Carotid baroreflex control of central and peripheral hemodynamics during recovery after moderate leg cycling exercise.

This study aimed to examine the carotid baroreflex (CBR) control of the central and peripheral hemodynamics after exercise using the neck pressure (NP) and neck suction (NS) technique. Sixteen healthy young male participants (age: 27 ± 1.5 yr) were in a supine position for 30 min preexercise, followed by 60 min of cycling exercise, and then returned to a supine position for an additional 60 min postexercise. Both pre- and postexercise, the CBR-mediated responses of the central and peripheral hemodynamics were evaluated using 5-s periods of NP and NS (-60, -40, or +40 mmHg). As the central hemodynamics measurements, heart rate (HR), mean arterial pressure (MAP), cardiac output, and total vascular conductance were assessed. To determine peripheral circulation, vascular conductance in active and inactive limbs was measured. Eight participants [responder (RE) group] showed substantial postexercise hypotension (PEH) during recovery from exercise (Δ MAP: approximately -5 ± 0.9 mmHg, < 0.05). The other eight participants did not display a reduction in MAP after exercise (non-RE group). In the non-RE group, the responsiveness of CBR-mediated changes in HR, MAP, and vascular conductance increased, particularly in response to -40 mmHg NS during postexercise compared with preexercise. However, in the RE group, any alterations in responsiveness to NP and NS were unchanged during PEH compared with preexercise. In conclusion, some normotensive individuals do not show PEH because the responsiveness of the CBR in central and peripheral hemodynamics following exercise is augmented, particularly to high blood pressure. The carotid baroreflex (CBR) control of central and peripheral hemodynamics was investigated after exercise in both the presence and absence of postexercise hypotension (PEH). In individuals with no PEH, the responsiveness of CBR-mediated changes in all hemodynamics was augmented after exercise, particularly to high blood pressure; conversely, the CBR responsiveness remained unchanged in individuals with PEH. These findings provide insight into the mechanism of CBR control after exercise.