This study evaluated the influence of central command and muscle afferent stimulation (mechanical and chemical) on the integrated arterial baroreflex control of the sinus node during dynamic exercise. Twenty-two healthy men performed voluntary knee extension and electrically induced dynamic knee extension under free-flow and arrested-flow (n = 18) conditions. Systolic arterial pressure (SAP) and pulse interval (PI) were measured continuously and noninvasively. The arterial baroreflex was evaluated by analyzing the slopes of sequences of three or more consecutive beats characterized by the SAP and PI of the following beat; both increased or decreased in a linear fashion. Compared with rest, both voluntary exercise and electrically induced exercise under arrested-flow conditions resulted in a maintained baroreflex sensitivity (BRS; 11.7 +/- 1.2 vs. 9.6 +/- 0.7 and 11.3 +/- 1.4 vs. 9.8 +/- 1.5 ms/mmHg, respectively; not significant), with an apparent rightward shift in the regression line relating SAP to PI. Electrically induced exercise under free-flow conditions resulted in a significant decrease in BRS (12.1 +/- 1.4 vs. 8.8 +/- 0.8 ms/mmHg; P < 0.05). These data suggest that the central command and muscle chemoreflex act to preserve the BRS, possibly "resetting" the baroreceptor-cardiac response relationship, whereas stimulation of mechanosensitive receptors appears capable of modifying the integrated baroreflex control of sinus node function in humans. The first two mechanisms seem, however, to overwhelm the latter to maintain BRS, thus permitting a concomitant increase in arterial pressure and heart rate.