Human upper airway and facial muscles support breathing, swallowing, speech, mastication, and facial expression, but their endurance performance in sustained contractions is poorly understood. The muscular fatigue typically associated with task failure during sustained contractions has both central and intramuscular causes, with the contribution of each believed to be task dependent. Previously we failed to show central fatigue in the nasal dilator muscles of subjects that performed intermittent maximal voluntary contractions (MVCs). Here we test the hypothesis that central mechanisms contribute to the fatigue of submaximal, sustained contractions in nasal dilator muscles. Nasal dilator muscle force and EMG activities were recorded in 11 subjects that performed submaximal contractions (20, 35, and 65% MVC) until force dropped to ≤90% of the target force for ≥3 s, which we defined as task failure. MVC and twitch forces (the latter obtained by applying supramaximal shocks to the facial nerve) were recorded before the trial and at several time points over the first 10 min of recovery. The time to task failure was inversely related to contraction intensity. MVC force was depressed by roughly 30% at task failure in all three trials, but recovered within 2 min. Twitch force fell by 30-44% depending on contraction intensity and remained depressed after 10 min of recovery, consistent with low-frequency fatigue. Average EMG activity increased with time, but never exceeded 75% of the maximal, pretrial level despite task failure. EMG mean power frequency declined by 20-25% in all trials, suggesting reduced action potential conduction velocity at task failure. In contrast, the maximal evoked potential did not change significantly in any of the tasks, indicating that the EMG deficit at task failure was due largely to mechanisms proximal to the neuromuscular junction. Additional experiments using the interpolated twitch technique suggest that subjects can produce about 92% of the maximal evocable force with this muscle, which is not a large enough deficit to explain the entire shortfall in the EMG at task failure. These data show that the nervous system fails to fully activate the nasal dilator muscles during sustained, submaximal contractions; putative mechanisms are discussed.
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