The mechanism for inspiratory extrathoracic airway obstruction is presumed to be encroachment on the airway by a flexible structure under the influence of the relative negative intraluminal pressure and Venturi effect attained during inspiration. During expiration, positive pressure tends to open the extrathoracic airway. Certainly, such effects are exaggerated during exercise. During quiet breathing, the glottis opens during inspiration and closes slightly during expiration.
Little is known about normal laryngeal movements during submaximal exercise, and extrapolations must be made from observations made during forced inspiratory and expiratory vital capacity maneuvers. Baier et al studied upper airway resistance and glottis opening in normal human subjects. They found that upper airway resistance falls with panting and with increasing lung volumes, and that upper airway resistance is lower during a forced inspiratory than forced expiratory maneuver. They also observed that the glottic opening is significantly larger during inspiration than expiration. This effect in normal subjects is probably due to reflex motions of the laryngeal musculature designed to tether the airway open, thus counteracting any forces tending to collapse it during inspiration. Of interest was the wide, fixed abduction of the vocal cords noted in this patient and WJM during both inspiratory and expiratory phases of ventilation with exercise.
A limited number of studies have addressed glottic resistance in pulmonary disease, with some surprising results. Lisboa et al studied pressure-flow curves in a group of asthmatic patients. They found a subset in whom inspiratory resistance exceeded expiratory resistance while panting. Inspiratory resistance fell when a helium-oxygen mixture was used, implying that the resistance originated in the large airways. They suggested a glottic source, perhaps caused by laryngospasm or laryngeal edema, although no direct observations of the glottis were made.
Higenbottam and Payne measured the glottic area in a group of patients with chronic obstructive pulmonary disease. They found the glottis to be abnormally narrow in forced inspiratory and expiratory vital capacity maneuvers compared with normal control subjects. In many patients, forced inspiration resulted in a decrease in the glottic area.
Thus, few data exist on the behavior of the larynx with exercise. During forced inspiration, the glottis normally opens widely, and opens to a lesser degree during forced expiration. Some early evidence suggests that glottic abnormalities are present in asthma and COPD; the extent to which they have physiologic significance is unknown.
A recent description by Christopher and co-workers of five cases of vocal-cord dysfunction presenting as asthma suggested a conversion reaction as the source of variable extrathoracic obstruction. In those patients, the true vocal cords were adducted so that the glottis narrowed to a small posterior chink, while the arytenoids maintained their lateral position. It is clear that the inspiratory narrowing of the supraglottic structures during only strenuous exercise in our patient is abnormal and different. The extent to which inflammation of the arytenoids from postnasal drip contributed to our patients symptoms is unclear, but symptoms did improve coincident with treatment, increased training, and warming of inspired air with the beginning of summer. There was no detectable functional disorder, and symptoms occurred only with running, whether during training or during a race.
Although gastroesophageal reflux may have caused similar inflammatory changes, she had no symptoms of reflux and was not taking any antacids or other treatment that might have improved the laryngeal erythema. Improvement in her symptoms was initially associated with progressive physical conditioning, and they improved further with the use of the topical nasal spray.
Find out more information about exercise-induced asthma in the video below:
Exercise-induced asthma is a common problem for the pulmonologist and allergist. By history, our patients symptoms were consistent with the diagnosis. This case illustrates that all that wheezes during exercise is not exercise-induced asthma. Physicians caring for asthmatic patients should be alert for other causes if the patient does not respond as expected to inhaled B2 aerosols and/or cromolyn sodium. A negative methacholine challenge test should suggest the absence at that time of hyperresponsive airways. A flow-volume loop during methacholine challenge or exercise may be helpful in spotting upper airway obstruction in patients complaining of wheezing, but developing stridor. Indirect or fiberoptic laryngoscopy will demonstrate any structural or functional abnormality present. These observations should be made especially if the patient complains of possible upper airway symptoms after careful questioning.