Department of Kinesiology and Health Education, University of Texas at Austin, Austin, TX, USA.
Department of Pharmacology and Physiology, George Washington University, DC, USA.
Exp Physiol. 2017 Oct 1;102(10):1300-1308. doi: 10.1113/EP086446. Epub 2017 Aug 24.
What is the central question of this study? Is there a difference in the cerebral vascular response to rebreathing-induced hypercapnia between obese and lean individuals? What is the main finding and its importance? The main finding is that obese individuals have an attenuated increase in cerebral vascular conductance during hypercapnia relative to lean individuals. This finding suggests cerebral vascular dysfunction in this population, which might contribute to the greater prevalence of cerebral vascular and neurocognitive disease in this population. Obesity increases the risk of cardiovascular disease by >45%. Furthermore, obesity is a contributory factor to cognitive impairment and Alzheimer's disease. The mechanisms accounting for this increased disease risk have not been clarified. This study tested the hypothesis that the total range of change (a) in cerebral blood velocity (CBV) and cerebral vascular conductance (CVCI) and the maximal (y0) CBV and CVCI achieved during rebreathing-induced hypercapnia would be attenuated in obese individuals. Sixteen lean and 15 obese individuals participated. The magnitude of rebreathing-induced hypercapnia was similar between groups (lean, ∆15 ± 3 mmHg versus obese, ∆15 ± 2 mmHg; P = 0.82). The total range of change in CBV during rebreathing (a; expressed as a percentage) was similar between groups (lean, 91 ± 24% versus obese, 76 ± 19%, P = 0.07), whereas the total range of change in CVCI during rebreathing (a; expressed as a percentage) was attenuated in the obese individuals (lean, 71 ± 20% versus obese, 51 ± 15%, P < 0.01). Likewise, the maximal increase in CBV during rebreathing (y0; expressed as a percentage) was similar between groups (lean, 189 ± 22% versus obese, 179 ± 20%, P = 0.20), whereas the maximal increase in CVCI during rebreathing (y0; expressed as a percentage) was attenuated in the obese individuals (lean, 172 ± 19% versus obese, 155 ± 17 %, P = 0.01). These data indicate that the cerebral vascular response to rebreathing-induced hypercapnia is attenuated in obese individuals. This impairment might be a factor contributing to the elevated cerebral vascular and neurocognitive disease risk in this population.
这项研究的核心问题是什么？肥胖者和瘦者在呼吸再吸入诱导的高碳酸血症时，脑血管反应是否存在差异？主要发现及其重要性是什么？主要发现是，与瘦者相比，肥胖者在高碳酸血症期间脑血管导水管的增加幅度较小。这一发现表明该人群存在脑血管功能障碍，这可能导致该人群中脑血管和神经认知疾病的发病率更高。肥胖使心血管疾病的风险增加超过 45%。此外，肥胖是认知障碍和阿尔茨海默病的一个促成因素。导致这种疾病风险增加的机制尚未阐明。本研究检验了这样一个假设，即呼吸再吸入诱导的高碳酸血症期间，（a）脑血流速度（CBV）和脑血管导水管（CVCI）的总变化范围以及达到的最大（y0）CBV 和 CVCI，在肥胖者中会减弱。16 名瘦者和 15 名肥胖者参与了研究。两组之间呼吸再吸入诱导的高碳酸血症的幅度相似（瘦者，∆15±3mmHg 与肥胖者，∆15±2mmHg；P=0.82）。呼吸再吸入过程中 CBV 的总变化范围（a；以百分比表示）在两组之间相似（瘦者，91±24%与肥胖者，76±19%，P=0.07），而呼吸再吸入过程中 CVCI 的总变化范围（a；以百分比表示）在肥胖者中减弱（瘦者，71±20%与肥胖者，51±15%，P<0.01）。同样，呼吸再吸入过程中 CBV 的最大增加量（y0；以百分比表示）在两组之间相似（瘦者，189±22%与肥胖者，179±20%，P=0.20），而呼吸再吸入过程中 CVCI 的最大增加量（y0；以百分比表示）在肥胖者中减弱（瘦者，172±19%与肥胖者，155±17%，P=0.01）。这些数据表明，肥胖者呼吸再吸入诱导的高碳酸血症时脑血管反应减弱。这种损伤可能是导致该人群中脑血管和神经认知疾病风险升高的一个因素。
