Sixty Days of Head‐Down Tilt Bed Rest Augments Muscle Sympathetic Nerve Activity Responses to Maximal End‐Inspiratory Apnea: Evaluation of Sympathetic Neural Recruitment Strategies
Authors: Klassen Stephen A. , De Abreu Steven , Denise Pierre , Shoemaker J. Kevin , Normand Hervé 
Published: November 2023

The objective of this study was to evaluate the impact of 60‐days head‐down tilt (−6°) bed rest (HDBR) on muscle sympathetic nerve activity (MSNA) responses to a maximal end‐inspiratory apnea (apnea) and the sympathetic neural recruitment strategies underlying the MSNA response. Thirteen male individuals (n = 13, 30 ± 2 yr, 180.7 ± 1.5 cm, 77.7 ± 1.8 kg, 23.8 ± 0.4 kg/m2) provided baseline MSNA data pre‐ and post‐HDBR, whereas eight participants provided complete apnea data as well. Heart rate (HR; ECG), blood pressure (Finometer) and MSNA (microneurography) were measured pre‐ and post‐HDBR, during ~3‐min of baseline and the last ~30‐s of a maximal end‐inspiratory apnea (apnea). Sympathetic action potentials (AP) were detected from the filtered raw MSNA signal using AP detection software. APs were binned based on peak‐to‐peak amplitude into clusters defined by Scott's rule. Values are mean ± SE. Apnea duration was 74 ± 5 s in the pre‐ and 85 ± 7 s in the post‐HDBR conditions (P = 0.09). Baseline mean arterial pressure (MAP; 104 ± 5 to 94 ± 4 mmHg, P = 0.04) and pulse pressure (PP; 59 ± 3 to 50 ± 4 mmHg, P < 0.01) were reduced with HDBR. MAP during apnea (112 ± 5 to 103 ± 4 mmHg, P = 0.14) was similar pre‐ and post‐HDBR, while PP during apnea (55 ± 3 to 49 ± 4 mmHg, P = 0.06) trended towards being reduced in the post‐HDBR session. HR was similar across testing sessions at baseline (66 ± 2 to 68 ± 5 bpm, P = 0.24) and during apnea (66 ± 2 to 70 ± 2 bpm, P = 0.17). Baseline integrated MSNA (burst frequency: 13 ± 2 to 18 ± 2 bursts/min; burst incidence: 20 ± 2 to 27 ± 4 bursts/100beats, all P > 0.05) and baseline AP indices (AP frequency: 62 ± 22 to 106 ± 27 spikes/min; AP incidence: 92 ± 31 to 159 ± 40 spikes/100 beats; AP/burst: 4 ± 0.8 to 6 ± 0.9 spikes/burst; active clusters/burst: 3 ± 0.3 to 3 ± 0.4 clusters/burst; total clusters: 7 ± 0.9 to 9 ± 0.6 clusters, all P > 0.05) were similar pre‐ and post‐ HDBR. However, the change in integrated MSNA burst frequency, from baseline to apnea, was greater post‐HDBR (Δ 28 ± 3 bursts/min) than pre‐HDBR (Δ 15 ± 2, P < 0.01). This exaggerated response to apnea post‐HDBR was a function of increased AP firing frequency (pre‐HDBR, post‐HDBR: Δ 94 ± 25, Δ 317 ± 55 AP/min, P < 0.01). Although the change in integrated burst amplitude, from baseline to apnea, was similar pre‐ (Δ 0.040 ± 0.01) and post‐HDBR (Δ0.080 ± 0.02, P = 0.15), AP analysis suggests that the change in the number of active sympathetic clusters per burst, from baseline to apnea, was greater post‐HDBR (Δ 1 ± 0.2 clusters/burst) than pre‐HDBR (Δ 0 ± 0.2 clusters/burst, P = 0.02), while the change in total sympathetic clusters, from baseline to apnea, trended towards greater recruitment post‐HDBR (Δ 2 ± 0.7 clusters) than pre‐HDBR (Δ 0 ± 0.5 clusters, P = 0.07). Also, the change in the number of APs per burst, from baseline to apnea, was greater post‐HDBR (Δ 3 ± 0.8) than pre‐HDBR (Δ 1 ± 0.4, P = 0.02). These findings suggest that reflex MSNA‐arousal imposed by apnea is exaggerated by 60‐days HDBR, primarily by mechanisms involving augmented AP firing rate with minimal contributions from recruitment of latent sub‐populations of sympathetic axons.

Support or Funding Information

This work was supported by Natural Sciences and Engineering Research Council of Canada (NSERC) Grant 217916‐2013 (awarded to J. K. Shoemaker).