Caffeine is ergogenic after supplementation
of oral creatine monohydrate

MIKE DOHERTY, PAUL M. SMITH, R. C. RICHARD DAVISON, and MICHAEL G. HUGHES Department of Sport, Exercise and Biomedical Sciences, University of Luton, Luton, UNITED KINGDOM ABSTRACT
DOHERTY, M., P. M. SMITH, R. C. R. DAVISON, and M. G. HUGHES. Caffeine is ergogenic after supplementation of oral creatine monohydrate. Med. Sci. Sports Exerc., Vol. 34, No. 11, pp. 1785–1792, 2002. Purpose: The purpose of this investigation was to assess
the acute effects of caffeine ingestion on short-term, high-intensity exercise (ST) after a period of oral creatine supplementation and caffeine abstinence. Methods: Fourteen trained male subjects performed treadmill running to volitional exhaustion (T
. Three trials were performed, one before 6 d of creatine loading (0.3 g·kgϪ1·dϪ1; baseline), and two further trials after the loading period. One hour before the postloading trials, caffeine (5 mg·kgϪ1) or placebo was orally ingested in a cross-over, double-blind fashion. Four measurements of rating of perceived exertion were taken, one every 30 s, during the first 120 s of the exercise. Blood samples were assayed for lactate, glucose, potassium, and catecholamines, immediately before and after exercise. Results: Body mass increased (P Ͻ 0.05) over the creatine supplementation period, and this increase was maintained for both
caffeine and placebo trials. There was no increase in the maximal accumulated oxygen deficit between trials; however, total V
significantly increased in the caffeine trial in comparison with the placebo trial (13.35 Ϯ 3.89 L vs 11.67 Ϯ 3.61 L). In addition, caffeineT (222.1 Ϯ 48.9 s) was significantly greater (P Ͻ 0.05) than both baseline (200.8 Ϯ 33.4 s) and placebo (198.3 Ϯ 45.4 s) T . RPE was also lower at 90 s in the caffeine treatment (13.8 Ϯ 1.8 RPE points) in comparison with baseline (14.6 Ϯ 1.9 RPE points).
Conclusion: As indicated by a greater T
, acute caffeine ingestion was found to be ergogenic after 6-d of creatine supplementation and caffeine abstinence. Key Words: ANAEROBIC CAPACITY, ERGOGENIC AIDS, PERCEPTUAL RESPONSE, FATIGUE.
Thereisagrowingbodyofresearchthathasobserved rinelevelsenhancedmuscleglycogenolysis,whichinturn the effects of caffeine on short-term, high-intensity drove anaerobic metabolism and muscle power output exercise (ST; i.e., an exercise intensity requiring Ͼ (1,6,7). More recent studies have dismissed this metabolic ) lasting from a few seconds up to ~ 6 min.
hypothesis and speculated that caffeine exerts its effect The mode of ST has included Wingate tests (both single during ST by direct action on muscle and/or the nervous (3,6) and repeated (15)), constant load tests to exhaustion system (3,4,10). One suggestion is that caffeine may atten- (3,10), and performance tests (4,7). Although some re- uate fatigue caused by loss of potassium (Kϩ) from skeletal searchers claim that caffeine exerts no effect on ST (27), a muscle and its accumulation in the extracellular space large number of studies have shown significant improve- (13,18,19). This could be achieved by an accelerated ments in power output (1,3), “anaerobic” capacity (3,10), Na2ϩ/Kϩ ATPase activity of inactive skeletal muscle lead- and other anaerobic-based performance measures (4,7,30).
ing to increased rates of Kϩ uptake (13,18,24). This may In a recent review, Graham (13) concluded that with ST indirectly result in enhanced motor unit activation and/or lasting at least 60 s, caffeine can be ergogenic. However, as enhanced force generated per motor unit (13,18,24).
yet, there is no clear explanation of how caffeine exerts its One aspect of caffeine’s ergogenic effects is a lower effect during ST. Earlier reports noted an elevated rise in rating of perceived exertion (RPE) at the same submaximal plasma epinephrine with a concomitant increase in blood exercise intensity in comparison with placebo (8,19,25). In lactate (1,6,7). It was hypothesized that the raised epineph- addition, other studies have shown that a greater amount ofwork 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 MEDICINE & SCIENCE IN SPORTS & EXERCISE® muscle contractions (21). Because fatigue has been defined Copyright 2002 by the American College of Sports Medicine as an acute impairment of exercise performance that in- Submitted for publication December 2001.
cludes both an increase in the perceived effort necessary to produce a power output and the eventual inability to main- Address for correspondence: Mike Doherty, University of Luton, Depart-ment of Sport, Exercise and Biomedical Sciences, Park Square, Luton, tain that power output (9), measuring perceptual response Beds LU1 3JU, United Kingdom; E-mail: [email protected].
during exercise performance can be beneficial (12). In com- parison with endurance-based studies, there have been no systematic attempts to investigate the perceptual response of their respective standard error of measurements were used to 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 thatRPE (Borg scale, 6 –20) displays a reliable linear response where SEM ϭ standard error of measurement and d ϭ the during the first 2 min of constant-load, ST treadmill running.
The authors concluded that the inclusion of RPE might add All sample size estimates were less than 10; however, 14 a new dimension to ST investigations and could contribute male volunteers, who had all been involved in two recent to an improved understanding of the perceptual response to 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 Another popular ergogenic aid that has been much used were 22.7 Ϯ 3.5 yr, 1.76 Ϯ 0.06 m, 70.6 Ϯ 8.8 kg, and, 58.1 (2,17,26,27). Not surprisingly, applied sport scientists have Ϯ 2.0 mL·kgϪ1·minϪ1, respectively. The procedures used begun to investigate the possible synergistic effects of caf- were approved by a departmental committee for ethics in feine and creatine on anaerobic exercise (26,27). A fre- research, and all participants provided written informed quently referred to study in this regard is by Vandenberghe consent. The subjects were recruited on the basis of their et al. (27), who investigated the effects of combining crea- tine monohydrate supplementation with caffeine ingestion uniformity in their caffeine habits. Caffeine consumption and hypothesized that caffeine, a potent sympathomimetic was estimated from a checklist of common foods and bev- agent, might facilitate the uptake of exogenous creatine by erages to be 920 Ϯ 370 mg·wkϪ1 (mean Ϯ SD). Although muscle tissue. Before and after 6 d of placebo, creatine the subjects continued to train over the duration of the study, monohydrate or a combination treatment of caffeine and they were instructed to refrain from physical activity for creatine monohydrate loading, a maximal intermittent exer- 24 h before the tests and to present themselves at the cise fatigue test of the knee extensors was performed. The laboratory in a 2-h postabsorptive state. Subjects were asked results showed that creatine loading improved dynamic to avoid caffeine-containing foods and beverages, 24 h torque production but that the ergogenic effect was com- before the first pretreatment MAOD. In addition, because a pletely eliminated when caffeine was taken with the creatine previous study (27) suggested there was an ergolytic inter- monohydrate. This suggests that caffeine, when ingested action between creatine loading and caffeine supplementa- with creatine monohydrate during 6 d of creatine loading, tion, the subjects were also asked to avoid caffeine-contain- interfered with the ergogenic effects of creatine. An alter- ing foods and beverages during the entire investigation.
native strategy to optimize the independent effects of crea- General design. All subjects were tested on four sep-
tine and caffeine and to minimize the interference of com- 1) Preliminary test session: measurement of V supplement with creatine while abstaining from caffeine for estimation of the treadmill speed equivalent to 125% the duration of the loading period. Ingestion of a single dose of caffeine would then be taken before exercise (i.e., as is 2) A pretreatment (i.e., creatine supplementation) MAOD the case in most caffeine studies). Thus, the purpose of the 3) A posttreatment MAOD (12–24 h after the end of present study was for subjects to complete 6 d of creatine loading and caffeine abstinence and to follow this with: 1) 4) A second posttreatment MAOD, 3–5 d after the first a single dose of caffeine taken 1 h before ST (i.e., treadmill Both posttreatment MAODs were preceded by either caf- trial. It was hypothesized that the caffeine trial would in- feine or placebo ingestion, 1 h before the start of the test, in crease both maximal accumulated oxygen deficit and run a cross-over, double-blind, randomized manner. After their time to exhaustion, and lower the RPE during the first 2 min final trial, subjects completed a questionnaire that asked whether they had abstained from caffeine for the duration oftheir participation in the study and whether they had expe-rienced any withdrawal symptoms. They were also asked whether they could identify the caffeine trial. An assump-tion made in this study was that muscle creatine levels were Subjects. From recent reliability studies conducted in
fully saturated after the supplementation period and that our laboratory (11,12), we estimated that the smallest worth- they remained so up to 5 d after supplementation.
while effects (16) for the maximal accumulated oxygen Creatine supplementation. All subjects undertook a
deficit (MAOD), run time to exhaustion (T creatine monohydrate loading program. This involved self- perceived exertion scores (Borg scale, 6 –20) at a running administration of creatine over a 6-d period. Subjects in- gested a total of 0.3 g·kgϪ1 of creatine monohydrate (Isostar and 1.0 RPE point, respectively. These effects, together with Creatine Direct, Westcott and Westcott Ltd., Clevedon, UK) Official Journal of the American College of Sports Medicine for each of 6 consecutive days. The daily dose was divided descriptor that adequately represented their RPE. In prac- into four sachets, each containing ~5 g of creatine mono- tice, this took no longer than 1–2 s and thus did not interfere hydrate. The subjects were instructed to consume their treat- with the exercise test. The treadmill velocity, i.e., range, ment at four regular intervals throughout the day by dis- 3.0 – 4.0 m⅐sϪ1 at 10.5% incline, was sufficiently slow to solving the contents of a single sachet in a supplied allow subjects to indicate RPE during the exercise without risk of injury. Subjects breathed through a Hans Rudolph no.
Caffeine and placebo ingestion. One hour before
2700 valve (Hans Rudolph, Kansas City, MO) and were the posttreatment MAODs, subjects consumed one of two connected to either a series of 200-L Douglas bags (i.e., beverages, either 1) 5 mg·kgϪ1 of caffeine (Roche, Welwyn preliminary assessment) or one 1000-L Douglas bag Garden City, UK) in 200 mL of an artificially sweetened (MAOD test) by means of short, lightweight wide-bore water drink (caffeine), or 2) 200 mL of artificially sweet- tubing. The MAOD test was terminated, together with the ened water drink (placebo). Subjects drank the assigned collection of expired air, when the subject could no longer beverage immediately and then relaxed in preparation for maintain the required running velocity. The time to exhaus- ) for the MAOD test was recorded to the nearest MAOD test. The calculated oxygen demand of supra-
0.1 s. One liter of air from each Douglas bag was drawn off maximal intensity exercise was determined using an extrap- for the determination of the fractions of oxygen and carbon olation method adapted from procedure 3 of the methods dioxide by using a paramagnetic oxygen analyzer (Ser- described by Medbø et al. (20). To relate V vomex 570A, Crowborough, UK) and an infrared carbon velocity, each subject performed three, 6-min discontinuous dioxide analyzer (Servomex PA404), both of which had treadmill (Powerjog, Cranlea & Co., Birmingham, UK) runs previously been calibrated against gases of known concen- of increasing exercise intensity approximating 80%, 85%, tration (15.1% O and 5% CO ; British Oxygen Co., Wem- bley, UK). The remaining volume of each sample was then tests were conducted on a 10.5% incline. On the basis of the measured with a Harvard dry-gas meter (Harvard Apparatus preliminary treadmill test and the relation between V running velocity, an individual linear regression equation ˙ O (L·minϪ1) obtained during the MAOD was derived for each subject. This was used to calculate the . The contribution of energy supply (anaerobic: running velocity required to elicit an exercise intensity aerobic) to the total energy demand was determined by calculating the proportion of MAOD and total V Subjects were informed that RPE was to be measured Blood analysis. Eight milliliters was taken from an
throughout the test but remained uninformed that the RPE antecubital forearm vein via a Monovette® blood collection measurements were to be taken every 30 s for the first 2 min system (Sarstedt, Numbrecht, Germany), immediately be- of the test. RPE was only taken for the first 2 min of the test fore and as soon as possible after each of the three MAOD because a previous study (12) revealed that the excessive tests. As soon as the subjects stopped exercising, they were and disorientating fatigue associated with high-intensity ex- led to a chair at the side of the treadmill and remained seated ercise ruled-out collection of RPE during the latter part (i.e., for the duration of the blood sampling. The venepuncture approximately the last minute) of the test. Before testing, and blood withdrawal then took between 30 and 60 s to subjects were reminded of the instructions on the use of the 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 trans- 1) Understand the definition of RPE and receive an ex- ferred to ice-cold lithium-heparin tubes and centrifuged with planation of the nature and use of the scale.
the plasma being stored at Ϫ70°C. The plasma was later 2) “Anchor” the top and bottom perceptual ratings to assayed for glucose and lactate (Analox GLM Instruments, previously experienced sensations of the easiest and most Hammersmith, UK), potassium (Beckman Synchron CX® system, Beckman Instruments, Inc., La Brea, CA), and 3) Ensure they gave an “all-over,” integrated rating, epinephrine and norepinephrine (HPLC with electrochemi- which included both muscular and cardiorespiratory cal detection). Pre-MAOD plasma caffeine was assayed by an enhanced turbidimetric inhibition immunoassay with a 4) Understand the subjective nature of the RPE scale; that minimum detection of 5 ␮mol·LϪ1 (Dade Behring Dimen- there are no “right” or “wrong” responses.
sion Analyzer, Marburg, Germany, using Syva® Emit Caf- The treadmill belt was adjusted to the predetermined feine Assay, Milton Keynes, UK). Final plasma data were velocity, and, when the subjects were ready, they lowered not corrected for changes in plasma volume.
themselves onto the moving treadmill belt. A digital stop Statistics. Data were tested with one-way repeated
clock was started to indicate the start of exercise and the ANOVAs (plasma caffeine, body mass, MAOD, T commencement of the collection of expired air. To ensure ˙ O ), and two-way repeated ANOVAs for all other accurate recording of RPE, a printed scale was presented dependent variables (Bonferroni, post hoc). The sphericity immediately in front of the subject on a large (0.91 ϫ assumption was checked by Mauchly’s test of sphericity. A 0.61 m) board. Subjects then pointed to the number or verbal paired t-test was used to determine whether there was an CAFFEINE, CREATINE, AND RUNNING PERFORMANCE Medicine & Science in Sports & Exerciseா TABLE 1. Comparison of mean (Ϯ SD) body mass, MAOD, total V˙O , T , and between reported caffeine consumption and any of the other contribution of the energy supply to total energy demands for each trial (N ϭ 14).
Body mass. 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 ϭ a Contribution of energy supply to the total energy demand.
* Significantly different from baseline (P Ͻ 0.05).
, total V˙O , and contribution of energy
** Significantly different from placebo (P Ͻ 0.05).
supply to total energy demands. There was no statis-
*** Significantly different from baseline and placebo (P Ͻ 0.05).
tical difference between the order in which the placebo andcaffeine trials were performed for either MAOD (5.56 Ϯ effect between the order in which the placebo and caffeine 1.74 L O Eq vs 5.23 Ϯ 1.55 L O Eq, mean Ϯ SD) or T trials were performed. Pearson product moment correlation (213.0 Ϯ 50.2 s vs 207.4 Ϯ 47.2 s, mean Ϯ SD) for first trial coefficients were used to determine the relationships be- versus second trial, respectively. Caffeine MAOD increased tween measured variables. Ninety-five percent confidence by 0.50 (0.0 –1.1) L O Eq and 0.49 (Ϫ0.1–1.1) L O Eq intervals were computed for all relevant statistics. An alpha (mean difference and lower and upper bound 95% confi- level of Յ 0.05 was chosen to indicate significance. All dence interval difference) in comparison with the baseline statistical procedures were performed using SPSS for Win- and placebo conditions, respectively (Table 1). However, dows, Version 9.0 (SPSS, Inc., Chicago, IL).
these differences did not reach statistical significance. Bycontrast, T 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 Caffeine concentrations. Plasma caffeine concentra-
condition compared with baseline and placebo conditions, tions were not detectable before the baseline or placebo respectively (Table 1). In addition, there was marked indi- trials. However, a mean caffeine concentration of 35 (Ϯ 8.8) ␮mol·LϪ1 was recorded before the caffeine trial. It should be noted that this moderate caffeine concentration is un- subjects failed to show any substantial change from the likely to have resulted in the IOC banned level of 12 baseline and placebo conditions (range Ϫ8 s to 3 s, Fig. 1).
␮mol·LϪ1 of urinary caffeine being attained (13). After the ˙ O was significantly increased in the caffeine trial in investigation, it was revealed that 7 of the 14 subjects comparison with the placebo trial (Table 1). However, there correctly identified the caffeine trial. All subjects main- were no statistically significant differences in the contribu- tained that they had abstained from caffeine consumption tion of energy supply to the total energy demands (Table 1).
for the duration of their participation in the study, and two Rating of perceived exertion. The RPE data at all
subjects claimed they had suffered from “headaches” as a four time points measured (i.e., 30 s, 60 s, 90 s, and 120 s) result of the caffeine abstention. There was no relationship and in all trials revealed a linear response to exercise dura- FIGURE 1—The individual T
response to
caffeine in comparison to the mean of the
baseline and placebo trials.

Official Journal of the American College of Sports Medicine FIGURE 2—Mean (؎ 95% confidence inter-
vals) rating of perceived exertion scores at
30-s intervals for the first 2 min of each trial.

F, baseline; , placebo; , caffeine trials.
*Caffeine trial significantly different from
baseline and placebo (P
< 0.05).
tion. There was a clear trend for RPE to be lower during the mance after caffeine ingestion (10). In addition, having caffeine trials at all time points; however, RPE only attained recently evaluated the reliability (from 3 trials) of T statistical significance at 90 s (Fig. 2).
in a group of similarly trained subjects (11), Metabolic data. There was a significant main effects
we are confident the improvement seen after the caffeine “time” increase in all variables from pre- to post-exercise in trial is worthwhile; the upper-bound 95% confidence inter- all trials (Table 2). Plasma epinephrine and plasma glucose val for the standard error of measurement in the reliability concentrations were higher in the postexercise caffeine assessment was 13.0 s. Although it is usual to have subjects treatment in comparison with the baseline and placebo trials whose performance is not enhanced after caffeine ingestion (Table 2). In contrast, plasma potassium did not increase (i.e., so-called, “nonresponders” (13)), it may well be that after caffeine ingestion compared with the baseline and for some of the nonresponders in the present study (N ϭ 5; placebo trials (Table 2). There was no difference in blood Fig. 1), there was some interference caused by the creatine lactate in any of the trials (Table 2).
supplementation. On the other hand, it is unlikely that theincrease in body mass accompanying creatine supplemen-tation (Table 1) contributed to the nonresponders perfor- DISCUSSION
mance as there was no association between improvement in The main finding from this study was that acute caffeine and the change in body mass (r ϭ Ϫ0.28, P ϭ 0.32). It ingestion (5 mg·kgϪ1) before a treadmill run to voluntary is possible that the effects of acute caffeine ingestion in the present study were influenced by the period of caffeine (0.5–20.7%; 95% confidence interval) in comparison with abstinence that accompanied the creatine supplementation.
baseline and placebo trials (Table 1). Because the caffeine This would be of most relevance to those subjects who have trial was performed within 5-d of a program of creatine a high caffeine consumption (Ͼ300 mg·dϪ1). However, supplementation, the results suggest that the ergogenic ef- there was no relationship between reported caffeine con- fects of caffeine during ST (1,3,4,7,10,30) were not altered (r ϭ 0.04, P ϭ 0.90). Wiles et al. (30) by either creatine loading or by the accompanying increase found no relationship between caffeine habits and the de- in body mass typically found with creatine loading (2,17).
gree of performance response in 1500-m runners (complet- ing the exercise in approximately the same time as our to a previous study that observed an enhanced ST perfor- subjects). Our data also support recent work where 0-, 2-, TABLE 2. Mean (Ϯ SD) for plasma data (N ϭ 14).
a Significant time (pre–post) main effects (P Ͻ 0.05).
b Significant interaction of caffeine with baseline and placebo conditions (P Ͻ 0.05).
CAFFEINE, CREATINE, AND RUNNING PERFORMANCE Medicine & Science in Sports & Exerciseா and 4-d withdrawal from caffeine showed no difference in was 0.5 km⅐hϪ1 slower than the athlete’s fastest 1500-m pace.
improved after creatine supplementation, i.e., in the placebo It is self-evident that a run to exhaustion at 125% V trial (Table 1). Although most studies have generally con- requires a very high degree of motivation. Given that cluded that creatine supplementation is ergogenic during is likely to have been achieved within the first 2 min repeated ST (2,27), there is limited support for (17) and of the MAOD test (20), the issue becomes one of how the against (2) creatine enhancing a single bout of high-intensity subjects in the caffeine trial were able to maintain such a exercise lasting ~3–5-min. Because there is also likely to be high exercise intensity for a further 20 s. It may well be variability in subject muscle creatine uptake after creatine that the improvement in exercise performance after caf- supplementation (14) (i.e., in addition to the variable re- feine was not due to alterations in energetics per se but to sponse to caffeine), future studies should investigate creat- the well-known stimulatory effects of caffeine on the ine uptake by direct muscle measurements to better quantify central nervous system (CNS; 5,13,21,23,25,28 –30). Rat- any interaction between caffeine, creatine, and exercise per- ing of perceived exertion, with its strong relation to formance. The wide individual variation of T factors indicating fatigue, is an important index in the (Fig. 1) reinforces statements alerting sportsmen and women evaluation of CNS drive and the extent of fatigue (22; pp.
to perform individual assessments of specific ergogenic aids 93–104). The RPE data (Fig. 2), although not fully con- before use and not to rely solely on generalisations from the clusive, are suggestive of a dampened perceptual re- sponse during ST after caffeine ingestion. In comparison Unlike previous studies, MAOD was not improved after with the many endurance-based caffeine studies that have either acute caffeine ingestion (10) or creatine loading (17).
observed a reduction in RPE at the same standardized The reason for the nonsignificant MAOD in comparison with exercise intensity after caffeine ingestion (5,8,19,25), thisstudy provides additional evidence that caffeine’s ergo- is possibly related to the MAOD being a less reliable genic effect during ST may also manifest itself via a measure. The reduced reliability may be because of the many dampened perceptual response (30), i.e., during the first single measurements associated with respiratory gas analysis 2 min of ST. Furthermore, it may be that the difference in used during MAOD in comparison with the one simple time perceptual response with caffeine to maximal exercise lasting between 3 and 5 min becomes even greater during although traditional measures of reliability (including coeffi- the last third of the exercise, that is, the part of the cient of variation and intraclass correlation coefficient) were exercise test where RPE was not monitored. The reason favorable, the 95% limits of agreement (95 LoA) revealed the why only the 90-s time point showed a significant reduc- MAOD to have relatively poor reliability. Based on the 95 tion may be the rather crude category RPE measure that LoA, it was estimated that a sample size of 20 was required to was used. Future studies investigating the connection detect a 10% change in MAOD (11). The sample size estima- between caffeine ingestion and perceived exertion may tion of the present study may therefore have underestimated the wish to use alternative, more sensitive visual analog number of subjects required to determine a change in MAOD.
Hopkins (16) concluded that, from a measurement sensitivity There are a number of theories relating caffeine to a perspective, the use of constant distance, constant work, and reduction in RPE in endurance-based studies. In a review of constant duration tests are more reliable than, and recom- this area, Spriet and Howlett (25) speculated that the low- mended over, constant exercise intensity tests to exhaustion ered RPE with caffeine could be due to a decrease in the (i.e., as used in this study). Where repeated trials use the same neuronal activation threshold of motoneurons and/or alter- supramaximal exercise intensity, one would expect that the ations in muscle contraction force. These mechanisms contribution of energy sources to the total energy demand would result in lowered sensory feedback from the exercis- would follow the same trend in all trials (20). Thus, it is ing muscle, and thus a reduced RPE, the first mechanism because more motor units would be recruited for a given increased in the caffeine trial in comparison with the placebo task and the second because force for a given stimulus trial. This is despite the fact that there were no changes in the would be greater (25). Of the measurements reported in this contribution of energy supply to the total energy demands study, the reduction in postexercise plasma [Kϩ] after the (Table 1; possibly because MAOD also increased along with caffeine treatment may be a possible link to improved mus- ˙ O but just failed to reach statistical significance). It may cle contractility. It has been suggested that Kϩ efflux from be that subjects either achieved a higher V skeletal muscle cells plays a role in the development of at a faster rate in the caffeine trial. Unfortunately, we muscle fatigue (24). Loss of Kϩ decreases the intracellular are only able to speculate on this because the protocol used in [Kϩ], which in turn reduces the muscle action potential and this study did not facilitate measurement of V excitability (13,18,24). These changes are likely to interfere with excitation-contraction coupling (13,18,24) and would been caused by stimulation of the sympathetic nervous system result in less motor unit activation and/or less force produc- (13), including an increased secretion of epinephrine, after the tion per motor unit (13,18,24). Other in vivo studies have caffeine trial (Table 2). Interestingly, Wiles et al. (30) also also shown less of an increase in plasma [Kϩ] after caffeine found that ingestion of 3 g of caffeinated coffee in 1500-m ingestion (18,19). It is speculated that caffeine, and/or the Official Journal of the American College of Sports Medicine associated increase in epinephrine (as reported in the present sensitive to tension or pressure, alterations in feedforward study), affects the washout of Kϩ from the active muscle information, and/or alterations in the central processing and/or the clearance of Kϩ by stimulating resting muscle of either feedforward or feedback information (23).
Na2ϩ/Kϩ ATPase to take up more Kϩ (13).
The increases in plasma epinephrine and plasma glu- Caffeine exerts a hypoalgesic effect during ischemic cose in the caffeine trial have been observed repeatedly in muscle contractions and acts as an analgesic adjuvant in previous research (1,6,7,19,29). However, the signifi- combination with other compounds (21). There is evi- cance of these changes is not clear. A recent review of dence that caffeine directly affects the release of ␤-en- this area suggests that such changes are coincidental with dorphins and other hormones and neurotransmitters that caffeine ingestion and do not in themselves elucidate how influence feelings of pain associated with some forms of caffeine provides an ergogenic effect (13). Unlike previ- exercise (25). However, some authors believe that CNS ous studies that have suggested a caffeine-induced epi- changes are not important and cite the caffeine-induced nephrine–lactate relationship (1,6,7), more recent work increases in muscle endurance reported in tetraplegic does not support this association (13,15). Our data also patients (28). In a recent study that used a constant- question the proposed positive relationship between sensation technique to determine whether caffeine (6 plasma epinephrine and plasma lactate.
mg·kgϪ1) influenced force sensation during 100 s of an Taken together with the results of other studies, this study isometric contraction of the quadriceps at 50% maximum demonstrates that acute ingestion of caffeine has ergogenic voluntary contraction, Plaskett and Cafarelli (23) found effects on ST regardless of whether or not creatine supple- that caffeine reduced force sensation during the first mentation precedes the caffeine ingestion. Our results sug- 10 –20 s of the contraction. In a separate experiment, gest that the ergogenic effects of caffeine are possibly re- Plaskett and Cafarelli (23) also observed a caffeine-in- lated to alterations in the perceptual response and/or the willing to maintain near-maximal activation longer due to The authors express their thanks to Karl Schroder for help with data collection, Neil Willmore for his expert technical assistance, alterations in muscle sensory processing (23). This may and Dr. John Wojdyla of the Luton and Dunstable Hospital, UK, for have been caused by feedback from mechanoreceptors REFERENCES
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Official Journal of the American College of Sports Medicine



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