AIMS: To test the influence of caffeine on the lower and upper motor neuron excitability. METHODS: In Experiment A, 18 healthy subjects received 200 mg of caffeine or placebo, in a randomized, double-blind, placebo-controlled design protocol. Mean F-waves amplitude, amplitude of the motor response evoked by magnetic stimulation (MEP), MEP duration, cortical silent period (CSP), central conduction time, and cortical threshold were evaluated. In Experiment B, 6 healthy controls received 400 mg of caffeine, the peripheral silent period (PSP) and CSP were evaluated. CSP was recorded bilaterally in biceps brachii (intensity 10% above threshold) and abductor digiti minimi (ADM) (intensity at 10% and 50% above threshold). Muscle contraction was above 50% of the maximum force in both experiments. Latencies were defined by a technician who was not aware of this investigation. Serum caffeine level was evaluated. RESULTS: In Experiment A, only the CSP, recorded in both ADM with intensity at 10% above threshold showed a significant change after caffeine (decrease of 17.1+/-34.0 ms, about 12% reduction). In Experiment B, PSP did not change, but CSP tested with intensities 10% above threshold was significantly decreased by 20.8+/-34.4 ms in ADM and 13.5+/-13.8 ms in biceps (about 13 and 16%, respectively). Serum caffeine level clearly increased after consumption but no correlation could be found between these levels and CSP reduction. CONCLUSIONS: In our investigation, caffeine elicited a consistent decrease of the CSP, suggesting that caffeine increases cortical neuronal excitability.
RCT Entities:
AIMS: To test the influence of caffeine on the lower and upper motor neuron excitability. METHODS: In Experiment A, 18 healthy subjects received 200 mg of caffeine or placebo, in a randomized, double-blind, placebo-controlled design protocol. Mean F-waves amplitude, amplitude of the motor response evoked by magnetic stimulation (MEP), MEP duration, cortical silent period (CSP), central conduction time, and cortical threshold were evaluated. In Experiment B, 6 healthy controls received 400 mg of caffeine, the peripheral silent period (PSP) and CSP were evaluated. CSP was recorded bilaterally in biceps brachii (intensity 10% above threshold) and abductor digiti minimi (ADM) (intensity at 10% and 50% above threshold). Muscle contraction was above 50% of the maximum force in both experiments. Latencies were defined by a technician who was not aware of this investigation. Serum caffeine level was evaluated. RESULTS: In Experiment A, only the CSP, recorded in both ADM with intensity at 10% above threshold showed a significant change after caffeine (decrease of 17.1+/-34.0 ms, about 12% reduction). In Experiment B, PSP did not change, but CSP tested with intensities 10% above threshold was significantly decreased by 20.8+/-34.4 ms in ADM and 13.5+/-13.8 ms in biceps (about 13 and 16%, respectively). Serum caffeine level clearly increased after consumption but no correlation could be found between these levels and CSP reduction. CONCLUSIONS: In our investigation, caffeine elicited a consistent decrease of the CSP, suggesting that caffeine increases cortical neuronal excitability.
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