Since tracheal traction decreased PTMlat and PTMant by a greater amount than ETPlat and ETPant, we conclude that the decrease in upper airway collapsibility mediated by lung volume related caudal tracheal traction is partially explained by reductions in ETP.

Carotid arteries subjected to 6 h of continuous peri-carotid tissue vibration displayed endothelial dysfunction, suggesting a direct plausible mechanism linking heavy snoring to the development of carotid atherosclerosis.