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Long-term intermittent hypoxia increases sympathetic activity and chemosensitivity during acute hypoxia in humans
Acute exposure to hypoxia stimulates oxygen sensitive chemoreceptors located peripherally in the carotid body and centrally in the brainstem. The physiological consequences of stimulation of these excitatory regions are many and include abrupt increases in ventilation and circulatory adjustments including increased sympathetic vasomotor outflow. When a chemoreceptor stimulus (i.e. increased CO2 and/or decreased O2)is used to drive ventilation in humans, sympathetic activity is increased in a dose–response fashion (Somers et al.1989; Morgan et al. 1995; Xie et al. 2000). Acute exposure to 20 min of combined hypoxia and hypercapnia causes increases in ventilation that are paralleled by increases in direct recordings of multiunit muscle sympathetic nerve activity (MSNA) (Morganet al.1995). After cessation of hypoxia and hypercapnia, ventilation and arterial oxyhaemoglobin saturation (SaO2) return to baseline values whereas the increases in sympathetic activity persist.
Lusina SJ, Kennedy PM, Inglis JT, McKenzie DC, Ayas NT, Sheel AW
Source: J Physiol