bluuebunny/crossref_metadata_2025_split huggingface dataset:
Metabolic and cardiovascular responses to chronic intermittent hypoxia and hypercapnia
Authors: do Carmo Jussara M. , da Silva Alexandre A. , Moak Sydney P. , Wang Zhen , Hall John E. 
Published: June 2021

Obstructive sleep apnea exposes individuals to chronic intermittent hypoxia‐hypercapnia (CIHH) episodes and it is associated with increases in sympathetic nervous system activity and blood pressure (BP). Previous experimental studies utilized mainly exposure to chronic intermittent hypoxia (CIH) alone without hypercapnia. In this study we examined if CIHH potentiates the pressor and metabolic responses compared to CIH alone. Sprague‐Dawley rats were instrumented with telemetry probes for measuring mean arterial pressure (MAP) and heart rate (HR) 24‐hrs/day. Rats (n=10) were exposed to CIH (7% O2, 8 hrs/day from 8:00–16:00 hours for 5 consecutive days) or CIHH (7% O2 plus 8% CO2, 8 hrs/day from 8:00–16:00 hours for 5 consecutive days). CIHH and CIH reduced food intake similarly (21±1 to 17±1 vs. 16±1 to 14±1 g/day) leading to a net cumulative decrease in food intake of −22 and −21g, respectively. No changes were observed in plasma glucose concentrations. However, MAP response to CIHH was attenuated by 30% compared to CIH alone (+7±1 vs. +10±1 mmHg). CIHH also induced bradycardia when compared to CIH alone (−24±4 vs. +3±4 bpm, respectively). These results show that combining hypoxia with hypercapnia attenuates the rise in MAP and reduces HR without altering blood glucose and food intake when compared to hypoxia alone. Thus, chronic intermittent hypoxia, but not intermittent hypercapnia, appears to contribute to elevated MAP in rats (NHLBI‐PO1HL51971, NIGMS P20GM104357, NIGMS U54GM115428)Support or Funding InformationNHLBI‐PO1HL51971, NIGMS P20GM104357, NIGMS U54GM115428This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Disproportional and paradoxical changes in blood pressure, heart rate and baroreflex under isoflurane anesthesia
Authors: Tsai Ching‐Yi , Chan Samuel H.H. 
Published: June 2021

For the biomedical researchers, the mandatory employment of anesthetics in experiments involving animals is often regarded as a major limitation because the results may be different from those obtained under a conscious state. For the anesthesiologists, whether patients may have been subjected to unnecessarily deep anesthesia that might jeopardize functions of the cardiovascular system and create inadvertent damage to the nervous system is a recurrent concern. Using isoflurane as the representative anesthetic agent, the goal of this study was to address the issue of whether general anesthetics induce their depressive actions equally on all aspects of cardiovascular functions and their regulations and whether the degree of depression is directly related to the doses. To mimic the clinical setting during surgery, changes of blood pressure (BP), heart rate (HR) and baroreflex in mice instrumented for radiotelemetry were recorded under a conscious state, to be followed by the delivery of incremental concentrations of isoflurane. We found that there was a significant but disproportional reduction in the cardiovascular parameters when C57BL/6 mice were subjected to 1.5% isoflurane anesthesia. Compared with the conscious state, the averaged reduction in BP or HR amounted to 23.5% or 20.5%. On the other hand, the experimental indices for baroreflex‐mediated sympathetic vasomotor tone or cardiac vagal baroreflex manifested a precipitous decline of 90.0% or 63.4%. On incremental concentrations of isoflurane up to a maximum of 4%, mice exhibited sustained BP and HR, alongside returning of both arms of the baroreflex towards the conscious level. We further found that bilateral adrenalectomy exerted minimal effects on the changes in BP, HR and baroreflex in mice subjected to incremental concentrations of isoflurane. It is therefore unlikely that norepinephrine and epinephrine released from the adrenal medulla may account for the disproportional and paradoxical changes in BP, HR and baroreflex under isoflurane anesthesia. These surprise observations offer at least two challenges to the general assumptions on general anesthesia. The effects of isoflurane on cardiovascular functions and their regulations are not exerted proportionally, and both baroreflex‐mediated sympathetic vasomotor tone and cardiac vagal baroreflex exhibit large functional capacity and plasticity in terms of regulating BP and HR.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Hypothalamic‐Pituitary‐Adrenal Axis Responses to an Acute Bout of Moderate Intensity Aerobic Exercise in Breast Cancer Survivors
Authors: Evans Elizabeth S , Little Jonathan , McNeill Kara T , Poole Cara , Bailey Stephen P 
Published: June 2021

The purpose of this investigation was to examine the effect of one 30‐minute bout of moderate intensity aerobic exercise on hypothalamic‐pituitary‐adrenal (HPA) axis hormone responses in women with and without a history of breast cancer. Study participants included 21 women between the ages of 40–75 years, 11 of whom had completed treatments for Stage I–III invasive breast cancer (breast cancer survivors) and 10 of whom did not have a history of cancer diagnosis or treatment (controls). Participants completed a 30‐minute session of aerobic exercise on the cycle ergometer at a workload corresponding to 60% of VO2peak. Blood samples were taken pre‐exercise, immediately post‐exercise, and 30 minutes post‐exercise. Plasma concentrations of corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol were measured at each time point using enzyme‐linked immunosorbent assay (ELISA) techniques (Biotang, Inc., Lexington, MA). Data were compared between groups using Mann‐Whitney U tests and across time using Wilcoxon Signed‐Rank tests. Physical characteristics (e.g. age, height, body mass, BMI, percent body fat and VO2peak) were similar between breast cancer survivors and controls (56 ± 8 years vs. 56 ± 7 years; 163.1 ± 5.3 cm vs. 165.7 ± 5.7 cm; 66.8 ± 9.9 kg vs. 77.0 ± 19.0 kg; 25.1 ± 4.1 kg/m2 vs. 28.1 ± 7.3 kg/m2; 31.1 ± 5.3% vs. 33.4 ± 6.6%; and 21.7 ± 6.8 mL/kg/min vs. 24.3 ± 9.8 mL/kg/min, respectively; p = 0.193–0.973). Cortisol was somewhat elevated immediately post‐exercise in breast cancer survivors relative to controls (Table 1, p = 0.085). CRH decreased significantly at 30 minutes post‐exercise relative to immediately post‐exercise values in breast cancer survivors (Table 1, p= 0.003). ACTH decreased somewhat at 30 minutes post‐exercise relative to immediately post‐exercise values in both groups (p = 0.091 and 0.059 for breast cancer survivors and controls, respectively). All other CRH, ACTH, and cortisol responses were similar between groups and across time (p = 0.114–0.929). These results suggest that one 30‐minute session of moderate intensity aerobic exercise has largely similar effects on hormonal responses of the HPA axis in women with and without a history of breast cancer. These preliminary findings continue to demonstrate that moderate aerobic exercise is well tolerated in breast cancer survivors, thus supporting current exercise recommendations for this population.Support or Funding InformationThis work was supported by Elon University Faculty Research and Development funds.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Predictors of feelings of energy differ from predictors of fatigue among graduate health sciences students
Authors: Boolani Ali , O'Connor Patrick , Reed Jeri , Ma Sai , Mondal Sumona 
Published: June 2021

BackgroundUntil recently many researchers have examined energy and fatigue as opposite ends of a bipolar spectrum rather than two separate unipolar moods. Studies have also focused on a single variable to study these mood states rather than examining multiple variables simultaneously. Therefore, the purpose of this study was to identify factors predicting feelings of energy and fatigue while simultaneously examining multiple domains related to these mood states in graduate health sciences students.MethodsSeventy‐seven subjects were recruited from a Physician Assistant, Physical Therapy and Occupational Therapy program at a small school in Northern New York. Subjects completed a series of surveys to measure mood, diet, mental work load intensity on school days and non‐school days, and physical activity. Subjects also completed the Trail‐making Test Part B task on an iPad and their Resting Metabolic Rate (RMR) and muscle oxygen consumption mVO2 was measured. A backwards linear regression was used to determine the relationship between energy, fatigue and multiple variables.ResultsThe predictor variables accounted for 46.1% and 22.7% of the variance in fatigue and energy, respectively. More fatigue was associated with worse sleep quality, more time spent sitting and higher perceived intensity of mental workload on non‐school days. More energy was associated with better sleep quality, higher muscle oxygen saturation, lower RMR, and faster psychomotor performance.ConclusionThe results of this study indicate that energy and fatigue are separate constructs that are predicted with different accuracy by different variables. Our results indicate that small lifestyle changes may be necessary to improve feelings of fatigue but comprehensive interventions may be necessary to improve feelings of energy. This study provides new insight into a multi‐domain approach to predicting energy and fatigue.Support or Funding InformationThere was no funding for this studyThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Exercise training ameliorates coronary endothelial dysfunction in atherosclerosis through endoplasmic reticulum stress and uncoupling protein‐2
Authors: Hong Junyoung , Park Eunkyung , Lee Jonghae , Park Yoonjung 
Published: June 2021

IntroductionProlonged endoplasmic reticulum (ER) stress, that has been known as an interrupted of ER homeostasis causing apoptosis and inflammation, is closely associated with cardiovascular diseases including atherosclerosis. Uncoupling protein (UCP)‐2 regulates mitochondrial reactive oxygen species (ROS) and its impairment may be associated with atherosclerosis. However, the role of ER stress and UCP‐2 in coronary endothelial dysfunction in atherosclerosis is unclear and no study has been conducted to determine the effect of exercise on ER stress and UCP‐2‐associated coronary arterioles dysfunction in atherosclerosis.MethodsWild type (WT), WT with exercise training, running on the treadmill for 12 weeks (WT‐EX), apolipoprotein E knockout (ApoE KO) and ApoE KO with exercise training (ApoE KO‐EX) mice were used for the study. To test coronary arterioles function, endothelium‐dependent (acetylcholine, ACh) vasodilation and endothelium‐independent nitroprusside (SNP) vasodilation of isolated and pressurized coronary arterioles were measured by a concentration‐dependent manner. The vessels were incubated with endothelial nitric oxide synthase (eNOS) inhibitor, NG‐nitro‐L‐arginine methyl ester (L‐NAME), ER stress inducer, tunicamycin, and uncoupling protein‐2 (UCP‐2) inhibitor, Genepin were incubated and ACh‐induced dilation were measured to investigate the underlying mechanisms.ResultsACh‐induced vasodilation was attenuated in ApoE KO compared to WT, but exercise training ameliorated the ACh‐induced vasodilatation in ApoE KO‐EX while endotheliumin‐dependent SNP‐induced vasodilation was not different among the groups. ACh‐induced vasodilation in the presence of L‐NAME, tunicamycin and Genepin were reduced in WT, WT‐EX and ApoE KO‐EX, but not in ApoE KO.ConclusionOur findings suggest that exercise alleviates endothelial dysfunction in atherosclerotic coronary arterioles through the NOS, UCP‐2, and ER stress signaling pathways.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Systolic Pressure Post‐Maximal Exercise is Associated with Arterial Stiffness and Baroreflex Sensitivity
Authors: Allie Kyleigh , Kilpatrick Julianna , Salvador Paolo , Rivas Eric 
Published: June 2021

BackgroundArterial stiffness is associated with cardiac dysfunction and coronary artery disease. The changes of stiffness post‐exercise is dependent on exercise intensity. Low intensity decreases stiffness while supramaximal exercise increases stiffness. The reason for the increase in stiffening occurring post‐maximal exercise is not well understood and may be due to central and peripheral stiffening or baroreflex resetting from maximal exercise.PurposeThis project tested the hypothesis that the acute increase in blood pressure post‐maximal aerobic exercise is due to central and peripheral arterial stiffness and changes in baroreflex sensitivity (indexed as Δ heart rate /Δ blood pressure).MethodsEight healthy active (7057±2910 steps/day) subjects (6M/2F, 25±6y, 74±17kg) completed a treadmill maximal aerobic exercise test (56.6±12.4mL·kg·min) and a time control standing condition in random order separated by at least 7 days. Heart rate (HR), peripheral blood pressure (SYS, DIA, MAP) stiffness (augmentation index; AIX, pulse wave velocity; PWV) and total vascular conductance (TVC), and central blood pressures (cSYS, cDIA) were measured at 30, 60, 90‐ and 120‐minutes post‐exercise in supine position and baroreflex sensitivity was examined at post‐30 minutes. A 2‐way repeated measures analysis of variance was used to examine interaction and main effects for condition x time. Pearson correlations determined relationships between blood pressures and stiffness measures, exercise capacity and physical activity.ResultsThe change (Δ) after maximal exercise compared to time control rest for HR (Δ13±15bpm), SYS (Δ4±9mmHg), MAP (Δ5±6mmHg), cSYS (Δ4±8mmHg) and PWV (Δ0.19±0.33cm/s) was greater from 30–120 min post‐maximal exercise (condition main effect, P≤0.03). Maximal aerobic exercise did not affect DIA, AIX, or TVC. Cardiac baroreflex sensitivity was increased to a greater extent after exercise (time control: 0.2±0.4 vs maximal exercise: 4.0±5.0 bpm/mmHg; P=0.02) and the ΔcSYS was strongly associated with the Δ arterial stiffness (PWV) accounting for 76% of the variance (P=0.0001).ConclusionThese data indicate that maximal aerobic exercise increases systemic and central systolic blood pressure that is associated with an increased stiffening that may reflect the resetting of cardiac baroreflex sensitivity acutely after maximal aerobic exercise. Further understanding of these mechanisms underlying changes in PWV following maximal exercise may be physiologically relevant to cardiac loading and examining an appropriate baroreflex response that could be impaired in disease states that requires further study.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Impact of dietary nitrate supplementation on the speed/duration relationship in mice with sickle cell anemia
Authors: Ferguson Scott Kohman , Stenmark Kurt R , Buehler Paul , Irwin David C. 
Published: June 2021

Sickle cell disease (SCD) compromises nitric oxide (NO) bioavailability and results in a plethora of cardiopulmonary and skeletal muscle complications causing severe exercise intolerance. It is now widely recognized that dietary nitrate can be reduced to nitrite and, subsequently, NO and impact hemodynamic and metabolic control during exercise. Therefore, the purpose of this investigation was to measure the impact of nitrate supplementation on exercise capacity as measured by the running speed/ exercise duration relationship (critical speed, CS) and the anaerobic work capacity (W′, the finite work capacity available above CS) in mice with SCD. We tested the hypothesis that dietary nitrate supplementation via beetroot juice (BR) would attenuate the exercise intolerance observed in mice with SCD. Ten wild‐type (WT) and 18 Berkley sickle‐cell mice (BERK) received either water (WT: n=10, BERK: n=10) or nitrate‐rich BR (BERK+BR: n=8, nitrate dose 1 mmol/kg/day) for five days). Following the supplementation period, all mice performed 4 constant‐speed treadmill tests that resulted in fatigue within 1.5 to 20 min. Time to fatigue vs. treadmill speed were fit to a hyperbolic model to determine CS. Speed and time to exhaustion for WT, BERK, and BERK+BR conformed to a hyperbolic relationship (WT: r2 = 0.93 ± 0.02, BERK: r2 = 0.97 ± 0.01, BERK+BR: r2= 0.97 ± 0.03, p>0.05). CS was significantly lower in BERK when compared to WT and BERK+BR with no significant difference between WT and BERK+BR (WT: 33.1 ± 1.5, BERK: 24.7 ± 0.7, BERK+BR: 31.9 ± 1.4 m/min, p<0.05). Additionally, the W′ was significantly higher in BERK relative to WT and BERK+BR (WT: 1456.2 ± 237.2, BERK: 2639.2 ± 106.8, BERK+BR: 1134.7 ± 156.7, P<0.05). To summarize, exercise tolerance, as measured via CS, was significantly lower in BERK mice relative to WT. However, BERK mice that had received a 5‐day dietary nitrate intervention exhibited no difference in exercise tolerance when compared to WT. In addition, the W′ was significantly higher in BERK mice relative to WT, but this difference was not observed in BERK+BR. The CS threshold is a well‐described fundamental feature of exercise energetics that represents the highest sustainable rate of aerobic metabolism and remains valid across species. Considering the lower CS in BERK mice and the ability of BR to restore CS in BERK mice, these results provide compelling support for the use of a dietary nitrate intervention to improve functionality in the SCD patient population.Support or Funding InformationFunded by NIH (R01HL125642) to DCI and Colorado Nutrition and Obesity Research Center (P30DK048520) award to SKF.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
CuZnSOD expressed specifically in neurons rescues mitochondrial function and calcium handling in muscles of Sod1KO mice
Authors: Su Yu , Macpherson Peter C.D. , Claflin Dennis R. , Van Remmen Holly , Brooks Susan V. 
Published: June 2021

BackgroundAging is accompanied by loss of muscle mass and force. The mechanism of the loss is not fully understood, but oxidative stress and mitochondrial dysfunction have been implicated as potential contributors. Mice deficient in CuZnSOD (Sod1−/− mice) show decreased ATP production and increased generation of reactive oxygen species by muscle mitochondria as well as muscle atrophy and weakness early in life that is reminiscent of that observed in old age in wild type (WT) mice. Thus, Sod1−/− mice represent a model of accelerated neuromuscular aging. Surprisingly, SynTgSod1−/− mice, which have Sod1 expression restored specifically in neurons, show none of the neuromuscular deficits observed in Sod1−/− mice. To investigate how neuron‐specific Sod1 expression rescues muscle mass and force in Sod1−/− mice, we examined contractile properties and mitochondrial function in muscles of SynTgSod1−/− mice.MethodLumbrical muscles were removed from 7–9 months old wild‐type, Sod1−/−, and SynTgSod1−/− mice, attached to a force transducer, and placed in an experimental chamber for the measurement of muscle contractile parameters and NADH fluorescence was recorded as a measure of mitochondrial redox status. Because mitochondrial function is regulated by calcium, we also examined intracellular calcium transients (ICT) using the fluorescent dye Mag‐fura2. Immunofluorescence techniques were used to examine neuromuscular junction (NMJ) structure and fiber type composition.ResultCompared with WT muscles, mitochondria of muscles of Sod1−/− mice were in a more reduced state at rest and became transiently more oxidized following a 5s maximum isometric contraction. Consistent with the idea that recovery of NADH may be driven by calcium activation of the TCA cycle, the peak of the ICT was reduced and the width prolonged in muscles of Sod1−/− mice. For all measures, muscles of SynTgSod1−/− and WT mice were not different. A shift in muscle fiber type composition observed in Sod1−/− mice was also restored in SynTgSod1−/− mice. Moreover, NMJ denervation and fragmentation was rescued in SynTg Sod1−/− mice.ConclusionOur finding of improved mitochondrial function in muscles of SynTgSod1−/− compared with Sod1−/− mice is consistent with the hypothesis that the mitochondrial dysfunction is an important contributor to the development of atrophy and weakness in Sod1−/− mice. Since SynTgSod1−/− mice are still lacking CuZnSOD in muscle, we conclude that appropriate neuronal function and intact innervation are key to maintaining muscle mitochondrial function and overall muscle size and strength.Support or Funding InformationSupported by NIH Grant AG051442 and the Second Xiangya Hospital of Central South University, ChinaThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.