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Objective: To explore the health perceptions of Black women in emerging adulthood and the degree to which perceptions align with core Health at Every Size (HAES) principles., Design: Semistructured interviews with Black women in emerging adulthood. Data were collected between June and July 2018 as part of a larger, mixed-methods study., Setting: Southern California., Participants: Forty-one Black women aged 18-24 years were recruited via a combination of convenience and respondent-drive sampling., Phenomenon of Interest: Health perceptions of young Black women and alignment with core HAES principles., Analysis: Data were analyzed using principles of inductive thematic analysis. Following analysis, data were further interpreted within the HAES framework., Results: Participants' insights resulted in 3 main themes: (1) health is multidimensional, (2) good health means taking care of yourself, and (3) systemic and environmental disparities affect Black women's health. These themes reflect 3 HAES principles of health enhancement, weight inclusivity, and eating for well-being., Conclusions and Implications: Findings provide preliminary support for aligning HAES principles and perceptions and health for Black women in emerging adulthood. Prioritizing holistic well-being, attention to individualized health needs and access to needed information and resources in efforts to improve health outcomes among members of this demographic may be promising., (Copyright © 2022 Society for Nutrition Education and Behavior. Published by Elsevier Inc. All rights reserved.)

Importance: Endurance exercise is effective in improving peak oxygen consumption (peak V̇o2) in patients with heart failure with preserved ejection fraction (HFpEF). However, it remains unknown whether differing modes of exercise have different effects., Objective: To determine whether high-intensity interval training, moderate continuous training, and guideline-based advice on physical activity have different effects on change in peak V̇o2 in patients with HFpEF., Design, Setting, and Participants: Randomized clinical trial at 5 sites (Berlin, Leipzig, and Munich, Germany; Antwerp, Belgium; and Trondheim, Norway) from July 2014 to September 2018. From 532 screened patients, 180 sedentary patients with chronic, stable HFpEF were enrolled. Outcomes were analyzed by core laboratories blinded to treatment groups; however, the patients and staff conducting the evaluations were not blinded., Interventions: Patients were randomly assigned (1:1:1; n = 60 per group) to high-intensity interval training (3 × 38 minutes/week), moderate continuous training (5 × 40 minutes/week), or guideline control (1-time advice on physical activity according to guidelines) for 12 months (3 months in clinic followed by 9 months telemedically supervised home-based exercise)., Main Outcomes and Measures: Primary end point was change in peak V̇o2 after 3 months, with the minimal clinically important difference set at 2.5 mL/kg/min. Secondary end points included changes in metrics of cardiorespiratory fitness, diastolic function, and natriuretic peptides after 3 and 12 months., Results: Among 180 patients who were randomized (mean age, 70 years; 120 women [67%]), 166 (92%) and 154 (86%) completed evaluation at 3 and 12 months, respectively. Change in peak V̇o2 over 3 months for high-intensity interval training vs guideline control was 1.1 vs -0.6 mL/kg/min (difference, 1.5 [95% CI, 0.4 to 2.7]); for moderate continuous training vs guideline control, 1.6 vs -0.6 mL/kg/min (difference, 2.0 [95% CI, 0.9 to 3.1]); and for high-intensity interval training vs moderate continuous training, 1.1 vs 1.6 mL/kg/min (difference, -0.4 [95% CI, -1.4 to 0.6]). No comparisons were statistically significant after 12 months. There were no significant changes in diastolic function or natriuretic peptides. Acute coronary syndrome was recorded in 4 high-intensity interval training patients (7%), 3 moderate continuous training patients (5%), and 5 guideline control patients (8%)., Conclusions and Relevance: Among patients with HFpEF, there was no statistically significant difference in change in peak V̇o2 at 3 months between those assigned to high-intensity interval vs moderate continuous training, and neither group met the prespecified minimal clinically important difference compared with the guideline control. These findings do not support either high-intensity interval training or moderate continuous training compared with guideline-based physical activity for patients with HFpEF., Trial Registration: ClinicalTrials.gov Identifier: NCT02078947.

Purpose of Review: In this review, our aim is to summarize the evidence of exercise interventions in heart failure. Addressing pathophysiology, we discuss training modalities and optimal dose finding in exercising patients with reduced (HFrEF) and preserved ejection fraction (HFpEF)., Recent Findings: While smaller studies showed a trend towards improved exercise capacity by high-intensity interval training in comparison with moderate continuous training in HFrEF, recent multicenter randomized trials were unable to confirm these findings. Considering the lack of effective drug therapies in HFpEF, exercise training plays an even more important role in this particular population. Exercise training in heart failure is beneficial in addition to medical and device therapy. Data are still mostly limited to HFrEF. Intensity should primarily be moderate at a daily base. The concept of "the higher the better" could not be confirmed for HFrEF. The overall concept of training is to maximally strain the periphery without straining the myocardium.

Background: Although systolic right ventricular (RV) dysfunction has been shown to be a potent predictor for adverse outcomes in patients with heart failure with preserved ejection fraction (HFpEF), RV functional abnormalities in the course of the syndrome are not well characterized. We, therefore, sought to assess load-independent and load-dependent systolic and diastolic characteristics of RV function in stable outpatients with HFpEF., Methods and Results: We invasively obtained RV and left ventricular pressure-volume loops in 24 HFpEF patients and 9 patients without heart failure symptoms with a conductance catheter during basal conditions and handgrip exercise. Transient preload reduction was used to extrapolate the RV end-systolic elastance and diastolic stiffness constant. HFpEF patients and controls showed similar left ventricular and RV dimensions and ejection fractions with elevated left ventricular filling pressures. In HFpEF patients, invasively determined load-independent RV contractility ( P =0.04) and load-independent passive RV stiffness constant β ( P <0.01) were elevated. Although RV relaxation and cardiac output were similar at baseline, HFpEF patients demonstrated a blunted increase in cardiac output under exercise ( P =0.01) associated with prolonged RV relaxation ( P =0.01), decrease in stroke volume ( P <0.01), higher RV-filling pressures ( P <0.01), and a marked increase in the end-diastolic pressure-volume relationship ( P <0.01)., Conclusions: In compensated stages of the HFpEF syndrome, systolic RV function is preserved, but diastolic abnormalities with intrinsic RV stiffness and prolonged RV relaxation are already present. Impaired diastolic RV reserve contributes to a blunted increase in cardiac output during exertion. Because impairments in diastolic function seem to be a biventricular phenomenon, RV diastolic dysfunction warrants further consideration when characterizing HFpEF patients., Clinical Trial Registration: https://www.clinicaltrials.gov. Unique identifier: NCT02459626., (© 2018 American Heart Association, Inc.)

Purpose of Review: Severe exercise intolerance and early fatigue are hallmarks of heart failure patients either with a reduced (HFrEF) or a still preserved (HFpEF) ejection fraction. This review, therefore, will provide a contemporary summary of the alterations currently known to occur in the skeletal muscles of both HFrEF and HFpEF, and provide some further directions that will be required if we want to improve our current understanding of this area., Recent Findings: Skeletal muscle alterations are well documented for over 20 years in HFrEF, and during the recent years also data are presented that in HFpEF muscular alterations are present. Alterations are ranging from a shift in fiber type and capillarization to an induction of atrophy and modulation of mitochondrial energy supply. In general, the molecular alterations are more severe in the skeletal muscle of HFrEF when compared to HFpEF. The alterations occurring in the skeletal muscle at the molecular level may contribute to exercise intolerance in HFrEF and HFpEF. Nevertheless, the knowledge of changes in the skeletal muscle of HFpEF is still sparsely available and more studies in this HF cohort are clearly warranted.

Until the late 1980s, physical exercise training was a contraindication in patients with heart failure. Extensive research has demonstrated that exercise training reverses heart failure-associated pathology at the clinical and molecular levels. Exercise training has emerged as a class I recommendation in all major national and international guidelines for the treatment of chronic heart failure. Knowledge gained in clinical trials and molecular research builds a strong case for exercise training as a key therapeutic component of an evidence-based treatment of chronic heart failure. It is long overdue to provide patients with an infrastructure that enables them to benefit from this class I intervention., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Unlabelled: Patients with advanced chronic heart failure (CHF) are characterized by progressive muscle wasting. The two E3-ligases Rnf28 and Atrogin-1 controlling the activation of the ubiquitinproteasome system might be of importance for the regulation of muscle size. Given the convincing effect of regular physical exercise training (ET) in CHF, it was the aim of the present trial to elucidate, whether ET affects both mentioned enzymes in CHF and whether this is associated with an increase in skeletal muscle mass., Methods: 37 patients with severe CHF were randomized to 12 weeks of ET or sedentary lifestyle (control). The expression of Rnf28 and Atrogin-1 in the skeletal muscle was analyzed by RT-PCR and Western blotting. Skeletal muscle cross sectional area (CSA) was measured by computed tomography., Results: In CHF patients ET led to a significant reduction in skeletal muscle mRNA transcription (from 14.3 ± 2.0 to 8.7 ± 1.4 arbitrary units; p<0.05 versus baseline and versus control for the change) and protein expression of Rnf28 (from 4.70 ± 1.35 to 2.84 ± 0.65 arbitrary units; p<0.05 versus baseline and versus control for the change). This was accompanied by a significant increase in total muscle CSA of both thighs (from 139.9 ± 5.2 to 149.2 ± 5.9 cm(2); p<0.05 versus baseline and versus control for the change). On the contrary, Atrogin-1 was not affected., Conclusion: In patients with advanced CHF, regular physical exercise training led to a decrease in Rnf28 expression in the skeletal muscle. This was linked to an increase in skeletal muscle cross sectional area, supporting the notion that ET has anti-catabolic properties in CHF., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

Background: Muscle wasting occurs in both chronic heart failure (CHF) and normal aging and contributes to exercise intolerance and increased morbidity/mortality. However, the molecular mechanisms of muscle atrophy in CHF and their interaction with aging are still largely unknown. We therefore measured the activation of the ubiquitin-proteasome system and the lysosomal pathway of intracellular proteolysis in muscle biopsies of CHF patients and healthy controls in two age strata and assessed the age-dependent effects of a 4-week endurance training program on the catabolic-anabolic balance., Methods and Results: Sixty CHF patients (30 patients aged ≤55 years, mean age 46±5 years; 30 patients aged ≥65 years, mean age 72±5 years) and 60 healthy controls (30 subjects aged ≤55 years, mean age 50±5 years; 30 subjects aged ≥65 years, mean age 72±4 years) were randomized to 4 weeks of supervised endurance training or to a control group. Before and after the intervention, vastus lateralis muscle biopsies were obtained. The expressions of cathepsin-L and the muscle-specific E3 ligases MuRF-1 and MAFbx were measured by real-time polymerase chain reaction and confirmed by Western blot. At baseline, MuRF-1 expression was significantly higher in CHF patients versus healthy controls (mRNA: 624±59 versus 401±25 relative units; P=0.007). After 4 weeks of exercise training, MuRF-1 mRNA expression was reduced by -32.8% (P=0.02) in CHF patients aged ≤55 years and by -37.0% (P<0.05) in CHF patients aged ≥65 years., Conclusions: MuRF-1, a component of the ubiquitin-proteasome system involved in muscle proteolysis, is increased in the skeletal muscle of patients with heart failure. Exercise training results in reduced MuRF-1 levels, suggesting that it blocks ubiquitin-proteasome system activation and does so in both younger and older CHF patients., Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00176319.

In the arterial wall nitric oxide (NO) is the key transmitter for endothelium-dependent regulation of vascular tone. It is produced in intact endothelial cells by endothelial NO synthase (eNOS) as the key enzyme from L-arginine. Endothelial NO generation is highly regulated by mechanical, humoral, and metabolic factors. The regulation of NO synthesis occurs at different levels: ENOS gene polymorphisms are related to eNOS expression and activity and may potentially increase coronary event rate, mRNA expression is influenced by estrogen status and shear stress, mRNA stability is enhanced by vascular endothelial growth factor (VEGF), and final enzyme activity is regulated by the phosphorylation status at serine/threonine residues. Released from endothelial cells NO is rapidly transported to the neighboring vascular smooth muscle cells (VSMCs), where it induces the production of cGMP as a second messenger. CGMP in turn increases Ca2+ uptake into intracellular calcium stores thereby lowering [Ca2+]i and inducing VSMC relaxation and vasodilation. On its way to the VSMCs NO may be prematurely degraded by reactive oxygen species. On the other hand, chronic endurance exercise with regular bouts of increased laminar flow along the endothelium has the potential to increase eNOS mRNA expression and phosphorylation via AKT (protein kinase B) and to reduce oxidative stress by improving antioxidative protection. The growing knowledge about the complex regulation of NO synthesis and degradation in cardiovascular diseases and its response to exercise has led to a new understanding of the protective effects of long-term habitual physical activity against atherosclerotic heart disease and vascular aging.

Endothelial progenitor cells (EPCs) are thought to participate in endothelial cell regeneration and neovascularization in either a direct or an indirect way. The number of circulating EPCs is influenced by many factors like disease status, medication, age, and fitness level and is an independent predictor of disease progression and cardiovascular events. Experimental as well as clinical studies during the last 10 years clearly demonstrated that physical exercise training has a beneficial effect on endothelial function, which is a clear predictive value for cardiovascular mortality. Over the last years mainly clinical studies provided solid evidence for an exercise training induced mobilization of EPCs from the bone marrow, thereby possibly influencing the regeneration of the endothelial cell layer. This review will discuss the mechanisms how exercise induces mobilization of EPCs from the bone marrow with a focus on the influence on the redox balance.

In clinical trials as well as in several animal experiments it is evident that physical exercise is a powerful tool to positively influence the development and/or progression of atherosclerosis and coronary artery disease (CAD). The main target of physical exercise seems to be the maintenance of an intact endothelial cell layer. Since the discovery that endothelial progenitor cells (EPCs) are present in the circulation and the knowledge that exercise, either as a single exercise bout or an exercise training program, have the potency to mobilize EPCs from the bone marrow, the contribution of the EPCs for the preservation or repair of the endothelial cell layer is still under debate. Either the EPCs differentiate into mature endothelial cells, or they stimulate via a paracrine mechanism mature endothelial cells to proliferate. It is still unclear, if the exercise-induced mobilization of EPCs is casually related to the improvement of endothelial function. This review will discuss the role of endothelial progenitor cells in the beneficial effects of physical exercise on atherosclerosis and coronary artery disease.

Background: The aim of this prospective, randomized study was to examine whether additional school exercise lessons would result in improved peak oxygen uptake (primary end point) and body mass index-standard deviation score, motor and coordinative abilities, circulating progenitor cells, and high-density lipoprotein cholesterol (major secondary end points)., Methods and Results: Seven sixth-grade classes (182 children, aged 11.1+/-0.7 years) were randomized to an intervention group (4 classes with 109 students) with daily school exercise lessons for 1 year and a control group (3 classes with 73 students) with regular school sports twice weekly. The significant effects of intervention estimated from ANCOVA adjusted for intraclass correlation were the following: increase of peak o(2) (3.7 mL/kg per minute; 95% confidence interval, 0.3 to 7.2) and increase of circulating progenitor cells evaluated by flow cytometry (97 cells per 1 x 10(6) leukocytes; 95% confidence interval, 13 to 181). No significant difference was seen for body mass index-standard deviation score (-0.08; 95% confidence interval, -0.28 to 0.13); however, there was a trend to reduction of the prevalence of overweight and obese children in the intervention group (from 12.8% to 7.3%). No treatment effect was seen for motor and coordinative abilities (4; 95% confidence interval, -1 to 8) and high-density lipoprotein cholesterol (0.03 mmol/L; 95% confidence interval, -0.08 to 0.14)., Conclusions: Regular physical activity by means of daily school exercise lessons has a significant positive effect on physical fitness (o(2)max). Furthermore, the number of circulating progenitor cells can be increased, and there is a positive trend in body mass index-standard deviation score reduction and motor ability improvement. Therefore, we conclude that primary prevention by means of increasing physical activity should start in childhood., Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Identifier: NCT00176371.

Exercise stimulates the release of hematopoietic and endothelial progenitor cells (EPC) from the bone marrow. However, no data are available concerning the time frame of EPC release during strenuous exercise. The aim of the present study was to investigate the time-dependent release of progenitor cells during strenuous exercise. Eighteen healthy young men cycled for 4 h continuously at 70% of their individual anaerobic threshold. Peripheral blood was drawn at 16 predefined time points during and after finishing cycling. A significant rise in heart rate and leukocytes was obvious, whereas lactate levels and hematocrit did not change. The amount of circulating progenitor cells, EPCs, mature endothelial cells (mECs), and microparticles, quantified by flow cytometry, showed a significant time-dependent increase at 210/240 min. In addition a very early rise in VEGF and later increase in IL-6, both measured by ELISA, were evident. All observed changes were normalized 24 h after finishing the test. In conclusion, strenuous activity in healthy individuals leads to a time-dependent increase in mECs, PCs, and EPCs that may be related to VEGF and IL-6.

Aims: Levels of endothelial progenitor cells (EPCs), that can be increased by regular exercise, correlate with vascular function. In the context of primary prevention, the impact of regular physical activity on the amount and function of EPC has not yet been investigated in school children., Methods: Four sixth grade classes of high school students (n=92) were randomly assigned to either the intervention group (IG) with daily physical exercise (45 min) at school or to the control group (CG) with conventional physical education (PE) (2 h/week). In addition, one sixth grade class at a high school focused on competitive sports (PE) served as a reference group. After 1 school year, exercise capacity and the amount and function of EPCs were evaluated., Results: After 1 year, a significantly higher Vo2max was evident in the intervention group. Nevertheless, exercise capacity did not reach the level of children from PE. In addition, exercise intervention was successful in increasing the amount of EPCs but failed to increase the migratory capacity of the cells., Conclusion: The result of this study shows, that intensified, supervised school sports leads to an increase in exercise capacity and EPCs in children. Nevertheless, its effect on primary prevention in cardiovascular disease has to be proven in further longitudinal studies.

Background: Chronic heart failure (CHF) is accompanied by an inflammatory activation which occurs both systemically and in the skeletal muscle. Exercise training has been shown to reduce the local expression of cytokines and inducible nitric oxide synthase (iNOS) in muscle biopsies of CHF patients. INOS-derived NO can inhibit oxidative phosphorylation and contribute to skeletal muscle dysfunction in CHF., Design: To investigate the correlation between changes in local iNOS expression associated with regular exercise and changes in aerobic enzyme activities in the skeletal muscle of patients with CHF. Twenty male CHF patients [ejection fraction 25% (SE 2), age 54 (SE 2) years] were randomized to a training (n=10) or a control group (C, n=10)., Methods: At baseline and after 6 months skeletal muscle iNOS expression was measured by real-time polymerase chain reaction. INOS protein and protein nitrosylation were assessed by immunohistochemistry. Cytochrome c oxidase (COX) activity was quantified electrochemically using the Clark oxygen electrode., Results: Exercise training led to a 27% increase in cytochrome c oxidase activity [from 21.8 (SE 3.2) to 27.7 (SE 3.5) nmol O2/mg per min, P=0.02 versus baseline]. Changes in iNOS expression and iNOS protein content were inversely correlated with changes in COX-activity (r=-0.60, P=0.01; r=-0.71, P<0.001)., Conclusions: The inverse correlation between iNOS expression/iNOS protein content and COX-activity indicates that local anti-inflammatory effects may contribute to improved muscular oxidative metabolism.

Background: Chronic heart failure (CHF) is associated with progressive muscle atrophy and reduced local expression of insulin-like growth factor I (IGF-I)., Design: The present study was designed to test the hypothesis that the local deficiency of IGF-I in the skeletal muscle of patients with CHF would respond to a 6-months aerobic training intervention. Therefore, 18 patients [mean age 52.4 (SD 4.8) years, left ventricular ejection function (LVEF) 27 (SD 6)%] were prospectively randomized to either 6 months of training or sedentary lifestyle., Methods: Serum levels of growth hormone (GH) were measured by immunofluorometric assay, IGF-I by competitive solid phase immunoassay. IGF-I expression was assessed in vastus lateralis biopsies by real-time PCR., Results: Exercise training led to a significant increase in peak oxygen uptake by 26% [from 20.3 (SD 3.3) ml/kg per min to 25.5 (SD 5.7) ml/kg per min, P=0.003 versus control]. Local expression of IGF-I increased significantly after exercise training by 81% [from 6.3 (SE 0.8) to 11.4 (SE 1.4) relative units, P=0.007 versus control] while IGF-I receptor expression was reduced by 33% [from 20.0 (SE 2.1) to 13.8 (SE 1.7) relative units, P=0.008 versus control]. Serum growth hormone (GH) rose modestly from 0.12 (SE 0.07) to 0.65 (SE 0.37) ng/ml in the training group (P=0.043 versus baseline), however, this change was not significant compared to the control group (P=0.848). IGF-I serum levels remained virtually unchanged., Conclusions: Exercise training improves local IGF-I expression without significant changes of systemic parameters of the GH/IGF-I axis. These findings indicate that exercise training has the therapeutic potential to attenuate peripheral skeletal muscle alterations in particular with respect to local IGF-I expression in patients with moderate CHF.

Background: In patients with stable coronary artery disease, physical exercise training (ET) improves endothelial dysfunction. A potential mechanism mediating the enhanced vasomotor function is a reduced breakdown of endothelium-derived nitric oxide by reactive oxygen species (ROS). The aim of the present study was to analyze the impact of ET on sources of ROS generation in the left internal mammary artery of patients with symptomatic coronary artery disease., Methods and Results: In left internal mammary artery rings sampled during bypass surgery from 45 patients randomized to either a training (n=22) or an inactive control (n=23) group, the mRNA expression of NAD(P)H oxidase subunits, NAD(P)H oxidase activity, and ROS production were assessed. In addition, endothelial function, expression of angiotensin II (Ang II) receptor type 1 and 2 (AT1-R and AT2-R), and Ang II-mediated vasoconstriction were determined. ET resulted in a significant lower expression of gp91phox (23.1+/-0.5 versus 69.1+/-18.1 arbitrary units, training versus control), p22phox (0.7+/-0.3 versus 2.0+/-0.5 arbitrary units), and Nox4 (2.7+/-1.2 versus 5.4+/-1.0 arbitrary units). Enzymatic activity (2.1+/-0.3 versus 4.9+/-0.4 mU/mg) and ROS generation (0.02+/-0.01 versus 0.06+/-0.02 arbitrary units) were significantly lower in the training compared with the control group. On a functional level, ET resulted in improved acetylcholine-mediated vasodilatation and a 49% reduction in Ang II-induced vasoconstriction, accompanied by lower AT1-R (3.7+/-0.8 versus 16.6+/-5.7 arbitrary units, training versus control) and higher AT2-R (7.8+/-2.5 versus 1.6+/-0.7 arbitrary units) mRNA expression., Conclusions: ET reduces vascular expression of NAD(P)H oxidase and AT1-R, resulting in decreased local ROS generation. These molecular effects converge in a reduced Ang II-mediated vasoconstriction.

Unlabelled: Background- Polymorphisms in the promoter (T-786C) and exon 7 (G894T) of the endothelial nitric oxide synthase (eNOS) gene were shown to be associated with reduced vascular NO production or increased proteolytic cleavage of eNOS. Therefore, we aimed to determine the effects of these polymorphisms on endothelial function and endothelial response to physical exercise in patients with coronary artery disease (CAD)., Methods and Results: Sixty-seven patients were randomized to either a training or a control group. At the beginning and after 4 weeks, acetylcholine-induced changes in average peak velocity (APV) of a coronary or mammary artery were invasively assessed by Doppler velocimetry. Polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism. At the beginning, in subjects with the wild-type (WT) variant, APV increased by 88+/-7% in response to acetylcholine. This response was significantly blunted in patients who were positive for the promoter (44+/-7%) or the exon 7 (62+/-9%) polymorphism. Four weeks of exercise training resulted in augmentation of an endothelium-dependent increase in APV by +36+/-12% in promoter polymorphism-positive patients but by +81+/-18% and +91+/-15% in WT variant- and exon 7 polymorphism-positive subjects, respectively., Conclusions: These results suggest that the presence of either one of the polymorphisms attenuates endothelium-dependent vasodilatation in CAD patients. Only the promoter polymorphism might have an adverse effect on training-induced improvement in endothelial function.