedly in previous research (1,6,7,19,29). However, the significance of these changes is not clear. A recent review of this area suggests that such changes are coincidental with caffeine ingestion and do not in themselves elucidate how caffeine provides an ergogenic effect (13). Unlike previous studies that have suggested a caffeine-induced epinephrine–lactate relationship (1,6,7), more recent work does not support this association (13,15). Our data also question the proposed positive relationship between plasma epinephrine and plasma lactate.
Taken together with the results of other studies, this study demonstrates that acute ingestion of caffeine has ergogenic effects on ST regardless of whether or not creatine supplementation precedes the caffeine ingestion. Our results suggest that the ergogenic effects of caffeine are possibly related to alterations in the perceptual response and/or the energetics of ST.
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