Cardiovascular and Respiratory Effects of Exposure to Experimental Models of Obstructive Sleep Apnoea-related Intermittent Hypoxia

Obstructive sleep apnoea (OSA) is a common chronic condition characterised by repetitive nocturnal upper airway collapse that evokes intermittent hypoxia (IH). Although animal research has demonstrated a causal relationship between IH and cardiovascular disease there is a relative paucity of human research. Using a variety of different models of OSA we investigated the effects of IH on respiratory control and oxidative stress. In addition, we attempted to use Doppler ultrasound to investigate the effects of hypoxic airway occlusions on the pulmonary circulation but concluded that it is not a feasible alternative to invasive catheterisation. In a number of studies we showed that the expression of respiratory plasticity following IH is only evident when arterial levels of CO2 are raised above normal levels. Furthermore, in stark contrast to previous findings in animals, exposure to acute continuous hypoxia also evokes respiratory plasticity in humans. In addition, we showed that combined postprandial hyperglycaemia and hyperlipidaemia augments the degree of oxidative stress during IH. Finally, we demonstrated that IH accentuates the magnitude of postprandial hyperglycaemia. These studies demonstrate the complexity of respiratory control in humans and they highlight significant species differences. Furthermore, they highlight a fascinating synergy between IH and the postprandial state.