Wingate performance and surface EMG frequency variables are not affected by caffeine ingestion.

The ergogenic effect of caffeine and its mechanism of action on short-term, high-intensity exercise are controversial. One proposed mechanism is caffeine's stimulatory effect on the central nervous system and thus, motor-unit excitation. The latter is non-invasively determined from surface electromyographic signal (EMG) frequency measures. The purpose of this study was to determine if power output and surface EMG frequency variables during high-intensity cycling were altered following caffeine ingestion. Eighteen recreationally active college males (mean +/- SD age, 21.5 +/- 1.8 y; height, 181.8 +/- 0.5 cm; body mass, 84.7 +/- 11.4 kg) performed the Wingate test (WG) after ingestion of gelatin capsules containing either placebo (PL; dextrose) or caffeine (CAFF; 5 mg/kg body mass). The trials were separated by 1 week and subjects were asked to withdraw from all caffeine-containing products for 48 h before each trial. From the resulting power-time records, peak power (PP; highest power output in 5 s), minimum power (MP; lowest power output in 5 s), and the percent decline in power (Pd) were calculated. Surface EMG records of the right vastus lateralis (VL) and the gastrocnemius (GA) muscles corresponding to the PP and MP periods were collected and used to determine the integrated electromyogram (IEMG), the mean (MNPF), and the median (MDPF) of the signal's power spectrum. A 2-way repeated measures analysis of variance (ANOVA) (treatment x time) was conducted to determine the effect of caffeine on these variables across levels of time. Caffeine ingestion had no effect on PP (PL, 1049 +/- 192 W; CAFF, 1098 +/- 198 W), MP (PL, 762 +/- 104 W; CAFF, 802 +/- 124 W), or the Pd (PL, 47% +/- 8.9%; CAFF, 48.2% +/- 7.3%) compared with the placebo. For both muscles, MNPF and MDPF diminished significantly (p < 0.001) across time and to a similar degree in both the CAFF and PL trials. Regardless of muscle, CAFF had no effect on the percent change in IEMG from the first 5 s to the last 5 s. For both treatments, the GA displayed a significantly (p < 0.05) greater pre vs. post percent decline in the EMG signal amplitude compared with the VL. These results indicate that caffeine does not impact power output during a 30 s high-intensity cycling bout. Furthermore, these data suggest that caffeine does not impact the neuromuscular drive as indicated by the similar IEMG scores between treatments. Similarly, caffeine does not seem to impact the frequency content of the surface EMG signal and thus the nature of recruited motor units before and after the expression of fatigue. The lack of decline in the IEMG in the VL despite the decline in power output over the course of the WG suggests a peripheral as opposed to a neural mechanism of fatigue in this muscle. The significant difference in the pre vs. post percent decline in the GA IEMG score further supports this notion. The pre vs. post decline in the IEMG noted in the GA may suggest a fatigue-triggered change in pedaling mechanics that may promote dominance of knee extensors with less reliance on plantar flexors.

RCT Entities:   Population Interventions Outcomes