TY - JOUR
T1 - The effect of lower body negative pressure on phase 1 cardiovascular responses at exercise onset in healthy humans
AU - Fontolliet, T
AU - Fagoni, N
AU - Bruseghini, Paolo
AU - Capelli, C
AU - Lador, F
AU - Moia, C1 Tam E
AU - Bringard, A
AU - Ferretti, G
PY - 2019
Y1 - 2019
N2 - We tested the hypothesis that vagal withdrawal and increased venous return interact in determining the rapid cardiac output response (Phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood dislocation to the heart by muscle pump action and simultaneously reduce resting vagal activity. At exercise start, we expected larger response amplitude for stroke volume and smaller for heart rate at progressively stronger LBNP levels, so that the cardiac output response would remain unchanged. Ten subjects performed 50 W exercise supine in Control condition and during -45 mmHg LBNP exposure. On single beat basis, we measured heart rate (HR), stroke volume (SV), and we calculated cardiac output (CO). We computed Phase I response amplitudes (A1) using an exponential model. SV A1 was higher under LBNP than in Control (p < 0.05). Conversely, the A1 of HR, was 23 ± 56 % lower under LBNP than in Control (although NS). Since these changes tended to compensate each other, the A1 for CO was unaffected by LBNP. The rapid SV kinetics at exercise onset is compatible with an effect of increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR kinetics. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, as hypothesized, one acting on SV, the other on HR
AB - We tested the hypothesis that vagal withdrawal and increased venous return interact in determining the rapid cardiac output response (Phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood dislocation to the heart by muscle pump action and simultaneously reduce resting vagal activity. At exercise start, we expected larger response amplitude for stroke volume and smaller for heart rate at progressively stronger LBNP levels, so that the cardiac output response would remain unchanged. Ten subjects performed 50 W exercise supine in Control condition and during -45 mmHg LBNP exposure. On single beat basis, we measured heart rate (HR), stroke volume (SV), and we calculated cardiac output (CO). We computed Phase I response amplitudes (A1) using an exponential model. SV A1 was higher under LBNP than in Control (p < 0.05). Conversely, the A1 of HR, was 23 ± 56 % lower under LBNP than in Control (although NS). Since these changes tended to compensate each other, the A1 for CO was unaffected by LBNP. The rapid SV kinetics at exercise onset is compatible with an effect of increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR kinetics. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, as hypothesized, one acting on SV, the other on HR
KW - cardiovascular responses
KW - lower body negative pressure
KW - cardiovascular responses
KW - lower body negative pressure
UR - https://publicatt.unicatt.it/handle/10807/215557
M3 - Conference article
SN - 1748-1716
VL - 227
SP - 175
EP - 176
JO - Acta Physiologica
JF - Acta Physiologica
IS - s718
ER -