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Many adults with major depressive disorder (MDD) do not receive effective treatment. The potential benefits of resistance exercise training (RET) are understudied and may be mechanistically related to cerebral blood flow changes., Purpose: To assess feasibility, acceptability, and preliminary efficacy of a 16-week, theory-informed RET trial for the treatment of MDD and explore changes in cerebral blood flow., Methods: Ten adults with DSM-5-diagnosed MDD were enrolled in a single-arm, 16-week, twice-weekly, whole-body RET intervention, consistent with US and WHO Physical Activity resistance exercise guidelines. To build intrinsic motivation and develop exercise-preparatory habits, motivators and commitment were discussed weekly. Screening, enrollment, and intervention attendance and compliance rates documented feasibility. At baseline and weeks 8, 16, and 26, current MDD diagnosis, clinician-rated, and self-reported symptom severity were evaluated along with cerebral blood flow which was assessed as middle cerebral artery (MCA) mean blood velocity, conductance, and pulsatility., Results: Nine participants completed the intervention. Strong feasibility and acceptability (98 % adherence, 93 % compliance, and 90 % retention) were found. MDD remission was reached by 8/9 participants at week 16 and persisted through week 26. There were large decreases in clinician-rated and self-reported symptoms at each assessment (Hedges' g = 0.84-2.13). There were small-to-moderate increases in MCA velocity (g = 0.32-0.57) and conductance (g = 0.20-0.76) across time, with minimal changes in pulsatility (all g < 0.21)., Conclusions: Preliminary results suggest RET for MDD treatment is feasible and plausibly efficacious, finding large antidepressant effects. A sufficiently powered randomized controlled trial to assess RET's efficacy for treating MDD via potential cerebrovascular mechanisms is warranted., Competing Interests: Declaration of competing interest None, (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Depression hinders obesity treatment; elucidating mechanisms may enable treatment enhancements., Objectives: The aim was to investigate whether changes in neural targets in the negative affect circuit following psychotherapy mediate subsequent changes in weight and behaviors., Methods: Adults (n = 108) with obesity and depression were randomly assigned to usual care or an intervention that delivered problem-solving therapy (PST) for depression over 2 mo. fMRI for brain imaging was performed at baseline and 2 mo. BMI, physical activity, and diet were measured at baseline and 12 mo. Mediation analysis assessed between-group differences in neural target changes using t test and correlations between neural target changes and outcome changes (simple and interaction effect) using ordinary least-squares regression., Results: Compared with usual care, PST led to reductions in left amygdala activation (-0.75; 95% CI: -1.49, -0.01) and global scores of the negative affect circuit (-0.43; -0.81, -0.06), engaged by threat stimuli. Increases in amygdala activation and global circuit scores at 2 mo correlated with decreases in physical activity outcomes at 12 mo in the usual-care group; these relations were altered by PST. In relation to change in leisure-time physical activity, standardized β-coefficients were -0.67 in usual care and -0.01 in the intervention (between-group difference: 0.66; 0.02, 1.30) for change in left amygdala activation and -2.02 in usual care and -0.11 in the intervention (difference: 1.92; 0.64, 3.20) for change in global circuit scores. In relation to change in total energy expenditure, standardized β-coefficients were -0.65 in usual care and 0.08 in the intervention (difference: 0.73; 0.29, 1.16) for change in left amygdala activation and -1.65 in usual care and 0.08 in the intervention (difference: 1.74; 0.85, 2.63) for change in global circuit scores. Results were null for BMI and diet., Conclusions: Short-term changes in the negative affect circuit engaged by threat stimuli following PST for depression mediated longer-term changes in physical activity. This trial was registered at www.clinicaltrials.gov as NCT02246413 (https://clinicaltrials.gov/ct2/show/NCT02246413)., (© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society for Nutrition.)

Background and Aims: Carotid extra-media thickness (EMT) encompasses arterial adventitia and perivascular adipose tissue (PAT). Adventitial remodeling and PAT may contribute independently to functional (stiffness) and structural (remodeling) changes in artery wall properties. Visceral adiposity may contribute to PAT, thereby affecting artery stiffness. We investigated the relationships between carotid artery stiffness, EMT, and visceral adiposity in young, healthy individuals., Methods: 135 healthy males (20 ± 2 yr, body mass index [BMI] 24.8 ± 3.3 kg/m 2 ) underwent anthropometric and vascular measures on two separate days. Visceral adiposity was assessed using waist circumference and sagittal abdominal diameter (SAD). Brachial and carotid systolic, diastolic, and pulsatile (PP) blood pressures were assessed using an oscillometric cuff and applanation tonometry, respectively. Carotid intima-media thickness (IMT) and EMT were assessed using Doppler ultrasound. Carotid artery stiffness was calculated as β-stiffness and calibrated to carotid pressures., Results: Separate stepwise multiple regression models demonstrated that carotid PP (β = 0.205) and EMT (β = 0.267) accounted for 12.6% of variance in β-stiffness, while carotid PP (β = 0.195) and SAD (β = 0.226) accounted for 10.5% of variance in EMT (p < 0.05). Mediation analyses revealed carotid PP partially mediated the relationship between a) EMT and β-stiffness, and b) SAD and EMT (p < 0.05)., Conclusions: Carotid PP and EMT, but not IMT, are related to carotid β-stiffness. Carotid PP and visceral adiposity (SAD) are related to EMT. Carotid PP partially mediates the association between a) EMT and carotid β-stiffness, and b) SAD and EMT. Our findings suggest visceral adiposity may detrimentally affect subclinical markers of cardiovascular disease risk (carotid PP, EMT) and contribute to artery stiffness., (Copyright © 2017 Elsevier B.V. All rights reserved.)

Background: High blood pressure (BP) may be associated with impaired cognitive function. BP is comprised of a steady (mean arterial pressure; MAP) and pulsatile (pulse pressure; PP) component. The purpose of this study was to examine the relationship between steady and pulsatile BP and cognition among adults ≥60years old., Methods: 2058 adults age 60-85years from the 1999-2002 NHANES were used in this analysis. MAP and PP were calculated from brachial BP as 1/3 systolic +2/3 diastolic BP, and systolic - diastolic BP, respectively. Cognition was assessed using the digit-symbol substitution test (DSST)., Results: Unadjusted multiple regression revealed although PP independently predicted DSST score (β=-0.21, p<0.05), MAP was only predictive when entered simultaneously with PP (β=0.06, p<0.05). Further adjustments for sociodemographics and medical history significantly improved prediction of DSST score (∆R 2 =0.37, p<0.05), and removed the association between MAP and DSST score, although PP remained a significant predictor (β=-0.07, p<0.05)., Conclusions: PP, but not MAP, was significantly and inversely related to cognitive function among a representative sample of adults aged ≥60years after controlling for sociodemographic information and medical history., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Unlabelled: Acute hypoxia results in local vasodilation that may temporarily unload the left ventricle (LV) through nitric oxide (NO)-mediated mechanisms. Whether increasing NO levels augments LV unloading and improves ventricular-vascular coupling in hypoxia remains unknown., Purpose: Investigate the effect of acute nitrate ingestion on central hemodynamic load in hypoxia., Methods: 20 Healthy men (23 ± 3 yrs, BMI 24.6 ± 2.8 kg m(-2)) consumed 70 mL of either a) 0.45 g nitrate (NIT) or b) an inert placebo (PLA) prior to 105 min of normobaric hypoxia (11.6 ± 0.1%) in this randomized, double-blind, crossover-design study. Wave reflection index (RIX; ratio of forward to reflected wave pressure), augmentation index (AIX75) and pulse wave velocity were calculated as measures of wave reflection magnitude and aortic stiffness, respectively, from the aortic blood pressure (BP) waveform. LV wasted pressure effort (WPE) was calculated as an index of LV work due to wave reflections. Subendocardial viability ratio (SEVR) was assessed a measure of myocardial O2 supply/demand ratio., Results: Aortic diastolic BP decreased in hypoxia compared to normoxia (p < 0.05). Aortic RIX, AIX75, and LV WPE significantly decreased in hypoxia compared to normoxia (p < 0.05). Aortic systolic BP, SEVR, and PWV were unaffected by hypoxia (p > 0.05). Compared to placebo, nitrate ingestion did not significantly alter central hemodynamics in hypoxia (p > 0.05)., Conclusions: Acute hypoxic exposure unloads the LV (WPE, AIX75, and RIX) without disturbing myocardial O2 supply-demand ratio (SEVR). Reductions in LV work with hypoxia are likely due to reductions in pressure from wave reflections as hypoxia had negligible effects on aortic stiffness. Nitrate ingestion did not affect the central hemodynamic response to acute systemic hypoxia., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Purpose: In premenopausal women, amenorrhea contributes to endothelial dysfunction. It is unknown whether this vascular functional change is associated with vascular structural change., Methods: This study examined regional and systemic vascular structure and function to gain insight into subclinical atherosclerotic risk in 10 amenorrheic athletes, 18 eumenorrheic athletes, and 15 recreationally active controls. Brachial flow-mediated dilation (FMD) and low flow mediated constriction (L-FMC) were used to measure global endothelial function. Carotid-femoral pulse wave velocity (PWV) was used to measure aortic stiffness. Doppler-ultrasound of the superficial femoral artery (SFA) was used to assess intima-media thickness (IMT) and vessel diameter as indicators of vascular remodeling., Results: Amenorrheic athletes had significantly lower brachial FMD adjusted for shear stimulus (6.9 ± 1.3%) compared with eumenorrheic athletes (11.0 ± 1.0%) and controls (11.0 ± 1.1%, p = 0.05). Brachial L-FMC (-1.8 ± 4.3%) and aortic PWV (5.0 ± 1.0 m/s) of amenorrheic athletes were similar to those of eumenorrheic athletes (L-FMC, -1.6 ± 4.6%; PWV, 4.6 ± 0.5 m/s) and controls (L-FMC, -1.5 ± 2.8%, p = 0.98; PWV, 5.4 ± 0.7 m/s, p = 0.15). SFA diameters were similar in amenorrheic athletes (5.7 ± 0.7 mm) and eumenorrheic athletes (5.7 ± 0.7 mm), but amenorrheic athletes had larger SFA diameters compared with controls (5.1 ± 0.6 mm, p = 0.04). In amenorrheic athletes, SFA IMT (0.31 ± 0.03 mm) was similar to that of eumenorrheic athletes (0.35 ± 0.07 mm) but significantly thinner compared to that of controls (0.38 ± 0.06, p = 0.01)., Conclusion: Vascular dysfunction in female amenorrheic athletes is not systemic. Parenthetically, amenorrhea may not prevent favorable peripheral vascular structural adaptations to habitual exercise training., (Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.)

Background: Brachial blood pressure (BP) reactivity to stress predicts large artery damage and future cardiovascular (CV) events. Central BP is an emerging risk factor associated with target organ damage (TOD). Currently, little is known about the central BP response to mental stress and its association to TOD., Methods and Results: Twenty-five healthy, non-obese adults completed a computerized mental stress test. Brachial and carotid systolic (S)BP reactivity to stress were calculated as SBP during stress minus resting SBP. Resting carotid intima-media thickness (IMT) was also measured. Carotid SBP reactivity to stress was significantly associated with carotid IMT, independent of age, sex, body mass index, non-high density lipoprotein cholesterol and brachial SBP reactivity to stress (r = 0.386, p < 0.05)., Conclusion: The relationship between carotid SBP reactivity and carotid IMT suggests that the central BP response to stress may prove to be an early risk marker for potential subclinical TOD., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)