Short-term physical inactivity impairs vascular function

Abstract

Introduction Sedentarism, also termed physical inactivity, is an independent risk factor for cardiovascular diseases. Mechanisms thought to be involved include insulin resistance, dyslipidemia, hypertension, and increased inflammation. It is unknown whether changes in vascular and endothelial function also contribute to this excess risk. We hypothesized that short-term exposure to inactivity would lead to endothelial dysfunction, arterial stiffening and increased vascular inflammation. Methods Five healthy subjects (4 males and 1 female) underwent 5 days of bed rest (BR) to simulate inactivity. Measurements of vascular function [flow-mediated vasodilation (FMD) to evaluate endothelial function; applanation tonometry to assess arterial resistance], inflammation and metabolism were made before BR, daily during BR and after 2 recovery days. Subjects maintained an isocaloric diet throughout. Results Bed rest led to significant decreases in brachial artery and femoral artery FMD [Brachial: 11 ± 3% pre-BR vs. 9 ± 2% end-BR, P=0.04; Femoral: 4 ± 1% vs. 2 ± 1%, P=0.04]. The central augmentation index increased with BR [−4 ± 9% vs. 5 ± 11%, P=0.03]. Diastolic blood pressure (DBP) increased [58 ± 7 mmHg vs. 62 ± 7 mmHg, P=0.02], while neither systolic blood pressure nor heart rate changed. 15-HETE, an arachidonic acid metabolite, increased but the other inflammatory and metabolic biomarkers were unchanged. Conclusions Our findings show that acute exposure to sedentarism results in decreased endothelial function, arterial stiffening, increased DBP, and an increase in 15-HETE. We speculate that inactivity promotes a vascular “deconditioning” state characterized by impaired endothelial function, leading to arterial stiffness and increased arterial tone. Although physiologically significant, the underlying mechanisms and clinical relevance of these findings need to be further explored.

Sedentary behavior is associated with impaired biomarkers in claudicants

“…Review study 36 has suggested that prolonged uninterrupted periods of being sedentary results in insufficient skeletal muscle contractions, which suppresses lipoprotein lipase activity, blunts triglyceride uptake, reduces HDL-C levels and glucose load, and increases insulin resistance. In addition, prior bedrest studies 38, 39 demonstrated that prolonged sedentary time leads to impaired vascular function manifest as endothelial dysfunction, arterial wall stiffening, and a narrowing of conduit artery diameter. All these factors contribute to the poor health prognosis in patients with PAD.…”

The Role of Deconditioning in the End-Stage Renal Disease Myopathy: Physical Exercise Improves Altered Resting Muscle Oxygen Consumption

“…Overall, findings in this study set ESRD as a condition entailing a risk for muscle function impairment similar or higher than that of other severe chronic disease like peripheral artery disease or a neurologic disease like multiple sclerosis. Along with higher rmVO 2 , physical inactivity and sedentarism induce vascular deconditioning, with reduced endothelium-dependent vasodilatation and increased arterial stiffness and vasoconstriction [21,22] , alterations which are almost universal in ESRD patients [23] . On the other hand, muscle deconditioning attributable to the burden of ESRD -including muscle wasting, anemia and other comorbidities -and the resulting sedentary lifestyle are recognized as a prevalent, major clinical problem in ESRD patients on dialysis [24] .…”

The Impact of Repetitive Long-duration Water Immersion on Vascular Function

“…Intensity of exercise may also affect arterial stiffness, which was shown to decrease significantly after high intensity interval exercise but not moderate continuous exercise [65]. Conversely, short-term bed rest (five days) resulted in decreased FMD and increased arterial stiffness [56]. Future work should identify the cause and time course of the transient increase in arterial stiffness parameters following WI.…”