A single bout of exercise is associated with post-exercise hypotension, changes in baroreflex sensitivity (BRS), and decreases in autonomic function lasting 20-60 minutes. These changes, in part, underline the increased occurrence of syncope at this time point. Furthermore, the baroreflex exhibits hysteresis; that is, it is less sensitive to falls in blood pressure (Gdown) than to rises in blood pressure (Gup). To better understand baroreflex changes following exercise, we aimed to characterize cardiac baroreflex hysteresis, and describe any alterations in terms of the respective contributions of the mechanical and neural segments of the baroreflex. Based on known changes in orthostatic tolerance, we hypothesized that hysteresis would be exacerbated following exercise due to greater post-exercise decreases in Gdown. In 9 healthy young humans (five male), we used bolus injections of sodium nitroprusside and phenylephrine hydrochloride to drive transient decreases and increases in blood pressure, respectively, in order to quantify BRS to rising and falling blood pressure (the modified Oxford technique). This intervention was completed before, and at 10, 30, and 60 minutes following 40 minutes of cycling at 60% of maximal oxygen consumption. Analysis of beat-to-beat blood pressure, R-R intervals, and carotid arterial diameter were used to determine the integrated cardiac baroreflex response; this was further quantified into two components – the “mechanical component” i.e., the transduction of systolic blood pressure into carotid stretch; and the “neural component” i.e., transduction of stretch into R-R interval changes. There were two principle findings of the present study: (1) Baroreflex hysteresis was exacerbated as reflected in a greater decrease in Gdown than Gup at 10 and 30 minutes post-exercise (paired t-test, Gdown vs. Gup; p < 0.05). The responsible mechanism of gain attenuation was different for rising versus falling blood pressure. The reduction in Gdown was mediated via selective reductions in the neural component, whereas, the reduction in Gup was mediated by selective reductions in the mechanical component. (2) The increased hysteresis following exercise was entirely attributable to increased neural, but not mechanical, hysteresis. The ability of the baroreflex to respond to hypotensive stimuli is likely attenuated following exercise due to reductions in neural baroreflex gain. These data have implications for the understanding of the occurrence of syncope following exercise. We suggest that despite vascular changes known to occur post-exercise, neural mechanisms are responsible for decreased orthostatic tolerance following exercise.