Pedrinolla Anna, Colosio Alessandro L, Magliozzi Roberta, Danese Elisa, Kirmizi Emine, Rossi Stefania, Pogliaghi Silvia, Calabrese Massimiliano, Gelati Matteo, Muti Ettore, Cè Emiliano, Longo Stefano, Esposito Fabio, Lippi Giuseppe, Schena Federico, Venturelli Massimo
Department of Neuroscience, Biomedicine, and Movement Science, Section of Movement Science, University of Verona, 37134 Verona, Italy.
Department of Neurological and Movement Sciences, Section of Neurology, University of Verona, 37134 Verona, Italy.
J Clin Med. 2020 Mar 27;9(4):918. doi: 10.3390/jcm9040918.
The interplay between chronic constraint and advanced aging on blood flow, shear-rate, vascular function, nitric oxide (NO)-bioavailability, microcirculation, and vascular inflammation factors is still a matter of debate. Ninety-eight individuals (Young, =28, 23±3yrs; Old, =36, 85±7yrs; Bedridden, =34, 88±6yrs) were included in the study. The bedridden group included old individuals chronically confined to bed (3.8±2.3yrs). A blood sample was collected and analyzed for plasma nitrate, and vascular inflammatory markers. Hyperemic response (∆peak) during the single passive leg movement (sPLM) test was used to measure vascular function. Skeletal muscle total hemoglobin was measured at the vastus lateralis during the sPLM test, by means of near infrared spectroscopy (NIRS). Bedridden subjects revealed a depletion of plasma nitrates compared with Old (-23.8%) and Young (-31.1%). Blood flow was lower in the Bedridden in comparison to Old (-20.1%) and Young (-31.7%). Bedridden presented lower sPLM ∆peak compared Old (-72.5%) and the Young (-83.3%). ∆peak of NIRS total hemoglobin was lower in the Bedridden compared to that in the Young (-133%). All vascular inflammatory markers except IL-6 were significantly worse in the Bedridden compared to Old and Young. No differences were found between the Old and Young in inflammatory markers. Results of this study confirm that chronic physical constraint induces an exacerbation of vascular disfunction and differential regulation of vascular-related inflammatory markers. The mechanisms involved in these negative adaptations seems to be associated with endothelial dysfunction and consequent diminished NO-bioavailability likely caused by the reduced shear-rate consequential to long-term reduction of physical activity.
长期限制活动与衰老对血流量、剪切率、血管功能、一氧化氮（NO）生物利用度、微循环及血管炎症因子的相互作用仍存在争议。本研究纳入了98名个体（年轻人，n = 28，23±3岁；老年人，n = 36，85±7岁；卧床者，n = 34，88±6岁）。卧床组包括长期卧床的老年人（3.8±2.3年）。采集血样并分析血浆硝酸盐及血管炎症标志物。单次被动腿部运动（sPLM）试验中的充血反应（∆峰值）用于测量血管功能。通过近红外光谱（NIRS）在sPLM试验期间测量股外侧肌的骨骼肌总血红蛋白。与老年人（-23.8%）和年轻人（-31.1%）相比，卧床受试者的血浆硝酸盐减少。与老年人（-20.1%）和年轻人（-31.7%）相比，卧床者的血流量较低。与老年人（-72.5%）和年轻人（-83.3%）相比，卧床者的sPLM ∆峰值较低。与年轻人相比，卧床者的NIRS总血红蛋白∆峰值较低（-133%）。与老年人和年轻人相比，卧床者除IL-6外的所有血管炎症标志物均显著更差。老年人和年轻人在炎症标志物方面未发现差异。本研究结果证实，长期身体限制会加剧血管功能障碍并导致血管相关炎症标志物的差异调节。这些负面适应所涉及的机制似乎与内皮功能障碍有关，进而可能由于长期体力活动减少导致剪切率降低，从而使NO生物利用度降低。
