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高强度运动后血液流动性受损的 L-精氨酸作用:体外评价。

Effects of L-arginine on impaired blood fluidity after high-intensity exercise: An in vitro evaluation.

机构信息

Department of Physical Analysis and Therapeutic Sciences, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Faculty of Early Childhood Education and Care, Ohkagakuen University, Aichi, Japan.

出版信息

Clin Hemorheol Microcirc. 2022;82(1):1-12. doi: 10.3233/CH-211201.

DOI:10.3233/CH-211201
PMID:35599472
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9741740/
Abstract

BACKGROUND

Exercise-induced impairment of blood fluidity is considered to be associated with thrombosis development. However, the effects of L-arginine on blood fluidity after exercise remain unclear.

OBJECTIVE

We investigated the mechanisms of impaired blood fluidity after high-intensity exercise, and examined whether L-arginine improves exercise-induced blood fluidity impairment in vitro.

METHODS

Ten healthy male participants performed 15 minutes of ergometer exercise at 70% of their peak oxygen uptake levels. Blood samples were obtained before and after exercise. L-arginine and NG-monomethyl-L-arginine acetate (L-NMMA)-a nitric oxide (NO) synthase inhibitor-were added to the post-exercise blood samples. Using Kikuchi's microchannel method, we measured the blood passage time, percentage of obstructed microchannels, and the number of adherent white blood cells (WBCs) on the microchannel terrace.

RESULTS

Exercise increased the hematocrit levels. The blood passage times, percentage of obstructed microchannels, and the number of adherent WBCs on the microchannel terrace increased after exercise; however, they decreased in a dose-dependent manner after the addition of L-arginine. L-NMMA inhibited the L-arginine-induced decrease in blood passage time.

CONCLUSIONS

High-intensity exercise impairs blood fluidity by inducing hemoconcentration along with increasing platelet aggregation and WBC adhesion. The L-arginine-NO pathway improves blood fluidity impairment after high-intensity exercise in vitro.

摘要

背景

运动引起的血液流动性受损被认为与血栓形成的发展有关。然而,精氨酸对运动后血液流动性的影响尚不清楚。

目的

我们研究了高强度运动后血液流动性受损的机制,并研究了精氨酸是否能改善体外运动引起的血液流动性受损。

方法

10 名健康男性参与者以 70%的峰值摄氧量在测功仪上运动 15 分钟。在运动前和运动后采集血液样本。将精氨酸和 NG-单甲基-L-精氨酸乙酸盐(L-NMMA)-一种一氧化氮(NO)合酶抑制剂-加入运动后的血液样本中。使用菊池微通道法测量血液通过时间、阻塞微通道的百分比和微通道平台上黏附的白细胞(WBC)的数量。

结果

运动增加了红细胞压积水平。运动后血液通过时间、阻塞微通道的百分比和微通道平台上黏附的白细胞数量增加;然而,加入精氨酸后,它们呈剂量依赖性下降。L-NMMA 抑制了精氨酸诱导的血液通过时间的减少。

结论

高强度运动通过诱导血液浓缩以及增加血小板聚集和白细胞黏附来损害血液流动性。精氨酸-NO 通路可改善体外高强度运动引起的血液流动性受损。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/8861879b33cb/ch-82-ch211201-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/2d328901e6be/ch-82-ch211201-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/8b9f0761f33c/ch-82-ch211201-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/cd987875e2b7/ch-82-ch211201-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/793c40964d33/ch-82-ch211201-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/8861879b33cb/ch-82-ch211201-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/2d328901e6be/ch-82-ch211201-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/8b9f0761f33c/ch-82-ch211201-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/cd987875e2b7/ch-82-ch211201-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/793c40964d33/ch-82-ch211201-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/75dd/9741740/8861879b33cb/ch-82-ch211201-g005.jpg

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