bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mechanisms of Gender Differences in Exercise Capacity
Authors: Oydanich Marko , Rynecki Nicole , Zhang Jie , Vatner Dorothy , Vatner Stephen 
Published: June 2021

The examination of gender differences has been a recent priority of the NIH. It is well documented that female rodents exhibit higher exercise capacity than their male counterparts. We confirmed this in C57 wild‐type(WT) mice, where female mice exhibited greater, p<0.05, maximal exercise capacity for running distance (469 ± 24 m) than age‐matched male WT mice (337 ± 14 m). The first goal was to examine whether these differences persisted with models of enhanced exercise capacity, e.g. exercise training and the adenylyl cyclase type 5 knockout (AC5 KO) mouse. When WT mice underwent chronic exercise‐training, female mice maintained their superiority over males, with females running a 32% greater distance (p<0.05) than age‐matched trained males. However, AC5 KO mice, which demonstrated enhanced exercise capacity, did not exhibit a gender difference, with female AC5 KO mice (695 ± 51 m) running similar distances to male AC5 KO mice (661 ± 45 m). The next goal was to determine mechanisms mediating these differences. After ovariectomy, WT female mice no longer demonstrated enhanced exercise compared with males. Conversely, chronic administration of estrogen to male mice improved their exercise performance and eliminated the gender differences with exercise. Next we investigated nitric oxide (NO), a downstream target of estrogen. Total NO synthase (NOS) activity was higher in female mice compared with male mice in both sedentary (207 ± 14 U/mg vs. 138 ± 4 U/mg, p<0.05) and exercise trained groups (338 ± 42 vs. 193 ± 15 U/mg, p<0.05). Ovariectomized females exhibited nitric oxide levels similar to males (165 ± 11 U/mg). Administration of L‐NAME, resulting in NO blockade, eliminated the gender differences in exercise performance. In AC5 KO mice NOS activity was not different in male and female mice and similar exercise performance in males and females was still observed after treatment with L‐NAME. Thus, both estrogen and nitric oxide are key mechanisms mediating the enhanced exercise performance in female mice.Support or Funding InformationThis study was supported by the National Institute of Health grant R01HL106511This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Voluntary Exercise Modifies Olfactory Circuits in Control‐ and Fat‐Fed Mice
Authors: Chelette Brandon , Thomas Abigail , Giachos Danielle , Gonzalez Daniel , Vinson Margaret , Fadool Debra 
Published: June 2021

Consumption of a fatty diet causes loss of olfactory sensory neurons (OSNs), loss of olfactory discrimination assessed by olfactometry and electroolfactogram, and increased inflammation in the olfactory epithelium. Because of potential anti‐inflammatory properties of voluntary exercise, we hypothesized it could mitigate the detrimental effects of a fatty diet on the olfactory system. Mice with reporters for the olfactroy receptor M72 (Olfr160) and those with resistance to diet‐induced obesity (Kv1.3−/−) were challenged with control (CF) vs. moderately‐high fat (MHF) diet for 6 months upon weaning, with (running wheel; RW) and without access (sedentary; SED) to a Med Associates vertical wireless running wheel and sensor. MHF/RW mice (n=10; mean 7 month body weight = 40.1 g) gained less body weight than MHF/SED (n=10; 33.3 g, p<0.001) and were able to clear plasma glucose as efficiently as CF/SED mice. Although mice of all treatment groups ran at the same velocity, those provided MHF diet (distance run/day = 11.2 km) increased running distance compared to both CF‐fed WT (n=10) and Kv1.3−/− (n=5) mice (6.85 km/day and 8.29 km/day respectively; p=0.02). Actogram analysis demonstrated that CF‐fed Kv1.3−/− and MHF/RW spend 20.2% and 28.3%, respectively, more time running and exhibit shorter pauses in running activity than CF/RW. Whole‐mount brain images were examined to evaluate M72 staining as quantified by the pixel density of the lateral glomerulus and projections. MHF/RW M72 pixel density was twice as much as MHF/SED mice, but CF/RW pixel density was 31.6% lower than that of CF/SED mice. Our results indicate that in addition to combating weight gain and glucose intolerance, voluntary exercise may reduce the detrimental effects of a MHF diet on olfaction, but exercise may also affect the olfactory system independent of diet composition.Support or Funding InformationThis was supported by NIH grant RO1 DC013080 from the NIDCD and a Dean's Arts and Sciences Scholarship in the Chemical Senses from FSU.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Impaired Oxygen Uptake Kinetics Related to Reduced Peripheral Oxygen Extraction in Heart Failure with Preserved Ejection Fraction
Authors: Hearon Christopher M. , Sarma Satyam , Dias Katrin A. , Hieda Michinari , Levine Benjamin D. 
Published: June 2021

BackgroundThe amount of time needed to increase oxygen utilization to sufficiently meet metabolic demand (V̇O2 kinetics) is impaired in heart failure (HF) with reduced ejection fraction, and is an independent predictor of HF mortality. However, it is not known if V̇O2 kinetics are slowed in heart HF patients with preserved ejection fraction (HFpEF). We tested the hypothesis that V̇O2 kinetics are slowed during submaximal exercise (equivalent to activities of daily living) in HFpEF patients, and that slower V̇O2 kinetics are related to impaired peripheral oxygen extraction.MethodsEighteen healthy controls (69±6 years, 10 females) and eighteen HFpEF patients (68±7 years, 10 females) were studied during submaximal (~30% predicted max) and peak treadmill exercise. Cardiac output (Qc, acetylene rebreathing), pulmonary oxygen uptake (V̇O2, Douglas bags), and arterial‐venous oxygen difference (a‐v O2 diff) were measured during exercise. Breath‐by‐breath V̇O2 uptake was measured continuously at the onset and throughout submaximal exercise, and V̇O2 kinetics quantified as the time needed to for V̇O2 to rise to ~63% of steady state V̇O2 (mean response time, MRT).ResultsDuring submaximal exercise, absolute oxygen demand was similar between groups (V̇O2: Control: 0.81±0.1, HFpEF: 0.85±0.2 L/min; P=0.54) however, HFpEF patients had substantially slowed V̇O2 kinetics (MRT: Control: 40.1±14.2, HFpEF: 65.4±27.7 s; P=0.002), and >50% greater accumulated oxygen deficit compared to controls (Control: 400±173, HFpEF: 693±392 mL; P=0.007). At peak exercise, HFpEF patients had lower relative V̇O2 (Control: 22.2±4.0, HFpEF: 14.6±3.1 mL/kg/min; P<0.001), preserved peak Qc (Control: 13.4±4.0, HFpEF: 13.9±3.5 L/min; P=0.68), and reduced peripheral oxygen extraction (a‐v O2 diff: Control: 12.7±2.9, HFpEF: 10.4±2.1 mL/dL; P=0.01). When stratified by MRT, HFpEF patients with a MRT >60s demonstrated impaired peripheral oxygen extraction that was apparent during submaximal exercise compared to HFpEF patients with a MRT <60s (submaximal a‐v O2 diff: MRT<60s: 9.7±2.1, MRT>60s: 7.9±1.1 mL/dL; P=0.03).ConclusionsHFpEF patients have slowed V̇O2 kinetics during exercise that are due in part to impaired peripheral oxygen utilization. This finding supports growing evidence that peripheral oxidative capacity is a primary contributor to exercise intolerance in HFpEF leading to substantial oxygen deficit even during activities of daily living. Further, MRT can lend important insight into the pathophysiology of exercise intolerance in individual HFpEF patients, and identify patients with severe peripheral limitations to exercise capacity.Support or Funding InformationNIH: AG017479, F32‐HL137285This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Exercise Pressor Reflex is attenuated and Coronary Exercise Hyperemia is improved by Peripheral Revascularization in Peripheral Arterial Disease
Authors: Miller Amanda Joy , Luck J Carter , Kim Danielle Jin‐Kwang , Leuenberger Urs A. , Aziz Faisal , Radtka John F. , Sinoway Lawrence I. , Muller Matthew D. 
Published: June 2021

Patients with peripheral arterial disease (PAD) have a greater blood pressure (BP) response to exercise or augmented exercise pressor reflex. Our recent work showed that PAD patients also have impaired coronary blood flow responses to exercise which may increase cardiovascular risk. We investigated the effects of leg revascularization procedures on the BP and coronary blood flow responses to exercise in PAD. Seventeen PAD patients (11 men, 66 ± 2 yr) performed single‐leg plantar flexion exercise for up to 6 minutes twice: 24 hr before and one month following leg revascularization. BP and heart rate (HR) were measured continuously and rate pressure product (systolic BP × HR) was calculated as an index of myocardial oxygen demand. Coronary blood velocity was obtained by transthoracic Doppler echocardiography. The mean BP response to plantar flexion exercise was attenuated by leg revascularization (pre revascularization: 15 ± 4 vs. post revascularization: 7 ± 3 mmHg, P = 0.025). The HR response to plantar flexion was also attenuated following leg revascularization (pre revascularization: 9 ± 1 vs. post revascularization: 6 ± 1 beats/min, P = 0.006). The change in coronary blood velocity with exercise was significantly greater at the post revascularization visit: 4 ± 1 vs. pre revascularization: −1 ± 2 cm/s (P = 0.038). The rate pressure product response to exercise tended to be lower following revascularization but this did not reach statistical significance (pre revascularization: 2796 ± 871 vs. post revascularization: 1766 ± 378 mmHg*beats/minute, P = 0.082). These data suggest that leg revascularization improves reflex control of BP, HR, and coronary blood flow in response to exercise in patients with PAD.Support or Funding InformationP01 HL134609 (Sinoway)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Stimulation of Peripheral Opioid Receptors during Acute Exercise Decreases Anxiety‐Like Behaviors in a Rat Model of Fibromyalgia
Authors: Williams Emily R. , Daniels Abigale B. , Ford Caleb M. , Horton Molly , Stocks Silas , Leal Anna K. 
Published: June 2021

Patients with fibromyalgia often experience comorbid anxiety. Studies show exercise training can decrease pain in patients with fibromyalgia as well as decrease anxiety in healthy populations. Evidence suggests endorphins acting on opioid receptors contribute to exercise‐induced analgesia, but the role of these receptors on anxiety has not been determined in patients with fibromyalgia. The purpose of this study was to compare the effects of sedentary behavior and exercise training on anxiety in a rat model of fibromyalgia and to determine the contribution of peripheral opioid receptors to the exercise‐induced response. Female Sprague Dawley rats were induced with fibromyalgia by acidic saline injections (0.1 mL; pH 4). To assess anxiety‐like behaviors, rats were placed in an open field arena (90 × 90 cm) for two minutes. The arena floor was marked with 20.5 cm grids and the number of grids crossed during the observation period was recorded: a decrease in grids crossed indicated increased anxiety. A group of sedentary rats (SED; n=8) were tested for anxiety 5 days/week for 4 weeks. Another group of treadmill‐trained rats (NAL; n=5) received injections of the nonspecific opioid receptor antagonist naloxone (120 μg in 0.1 mL saline) in both gastrocnemius muscles ten minutes prior to moderate‐intensity (15 m/sec) treadmill running (4 weeks; 5 days/week; 30 min/day). NAL rats were observed in the open field arena before (PRE) and after (POST) each running bout. Mean grids crossed for SED rats in the open field were 21.3 ± 2.4 for week 1, 23.7 ± 2.9 for week 2, 29.7 ± 2.9 for week 3, and 28.0 ± 3.0 for week 4. While NAL PRE grids crossed were not different from SED grids crossed, the POST grids crossed for NAL rats decreased for all weeks: 16.5 ± 2.0 (PRE) and 10.1 ± 1.9 (POST) for week 1, 24.0 ± 1.9 (PRE) and 12.4 ± 1.4 (POST) for week 2, 21.8 ± 1.9 (PRE) and 10.4 ± 1.7 (POST) for week 3, and 23.6 ± 2.2 (PRE) and 13.2 ± 1.8 (POST) for week 4 (all p<0.05). Further, NAL POST grids crossed were significantly different from SED grids crossed for weeks 1, 2, 3 and 4 (p<0.05). While our data does not show a long‐term effect of exercise training on anxiety, it does suggest that stimulation of peripheral opioid receptors during acute exercise decreases anxiety‐like behaviors in the rat model. In conclusion, this study provides evidence that peripheral, in addition to central, opioid receptors contribute to an exercise‐induced decrease in anxiety and that even one exercise bout is beneficial when compared to sedentary behavior.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Cerebral oxygenation in Metabolic Syndrome patients during mental task and muscle metaboreflex activation
Authors: roberto silvana , doneddu azzurra , pinna virginia , milia raffaele , ghiani giovanna , lecis romina , velluzzi fernanda , magnani sara , sainas gianmarco , guicciardi marco , crisafulli antonio 
Published: June 2021

The post‐exercise muscle ischemia (PEMI) is a well established method to study the cardiovascular adjustments to exercise since it enhances sympathetic tone thereby recruiting the hemodynamic reserves. Thus, PEMI can reveal cardiovascular diseases1,2. Our hypothesis was that, in patients suffering from Metabolic Syndrome (MS), cerebral oxygenation decreased during the metaboreflex elicited by PEMI, because of an exaggerated sympathetic response which could vasoconstrict the cerebral circulation3. Furthermore, we hypothesized that in these patients, the cerebral oxygenation could be further impaired by superimposing a mental task (MT) to PEMI. To this aim, variation in cerebral circulation of MS patients was compared with that of healthy controls during contemporary PEMI and MT.Two groups were enrolled: one composed of 15 subjects (7 women, age 53.5±10.7 yrs.) suffering from MS and a control group (CTL) composed of 14 healthy subjects (6 women, age 50.86±8.2 yrs). Both groups underwent 5 different tests each lasting 12 min: PEMI, control exercise recovery (CER), PEMI+MT, CER+MT, and MT alone. During each session, cerebral oxygenation (COx) was measured by Near Infrared Spectroscopy (NIRS) by applying sensors to the skin of the forehead.Data analysis found no significant differences in COx between groups during any test. No reduction in COx were observed during the PEMI test (CTL 100.9±3.3% vs MS 102.5±1.9%) and the MT test (CTL 101.5±2.2% vs MS 102±1.8%) in both groups. Moreover, the addiction of MT to the PEMI test did not cause any impairment in COx.Contrary to our hypothesis, results of the present study indicate that in patients with MS there is no impairment in COx during sympathetic activation obtained by PEMI. Furthermore, no significant reduction was found in the COx when adding MT to the PEMI test. It was concluded that COx is not impaired in patients suffering from MS when sympathetic tone is augmented.Support or Funding InformationThis study was supported by the “Fondazione di Sardegna”This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
The Association between Oxidized Low Density Lipoprotein Concentration and Paraoxonase‐1 Activity, Total Antioxidant Capacity, and Low Density Lipoprotein Concentration in Highly Trained Individuals
Authors: Robison Charles E. , Davis Paul G. , Goldfarb Allan , Mellick Paul 
Published: June 2021

Physical fitness is associated with reduced risk factors for cardiovascular disease, in particular oxidized low‐density lipoprotein (ox‐LDL). Therefore determinants of ox‐LDL in fit individuals are important to understand. Antioxidant defenses and the concentration of low‐density lipoprotein (LDL) are associated with ox‐LDL concentration, however the relative importance of these variables is not fully understood. Paraoxonase 1 (PON1) is an antioxidant enzyme capable of preventing the oxidation of LDL. Moreover, total antioxidant capacity (TAC) is an assessment of the broad antioxidant status of the blood.PURPOSEOur purpose was to measure the association between ox‐LDL concentration and PON1 activity, TAC, and LDL concentration in highly trained individuals.METHODSParticipants were instructed to refrain from exercise for 48 hours prior to blood sampling. Following a 12‐hour fast venous blood was taken at rest to determine ox‐LDL in plasma, PON1 in serum, and TAC in serum. LDL concentration was estimated using the Friedewald formula. Pearson Product Moment correlations were used to assess the relationships between ox‐LDL concentration and PON1 activity, ox‐LDL concentration and TAC, and ox‐LDL concentration and LDL concentration.RESULTSFifteen individuals (12 males, 3 females) who had high cardiorespiratory fitness (VO2max= 54.8 ± 1.7 ml×kg−1×min−1) completed the study. We found no association between ox‐LDL concentration and PON1 activity (r= 0.08, p = 0.78) and no association between ox‐LDL concentration and TAC (r= −0.15, p= 0.58). However there was a significant association between ox‐LDL concentration and LDL concentration (r= 0.82, p < 0.001).CONCLUSIONThis indicates that in highly trained individuals LDL concentration may be more important than antioxidant defenses in the development of circulating ox‐LDL concentration.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Relationships between injury years and thermoregulatory responses during heat stress in spinal cord injury persons.
Authors: Kamijo Yoshi‐ichiro , Shibasaki Manabu , Kinoshita Tokio , Moriki Takashi , Nakamura Takeshi , Kouda Ken , Tajima Fumihiro 
Published: June 2021

Thermoregulatory responses via sympathetic nerve activity during heat stress are absent or impaired in persons with spinal cord injury. However, relationships between their injury years and responses of sweating and cutaneous vasodilation to increased core temperature remained unknown. Six of cervical (CSCI; N=6; level of C5‐7; injury years of 1–22 yrs) and 8 thoraciolumbal (SCI; N=8; Th4‐L1; 1–24 yrs) spinal cord injury persons and 10 healthy subjects (AB; able‐body) were recruited. They wore water‐perfused suits with taking a supine position and 33‐degree C water was perfused into the suits to make a whole body thermoneutral condition, while all devices were applied. After 10‐min measurements during thermoneutral condition, heat stress was performed with infusion of 47‐degree C water until esophageal temperature (thermocouples) increased by 1 degree C. Mean arterial pressure (MAP; the brachial artery; Korotkoff's method), mean skin (Tsk) and local chest temperatures (Tchest; thermocouples), sweat rate (SR; capacitance hygrometry) and skin blood flow (SkBF; laser‐Doppler velocimetry) on the chest. Cutaneous vascular conductance (CVC) were calculated as SkBF divided by MAP. Tsk was about 35 degree C in all groups and increased by 3 degree C. Tchest increased by 1.4 degree C during heat stress. CVC increased by 4 times as baseline in AB, 3 times in SCI during heat stress, but no increase was observed in CSCI. Patterns of SR in all groups were similar to CVC. Maximal response of CVC [control/degrees] was tended to be negatively correlated, but that of SR [mg/cm2/min] was positively correlated with injury years. In conclusion, thermoregulatory responses to increased core temperature were absent in CSCI and impaired in SCI. In SCI, sweating response on the chest, where sympathetic nerve activity is intact, is possibly enhanced to compensate for reduced cutaneous vasodilation with increased injury year.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Prior Viral Illness Exacerbates the Severity of Lung Injury in a Mice Heat Stroke Model
Authors: Plamper Mark l. , Dineen Shauna M. , King Michelle A. , Leon Lisa R. 
Published: June 2021

Heat Stroke (HS) is a common threatto both civilian and warfighter populations, however the mechanisms underlying tissueinjury are unknown. Acute respiratory distress syndrome (ARDS) is often seen with the adverse sequelae that follows HS, and correlates with mortality. Further, anecdotal evidence suggests that prior illness can increase the severity of multi‐organ injury in HS. To examine the effect of a recent viral illness on the severity of ARDS following HS, male C57BL/6J mice (body weight 23.0 ± 0.3g)were intraperitoneally injected with Polyinosinic: Polycytidylic acid (PIC; 100μg) or saline (SAL; 100 μl) 48‐h prior to heat exposure (HE; 39.5 ±0.1°C). Miceremained in HE until core temperature (Tc; ±0.1°C; radio telemetry) reached Tc Max of 42.4°C. Control mice were injected with saline or PIC, but never exposed to the heat. Lung tissue was collected for analysis of inflammatory biomarkers indicative of ARDS and cell death at Tc Max and at 1 day post HE (1d). Monocyte chemoattractant protein‐1 (MCP‐1; a predictor of ARDS severity) was upregulated in control mice injected with PIC alone (P=0.003 at Tc Max; P<0.001 at 1d)and HE exacerbated this response at both Tc Max and 1d (P<0.001 and P=0.029 respectively). Interestingly, eotaxin (an eosinophil‐specific chemoattractant)was suppressed at Tc Max following HE in both PIC and SAL groups (P<0.001). PIC in the absence of HE did not alter expression at Tc Max, however eotaxin was significantly upregulated in this group at 1d (P=0.041). To determine the extent of lung injury, a cell death assay was conducted. Unexpectedly, at Tc Max no differences in cell death were seen between groups; however, at 1d cell death was significantly augmented in those that received PIC alone (P=0.001) and those that received PIC prior to HE (P=0.002). In conclusion, PIC injection 48‐h prior to HE increases severity of lung tissue injury with the magnitude and time course of inflammatory changes was unique to each biomarker. Author views not official US Army or DOD policy.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.