Division of Geriatrics, Department of Internal Medicine, University of Utah, Salt Lake City, Utah, United States.
Geriatric Research, Education, and Clinical Center, George E. Wahlen Department of Veterans Affairs Medical Center, Salt Lake City, Utah, United States.
J Appl Physiol (1985). 2023 Jun 1;134(6):1508-1519. doi: 10.1152/japplphysiol.00045.2023. Epub 2023 May 11.
Heart failure with preserved ejection fraction (HFpEF) is characterized by reduced ability to sustain physical activity that may be due partly to disease-related changes in autonomic function that contribute to dysregulated cardiovascular control during muscular contraction. Thus, we used a combination of static handgrip exercise (HG) and postexercise ischemia (PEI) to examine the pressor response to exercise and isolate the skeletal muscle metaboreflex, respectively. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were assessed during 2-min of static HG at 30 and 40% of maximum voluntary contraction (MVC) and subsequent PEI in 16 patients with HFpEF and 17 healthy, similarly aged controls. Changes in MAP were lower in patients with HFpEF compared with controls during both 30%MVC (Δ11 ± 7 vs. Δ15 ± 8 mmHg) and 40%MVC (Δ19 ± 14 vs. Δ30 ± 8 mmHg), and a similar pattern of response was evident during PEI (30%MVC: Δ8 ± 5 vs. Δ12 ± 8 mmHg; 40%MVC: Δ13 ± 10 vs. Δ18 ± 9 mmHg) (group effect: = 0.078 and = 0.017 at 30% and 40% MVC, respectively). Changes in HR, CO, and TPR did not differ between groups during HG or PEI ( > 0.05). Taken together, these data suggest a reduced pressor response to static muscle contractions in patients with HFpEF compared with similarly aged controls that may be mediated partly by a blunted muscle metaboreflex. These findings support a disease-related dysregulation in neural cardiovascular control that may reduce an ability to sustain physical activity in HFpEF. The current investigation has identified a diminution in the exercise-induced rise in arterial blood pressure (BP) that persisted during postexercise ischemia (PEI) in an intensity-dependent manner in patients with heart failure with preserved ejection fraction (HFpEF) compared with older, healthy controls. These findings suggest that the pressor response to exercise is reduced in patients with HFpEF, and this deficit may be mediated, in part, by a blunted muscle metaboreflex, highlighting the consequences of impaired neural cardiovascular control during exercise in this patient group.
射血分数保留的心力衰竭（HFpEF）的特征是身体活动能力降低，部分原因可能是自主功能的疾病相关变化，导致肌肉收缩期间心血管控制失调。因此，我们使用静态握力运动（HG）和运动后缺血（PEI）的组合，分别检查运动时的升压反应并分离骨骼肌代谢反射。在 16 例 HFpEF 患者和 17 例年龄匹配的健康对照者中，评估了 2 分钟的 30%和 40%最大自主收缩（MVC）的静态 HG 期间的平均动脉压（MAP）、心率（HR）、心输出量（CO）和总外周阻力（TPR），以及随后的 PEI。与对照组相比，HFpEF 患者在 30%MVC（Δ11 ± 7 对 Δ15 ± 8 mmHg）和 40%MVC（Δ19 ± 14 对 Δ30 ± 8 mmHg）期间的 MAP 变化均较低，PEI 期间也出现类似的反应模式（30%MVC：Δ8 ± 5 对 Δ12 ± 8 mmHg；40%MVC：Δ13 ± 10 对 Δ18 ± 9 mmHg）（组间差异：= 0.078 和 = 0.017 在 30%和 40% MVC 时）。HG 或 PEI 期间，HR、CO 和 TPR 的变化在两组之间无差异（> 0.05）。总之，与年龄匹配的对照组相比，HFpEF 患者的静态肌肉收缩升压反应降低，这可能部分是由于肌肉代谢反射减弱所致。这些发现支持神经心血管控制的疾病相关失调，这可能会降低 HFpEF 患者维持身体活动的能力。目前的研究在 HFpEF 患者中发现，与年龄较大的健康对照组相比，在保留射血分数的心力衰竭（HFpEF）患者中，运动诱导的动脉血压（BP）升高在运动后缺血（PEI）期间以强度依赖性方式减弱。这些发现表明，HFpEF 患者的运动升压反应降低，这种缺陷部分可能是由于肌肉代谢反射减弱所致，突出了该患者群体在运动期间神经心血管控制受损的后果。
