Department of Physical Therapy and Rehabilitation Science, Carver College of Medicine, University of Iowa, Iowa City, IA, 52242, USA.
Abboud Cardiovascular Research Center, Carver College of Medicine, University of Iowa, Iowa City, IA, 52242, USA.
Eur J Appl Physiol. 2020 Jun;120(6):1357-1369. doi: 10.1007/s00421-020-04368-8. Epub 2020 Apr 17.
Blood flow (BF) and vasodilator responses to knee-extension exercise are attenuated in older adults across an exercise transient (onset, kinetics, and steady-state), and reduced nitric oxide bioavailability (NO) has been hypothesized to be a primary mechanism contributing to this attenuation. We tested the hypothesis acute dietary nitrate (NO) supplementation (~ 4.03 mmol NO and 0.29 mmol NO) would improve leg vasodilator responses across an exercise transient during lower limb exercise in older adults.
Older (n = 10) untrained adults performed single and rhythmic knee-extension contractions at 20% and 40% work-rate maximum (WR) prior to and 2-h after consuming a NO or placebo beverage in a double-blind, randomized fashion. Femoral artery BF was measured by Doppler ultrasound. Vascular conductance was calculated using BF and mean arterial pressure.
Acute ingestion of dietary NO enhanced plasma [NO] and [NO] (P < 0.05). Neither dietary NO or placebo enhanced vasodilator responses at the onset of exercise or during steady state at 20% and 40% WR (P > 0.05). Leg vasodilator kinetics during rhythmic exercise remained unchanged following NO and placebo ingestion (P > 0.05).
The key findings of this study are that despite increasing plasma [NO] and [NO] acute dietary NO intake had no effect on (1) rapid hyperaemic or vasodilator responses at the onset of exercise; (2) hyperaemic and vasodilator responses during steady-state submaximal exercise; or (3) kinetics of vasodilation preceding steady-state responses. Collectively, these findings suggest that low dose dietary NO supplementation does not improve hyperaemic and vasodilator responses across an exercise transient in older adults.
在运动暂态(起始、动力学和稳态)中,老年人的膝关节伸展运动时血流量(BF)和血管舒张反应减弱,并且减少的一氧化氮生物利用度(NO)被假设为导致这种减弱的主要机制。我们测试了假设,即急性膳食硝酸盐(NO)补充剂(约 4.03 mmol NO 和 0.29 mmol NO)会改善老年人下肢运动期间运动暂态过程中的腿部血管舒张反应。
10 名未经训练的老年人以 20%和 40%的最大工作率(WR)进行单次和节律性膝关节伸展收缩,然后在双盲、随机方式下饮用 NO 或安慰剂饮料之前和之后 2 小时进行。通过多普勒超声测量股动脉 BF。使用 BF 和平均动脉压计算血管传导。
急性摄入膳食 NO 可增强血浆 [NO] 和 [NO](P < 0.05)。无论是 NO 还是安慰剂饮食都没有增强 20%和 40% WR 运动起始时或稳态时的血管舒张反应(P > 0.05)。在 NO 和安慰剂摄入后,节律性运动期间腿部血管舒张动力学保持不变(P > 0.05)。
本研究的主要发现是,尽管增加了血浆 [NO] 和 [NO],但急性膳食 NO 摄入对(1)运动起始时的快速充血或血管舒张反应;(2)稳态亚最大运动期间的充血和血管舒张反应;或(3)稳态反应前的血管舒张动力学没有影响。总之,这些发现表明,低剂量膳食 NO 补充剂不能改善老年人运动暂态过程中的充血和血管舒张反应。