A new perspective on cardiovascular function and dysfunction during endurance exercise: identifying the primary cause of cardiovascular risk.

IF 4.2 2区 医学 Q1 SPORT SCIENCES Biology of Sport Pub Date : 2024-10-01 Epub Date: 2024-04-09 DOI:10.5114/biolsport.2024.134757
Amine Souissi, Ismail Dergaa, Samia Ernez Hajri, Karim Chamari, Helmi Ben Saad
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Abstract

Exercise mechanical efficiency typically falls within the range of approximately 20 to 25%. This means that a great part of the metabolic energy converted to generate movement is released as heat. Therefore, the rise in core temperature during endurance exercise in humans is proportional to generated work. Cutaneous vasodilation occurs when the core temperature threshold is reached. The rise in heart rate in response to thermal stress is a cardiovascular response that increases cardiac output and skin blood flow. The cardiovascular response during endurance exercise is a complex phenomenon potentially influenced by the involvement of nitric oxide in active thermoregulatory vasodilation. Excessive exercise can create high oxidative stress by disrupting the balance between free radicals' production and scavenging, resulting in impaired cardiovascular function. The above considerations are related to the severity and duration of endurance exercise. The first focus of this narrative review is to provide an updated understanding of cardiovascular function during endurance exercise. We aim to explore the potential role of oxidative stress in causing cardiovascular dysfunction during endurance exercise from a fresh perspective. Additionally, we aim to identify the primary factors contributing to cardiovascular risk during strenuous prolonged exercise by highlighting recent progress in this area, which may shed light on previously unexplained physiological responses. To ascertain the effect of endurance exercise on cardiovascular function and dysfunction, a narrative review of the literature was undertaken using PubMed, ScienceDirect, Medline, Google Scholar, and Scopus. The review highlighted that high oxidative stress (due to high levels of catecholamines, shear stress, immune system activation, and renal dysfunction) leads to a rise in platelet aggregation during endurance exercise. Importantly, we clearly revealed for the first time that endothelial damage, vasoconstriction, and blood coagulation (inducing thrombosis) are potentially the primary factors of cardiovascular dysfunction and myocardial infarction during and/or following endurance exercise.

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耐力运动期间心血管功能和功能障碍的新视角:确定心血管风险的主要原因。
运动的机械效率通常在 20% 到 25% 之间。这意味着,产生运动所转换的大部分新陈代谢能量都以热量的形式释放出来。因此,人体耐力运动时核心温度的升高与产生的功成正比。当达到核心温度阈值时,皮肤血管就会扩张。对热应激反应的心率上升是一种心血管反应,可增加心输出量和皮肤血流量。耐力运动时的心血管反应是一个复杂的现象,可能受到一氧化氮参与主动热调节血管扩张的影响。过度运动会破坏自由基产生和清除之间的平衡,从而产生高氧化应激,导致心血管功能受损。上述考虑因素与耐力运动的强度和持续时间有关。本综述的第一个重点是提供对耐力运动期间心血管功能的最新认识。我们旨在从一个全新的角度探讨氧化应激在耐力运动期间导致心血管功能障碍的潜在作用。此外,我们还希望通过重点介绍该领域的最新进展,找出导致长时间剧烈运动时心血管风险的主要因素,从而揭示以前无法解释的生理反应。为了确定耐力运动对心血管功能和功能障碍的影响,我们使用 PubMed、ScienceDirect、Medline、Google Scholar 和 Scopus 对文献进行了叙述性综述。综述强调,高氧化应激(由于高浓度儿茶酚胺、剪切应力、免疫系统激活和肾功能障碍)会导致耐力运动期间血小板聚集的增加。重要的是,我们首次清楚地揭示了内皮损伤、血管收缩和血液凝固(诱发血栓形成)可能是耐力运动期间和/或之后导致心血管功能障碍和心肌梗死的主要因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Biology of Sport
Biology of Sport 生物-运动科学
CiteScore
8.20
自引率
12.50%
发文量
113
审稿时长
>12 weeks
期刊介绍: Biology of Sport is the official journal of the Institute of Sport in Warsaw, Poland, published since 1984. Biology of Sport is an international scientific peer-reviewed journal, published quarterly in both paper and electronic format. The journal publishes articles concerning basic and applied sciences in sport: sports and exercise physiology, sports immunology and medicine, sports genetics, training and testing, pharmacology, as well as in other biological aspects related to sport. Priority is given to inter-disciplinary papers.
期刊最新文献
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