Reanalysis of the refractory period in exertional asthma

1981 ◽  
Vol 50 (3) ◽  
pp. 503-508 ◽  
Author(s):  
D. R. Stearns ◽  
E. R. McFadden ◽  
F. J. Breslin ◽  
R. H. Ingram
Keyword(s):  
Refractory Period ◽  
Voluntary Hyperventilation ◽  
Short Intervals ◽  
Exercise Challenge ◽  
Repeated Exercise ◽  
Time Periods ◽  
Exercise Induced

In an effort to determine whether the refractory period in exercise-induced asthma derived from mediator consumption we had seven asthmatic subjects repeatedly perform both exercise and eucapnic hyperventilation at matched minute ventilations under precisely controlled inspired air conditions. We reasoned that, if airway cooling were causing an agent to be released whose depletion resulted in less responsiveness, we should be able to observe this phenomenon irrespective of how cooling was produced. Repetitive exercise at short intervals produced a diminution in the obstructive response that disappeared when the interval between challenges was extended to 2 h. However, the degree of obstruction that occurred after voluntary hyperventilation remained constant irrespective of when the provocations were performed and equaled that seen with the first and last exercise challenge. Because the thermal burdens were identical for each challenge and all time periods, these results are incompatible with mediator depletion and suggest that it may be the secondary sympathoadrenal consequences of repeated exercise that cause the airways to temporarily lose their responsivity.

scholarly journals Exercise-Induced Bronchoconstriction Diagnostics: Impact of a Repeated Exercise Challenge Test

2014 ◽  
Vol 04 (02) ◽  
pp. 55-63
Author(s):  
Maj R. Angell ◽  
Liv Berit Augestad ◽  
Thorbjørn S. Haugen ◽  
Anne Frostad ◽  
Thor Arne Grønnerød ◽  
...  
Keyword(s):  
Challenge Test ◽  
Exercise Challenge ◽  
Repeated Exercise ◽  
Exercise Induced

Urinary excretion of lipid mediators in response to repeated eucapnic voluntary hyperpnea in asthmatic subjects

2015 ◽  
Vol 119 (3) ◽  
pp. 272-279 ◽  
Author(s):  
Johan R. Bood ◽  
Britt-Marie Sundblad ◽  
Ingrid Delin ◽  
Marcus Sjödin ◽  
Kjell Larsson ◽  
...  
Keyword(s):  
Mast Cell ◽  
Urinary Excretion ◽  
Refractory Period ◽  
Ultra Performance Liquid Chromatography ◽  
Lipid Mediators ◽  
Similar Degree ◽  
Cysteinyl Leukotrienes ◽  
Repeated Exercise ◽  
Urinary Levels ◽  
Exercise Induced

Exercise-induced bronchoconstriction displays refractoriness manifested as a decreased response to repeated exercise challenge within hours. The refractoriness may be attenuated by inhibition of the biosynthesis of prostaglandins (PG). The aim of the study was to determine which PGs and other lipid mediators are excreted during the refractory period. First, 16 subjects with mild stable asthma performed two repeated 4-min challenges with eucapnic voluntary hyperpnea (EVH) 1 and 3 h apart. There was a similar degree of refractoriness in both protocols (∼15% protection). The 1-h interval was too short to study mediator excretion because the urinary levels did not return to baseline before the second challenge. With the 3-h protocol, there was increased urinary excretion of cysteinyl-leukotrienes and metabolites of the mast cell product PGD2 after both challenges. Next, another eight subjects performed two 6-min challenges with EVH 3 h apart, which produced a greater bronchoconstrictor response than the 4-min protocol (30.0 ± 5.4 vs. 17.7 ± 1.5%; P = 0.0029) and a greater degree of refractoriness (∼30%). Analysis by ultra-performance liquid chromatography triple quadrupole mass spectrometry confirmed excretion of the bronchoconstrictor cysteinyl-leukotrienes and PGD2 during both challenges. In addition, there was increased excretion of the bronchoprotective PGE2, and also of the main metabolite of PGI2. This is the first report of excretion of PGE2 and PGI2 during the refractory period to EVH challenge, suggesting that they may mediate the refractoriness. Maintained excretion of PGD2 and leukotriene E4 following the repeat challenge argues against mast cell mediator depletion as the mechanism of refractoriness.

Exercise-Induced Asthma and the Refractory Period

2015 ◽  
pp. 298-301
Author(s):  
S. Godfrey ◽  
E. Bar-Yishay ◽  
I. Ben-Dov ◽  
C. Springer
Keyword(s):  
Refractory Period ◽  
Exercise Induced

Exercise-Induced Alterations in Phospholipid Hydrolysis, Airway Surfactant and Eicosanoids and their Role in Airway Hyperresponsiveness in Asthma

2021 ◽  
Author(s):  
Ryan Conrad Murphy ◽  
Ying Lai ◽  
James D Nolin ◽  
Robier A Aguillon Prada ◽  
Arindam Chakrabarti ◽  
...  
Keyword(s):  
Osmotic Stress ◽  
Airway Hyperresponsiveness ◽  
Apical Surface ◽  
Phospholipase Activity ◽  
Absolute Change ◽  
Phospholipid Hydrolysis ◽  
Exercise Challenge ◽  
Surfactant Degradation ◽  
Exercise Induced ◽  
Phospholipid Structure

The mechanisms responsible for driving endogenous airway hyperresponsiveness (AHR) in the form of exercise-induced bronchoconstriction (EIB) are not fully understood. We examined alterations in airway phospholipid hydrolysis, surfactant degradation, and lipid mediator release in relation to AHR severity and changes induced by exercise challenge. Paired induced sputum (n=18) and bronchoalveolar lavage (BAL) fluid (n=11) were obtained before and after exercise challenge in asthmatic subjects. Samples were analyzed for phospholipid structure, surfactant function and levels of eicosanoid and secreted phospholipase A2 group 10 (sPLA2-X). A primary epithelial cell culture model was used to model effects of osmotic stress on sPLA2-X. Exercise challenge resulted in increased surfactant degradation, phospholipase activity, and eicosanoid production in sputum samples of all patients. Subjects with EIB had higher levels of surfactant degradation and phospholipase activity in BAL fluid. Higher basal sputum levels of cysteinyl leukotrienes (CysLTs) and prostaglandin D2 (PGD2) were associated with direct AHR and both the post-exercise and absolute change in CysLTs and PGD2 levels were associated with EIB severity. Surfactant function was either abnormal at baseline or became abnormal after exercise challenge. Baseline levels of sPLA2-X in sputum and the absolute change in amount of sPLA2-X with exercise were positively correlated with EIB severity. Osmotic stress ex vivo resulted in movement of water and release of sPLA2-X to the apical surface. In summary, exercise challenge promotes changes in phospholipid structure and eicosanoid release in asthma, providing two mechanisms that promote bronchoconstriction, particularly in individuals with EIB who have higher basal levels phospholipid turnover.

scholarly journals Altered ventricular mechanics after 60 min of high-intensity endurance exercise: insights from exercise speckle-tracking echocardiography

2015 ◽  
Vol 308 (8) ◽  
pp. H875-H883 ◽  
Author(s):  
Glenn M. Stewart ◽  
Akira Yamada ◽  
Luke J. Haseler ◽  
Justin J. Kavanagh ◽  
Gus Koerbin ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Cardiac Troponin ◽  
Troponin T ◽  
High Sensitivity ◽  
Left Ventricular ◽  
Cardiac Troponin T ◽  
Low Intensity ◽  
Exercise Challenge ◽  
Exercise Induced ◽  
Low Intensity Exercise

Transient reductions in myocardial strain coupled with cardiac-specific biomarker release have been reported after prolonged exercise (>180 min). However, it is unknown if 1) shorter-duration exercise (60 min) can perturb cardiac function or 2) if exercise-induced reductions in strain are masked by hemodynamic changes that are associated with passive recovery from exercise. Left ventricular (LV) and right ventricular global longitudinal strain (GLS), LV torsion, and high-sensitivity cardiac troponin T were measured in 15 competitive cyclists (age: 28 ± 3 yr, peak O2 uptake: 4.8 ± 0.6 l/min) before and after a 60-min high-intensity cycling race intervention (CRIT60). At both time points (pre- and post-CRIT60), strain and torsion were assessed at rest and during a standardized low-intensity exercise challenge (power output: 96 ± 8 W) in a semirecumbent position using echocardiography. During rest, hemodynamic conditions were different from pre- to post-CRIT60 (mean arterial pressure: 96 ± 1 vs. 86 ± 2 mmHg, P < 0.001), and there were no changes in strain or torsion. In contrast, during the standardized low-intensity exercise challenge, hemodynamic conditions were unchanged from pre- to post-CRIT60 (mean arterial pressure: 98 ± 1 vs. 97 ± 1 mmHg, not significant), but strain decreased (left ventricular GLS: −20.3 ± 0.5% vs. −18.5 ± 0.4%, P < 0.01; right ventricular GLS: −26.4 ± 1.6% vs. −22.4 ± 1.5%, P < 0.05), whereas LV torsion remained unchanged. Serum high-sensitivity cardiac troponin T increased by 345% after the CRIT60 (6.0 ± 0.6 vs. 20.7 ± 6.9 ng/l, P < 0.05). This study demonstrates that exercise-induced functional and biochemical cardiac perturbations are not confined to ultraendurance sporting events and transpire during exercise that is typical of day-to-day training undertaken by endurance athletes. The clinical significance of cumulative exposure to endurance exercise warrants further study.

Exercise, physical activity, and asthma

2017 ◽  
Author(s):  
Helge Hebestreit ◽  
Susi Kriemler ◽  
Thomas Radtke
Keyword(s):  
Physical Activity ◽  
Challenge Test ◽  
Well Being ◽  
Physical Activities ◽  
Shortness Of Breath ◽  
Chest Tightness ◽  
Exercise Challenge ◽  
Typical History ◽  
Children With Asthma ◽  
Exercise Induced

The incidence of asthma in children varies among countries and can be estimated to range between 5% and 20%. Exercise-induced asthma (EIA) is common in patients with asthma but can also occur in some children without asthma. Typical symptoms of EIA include cough, chest tightness, and shortness of breath shortly after exercise. The pathophysiology of EIA is not completely understood, but it has been shown that airway cooling and drying with increased ventilation during exercise and airway re-warming after exercise play a pivotal role. In addition, a lack of physical activity may also contribute to EIA. Regular exercise may increase fitness and psychological well-being but may also positively influence airway inflammation in children with asthma. The diagnosis of EIA is based on the typical history and may be verified by an exercise challenge test. Every child with EIA should be able to engage in all type of physical activities.

scholarly journals Physiological Changes at Altitude in Nonasthmatic and Asthmatic Subjects

2004 ◽  
Vol 11 (3) ◽  
pp. 197-199 ◽  
Author(s):  
Dianna Louie ◽  
Peter D Paré
Keyword(s):  
Peak Expiratory Flow ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Physiological Changes ◽  
High Altitudes ◽  
Exercise Challenge ◽  
Per Se ◽  
Expiratory Flow ◽  
Exercise Induced ◽  
Very High

Exercised-induced asthma is not due to exercise itself per se, but rather is due to cooling and/or drying of the airway because of the increased ventilation that accompanies exercise. Travel to high altitudes is accompanied by increased ventilation of cool, often dry, air, irrespective of the level of exertion, and by itself, this could represent an 'exercise' challenge for asthmatic subjects. Exercise-induced bronchoconstriction was measured at sea level and at various altitudes during a two-week trek through the Himalayas in a group of nonasthmatic and asthmatic subjects. The results of this study showed that in mild asthmatics, there was a significant reduction in peak expiratory flow at very high altitudes. Contrary to the authors' hypothesis, there was not a significant additional decrease in peak expiratory flow after exercise in the asthmatic subjects at high altitude. However, there was a significant fall in arterial oxygen saturation postexercise in the asthmatic subjects, a change that was not seen in the nonasthmatic subjects. These data suggest that asthmatic subjects develop bronchoconstriction when they go to very high altitudes, possibly via the same mechanism that causes exercise-induced asthma.

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