The objective of this study was to evaluate the changes in the portal vein cross-sectional area (PV CSA) and flow during a stand test associated with orthostatic intolerance. Eighteen subjects underwent a 90-day head-down tilt (HDT) bed rest at 6 degrees: 9 controls (Con) and 9 with flywheel exercise countermeasures (CM). At post-HDT, nine subjects (5 CM, 4 Con) were tolerant, and nine were intolerant. The PV CSA was measured by echography. We found that at HDT day 85, the PV CSA at rest had increased less in the CM subjects than in the Con (+12 vs. +27% from pre-HDT supine; P < 0.05), whereas it increased similarly in tolerant and intolerant subjects (23 and 16%, respectively). Two days after the HDT, there was a decrease in the PV CSA supine compared with the pre-HDT PV CSA supine that was similar for all groups (Con: -11%, CM: -21%; tolerant: -10%, intolerant: -16%; P < 0.05). The PV CSA decreased significantly less from supine to standing in the Con than in the CM group (-2 vs. -10% compared with the pre-HDT stand test; P < 0.05). The PV CSA also decreased significantly from supine to standing compared with the pre-HDT stand test in the tolerant group but not in the intolerant group (-20 vs. +2%; P < 0.05). From these findings, we conclude the following. 1) Because the portal vein is the only output from the splanchnic vascular area, we suggest that the lower reduction in the PV CSA and flow associated with orthostatic intolerance was related to a lower splanchnic arterial vasoconstriction. 2) The flywheel exercise CM helped to reduce the distention of the splanchnic network at rest and to maintain partially the splanchnic vasoconstriction, but it did not reduce the orthostatic intolerance.
Our understanding of the impact of long-duration head-down bed rest (HDBR) on sympathetic neurovascular regulation during orthostatic stress remains incomplete. Through retrospective analysis of the WISE-2005 long-duration bed rest trial, this study aimed to investigate the impact of 60 days of -6° HDBR on the transduction of integrated muscle sympathetic nerve activity (MSNA; peroneal microneurography) into total peripheral resistance (TPR; Finometer Modelflow) responses during rest and graded lower body negative pressure (LBNP; -20, -30, and -45 mmHg). Signal averaging quantified sympathetic transduction for 12 cardiac cycles (ECG) following integrated MSNA bursts in healthy females ( n = 12; 25-40 years). Mixed-effects modeling and post-hoct-tests assessed the impact of HDBR on sympathetic transduction during rest (5-min) and graded LBNP (3-min per level). Data are presented as mean ± SD. Long-duration HDBR did not affect resting total MSNA (pre-HDBR: 909 ± 368 AU/min, post-HDBR: 910 ± 254 AU/min; p = 0.999). HDBR did not affect total MSNA responses to -20 mmHg LBNP (pre-HDBR: 1430 ± 599 AU/min, post-HDBR: 1823 ± 433 AU/min), -30 mmHg LBNP (pre-HDBR: 1574 ± 549 AU/min, post-HDBR: 1924 ± 587 AU/min), or -45 mmHg LBNP (pre-HDBR: 1950 ± 819 AU/min, post-HDBR: 2328 ± 880 AU/min; p = 0.191). HDBR did not affect resting sympathetic transduction to TPR (pre-HDBR: 0.002 ± 0.16 mmHg/L/min, post-HDBR: -0.091 ± 0.12 mmHg/L/min; p = 0.296). However, HDBR augmented TPR transduction responses to graded LBNP (HDBR-by-LBNP interaction: p = 0.050). Pre-HDBR, TPR transduction responses were unchanged with graded LBNP (all p > 0.05). In contrast, post-HDBR, TPR transduction responses increased progressively with graded LBNP (rest: -0.09 ± 0.12 mmHg/L/min, -20 mmHg: 0.22 ± 0.31 mmHg/L/min, -30 mmHg: 0.30 ± 0.34 mmHg/L/min, -45 mmHg: 0.44 ± 0.12 mmHg/L/min; all p < 0.005). The same effect of HDBR was observed when sympathetic transduction of mean arterial pressure was analyzed (data not shown). These data suggest that long-duration HDBR augments sympathetic neurovascular responses to integrated MSNA bursts during orthostatic stress among females. This work was supported by the Canadian Space Agency, the French “Centre National d’Etudes Spatiales”, the European Space Agency, and the National Aeronautics and Space Administration of the USA. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Lower body negative pressure (LBNP) and head down bed rest (HDBR) are protocols used to simulate hypovolemia and cardiovascular deconditioning, causing an alteration of autonomic control of circulation. The objective of this study was to investigate the combined effects of LBNP and bed rest on cardiac baroreflex sensitivity (BRS). RR and systolic blood pressure (SBP) recordings from seven volunteers were analyzed during a mild LBNP protocol consisting of three different levels of LBNP (-10 mmHg, -20 mmHg, -30 mmHg) before (pre-HDBR) and on day 50 of a HDBR study. Spectra of RR and SBP were computed and BRS was assessed in the low frequency (LF) and high frequency (HF) bands through a bivariate model that takes into account the causal relationships between heart rate (HR) and arterial blood pressure. HR significantly increased from BL in HDBR for LBNP≤-20 mmHg. BRS gain decreased significantly in the LF band with increasing levels of LBNP in both conditions. BRS gain was significantly lower on day 50 of HDBR with respect to pre-HDBR at -20 mmHg. These data suggest that BRS in the LF range is reduced in bed rest, and these changes may be due primarily to a reduction in plasma volume associated with bed rest, which impact the physiological responses of autonomic control of circulation.
The objectives to determine both the contribution to orthostatic intolerance (OI) of calf venous volume during a stand-test, and the effects of a combined eccentric-concentric resistance exercise countermeasure on both vein response to orthostatic test and OI, after 90-day head-down tilt bed-rest (HDT). The subjects consisted of a control group (Co-gr, n = 9) and an exercise countermeasure group (CM-gr, n = 9). Calf volume and vein cross-sectional area (CSA) were assessed by plethysmography and echography during pre- and post-HDT stand-tests. From supine to standing (post-HDT), the tibial and gastrocnemius vein CSA increased significantly in intolerant subjects (tibial vein, +122% from pre-HDT; gastrocnemius veins, +145%; P < 0.05) whereas it did not in tolerant subjects. Intolerant subjects tended to have a higher increase in calf filling volume than tolerant subjects, in both sitting and standing positions. The countermeasure did not reduce OI. Absolute calf volume decreased similarly in both groups. Tibial and gastrocnemius vein CSA at rest did not change during HDT in either group. During the post-HDT stand-test, the calf filling volume increased more in the CM-gr than in the Co-gr both in the sitting (+1.3 +/- 5.1%, vs. -7.3 +/- 4.3%; P < 0.05) and the standing positions (+56.1 +/- 23.7% vs. +1.6 +/- 9.6%; P < 0.05). The volume ejected by the muscle venous pump increased only in the CM-gr (+38.3 +/- 21.8%). This study showed that intolerant subjects had a higher increase in vein CSA in the standing position and a tendency to present a higher calf filling volume in the sitting and standing positions. It also showed that a combined eccentric-concentric resistance exercise countermeasure had no effects on either post-HDT OI or on the venous parameters related to it.
The objective was to check, during a lower body negative pressure (LBNP) test, new vascular parameters for the detection of orthostatic intolerance induced by head-down-tilt (HDT) and spaceflight.The lower-limb volume flow and vascular resistance were evaluated by Doppler ultrasound. The HDT population consisted of two groups: control [6 subjects resting in a HDT (-6 degrees) position for 28 d] and countermeasure (6 subjects also in HDT for 28 d, but with repeated LBNP and exercise). The LBNP orthostatic test (four steps: -20, -30, -40, -50 mm Hg, of 3 min each) was performed before, during, and after the HDT. For the 14-d spaceflight (Antares) the cosmonaut underwent the LBNP test (10 min at -25 mm Hg and 10 min at -45 mm Hg), at preflight (3 times), inflight (day 11), and postflight (twice).HDT--As the LBNP pressure decreased, the femoral blood flow decreased and the lower-limb vascular resistances increased in both HDT groups. In the control group the femoral flow was less reduced, at each of the 4 levels of depressure (p < 0.01). The amplitude of the leg vascular resistances was reduced at -40 mm Hg, and at -50 mm Hg, on HDT day 15 in both groups (before LBNP, after 1 week's exercise for the countermeasure group), and on post-HDT day 1 (p < 0.01) only in the control group. The femoral vascular resistance response had completely recovered in the countermeasure group on post-HDT day 1. During the post-HDT tilt table test, all 6 controls had a drop in blood pressure of 20 mm Hg (4 subjects) or 10 mm Hg (2 subjects); 3 had pre-syncopal symptoms. The HDT countermeasure subjects had neither any clinical signs of orthostatic intolerance nor any blood pressure drop. 14d-Spaceflight--During the flight, the cosmonaut did not use any countermeasures (exercise, LBNP). On flight day +11, and on postflight day 3, the femoral vascular resistance response to LBNP was decreased as observed in the control group on HDT day +15 and post HDT. On postflight day 7, the femoral response had completely recovered. The middle cerebral flow response to the various pre-, in-, and postflight LBNP tests consisted of a slight decrease of the cerebral flow together with resistances of comparable amplitude (-10 to -20%) to those measured during the same LBNP test in the HDT control group.The femoral hemodynamics are much more disturbed than the cerebral ones in vascular deconditioning. The assessment of the lower limb vascular reactivity will be of interest in predicting orthostatic intolerance, and checking the efficiency of counter-measures.
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