Purpose <p>We aimed to clarify the mechanism for presyncope, defined as the gradual onset of hypotension, starting some minutes before vasovagal syncope. Although there is a fall in cardiac output and usually vasodilatation, the control of sympathetic activity during presyncope is uncertain.</p> Methods <p>We retrospectively compared haemodynamics and muscle sympathetic nerve activity levels from positive tilt tests (without provocation) in patients with known vasovagal syncope (age 41 ± 3 years, 13 female, <i>n</i> = 27) to controls (age 39 ± 3 years, 8 female, <i>n</i> = 13). We used sequence methods to measure vascular sympathetic and cardiovagal baroreflex gain at baseline (lying supine) during tilt, presyncope and recovery.</p> Results <p>Patients were tilted for 18.1 ± 1&#xa0;min, and mean arterial pressure fell to 62 ± 3&#xa0;mmHg before tilt-back. At baseline and early tilt, all haemodynamic variables were similar to controls, however sympathetic baroreflex gain was increased: −2.7 ± 0.2 bursts/100 beats/mmHg versus −2.0 ± 0.3 (<i>p</i> = 0.03). Cardiovagal baroreflex gain was increased at baseline 11.8 ± 0.6&#xa0;ms/mmHg versus 9.3 ± 0.8 (<i>p</i> = 0.02). During early presyncope (from 8 to 4&#xa0;min before tilt-back), sympathetic baroreflex gain fell to −2.4 bursts/100 b/mmHg and thereafter to −0.5 ± 0.3 (<i>p</i> = 0.01) during late presyncope, before losing correlation with mean arterial pressure. In some patients, the regression coefficient reversed before correlation was lost (<i>n</i> = 8) but this did not result in lower levels of nerve activity. At tilt-back, nerve activity fell below baseline levels in at least 63% of patients.</p> Conclusion <p>Presyncope appeared to be initiated by a fall in sympathetic baroreflex gain despite increased levels at baseline and early tilt.</p>