Abstract
Baroreflex function is impaired in patients with obstructive sleep apnoea. We tested the hypothesis that short-term exposure to repetitive hypoxic apnoeas (RHA) produces prolonged impairment in baroreflex function. Baroreflex function was determined using the modified Oxford technique in 14 subjects (26 +/- 1 years). Baroreflex sensitivity (BRS) was quantified from the R-R interval-systolic blood pressure (BP; cardiovagal BRS), heart rate-systolic BP (HR BRS) and muscle sympathetic nerve activity (MSNA)-diastolic BP (sympathetic BRS) relations. RHA involved subjects performing repetitive end-expiratory apnoeas (20 s) every minute for 30 min during intermittent hypoxia to accentuate oxygen desaturation. After RHA, BP and MSNA at rest were elevated. BRS was measured approximately 7 (Post 1), approximately 30 (Post 2) and approximately 50 min (Post 3) after RHA to provide insight into the temporal pattern of responses. Cardiovagal BRS (16.8 +/- 1.3, 16.5 +/- 1.6, 17.6 +/- 2.0 and 17.4 +/- 1.5 ms mmHg(-1) for Pre, Post 1, Post 2 and Post 3, respectively), HR BRS (-1.1 +/- 0.1, -1.1 +/- 0.1, -1.3 +/- 0.1 and -1.4 +/- 0.1 beats min(-1) mmHg(-1)) and sympathetic BRS (-4.5 +/- 0.6, -4.4 +/- 0.7, -3.7 +/- 0.5 and -4.7 +/- 1.0 arbitrary units (au) beat(-1) mmHg(-1)) were unchanged by RHA. In contrast, the operating points of the baroreflexes were shifted rightward (to higher levels of BP) and upward (to higher levels of heart rate and MSNA) after RHA (P < 0.05). Time control studies performed in five additional subjects showed no change in any of the measured variables over time. Collectively, these data indicate that short-term exposure to RHA shifts ('resets') the baroreflex stimulus-response curve to higher levels of BP without influencing BRS for extended periods of time.