Division of Experimental Medicine and Immunotherapeutics, Department of Medicine, University of Cambridge, Cambridge, United Kingdom.
J Hypertens. 2024 Nov 1;42(11):2011-2017. doi: 10.1097/HJH.0000000000003830. Epub 2024 Aug 8.
Obesity and hypertension share a well known association. However, the mechanisms underlying their relationship are not well understood. Our goal was to assess the feasibility of a longitudinal, interventional weight gain study with detailed cardiovascular measurements in humans.
Sixteen healthy, normotensive, young, male volunteers (28 ± 7 years) were enrolled. Body composition, biochemical and cardiovascular data were obtained at baseline, and after an 8-week period of overfeeding (800-1000 kcal/day). Blood pressure (BP), cardiac output (CO) and peripheral vascular resistance (PVR) were determined, as were the minimum forearm vascular resistance (MFVR), forearm blood flow (FBF) response to mental stress and heart rate variability (HRV) parameters.
Overfeeding resulted in a median weight gain of 5.6 kg [interquartile range (IQR) 4.6-6.4 kg; P < 0.001]. Seated systolic and diastolic BP were significantly increased by 10 ± 9 and 4 ± 6 mmHg, respectively, after weight gain ( P < 0.001 and P = 0.011, respectively). CO also increased and PVR decreased significantly as a result of weight gain ( P = 0.032 and P = 0.044, respectively). MFVR was also significantly decreased after weight gain ( P = 0.023). The FBF response to mental stress was blunted significantly ( P = 0.002), and sympathovagal balance and responsiveness to orthostatic challenge altered moderately after weight gain.
Our overfeeding regimen resulted in moderate weight gain and significant increases in BP. An increase in CO is likely to be the dominant mechanism underlying the observed BP changes, with decreases in PVR partially compensating for these effects. Experimental weight gain, coupled with detailed cardiovascular phenotyping, is a feasible model to examine potential mechanisms underlying obesity-associated hypertension in young adults.
肥胖和高血压有着众所周知的关联。然而，它们之间关系的机制尚不清楚。我们的目标是评估在人类中进行一项具有详细心血管测量的纵向、干预性体重增加研究的可行性。
纳入了 16 名健康、血压正常、年轻的男性志愿者（28±7 岁）。在基线时和 8 周的过度喂养（800-1000 千卡/天）后，获得身体成分、生化和心血管数据。测定血压（BP）、心输出量（CO）和外周血管阻力（PVR），以及最小前臂血管阻力（MFVR）、前臂血流（FBF）对精神压力的反应和心率变异性（HRV）参数。
过度喂养导致体重中位数增加 5.6kg[四分位距（IQR）4.6-6.4kg；P<0.001]。体重增加后，坐位收缩压和舒张压分别显著增加 10±9 和 4±6mmHg（P<0.001 和 P=0.011）。CO 也因体重增加而显著增加，PVR 也显著降低（P=0.032 和 P=0.044）。体重增加后，MFVR 也显著降低（P=0.023）。精神压力下的 FBF 反应明显减弱（P=0.002），且体重增加后交感神经迷走神经平衡和对直立挑战的反应适度改变。
我们的过度喂养方案导致体重适度增加和血压显著升高。CO 的增加可能是观察到的 BP 变化的主要机制，而 PVR 的降低部分补偿了这些影响。实验性体重增加，加上详细的心血管表型分析，是研究年轻人肥胖相关高血压潜在机制的可行模型。
