Abstract：
Hypertension is a widespread disease that, if persistent, increases the risks of coronary heart disease mortality and morbidity. Slow breathing is a recommended blood pressure-lowering strategy though the mechanisms mediating its effects are unknown.
This review aims to evaluate autonomic and vascular function as potential mediators driving BP adaptive responses with slow breathing.
We searched EBSCO host, Web of Science, Cochrane Central Register of Controlled Trials, and PubMed using key words for optimized search results.
Nineteen studies were included in this review (11 device-guided; 8 non-device-guided breathing). Though some studies showed increased vagally mediated components of heart rate variability during slow breathing, results from acute and long-term studies were incongruent. Increases in baroreflex sensitivity (BRS) following a single device-guided slow breathing bout were noted in normotensive and hypertensive adults. Long-term (4 weeks to 3 months) effects of slow breathing on BRS were absent. Device-guided breathing resulted in immediate reductions in muscle sympathetic nerve activity (MSNA) in normo- and hyper-tensive adults though results from long-term studies yielded inconsistent findings. Non-device-guided slow breathing posed acute and chronic effects on vascular function with reductions in arterial stiffness in adults with type I diabetes and increases in microvascular endothelial function in adults with irritable bowel syndrome. Non-device guided breathing also reduced pro-inflammatory cytokines in healthy and hypertensive adults in acute and chronic studies. No adverse effects or non-adherence to treatment were noted in these trials.
Device-guided slow breathing is a feasible and effective modality in improving BRS, HRV, and arterial stiffness though its long-term effects are obscure. Though less evidence exists supporting the efficacy of non-device-guided slow breathing, acute and chronic studies demonstrate improvements in vascular function and inflammatory cytokines. More studies are needed to further explore the long-term effects of slow breathing in general and non-device-guided breathing in particular.
This review aims to evaluate autonomic and vascular function as potential mediators driving BP adaptive responses with slow breathing.
We searched EBSCO host, Web of Science, Cochrane Central Register of Controlled Trials, and PubMed using key words for optimized search results.
Nineteen studies were included in this review (11 device-guided; 8 non-device-guided breathing). Though some studies showed increased vagally mediated components of heart rate variability during slow breathing, results from acute and long-term studies were incongruent. Increases in baroreflex sensitivity (BRS) following a single device-guided slow breathing bout were noted in normotensive and hypertensive adults. Long-term (4 weeks to 3 months) effects of slow breathing on BRS were absent. Device-guided breathing resulted in immediate reductions in muscle sympathetic nerve activity (MSNA) in normo- and hyper-tensive adults though results from long-term studies yielded inconsistent findings. Non-device-guided slow breathing posed acute and chronic effects on vascular function with reductions in arterial stiffness in adults with type I diabetes and increases in microvascular endothelial function in adults with irritable bowel syndrome. Non-device guided breathing also reduced pro-inflammatory cytokines in healthy and hypertensive adults in acute and chronic studies. No adverse effects or non-adherence to treatment were noted in these trials.
Device-guided slow breathing is a feasible and effective modality in improving BRS, HRV, and arterial stiffness though its long-term effects are obscure. Though less evidence exists supporting the efficacy of non-device-guided slow breathing, acute and chronic studies demonstrate improvements in vascular function and inflammatory cytokines. More studies are needed to further explore the long-term effects of slow breathing in general and non-device-guided breathing in particular.
摘要：
背景：高血压是一种广泛的疾病，如果持续，增加冠心病死亡率和发病率的风险。缓慢呼吸是一种推荐的降血压策略，尽管介导其作用的机制尚不清楚。
目的：这篇综述旨在评估自主神经和血管功能作为驱动缓慢呼吸的BP适应性反应的潜在介质。
方法：我们搜索了EBSCO主机，WebofScience,Cochrane中央控制试验登记册,和PubMed使用关键字来优化搜索结果。
结果：本综述纳入了19项研究（11项器械指导；8项非器械指导呼吸）。尽管一些研究表明，缓慢呼吸过程中迷走神经介导的心率变异性成分增加，急性和长期研究的结果不一致.在血压正常和高血压成人中，单次设备引导的缓慢呼吸发作后，压力反射敏感性（BRS）增加。慢呼吸对BRS的长期（4周至3个月）影响不存在。设备引导的呼吸导致正常和高强度成年人的肌肉交感神经活动（MSNA）立即减少，尽管长期研究的结果不一致。非器械引导的慢呼吸对I型糖尿病成人血管功能有急性和慢性影响,动脉僵硬度降低,肠易激综合征成人微血管内皮功能增加。在急性和慢性研究中，非器械引导的呼吸也降低了健康和高血压成人的促炎细胞因子。在这些试验中没有注意到不良反应或不坚持治疗。
结论：设备引导的慢呼吸是改善BRS的可行和有效的方式，HRV,和动脉僵硬，尽管其长期影响是模糊的。尽管存在较少的证据支持非器械引导的慢呼吸的疗效，急性和慢性研究表明血管功能和炎症细胞因子的改善.需要更多的研究来进一步探索缓慢呼吸在一般情况下的长期影响，特别是非设备引导呼吸。
目的：这篇综述旨在评估自主神经和血管功能作为驱动缓慢呼吸的BP适应性反应的潜在介质。
方法：我们搜索了EBSCO主机，WebofScience,Cochrane中央控制试验登记册,和PubMed使用关键字来优化搜索结果。
结果：本综述纳入了19项研究（11项器械指导；8项非器械指导呼吸）。尽管一些研究表明，缓慢呼吸过程中迷走神经介导的心率变异性成分增加，急性和长期研究的结果不一致.在血压正常和高血压成人中，单次设备引导的缓慢呼吸发作后，压力反射敏感性（BRS）增加。慢呼吸对BRS的长期（4周至3个月）影响不存在。设备引导的呼吸导致正常和高强度成年人的肌肉交感神经活动（MSNA）立即减少，尽管长期研究的结果不一致。非器械引导的慢呼吸对I型糖尿病成人血管功能有急性和慢性影响,动脉僵硬度降低,肠易激综合征成人微血管内皮功能增加。在急性和慢性研究中，非器械引导的呼吸也降低了健康和高血压成人的促炎细胞因子。在这些试验中没有注意到不良反应或不坚持治疗。
结论：设备引导的慢呼吸是改善BRS的可行和有效的方式，HRV,和动脉僵硬，尽管其长期影响是模糊的。尽管存在较少的证据支持非器械引导的慢呼吸的疗效，急性和慢性研究表明血管功能和炎症细胞因子的改善.需要更多的研究来进一步探索缓慢呼吸在一般情况下的长期影响，特别是非设备引导呼吸。
