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1.
Trials ; 23(1): 182, 2022 Mar 01.
Article in English | MEDLINE | ID: mdl-35232475

ABSTRACT

BACKGROUND: Individuals with metabolic syndrome (MetS) are at a greater risk for developing atherosclerotic cardiovascular disease (ASCVD) than those without MetS, due to underlying endothelial dysfunction, dyslipidemia, and insulin resistance. Exercise is an effective primary and secondary prevention strategy for MetS; however, less than 25% of adults meet the minimum stated public recommendations. Barriers often identified are lack of enjoyment and lack of time. High-intensity functional training (HIFT), a time-efficient modality of exercise, has shown some potential to elicit positive affectivity and elicit increased fitness and improved glucose metabolism. However, the effects of HIFT on dyslipidemia and endothelial dysfunction have not been explored nor have the effects been explored in a population with MetS. Additionally, no studies have investigated the minimal dose of HIFT per week to see clinically meaningful changes in cardiometabolic health. The purpose of this study is to (1) determine the dose-response effect of HIFT on blood lipids, insulin resistance, and endothelial function and (2) determine the dose-response effect of HIFT on body composition, fitness, and perceived enjoyment and intention to continue the exercise. METHODS/DESIGN: In this randomized, dose-response trial, participants will undergo a 12-week HIFT intervention of either 1 day/week, 2 days/week, or 3 days/week of supervised, progressive exercise. Outcomes assessed at baseline and post-intervention will be multiple cardiometabolic markers, and fitness. Additionally, the participant's affective response will be measured after the intervention. DISCUSSION: The findings of this research will provide evidence on the minimal dose of HIFT per week to see clinically meaningful improvements in the risk factors of MetS, as well as whether this modality is likely to mitigate the barriers to exercise. If an effective dose of HIFT per week is determined and if this modality is perceived positively, it may provide exercise specialists and health care providers a tool to prevent and treat MetS. TRIAL REGISTRATION: ClinicalTrials.gov NCT05001126 . August 11, 2021.


Subject(s)
High-Intensity Interval Training , Metabolic Syndrome , Adult , Cardiometabolic Risk Factors , Exercise/physiology , Female , Humans , Male , Metabolic Syndrome/diagnosis , Metabolic Syndrome/prevention & control , Pleasure , Randomized Controlled Trials as Topic
3.
J Hum Hypertens ; 25(1): 57-62, 2011 Jan.
Article in English | MEDLINE | ID: mdl-20336149

ABSTRACT

Prehypertension is associated with significant damage to the coronary vasculature and increased rates of adverse cardiovascular events. Circulating endothelial progenitor cells (EPCs) are critical to vascular repair and the formation of new blood vessels. We tested the hypothesis that prehypertension is associated with EPC dysfunction. Peripheral blood samples were collected from 83 middle-aged and older adults (51 male and 32 female): 40 normotensive subjects (age 53±2 years; BP 111/74±1/1 mm Hg) and 43 prehypertensive subjects (age 54±2 years; 128/77±1/1 mm Hg). EPCs were isolated from peripheral blood, and EPC colony-forming capacity (colony-forming unit (CFU) assay), migratory activity (Boyden chamber) and apoptotic susceptibility (active caspase-3 concentrations) were determined. There were no significant differences in the number of EPC CFUs (10±2 vs 9±1), EPC migration (1165±82 vs 1120±84 fluorescent units) or active intracellular caspase-3 concentrations (2.7±0.3 vs 2.3±0.2 ng ml⁻¹) between the normotensive and prehypertensive groups. When groups were stratified into low prehypertension (n=27; systolic blood pressure: 120-129 mm Hg) and high prehypertension (n=16; 130-139 mm Hg), it was found that EPCs from the high prehypertensive group produced fewer (∼65%, P<0.05) CFUs compared with the low prehypertensive (4±1 vs 12±2) and normotensive adults. In conclusion, EPC colony-forming capacity is impaired only in prehypertensive adults with systolic BP greater than 130 mm Hg. Prehypertension is not associated with migratory dysfunction or enhanced apoptosis of EPCs.


Subject(s)
Endothelium, Vascular/cytology , Prehypertension/blood , Stem Cells/cytology , Stem Cells/physiology , Apoptosis/physiology , Case-Control Studies , Caspase 3/metabolism , Cell Movement/physiology , Colony-Forming Units Assay , Female , Humans , Male , Middle Aged
4.
Int J Obes (Lond) ; 33(2): 219-25, 2009 Feb.
Article in English | MEDLINE | ID: mdl-19079361

ABSTRACT

OBJECTIVE: To investigate whether adiposity influences endothelial progenitor cell (EPC) number and colony-forming capacity. DESIGN: Cross-sectional study of normal weight, overweight and obese adult humans. PARTICIPANTS: Sixty-seven sedentary adults (aged 45-65 years): 25 normal weight (body mass index (BMI) or=30 kg/m(2); 18 males/6 females). All participants were non-smokers and free of overt cardiometabolic disease. MEASUREMENTS: Peripheral blood samples were collected and circulating EPC number was assessed by flow cytometry. Putative EPCs were defined as CD45(-)/CD34(+)/VEGFR-2(+)/CD133(+) or CD45(-)/CD34(+) cells. EPC colony-forming capacity was measured in vitro using a colony-forming unit (CFU) assay. RESULTS: Number of circulating putative EPCs (either CD45(-)/CD34(+)/VEGFR-2(+)/CD133(+) or CD45(-)/CD34(+) cells) was lower (P<0.05) in obese (0.0007+/-0.0001%; 0.050+/-0.006%) compared with overweight (0.0016+/-0.0004%; 0.089+/-0.019%) and normal weight (0.0015+/-0.0003%; 0.082+/-0.008%) adults. There were no differences in EPC number between the overweight and normal weight groups. EPC colony formation was significantly less in the obese (6+/-1) and overweight (4+/-1) compared with normal weight (9+/-2) adults. CONCLUSION: These results indicate that: (1) the number of circulating EPCs is lower in obese compared with overweight and normal weight adults; and (2) EPC colony-forming capacity is blunted in overweight and obese adults compared with normal weight adults. Impairments in EPC number and function may contribute to adiposity-related cardiovascular risk.


Subject(s)
Endothelial Cells/physiology , Obesity/pathology , Stem Cells/physiology , Aged , Body Mass Index , Cell Count , Colony-Forming Units Assay , Cross-Sectional Studies , Endothelial Cells/cytology , Female , Flow Cytometry , Humans , Male , Middle Aged , Overweight/pathology , Stem Cells/cytology
5.
Clin Pharmacol Ther ; 83(1): 122-9, 2008 Jan.
Article in English | MEDLINE | ID: mdl-17522594

ABSTRACT

We examined the effect of -58 C/T and BE1 +9/-9 polymorphisms in the bradykinin B2 receptor gene on forearm vascular resistance (FVR) before and during intrabrachial artery infusion of the B2 receptor-, endothelium-dependent agonist bradykinin and the endothelium-independent agonist sodium nitroprusside in 228 normotensive subjects. In 166 white Americans, systolic blood pressure (SBP) and pulse pressure were highest in the BE1 +9/+9 group (118+/-2 and 51+/-2 mm Hg, respectively; P<0.05 versus -9/-9 for either), intermediate in the +9/-9 group (114+/-1 and 49+/-1 mm Hg, P<0.05 versus -9/-9 for pulse pressure), and lowest in the -9/-9 group (110+/-2 and 44+/-2 mm Hg). In 62 black Americans, FVR was 25% higher in the BE1 +9/+9 group compared with the BE1 +9/-9 and -9/-9 groups at baseline (P=0.038) or during bradykinin (P=0.03). Increased SBP or vascular resistance may contribute to increased left ventricular mass reported previously in individuals with the BE1+9/+9 genotype.


Subject(s)
Black or African American/genetics , Blood Pressure/genetics , Forearm/blood supply , Polymorphism, Genetic , Receptor, Bradykinin B2/genetics , Vascular Resistance/genetics , White People/genetics , Adult , Blood Flow Velocity/drug effects , Blood Pressure/drug effects , Bradykinin/administration & dosage , Dose-Response Relationship, Drug , Female , Gene Frequency , Genotype , Humans , Infusions, Intra-Arterial , Male , Nitroprusside/administration & dosage , Phenotype , Receptor, Bradykinin B2/agonists , Regional Blood Flow/genetics , Vascular Resistance/drug effects , Vasodilator Agents/administration & dosage
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