From the Bristol Heart Institute (BHI) CardioNomics Research Group, Clinical Research and Imaging Centre, School of Physiology, Pharmacology, Neuroscience (B.C., M.B., T.H., J.F.R.P., E.C.H.).
Department of Cardiology, Bristol Heart Institute, University Hospitals Bristol National Health Service (NHS) Foundation Trust, United Kingdom (A.E.B., A.K.N.).
Hypertension. 2018 Jul;72(1):102-109. doi: 10.1161/HYPERTENSIONAHA.118.11076.
An exaggerated blood pressure (BP) response to maximal exercise is an independent risk factor for cardiovascular events and mortality. It is unclear whether treating BP to guideline recommended levels could normalize the rise in BP during exercise, which is mediated by the metaboreflex. We aimed to assess the BP response to incremental exercise testing and metaboreflex activation in treated-controlled hypertension (n=16), treated-uncontrolled hypertension (n=16), and untreated hypertension (n=11) and 16 control participants with normal BP (n=16). All groups were matched for age and body mass index. BP was measured during an incremental Vo peak test on a cycle ergometer and during metaboreflex isolation using postexercise ischemia. Data were analyzed using 2-way ANOVA with Tukey test for multiple comparisons. Aerobic fitness was similar among groups (=0.97). The rise in absolute systolic BP from baseline at peak exercise was similar in controlled, uncontrolled, and untreated hypertension but greater compared with normotensive controls (Δ71±3, 81±7, 79±8.5 versus 47±5 mm Hg; =0.0001). Metaboreflex sensitivity was also similar in controlled, uncontrolled, and untreated hypertension but augmented compared with normotensive controls (Δsystolic BP: 21±2, 28±2, 25±3 versus 12±2 mm Hg; <0.0001). An amplified pressor response to exercise occurred in patients taking antihypertensive medication, despite having controlled BP at rest and was potentially caused (in part) by enhanced metaboreflex sensitivity. Poor BP control during exercise, partially mediated by the metaboreflex, may contribute to the heightened risk of an adverse cardiovascular event even in treated-controlled patients.
血压(BP)对最大运动的反应过度是心血管事件和死亡的独立危险因素。目前尚不清楚将 BP 控制在指南推荐水平是否可以使运动期间 BP 的升高正常化,而这种升高是由代谢反射介导的。我们旨在评估经治疗的高血压控制组(n=16)、经治疗的未控制高血压组(n=16)、未经治疗的高血压组(n=11)和 16 名血压正常的对照组(n=16)的递增运动测试和代谢反射激活时的 BP 反应。所有组均按年龄和体重指数匹配。BP 在循环测功计上进行递增 Vo 峰值测试期间以及在运动后缺血期间进行代谢反射隔离时进行测量。使用双因素方差分析和 Tukey 检验进行多重比较对数据进行分析。各组的有氧健身能力相似(=0.97)。从基线到峰值运动时绝对收缩压的升高在控制组、未控制组和未治疗组中相似,但与正常血压对照组相比更大(Δ71±3、81±7、79±8.5 与 47±5 mmHg;=0.0001)。代谢反射敏感性在控制组、未控制组和未治疗组中也相似,但与正常血压对照组相比增强(Δ收缩压:21±2、28±2、25±3 与 12±2 mmHg;<0.0001)。尽管在休息时血压得到控制,但服用抗高血压药物的患者在运动时出现了更强的升压反应,这可能部分是由于代谢反射敏感性增强所致。运动期间血压控制不佳,部分由代谢反射介导,即使在经治疗的控制组患者中,也可能导致心血管不良事件的风险增加。