Abstract:
:Exercise induced bronchospasm (EIB) affects approximately 10% of normal individuals with higher prevalence rates among children, obese adults, and competitive athletes. Although hyperpnea with dry air is the best known cause, the problem is multifactorial with atopy, asthma and chlorine all playing established roles. To date, no clear mechanism has connected musculoskeletal loading with the ensuing pulmonary compromise. This paper reviews evidence that impact-driven pulses in subchondral bone pressure may push osseous fat cells into the local venous sinusoids. The resultant showers of microemboli must then travel to the lung where lysis of membrane phospholipids leads to leukotriene formation with resultant inflammation and bronchial hypersensitivity. Concurrently, the same emboli deliver triglyceride fuels for further physical activity. Thus, pulmonary microemboli derived from osseous fat may resolve the seeming paradox of athletic excellence in persons afflicted with exercise-induced bronchospasm.
journal_name
Med Hypothesesjournal_title
Medical hypothesesauthors
Simkin PA,Snitily BKdoi
10.1016/j.mehy.2015.08.014subject
Has Abstractpub_date
2015-11-01 00:00:00pages
694-8issue
5eissn
0306-9877issn
1532-2777pii
S0306-9877(15)00319-9journal_volume
85pub_type
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