Lung volume modulation of sternohyoid muscle function: an anesthetized rat model

Lung volume change modifies pharyngeal airway patency by altering breathing-related passive force transmission between lower and upper airways (via tracheal and other connections). We hypothesize that such force transmission may also impact active upper airway dilator muscle function by altering resting muscle length. The aim of this study was to determine the relationship between end-expiratory lung volume (EELV) and the ability of sternohyoid muscle (SH) contraction to alter pharyngeal airway patency. Eleven supine, anesthetized, spontaneously breathing Wistar rats with sealed snout mask to monitor airflow ([Formula: see text]) and mask pressure (P_M) were positioned in head-out plethysmograph (P_BOX). Graded changes in P_BOX (±8 cmH₂O) were applied, and tracheal pressure (P_tr), SH length (SHL), and tension (SHT_P) were monitored. Change in EELV (ΔEELV) and upper-airway resistance (R_UA-passive) (%baseline) were calculated. Electrical stimulation of SH at each P_BOX was performed, and changes in SH tension (SHT_A) and <i>R</i>_UA (Δ<i>R</i>_UA = <i>R</i>_UA-Passive - <i>R</i>_UA-Active) were calculated. Data were analyzed using mixed-effects models. Increasing EELV increased SHL by 0.062 mm/mL (0.037-0.086) [mean (95% CI)], increased SHT_P by 5.42 mN/mL (3.96-6.87), and decreased <i>R</i>_UA-passive by 4%/mL (1.1-7.4), whereas decreasing EELV decreased SHL by 0.31 mm/mL (0.14-0.49), SHT_P by 17.8 mN/mL (11.7-23.9), and increased <i>R</i>_UA-passive by 132%/mL (95.6-168.3). Increasing EELV decreased SHT_A by 19.7%/mL (10.6-28.8) and Δ<i>R</i>_UA by 60.1%/mL (27.1-93.1), whereas decreasing EELV also decreased both SHT_A by 57.5%/mL (31.4-84.2) and Δ<i>R</i>_UA by 139.0%/mL (46.8-231.2) (all <i>P</i> < 0.05). Maximal SHT_A and Δ<i>R</i>_UA occurred at baseline EELV. We conclude that although shifts in EELV impact passive upper airway function, they also negatively impact active SH pharyngeal dilator function, potentially via generation of a suboptimal resting SHL.<b>NEW & NOTEWORTHY</b> This study identifies a previously unrecognized mechanism linking lung volume to upper airway patency. We show that lung volume alters both passive and active force generation in the sternohyoid muscle, thereby modulating its impact on upper airway airflow. These findings are likely to inform on emerging therapies for obstructive sleep apnea, involving targeted stimulation of upper airway dilator muscles.