Effect of acute dietary nitrate supplementation on sympathetic vasoconstriction at rest and during exercise

急性膳食硝酸盐补充对静息和运动时交感神经血管收缩的影响

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作者:Christopher J de Vries, Darren S DeLorey

Abstract

Dietary nitrate ( NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> ) supplementation has been shown to reduce resting blood pressure. However, the mechanism responsible for the reduction in blood pressure has not been identified. Dietary NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> supplementation may increase nitric oxide (NO) bioavailability, and NO has been shown to inhibit sympathetic vasoconstriction in resting and contracting skeletal muscle. Therefore, the purpose of this study was to investigate the hypothesis that acute dietary NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> supplementation would attenuate sympathetic vasoconstrictor responsiveness at rest and during exercise. In a double-blind randomized crossover design, 12 men (23 ± 5 yr) performed a cold-pressor test (CPT) at rest and during moderate- and heavy-intensity alternate-leg knee-extension exercise after consumption of NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> rich beetroot juice (~12.9 mmol NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> ) or a NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> -depleted placebo (~0.13 mmol NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> ). Venous blood was sampled before and 2.5 h after the consumption of beetroot juice for the measurement of total plasma nitrite/ NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> [NOx]. Beat-by-beat blood pressure was measured by Finometer. Leg blood flow was measured at the femoral artery via Doppler ultrasound, and leg vascular conductance (LVC) was calculated. Sympathetic vasoconstrictor responsiveness was calculated as the percentage decrease in LVC in response to the CPT. Total plasma [NOx] was greater (P < 0.001) in the NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> (285 ± 120 µM) compared with the placebo (65 ± 30 µM) condition. However, mean arterial blood pressure and plasma catecholamines were not different (P > 0.05) between NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> and placebo conditions at rest or during moderate- and heavy-intensity exercise. Sympathetic vasoconstrictor responsiveness (Δ% LVC) was not different (P > 0.05) between NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> and placebo conditions at rest ( NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> : -33 ± 10%; placebo: -35 ± 11%) or during moderate ( NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> : -18 ± 8%; placebo: -20 ± 10%)- and heavy ( NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> : -12 ± 8%; placebo: -11 ± 9%)-intensity exercise. These data demonstrate that acute dietary NO-3<math><mrow><mtext>N</mtext><msubsup><mtext>O</mtext><mn>3</mn><mo>-</mo></msubsup></mrow></math> supplementation does not alter sympathetic vasoconstrictor responsiveness at rest or during exercise in young healthy males. NEW & NOTEWORTHY Dietary nitrate may increase nitric oxide bioavailability, and nitric oxide has been shown to attenuate sympathetic vasoconstriction in resting and contracting skeletal muscle and enhance functional sympatholysis. However, the effect of dietary nitrate on sympathetic vasoconstrictor responsiveness is unknown. Acute dietary nitrate supplementation did not alter blood pressure or sympathetic vasoconstrictor responsiveness at rest or during exercise in young healthy males.

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