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Original Research

Caffeine and Sprinting Performance

Dose Responses and Efficacy

Glaister, Mark; Patterson, Stephen D.; Foley, Paul; Pedlar, Charles R.; Pattison, John R.; McInnes, Gillian

Author Information
Journal of Strength and Conditioning Research: April 2012 - Volume 26 - Issue 4 - p 1001-1005
doi: 10.1519/JSC.0b013e31822ba300
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Caffeine, a trimethylxanthine, is one of the most commonly consumed drugs in the world, with no apparent long-term adverse health effects (18). Despite being previously on the World Anti-Doping Agency (WADA) list of controlled substances (>12 μg·ml−1 in urine was considered a doping offense), its removal in 2004 opened up the opportunities for athletes to exploit its ergogenic potential. Research into the effects of caffeine on athletic performance has been focused largely around endurance exercise, particularly since early research hypothesized a glycogen-sparing mode of action. Although evidence of a positive effect on endurance is considerable (5), the shift to a central nervous system mediated mode of action (via adenosine receptor antagonism) has led researchers to also consider the effects of caffeine on shorter and more intense exercise paradigms. Research into the effects of caffeine on speed-endurance events (60–180 seconds) and multiple sprint events tends to support a positive effect (8). Indeed, in a recent investigation, caffeine supplementation was found to increase sprint performance in the early stages of a 12 × 30-m multiple sprint test (11). Moreover, the magnitude of the improvement in fastest sprint time was evenly distributed across each 10-m split, suggesting potential benefits over longer sprint durations and single sprint events. In contrast, research into the effects of caffeine on single bouts of brief maximal work (primarily focused on 30-second Wingate anaerobic tests) generally, though not always (1,23), fails to show any performance effects (3,7,15–17,22,24). However, the possibility of pacing strategies influencing sprint durations of around 30 seconds, even in well-trained individuals, is a confounding factor (25). Indeed, several factors such as poor sample sizes; use of untrained participants; failure to test resting plasma or urine caffeine concentrations; inadequate placebos; and the use of fixed rather than relative caffeine doses may explain why research into the effects of caffeine on high-intensity exercise has many contradictions.

The primary aim of this study was to address the aforementioned methodological limitations to investigate the effects of acute caffeine ingestion on brief (10 seconds) maximal sprint cycling performance. In addition, the study aimed to investigate whether, as with endurance performance, effects followed a dose-related response (4,14). Finally, several investigations have observed elevations in blood lactate after caffeine supplementation. If those elevations cannot be explained by a caffeine-induced increase in lactate production by the working muscles (13), then supplementation should lead to an increase in resting blood lactate concentrations. Therefore, a final aim of this study was to investigate the effects of caffeine supplementation on resting blood lactate concentrations.


Experimental Approach to the Problem

All the subjects completed 7 maximal 10-second sprint trials on an electromagnetically braked cycle ergometer (Lode Excalibur Sport, Groningen, Holland), which was fitted with standard pedals, toe clips, and straps and interfaced with a computer to enable high-frequency logging of the flywheel angular velocity. A 10-second sprint was chosen to reduce the potential for pacing strategies previously identified in longer sprints (25). The reliability coefficient of the 10-second cycle sprint test has previously been reported as 0.96 (25). The saddle height and handlebar position for each subject were determined before the first trial and remained constant for all subsequent trials. Trial 1 was a familiarization test to limit the effects of learning on the outcome of the experiment and involved no blood sampling. In the remaining trials, which were randomized and conducted in a double-blind manner, the subjects consumed a gelatine capsule containing 2, 4, 6, 8, or 10 mg·kg bm1 (bm is body mass) of caffeine (My Protein, Manchester, United Kingdom) or the same volume (4 mg·kg bm1) and color of placebo (maltodextrin: My Protein). All the trials were completed at approximately the same time of the day with a minimum of 48 hours between each. The subjects were instructed to maintain their normal diet throughout the testing period, to avoid food and drink in the hour before testing, and to avoid strenuous exercise 24 hours before each trial. The subjects were provided with a list of dietary sources of caffeine and asked to refrain from consuming these 48 hours before each trial. A questionnaire was used to establish typical daily caffeine consumption.


Seventeen male strength and conditioning and sport science students volunteered for the study, which was approved by the St. Mary's University College Ethics Committee. Before testing, the subjects received written and verbal instructions regarding the nature of the investigation and completed a training history questionnaire, which indicated that all had been actively involved in sport for approximately 12 years. Times spent training and competing each week were reported as 8.8 ± 7.2 and 3.9 ± 4.2 hours, respectively. Before commencement of the study, all the subjects completed a health-screening questionnaire and provided written informed consent. Mean ± SD for age, height, bm, and body fat (10) of the subjects were 24 ± 6 years, 1.82 ± 0.06 m, 82.2 ± 6.9 kg, and 13.5 ± 3.4%, respectively.


All testing was conducted in a laboratory that was thermostatically controlled at 18°C. On arrival at the testing facility, and after approximately 5 minutes of seated rest, resting blood samples (∼5 ml) were drawn from a branch of the basilic vein and collected in plain siliconized tubes. At the same time, blood samples were obtained from the earlobe via capillary puncture for the evaluation of blood lactate. The subjects then consumed the supplement after which they rested for 50 minutes before the same blood sampling procedures were repeated. Venous blood samples were allowed to clot at room temperature before being centrifuged at 2,000 rpm for 20 minutes, with subsequently decanted serum samples frozen at −20°C until analyzed for caffeine content using high-performance liquid chromatography. Capillary blood samples were analyzed for lactate content using an automated analyzer (Biosen C-Line, EKF Diagnostic, Ebendorfer Chaussee 3, Germany). The analyzer was calibrated before all the trials in accordance with the manufacturer's instructions.

After blood sampling procedures were completed, the subjects performed a standardized warm-up comprising 3.5 minutes of cycling at 120 W using a cadence of 80 rpm after which the subjects were asked to indicate on a 20-cm visual analog scale (ranging from ‘not ready’ to ‘very ready’) their perceived readiness to perform the forthcoming 10-second sprint. The subjects then performed two 5-second maximal practice sprints interspersed with 30 seconds of passive recovery, followed by another minute of cycling at 120 W (Figure 1). On completion of the warm-up and starting from a stationary position, the subjects performed a 10-second maximal sprint against a torque factor of 0.7 N·m·kg bm−1. The Subjects were verbally encouraged to give maximal effort during all the trials. After each trial, the subjects completed a cool-down by cycling at 120 W for a minimum of 2 minutes.

Figure 1
Figure 1:
Schematic of the experimental protocol to investigate the effects of caffeine supplementation on 10-second sprint cycling performance.

Statistical Analyses

All data were analyzed using the Statistical Package for the Social Sciences (SPSS Inc., Chicago, IL, USA). Measures of centrality and spread are presented as mean ± SD. The effects of supplementation on serum caffeine concentrations and blood lactate were analyzed using a 2-way (time × dose) analysis of variance (ANOVA). The effects of caffeine dose on perceived readiness and on key sprint performance outcomes of peak power, mean power, and time to peak power were analyzed using a 1-way ANOVA. The value of α was set at 0.05 for all comparisons, and significant effects were followed up using Bonferroni-adjusted post hoc analyses. The above analyses provided 95% confidence limits for all outcomes.


Analysis of the caffeine questionnaire data revealed that normal mean daily caffeine consumption of the subjects was 261 ± 224 mg (range: 10–677 mg). Analysis of the serum data (Table 1) revealed significant effects of time (F(1,16) = 297.64, p < 0.001), dose (F(2.7, 43.3) = 32.89, p < 0.001), and time × dose (F(2.7, 42.7) = 33.48, p < 0.001). Post hoc analyses showed that there were no significant differences in baseline serum caffeine concentrations obtained before each trial. In contrast, apart from placebo (p = 0.299), significant increases in serum caffeine concentrations were observed between baseline and postsupplementation samples (p < 0.001). The time × dose interaction supported a dose-response effect of supplementation with higher doses producing higher serum caffeine concentrations; though not all post hoc comparisons were statistically significant (Table 1). Blood lactate decreased significantly (F(1,16) = 18.32, p < 0.001) from baseline to postsupplementation (mean change: 0.22 mmol·L−1; 95% likely range: 0.11–0.34 mmol·L−1), but there was no effect of caffeine dose (F(5,80) = 0.76, p = 0.581) and no time × dose interaction (F(5,80) = 1.74, p = 0.135) (Table 1). There was a significant effect of supplementation on perceived readiness (F(5,80) = 5.30, p < 0.001), with placebo resulting in significantly lower scores than the 2, 8, and 10 mg·kg bm−1 caffeine doses (Table 1). Supplementation had no significant effect on sprint performance measures of peak power (F(5,80) = 1.88, p = 0.108), mean power (F(5,80) = 0.80, p = 0.552), or time to peak power (F(3.63,58.15) = 1.68, p = 0.172) (Table 2).

Table 1
Table 1:
The effects of various doses of caffeine supplementation on presprint measures of serum caffeine concentration, blood lactate, and perceived readiness.*†‡
Table 2
Table 2:
The effects of caffeine supplementation on measures of maximal 10-second sprint cycling performance.*†


The principal aim of this study was to examine the effects of caffeine supplementation on short-duration maximal-intensity sprint cycling. The main finding was that caffeine had no significant effect on any of the measures of sprinting performance. The absence of any significant effect of caffeine on short-duration (≤30 seconds) sprinting performance confirms a number of previous reports (3,7,15–17,22,24) but contrasts with others (1,23). Although the majority of studies support the absence of an effect of caffeine on sprinting performance, it is difficult to explain why this is not always the case. However, the fact that there was no dose-response effect of caffeine on performance suggests that between-protocol differences in dosing strategies are unlikely to be a confounding factor. The possibility that caffeine habituation may have influenced the results also seems unlikely given the habitual caffeine consumption range of the participants in this study and the absence of any corresponding effect on performance. Previous research on graded exercise performance (9), low-frequency stimulated contraction force (21), and multiple sprint work (11) have failed to find a relationship between caffeine habituation and subsequent effects on performance. Overall, there appear to be no common factors that explain the discrepant results regarding the effects of caffeine on sprinting performance, though a failure to measure resting serum or urine caffeine concentrations in several studies (1,7,15–17,24) is a concern.

One of the biggest problems when conducting research into responses to caffeine supplementation is that of blinding subjects to the treatment. Given the pronounced side effects of ‘jitteriness’ and ‘nervousness’ that generally accompany acute caffeine administration (20), it is often the case that subjects are able to determine when they have taken the supplement. Moreover, manifestation of those same side effects makes it difficult for researchers to also maintain a blind perspective. In this study, differences in perceived readiness scores between caffeine and placebo trials suggest that subjects were aware of when they had taken caffeine. However, despite this, the subjects seemed unable to identify differences between the various doses used. Moreover, the absence of any subsequent effect of caffeine on performance suggests that knowledge of the supplement did not influence their motivation to give a maximal effort. Although the same may not have been the case if the duration of the sprints had been extended (25), the absence of an effect of caffeine on most 30-second sprint trials (3,7,15–17) diminishes the possibility of a placebo effect (2) influencing the results.

A secondary aim of this study was to examine the effects of caffeine on resting blood lactate concentration. Many studies have shown a caffeine-induced increase in blood lactate during constant-intensity exercise (12). However, caffeine has been found to have no effect on lactate release by the working muscles (6,13), suggesting that either lactate clearance by the liver or resting muscle is inhibited or that lactate release by other tissues is increased (13). The results of this study are contrary to both these suggestions in that regardless of the dosage used, caffeine had no significant effect on resting blood lactate; moreover, values significantly reduced across the 50-minute pretrial resting period, most likely because of slightly elevated levels on arrival at the laboratory. Although it is possible that subtle differences in exercise intensity as a result of caffeine supplementation could explain many of the aforementioned elevations in blood lactate observed in several investigations, more research is needed to clarify.

In summary, the results of this study suggest, in conjunction with a number of previous reports, that caffeine supplementation has no significant effect on short-duration (≤30 seconds) sprinting performance. Moreover, the absence of any effect on performance does not appear to be dose related. Given that caffeine appears to exert its effect via a central mechanism and that the effects of caffeine on endurance exercise are well established, further research with rigorous methodological control is required to clarify the duration of exercise for which caffeine ceases to be ergogenic. Finally, if caffeine does indeed have no effect on sprinting performance, it is difficult to reconcile the positive effects of caffeine in some tests of repeated sprint performance, particularly because such effects have been observed from the start of each protocol (11,19).

Practical Applications

The removal of caffeine from the WADA list of controlled substances in 2004 opened up opportunities for athletes to exploit its ergogenic effects. In contrast to its established positive effects on endurance exercise, the results of this study show that caffeine has no effect on short-duration sprinting performance, regardless of the dosage used.


The authors would like to express their gratitude to all the participating subjects for their enthusiasm and commitment to this investigation and to St. Mary's University College, School of Human Sciences Research Support Fund for funding this research.


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methylxanthine; Wingate; supplementation; ergogenic

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