Both obesity and sleep apnea are prevalent health conditions that frequently coaggregate. Obesityassociated inflammation may influence asthma control; the relation of sleep apnea to asthma or allergic rhinitis may be bidirectional. Both obesity and sleep apnea are associated with augmented levels of inflammation and oxidative stress, and it is biologically plausible that the proinflammatory effects of one disorder influence the expression of the other disorder. This article elucidates mechanistic associations among obesity, sleep apnea, and systemic inflammation; highlights interrelationships between these factors with cardiopulmonary disease; and identifies specific areas for future research directions.
KeywordsSleep apnea; obesity; inflammation; asthma Sleep apnea, characterized by loud snoring and daytime sleepiness, is a prevalent disorder, affecting upwards of 2% to 4% of the population. 1 It is caused by episodes of repetitive partial or complete upper airway collapse during sleep, which causes sleep disruption and fragmentation, as well as intermittent hypoxia, ventilatory overshoot hyperoxia, sympathetic nervous system surges, alterations in intrathoracic pressure, and local airway edema and inflammation. Sleep apnea also frequently coaggregates with obesity, and both conditions may independently or synergistically influence cardiopulmonary function and systemic inflammation. Moreover, sleep apnea and accompanying obesity may share common inflammatory pathways with asthma and allergic rhinitis. The relation of sleep apnea to asthma or allergic rhinitis may be bidirectional. To date, most research has been directed at understanding the links among sleep apnea, systemic inflammation, and cardiac responses. In this article, we present mechanistic associations between sleep apnea, obesity, and systemic inflammation. We highlight interrelationships between these factors and pulmonary as well as cardiac disease and identify specific areas for future research directions.
Systemic responsesOne mechanism by which sleep apnea may contribute to systemic inflammation is through increased sympathetic nervous system activation, which may be induced by upper airway closure, hypoxia, hypercarbia, and/or arousals associated with the respiratory disturbances. Sleep apnea-related enhanced sympathetic nervous system activity likely plays a pathophysiologic role in the development of the acute increases in blood pressure commonly observed at the termination of apneas. It is also implicated in the pathogenesis of sustained systemic hypertension. Augmented sympathetic nervous system activity also appears to be associated with cytokine expression and oxidative stress. 2 In addition, elevated catecholamine levels may undergo auto-oxidation, and this has been considered to be a cause of catecholamine-induced cardiomyopathy, which may account for cardiovascular disease complications in individuals with sleep apnea.Cyclical episodes of hypoxia-reoxygenation, analogous to cardiac ischemia/reoxygenation injury, occur repetit...