Sitting decreases endothelial microparticles but not circulating angiogenic cells irrespective of lower leg exercises: a randomized cross-over trial.

Abstract

What is the central question of this study? What are the cellular and molecular determinants of increased risk for cardiovascular disease from prolonged sitting? What is the main finding and its importance? Prolonged sitting, independent of calf raise interruption strategies, decreases microparticle counts linked to endothelial activation and apoptosis. An acute bout of prolonged sitting appears to promote paradoxical decreases in microparticle counts, but the implications are not yet clear. Repeated exposure to prolonged sitting increases the risk for cardiovascular disease. However, the cellular links by which repeated exposure to prolonged sitting lead to increased cardiovascular risk have not been fully elucidated, with markers of vascular damage and repair such as microparticles (MPs) and circulating angiogenic cell (CACs) being promising targets. The objective of the study was to examine the effects of 3h of sitting with or without intermittent calf raises on annexin V+ /CD34+ , annexin V+ /CD62E+ , and annexin V+ /CD31+ /42b- MP populations linked to CAC paracrine activity, endothelial activation and apoptosis, respectively, as well as CD14+ /31+ , CD3+ /31+ , and CD34+ CACs, which are linked to endothelial repair. In a random order, 20 sedentary participants (14 females, 22±3 years) remained seated for 180min with or without performing 10 calf raises every 10min. Blood samples were obtained after 20min of quiet rest in the supine position before and after sitting. Overall, sitting decreased annexin V+ /CD34+ MPs (-12±5eventsµl-1 , P<0.01), annexin V+ /CD62E+ MPs (-17±4eventsµl-1 , P<0.001), and annexin V+ /CD31+ /42b- MPs (-22±6eventsµl-1 , P<0.001) regardless of condition. There were no differences in endothelin-1 plasma concentration, CD14+ /31+ , CD34+ or CD3+ /31+ CAC frequencies. Sitting did not alter CAC number, but decreased MPs linked to endothelial activation, apoptosis and CAC paracrine activity in a manner that was independent of muscle contraction. These findings support changes in markers of endothelial activation and apoptosis with sedentary behaviour and provide new insights into altered intercellular communication with physical inactivity such as prolonged sitting.