Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, C040

Oral Communications

The influence of high altitude exposure on sympathetic baroreflex function in humans: a comparison of lowlanders and Nepalese Sherpa

L. L. Simpson1, S. A. Busch3, M. Stembridge2, S. J. Oliver1, P. N. Ainslie4, C. D. Steinback3, J. Moore1

1. School of Sport, Health and Exercise Sciences, Bangor University, Walsall, United Kingdom. 2. School of Sport and Health Sciences, Cardiff Metropolitan University, Cardiff, United Kingdom. 3. Faculty of Kinesiology, Sport, and Recreation, University of Alberta, Edmonton, Alberta, Canada. 4. Centre for Heart, Lung, and Vascular Health, University of British Columbia Okanagan, Kelowna, British Columbia, Canada.


Muscle sympathetic neural activity (MSNA) contributes to blood pressure regulation. Microneurographic studies have shown sustained high altitude hypoxia is accompanied by heightened MSNA; however, the influence on baroreflex control of MSNA and blood pressure remains unknown. We investigated sympathetic baroreflex function in 10 lowlanders and 7 Nepalese Sherpa. Lowlanders were studied at low altitude (LA; 344m) and high altitude (HA; 5050m), with Sherpa only studied at HA. Indices of sympathetic baroreflex function (i.e. ‘operating pressure', ‘set point' and ‘gain') were determined from beat-by-beat changes in diastolic blood pressure (DBP, photoplethysmography) and corresponding MSNA (microneurography) during supine rest, and during boluses of vasodilator sodium nitroprusside and vasoconstrictor phenylephrine (modified Oxford test). Values are means and 95% confidence intervals, compared using paired and unpaired T-tests. In lowlanders, the sympathetic baroreflex ‘operating' DBP was unchanged at HA compared to LA (71 [64-78] vs 68 [64-73] mmHg, P=0.56); however, the corresponding MSNA burst frequency (29 [22-36] vs 10 [7-12] bursts/min, P=0.0004) and MSNA burst incidence (i.e. ‘set point,' 45 [34-56] vs 18 [13-24] bursts/100HB, P=0.0007) were increased. Sympathetic baroreflex gain was unchanged (-2.6 [-1.8- -3.5] vs -2.3 [-1.8- -2.8] %/mmHg, P=0.30). In lowlanders, breathing 100% oxygen for 5 minutes at HA (n=9), to silence peripheral chemoreceptor drive, did not influence DBP (74 [66-82] vs 72 [65-79] mmHg, P=0.22), MSNA burst frequency (26 [18-35] vs 30 [22-38] bursts/min, P=0.33), MSNA burst incidence (45 [33-57] vs 44 [31-56] bursts/100HB, P=0.78), or sympathetic baroreflex gain (-2.5 [-1.7- -3.2] vs -2.8 [-2.0- -3.6] %/mmHg, P=0.16). Compared to lowlanders at HA, Sherpa had a similar baroreflex operating DBP (66 [59-73] mmHg, P=0.28); however MSNA burst frequency (22 [12-33] bursts/min, P=0.05) and MSNA burst incidence (30 [17-43] bursts/100HB, P=0.02) were lower. Sympathetic baroreflex gain was similar (-2.6 [-1.8- -3.4] %/mmHg, P=0.94) to lowlanders at HA. Our data show that sustained HA exposure in lowlanders is accompanied by an upward resetting of the sympathetic baroreflex, with no difference in the operating pressure, or the responsiveness of MSNA to changes in blood pressure. In Sherpa, the sympathetic baroreflex set point is lower, with a similar operating pressure and reflex responsiveness, compared to lowlanders at HA. Furthermore, the inability of acute hyperoxia to influence sympathetic baroreflex set point, suggests that mechanisms other than the peripheral chemoreflex could play a role in baroreflex resetting in lowlanders at HA. In conclusion, sustained HA exposure modifies sympathetic baroreflex function in lowlanders; however, the underlying mechanism(s) remain to be delineated.

Where applicable, experiments conform with Society ethical requirements