Neuromechanical features of the cardiac baroreflex after exercise.

A single bout of exercise is associated with postexercise hypotension, transient decreases in autonomic function, and changes in baroreflex sensitivity. The baroreflex is less sensitive to falling blood pressure than to rising blood pressure; we characterized the cardiac baroreflex in terms of hysteresis and its mechanical and neural components. We hypothesized that hysteresis would be exacerbated postexercise because of a greater relative decrease in falling blood pressure. In 10 healthy young humans (5 men), we used bolus injections of sodium nitroprusside and phenylephrine hydrochloride to drive transient decreases and increases in blood pressure, respectively, to quantify cardiac baroreflex sensitivity to falling and rising blood pressure. This was completed before and at 10, 30, and 60 minutes after 40 minutes of cycling at 60% estimated maximal oxygen consumption. Analyses of beat-to-beat blood pressure, R-R intervals and heart rate, and carotid artery diameter were used to determine the integrated cardiac baroreflex response; this was further quantified into a mechanical component (systolic blood pressure versus carotid diameter) and a neural component (carotid diameter versus R-R interval). There were 2 principle findings: after aerobic exercise baroreflex sensitivity is reduced and hysteresis manifests, and the reduction in sensitivity to falling blood pressure is mediated by decreased mechanical and neural gains, whereas the decreased baroreflex sensitivity to rising blood pressure is mediated by a reduced mechanical gain only. We suggest that impaired neural transduction of the cardiac baroreflex, and its influence on hysteresis, plays an important role in transient autonomic dysfunction after exercise.