This study analysed the effect of selective beta(1)-blockade on neuromuscular recruitment characteristics during progressive endurance exercise. Ten healthy subjects ingested a selective beta(1)-blocker, acebutolol (200 mg b.d.), for 7 days (for one of two cycling trials), with a 10-day wash-out period between trials. On the last day of acebutolol ingestion subjects performed three successive 15-min rides at 30%, 50% and 70% of their peak power output and then cycled at increasing (15 W min(-1)) work rates to exhaustion. Force output, heart rate, submaximal VO(2), rate of perceived exertion (RPE), electromyographic (EMG) data and blood lactate were captured during the cycling activity. Peak work rate [270 (111) W vs 197 (75) W, CON vs BETA, P <0.01], time to exhaustion [49.7 (23.2) min vs 40.3 (23.7) min, CON vs BETA, P <0.05] and heart rate [mean, for the full ride 135.5 (38.3) beats min(-1) vs 111.5 (30.0) beats min(-1) CON vs BETA, P <0.05] were significantly lower for the group who ingested beta(1)-blockade (BETA) compared to the control group (CON). Although not significant, submaximal VO(2)was reduced in BETA during the ride, while RPE was significantly higher during the ride for BETA (P <0.01). Mean integrated electromyography was higher in the BETA group although these differences were not significant. Mean power frequency values of the BETA group showed a significant (P <0.05) shift to the upper end of the spectrum in comparison to the control group. Lactate values [11.7 (3.5) mmol x l(-1) vs 7.1 (4.1) mmol x l(-1)CON vs BETA] were significantly lower (P <0.05) at exhaustion in BETA. Significant reductions in cycling performance were found when subjects ingested beta(1)-blockers. This study has shown significant shifts to the upper end of the EMG frequency spectrum after beta(1)-blocker ingestion, which could be caused by a change in neuromuscular recruitment strategy to compensate for the impaired submaximal exercise performance.