The aim of this study was to determine if inducing metabolic alkalosis would alter neuromuscular control after 50 min of standardized submaximal cycling. Eight trained male cyclists (mean age 32 years, s = 7; [Vdot]O(2max) 62 ml . kg(-1) x min(-1), s = 8) ingested capsules containing either CaCO(3) (placebo) or NaHCO(3) (0.3 g x kg(-1) body mass) in eight doses over 2 h on two separate occasions, commencing 3 h before exercise. Participants performed three maximal isometric voluntary contractions (MVC) of the knee extensors while determining the central activation ratio by superimposing electrical stimulation both pre-ingestion and post-exercise, followed by a 50-s sustained maximal contraction in which force, EMG amplitude, and muscle fibre conduction velocity were assessed. Plasma pH, blood base excess, and plasma HCO(3) were higher (P < 0.01) during the NaHCO(3) trial. After cycling, muscle fibre conduction velocity was higher (P < 0.05) during the 50-s sustained maximal contraction with NaHCO(3) than with placebo (5.1 m x s(-1), s = 0.4 vs. 4.2 m x s(-1), s = 0.4) while the EMG amplitude remained the same. Force decline rate was less (P < 0.05) during alkalosis-sustained maximal contraction and no differences were shown in central activation ratio. These data indicate that induced metabolic alkalosis can increase muscle fibre conduction velocity following prolonged submaximal cycling.