Effect of airway inflammation on short-latency reflex inhibition to inspiratory loading in human scalene muscles.

The short-latency reflex inhibition of human inspiratory muscles produced by loading is prolonged in asthma and obstructive sleep apnoea, both diseases involving airway and systemic inflammation. Both diseases also involve repetitive inspiratory loading. Although airway mucosal afferents are not critical components of the normal reflex arc, during airway inflammation, prolongation of the reflex may be caused by altered mucosal afferent sensitivity, or altered central processing of their inputs. We hypothesised that acute viral airway inflammation would replicate the reflex abnormality. The reflex was tested in 9 subjects with a "common cold" during both the acute infection and when well. Surface electrodes recorded electromyographic (EMG) activity bilaterally from scalene muscles. Latencies of the inhibitory response (IR) did not differ significantly (IR peak 67 vs 70 ms (p=0.12), and IR offset 87 vs 90 ms (p=0.23), between the inflamed and well conditions, respectively). There was no difference in any measure of the size of the reflex inhibition.