Streeter Daniel M, Trautman Kara A, Bennett Tylor W, McIntosh Lauren E, Grier James W, Stastny Sherri N, Hackney Kyle J
Muscle, Metabolism, and Ergogenics Workgroup, Department of Health, Nutrition, and Exercise Sciences, North Dakota State University, Fargo, North Dakota, USA.
Department of Biological Sciences, North Dakota State University, Fargo, ND, USA.
Int J Exerc Sci. 2019 May 1;12(2):701-713. doi: 10.70252/SQVU9671. eCollection 2019.
The purpose of this study was to examine the acute endothelial, cardiovascular, and performance responses to L-arginine intake by assessing flow-mediated dilation (FMD) and various indicators (e.g., heart rate, heart rate variability (HRV), blood pressure, torque) both before and after resistance exercise. Thirty (15 male, 15 female) physically active participants (mean ± SD: age 20.4 ± 1.8 years, height 176.9 ± 10.2 cm, body mass 76.0 ± 12.2 kg) volunteered for a randomized, cross-over, double-blind, placebo-controlled clinical trial. Participants completed five sets of elbow extension-flexion exercise after consumption of either 3 g L-arginine or 3 g of placebo. There was a significant decline in post-exercise elbow extension ( = 0.014) and flexion peak torque ( < 0.001). FMD response after exercise was ~5.8% less than before resistance exercise (L-arginine and placebo data pooled, < 0.001). Baseline brachial artery diameter significantly increased post-FMD ( < 0.001), post-resistance exercise ( < 0.001), and post-resistance exercise FMD ( < 0.001). There were significant time effects for HRV when expressed as the square root of the mean of the sum of squares of differences between adjacent RR intervals (RMSSD) or the proportion of differences between adjacent normal (NN) RR intervals that exceed 50 ms (pNN50) (all -values < 0.05), but there were no treatment or interaction effects (all -values > 0.05). We conclude the increased vasodilation due to acute resistance exercise was not enhanced by acute supplementation with L-arginine nor was exercise performance augmented. Further, the relative contribution of sympathetic nervous system input increased with resistance exercise but was not influenced by the addition of L-arginine.
本研究的目的是通过评估阻力运动前后的血流介导的血管舒张（FMD）以及各种指标（如心率、心率变异性（HRV）、血压、扭矩），来研究摄入L-精氨酸后急性内皮、心血管和运动表现的反应。30名（15名男性，15名女性）身体活跃的参与者（平均±标准差：年龄20.4±1.8岁，身高176.9±10.2厘米，体重76.0±12.2千克）自愿参加一项随机、交叉、双盲、安慰剂对照的临床试验。参与者在摄入3克L-精氨酸或3克安慰剂后完成五组肘部屈伸运动。运动后肘部伸展（P = 0.014）和屈曲峰值扭矩（P < 0.001）显著下降。运动后的FMD反应比阻力运动前减少了约5.8%（L-精氨酸和安慰剂数据合并，P < 0.001）。肱动脉基线直径在FMD后（P < 0.001）、阻力运动后（P < 0.001）和阻力运动后FMD时（P < 0.001）显著增加。当以相邻RR间期差异平方和的平均值的平方根（RMSSD）或相邻正常（NN）RR间期差异超过50毫秒的比例（pNN50）表示HRV时，存在显著的时间效应（所有P值< 0.05），但没有治疗或交互效应（所有P值> 0.05）。我们得出结论，急性补充L-精氨酸并不能增强急性阻力运动引起的血管舒张增加，也不能增强运动表现。此外，交感神经系统输入的相对贡献随着阻力运动增加，但不受添加L-精氨酸的影响。
