School of Kinesiology and Health Studies, Queen's University, Kingston, Ontario, Canada.
School of Kinesiology and Health Studies, Queen's University, Kingston, Ontario, Canada
J Appl Physiol (1985). 2017 Sep 1;123(3):594-605. doi: 10.1152/japplphysiol.00953.2016. Epub 2017 Jun 8.
Recently, dietary nitrate supplementation has been shown to improve exercise capacity in healthy individuals through a potential nitrate-nitrite-nitric oxide pathway. Nitric oxide has been shown to play an important role in compensatory vasodilation during exercise under hypoperfusion. Previously, we established that certain individuals lack a vasodilation response when perfusion pressure reductions compromise exercising muscle blood flow. Whether this lack of compensatory vasodilation in healthy, young individuals can be restored with dietary nitrate supplementation is unknown. Six healthy (21 ± 2 yr), recreationally active men completed a rhythmic forearm exercise. During steady-state exercise, the exercising arm was rapidly transitioned from an uncompromised (below heart) to a compromised (above heart) position, resulting in a reduction in local pressure of -31 ± 1 mmHg. Exercise was completed following 5 days of nitrate-rich (70 ml, 0.4 g nitrate) and nitrate-depleted (70 ml, ~0 g nitrate) beetroot juice consumption. Forearm blood flow (in milliliters per minute; brachial artery Doppler and echo ultrasound), mean arterial blood pressure (in millimeters of mercury; finger photoplethysmography), exercising forearm venous effluent (ante-cubital vein catheter), and plasma nitrite concentrations (chemiluminescence) revealed two distinct vasodilatory responses: nitrate supplementation increased (plasma nitrite) compared with placebo (245 ± 60 vs. 39 ± 9 nmol/l; < 0.001), and compensatory vasodilation was present following nitrate supplementation (568 ± 117 vs. 714 ± 139 ml ⋅ min ⋅ 100 mmHg; = 0.005) but not in placebo (687 ± 166 vs. 697 ± 171 min ⋅ 100 mmHg; = 0.42). As such, peak exercise capacity was reduced to a lesser degree (-4 ± 39 vs. -39 ± 27 N; = 0.01). In conclusion, dietary nitrate supplementation during a perfusion pressure challenge is an effective means of restoring exercise capacity and enabling compensatory vasodilation. Previously, we identified young, healthy persons who suffer compromised exercise tolerance when exercising muscle perfusion pressure is reduced as a result of a lack of compensatory vasodilation. The ability of nitrate supplementation to restore compensatory vasodilation in such noncompensators is unknown. We demonstrated that beetroot juice supplementation led to compensatory vasodilation and restored perfusion and exercise capacity. Elevated plasma nitrite is an effective intervention for correcting the absence of compensatory vasodilation in the noncompensator phenotype.
最近的研究表明，通过硝酸盐-亚硝酸盐-一氧化氮途径，膳食硝酸盐补充可以改善健康个体的运动能力。一氧化氮在低灌注下运动时的代偿性血管扩张中起着重要作用。之前，我们已经确定在灌注压降低导致运动肌肉血流减少时，某些个体缺乏血管扩张反应。在健康的年轻个体中，这种缺乏代偿性血管扩张是否可以通过膳食硝酸盐补充来恢复尚不清楚。六名健康（21 ± 2 岁）、有规律运动的男性完成了一项节律性前臂运动。在稳态运动期间，运动手臂迅速从未受影响（低于心脏）的位置转变为受影响（高于心脏）的位置，导致局部压力降低 -31 ± 1mmHg。在 5 天的富含硝酸盐（70ml，0.4g 硝酸盐）和硝酸盐耗尽（70ml，~0g 硝酸盐）甜菜根汁消耗后完成运动。前臂血流量（每分钟毫升；肱动脉多普勒和超声）、平均动脉血压（毫米汞柱；手指光容积描记法）、前臂静脉流出物（肘前静脉导管）和血浆亚硝酸盐浓度（化学发光）揭示了两种不同的血管扩张反应：与安慰剂相比，硝酸盐补充增加了（血浆亚硝酸盐）（245 ± 60 对 39 ± 9nmol/L；<0.001），并且在硝酸盐补充后存在代偿性血管扩张（568 ± 117 对 714 ± 139ml ⋅ min ⋅ 100mmHg；=0.005），而不是在安慰剂中（687 ± 166 对 697 ± 171min ⋅ 100mmHg；=0.42）。因此，峰值运动能力的降低幅度较小（-4 ± 39 对-39 ± 27N；=0.01）。总之，在灌注压挑战期间，膳食硝酸盐补充是一种恢复运动能力和实现代偿性血管扩张的有效方法。之前，我们发现当运动肌肉灌注压由于缺乏代偿性血管扩张而降低时，年轻健康的个体运动耐量会受到损害。硝酸盐补充恢复非补偿者代偿性血管扩张的能力尚不清楚。我们证明，甜菜根汁补充可导致代偿性血管扩张，并恢复灌注和运动能力。升高的血浆亚硝酸盐是纠正非补偿者中缺乏代偿性血管扩张的有效干预措施。
