The Vascular Side of Chronic Bed Rest: When a Therapeutic Approach Becomes Deleterious

Abstract

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, n = 28, 23 ± 3 yrs; Old, n = 36, 85 ± 7 yrs; Bedridden, n = 34, 88 ± 6 yrs) were included in the study. The bedridden group included old individuals chronically confined to bed (3.8 ± 2.3 yrs). 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.

Altered Vascular Endothelium-Dependent Responsiveness in Frail Elderly Patients Recovering from COVID-19 Pneumonia: Preliminary Evidence

“…First, the bed-rest experienced by the patients during their long-term hospitalization. For instance, a previous study [27] described the reduction of peripheral blood flow and endothelial function due to inactivity, which is in line with our finding. Second, the advanced age of the patients may have influenced our results, which may reflect the natural age-related reduction of endothelial function [28].…”

From Cultured Vascular Cells to Vessels: The Cellular and Molecular Basis of Vascular Dysfunction in Space

“…Regular exercise is associated with metabolic and cardiovascular adaptations which improve general health, including vascular function ( Boeno et al, 2019 ). Accordingly, chronic physical constraint obtained by bed rest exacerbates vascular, and in particular, endothelial dysfunction ( Pedrinolla et al, 2020 ). Indeed, physical training, and especially aerobic exercise, improves intracellular redox balance and mitochondrial health, reduces the levels of systemic inflammatory markers, ameliorates endothelial function and also modulates the circadian clocks thus resynchronizing vascular clock misalignment ( Silva et al, 2021 ).…”

Regulation of microRNAs in Satellite Cell Renewal, Muscle Function, Sarcopenia and the Role of Exercise

“…Recently, attention has been directed to the role of inflammation in the development of sarcopenia. Increased inflammation in the elderly, the so-called inflammaging, is driven by the expression of proinflammatory cytokines activated by transcription factor nuclear factor-kappa B (NF-κB) and response to oxidative stress and has been considered a crucial mediator of muscle wasting in sarcopenia [47][48][49]. Increasing evidence shows that mitochondrial dysfunction is a cause of sarcopenia, contributing to inflammation via reactive oxygen species (ROS) production and NF-κB activation, accelerating the aging process of skeletal muscle [50].…”