Adams Jose A, Uryash Arkady, Lopez Jose R, Sackner Marvin A
Division of Neonatology, Mount Sinai Medical Center, Miami Beach, FL, United States.
Department of Research, Mount Sinai Medical Center, Miami Beach, FL, United States.
Front Physiol. 2021 Feb 23;12:638491. doi: 10.3389/fphys.2021.638491. eCollection 2021.
Diabetes has reached worldwide epidemic proportions, and threatens to be a significant economic burden to both patients and healthcare systems, and an important driver of cardiovascular mortality and morbidity. Improvement in lifestyle interventions (which includes increase in physical activity via exercise) can reduce diabetes and cardiovascular disease mortality and morbidity. Encouraging a population to increase physical activity and exercise is not a simple feat particularly in individuals with co-morbidities (obesity, heart disease, stroke, peripheral vascular disease, and those with cognitive and physical limitations). Translation of the physiological benefits of exercise within that vulnerable population would be an important step for improving physical activity goals and a stopgap measure to exercise. In large part many of the beneficial effects of exercise are due to the introduction of pulsatile shear stress (PSS) to the vascular endothelium. PSS is a well-known stimulus for endothelial homeostasis, and induction of a myriad of pathways which include vasoreactivity, paracrine/endocrine function, fibrinolysis, inflammation, barrier function, and vessel growth and formation. The endothelial cell mediates the balance between vasoconstriction and relaxation via the major vasodilator endothelial derived nitric oxide (eNO). eNO is critical for vasorelaxation, increasing blood flow, and an important signaling molecule that downregulates the inflammatory cascade. A salient feature of diabetes, is endothelial dysfunction which is characterized by a reduction of the bioavailability of vasodilators, particularly nitric oxide (NO). Cellular derangements in diabetes are also related to dysregulation in Ca handling with increased intracellular Caoverload, and oxidative stress. PSS increases eNO bioavailability, reduces inflammatory phenotype, decreases intracellular Ca overload, and increases antioxidant capacity. This narrative review and perspective will outline four methods to non-invasively increase PSS; Exercise (the prototype for increasing PSS), Enhanced External Counterpulsation (EECP), Whole Body Vibration (WBV), Passive Simulated Jogging and its predicate device Whole Body Periodic Acceleration, and will discuss current knowledge on their use in diabetes.
糖尿病已成为全球性的流行病,对患者和医疗系统构成重大经济负担,也是心血管疾病死亡率和发病率上升的重要因素。改善生活方式干预措施(包括通过锻炼增加身体活动)可以降低糖尿病和心血管疾病的死亡率及发病率。鼓励人们增加身体活动和锻炼并非易事,尤其是对于患有合并症(肥胖、心脏病、中风、外周血管疾病以及有认知和身体限制的人)的个体。将锻炼对生理的益处转化到这一脆弱人群中,对于实现身体活动目标以及作为锻炼的临时措施而言,将是重要的一步。在很大程度上,锻炼的许多有益效果归因于向血管内皮引入脉动剪切应力(PSS)。PSS是内皮细胞稳态的著名刺激因素,可诱导多种途径,包括血管反应性、旁分泌/内分泌功能、纤维蛋白溶解、炎症、屏障功能以及血管生长和形成。内皮细胞通过主要的血管舒张剂内皮衍生一氧化氮(eNO)介导血管收缩和舒张之间的平衡。eNO对于血管舒张、增加血流量至关重要,并且是下调炎症级联反应的重要信号分子。糖尿病的一个显著特征是内皮功能障碍,其特点是血管舒张剂,尤其是一氧化氮(NO)的生物利用度降低。糖尿病中的细胞紊乱还与钙处理失调、细胞内钙超载增加以及氧化应激有关。PSS可提高eNO的生物利用度,减少炎症表型,降低细胞内钙超载,并提高抗氧化能力。本叙述性综述及观点将概述四种非侵入性增加PSS的方法;锻炼(增加PSS的典型方式)、增强型体外反搏(EECP)、全身振动(WBV)、被动模拟慢跑及其相关设备全身周期性加速,并将讨论目前关于它们在糖尿病治疗中应用的知识。