The Effects of Machine-Weight and Free-Weight Resistance Exercise on Hemodynamics and Vascular Function

International Journal of Exercise Science 13(2): 526-538, 2020. The purpose of this study was to examine hemodynamic and vascular responses between machine-weight and free-weight exercise. Resistance-trained individuals were assigned to a machine-weight (n= 13) or free-weight (n= 15) group. Groups completed two visits consisting of their assigned exercise condition and a control (CON). A 2 x 2 x 3 repeated measures ANOVA was used to test the effects of group across condition and time on the hemodynamic parameters [cardiac output (CO), heart rate (HR), total peripheral resistance (TPR), mean arterial pressure (MAP), and stroke volume (SV)]. A 2 x 2 x 2 repeated measures ANOVA was used to test the effects of group across condition and time on the hemodynamic variable, forearm vascular conductance (FVC), as well as on vascular measures [forearm blood flow (FBF), blood flow peak, and total reactive hyperemia (RH)]. Main effects were analyzed using pairwise comparisons. The results of the present study demonstrate that both machine-weight and free-weight exerciseproduce similar (p \u3e 0.05)alterations in hemodynamics and vascular function. Specifically, during recovery both groups demonstrated significant (p ≤ 0.05) increases in measures of hemodynamics such as CO, HR and FVC, as well as significant (p ≤ 0.05) decreases in TPR, MAP, and SV. Measures of vascular function such as FBF, blood flow peak, and total RH were also significantly (p ≤ 0.05) increased during recovery.Therefore, this study suggests that either machine weight or free-weight exercise may induce acute hemodynamic and vascular benefits, which may reduce the risk of cardiovascular disease (CVD) and CVD events

Hemodynamic response and pulse wave analysis after upper- and lower-body resistance exercise with and without blood flow restriction

Resistance exercise (RE) has been shown to elevate hemodynamics and pulse wave reflection. However, the effects of acute RE with blood flow restriction (BFR) on hemodynamics and pulse wave reflection are unclear. The purpose of this study was to evaluate the differences between upper- and lower-body RE with and without BFR on hemodynamics and pulse wave reflection. Twenty-three young resistance-trained individuals volunteered for the study. Hemodynamics and pulse wave reflection were assessed at rest, 10, 25, 40, and 55 minutes after either upper- or lower-body with or without BFR. The upper-body RE (URE) consisted of the latissimus dorsi pulldown and chest press; the lower-body RE (LRE) consisted of knee extension and knee flexion. The BFR condition consisted of four sets of 30, 15, 15, and 15 repetitions at 30% 1-repetition maximum (1RM) while the without BFR condition consisted of four sets of 8 repetitions at 70% 1RM. Heart rate, rate pressure product, and subendocardial viability ratio significantly (p\u3c0.05) increased after all exercises. Brachial and aortic systolic blood pressure (BP) significantly (p\u3c0.05) elevated after LRE while brachial and aortic diastolic BP significantly (p\u3c0.05) reduced after URE. Augmentation pressure, augmentation index (AIx), AIx normalized at 75 bpm, and wasted left ventricular pressure energy significantly (p\u3c0.05) increased after URE while transit time of reflected wave significantly (p\u3c0.05) decreased after LRE. URE places greater stress on pulse wave reflection while LRE results in greater responses in BP. Regardless of URE or LRE, the cardiovascular responses between BFR and without BFR are similar

The Effects of Machine-Weight and Free-Weight Resistance Exercise on Hemodynamics and Vascular Function

The purpose of this study was to examine hemodynamic and vascular responses between machine-weight and free-weight exercise. Resistance-trained individuals were assigned to a machine-weight (n = 13) or free-weight (n = 15) group. Groups completed two visits consisting of their assigned exercise condition and a control (CON). A 2 × 2 × 3 repeated measures ANOVA was used to test the effects of group across condition and time on the hemodynamic parameters [cardiac output (CO), heart rate (HR), total peripheral resistance (TPR), mean arterial pressure (MAP), and stroke volume (SV)]. A 2 × 2 × 2 repeated measures ANOVA was used to test the effects of group across condition and time on the hemodynamic variable, forearm vascular conductance (FVC), as well as on vascular measures [forearm blood flow (FBF), blood flow peak, and total reactive hyperemia (RH)]. Main effects were analyzed using pairwise comparisons. The results of the present study demonstrate that both machine-weight and free-weight exercise produce similar (p \u3e 0.05) alterations in hemodynamics and vascular function. Specifically, during recovery both groups demonstrated significant (p ≤ 0.05) increases in measures of hemodynamics such as CO, HR and FVC, as well as significant (p ≤ 0.05) decreases in TPR, MAP, and SV. Measures of vascular function such as FBF, blood flow peak, and total RH were also significantly (p ≤ 0.05) increased during recovery. Therefore, this study suggests that either machine weight or free-weight exercise may induce acute hemodynamic and vascular benefits, which may reduce the risk of cardiovascular disease (CVD) and CVD events

Changes in Endothelial Function after Acute Resistance Exercise Using Free Weights

We determined the effects of an acute bout of free-weight resistance exercise (ARE) on cardiovascular hemodynamics and endothelial function in resistance-trained individuals. Nineteen young, healthy, resistance-trained individuals performed two randomized sessions consisting of ARE or a quiet control (CON). The ARE consisted of three sets of 10 repetitions at 75% 1-repetition maximum for the squat, bench press, and deadlift. Cardiovascular hemodynamics was assessed using finger photoplethysmography. Forearm blood flow (FBF), and vasodilatory capacity markers, were assessed using venous occlusion plethysmography. Forearm vascular conductance was calculated by the division of mean FBF by mean arterial pressure. A two-way ANOVA was used to compare the effects of condition (ARE, CON) across time (rest, recovery). There were significant (p ≤ 0.05) decreases in mean arterial pressure and total peripheral resistance across conditions and time. There were significant condition-by-time interactions (p ≤ 0.05) for heart rate, stroke volume, and cardiac output after the ARE compared to the CON and rest. FBF was significantly (p = 0.001) increased during the recovery from ARE, as well as vasodilatory capacity markers such as peak blood flow (p = 0.05) and reactive hyperemia-induced blood flow (p = 0.0001). These data suggest that whole-body free-weight exercises acutely reduced blood pressure while simultaneously augmenting FBF, and vasodilatory capacity markers

Vascular Responses to High-Intensity Battling Rope Exercise between the Sexes

The purpose of the study was to assess high-intensity battling rope exercise (HI-BRE) on hemodynamics, pulse wave reflection and arterial stiffness during recovery and between sexes. Twenty-three young, healthy resistance-trained individuals (men: n = 13; women: n = 10) were assessed for all measures at Rest, as well as 10-, 30-, and 60-minutes following HI-BRE. A one-way repeated measures ANOVA was used to analyze the effects of HI-BRE across time (Rest, 10, 30, and 60-minutes) on all dependent variables. Significant main effects were analyzed using paired t-tests with a Sidak correction factor. Significance was accepted a priori at p 0.05. There were significant reductions in hemodynamic measures of diastolic blood pressure (BP) in women, but not men following HI-BRE at 30 minutes. Further, measures of pulse wave reflection, specifically those of the augmentation index (AIx) and wasted left ventricular energy (ΔEw), were significantly increased in both men and women for 60 minutes, but changes were significantly attenuated in women suggesting less ventricular work. There were also significant increases in arterial stiffness in regard to the aorta and common carotid artery that were fully recovered by 30 and 60 minutes, respectively with no differences between men and women. Thus, the primary findings of this study suggest that measures of hemodynamics and pulse wave reflection are collectively altered for at least 60 minutes following HI-BRE, with women having attenuated responses compared to men

On the possibility of a metallic phase in granular superconducting films

We investigate the possibility of finding a zero-temperature metallic phase in granular superconducting films. We are able to identify the breakdown of the conventional treatment of these systems as dissipative Bose systems. We do not find a metallic state at zero temperature. At finite temperatures, we find that the system exhibit crossover behaviour which may have implications for the analysis of experimental results. We also investigate the effect of vortex dissipation in these systems.Comment: 7 pages, ReVTeX3.0, 3 EPS figure

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Abstract Background Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Publisher Copyright: © 2022, The Author(s).Background: Genetic variants within nearly 1000 loci are known to contribute to modulation of blood lipid levels. However, the biological pathways underlying these associations are frequently unknown, limiting understanding of these findings and hindering downstream translational efforts such as drug target discovery. Results: To expand our understanding of the underlying biological pathways and mechanisms controlling blood lipid levels, we leverage a large multi-ancestry meta-analysis (N = 1,654,960) of blood lipids to prioritize putative causal genes for 2286 lipid associations using six gene prediction approaches. Using phenome-wide association (PheWAS) scans, we identify relationships of genetically predicted lipid levels to other diseases and conditions. We confirm known pleiotropic associations with cardiovascular phenotypes and determine novel associations, notably with cholelithiasis risk. We perform sex-stratified GWAS meta-analysis of lipid levels and show that 3–5% of autosomal lipid-associated loci demonstrate sex-biased effects. Finally, we report 21 novel lipid loci identified on the X chromosome. Many of the sex-biased autosomal and X chromosome lipid loci show pleiotropic associations with sex hormones, emphasizing the role of hormone regulation in lipid metabolism. Conclusions: Taken together, our findings provide insights into the biological mechanisms through which associated variants lead to altered lipid levels and potentially cardiovascular disease risk.Peer reviewe

Implicating genes, pleiotropy, and sexual dimorphism at blood lipid loci through multi-ancestry meta-analysis

Funding GMP, PN, and CW are supported by NHLBI R01HL127564. GMP and PN are supported by R01HL142711. AG acknowledge support from the Wellcome Trust (201543/B/16/Z), European Union Seventh Framework Programme FP7/2007–2013 under grant agreement no. HEALTH-F2-2013–601456 (CVGenes@Target) & the TriPartite Immunometabolism Consortium [TrIC]-Novo Nordisk Foundation’s Grant number NNF15CC0018486. JMM is supported by American Diabetes Association Innovative and Clinical Translational Award 1–19-ICTS-068. SR was supported by the Academy of Finland Center of Excellence in Complex Disease Genetics (Grant No 312062), the Finnish Foundation for Cardiovascular Research, the Sigrid Juselius Foundation, and University of Helsinki HiLIFE Fellow and Grand Challenge grants. EW was supported by the Finnish innovation fund Sitra (EW) and Finska Läkaresällskapet. CNS was supported by American Heart Association Postdoctoral Fellowships 15POST24470131 and 17POST33650016. Charles N Rotimi is supported by Z01HG200362. Zhe Wang, Michael H Preuss, and Ruth JF Loos are supported by R01HL142302. NJT is a Wellcome Trust Investigator (202802/Z/16/Z), is the PI of the Avon Longitudinal Study of Parents and Children (MRC & WT 217065/Z/19/Z), is supported by the University of Bristol NIHR Biomedical Research Centre (BRC-1215–2001) and the MRC Integrative Epidemiology Unit (MC_UU_00011), and works within the CRUK Integrative Cancer Epidemiology Programme (C18281/A19169). Ruth E Mitchell is a member of the MRC Integrative Epidemiology Unit at the University of Bristol funded by the MRC (MC_UU_00011/1). Simon Haworth is supported by the UK National Institute for Health Research Academic Clinical Fellowship. Paul S. de Vries was supported by American Heart Association grant number 18CDA34110116. Julia Ramierz acknowledges support by the People Programme of the European Union’s Seventh Framework Programme grant n° 608765 and Marie Sklodowska-Curie grant n° 786833. Maria Sabater-Lleal is supported by a Miguel Servet contract from the ISCIII Spanish Health Institute (CP17/00142) and co-financed by the European Social Fund. Jian Yang is funded by the Westlake Education Foundation. Olga Giannakopoulou has received funding from the British Heart Foundation (BHF) (FS/14/66/3129). CHARGE Consortium cohorts were supported by R01HL105756. Study-specific acknowledgements are available in the Additional file 32: Supplementary Note. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.Peer reviewedPublisher PD

Global age-sex-specific mortality, life expectancy, and population estimates in 204 countries and territories and 811 subnational locations, 1950–2021, and the impact of the COVID-19 pandemic: a comprehensive demographic analysis for the Global Burden of Disease Study 2021

Background: Estimates of demographic metrics are crucial to assess levels and trends of population health outcomes. The profound impact of the COVID-19 pandemic on populations worldwide has underscored the need for timely estimates to understand this unprecedented event within the context of long-term population health trends. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 provides new demographic estimates for 204 countries and territories and 811 additional subnational locations from 1950 to 2021, with a particular emphasis on changes in mortality and life expectancy that occurred during the 2020–21 COVID-19 pandemic period. Methods: 22 223 data sources from vital registration, sample registration, surveys, censuses, and other sources were used to estimate mortality, with a subset of these sources used exclusively to estimate excess mortality due to the COVID-19 pandemic. 2026 data sources were used for population estimation. Additional sources were used to estimate migration; the effects of the HIV epidemic; and demographic discontinuities due to conflicts, famines, natural disasters, and pandemics, which are used as inputs for estimating mortality and population. Spatiotemporal Gaussian process regression (ST-GPR) was used to generate under-5 mortality rates, which synthesised 30 763 location-years of vital registration and sample registration data, 1365 surveys and censuses, and 80 other sources. ST-GPR was also used to estimate adult mortality (between ages 15 and 59 years) based on information from 31 642 location-years of vital registration and sample registration data, 355 surveys and censuses, and 24 other sources. Estimates of child and adult mortality rates were then used to generate life tables with a relational model life table system. For countries with large HIV epidemics, life tables were adjusted using independent estimates of HIV-specific mortality generated via an epidemiological analysis of HIV prevalence surveys, antenatal clinic serosurveillance, and other data sources. Excess mortality due to the COVID-19 pandemic in 2020 and 2021 was determined by subtracting observed all-cause mortality (adjusted for late registration and mortality anomalies) from the mortality expected in the absence of the pandemic. Expected mortality was calculated based on historical trends using an ensemble of models. In location-years where all-cause mortality data were unavailable, we estimated excess mortality rates using a regression model with covariates pertaining to the pandemic. Population size was computed using a Bayesian hierarchical cohort component model. Life expectancy was calculated using age-specific mortality rates and standard demographic methods. Uncertainty intervals (UIs) were calculated for every metric using the 25th and 975th ordered values from a 1000-draw posterior distribution. Findings: Global all-cause mortality followed two distinct patterns over the study period: age-standardised mortality rates declined between 1950 and 2019 (a 62·8% [95% UI 60·5–65·1] decline), and increased during the COVID-19 pandemic period (2020–21; 5·1% [0·9–9·6] increase). In contrast with the overall reverse in mortality trends during the pandemic period, child mortality continued to decline, with 4·66 million (3·98–5·50) global deaths in children younger than 5 years in 2021 compared with 5·21 million (4·50–6·01) in 2019. An estimated 131 million (126–137) people died globally from all causes in 2020 and 2021 combined, of which 15·9 million (14·7–17·2) were due to the COVID-19 pandemic (measured by excess mortality, which includes deaths directly due to SARS-CoV-2 infection and those indirectly due to other social, economic, or behavioural changes associated with the pandemic). Excess mortality rates exceeded 150 deaths per 100 000 population during at least one year of the pandemic in 80 countries and territories, whereas 20 nations had a negative excess mortality rate in 2020 or 2021, indicating that all-cause mortality in these countries was lower during the pandemic than expected based on historical trends. Between 1950 and 2021, global life expectancy at birth increased by 22·7 years (20·8–24·8), from 49·0 years (46·7–51·3) to 71·7 years (70·9–72·5). Global life expectancy at birth declined by 1·6 years (1·0–2·2) between 2019 and 2021, reversing historical trends. An increase in life expectancy was only observed in 32 (15·7%) of 204 countries and territories between 2019 and 2021. The global population reached 7·89 billion (7·67–8·13) people in 2021, by which time 56 of 204 countries and territories had peaked and subsequently populations have declined. The largest proportion of population growth between 2020 and 2021 was in sub-Saharan Africa (39·5% [28·4–52·7]) and south Asia (26·3% [9·0–44·7]). From 2000 to 2021, the ratio of the population aged 65 years and older to the population aged younger than 15 years increased in 188 (92·2%) of 204 nations. Interpretation: Global adult mortality rates markedly increased during the COVID-19 pandemic in 2020 and 2021, reversing past decreasing trends, while child mortality rates continued to decline, albeit more slowly than in earlier years. Although COVID-19 had a substantial impact on many demographic indicators during the first 2 years of the pandemic, overall global health progress over the 72 years evaluated has been profound, with considerable improvements in mortality and life expectancy. Additionally, we observed a deceleration of global population growth since 2017, despite steady or increasing growth in lower-income countries, combined with a continued global shift of population age structures towards older ages. These demographic changes will likely present future challenges to health systems, economies, and societies. The comprehensive demographic estimates reported here will enable researchers, policy makers, health practitioners, and other key stakeholders to better understand and address the profound changes that have occurred in the global health landscape following the first 2 years of the COVID-19 pandemic, and longer-term trends beyond the pandemic