In a series of investigations conducted nearly 20 years ago, Costill and coworkers (10,13,22) were the first to report that the ingestion of moderate doses of caffeine (∼5 mg·kg−1) improved the performance of well-trained athletes in exercise tests lasting ∼1 h. In those studies, caffeine ingested ∼1 h before exercise stimulated lipolysis, enhanced rates of fat oxidation (as estimated from respiratory gas exchange measurements), and decreased the utilization of muscle glycogen (10,13,22).
Recently, several well-controlled studies utilizing both short-term (<10 min) and prolonged (>60 min) exercise protocols have confirmed and extended the earlier findings of Costill’s group (5,16–18,23,26,31). Spriet et al. (31) reported that a high dose of caffeine (9 mg·kg−1) decreased the rate of muscle glycogen utilization by ∼55% while cycling at 80% of maximal oxygen uptake (V̇O2max). Interestingly, the “glycogen-sparing” effect of caffeine was restricted to the initial 15 min of exercise (31). It was hypothesized that the spared glycogen was subsequently available for oxidation during the latter stages of exercise, thus prolonging cycling time to exhaustion. These researchers did not measure rates of substrate oxidation during the period of glycogen sparing, but respiratory gas exchange measures taken after 15 min and throughout the remainder of the exercise bout revealed that rates of fat oxidation were decreased with caffeine ingestion compared with the placebo condition (31). These results are consistent with the possibility that the ergogenic effect of caffeine is not due exclusively to enhancement of fat oxidation.
Further evidence of a nonmetabolic mechanism for caffeine-induced improvements in performance was provided by Jackman et al. (23). These workers reported that caffeine (6 mg·kg−1) prolonged high-intensity cycling time to exhaustion from 4 min 7 s to 4 min 56 s, and that this effect was not associated with any reduction in the rate of muscle glycogenolysis. Taken collectively, these findings strongly suggest that any improvements in short-term athletic performance are independent of a metabolic effect of caffeine. Instead, alternative mechanism(s) for performance enhancement could be due to altered central nervous system (CNS) function (7,11,29,32), improved neuromuscular function (24,34), or a direct effect of caffeine on skeletal muscle ion homeostasis (26). Accordingly, the aim of the current study was to investigate the effect of varying doses of caffeine on the performance of well-trained rowers utilizing a highly reliable laboratory test (28) that simulates the physiological demands of competition (19). As we wished to identify the mechanism(s) that might explain any differences in performance between the treatments, measures of whole body metabolism and the subject’s perception of effort were also determined.
Eight well-trained male rowers were recruited to participate in the study, which was approved by the Human Research Ethics Committee of RMIT University. The experimental procedures and possible risks of the study were explained to each subject who gave their written informed consent. All subjects regularly performed a significant portion of their training, as well as race selection on the Concept II rowing ergometer (Model B, Morrisville, VT) and were familiar with the criterion performance measure chosen for this investigation.
All subjects were required to complete three familiarization testing sessions before undertaking the subsequently described experimental trials on a Concept II rowing ergometer. The aim of this preliminary testing was to determine the reliability of each rower’s 2000-m time-trial performance. In these sessions, subjects undertook a standardized submaximal row consisting of 4 min of rowing at a workload that elicited ∼60% of individual peak heart rate (HRpeak) followed by 1-min rest and then 6 min of rowing at a constant power output, which elicited ∼80% of HRpeak (∼75% of V̇O2peak). After the completion of the submaximal row, subjects rested for 3 min before completing a 2000-m time trial.
Nutritional and training control.
Nutritional status was controlled during the 24 h before each experimental trial (described subsequently) by providing subjects with a standard diet of 50 kcal·kg−1 of body mass, composed of 63% carbohydrate (8 g·kg−1), 20% fat, and 17% protein. In addition, subjects were requested to abstain from ingesting foods or beverages containing caffeine or alcohol for the 72 h before an experiment. Each subject kept a training diary for 48 h before the first test; they then attempted to replicate their training for the subsequent trials.
Each subject completed a random order of three experimental trials, which were separated by at least 3, but no more than 7 d. For a given subject, each trial was conducted at the same time of day. All treatments were administered in a double-blind fashion.
Subjects reported to the laboratory after a fast of 8–12 h. A baseline urine sample was obtained for subsequent determination of urinary caffeine concentration. Subjects were then weighed on electronic scales (Wedderburn Tanita BWB-620, Japan) before a 20-gauge Teflon catheter (Terumo, Tokyo, Japan) was inserted into a forearm vein. A 10-mL blood sample was drawn, and the catheter was flushed with 5 mL of 0.9% sterile saline solution to keep the catheter patent. This process was repeated after each blood draw.
Subjects then ingested 3 mL·kg−1 of water with a capsule containing either 6 mg·kg−1 caffeine, 9 mg·kg−1 caffeine, or a placebo containing ∼500 mg of glucose. Blood samples (10 mL) were drawn 30 and 45 min post ingestion, after which subjects began a standardized submaximal row (described previously) on the ergometer. Throughout the final 6 min of the warm-up, subjects breathed through a mouthpiece attached to a Quark b2 metabolic cart (Cosmed, Rome, Italy). Expired gas was passed through a flow meter, an O2 analyzer, and a CO2 analyzer. The flow meter was calibrated with a 3 L Hans-Rudolph syringe (Kansas City, MO). The gas analyzers were calibrated with gases of known concentrations (4.00% CO2 and 16.00% O2). The flow meter and gas analyzers were connected to a computer, which calculated minute ventilation (V̇E), oxygen consumption (V̇O2), carbon dioxide production (V̇CO2), and respiratory exchange ratio (RER) from conventional equations. From V̇CO2 and V̇O2 values, the instantaneous rates of total carbohydrate and fat oxidation rates were estimated. Immediately after the warm-up, a blood sample (5 mL) was drawn and ratings of perceived exertion (RPE) were obtained (3). Subjects then rested for 3 min before undertaking a 2000-m time trial.
Throughout each time trial subjects breathed through the previously described gas collection system. The only feedback given was their stroke rate and the distance remaining. Heart rate was measured by telemetry and stored every 5 s using a Polar Accurex Plus (Polar Electro OY, Kemple, Finland). The time to complete the 2000-m time trial was recorded along with the time to complete each consecutive 100-m of the trial. Average power output for the 2000-m time trial was obtained upon completion of the row. Measures of RPE were obtained immediately after the time trial.
Blood samples were divided into two aliquots: 5 mL was transferred into an EDTA tube for the immediate determination of blood lactate and glucose concentration, and 5 mL of whole blood was placed into nontreated tubes containing 60 μL of ethylene glycol-bis(-aminoethyl ether)–N,N,N′,N′-tetraacetic acid and reduced glutathione and was spun in a centrifuge (J6-MC Beckman Centrifuge, Beckman Instruments, CA) at 900 g for 15 min at 4°C. The plasma was stored at −80°C, and later analyzed for plasma free fatty acid (FFA) concentration by a spectrophotometer (Cary IE UV-Vis Spectrophotometer, Melbourne, Australia), using an enzymatic colorimetric method (half micro test, Boehringer Mannheim 1383175, GmbH, Mannheim, Germany). Blood lactate and blood glucose concentrations were analyzed in triplicate using automated analyzers (Yellow Springs Instruments 2300 Stat Plus Glucose and L-Lactate Analyzer, Yellow Springs, OH). Hematocrit and hemoglobin concentration were measured using a Cobas Micros CT cell counter (Roche Diagnostic Systems, Montpellier, France) to estimate changes in plasma volume (12).
Further blood samples (5 mL) were drawn 3, 5, 10, 15, and 30-min after each experimental time trial and immediately analyzed for blood lactate and glucose concentration. During the recovery, subjects were allowed ad libitum access to water. Before leaving the laboratory, subjects provided a urine sample and were questioned by the principal investigator as to what treatment they had thought they had received. The results of all experimental trials were not disclosed to each subject until the completion of the study.
Pre- and post-exercise urine samples were stored at −80°C, and later analyzed for urinary caffeine concentration using high performance liquid chromatography (HPLC; ICI Instruments, Melbourne, Australia), using a method modified from Aldridge et al. (1). A urine sample (1 mL) was thawed and transferred to a nontreated tube, and the pH was adjusted to >9.0 by addition of NaOH. Dichloromethane (1 mL) was added to the urine sample (1 mL); the solution was mixed for 20-min and centrifuged for 10 min at 4000 revolutions·min−1 at 0°C. The organic phase was then dried at 40°C under a constant stream of oxygen-free N2. Residuals were then resuspended in 1 mL of HPLC mobile phase solvent (65% distilled water: 25% methanol:10% acetonitrile: 1% glacial acetic acid); 200 μL was then transferred to a sample tube and 10 μL was injected into an Alltech column (Platinum C18, 100 A, 5 u, 250 × 4.6 mm). Caffeine was measured at a wavelength of 273 nm.
Changes in the mean of variables and/or treatments and measures of within-subject variability were estimated using a mixed modeling procedure (Proc Mixed) in the Statistical Analysis System (SAS Institute, Cary, NC). The same procedure provided 95% confidence limits (the likely range of the true value) for all estimates. For all analyses, the identity of subjects was a random effect. For the analysis of reliability of performance time in the three familiarization trials, the identity of the trial (first, second, third) was included as a fixed effect to account for any learning or habituation effects between trials. For the analysis of all outcome variables in the crossover trials, the identity of the caffeine or placebo treatment was a fixed effect; identity of the trial was included in these analyses to account for any learning or habituation effects. An extra random effect was included for the caffeine trials to account for individual differences (variation between individuals) in the effect of caffeine. The analysis is based on the assumption that there was no difference in an individual’s response to either dose of caffeine, other than random error. The individual differences were expressed as a standard deviation of the mean effect of caffeine, free of error of measurement.
We also performed an analysis that combined baseline and treatment trials to determine the effect of the treatments on performance time relative to baseline. We excluded the first trial, because pairwise analyses of trials showed that there was an increase in reliability for trials 2 and 3 (CV = 0.7%) relative to trials 1 and 2 (CV = 0.9%). When we discovered markedly greater error of measurement in this analysis than in separate analyses of the baseline trials or the treatment trials, we included an extra random effect to account for individual differences in the change in performance between the baseline and the treatment trials.
The centrality and spread of values of variables are shown throughout as mean ± standard deviation (SD). Individual differences in treatment or learning effects are shown as standard deviations of the change in the mean; these standard deviations represent typical variation in the effect between subjects, and they are free of random error of measurement. The precision of estimates of outcome statistics are shown as the 95% confidence interval (95%CI), which defines the likely range of the true value in the population from which we drew our sample.
Familiarization time trials.
The performance time for the first 2000-m time trial was 416 ± 16 s. The time for Trial 2 was 0.1% slower (95%CI = −1.2 to 1.0%), but there was a slight improvement of 0.9% (95%CI = −0.1 to 2.0%) in trial 3 relative to trial 2. The typical error between trials 1 and 2 was similar to that between trials 2 and 3; for the three trials combined it was 0.9% (95%CI = 0.4–1.8%).
Metabolic data averaged during the last 5 min of the submaximal row are presented in Table 1. As intended, power output sustained by subjects was similar for all three trials. There were no significant differences between treatments for V̇O2, HR, or RPE, but there was a tendency for V̇O2 to be higher and RER to be lower with the caffeine treatments. V̇E was significantly elevated with the higher caffeine dose (102 ± 18 vs 99 ± 17 and 94 ± 19 L·min−1 for the high and low doses and placebo, respectively;P = 0.02).
2000-m time trial.
Relative to placebo, ingestion of the lower dose of caffeine resulted in a 1.3% improvement in time to complete the 2000 m (95%CI = 0.4–2.1%, P = 0.01), whereas the higher dose resulted in a 1.0% improvement in performance (95%CI = 0.2–1.9%, P = 0.03). The average of the two caffeine trials was 1.2% faster than the placebo trial (95%CI = 0.4–1.9%, P = 0.006). Individual differences for this effect were represented by a standard deviation of 0.9% (95%CI = 1.5 to −0.9%, P = 0.34).
Relative to the mean of the two baseline trials, the placebo trial was a little slower (0.4%, 95%CI = −1.6 to 2.5%, P = 0.75), and the mean of the caffeine trials was somewhat faster (0.7%, 95%CI = −1.3 to 2.7%, P = 0.45). There were large differences between individuals in the change in performance between baseline and treatment trials: a standard deviation of 2.5% (95%CI = −0.9 to 3.7, P = 0.09).
Changes in mean power between time trials were in the opposite direction to the changes in time and were approximately 2.4 times as large. For example, mean power for the average of the two caffeine trials was 2.7% greater than mean power in the placebo trial (95%CI = 0.4–5.0%, P = 0.03).
Caffeine ingestion had no significant effect on V̇O2, RER, V̇E, and HR during or RPE and changes in plasma volume immediately after the 2000-m time trial (Table 2). As with submaximal exercise, there was a tendency for higher V̇O2 and lower RER with caffeine relative to placebo.
Blood lactate concentration was similar at rest for all treatments (∼1 mM). After the submaximal exercise lactate concentration rose to 3–4 mM, and after the time trial it reached 10–12 mM; on average, it was 22% higher with caffeine than with placebo (95%CI 13–30%, P = 0.0003), but there was little difference between the two doses of caffeine.
Blood glucose concentration showed a time course similar to that of blood lactate concentration, and the effect of the treatments was similar. There was little difference at rest (∼ 4 mM), but there was a marked hyperglycemia after the 2000-m time trial for all treatments (6–9 mM). On average, blood glucose was 13% higher with caffeine than with placebo (95%CI 5–21%, P = 0.007), and there was a tendency for a higher concentration with the higher dose of caffeine.
Figure 1 shows that resting plasma FFA concentrations were similar for all treatments. However, ingestion of caffeine resulted in a ∼50% increase in plasma FFA concentration with the lower dose of caffeine (P = 0.12), and a ∼100% increase with the higher dose (P = 0.02).
Urinary caffeine concentration.
Urinary caffeine concentrations at rest and after exercise are shown in Figure 2. Resting urinary caffeine concentrations were similar for the three experimental treatments. As expected, there was a marked increase in postexercise urinary caffeine concentration following caffeine ingestion.
The first major finding of this study was that, under controlled laboratory conditions, the ingestion of 6–9 mg·kg−1 of caffeine 1 h before exercise leads to an improvement in 2000-m simulated rowing time trial performance in well-trained oarsmen. The magnitude of the improvement (∼1% for performance time or ∼3% for mean power) is likely to be worthwhile for competitive rowers (21).
The individual differences in the effect of caffeine were of magnitude similar to the mean effect, but there was considerable uncertainty in this estimate. A larger sample size or more trials with each treatment would be needed before we could conclude confidently that there is a substantial graded response to caffeine between individuals.
Individual differences in performance time as the subjects moved from baseline to treatment trials were relatively large (∼2%), although still lacking a little in precision. Blinding the subjects to the treatment apparently made some of them try consistently harder in the three treatment trials, whereas others made consistently less effort. This extra source of variation explains the relatively poor precision for the estimate of effect of the treatments relative to baseline performance. A similar increase in variability of endurance performance with blinding has been noted recently (6). More research is needed to confirm this effect, because the findings of studies in which some subjects make less than their best effort may not apply to the performance of presumably more highly motivated athletes in competitive events.
Other workers have also reported that short-term, high-intensity exercise capacity is improved after caffeine ingestion. Wiles et al. (33) reported that the ingestion of 3 g of caffeinated coffee resulted in a 4.2-s improvement in 1500-m treadmill running time. In that study, subjects ran the final 400 m 0.6 km·h−1 faster after caffeine ingestion compared with placebo. Collomp et al. (8,9) and Jackman et al. (23) have also reported performance enhancements in short-term, high-intensity exercise after caffeine ingestion. For example, trained swimmers increased the velocity of two 100-m swims by an average of 3% after the ingestion of 250 mg of caffeine (9).
On the other hand, several researchers have reported no effect of moderate doses of caffeine on maximal exercise performance in protocols lasting up to 20 min (for reviews see 30). There are several possible explanations for the discrepancy in the results between the various investigations.
First, a number of studies have used untrained (2,9) or moderately trained subjects (7,13,15,23) who were not familiar with the performance test. Highly trained athletes have genetic endowment, training history, and training program that differ from untrained or subelite athletes, and it is likely that a treatment would produce different effects on performance in such groups (21). Furthermore, well-trained subjects are likely to perform more reliably in any chosen performance task, particularly if they frequently undergo testing and training sessions on the same ergometer that is used for testing (21,28). In this respect it is worth noting that none of the previous studies of the effects of caffeine on exercise capacity have reported the reliability of the criterion performance measure.
Second, many studies fail to adequately control for replication of training and dietary status before and between trials. Such control is particularly important in the 1–2 d immediately before an experiment (21). During studies of the effects of caffeine on performance, attention must be given to controlling caffeine consumption in the 3–4 d before exercise test. Indeed, Fisher et al. (14) have shown that the effects of caffeine on performance are attenuated in caffeine habituated individuals, and so in the present investigation, subjects abstained from caffeine ingestion 72 h before an experiment. Other studies examining caffeine’s effect on short-term, high-intensity exercise have implemented a similar period of abstinence (2,8,9,27) but failed to report either resting urinary or plasma caffeine concentration. Therefore, it is difficult to establish how well subjects followed pretrial instructions regarding caffeine abstinence. On the basis of resting urinary caffeine concentration (see Fig. 2), subjects in the present study complied well with our requests for caffeine abstinence.
To the best of our knowledge, there has been no previous study of the dose-response of caffeine on high-intensity, short-term endurance performance. We found that the moderate (6 mg·kg−1) dose resulted in a slightly faster performance time. This finding is in agreement with some (4,17) but not all (14,16,23) studies of the effect of caffeine on exercise performance. Ingested caffeine is rapidly absorbed into the bloodstream and demonstrates dose-dependent increases in plasma caffeine concentration (17). However, at the higher (∼9 mg·kg−1) dose at least one-third of athletes tested have urinary caffeine concentrations at or above 12 mg·L−1 (for review see 30), which exceeds the limit set by the International Olympic Committee (IOC). In the current study, the mean urinary caffeine concentration after ingestion of 9 mg·kg−1 was ∼14 mg·L−1. It should be noted that the between subject variation in urinary caffeine concentration to caffeine ingestion is large (4,27,30). Therefore, the recommendation to competitive male athletes who wish to use caffeine to enhance their performance should be to trial doses of up to ∼6 mg·kg−1 in a variety of training situations.
Caffeine ingestion has been shown to increase fat oxidation (10) and spare muscle glycogen stores during moderate- to high-intensity endurance exercise (5,13,31). This “metabolic” theory has gained wide spread acceptance as the major mechanism by which caffeine improves endurance performance (30). However, intense aerobic exercise lasting up to 1 h is unlikely to be limited by muscle glycogen availability (20). In the present study, we found substantial shifts in the rates of substrate oxidation during a standardized submaximal workbout undertaken before the all-out performance row, but during the time trial RER values were similar. The improvement in 2000-m rowing performance was therefore likely to be independent of any effect of caffeine on substrate mobilization. Rather, the mechanism for a performance enhancement is likely to be an effect on the CNS or a direct effect on skeletal muscle. It is well known that caffeine affects the CNS (7,11,25,32) by eliciting greater motor unit recruitment and alterations in neurotransmitter function (24,34). Caffeine could also affect the CNS in ways that cause it to overrule fatigue signals during exercise (7,32). However, the fact that most of the subjects in the present study failed to correctly identify the trials in which they ingested caffeine suggest that any effect on the CNS was subtle and not obvious to the subjects themselves.
In conclusion, we observed a worthwhile enhancement of performance when highly trained rowers ingested caffeine before a reliable, short-term high-intensity endurance test under experimental conditions in which diet and training were well controlled. The higher dose of caffeine resulted in urinary caffeine concentrations that sometimes exceeded the limit permitted by the IOC, whereas the lower dose elicited a similar performance enhancement without exceeding the legal limit.
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