Diet and exercise in the management of obstructive sleep apnoea and cardiovascular disease risk

 

Abstract

Obstructive sleep apnoea (OSA) is associated with increased cardiovascular disease (CVD) morbidity and mortality. It is accepted that OSA and obesity commonly coexist. The American Academy of Sleep Medicine recommends dietary-induced weight loss and exercise as lifestyle treatment options for OSA. However, most clinical trials upon which this recommendation is based have focused on establishing the effectiveness of calorie-restricted, often low-fat diets for improving OSA severity, whereas less attention has been given to the means through which weight loss is achieved (e.g. altered dietary quality) or whether diet or exercise mediates the associations between reduced weight, improved OSA severity and the CVD substrate. The current evidence suggests that the benefits of a low-carbohydrate or Mediterranean diet in overweight and obese individuals go beyond the recognised benefits of weight reduction.

Introduction:

Obstructive sleep apnoea (OSA) is characterised by repeated episodes of extrathoracic upper airway obstruction or reductions in breath amplitude that result in intra-arterial hypoxaemia and hypercapnia and transient arousals from sleep, leading to fragmented sleep. The prevalence of OSA among middle-aged adults is estimated to be 24% in males and 9% in females, with 7% of the general population estimated to have moderate to severe OSA. Moreover, OSA is increasingly being recognised as a cause of cardiovascular mortality

Biological pathways linking OSA and CVD

Epidemiological and prospective studies clearly support a causative link between OSA and various manifestations of CVD. The multiple pathways through which OSA sets up the CVD substrate are incredibly complex and have been reviewed elsewhere. We provide a brief discussion of these pathways in order to highlight the potential targets for treatment.

Sleep fragmentation occurs with obstructive apnoea and may induce severe intermittent hypoxaemia and carbon dioxide retention during sleep. As a result, the normal structured autonomic and haemodynamic response to sleep is disrupted. Repetitive apnoeas are accompanied by sympathetic activation and consequent vasoconstriction due to the combined influence of hypercapnia and hypoxia. Patients with sleep apnoea have high levels of nerve activity during wakefulness and sleep, with blood pressure increasing markedly toward the end of apnoea events