bluuebunny/crossref_metadata_2025_split huggingface dataset:
EXERCISE TRAINING ASSOCIATED WITH DIETARY ADJUSTMENT INDUCES METABOLIC AND CARDIOVASCULAR BENEFITS IN HIGH‐FAT‐FED MENOPAUSE RATS
Authors: dos Santos Adriano , da Costa Santos Nicolas , do Nascimento‐Carvalho Bruno , Carvalho Sabrina Leonardo , Mello‐Silva Fernanda Queiroz , Stabile Gabriel Correia , Izaías João Eduardo , Irigoyen Maria‐Claudia , De Angelis Kátia , Scapini Kátia Bilhar , Sanches Iris Callado 
Published: June 2021

IntroductionConsidering the increase in cardiometabolic risk after menopause, and that diet and exercise training (ET) are the pillars of prevention/treatment strategies, the objective of this study was to evaluate the metabolic, hemodynamic and autonomic effects of exercise training in an experimental model of menopausal undergoing a high‐fat diet followed by dietary adjustment. Twenty female C57BL/6J mice (8 weeks aged), all oophorectomized (bilateral ovarian removal) divided into 4 experimental groups (n = 5) were used: sedentary submitted to a high‐fat diet (OSD), sedentary submitted to 4 weeks of high‐fat diet and 4 weeks of control diet (OSRa), trained submitted to a high‐fat diet (OTD), trained submitted to 4 weeks of high‐fat diet and 4 weeks of control diet (OTRa). Oophorectomy was performed at the end of the 4th week of the protocol. Fasting glycemia and oral glucose tolerance were evaluated. ET had duration of 4 weeks (6th to 9th week of protocol, 5 days/week, 1 hour/day, intensity 50–70% of the maximum treadmill test). At the end of the protocol, the animals were cannulated for direct recording of arterial pressure (AP), after which baroreflex sensitivity and cardiovascular autonomic modulation were analyzed.RESULTSDietary adjustment promoted a reduction in glycemia and a better glucose tolerance, associated with reduction in cardiac sympathetic modulation (LF‐PI: OSD: 0.54±0.02; OSRa: 0.37±0.06; OTD: 3.0±0.02, OTRa: 0.19±0.02 ms2) and vascular (LF‐SAP: OSD: 11.3±1.7, OSRa: 3.6±0.9, OTD: 1.6±0.2; OTR:3.0±0.5mmHg2). ET, with or without dietary adjustment, increased physical capacity, reduced heart rate, improved baroreflex sensitivity, increased cardiac parasympathetic modulation (HF‐PI: OSD: 0.47±0.04, OSRa: 0,63±0.07, OTD: 0.86±0.02, OTRa: 0.75±0.07 ms2) and reduction of cardiac and vascular sympathetic modulation. However, only the association of ET with dietary adjustment was able to promote reduction in body weight, glycemia, improvement in glucose tolerance, reduction in blood pressure (mean AP: OSD: 123±2.1, OSRa: 114±0.8; OTD: 120±1.4; OTR: 110±4.0 mmHg), and further increase in parasympathetic modulation. Thus, the association of ET with dietary adjustment may be considered an important behavior for the management of cardiovascular risk in the association of obesity with ovarian deprivation.Support or Funding InformationCoordenação de Aperfeiçoamento de Pessoal de Nível Superior ‐ Brazil (CAPES) ‐ Funding Code: 001.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Effects of Expiratory Muscle Strength Training on Run Performance in Healthy College Students
Authors: Bernard Jeffrey R , Thao Nou , Sanders Krystle K , Liao Yi‐Hung 
Published: June 2021

PurposeExpiratory muscle strength training (EMST) is a novel and noninvasive intervention to improve expiratory capacity. EMST programs have been shown to benefit individuals who have difficulty breathing, swallowing, and coughing by improving expiratory muscle strength. However, it is unclear if EMST can benefit those without impaired respiratory capacity. Thus, the purpose of this study was to investigate the effects of EMST on run performance in healthy college students.MethodsThis was a repeated measure study design in which participants performed body composition, maximal expiratory pressure (PEmax), VO2max, and 5K run time before and after 4‐weeks of training. In addition, blood samples were obtained immediately before and after the 5K to measure lactic acid, glucose, and epinephrine. Twenty‐one college students were recruited and matched, based on their pre‐VO2max, into 1 of 3 treatment groups (n=7 for each): 1) EMST, 2) aerobic training (AT), or 3) EMST‐AT (combined EMST and aerobic training). EMST was performed 5 d/wk starting at 75% PEmax and progressively increased the resistance throughout the 4‐weeks. AT was performed 4 d/wk for 4‐weeks by progressively increasing run volume up to 5K. EMST‐AT performed both interventions.ResultsThere were no differences among treatment groups for the pre‐measurements. Body composition did not significantly change throughout the study. After 4‐weeks of training all groups improved PEmax, VO2max, and 5K run time. However, the improvement in PEmax was significantly greater for both EMST and EMST‐AT compared to AT. Although there was a trend for improved VO2max and 5K run time for AT and EMST‐AT compared to EMST, the differences were not statistically significant. There were no differences found for the blood variables among treatment groups.ConclusionEMST appears to provide similar benefits to that of short‐term aerobic training in healthy college students. However, the long‐term benefits of EMST compared to aerobic training warrant further investigation.Support or Funding InformationThis study was funded, in part, by a Research Scholarship and Creative Activities (RSCA) grant from California State University, Stanislaus.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Whole body exercise training improves blood pressure and postural balance responses during orthostatic stress onset in older women
Authors: Ferreira Luana Farinazzo , Rodrigues Gabriel Dias , Soares Pedro Paulo Silva 
Published: June 2021

The purpose of the current study was to investigate the effects of whole body exercise training on spontaneous baroreflex sensitivity at rest, blood pressure and postural balance responses during orthostatic onset in older women. The sample composed by eight healthy older women (65±3 yrs.). R‐R intervals and blood pressure were continuously measured from a standard electrocardiogram (ECG) and infrared finger plethysmography, respectively, at rest (10min) and during orthostatic position (7min). Spontaneous baroreflex sensitivity at rest was obtained by spectral method in the low‐frequency component of R‐R and systolic blood pressure time series (αLF). The nadir point was considered the lower value of mean arterial pressure (MAP) during transition from supine to orthostatic position. The percentage changes (%ΔMAP) from supine to orthostatic nadir were calculated. The time of MAP oscillations during orthostatic onset (MAPtime) was calculated by the sum of time to nadir and time to recovery (nearest value of MAP at rest). In addition, during the ORT onset (15s) the center of pressure displacements (COP) were acquired by a force plate, and COP distance and speed were calculated. The whole body exercise training protocol (rowing ergometer) consisted of three weekly sessions (30 minutes) at 60–80% of maximal heart rate (defined by a previous maximal exercise test) for 10 weeks. The volunteers were evaluated pre and post‐trainning. Student‐t tests for paired samples was employed (p≤0.05) to compare all variables. At rest, αLF (pre= 3.9 ±1.7 vs. post= 5.3 ±1.1 ms2 p<0.001) increased post‐training and MAP (pre= 85.1 ±10.3 vs. post= 77.4 ±7.8 mmHg p< 0.02) decreased. No differences in CO (pre= 4.526 ±0.7697 vs. post= 5.058 ±2.104 L/min p=0.02) and SV (pre= 66.33 ±19.94 vs. post= 72.18 ±29.67 mL p=0.01) were found at rest. Although %ΔMAP (pre= −0.3 ±0.2 vs. post= −0.3 ±0.16 mmHg p< 0.19) was not different pre and post training, MAPtime (pre= 14.16 ±3.996 vs. post= 10.94 ±5.637 seconds p<0.04) decreased post‐training protocol. Moreover. COP distance (pre= 673.7 ±74.9 vs. post= 560.3 ±95.1 mm p< 0.03) and speed (pre= 44.9 ±4.9 vs. post= 37.3 ±6.3 mm/s p<0.03) were lower post‐training. Whole body exercise training improves spontaneous baroreflex sensitivity at rest mean arterial pressure and postural balance adjustments during orthostatic stress onset in older women. Research ethics committee (CEP‐851.371/14).Support or Funding InformationFoundation for Research Support of the State of Rio de Janeiro ‐ FAPERJ (E‐6/110.079/2013), Coordination for the Improvement of Higher Education Personnel ‐ CAPES.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Taurine supplementation restores pancreatic and mesenteric endothelial function in protein malnourished mice
Authors: Davel Ana Paula , Carneiro Everardo Magalhães , Vettorazzi Jean , Guizoni Daniele Mendes 
Published: June 2021

Protein malnutrition predisposes to type 2 diabetes and hypertension. Reduced endothelium‐mediated vasodilation is a risk factor for cardiometabolic disorders, increasing vascular resistance and impairing pancreatic islet blood flow and insulin secretion. Therefore, restoring endothelial function could be relevant for malnourished individuals. Diet supplementation with taurine has been reported to be an antihypertensive and vasculoprotective therapy. In the present study we evaluated the effects of taurine supplementation on the protein restriction‐induced vasodilator endothelial dysfunction in two different vascular beds: small mesenteric arteries, that contribute for total vascular resistance, and intralobular pancreatic artery, responsible for pancreatic blood flow. For this, male post‐weaned mice fed a normal‐ (14%, NP) or an isocaloric low‐protein (6%, LP) diet for 90 days. Concomitantly, half of the LP mice received 2.5% taurine supplementation in drinking water. Blood pressure (BP) was higher in LP mice when compared to NP, which was reversed by taurine supplementation. Vascular function was evaluated by using a wire myograph and no changes in vessel internal diameter among groups were found. The endothelium‐dependent relaxation to acetylcholine (ACh) was significantly reduced by LP diet and normalized by taurine supplementation in both mesenteric and pancreatic arteries. Next, we investigated the involvement of nitric oxide synthase (NOS)‐derived NO and the endothelium derived‐hyperpolarization (EDH) by incubating the vessels with L‐NAME and 20 mM KCl, respectively. L‐NAME reduced the relaxation to ACh in both arteries. However, L‐NAME abolished differences among groups only in mesenteric arteries, suggesting a role for NOS‐derived NO in the LP‐induced endothelial dysfunction in the mesenteric bed. In intralobular pancreatic arteries, LP diet‐induced endothelial dysfunction was associated with reduced EDH. Taurine supplementation reversed the impaired NOS and EDH contribution to ACh‐induced relaxation. The relaxation to sodium nitroprusside was not modified by LP diet or taurine, suggesting no changes in vascular smooth muscle responsiveness. In conclusion, our data revealed that post‐weaning protein restriction induces endothelial dysfunction in mesenteric and pancreatic arteries by different pathways: in resistance mesenteric arteries results in impaired NOS‐derived NO, while in pancreatic vessels there is an impair in EDH. Interestingly, diet supplementation with taurine restores the endothelial function in both mesenteric and pancreatic vessels and reduces BP in protein‐restricted mice. Therefore, taurine emerges as a potential therapy for vascular dysfunction associated with malnutrition.Support or Funding InformationSão Paulo Research Foundation‐FAPESPThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Neurovascular Coupling is Blunted in Atrial Fibrillation
Authors: Junejo Rehan T. , Phillips Aaron , Lucas Samuel J. E. , van Lieshout Johannes J. , Lip Gregory Y. H. , Fisher James P. 
Published: June 2021

People with atrial fibrillation are at an increased risk of stroke, cognitive decline and dementia. We recently identified that individuals with atrial fibrillation exhibit a reduced cerebrovascular reactivity to carbon dioxide, indicative of a diminished cerebral vasodilatory reserve. In this study we sought to determine whether neurovascular coupling (NVC) is blunted in atrial fibrillation in comparison with age‐matched, hypertensive and healthy control participants.Posterior (PCA) and middle cerebral artery (MCA) flow velocity (Vm), along with beat‐to‐beat mean arterial pressure (MAP), were measured during a NVC assessment consisting of five cycles of visual stimulation (reading) for 30 s followed by 30 s with both eyes‐closed in 12 patients with atrial fibrillation (69 [7] yr; mean [SD], 3 women), 13 patients with hypertension (67 [5] yr, 4 women) and 12 healthy control participants (63 [10] yr, 4 women). Cerebrovascular conductance indices (CVCi) were calculated as PCA Vm/MAP and MCA Vm/MAP. NVC was denoted by the peak response observed during visual stimulation and is expressed as a percentage change from the eyes‐closed period.Resting PCA Vm and MCA Vm were not different between the atrial fibrillation (31 [7] and 49 [12] cm/s), hypertension (33 [8] and 55 [12] cm/s), and healthy control (36 [8] and 55 [12] cm/s) groups (P>0.05). Visual stimulation evoked an increase in PCA CVCi in all groups, but the magnitude of the hyperemic response was blunted in patients with atrial fibrillation (18 [8] %) and hypertension (17 [8] %), in comparison with healthy controls (26 [9] %) (P<0.05). Visual stimulation evoked a greater increase in MCA CVCi in the atrial fibrillation group (17 [6] %), than patients with hypertension (10 [4] %) and healthy controls (13 [6] %) (P<0.05). Thus, when peak PCA CVCi responses were considered following subtraction of the peak MCA CVCi responses (i.e., the “non‐selective” effect of the NVC test), a significantly diminished response was observed in the atrial fibrillation group (1 [8] %) compared the hypertension (7 [9] %) and healthy control groups (13 [9] %) (P<0.01).In summary, individuals with atrial fibrillation exhibit a blunted NVC response to visual stimulation when compared to age‐matched, healthy control and hypertensive participants. Additional studies are required to identify the mechanisms for the attenuated cerebral perfusion response of the occipital lobe to visual stimulation in atrial fibrillation (e.g., attenuated neuronal activation, altered cerebrovascular vasodilatory signaling).Support or Funding InformationFunded by BHF project grant PG/15/45/31579.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Compromised endothelial function in transgender men taking testosterone
Authors: Stachenfeld Nina , Leone Cheryl , Gulanski Barbara 
Published: June 2021

Approximately 0.6% or 1.4 million people identify as transgender or having a current gender identity that differs from the sex assigned at birth. Transgender men (TGM) are persons assigned female at birth with a male gender identity. In TGM, testosterone therapy may be associated with increased blood pressure (BP), lipids, triglycerides, LDL cholesterol and decreased HDL‐cholesterol. Androgen excess is a major driver of endothelial dysfunction among cisgender females (CGF), and endothelial dysfunction is an early sign of atherosclerosis and hypertension. We therefore examined endothelial function in TGM receiving testosterone. We hypothesized that endothelial function in TGM would be attenuated compared to CGF of similar age and BMI. We compared 4 TGM (age 26 ± 5 y; BMI 26.3 ± 3.2 kg/m2) receiving testosterone (T) to 8 CGF (25 ± 4 y; BMI 25.7 ± 6.8 kg/m2) during the early follicular phase of their menstrual cycle. We evaluated brachial vasodilatory responses following stimuli designed to elicit shear stress using 5‐min occlusion to determine endothelial function (flow mediated vasodilation, FMD). As expected, total T was increased in the TGM compared to CGF (457.4 ± 119.8 vs. 1.9 ± 1.1 ng/dL), as was free T (72. ± 7.5 vs. 1.5 ± 0.9 pg/dL). Blood lipids, including LDL (98.6 ± 38.5 mg/dL), HDL (51.5 ± 11.1 mg/dL) and triglycerides (79.0 ± 31.9 mg/dL) as well as HbA1c (4.9 ± 0.1%) were within normal ranges in the TGM. Systolic BP (SBP) was elevated in 2/4 TGM and 3/8 CGF; MAP was similar between groups (90 ± 21 and 90 ± 10 mm Hg). However, FMD was attenuated in the TGM (3.7 ± 3.5 %) compared to the CGF (9.2 ± 1.2 %, P=0.001) indicating markedly diminished endothelial function in TGM receiving androgen treatment. Further, endothelial dysfunction was independent of other risk factors associated with cardiovascular disease including hyperlipidemia, diabetes and hypertension. In transgender men, the androgen‐dominant hormonal milieu appears to impair endothelial function. Endothelial dysfunction precedes clinically detectable atherosclerotic plaques in the coronary arteries and is an important marker for cardiovascular risk. Therefore, attention to cardiovascular risk factors should be integral to the care of transgender men.Support or Funding InformationR01 HL135089This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Effect of iNOS on Cutaneous Thermal Hyperemia in Non‐Hispanic Blacks versus Non‐Hispanic Whites
Authors: Miller James , Hollowed Casey , Otis Jeff , Hayat Matthew , Quyyumi Arshed , Wong Brett 
Published: June 2021

Non‐Hispanic Blacks exhibit a blunted cutaneous microvascular response to local heating due, in part, to a decrease in nitric oxide (NO) bioavailability compared to non‐Hispanic Whites. Inducible NO synthase (iNOS) is known to contribute to vascular dysfunction; however, it is unknown whether iNOS contributes to microvascular dysfunction in NHB. The purpose of this study was to examine the role of iNOS on cutaneous microvascular function in NHB vs. NHW. Young, healthy non‐Hispanic Black and White participants (n = 4 per group) were instrumented with 2 microdialysis fibers for infusion of lactated Ringer's solution (control) and 0.1 mM 1400W (iNOS inhibitor), respectively. Following Ringer's and 1400W infusion, local skin temperature was increased via rapid local heating to 39°C at a rate of 0.1°C s−1. Once skin blood flow plateaued, 20 mM L‐NAME was infused to quantify endothelial NO synthase (eNOS)‐dependent vasodilation to the local heating response. Following L‐NAME infusion, the local heaters were increased to 43°C and 54mM of sodium nitroprusside was infused to elicit maximal endothelium‐independent cutaneous vasodilation. Skin blood flow was measured via laser‐doppler flowmetry (LDF) throughout the local heating protocol. Cutaneous vascular conductance (CVC) was calculated as LDF flow divided by mean arterial pressure and normalized to maximum (%CVCmax). iNOS inhibition minimally increased the initial peak in non‐Hispanic Blacks (33±6 vs. 41±8 %CVCmax) but had no effect in non‐Hispanic Whites (53±9 vs. 55±6 %CVCmax), suggesting an increased sensory nerve response in non‐Hispanic Blacks following blockade. Inhibition of iNOS (66±10 %CVCmax) did not alter microvascular function compared to control (70±14 %CVCmax) in non‐Hispanic Whites; however, microvascular function increased (47±11 vs. 60±10 %CVCmax) in non‐Hispanic Blacks, suggesting an increase in basal iNOS concentrations. Notably, iNOS inhibition in non‐Hispanic Blacks increased %CVCmax to a level similar to non‐Hispanic Whites. The %NO‐dependent vasodilation did not change in non‐Hispanic Whites with infusion of 1400W (60±5 vs. 61±5 %); however, infusion of 1400W increased the %NO‐dependent vasodilation in non‐Hispanic Blacks (44±6 vs. 57±3 %), suggesting increased levels of circulating iNOS impairs endothelial‐dependent vasodilation. These findings indicate iNOS‐derived NO contributes to reduced eNOS‐dependent microvascular vasodilation in young, healthy non‐Hispanic Blacks.Support or Funding InformationGrant Number: 1R01HL141205‐01This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Determinants of Peak Oxygen Uptake in Patients with Chronic Obstructive Pulmonary Disease: Looking Beyond the Lungs
Authors: Broxterman Ryan M , Nelson Ashley D , Lawrenson Lesley , Poole Jennifer G , Hoff Jan , Wagner Peter D , Richardson Russell S 
Published: June 2021

Peak oxygen uptake (V̇O2peak), a primary determinant of prognosis, mortality, and quality of life, is diminished in patients with chronic obstructive pulmonary disease (COPD). Of importance, even after lung function is restored, by lung transplant, V̇O2peak remains markedly attenuated, emphasizing the critical importance of peripheral dysfunction in this pathology. However, the peripheral determinants of V̇O2peak in patients with COPD remain poorly understood. Therefore, the purpose of this investigation was to assess the peripheral determinants of V̇O2peak in patients with COPD, to better understand disease‐related peripheral adaptations. Oxygen transport and utilization at peak single‐leg knee‐extensor exercise were assessed from arterial and femoral venous oxygenation measurements and leg blood flow (by thermodilution) in 8 patients with COPD (FEV1 = 0.9 ± SE 0.1 L, 30% of predicted) and 8 well‐matched control subjects. This exercise modality was utilized to minimize cardiopulmonary exercise limitations. Muscle convective O2 delivery (0.44 ± 0.06 vs. 0.69 ± 0.07 l/min, p<0.05) and muscle diffusive O2 conductance (6.6 ± 0.8 vs. 10.4 ± 0.9 ml/min/mmHg, p<0.05) were both ~1/3 lower in COPD patients than control subjects, resulting in a significantly attenuated leg V̇O2peak in the patients (0.27 ± 0.04 vs. 0.42 ± 0.05 l/min, p<0.05). Thus, in an exercise paradigm that minimizes cardiopulmonary limitations, the convective and diffusive components of oxygen transport within skeletal muscle, key determinants of V̇O2peak, are markedly diminished in patients with COPD. These findings emphasize the importance of peripheral factors, beyond the lungs, that limit exercise capacity, exacerbate inactivity, and increase the risk for cardiovascular disease in patients with COPD.Support or Funding InformationSupported by National Heart, Lung, and Blood Institute Grant HL‐091830This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.