Effects of Prolonged Head-Down Bed Rest on Cardiac and Vascular Baroreceptor Modulation and Orthostatic Tolerance in Healthy Individuals

Abstract

Orthostatic intolerance commonly occurs after prolonged bed rest, thus increasing the risk of syncope and falls. Baroreflex-mediated adjustments of heart rate and sympathetic vasomotor activity (muscle sympathetic nerve activity – MSNA) are crucial for orthostatic tolerance. We hypothesized that prolonged bed rest deconditioning alters overall baroreceptor functioning, thereby reducing orthostatic tolerance in healthy volunteers. As part of the European Space Agency Medium-term Bed Rest protocol, 10 volunteers were studied before and after 21 days of −6° head down bed rest (HDBR). In both conditions, subjects underwent ECG, beat-by-beat blood pressure, respiratory activity, and MSNA recordings while supine (REST) and during a 15-min 80° head-up tilt (TILT) followed by a 3-min −10 mmHg stepwise increase of lower body negative pressure to pre-syncope. Cardiac baroreflex sensitivity (cBRS) was obtained in the time (sequence method) and frequency domain (spectrum and cross-spectrum analyses of RR interval and systolic arterial pressure – SAP, variability). Baroreceptor modulation of sympathetic discharge activity to the vessels (sBRS) was estimated by the slope of the regression line between the percentage of MSNA burst occurrence and diastolic arterial pressure. Orthostatic tolerance significantly decreased after HDBR (12 ± 0.6 min) compared to before (21 ± 0.6 min). While supine, heart rate, SAP, and cBRS were unchanged before and after HDBR, sBRS gain was slightly depressed after than before HDBR (sBRS: −6.0 ± 1.1 versus −2.9 ± 1.5 burst% × mmHg −1 , respectively). During TILT, HR was higher after than before HDBR (116 ± 4 b/min versus 100 ± 4 b/min, respectively), SAP was unmodified in both conditions, and cBRS indexes were lower after HDBR ( α index: 3.4 ± 0.7 ms/mmHg; BRS SEQ 4.0 ± 1.0) than before ( α index: 6.4 ± 1.0 ms/mmHg; BRS SEQ 6.8 ± 1.2). sBRS gain was significantly more depressed after HDBR than before (sBRS: −2.3 ± 0.7 versus −4.4 ± 0.4 burst% × mmHg −1 , respectively). Our findings suggest that baroreflex-mediated adjustments in heart rate and MSNA are impaired after prolonged bed rest. The mechanism likely contributes to the decrease in orthostatic tolerance.

Cardiac adaptations to 60 day head‐down‐tilt bed rest deconditioning. Findings from the AGBRESA study

“…Previous studies showed worsened cardiopulmonary fitness and orthostatic tolerance. 8 Yet we did not observe sustained reductions in left ventricular function assessed by systolic strain analysis in line with shorter duration bed rest studies. 9 Finally, myocardial mass did not change significantly, suggesting that cardiac atrophy is not a general feature during physical deconditioning and cannot be seen as risk factor for developing chronic heart failure.…”

Tolerability of daily intermittent or continuous short-arm centrifugation during 60-day 6o head down bed rest (AGBRESA study)

“…However, in both groups the incidence was very low, potentially due to the fact that subjects were permitted to perform isometric leg muscle pump exercises when experiencing symptoms. In the absence of countermeasures, bed rest deconditioning is associated with markedly reduced orthostatic tolerance [ 37 ]. Interestingly, we did not observe worsening tolerability of short-arm centrifugation over time suggesting that daily artificial gravity may have maintained orthostatic tolerance but this requires further evaluation including specific testing of orthostatic tolerance during bed rest [ 19 ].…”

Autonomic dysfunction in ‘long COVID’: rationale, physiology and management strategies

“…Prolonged bedrest (there have been extensive studies of head-down bedrest simulating chronic weightlessness in astronauts) leads to reduced cardiac output and stroke volume, hypovolaemia, baroreflex impairment, and withdrawal of the sympathetic neural response. [12][13][14][15]…”