This work delineates the normal oscillation and responsiveness of circulating monocytes and T lymphocytes in ten human volunteers over circadian time. Under normal circadian parameters, bimodal cytokine secretion was observed with the night peak caused by an increased responsiveness of monocytes, and the day peak corresponding to a higher absolute number of monocytes. T lymphocytes demonstrated an evening peak caused by both higher cell count and responsiveness. When subjected to a night shift schedule (acute circadian disruption) monocyte and T cells circulating phase was not changed but the responsiveness of both cell types was advanced (earlier expression of cytokine) after stimulation. This suggests that acute changes in sleep-wake cycles alter the cell intrinsic responsiveness to stimulation whereas parameters governing circulation may lag behind.

The preBotzinger complex in rats is a respiratory neuronal network driving inspiratory rhythm. Chronic intermittent hypoxia (as is the case in OSA) causes irregular firing of the preBotzinger complex. Dysrhythmia in the preBotzinger complex loosens the coupling of neuronal transmission with XIIn. Lipid peroxidation is increased in both the preBotzinger complex and XIIn as a result of chronic intermittent hypoxia. Treatment with antioxidant can reverse the instability in neuronal coupling caused by the exposure hypoxia. This work demonstrates the effect of hypoxia on rhythmic breathing in a salient neuronal network and provides a possible therapeutic strategy to re-establish rhythmic neuronal connectivity in this pathway.