The first rapid phase of the cardiac output (CO) kinetics at the onset of exercise is generally attributed to the sudden withdrawal of vagal tone. We hypothesized that a mechanical effect related to sudden increase in venous return at exercise onset might also play a role, by increasing stroke volume (SV) via the Frank-Starling mechanism. If this is so, applying increasing levels of lower body negative pressure (LBNP) would generate a progressively greater increase in phase I amplitude (A1) of SV at exercise onset, which may also affect A1 for CO. 8 subjects performed 3 transitions at 50 W in supine position, with 0 (control), -15, -30 and -45 mmHg of LBNP. The pulse pressure profile waveform of a left hand's finger was continuously recorded using Portapres device, allowing calculation of beat-by-beat CO, SV and heart rate (HR). Amplitude A1 of SV was significantly increased from 0 to -45 mmHg of LBNP. By contrast, A1 of HR was reduced with increasing LBNP level. As a consequence, A1 of CO exhibited only a trend (p = 0.06) to increase. The time constant of phase 1 was unaffected by LBNP exposure for either SV, HR or CO. The tested hypothesis was supported by the results in so far as A1 of SV was increased. However, this change did not translate into an equivalent change in CO, because of the concomitant reduction of A1 of HR. We conclude that the A1 of CO kinetics is indeed under dual control: neural and mechanical.