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Short‐term intermittent hypoxia enhances ventilatory chemoreflex sensitivity in humans

Short‐term intermittent hypoxia (IH, one episode/min for 30 min) raises basal sympathetic nerve activity and blood pressure, and enhances sympathetic vasoconstrictor nerve responses to acute hypoxia. We investigated whether the enhanced sympathetic activation in response to acute hypoxia following IH is also accompanied by enhanced ventilatory chemosensitivity. To this end we examined the effects of IH (30 episodes, SaO2 nadir 80–85%) on sympathetic vasoconstrictor nerve activity and ventilation in young healthy humans (5 male, 6 female). Muscle sympathetic nerve activity (MSNA, peroneal microneurography) and ventilatory responses to inhalation of 100% N2 (2–8 breaths) pre‐and post‐IH were compared. In addition, the effects of IH on the blood pressure and MSNA responses to static handgrip to fatigue (HG, at 30% of maximal voluntary contraction) and post‐HG circulatory arrest (CA) were also assessed. Compared to pre‐IH, post‐IH mean blood pressure (89±4 vs. 92±3 mmHg; n=11), MSNA (12.1±1.9 vs. 16.8±2.6 bursts/min; n=9), and ventilatory chemoreflex sensitivity (−0.184±0.032 vs. −0.285±0.051 L/min/%SaO2; n=11) were all increased (P<0.05) whereas the blood pressure and MSNA responses to HG and post‐HG CA were unaffected (n=9; P=NS). These data suggest that short‐term IH in healthy humans selectively enhances ventilatory chemoreflex sensitivity. (Supported by P01 HL09670 and UL1 TR000127)