Acute beetroot juice supplementation on sympathetic nerve activity: a randomized, double-blind, placebo-controlled proof-of-concept study

Acute dietary nitrate (NO3-) supplementation reduces resting blood pressure in healthy normotensives. This response has been attributed to increased nitric oxide bioavailability and peripheral vasodilation, although nitric oxide also tonically inhibits central sympathetic outflow. We hypothesized that acute dietary NO3- supplementation using beetroot (BR) juice would reduce blood pressure and muscle sympathetic nerve activity (MSNA) at rest and during exercise. Fourteen participants (7 men and 7 women, age: 25 +/- 10 yr) underwent blood pressure and MSNA measurements before and after (165-180 min) ingestion of 70ml high-NO3- (similar to 6.4 mmol NO3- ) BR or NO3--depleted BR placebo (PL; similar to 0.0055 mmol NO3-) in a double-blind, randomized, crossover design. Blood pressure and MSNA were also collected during 2 min of static handgrip (30% maximal voluntary contraction). The changes in resting MSNA burst frequency (-3 +/- 5 vs. 3 +/- 4 bursts/min, P = 0.001) and burst incidence (-4 +/- 7 vs. 4 +/- 5 bursts/100 heart beats, P = 0.002) were lower after BR versus PL, whereas systolic blood pressure (-1 +/- 5 vs. 2 +/- 5 mmHg, P = 0.30) and diastolic blood pressure (4 +/- 5 vs. 5 +/- 7 mmHg, P = 0.68) as well as spontaneous arterial sympathetic baroreflex sensitivity (P = 0.95) were not different. During static handgrip, the change in MSNA burst incidence (1 +/- 8 vs. 8 +/- 9 bursts/ 100 heart beats, P = 0.04) was lower after BR versus PL, whereas MSNA burst frequency (6 +/- 6 vs. 11 +/- 10 bursts/min, P = 0.11) as well as systolic blood pressure (11 +/- 7 vs. 12 +/- 8 mmHg, P = 0.94) and diastolic blood pressure (11 +/- 4 vs. 11 +/- 4 mmHg, P = 0.60) were not different. Collectively, these data provide proof of principle that acute BR supplementation can decrease central sympathetic outflow at rest and during exercise. Dietary NO3- supplementation may represent a novel intervention to target exaggerated sympathetic outflow in clinical populations.