Macrovascular and microvascular responses to prolonged sitting with and without bodyweight exercise interruptions: A randomized cross-over trial

2021 ◽  
pp. 1358863X2110533
Author(s):  
Masahiro Horiuchi ◽  
Lee Stoner
Keyword(s):  
Vascular Function ◽  
Disease Risk ◽  
Microvascular Complications ◽  
Reactive Hyperemia ◽  
Cardiovascular Disease Risk ◽  
Medial Gastrocnemius ◽  
Stiffness Index ◽  
Tissue Oxygen Saturation ◽  
Significant Interaction Effect ◽  
Prolonged Sitting

Exposure to uninterrupted prolonged sitting leads to macro- and microvascular complications, which can contribute to increased cardiovascular disease risk. This study investigated the macrovascular and microvascular responses to 3 h of sitting that was: (i) uninterrupted (CON); and (ii) interrupted every 20 min with 1 min light intensity half squats plus calf raises (EX). Twenty healthy participants (21 [SD: 2] years; 21.5 [SD: 1.6] kg/m2) were recruited to participate in this randomized cross-over trial. Macrovascular function was quantified using brachial–ankle pulse wave velocity (baPWV) and the lower- and upper-limb arterial stiffness index (ASI). Microvascular function was quantified as the medial gastrocnemius tissue oxygen saturation (StO2) area under the curve (AUC) during reactive hyperemia. The baPWV did not significantly change with time ( p = 0.594) or by condition ( p = 0.772). The arm ASI increased by 3.6 (95% CI: 0.7 to 6.6, effect size [ES] = 0.27) with a nonsignificant condition effect ( p = 0.219). There was a significant interaction effect for leg ASI ( p = < 0.001), with ASI increasing (impairment) by 18.7 (95% CI: 12.1 to 25.3, ES = 0.63) for CON and decreasing (improvement) by −11.9 (95% CI: −18.5 to −5.3, ES = 0.40) for EX compared to presitting. Similarly, the AUC decreased (detrimental) by 18% (Δ = −321, 95% CI: −543 to −100, ES = 0.32) for CON and increased by 32% (Δ = 588, 95% CI: 366 to 809, ES = 0.59) for EX. The leg ASI was inversely associated with StO2 AUC (interclass correlation coefficient: −0.66, 95% CI: −0.51 to −0.77). These preliminary findings suggest that regularly interrupting prolonged sitting with simple bodyweight exercises may help to preserve lower-limb vascular function.

Arterial Stiffness Responses to Prolonged Sitting Combined with a High Glycemic Index Meal: A Double-Blind, Randomized Cross-Over Trial

2021 ◽  
Author(s):  
Elizabeth Kelsch ◽  
Jake C. Diana ◽  
Kathryn Burnet ◽  
Erik D. Hanson ◽  
Simon F. Fryer ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Glycemic Index ◽  
Mixed Models ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Vascular Health ◽  
Double Blind ◽  
Prolonged Sitting ◽  
Healthy Participants ◽  
Low Glycemic Index

Regular exposure to uninterrupted prolonged sitting and the consumption of high glycemic meals (HGI) is independently associated with increased cardiovascular disease risk. Sitting for as little as 1-hour can impair the health of both peripheral and central arteries. However, it is currently unknown whether combined acute exposure to uninterrupted prolonged sitting and a HGI meal is more detrimental to global (peripheral and central) vascular health. The purpose of this study was to investigate the effect of prolonged sitting (3 hours), following the consumption of a HGI or low glycemic index (LGI) meal, on global pulse wave velocity (G-PWV). METHODS: Eighteen healthy participants (70% female, mean standard deviation [SD] age: 22.6 [3.1] years old, BMI: 25.5 [6.1] kg/m2) sat for 3 hours after consuming a HGI or LGI meal. G-PWV was assessed by incorporating three PWV measures (carotid-femoral, brachial-femoral, femoral-ankle). The effects of time (PRE vs. POST) and condition (LGI vs. HGI) were analyzed using linear mixed models. RESULTS: Following prolonged sitting, G-PWV increased by 0.29 m/s (i.e., PRE vs. POST). However, the condition (P=0.987) and time x condition (P=0.954) effects were non-significant. DISCUSSION: The current findings support previous research showing an increase in arterial stiffness with prolonged sitting. However, in young and healthy adults, the arterial stiffness response was not worsened through HGI consumption.

Sleep deprivation and endothelial function: reconciling seminal evidence with recent perspectives

2021 ◽  
Vol 320 (1) ◽  
pp. H29-H35
Author(s):  
Joshua M. Cherubini ◽  
Jem L. Cheng ◽  
Jennifer S. Williams ◽  
Maureen J. MacDonald
Keyword(s):  
Cardiovascular Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Sleep Deprivation ◽  
Vascular Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Health Concern ◽  
Short Sleep ◽  
Inadequate Sleep

Sleep is critical for the maintenance of physiological homeostasis and, as such, inadequate sleep beckons a myriad of pathologies. Sleep deprivation is a growing health concern in contemporary society since short sleep durations are associated with increased cardiovascular disease risk and atherosclerotic plaque development. Vascular endothelial dysfunction is an antecedent to atherosclerosis and cardiovascular disease. Herein, we review seminal literature indicating that short sleep durations attenuate endothelial function and explore more recent evidence indicating that sleep deprivation perturbs autonomic balance and the circadian rhythmicity of peripheral vascular clock components. We further examine literature that indicates a mechanistic link between short sleep duration and endothelial dysfunction and subsequent morbidity. Understanding the mechanisms that regulate endothelial function in the context of sleep deprivation facilitates the development and optimization of interventions, such as exercise, that mitigate the ramifications of inadequate sleep on vascular function and cardiovascular health. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/sleep-deprivation-and-endothelial-function/

scholarly journals Carotid β-stiffness index is associated with slower processing speed but not working memory or white matter integrity in healthy middle-aged/older adults

2017 ◽  
Vol 122 (4) ◽  
pp. 868-876 ◽  
Author(s):  
Lyndsey E. DuBose ◽  
Michelle W. Voss ◽  
Timothy B. Weng ◽  
James D. Kent ◽  
Kaitlyn M. Dubishar ◽  
...  
Keyword(s):  
Working Memory ◽  
Carotid Artery ◽  
Processing Speed ◽  
Aortic Stiffness ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Stiffness Index ◽  
Middle Aged ◽  
Artery Stiffness ◽  
Memory Cost

Aging is associated with increased carotid artery stiffness, a predictor of incident stroke, and reduced cognitive performance and brain white matter integrity (WMI) in humans. Therefore, we hypothesized that higher carotid stiffness/lower compliance would be independently associated with slower processing speed, higher working memory cost, and lower WMI in healthy middle-aged/older (MA/O) adults. Carotid β-stiffness ( P < 0.001) was greater and compliance ( P < 0.001) was lower in MA/O ( n = 32; 64.4 ± 4.3 yr) vs. young ( n = 19; 23.8 ± 2.9 yr) adults. MA/O adults demonstrated slower processing speed (27.4 ± 4.6 vs. 35.4 ± 5.0 U/60 s, P < 0.001) and higher working memory cost (−15.4 ± 0.14 vs. −2.2 ± 0.05%, P < 0.001) vs. young adults. Global WMI was lower in MA/O adults ( P < 0.001) and regionally in the frontal lobe ( P = 0.020) and genu ( P = 0.009). In the entire cohort, multiple regression analysis that included education, sex, and body mass index, carotid β-stiffness index (B = −0.53 ± 0.15 U, P = 0.001) and age group (B = −4.61 ± 1.7, P = 0.012, adjusted R2 = 0.4) predicted processing speed but not working memory cost or WMI. Among MA/O adults, higher β-stiffness (B = −0.60 ± 0.18, P = 0.002) and lower compliance (B = 0.93 ± 0.26, P = 0.002) were associated with slower processing speed but not working memory cost or WMI. These data suggest that greater carotid artery stiffness is independently and selectively associated with slower processing speed but not working memory among MA/O adults. Carotid artery stiffening may modulate reductions in processing speed earlier than working memory with healthy aging in humans. NEW & NOTEWORTHY Previously, studies investigating the relation between large elastic artery stiffness, cognition, and brain structure have focused mainly on aortic stiffness in aged individuals with cardiovascular disease risk factors and other comorbidities. This study adds to the field by demonstrating that the age-related increases in carotid artery stiffness, but not aortic stiffness, is independently and selectively associated with slower processing speed but not working memory among middle-aged/older adults with low cardiovascular disease risk factor burden.

scholarly journals Differential Mitochondrial Adaptation in Primary Vascular Smooth Muscle Cells from a Diabetic Rat Model

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Amy C. Keller ◽  
Leslie A. Knaub ◽  
P. Mason McClatchey ◽  
Chelsea A. Connon ◽  
Ron Bouchard ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Mitochondrial Function ◽  
High Glucose ◽  
Vascular Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Muscle Cells ◽  
Nutrient Stress

Diabetes affects more than 330 million people worldwide and causes elevated cardiovascular disease risk. Mitochondria are critical for vascular function, generate cellular reactive oxygen species (ROS), and are perturbed by diabetes, representing a novel target for therapeutics. We hypothesized that adaptive mitochondrial plasticity in response to nutrient stress would be impaired in diabetes cellular physiology via a nitric oxide synthase- (NOS-) mediated decrease in mitochondrial function. Primary smooth muscle cells (SMCs) from aorta of the nonobese, insulin resistant rat diabetes model Goto-Kakizaki (GK) and the Wistar control rat were exposed to high glucose (25 mM). At baseline, significantly greater nitric oxide evolution, ROS production, and respiratory control ratio (RCR) were observed in GK SMCs. Upon exposure to high glucose, expression of phosphorylated eNOS, uncoupled respiration, and expression of mitochondrial complexes I, II, III, and V were significantly decreased in GK SMCs (p<0.05). Mitochondrial superoxide increased with high glucose in Wistar SMCs (p<0.05) with no change in the GK beyond elevated baseline concentrations. Baseline comparisons show persistent metabolic perturbations in a diabetes phenotype. Overall, nutrient stress in GK SMCs caused a persistent decline in eNOS and mitochondrial function and disrupted mitochondrial plasticity, illustrating eNOS and mitochondria as potential therapeutic targets.

scholarly journals ABNORMALITY OF LIPID METABOLISM IN PATIENTS WITH DIABETES MELLITUS TYPE 1 AND POOR GLYCEMIC CONTROL WITH AND WITHOUT DIABETIC MICROANGIOPATHIES

2016 ◽  
Vol 1 (6) ◽  
pp. 113-117
Author(s):  
Хамнуева ◽  
Larisa Khamnueva ◽  
Съемщиков ◽  
Vladimir Syomshchikov ◽  
Чугунова ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Lipid Metabolism ◽  
Glycemic Control ◽  
Disease Risk ◽  
Microvascular Complications ◽  
Cardiovascular Disease Risk ◽  
Poor Glycemic Control ◽  
High Density Lipoproteins ◽  
Very Low Density Lipoproteins

Hyperglycemia and dyslipidemia are common metabolic abnormalities in adults with type 1 diabetes mellitus (T1DM) and both increase cardiovascular disease risk. Normalization of lipid metabolism is a mandatory element in preven-tion of diabetic micro- and macroangiopathies in patients with T1DM and it is directly related to improvement of health outcome. We aimed to investigate serum lipid profiles in patients with T1DM and poor glycemic control. Among observed patients with T1DM, 76% were classified as having dyslipidemia, dyslipidemia rate was higher in patients with diabetic microangiopathies. Patients with T1DM and microvascular complications, arterial hypertension (AH) and the level of glycated hemoglobin (HbA1c) &#62;8% had significantly higher levels of total cholesterol (TC), very low density lipoproteins (VLDL), triglycerides (TG) and non-high density lipoproteins (non-HDL). Therefore, management of patients with T1DM at the outpatient stage requires a strict control of lipid metabolism.

scholarly journals Arterial Stiffness Parameters Correlate with Estimated Cardiovascular Risk in Humans: A Clinical Study

2019 ◽  
Vol 16 (14) ◽  
pp. 2547 ◽  
Author(s):  
Małgorzata Tąpolska ◽  
Maciej Spałek ◽  
Urszula Szybowicz ◽  
Remigiusz Domin ◽  
Karolina Owsik ◽  
...  
Keyword(s):  
Cardiovascular Risk ◽  
Arterial Stiffness ◽  
Cardiovascular Events ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Normal Weight ◽  
Stiffness Index ◽  
Individual Risk ◽  
Cross Sectional ◽  
Reflection Index

Arterial stiffness is said to be a novel predictor of cardiovascular events. This study investigated the correlation between arterial stiffness parameters and the estimated cardiovascular disease risk (RISK) in a Polish cohort of patients divided by age, sex, and body-mass index (BMI). The cross-sectional study enrolled 295 patients who met the inclusion criteria. Subjects were divided into three age groups, four weight groups, and by gender. The stiffness of the vessels was assessed by the measurement of the stiffness index (SI) and reflection index (RI). An individual 10-year RISK was calculated for each patient using the Heart Risk Calculator algorithm by the American Heart Association. A correlation between the SI and estimated RISK was observed (rS 0.42, p < 0.05). The strongest relationship was presented for women, the age group 40–54, and individuals with normal weight. The correlation between RI and calculated RISK was observed (rS 0.19, p < 0.05), the highest correlation was noticed for people aged 40–54 and obese. In conclusion, both SI and RI are correlated with estimated cardiovascular risk, however SI seems to be more useful than RI to predict the individual risk of future cardiovascular events. Both of these can be measured using non-invasive techniques, which demonstrates their potential utility in clinical practice.

scholarly journals Analysis of the vascular responses in a murine model of polycystic ovary syndrome

2013 ◽  
Vol 218 (2) ◽  
pp. 205-213 ◽  
Author(s):  
Sieneke Labruijere ◽  
E Leonie A F van Houten ◽  
René de Vries ◽  
Usha M Musterd-Bagghoe ◽  
Ingrid M Garrelds ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Polycystic Ovary Syndrome ◽  
Vascular Function ◽  
Disease Risk ◽  
Polycystic Ovary ◽  
Cardiovascular Disease Risk ◽  
Endothelial Damage ◽  
Reproductive Age ◽  
Enos Expression ◽  
Ovary Syndrome

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of the reproductive age, but the exact pathophysiological mechanisms involved remain unclear. Cardiovascular disease risk is increased in PCOS patients and endothelial damage has been observed. We recently developed a mouse model of PCOS with reproductive and metabolic characteristics resembling those observed in women with PCOS. In this model we studied vascular function with particular emphasis on markers of vascular endothelial function. Animals were treated for 90 days with dihydrotestosterone (DHT; 27.5 μg/day) or placebo using subcutaneous continuous-release pellets. Aortas were isolated for isometric force recordings in organ baths to investigate endothelial and vascular smooth muscle characteristics. Lungs were used to analyze endothelial nitric oxide synthase (eNOS) expression and phosphorylation. Asymmetric dimethylarginine (ADMA) levels were investigated in serum to assess endothelial damage. Expression of androgen receptor (Ar) mRNA was studied in aortas. DHT treatment (compared with placebo) induced i) a significant decrease in acetylcholine-induced aortic relaxations, with no change in calcitonin gene-related peptide- or sodium nitroprusside-induced relaxations, as well as 5-hydroxytryptamine-induced contractions; ii) no change in eNOS expression/phosphorylation in lungs or in plasma ADMA levels; and iii) a twofold increase in aortic AR expression. Our results suggest that, in DHT-exposed mice, hyperandrogenemia specifically decreases endothelium-dependent vasorelaxation without deterioration of smooth muscle function. This study may initiate further investigations to elucidate underlying mechanism for the phenotype that is present in these animals, as well as in PCOS patients.

scholarly journals Cyclo-Oxygenase (COX) Inhibitors and Cardiovascular Risk: Are Non-Steroidal Anti-Inflammatory Drugs Really Anti-Inflammatory?

2019 ◽  
Vol 20 (17) ◽  
pp. 4262 ◽  
Author(s):  
Shanzana Khan ◽  
Karen L. Andrews ◽  
Jaye P. F. Chin-Dusting
Keyword(s):  
Vascular Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Western World ◽  
Cox Inhibitors ◽  
Analgesic Effects ◽  
Overwhelming Evidence ◽  
Clinical Literature ◽  
Anti Inflammatory ◽  
Coronary Events

Cyclo-oxygenase (COX) inhibitors are among the most commonly used drugs in the western world for their anti-inflammatory and analgesic effects. However, they are also well-known to increase the risk of coronary events. This area is of renewed significance given alarming new evidence suggesting this effect can occur even with acute usage. This contrasts with the well-established usage of aspirin as a mainstay for cardiovascular prophylaxis, as well as overwhelming evidence that COX inhibition induces vasodilation and is protective for vascular function. Here, we present an updated review of the preclinical and clinical literature regarding the cardiotoxicity of COX inhibitors. While studies to date have focussed on the role of COX in influencing renal and vascular function, we suggest an interaction between prostanoids and T cells may be a novel factor, mediating elevated cardiovascular disease risk with NSAID use.

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