Central and peripheral mechanisms underlying postexercise hypotension: a scoping review

医学 压力反射 血压 奇纳 内科学 血管阻力 科克伦图书馆 心脏病学 人口 血流动力学 血管舒张 物理疗法 随机对照试验 心率 环境卫生 精神科 心理干预
作者
Iedda Almeida Brasil,J Silva,Linda S. Pescatello,Paulo Farinatti
出处
期刊:Journal of Hypertension [Lippincott Williams & Wilkins]
卷期号:42 (5): 751-763
标识
DOI:10.1097/hjh.0000000000003702
摘要

Blood pressure (BP) reduction occurs after a single bout of exercise, referred to as postexercise hypotension (PEH). The clinical importance of PEH has been advocated owing to its potential contribution to chronic BP lowering, and as a predictor of responders to exercise training as an antihypertensive therapy. However, the mechanisms underlying PEH have not been well defined. This study undertook a scoping review of research on PEH mechanisms, as disclosed in literature reviews. We searched the PubMed, Web of Science, Scopus, Cumulated Index to Nursing and Allied Health Literature (CINAHL), Cochrane Library, and Sport Discus databases until January 2023 to locate 21 reviews – 13 narrative, four systematic with 102 primary trials, and four meta-analyses with 75 primary trials involving 1566 participants. We classified PEH mechanisms according to major physiological systems, as central (autonomic nervous system, baroreflex, cardiac) or peripheral (vascular, hemodynamic, humoral, and renal). In general, PEH has been related to changes in autonomic control leading to reduced cardiac output and/or sustained vasodilation. However, the role of autonomic control in eliciting PEH has been challenged in favor of local vasodilator factors. The contribution of secondary physiological outcomes to changes in cardiac output and/or vascular resistance during PEH remains unclear, especially by exercise modality and population (normal vs. elevated BP, young vs. older adults). Further research adopting integrated approaches to investigate the potential mechanisms of PEH is warranted, particularly when the magnitude and duration of BP reductions are clinically relevant. (PROSPERO CRD42021256569).

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