Rationale: Partial neuromuscular transmission failure by acetylcholine receptor blockade (neuromuscular blockade) or antibody mediated functional loss (myasthenia gravis), even with a magnitude of muscle weakness that does not evoke respiratory symptoms, can evoke dysphagia, decreased inspiratory airflow, and increases the risk of susceptible patients to develop severe pulmonary complications. Objectives: To assess whether impaired neuromuscular transmission predisposes to inspiratory upper airway collapse we assessed in healthy awake volunteers supraglottic airway diameter and volume by respiratory-gated magnetic resonance imaging, upper airway dilator muscle function (genioglossus force and EMG), changes in lung volume, respiratory timing, and peripheral muscle function before, during, and after partial neuromuscular blockade. Measurements and main results: Partial neuromuscular blockade (train-of-four (TOF) ratio: 0.5 and 0.8) was associated with: (1) a decrease of inspiratory retropalatal and retroglossal upper airway volume to 66±22 and 82±12 % of baseline that was significantly more intense in the retropalatal area, (2) an attenuation of the normal increase in anterior-posterior upper airway diameter during forced inspiration to 74±18% of baseline, (3) a decrease in genioglossus activity during maximum voluntary tongue protrusion to 39±19% (TOF 0.5) and 73±29% (TOF 0.8) of baseline, and (4) no effects on upper airway size during expiration, lung volume, and respiratory timing. Conclusions: Thus, impaired neuromuscular transmission, even to a degree insufficient to evoke respiratory symptoms, markedly impairs upper airway dimensions and function. This may be explained by an impairment of the balance between upper airway dilating forces and negative intraluminal pressure generated during inspiration by respiratory "pump" muscles.