Chest
Original ResearchAsthmaExercise-Induced Asthma May Be Associated With Diminished Sweat Secretion Rates in Humans
Section snippets
Materials and Methods
These studies were approved by our institutional review board, and all volunteers gave written informed consent. We recruited 56 subjects who had been referred to our medical center for the evaluation of signs and symptoms suggestive of new-onset, exercise-induced asthma. Subjects were otherwise healthy, young, male and female US Navy and Marine Corps personnel between 18 and 32 years of age. This evaluation included the measurement of bronchiolar reactivity to methacholine. No patients were
Results
Fifty-six otherwise healthy subjects with signs and symptoms suggestive of exercise-induced bronchospasm volunteered for this study. Twenty-two subjects were classified as having a positive MCT result using standard clinical criteria4, 13 (ie, they had at least a 20% fall in their FEV1 over baseline measurements following methacholine challenge), and 34 subjects had a minimal response, if any, to methacholine challenge. As shown in Figure 1, there were wide-ranging differences in the
Discussion
It has been shown that targeted disruption of the gene encoding Aqp5 results in mice with decreased osmotically dependent water movement into, and out of, alveoli, but the loss of Aqp5 did not modify hydrostatically driven lung edema or active alveolar fluid reabsorption. Furthermore, lower airway humidification, as determined by the moisture content of the expired air, was reduced by only 3 to 4% in mice that lacked both Aqp5 and Aqp1.10, 11 On the basis of these two reports,10, 11 one would
Acknowledgment
We thank Justin Clark, MD, from the University of Michigan, for providing the measurements of sweat sodium concentrations. Also, the following individuals from the Naval Medical Center San Diego contributed to our work: Ryan Woodman for drawing our graphs; Debra James, Waine Macallister, and Suzana Hazeldon for the editorial assistance; and Robert Riffenburgh, PhD, for statistical analyses. Dr. Lockette has had full access to all of the data in the study and takes responsibility for the
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Cited by (23)
Exercise-induced bronchoconstriction in elite or endurance athletes:: Pathogenesis and diagnostic considerations
2020, Annals of Allergy, Asthma and ImmunologyCitation Excerpt :In a study among elite swimmers, severe airway hyperresponsiveness correlated to increased parasympathetic activity parameters.63 A significant correlation also has been observed among patients with EIB and reduced sweat secretion, salivary flow, and eye tearing compared with patients without EIB.64 The airway epithelium serves as an important barrier to inhaled allergens, PM, pollutants, and pathogens, and a loss of integrity of this barrier is a significant mechanism of bronchoconstriction in patients with EIBwa.65
Infant rhinitis and watery eyes predict school-age exercise-induced wheeze, emergency department visits and respiratory-related hospitalizations
2018, Annals of Allergy, Asthma and ImmunologyCitation Excerpt :Exercise-induced bronchoconstriction, the process that underlies exercise-induced wheeze (EIW), occurs in 5% to 15% of the general population4,5 and 40% to 90% of the asthmatic population.6 EIW is thought to be related to parasympathetic nerve stimulation by osmotic cellular changes or airway cooling.7–10 Therefore, rhinitis, watery eyes, and EIW may share these physiologic responses that are independent of an allergic pathway.
Exploratory study comparing dysautonomia between asthmatic and non-asthmatic elite swimmers
2015, Revista Portuguesa de PneumologiaCitation Excerpt :Previous studies supporting this hypothesis of dysautonomy associated with training match our findings. Pichon et al. demonstrated that subjects with an increased AHR had a higher vagal tone,14 which was corroborated by Park et al. findings of a relationship between AHR to methacholine and a diminished sweat secretion, tearing and salivary flow rate in healthy athletes.15 All these studies have used AHR as an outcome measure, rather than asthma status.
Pathogenesis of Exercise-Induced Bronchoconstriction
2013, Immunology and Allergy Clinics of North AmericaCitation Excerpt :Using sputum percent solids as a marker for airway hydration, Loughlin and colleagues reported that airway hydration is significantly reduced at baseline in clinically stable asthmatics.40 Further, athletes with excessive bronchial reactivity have been found to have a reduced ability to sweat.41 Since respiratory gland epithelium and sweat gland epithelium share identical mechanisms of muscarinic receptor (m3 subtype)-dependent sodium, chloride, and water secretion, this latest result may indicate a general deficiency in body fluid homeostasis regulation in those individuals with EIB.
Where to from Here for Exercise-Induced Bronchoconstriction. The Unanswered Questions
2013, Immunology and Allergy Clinics of North AmericaCitation Excerpt :Several lines of human-based research suggest that disorders of water transport may be a contributor to EIB. A problem in airway fluid regulation has been proposed to lead to mucus hypersecretion and mucosal edema,32 and in exacerbation of the dehydration stress to the airways during exercise hyperpnoea.33,34 It has been proposed that the protective effect of the cromones may play a role in epithelial volume regulation through an action on chloride ion channels.35
Neutrophilic inflammation is associated with altered airway hydration in stable asthmatics
2010, Respiratory MedicineCitation Excerpt :Deletion of the aquaporin 5 water channel gene in mice results in reduced airway hydration and a greater sensitivity to bronchoconstrictor challenge agents.3 A recent study in humans demonstrated a negative correlation between fluid secretion rates in tears and sweat18 and sensitivity to methacholine-induced bronchoconstriction. These data suggested that individuals who have difficulty rehydrating airway secretions after a dehydrating exercise challenge may be at greater risk for subsequent bronchoconstriction.
The comments expressed represent the personal opinions of the authors and they do not necessarily reflect the views of the Department of the Navy or the Department of Defense.
The authors have reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).