Left ventricular volumes and hemodynamic responses to postexercise ischemia in healthy humans
Left ventricular volumes and hemodynamic responses to postexercise ischemia in healthy humans
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DOI：
10.1097/00005768-200006000-00012
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发表时间：
2000-06-01
期刊：
影响因子：
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通讯作者：
Da Nóbrega, ACL
中科院分区：
文献类型：
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作者：
Bastos, BG;Williamson, JW;Da Nóbrega, ACL
目的：本研究的目的是确定运动后循环阻断（OCCL）期间心血管调节的心脏机制。方法：心率（HR）、平均动脉压（MAP）、左心室舒张末期（EDV）和收缩末期容积（ESV）、每搏输出量（SV）、心输出量（CO），和总外周血管阻力（总外周阻力（TPR））进行了评估，在9名健康志愿者在休息和静态运动的30%的最大随意收缩，然后无论是OCCL 3分钟或非随机交叉方案中的OCCL。结果：握力时HR（+ 20%; P < 0.001），CO（+ 11%; P = 0.003）。平均动脉压（+ 18%; P = 0.001），TPR（+6%; P = 0.004）增加，SV（-8%; P = 0.001）和EDV（-5%; P < 0.001）降低，而ESV无变化（P > 0.05）。这些反应在不同条件下相似（P > 0.05）。在OCCL期间，HR、SV和CO恢复至基线水平，而MAP（+ 19%; P < 0.001）和TPR（+9%; P = 0.004）仍然升高。EDV（+ 12%; P < 0.001）和ESV（+ 23%：P < 0.001）平行增加，高于静息值。结论：OCCL时肌肉代谢受体激活，通过升高TPR而增加MAP。尽管后负荷增加，ESV增加，CO和SV保持与静息值相似，因为EDV也增加，这意味着Frank-Starling机制的参与。
Purpose: The purpose of this study was to determine the cardiac mechanisms involved in cardiovascular adjustments during postexercise circulatory occlusion (OCCL). Method: Heart rate (HR), mean arterial pressure (MAP), left ventricular end-diastolic (EDV) and end-systolic volumes (ESV), stroke volume (SV), cardiac output (CO), and total peripheral vascular resistance (total peripheral resistance (TPR)) were assessed in nine healthy volunteers during rest and static exercise at 30% of maximum voluntary contraction followed by either OCCL for 3 min or non-OCCL in a randomized crossover protocol. Results: During handgrip, HR (+ 20%; P < 0.001), CO (+ 11%; P = 0.003). MAP (+ 18%; P = 0.001), and TPR (+ 6%; P = 0.004) increased, SV (- 8%; P = 0.001) and EDV (-5%; P < 0.001) decreased, while ESV did not change (P > 0.05). These responses were similar between conditions (P > 0.05). During OCCL, HR, SV, and CO returned to baseline, whereas MAP (+ 19%; P < 0.001) and TPR (+9%; P = 0.004) remained elevated. EDV (+ 12%; P < 0.001) and ESV (+ 23%: P < 0.001) increased in parallel above resting values. Conclusion: Activation of muscle metaboreceptors during OCCL increased MAP by elevating TPR. Despite the higher afterload and increased ESV, CO and SV were kept similar to resting values because EDV also increased, implying me involvement of the Frank-Starling mechanism.