The influence of cyclist’s performance level on caffeine-induced increases in neuromuscular fatigue after a 4-km cycling TT was investigated. Nineteen cyclists performed a 4-km cycling TT one hour after ingesting caffeine (5 mg‧kg-1) or placebo (cellulose). Changes from baseline to post-exercise in voluntary activation (VA) and potentiated 1 Hz force twitch (Qtw,pot) were used as markers of central and peripheral fatigue, respectively. Participants were classified as “high-performing” (HP, n=8) or “low-performing” (LP, n=8) in accordance with their performance in placebo trial. Compared with placebo, caffeine increased the power, the anaerobic mechanical power and the anaerobic work, reducing the time to complete the trial for both groups (p<0.05). There was a group vs. supplement and group vs. supplement vs. trial interaction for Qtw,pot, where the post-exercise reduction was higher after caffeine compared with placebo in LP (Qtw,pot=–34±17 vs. –21±11%, p=0.02) but not in HP (Qtw,pot=–22±8 vs. –23±10%, p=0.64). There was no effect of caffeine on VA, but there was a group vs. trial interaction with lower post-exercise values in LP than in HP (p=0.03). Caffeine-induced improvement on 4-km cycling TT performance seems to be at the expense of greater locomotor muscle fatigue in low- but not in high-performing cyclists. BULLET POINTS -Caffeine improves exercise performance at the expense of a greater end-exercise peripheral fatigue in low-performing athletes. -Caffeine-induced improvement on exercise performance does not affect end-exercise peripheral fatigue in high-performing athletes. -High-performing athletes seems to have augmented tolerance to central fatigue during a high-intensity time-trial.

Purpose: In the present study, we tested the hypothesis that caffeine would increase endurance performance via attenuation of neural and muscular determinants of performance fatigability during high-intensity, whole-body exercise. Methods: Ten healthy males cycled until exhaustion (89% ± 2% of VO 2max ) after the ingestion of caffeine or placebo. During another four visits, the same exercise was performed after either caffeine or placebo ingestion but with exercise discontinued after completing either 50% or 75% of the duration of placebo trial. An additional trial with caffeine ingestion was also performed with interruption at the placebo time to exhaustion (isotime). Performance fatigability was measured via changes in maximal voluntary contraction, whereas neural and muscular determinants of performance fatigability were quantified via preexercise to postexercise decrease in quadriceps voluntary activation (VA) and potentiated twitch force, respectively. Results: Compared with the placebo, caffeine increased time to exhaustion (+14.4 ± 1.6%, P = 0.017, 314.4 ± 47.9 vs 354.9 ± 40.8 s). Caffeine did not change the rate of decline in maximal voluntary contraction (P = 0.209), but caffeine reduced the twitch force decline at isotime when stimulating at single twitch (−58.6 ± 22.4 vs À45.7 ± 21.9%, P = 0.014) and paired 10 Hz electrical stimuli (−37.3 ± 13.2 vs À28.2 ± 12.9%, P = 0.025), and reduced the amplitude of electromyography signal during cycling at isotime (P = 0.034). The decline in VA throughout the trial was lower (P = 0.004) with caffeine (−0.5 ± 4.2%) than with placebo (−5.8 ± 8.5%). Caffeine also maintained peripheral oxygen saturation at higher levels (95.0 ± 1.9%) than placebo (92.0 ± 6.2%, P = 0.016). Conclusions: Caffeine ingestion improves performance during high-intensity, whole-body exercise via attenuation of exercise-induced reduction in VA and contractile function.

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