Exercise Induced Asthma Essay Research Paper

Exercise Induced Asthma Essay, Research Paper

“Asthma is a pulmonary disease with the following characteristics: 1) airway obstruction that is reversible in most patients either spontaneously or with treatment; 2) airway inflammation; and 3) increased airway responsiveness to a variety of stimuli” (Enright, 1996, p. 375). There presently exist many varieties of asthma that differ in the severity, means of induction, and methods of treatment. One type is exercise-induced asthma. “Exercise-induced asthma (EIA) is a temporary increase in airway resistance and acute narrowing of the airway that occurs after several minutes of strenuous exercise, usually after the exercise had ceased” (Spector, 1993, p. 571). Perfectly healthy individuals with no history of asthma or allergies can experience EIA. EIA can be found in 5.6%-25% of the general population and in 40%-90% of asthmatics (Randolph, 1997). EIA has been recognized for over 300 years, but only recently have it’s pathophysiology, diagnosis, and treatment been studied in detail.

EIA was discovered as early as the first century AD when it was observed by Aretaeus the Cappadocian that “if from running, gymnastic exercises, or any other work, the breathing becomes difficult, it is called Asthma” (Randolph, 1997, p. 54). After that, no further research or emphasis was placed on EIA until 1698 when Sir John Floyer, an asthma sufferer, wrote the Treatise on Asthma in which he reported the first delineation of asthmogenic activities. In 1864 Salter recognized that EIA was exacerbated by cold air, and in 1962 Jones determined the pattern of bronchodilation followed by bronchoconstriction that is characteristic of EIA. Such strokes stimulated additional research, and in 1984 and 1988 the Olympic authorities began to screen athletes for EIA before competition. Subsequently, in 1990 the U.S. Olympic Committees published the guidelines for banned and accepted medications for asthma (Randolph, 1997). The results of these studies provided the basis on which to classify EIA. This basis includes airway constriction within the first 6-12 minutes of vigorous exercise, a peak at about 5-10 minutes after exercise, and recovery that is usually spontaneous and within 60 minutes, except in severe cases where it may require up to 3 hours (Enright, 1996; Spector, 1993).

The exact causes of EIA are unknown, but according to Storms (1999), there are two theories of the possible pathogenesis of EIA:

The first is the water loss theory which states that the hyperventilation associated with

strenuous exercise leads to loss of water through the epithelium of the bronchial mucosa.

This loss of water leads to changes in intracellular osmolarity, pH, and temperature through

mechanisms currently unknown, producing the signs and symptoms of EIA. (p. S35)

This theory states that as exercise begins, rate of breathing increases rapidly, and in order for the air to be warmed and saturated with water as it is inhaled, water vapor from the respiratory epithelium must be contributed. This contribution leads to hyperosmolarity of the epithelium, which causes bronchoconstriction through a series of undetermined events. This can be supported by the fact that inhaling hyperosmolar saline at rest will cause bronchoconstriction.

Storms (1999) states the following:

The second hypothesis, the thermal expenditure or respiratory heat exchange theory, states

that EIA results from heat transfer from the bronchiolar blood vessels in the pulmonary

vascular bed with heat loss during exercise; after the exercise, the heat transfer is followed by

a rewarming of the bronchiolar blood vessels, which causes dilation and hyperemia of the

vessels; this then leads to EIA by mechanisms unknown. (p. S35)

This theory states that heat is lost from the upper and lower airways during exercise, and this loss causes the bronchial vasculature to dilate and engorge in order to rewarm the epithelium. This engorgement, in turn, causes the airways to be impinged and narrowed, causing the symptoms of EIA. Support for this theory comes from the observation that inhaling warm air after exercise worsens the bronchoconstriction and inhaling cold air, lessens it (Tan & Spector, 1998).

EIA follows the typical pattern of bronchodilation at the beginning of exercise, followed by bronchoconstriction, and then recovery. During the first 2 to 3 minutes of strenuous exercise bronchodilation occurs, however, after 5 minutes of exercise at 80% or more of maximal heart rate, bronchoconstriction occurs. “Pulmonary function classically declines 8-15 minutes after exercise has ceased” (Spector, 1993, p. 572). Recovery is usually spontaneous and occurs within 60 minutes. “Factors influencing EIA severity include the type, intensity, duration of exercise, environmental conditions (temperature, humidity, and air pollution) and the interval since the last attack” (Enright, 1996, p. 377). According to Hansen-Flaschen and Schotland (1998), “the greater the ventilatory response and the colder and dryer the inspired air, the more likely and severe is the resulting bronchoconstriction” (p. 192).

EIA may or may not be classified by a refractory period ranging from between 40 minutes to 3 hours after the initial exercise challenge (Smith & LaBotz, 1998; Tan & Spector, 1998).

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