Author(s): EWALTS, M., GRIFFITHS, T.D., DOUGLAS, A., JENKINS, E., OLIVER, S., STEMBRIDGE, M., MOORE, J., Institution: BANGOR UNIVERSITY, UK, Country: NETHERLANDS, Abstract-ID: 2090

INTRODUCTION:
During exercise, increased sympathetic vasomotor outflow optimizes blood flow to exercising muscles and maintains blood pressure. Several mechanisms activate vasomotor outflow during exercise, including central command, muscle afferent feedback, and the arterial baroreceptor reflex. We have shown that a sustained increase in pulmonary arterial pressure, like that displayed during exercise, elicits sympathetic activation in experimental animals and humans exposed to high altitude hypoxia. The aim of this study was to investigate an additional mechanism of exercise induced sympathetic activation, which potentially arises from mechanoreceptors located in the pulmonary arterial system.
METHODS:
To address our aim, 12 healthy individuals (F=2; 28±7 years old) were studied under hypoxic conditions, a setting designed to elevate pulmonary arterial systolic pressure (PASP) above normal. The experiment comprised of three conditions: i) rest in acute hypoxia (FiO2=12.5%; baseline); ii) mild intensity exercise (RPE 11-12) in acute hypoxia (EX) and iii) mild intensity exercise in acute hypoxia combined with inhalation of vasodilator nitric oxide (iNO, 40 ppm) to selectively reduce PASP (EX reduced PASP). Muscle sympathetic nerve activity (MSNA; microneurography), ventilation (VE; breath-by-breath online gas collection system), blood pressure (BP; photoplethysmography) and heart rate (HR) were measured continuously, and ratings of perceived exertion was assessed in the final minute of exercise. PASP was measured using Doppler echocardiography. Vascular-sympathetic baroreflex gain was determined using spontaneous baroreflex sensitivity. To detect differences between conditions, a one-way repeated measures ANOVA was performed, followed by Bonferroni corrected T-tests. A statistical level of p<0.05 was accepted. All data are expressed as mean±SD.
RESULTS:
PASP increased during exercise (baseline 28±7 vs. EX 42±9 mmHg; P<0.001) and was lower in EX reduced PASP vs EX (42±9 vs. 36±8 mmHg; P=0.018). MSNA burst frequency increased by 61% during exercise (baseline 21±7 vs. EX 34±9 burst/min; P=0.001), which was partially reversed (12%) by reducing PASP with iNO during exercise (EX 34±9 vs. EX reduced PASP 30±9 burst/min; P=0.027). Reducing PASP during exercise also reduced MSNA operating point (burst incidence; 28±9 vs. 25±8 bursts/100Hb; P=0.030), without changing diastolic operating pressure (79±16 vs. 78±12 mmHg; P=0.307), or spontaneous vascular-sympathetic baroreflex gain (P=0.726). Reducing PASP during exercise had no effect on HR (P=0.999), VE (p=0.159), workload (P=0.701) or RPE (P=0.667).
CONCLUSION:
Lowering PASP reduced sympathetic outflow and reset vascular sympathetic baroreflex control of MSNA downward during hypoxic exercise. Our findings indicate that, in addition to established neural mechanisms, an input from pulmonary arterial mechanoreceptors contributes to sympathetic activation and arterial baroreceptor reflex resetting during exercise.