Abstract

Caffeine is usually consumed in the form of tea, coffee, chocolate products as well as carbonated beverages and is one of the most popular drugs [1]. There is evidence that caffeine increases endurance and short-term, high-intensity exercise performance [2]. However, the effect of caffeine on maximal voluntary contraction strength and neural activation during different contraction modes is less clear. PURPOSE: Therefore, this study investigated effects of caffeine ingestion (8 mg/kg) on maximum voluntary torque (MVT) and neural activation of the quadriceps muscle during isometric, concentric and eccentric contractions. METHODS: Fourteen subjects ingested caffeine and placebo in a randomized, controlled, counterbalanced, double-blind crossover design. Neuromuscular tests were performed before and 1 h after oral caffeine and placebo intake. MVTs were measured and the interpolated twitch technique was applied during isometric, concentric and eccentric contractions to assess voluntary activation. Furthermore, normalized root mean square of the EMG signal was calculated and evoked spinal reflex responses (H-reflex evoked at rest and during weak isometric voluntary contraction) as well as contractile properties of the quadriceps were analyzed. RESULTS: Caffeine increased MVT by 26.4 N•m (+13.7%, 95%CI: 9.3-43.5 N•m, P = 0.004), 22.5 N•m (+13.9%, 95%CI: 3.1-42.0 N•m, P = 0.025) and 22.5 N•m (+11.7%, 95%CI: 2.2-42.7 N•m, P = 0.032) for isometric, concentric and eccentric contractions. Strength enhancements were associated with increases in voluntary activation. Isometric explosive voluntary strength and neural activation at the onset of contraction were significantly increased following caffeine ingestion. Changes in spinal reflex responses and contractile properties were not observed. CONCLUSIONS: Data suggest that caffeine ingestion induced acute neural adaptations that were responsible for the increased strength and neural activation regardless of the contraction mode. The results indicate that strength gains were due to alterations of excitability at the supraspinal site rather than changes in spinal excitability. REFERENCES 1. Harland BF, Nutrition. 16:522-6, 2000. 2. Burke LM, Appl Physiol Nutr Metab. 33:1319-34, 2008.

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