Resetting of the arterial baroreflex is mediated by central (central command) or peripheral (exercise pressor reflex) mechanisms. The purpose of this study was to determine the effect of somatosensory input from skeletal muscle receptors on resetting of the carotid baroreceptor reflex. Resetting of the baroreflex was determined by measuring carotid sinus threshold pressure (Pth) during a ramp protocol that consisted of a linear increase in sinus pressure from 50 to 250 mmHg at approximately 3 mmHg/s. Experiments were performed in seven alpha-chloralose-anesthetized and vagotomized dogs. To determine the effect of skeletal muscle afferent input on resetting, electrically induced muscle contraction was used to activate mechanically and metabolically senstive afferent fibers, whereas passive stretch of the hindlimb was used to activate predominantly mechanically sensitive afferent fibers. Pth for heart rate (HR) and arterial blood pressure (BP) during the control ramp protocol was 110 +/- 4 and 118 +/- 7 mmHg, respectively. Electrically induced muscle contraction increased hindlimb tension (5.7 +/- 0.4 kg) and significantly increased Pth-HR and Pth-BP above control (135 +/- 6 and 141 +/- 5 mmHg, respectively; P < 0.05). Muscle paralysis prevented the increase in Pth-HR and Pth-BP during ventral root stimulation (104 +/- 7 and 116 +/- 5 mmHg, respectively; P = not significant). Passive muscle stretch (n = 3) increased hindlimb tension (5.9 +/- 0.9 kg) and significantly increased Pth-BP (125 +/- 21 vs. 159 +/- 16 mmHg, control vs. contraction; P < 0.05). There was no difference in the magnitude of Pth resetting between muscle contraction or stretch. The present study demonstrates that activation of skeletal muscle afferent fibers, by either muscle contraction or stretch, increases Pth of the carotid baroreflex. Therefore, neural input from skeletal muscle receptors resets the carotid baroreflex in a manner similar to that ascribed by central command.