Human Health and Nutritional Sciences, University of Guelph, 50 Stone Road East, Guelph, ON, N1G 2W1, Canada.
Department of Medicine, Northwestern University, Chicago, USA.
Eur J Appl Physiol. 2021 Sep;121(9):2437-2447. doi: 10.1007/s00421-021-04715-3. Epub 2021 May 18.
Limb immobilization causes local vasculature to experience detrimental adaptations. Simple strategies to increase blood flow (heating, fidgeting) successfully prevent acute (≤ 1 day) impairments; however, none have leveraged the hyperemic response over prolonged periods (weeks) mirroring injury rehabilitation. Throughout a 14-day unilateral limb immobilization, we sought to preserve vascular structure and responsiveness by repeatedly activating a reactive hyperemic response via blood flow restriction (BFR) and amplifying this stimulus by combining BFR with electric muscle stimulation (EMS).
Young healthy adults (M:F = 14:17, age = 22.4 ± 3.7 years) were randomly assigned to control, BFR, or BFR + EMS groups. BFR and BFR + EMS groups were treated for 30 min twice daily (3 × 10 min ischemia-reperfusion cycles; 15% maximal voluntary contraction EMS), 5 days/week (20 total sessions). Before and after immobilization, artery diameter, flow-mediated dilation (FMD) and blood flow measures were collected in the superficial femoral artery (SFA).
Following immobilization, there was less retrograde blood velocity (+ 1.8 ± 3.6 cm s, P = 0.01), but not retrograde shear (P = 0.097). All groups displayed reduced baseline and peak SFA diameter following immobilization (- 0.46 ± 0.41 mm and - 0.43 ± 0.39 mm, P < 0.01); however, there were no differences by group or across time for FMD (% diameter change, shear-corrected, or allometrically scaled) nor microvascular function assessed by peak flow capacity.
Following immobilization, our results reveal (1) neither BFR nor BFR + EMS mitigate artery structure impairments, (2) intervention-induced shear stress did not affect vascular function assessed by FMD, and (3) retrograde blood velocity is reduced at rest offering potential insight to mechanisms of flow regulation. In conclusion, BFR appears insufficient as a treatment strategy for preventing macrovascular dysfunction during limb immobilization.
肢体固定会导致局部血管发生有害的适应性改变。增加血流量的简单策略(加热、烦躁)可成功预防急性(≤ 1 天)损伤;然而,没有一种策略能够利用充血反应来模拟损伤康复的长时间(数周)过程。在为期 14 天的单侧肢体固定期间,我们试图通过血流限制(BFR)反复激活反应性充血反应,并通过 BFR 与电肌肉刺激(EMS)相结合来放大这种刺激,从而保持血管结构和反应性。
年轻健康成年人(M:F=14:17,年龄=22.4±3.7 岁)被随机分配到对照组、BFR 组或 BFR+EMS 组。BFR 和 BFR+EMS 组每天治疗 2 次,每次 30 分钟(3×10 分钟缺血再灌注循环;15%最大自主收缩 EMS),每周 5 天(共 20 次)。在固定前后,收集股浅动脉(SFA)的动脉直径、血流介导的扩张(FMD)和血流测量值。
固定后,逆行血流速度增加(+1.8±3.6cm/s,P=0.01),但逆行剪切力无变化(P=0.097)。所有组固定后基础和峰值 SFA 直径均减小(-0.46±0.41mm 和-0.43±0.39mm,P<0.01);然而,组间或随时间推移,FMD(直径变化百分比、剪切校正或比例缩放)或通过峰值流量能力评估的微血管功能均无差异。
固定后,我们的结果显示:(1)BFR 或 BFR+EMS 均不能减轻动脉结构损伤;(2)干预诱导的剪切力未影响通过 FMD 评估的血管功能;(3)休息时逆行血流速度降低,这为血流调节机制提供了潜在的见解。总之,BFR 似乎不足以作为预防肢体固定期间大血管功能障碍的治疗策略。