Obstructive sleep apnoea and exercise functional capacity: time to move?

Obstructive sleep apnoea (OSA) is defined by repetitive episodes of obstructive respiratory events, characterised by marked reduction (hypopnoea) or cessation of respiration (apnoea) due to upper airway obstruction during sleep. Each respiratory event leads to episodes of asphyxia and progressive but futile generation of excessive negative intrathoracic pressure. The patient is typically self-rescued by an arousal from sleep that leads to opening of the airway and resumption of breathing [1]. OSA is common in the general population across the whole human life span from infants to the elderly [2]. There is good evidence built over the past 30 years that OSA may trigger a cascade of mechanisms that are harmful to the cardiovascular and metabolic system, including sympathetic over activity, oxidative stress, endothelial dysfunction and insulin resistance. OSA is also associated with hypertension, arrhythmias, progression of atherosclerosis and increased cardiovascular mortality due to acute myocardial infarction and stroke [3–6]. Despite all these evidence, the impact of OSA on cardiorespiratory fitness (CRF) is controversial. This is an important question because low levels of CRF have been associated with a high risk of cardiovascular disease and all-cause mortality [7–9]. CRF is a potentially stronger predictor of mortality than established cardiovascular risk factors [9, 10]. Although CRF can be quantified by different means, including metabolic equivalents ...
Source: European Respiratory Journal - Category: Respiratory Medicine Authors: Tags: Editorials Source Type: research