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Annals of the American Thoracic Society Dec 2014
Review
Topics: Asthma, Exercise-Induced; Bronchoconstriction; Exercise; Exercise Test; Humans
PubMed: 25549031
DOI: 10.1513/AnnalsATS.201409-427OT -
Annals of Allergy, Asthma & Immunology... May 2013To review the literature regarding the pathophysiology of exercise-induced bronchoconstriction (EIB). (Review)
Review
OBJECTIVE
To review the literature regarding the pathophysiology of exercise-induced bronchoconstriction (EIB).
DATA SOURCES
The databases of PubMed, Ovid MEDLINE, and Scopus were searched for articles using the subject headings and/or keywords asthma, exercise-induced/etiology, exercise, mechanism, pathogenesis, and bronchoconstriction.
STUDY SELECTIONS
Articles were selected based on their relevance to the focus of this review, with emphasis on the specific pathophysiologic mechanisms of EIB.
RESULTS
EIB occurs in response to the loss of water from the lower airways that results from heating and humidifying large volumes of air in a short period. The resulting hyperosmolar environment activates various cellular mechanisms to release mediators from mast cells, eosinophils, epithelial cells, and sensory nerves. These mediators, in turn, lead to airway smooth muscle contraction and bronchoconstriction. Airway hyperresponsiveness in elite athletes may develop from a process of airway injury and changes in the contractile properties of airway smooth muscle.
CONCLUSION
EIB commonly affects individuals with and without clinically recognized asthma, especially those who participate in competitive athletics. Through years of research, the pathophysiology of EIB is now better understood and involves a complex interaction between several different cell types and mediators. Continued research to improve the knowledge regarding the mechanisms of EIB should aid the identification, diagnosis, and treatment of this common condition.
Topics: Athletes; Bronchoconstriction; Exercise; Humans; Lung Injury
PubMed: 23621999
DOI: 10.1016/j.anai.2013.02.002 -
Nihon Rinsho. Japanese Journal of... Oct 2016Exercise-induced bronchoconstriction(EIB) is defined as a transient airway obstruction that follows a modest period of high intensity exercise. Accumulating evidence... (Review)
Review
Exercise-induced bronchoconstriction(EIB) is defined as a transient airway obstruction that follows a modest period of high intensity exercise. Accumulating evidence demonstrated that EIB is reported not only among patients with asthma (EIBA), but also observed in a signifi- cant number of individuals without a known diagnosis of asthma (EIBWA). Accordingly, most recent guidelines have been largely revised. Since EIBA have different pathological back- ground from that in EIBwA, EIBA and EIBwa might have distinct responses to treatment and prevention despite using similar therapeutic strategies. This article aims to present a brief review on the current understandings of clinical features, pathogenesis, and management of both types of EIB.
Topics: Bronchoconstriction; Exercise; Humans
PubMed: 30551281
DOI: No ID Found -
The Journal of Allergy and Clinical... Jun 2021The airway smooth muscle (ASM) cell plays a central role in the pathogenesis of asthma and constitutes an important target for treatment. These cells control muscle tone... (Review)
Review
The airway smooth muscle (ASM) cell plays a central role in the pathogenesis of asthma and constitutes an important target for treatment. These cells control muscle tone and thus regulate the opening of the airway lumen and air passage. Evidence indicates that ASM cells participate in the airway hyperresponsiveness as well as the inflammatory and remodeling processes observed in asthmatic subjects. Therapeutic approaches require a comprehensive understanding of the structure and function of the ASM in both the normal and disease states. This review updates current knowledge about ASM and its effects on airway narrowing, remodeling, and inflammation in asthma.
Topics: Airway Remodeling; Animals; Asthma; Biomarkers; Bronchoconstriction; Disease Susceptibility; Gene Expression Regulation; Humans; Muscle, Smooth; Myocytes, Smooth Muscle
PubMed: 34092351
DOI: 10.1016/j.jaci.2021.03.035 -
Experimental Biology and Medicine... Jun 2021Asthma is a chronic inflammatory lung disease affecting approximately 7.7% of the US population. Sex differences in the prevalence, incidence, and severity of asthma... (Review)
Review
Asthma is a chronic inflammatory lung disease affecting approximately 7.7% of the US population. Sex differences in the prevalence, incidence, and severity of asthma have been widely described throughout the lifespan, showing higher rates in boys than girls before puberty, but a reversed pattern in adults. Asthma is often associated with atopy, i.e. the tendency to develop allergic diseases, and can be worsened by environmental stimuli and/or exercise. While not exclusive to patients with asthma, exercise-induced bronchoconstriction (EIB) is a common complication of athletes and individuals who exercise regularly. Currently, there is limited research on sex differences in EIB and its relationship with atopy and asthma in men and women. In this minireview, we summarize the available literature on this topic. Overall, the collective knowledge supports the notion that physiological changes triggered during exercise affect males and females differently, suggesting an interaction among sex, exercise, sex hormones, and atopic status in the course of EIB pathophysiology. Understanding these differences is important to provide personalized management plans to men and women who exercise regularly and suffer from underlying asthma and/or atopy.
Topics: Animals; Asthma; Athletes; Bronchoconstriction; Exercise; Humans; Prevalence; Sex Characteristics
PubMed: 33794694
DOI: 10.1177/15353702211003858 -
Clinical Reviews in Allergy & Immunology 2006Until recently, researchers believed that tolerance or tachyphylaxis to the bronchodilator effects of beta-agonists did not occur. However, recent studies examining the... (Review)
Review
Until recently, researchers believed that tolerance or tachyphylaxis to the bronchodilator effects of beta-agonists did not occur. However, recent studies examining the recovery from bronchoconstriction have clearly shown that an impaired response to beta-agonists occurs in patients who have been using regular beta-agonist treatment. This tolerance develops with both long- and short-acting beta-agonists and is not affected by treatment with inhaled steroids. It develops rapidly, reaching a maximum within 1 wk of starting beta-agonists, and has been demonstrated after methacholine, hypertonic saline, mannitol, and exercise-induced bronchoconstriction. The observed reduction in the bronchodilator response is proportional to the severity of bronchoconstriction. Therefore, although individuals with stable asthma show little evidence of tolerance, those with severe bronchospasm have a markedly reduced bronchodilator response to beta-agonists. Almost all asthmatics show evidence of tolerance when tested in the setting of bronchoconstriction, although the extent of this tolerance varies. The reasons for this interindividual variation are not understood. Bronchodilator tolerance is difficult to study in the clinical setting because nearly every patient has used multiple doses of beta-agonist before seeking medical attention. However, there is compelling evidence that the response to rescue beta-agonist treatment is reduced in those who use regular long- or short-acting beta-agonists. The extent to which this phenomenon contributes to asthma morbidity and mortality remains to be determined.
Topics: Bronchoconstriction; Bronchodilator Agents; Drug Tolerance; Humans; Recovery of Function
PubMed: 17085792
DOI: 10.1385/CRIAI:31:2:181 -
The European Respiratory Journal Feb 1997Airway obstruction in asthma and chronic obstructive pulmonary disease (COPD) is often associated with lung hyperinflation. In this review, we examine the mechanisms... (Review)
Review
Airway obstruction in asthma and chronic obstructive pulmonary disease (COPD) is often associated with lung hyperinflation. In this review, we examine the mechanisms that may cause functional residual capacity (FRC), residual volume (RV) and total lung capacity (TLC) to increase during acute and chronic airway obstruction. Normally, FRC at rest is determined by the static characteristics of the lung and chest wall. When airways narrow, FRC may be also be determined by dynamic factors. There are data suggesting that expiratory flow limitation during tidal breathing represents the starting trigger for FRC to increase, in order to allow breathing at higher flows. Indeed, the increase in FRC during induced bronchoconstriction in asthma is closely associated with the occurrence of flow limitation, i.e. the achievement of maximum flow during tidal breathing. Conversely, the decrease in FRC following bronchodilatation in COPD is closely associated with flow limitation disappearing or occurring at lower lung volumes. In normal young people, RV is determined by the static characteristics of the chest wall. During bronchoconstriction RV may also be determined by dynamic factors; therefore, changes in flow or airway calibre at low lung volumes may modulate RV during bronchoconstriction. During acutely induced bronchoconstriction, RV achieved with an expiration from TLC is less than with an expiration from tidal breathing, and this effect appears to be linked to the bronchodilator effect of the deep inhalation. The reasons for the increase in TLC during airway narrowing are not clear, but the duration of the bronchoconstriction by itself may play a role.
Topics: Bronchoconstriction; Forced Expiratory Flow Rates; Functional Residual Capacity; Humans; Lung; Lung Diseases, Obstructive; Residual Volume; Total Lung Capacity
PubMed: 9042651
DOI: 10.1183/09031936.97.10020468 -
Wiley Interdisciplinary Reviews.... Sep 2016Understanding lung and airway behavior presents a number of challenges, both experimental and theoretical, but the potential rewards are great in terms of both potential... (Review)
Review
Understanding lung and airway behavior presents a number of challenges, both experimental and theoretical, but the potential rewards are great in terms of both potential treatments for disease and interesting biophysical phenomena. This presents an opportunity for modeling to contribute to greater understanding, and here, we focus on modeling efforts that work toward understanding the behavior of airways in vivo, with an emphasis on asthma. We look particularly at those models that address not just isolated airways but many of the important ways in which airways are coupled both with each other and with other structures. This includes both interesting phenomena involving the airways and the layer of airway smooth muscle that surrounds them, and also the emergence of spatial ventilation patterns via dynamic airway interaction. WIREs Syst Biol Med 2016, 8:459-467. doi: 10.1002/wsbm.1349 For further resources related to this article, please visit the WIREs website.
Topics: Bronchoconstriction; Humans; Lung; Lung Diseases; Models, Biological; Parenchymal Tissue; Respiratory Muscles
PubMed: 27348217
DOI: 10.1002/wsbm.1349 -
British Journal of Clinical Pharmacology 19901. Inhaled adenosine and its parent nucleotide, adenosine 5'-monophosphate (AMP) provoke bronchoconstriction in atopic and asthmatic individuals but not in normal... (Review)
Review
1. Inhaled adenosine and its parent nucleotide, adenosine 5'-monophosphate (AMP) provoke bronchoconstriction in atopic and asthmatic individuals but not in normal subjects. 2. In clinical studies, histamine H1-receptor antagonists, cyclo-oxygenase inhibitors and the mast cell 'stabilising' drugs, sodium cromoglycate and nedocromil, protect against the effects of adenosine bronchoprovocation suggesting the involvement of secondary mast cell mediator release. 3. Adenosine and its analogues potentiate histamine and leukotriene release from mast cells activated by other stimuli in vitro, and may also increase net mediator release from mast cells by counteracting the inhibitory effect of circulating adrenaline. 4. Although adenosine fulfils many of the criteria required for a mediator in asthma, its importance is not fully understood, and the mechanisms by which it provokes bronchoconstriction in asthmatic subjects is far from concluded. 5. Two possibilities are that either adenosine acts directly on luminal mast cells to upregulate histamine secretion, or it acts to initiate neuronal reflexes which stimulate histamine release indirectly and possibly activate peptidergic and/or cholinergic pathways.
Topics: Adenosine; Animals; Asthma; Bronchoconstriction; Humans
PubMed: 2268511
DOI: 10.1111/j.1365-2125.1990.tb05474.x -
The New England Journal of Medicine Sep 2011
Topics: Animals; Asthma; Bronchi; Bronchoconstriction; Female; Humans; Male
PubMed: 21992136
DOI: 10.1056/NEJMc1107353