The Refractory Period after Exercise Induced Asthma

1977 ◽  
Vol 52 (2) ◽  
pp. 11P-11P ◽  
Author(s):  
A. T. Emunds ◽  
M. Tooley ◽  
S. Godfrey
Keyword(s):  
Refractory Period ◽  
Exercise Induced

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

Refractory Period After Exercise-induced Asthma Unexplained by Respiratory Heat Loss1,2

1982 ◽  
Vol 125 (5) ◽  
pp. 530-534 ◽  
Author(s):  
Issahar Ben-Dov ◽  
Ephraim Bar-Yishay ◽  
Simon Godfrey
Keyword(s):  
Refractory Period ◽  
Exercise Induced

scholarly journals Histamine reactivity during the refractory period after exercise induced asthma.

Thorax ◽  
1984 ◽  
Vol 39 (12) ◽  
pp. 919-923 ◽  
Author(s):  
A G Hahn ◽  
S G Nogrady ◽  
D M Tumilty ◽  
S R Lawrence ◽  
A R Morton
Keyword(s):  
Refractory Period ◽  
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.

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.

Pathogenetic Mechanisms of Exercise Induced Asthma and the Refractory Period

1987 ◽  
Vol 29 (5) ◽  
pp. 706-709 ◽  
Author(s):  
Nick G. Belcher ◽  
Steve O'Hickey ◽  
Jonathan P. Arm ◽  
Tak H. Lee
Keyword(s):  
Refractory Period ◽  
Pathogenetic Mechanisms ◽  
Exercise Induced

Pathogenetic Mechanisms of Exercise-Induced Asthma and the Refractory Period

1988 ◽  
Vol 9 (3) ◽  
pp. 199-201 ◽  
Author(s):  
Nick G. Belcher ◽  
Steve O'Hickey ◽  
Jonathan P. Arm ◽  
Tak H. Lee
Keyword(s):  
Refractory Period ◽  
Pathogenetic Mechanisms ◽  
Exercise Induced
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