Refractory Period After An Initial Exercise example essay topic

"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 Flower, 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). Th 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 os molarity, pH, and temperature through mechanisms currently unknown, producing the signs and symptoms of EIA. (p.

S 35) 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. S 35) 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).

"Approximately 40% to 50% of patients with EIA experience a 2-hour to 4-hour refractory period after an initial exercise task" (Spector, 1993, p. 575). As stated by Tan and Spector (1998), "if the individual attempts to exercise again after the symptoms subside, he or she will experience fewer symptoms the second time. This has been referred to as the refractory period" (p. 4). During this period, the effects of the exercise challenge are not as substantial as the initial trial; however, other factors such as allergens and air pollutants can cause the refractory period to become obsolete because of the hyper reactivity of the airways (Smith & LaBotz, 1998; Tan & Spector, 1998). Common symptoms of EIA include, but are not limited to, chest tightness, shortness of breath, fatigue, coughing, and wheezing. Less common symptoms include stomachache, headache, muscle cramps, and the feeling of being "out of shape" (Enright, 1996; Randolph, 1997; Storms, 1999; Tan & Spector, 1998).

These symptoms typically emerge after 8-10 minutes of strenuous exercise and continue for up to one hour after exercise has ceased. The severity of the symptoms again depends on the duration, intensity, and volume of exercise. With increased exposure to allergens and air pollutants, bronchial reactivity is increased, causing more severe bronchospasm. Good conditioning and aerobic fitness, along with proper medications, can greatly lessen the effect of EIA. This is due to the fact that conditioned athletes and those who exercise regularly do not have rapid and abrupt increases in respiratory rate, which is a cause of EIA (Tan & Spector, 1998). Diagnosis of EIA is determined through spirometry measurements of peak expiratory flow rate (PEFR) and forced expiratory volume in one second (FEV 1) before and after an exercise challenge.

For all possible cases of EIA a complete family and personal history must be obtained prior to testing. Sometimes the history is enough to make a diagnosis, but, in some cases, especially those of athletes, spirometry testing must be done. In the case of PEFR and FEV 1, a fall of 10%-15% from the resting rate is diagnostic of EIA (Enright, 1996). The methods of testing through an exercise challenge include free running, treadmill, and cycle ergometer (Enright, 1996; Randolph, 1997; Tan & Spector, 1998). In a free running test, the athlete runs for 6-8 minutes to maintain heart rate at 180 or above. This is the most inexpensive and valuable test because of the high asthmogenic quality of running (Randolph, 1997).

The cycle ergometer is less asthmogenic than running and also more expensive, but still allows for adequate diagnosis of EIA. With the cycle ergometer, 4 minutes of work at 80%-90% of the individual's target heart rate or 50%-60% of predicted maximal oxygen consumption (VO 2 max) can trigger a response (Tan & Spector, 1998). The last method of testing is the standard treadmill in which the individual attains a workload at a target heart rate of 180 or more in the first few minutes and then maintains this for 6-8 minutes while speed and grade are manipulated to maintain the heart rate throughout the entire exercise challenge (Randolph, 1997). According to Randolph (1997), "the most important elements in a successful exercise challenge are the level of ventilation, the heat and water contained in inspired air, and the degree of warm down at the conclusion of the challenge" (p. 71).

There are pharmacological and nonpharmacological treatments for EIA. The most common pharmacological treatment is a bronchodilator, or beta agonist inhaler. Beta agonists are 80%-95% effective in protecting against exercise induced symptoms and have been the most popular and effective method of treatment and prevention of EIA (Enright, 1996; Randolph, 1997; Smith & LaBotz, 1998; Spector, 1993; Storms, 1999; Tan & Spector, 1998). The beta agonists act immediately upon inhalation and result in bronchodilation for 4-6 hours. Bronchodilators should be administered 2-4 puffs at a time, 15 minutes before exercise or during acute attacks of bronchospasm (Enright, 1996; Randolph, 1997; Smith & LaBotz, 1998). The most frequently used beta agonists, and ones approved by the US Olympics committee, are albuterol and terbutaline (Enright, 1996; Randolph, 1997; Smith & LaBotz, 1998; Tan & Spector, 1998).

Recently, a longer lasting beta agonist has been researched called salmeterol. The effects last up to 12 hours, and it must be taken 30-60 minutes prior to exercise, or as a chronic preventative medication for individuals with EIA (Enright, 1996; Randolph, 1997; Smith & LaBotz, 1998; Tan & Spector, 1998). Salmeterol is not approved by the US Olympics committee. Other commonly prescribed agents for the prevention and treatment of EIA include inhaled mast cell stabilizers, or antiinflammatories, such as cromolyn sodium and nedocromil. These are 70%-85% effective in individuals with EIA and result in bronchodilation for 1-2 hours (Randolph, 1997; Spector, 1993). Antiinflammatories, which inhibit bronchoconstriction, should be administered in 2-4 puffs, 15-30 minutes before exercise.

Cromolyn sodium and nedocromil are not beta agonists, do not last as long, and are not as effective as beta agonists in the prevention of EIA. Nedocromil has also been known to have a foul taste, and, therefore, is not prescribed as often as other medications (Randolph, 1997; Smith & LaBotz, 1998). Antiinflammatories have been approved for use by the US Olympic Committee. Nonpharmacological prevention and treatment of EIA involves climate control, appropriate activity selection, refractory period considerations, and physical conditioning (Randolph, 1997; Smith & LaBotz, 1998; Spector, 1993).

Cold, dry conditions are prime activators of bronchoconstriction, which leads to EIA. Avoiding these conditions or protecting against them is ideal. Different activities have variable ranges of asthmogenicity and their recognition will help prevent EIA. If an individual is known to experience a refractory period after an initial exercise challenge, it is suggested that this individual induce a refractory period during the performance of an activity. This refractory period can be induced by engaging in an initial exercise challenge 40 minutes to 3 hours before competition, based on the individual's known refractory length. This allows him or her to perform at a higher level with decreased or absent symptoms of EIA.

Lastly, physical conditioning is an important aspect of prevention of EIA in that an individual in better shape does not undergo such an abrupt change in respirations and bronchial obstruction (Enright, 1996; Randolph, 1997; Smith & LaBotz, 1998; Spector, 1993; Tan & Spector, 1998). General guidelines for decreasing symptoms of EIA are to warm up before the actual exercise challenge, cover the mouth and nose in cold weather, exercise in warm, humidified environments whenever possible, and warm down or gradually decrease the intensity of exercise (Enright, 1996; Randolph, 1997; Smith & LaBotz, 1998; Spector, 1993; Tan & Spector, 1998). In conclusion, EIA is a condition in which exercise induces bronchoconstriction, which causes difficulty breathing. EIA is found in athletes, children, adults and recreational individuals.

The exact causes of EIA are unknown, but there are two theories as to its pathophysiology, which involve water or heat loss through the bronchial epithelium. Prevention and management of EIA can be achieved through pharmacological or nonpharmacological means. Bronchodilators are the most common form of pharmacological treatment, along with antiinflammatories. Education, proper conditioning, climate conditions, activity selection, and refractory period considerations are all important aspects of nonpharmacological management of EIA. With all of these considerations, and early recognition and treatment, an individual should be able to perform at a maximum competitive level with minimal or no symptoms. Famous athletes such as Jackie Joyner-Ker see, Dennis Rodman, and the Ohio bobcats free safety, Duffer Duffy, all perform at different levels of competition with EIA.

Bibliography

Bibliography

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Exercise-induced asthma and the asthmatic athlete. Wisconsin Medical Journal, 95 (6), 375-378. Hansen-Flaschen, J., & Schotland, H. (1998).
New treatments for exercise-induced asthma. The New England Journal of Medicine, 339 (3), 192-193. Randolph, C. (1997).
Exercise-induced asthma: Update on pathophysiology, clinical diagnosis, and treatment. Current Problems in Pediatrics, 27 (2), 53-77. Smith, B.W., & LaBotz, M. (1998).
Pharmacologic treatment of exercise-induced asthma. Clinics in Sports Medicine, 17 (2), 343-363. Spector, S.L. (1993).
Update on exercise-induced asthma. Annals of Allergy, 71 (6), 571-577. Storms, W.W. (1999).
Exercise-induced asthma: Diagnosis and treatment for the recreational or elite athlete. Medicine and Science in Sports and Exercise, 31 (1), S 33-38. Tan, R.A., & Spector, S.L. (1998).