Aortic distensibility is reduced during intense lower body negative pressure and is related to low frequency power of systolic blood pressure.

As sympathetic activity approximately doubles during intense lower body negative pressure (LBNP) of -60 mmHg or greater, we examined the relationship between surrogate markers of sympathetic activation and central arterial distensibility during severe LBNP. Eight participants were exposed to progressive 8-min stages of LBNP of increasing intensity (-20, -40, -60, and -80 mmHg), while recording carotid-femoral pulse wave velocity (cPWV), stroke volume (SV), heart rate, and beat-by-beat blood pressure. The spectral power of low frequency oscillations in SBP (SBP(LF)) was used as a surrogate indicator of sympathetically modulated vasomotor modulation. Total arterial compliance (C) was calculated as C = SV/pulse pressure. Both cPWV and C were compared between baseline, 50 % of the maximally tolerated LBNP stage (LBNP(50)), and the maximum fully tolerated stage of LBNP (LBNP(max)). No change in mean arterial pressure (MAP) occurred over LBNP. An increase in cPWV (6.5 ± 2.2; 7.2 ± 1.4; 9.0 ± 2.5 m/s; P = 0.004) occurred during LBNP(max). Over progressive LBNP, SBP(LF) increased (8.5 ± 4.6; 9.3 ± 5.8; 16.1 ± 12.9 mmHg(2); P = 0.04) and C decreased significantly (18.3 ± 6.8; 14.3 ± 4.1; 11.6 ± 4.8 ml/mmHg × 10; P = 0.03). The mean correlation (r) between cPWV and SBP(LF) was 0.9 ± 0.03 (95 % CI 0.79-0.99). Severe LBNP increased central stiffness and reduced total arterial compliance. It appears that increased sympathetic vasomotor tone during LBNP is associated with reduced aortic distensibility in the absence of changes in MAP.