LBNP Effect On Rapid Changes In Stroke Volume And Cardiac Output At Exercise Onset

PURPOSE: The kinetics of cardiac output (CO) at the onset of exercise is characterized by two phases. The first rapid phase (phase I), which has a time constant of less than 5 s, is generally attributed to the sudden withdrawal of vagal tone. Yet the hypothesis was put forward that a mechanical effect related to sudden increase in venous return at exercise start might also play a role, especially by increasing stroke volume (SV) via the Frank-Starling mechanism. If the latter was the case, then application of increasing levels of lower body negative pressure (LBNP) would generate a progressively greater increase in phase I amplitude (A1) of SV at exercise start, which may also affect A1 for CO. METHODS: To test this hypothesis, 8 healthy subjects (24.8 ± 5.0 years) repeated 3 transitions of 5 min moderate (50 W) pedaling exercise in supine position, with 0 (control), -15, -30 and -45 mmHg of LBNP. The pulse pressure waveform of a left hand’s finger was continuously recorded using Portapres device, allowing calculation of CO, SV and heart rate (HR) on a beat-by-beat basis using Modelflow method (Wesseling et al., 1993). After superimposition of the 3 transitions, kinetics of CO, SV and HR were fitted using bi-exponential model, and the amplitude of phase one (A1) amongst the 4 conditions was compared using repeated ANOVA (with Tukey post-hoc test). RESULTS: A1 of SV was significantly increased from 7.5 ± 3.7 and 9.5 ± 3.8 to 16.7 ± 12.4 and 21.4 ± 7.9 ml, for 0 (control), -15, -30 and -45 mmHg of LBNP respectively. By contrast, A1 of HR was reduced (p = 0.05) with increasing LBNP level. As a consequence, A1 of CO exhibited only a trend (p = 0.06) to increase from 1.93 ± 0.79 to 2.42 ± 0.72, 3.01 ± 1.47 and 3.19 ± 0.82 l.min-1, for 0 (control), -15, -30 and -45 mmHg of LBNP respectively. The time constant of phase 1 was ranged between 1.5 and 3.5 s and remained unaffected by LBNP exposure for either SV, HR or CO. CONCLUSIONS: 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, possibly due to a weaker vagal activity during LBNP exposure before exercise started. We conclude that the amplitude of the first phase of CO kinetics is indeed under dual control: neural and mechanical