Exercise-Induced Bronchoconstriction (EIB/EIA) Condition

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A Exercise-Induced Bronchoconstriction (EIB/EIA) Condition is an asthma condition that is triggered by exercise.

References

2015

  • (Wikipedia, 2015) ⇒ http://en.wikipedia.org/wiki/Bronchoconstriction#Exercise-induced_bronchoconstriction Retrieved:2015-11-11.
    • More generally termed exercise-induced asthma, the preferred and more accurate term exercise-induced bronchoconstriction better reflects underlying pathophysiology. It is also preferred due to the former term giving the false impression that asthma is caused by exercise.

      In a patient with EIB, exercise initially follows the normal patterns of bronchodilation. However, by three minutes, the constriction sets in, which peaks at around 10–15 minutes, and usually resolves itself by an hour. During an episode of this type of bronchorestriction, the levels of inflammatory mediators, particularly leukotrienes, histamine, and interleukin, increase. TH2-type lymphocytes are activated, with an increase in T cells expressing CD25 (IL-2R), and B cells expressing CD 23, causing increased production of IgE. After exercise, the conditions will fade within one to three minutes. In most sufferers of EIB, this is followed by a refractory period, of generally less than four hours, during which if exercise is repeated, the bronchorestriction is less emphasised. This is probably caused by the release of prostaglandins.

      The underlying cause of this type of bronchoconstriction appear to be the large volume of cool, dry air inhaled during strenuous exercise. The condition appears to improve when the air inhaled is more fully humidified and closer to body temperature.

      This specific condition, in the general population, can vary between 7 and 20 percent. This increases to around 80 percent in those with symptomatic asthma. In many cases, however, the constriction, even during or after strenuous exercise, is not clinically significant except in cases of severe to moderate emphysema.

      In May 2013, the American Thoracic Society issued the first treatment guidelines for EIB. [1]

  1. ↑ http://www.atsjournals.org/doi/abs/10.1164/rccm.201303-0437ST

2014

  • (Wikipedia, 2014) ⇒ http://en.wikipedia.org/wiki/Exercise-induced_bronchoconstriction Retrieved:2014-8-18.
    • Exercise-induced asthma, or E.I.A., occurs when the airways narrow as a result of exercise. The preferred term for this condition is exercise-induced bronchoconstriction (EIB); exercise does not cause asthma, but is frequently an asthma trigger.


  • (Wikipedia, 2014) ⇒ http://wikipedia.org/wiki/Asthma#Classification Retrieved:2014-8-18.
    • QUOTE: Exercise can trigger bronchoconstriction in both people with and without asthma.[1] It occurs in most people with asthma and up to 20% of people without asthma. In athletes is diagnosed more commonly in elite athletes, with rates varying from 3% for bobsled racers to 50% for cycling and 60% for cross-country skiing. While it may occur with any weather conditions it is more common when it is dry and cold.[2] Inhaled beta2-agonists do not appear to improve athletic performance among those without asthma[3] however oral doses may improve endurance and strength.[4][5]
  1. ↑ Khan, DA (Jan–Feb 2012). "Exercise-induced bronchoconstriction: burden and prevalence". Allergy and asthma proceedings : the official journal of regional and state allergy societies 33 (1): 1–6. doi:10.2500/aap.2012.33.3507. PMID 22370526. 
  2. ↑ Template:Harvnb
  3. ↑ Carlsen, KH; Anderson, SD; Bjermer, L; Bonini, S; Brusasco, V; Canonica, W; Cummiskey, J; Delgado, L; Del Giacco, SR; Drobnic, F; Haahtela, T; Larsson, K; Palange, P; Popov, T; van Cauwenberge, P; European Respiratory, Society; European Academy of Allergy and Clinical, Immunology; GA(2)LEN, (May 2008). "Treatment of exercise-induced asthma, respiratory and allergic disorders in sports and the relationship to doping: Part II of the report from the Joint Task Force of European Respiratory Society (ERS) and European Academy of Allergy and Clinical Immunology (EAACI) in cooperation with GA(2)LEN". Allergy 63 (5): 492–505. doi:10.1111/j.1398-9995.2008.01663.x. PMID 18394123. 
  4. ↑ Kindermann, W (2007). "Do inhaled beta(2)-agonists have an ergogenic potential in non-asthmatic competitive athletes?". Sports medicine (Auckland, N.Z.) 37 (2): 95–102. doi:10.2165/00007256-200737020-00001. PMID 17241101. 
  5. ↑ Pluim, BM; de Hon, O; Staal, JB; Limpens, J; Kuipers, H; Overbeek, SE; Zwinderman, AH; Scholten, RJ (Jan 1, 2011). "β₂-Agonists and physical performance: a systematic review and meta-analysis of randomized controlled trials". Sports medicine (Auckland, N.Z.) 41 (1): 39–57. doi:10.2165/11537540-000000000-00000. PMID 21142283. 

2013

2000

The mechanism whereby EIA occurs is thought to relate to the consequences of heating and humidifying large volumes of air during exercise. In 1978 airway cooling was identified as an important stimulus for EIA; however, severe EIA also occurred when hot dry air was inspired, and there was no abnormal cooling of the airways. In 1986 the thermal hypothesis proposed that cooling of the airways needed to be followed by rapid rewarming and that these two events caused a vasoconstriction and a reactive hyperemia of the bronchial microcirculation, together with edema of the airway wall, causing the airways to narrow after exercise. The osmotic, or airway-drying, hypothesis developed from 1982-1992 because neither airway cooling nor rewarming appeared to be necessary for EIA to occur. As water is evaporated from the airway surface liquid, it becomes hyperosmolar and provides an osmotic stimulus for water to move from any cell nearby, resulting in cell volume loss. It is proposed that the regulatory volume increase, after cell shrinkage, is the key event resulting in release of inflammatory mediators that cause airway smooth muscle to contract and the airways of asthmatic subjects to narrow. This event may or may not be associated with airway edema. The osmotic and thermal theories come together by considering that inspiration of cold air not only cools the airways but also increases the numbers of airway generations becoming dehydrated in the humidifying process.

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