bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rapid Onset Vasodilation in the Leg is Greater in Habitual Endurance Runners
Authors: Coolbaugh Crystal , Bush Emily , Sabin Shea , Scott Brent , Damon Bruce , Towse Theodore 
Published: November 2023

Although the beneficial effects of habitual physical activity on the peripheral vasculature are well‐established, activity‐dependent differences in the blood flow response to single muscle contractions have been largely ignored. Therefore, the purpose of this study was to determine if habitual endurance running (average training volume > 50 miles/week for ≥ 3 years) alters contraction‐induced rapid vasodilation in a limb‐specific manner. Trained (n = 8, 24 ± 3 years) and untrained (n = 4, 24 ± 1 years) men performed 1‐s maximal voluntary contractions in the leg (dorsiflexion) and forearm (hand‐grip). A physical activity recall questionnaire and 7‐day accelerometer recordings were used to confirm differences in training status between groups (p < 0.001). Anterior tibial and brachial arterial blood flow (ml/min) were measured with Doppler ultrasound for 30‐s prior, during, and 90‐s following the muscle contraction. Trained men demonstrated a greater increase in arterial flow in the leg (peak 5.8 ± 0.66‐fold above rest) compared with untrained men (peak 3.5 ± 0.37‐fold above rest; p = 0.04). In contrast, postcontractile blood flow responses in the arm were similar despite training status (Trained: peak 2.8 ± 0.41‐fold above rest; Untrained: peak 3.2 ± 1.1‐fold above rest, p = 0.86). Our data demonstrate that the magnitude of the postcontractile blood flow response to brief muscle contractions is greater in the legs of habitual endurance runners compared with untrained men. Collectively, these findings indicate that quantification of physical activity is necessary to properly interpret differences in contraction‐induced rapid vasodilation due to aging or disease.Support or Funding InformationFunding: NIH/NIBIB T32 EB001628; CTSA UL1TR000445
Is A 90 Min Recovery Period Following Fatiguing Handgrip Exercise Enough To Ensure Maximal Performance During A Critical Impulse Test (CIT) Or Incremental Exercise Test (IET)?
Authors: Fenuta Alyssa M. , Tschakovsky Michael E. 
Published: November 2023

IntroductionThe critical impulse (CIT) and incremental exercise (IET) tests are used to quantify important performance capacity indices. The CIT requires maximal effort for 10 min enabling determination of the highest work rate sustainable by aerobic metabolism (CI) and anaerobic work capacity (W’). The IET involves 25 N increases every 3.5 min enabling determination of peak work rate (VO2). Since these protocols are fatiguing, methodological considerations must be made when both parameters are assessed in a single session to ensure the second test performance is not compromised.PurposeTo establish the reproducibility of the CIT and IET performance and to determine if 90 min of rest between trials allowed complete performance recovery.Methods12 healthy recreationally active adults (24.3±3.9 yrs; 24.2±3.9 kg/m2) completed rhythmic isometric forearm handgripping (1s contraction:2s relaxation) while supine with exercising muscles at heart level. Day 1 consisted of completing one exercise test followed 90 min later by the other. The order of test presentation was reversed on Day 2. Pre‐test maximal voluntary contractions (MVCs) were completed prior to each trial. CI was calculated as the average contraction impulse of the last 30s of the CIT and W’ was calculated as the area under the curve between CI and the maximal effort contractions over the course of the test. Peak IET Performance was calculated as the average impulse of final stage contractions. Total IET Work was calculated as the cumulative impulse from first to final contraction. Fatigue during the CIT and IET protocols were measured as the relative change in impulse from the pre‐test MVC to CI or Peak IET Performance respectively.ResultsWhether the CIT was preceded by the IET or not did not affect CIT performance: CI (p=0.2;ICC=0.9;CV=8.8) and W’ (p=0.5;ICC=0.9; CV=8.3%). Whether the IET was preceded by a CIT or not did not affect Peak IET Performance (p=0.6; ICC=1.0;CV=5.0) or Total IET Work (p=0.1;ICC=0.9;CV=11.5%). Total IET Work and W’ were equally reproducible (CV=8.0% vs. CV=7.0%; p=0.7). The impulse at the end of the CIT was ~86.6%±3.3% of the impulse at the end of the IET. Fatigue was greater during the CIT versus IET (−56.8% vs. −48.6%) (p<0.001). There was a strong correlation between CIT and Peak IET Performance (R2= 0.8; p<0.001) and W’ and Total IET Work (R2= 0.8; p<0.001).ConclusionPerformance for both exercise tests demonstrates good day‐to‐day repeatability and 90 min of recovery is adequate to ensure peak performance in both tests. Therefore, to assess both CIT and Peak IET Performance in one session it is recommended at least 90 min of recovery be provided to ensure the prior fatiguing protocol does not compromise subsequent maximal performance.Support or Funding InformationAlyssa M. Fenuta, MSc, is supported by Queen's University School of Graduate Studies Bruce Mitchell Academic Leadership Award.
Effects of hypoxia with matched convective O2 delivery on fatigue and O2 on‐kinetics in canine skeletal muscle in situ
Authors: Ferguson Brian S , McDonald James R , Mowry Francesca , Sun Yi , Rasica Letizia , Porcelli Simone , Hogan Michael C , Grassi Bruno , Gladden Bruce 
Published: November 2023

PURPOSEFactors influencing maintenance of force development (i.e., fatigue) remain incompletely understood. Previous research in the perfused canine gastrocnemius‐superficial digital flexor muscle complex (GS) (e.g., Barclay. J Appl Physiol 61(3):1084–90, 1986) has suggested that higher blood flow, independent of O2 delivery diminishes the fatigue rate. The aim of this investigation was to evaluate skeletal muscle fatigue development at two different metabolic rates in the GS while blood flow was varied but O2 delivery held constant.METHODSCanine GS (n=14) were surgically isolated and electrically stimulated via the sciatic nerve (8V, 0.2ms duration, 50Hz, 200ms train) generating tetanic contractions at either 2 contractions every 3 seconds (~70% VO2peak, n=7) or 1 contraction every second (~100% VO2peak, n=7). Fractional O2 was manipulated with additional nitrogen to the inspired air for final concentrations of ≈21, 12, and 8% O2. Convective O2 delivery to the muscle [blood flow (Q) x arterial O2 content (CaO2)] was held constant by elevating muscle blood flow via a perfusion pump. Muscle developed force was monitored over 3‐min periods of stimulation (sufficient time for significant fatigue to occur) while O2 and blood gases were measured.RESULTSArterial PO2 prior to the different trials at 70% VO2peak was 105±13, 41±2, and 27±1 torr, and for 100% VO2peak was 101±15, 45±4, and 33±5 torr for 21, 12, and 8% inspired O2 respectively. Convective O2 delivery was not different (p≥0.05) among the three O2 fractions; 70% VO2peak = 202±58, 206±57, and 205±49 mL O2·kg−1·min−1; 100% VO2peak = 282±31, 284±43, and 285±52 mL O2·kg−1·min−1 for 21, 12, and 8% respectively. During the 70% VO2peak trials, fatigue was minor for all conditions with 8% inspired O2 fatigue index (FI) = 5.3±3.1% being greater than during the 21% inspired O2, FI = 1.9±1.2% (p≤0.05). During 100% VO2peak, fatigue was much more marked, 22.5±4.8, 22.3±7.5, and 27.8±2.1% for 21, 12, and 8% trials, but not significantly different across conditions (p≥0.05).CONCLUSIONSBlood flow independent of O2 delivery had minimal to no effect on the development of fatigue in isolated perfused skeletal muscle stimulated to 70% VO2peak and 100% VO2peak. This was the case despite large differences in arterial and venous PO2, and therefore, likely mean capillary PO2. These results differ from previous work which found effects of blood flow on fatigue that were independent of O2 delivery.
Prediction of Mountain Marathon Performance with Anaerobic Capacity
Authors: Rogers Michael J , Rietchel Lauren J , Singh Prabhjot K , Foster Ian J , Wookey Alison L , White Matthew D 
Published: November 2023

PURPOSEAnaerobic capacity, aerobic capacity and morphology were assessed for their potential effects on race performance during a 50 km mountain ultra‐marathon.HYPOTHESISIt was hypothesized that anaerobic and aerobic capacities would be the best predictors of finishing times in this ultra‐marathon.METHODSTen healthy males were recruited to participate in this study. Their average height was 1.76±0.09 m, body mass was 70.75±8.04 kg, Body Mass Index was 22.9±1.85 kg·m−2, body fat percentage was 21.98±4.75 %, and age was 47.6±11.0 years. The office of research ethics at SFU approved the study and each volunteer gave a signed consent prior to participation. Each volunteer's anaerobic capacity was evaluated using a Wingate test on a seated cycle ergometer and aerobic capacity was assessed by indirect calorimetry with a breath‐by‐breath metabolic cart during an incremental test from rest to the point of exhaustion on a treadmill. Predictions of race finishing times were assessed using both stepwise multiple linear regression as well as ANCOVA with body mass as the covariate. The independent variables included mean power, peak power, minimum power, time to peak power, time to fatigue, body fat percentage, body mass, lean body mass and maximal oxygen consumption (VO2MAX).RESULTSDuring the Wingate test mean power was 531.70±88.92 W, peak power was 854.30±193.97 W, time to peak power was 3.25±2.44 s and rate to fatigue was 18.01±4.93 s. During the incremental treadmill test VO2MAX_ABS was 4.01±0.65 L·min−1 and VO2MAX_REL was56.70±6.24 L·min−1·kg body mass−1. The stepwise multiple linear regression indicated that peak power (R2=0.59, p<0.05) or residuals from peak power plotted as a function of body mass (R2=0.54, p<0.05) were significant predictors of race performance in this mountain marathon.CONCLUSIONThese preliminary results support that in a mountain ultra‐marathon a significant fraction of the variance in performance is predicted by peak power as determined in a Wingate anaerobic test.Support or Funding InformationSupported by the Natural Sciences and Engineering Research Council of Canada (NSERC) and the Canadian Foundation for Innovation (CFI)
Exercise pressor reflex response to static and dynamic skeletal muscle stretch
Authors: Venturelli Massimo , Cè Emiliano , Limonta Eloisa , Rampichini Susanna , Bisconti Angela V. , Devoto Michela , Esposito Fabio 
Published: November 2023

Passive static stretching (SS), arterial occlusion (C), and the combination of both procedures (SS+C) has been used to stimulate group III and IV afferents of the exercise pressor reflex. However, the effects of dynamic passive stretching (DS) and arterial occlusion (DS+C) on the exercise pressor reflex are not fully elucidated. Therefore, the aim of the present study was to compare central and peripheral hemodynamic response to DS, SS, DS+C, and SS+C.In twelve healthy volunteers, femoral blood flow (FBF), heart rate (HR), cardiac output (CO), and mean arterial pressure (MAP) were assessed during DS and SS of the quadriceps muscle. The same procedures were repeated with arterial occlusion of lower limb (upper‐thigh cuff inflated at 250 mmHg).FBF increased significantly in both DS and SS by 365±98 and 377±102 ml/min, respectively. This hyperaemia was reduced during DS+C and SS+C by 11±98 and 5±87ml/min. The increase in HR was similar in all conditions (~4.2 bpm for DS, SS, DS+C, and SS+C; p < 0.05). Likewise, the change in CO was ~0.30 l/min p < 0.05. MAP dropped by −4.7±1.2 and −4±1.4 mmHg (p < 0.05) during DS and SS, while it increased by 3.7±1.6, and 4.8±1.3 mmHg for DS+C and SS+C (p < 0.05).Data from the current study indicated a similar group III afferents response to DS, SS (i.e., equal HR and CO changes). HR and CO findings during DS+C and SS+C suggested no evidence of interaction between group III and IV afferents. Conversely, the MAP reduced only during DS and SS, because of a limb induced‐hyperaemia.
Transiently augmented endothelium dependent vasodilatory capacity following repeated 6‐hour air dives
Authors: Morgan Richard Garrett , Bergeron Elizabeth , Shykoff Barbara E , Florian John P. 
Published: November 2023

BackgroundMilitary divers routinely participate in operations that involve long duration (≥ 6hr) air dives at shallow (≤ 60 FSW) depths that are repeated daily until mission completion. These dive operations have been linked to impairments in aerobic exercise performance and orthostatic tolerance after egress from the water. Alterations in endothelium‐dependent vasodilation and blood flow may play a role in cardiovascular dysfunction associated with long duration repeated air dives.MethodsTo test this unexplored hypothesis, we measured reactive hyperemia index (RHI), mean arterial pressure (MAP) and resting heart rate (RHR) using the Endo‐PAT2000 plethysmographic peripheral arterial tone (PAT) device in 11 military divers (21–40y) before and after single 6hr air dives at 15 FSW and 6hr air dives at 15 FSW repeated daily for four days. We compared pre and post RHI, MAP and RHR from a single dive and between repeated dives.ResultsWe found no differences in RHI, MAP or RHR following completion of a single 6hr air dive at 15 FSW (all P ≥ 0.39). Over the course of four dives repeated daily, we found a main effect of dive day for RHI (P = 0.03), such that pre‐ and post‐dive RHI increased by at least 30% between dives one and three, but returned to baseline by dive four. There was no effect of dive on RHI, determined by pre‐ and post‐dive testing, during each dive day (P = 0.26). We found no effect of dive or dive day on MAP (all P ≥ 0.15); however, pre‐dive RHR was 4–6 bpm higher on the fourth dive day than the second and first day (all P < 0.01), and post‐dive RHR was ~4 bpm lower than pre‐dive RHR across all dive days (P < 0.02).ConclusionsThese findings demonstrate that repeated shallow air dives lead to transiently augmented vasodilatory capacity with a parallel increase in RHR. Increased RHI may help maintain perfusion to the periphery following immersion‐induced diuresis and subsequent reductions in blood volume, while a compensatory increase in RHR occurs to maintain mean arterial pressure.Support or Funding InformationNAVSEA DSBDP and ONR
The Impact of Acute Isocapnic Hypoxia on Reactive Hyperemia in Young, Healthy Humans
Authors: Kelsch Elizabeth A , Keller Joshua L , Crecelius Anne R 
Published: November 2023

Acute hypoxic exposure results in a number of significant physiological responses, including vasodilation in vascular beds of the skeletal muscle. The objective of this study was to investigate the effects of acute hypoxic exposure on microvascular function in young healthy humans, as determined by reactive hyperemia (RH). We first hypothesized that brief exposure to isocapnic hypoxia just prior to arterial occlusion would exaggerate the reactive hyperemic response, given hypoxic vasodilation may cause an increased oxygen mismatch. Second, we hypothesized continuous isocapnic hypoxia prior to and throughout arterial occlusion would attenuate the reactive hyperemic response given chronic exposure has been linked to vascular dysfunction. We tested subjects between the ages of 20 and 23 (n=6) with three counterbalanced trials: control, prior hypoxic exposure, and prolonged hypoxic exposure. Subjects were monitored for end‐tidal CO2 (gas analyzer), O2 saturation (pulse oximetry), heart rate (ECG) and blood pressure (sphygmomanometry). Forearm blood flow (FBF) measurements using venous occlusion plethysmography were made prior to and following 5 minutes of forearm ischemia (RH). During experimental trials, subjects breathed hypoxic gas to decrease arterial O2 saturation to ~85% and isocapnia was maintained via a rebreathe system. Peak RH FBF was slightly increased after brief hypoxic exposure compared to normoxia (43.2±4.2 vs 40.3±6.2 ml/dl/min). However, in continuous hypoxia, peak RH FBF (39.6±3.9 ml/dl/min) was similar to normoxia. The total area under the curve during RH was similar in all three trials (normoxia: 156±9 ml; brief: 152±6 ml; continuous: 154±14 ml). Continuous hypoxia resulted in increased heart rate as compared to brief hypoxia and normoxia. The present results suggest that a brief period of hypoxia prior to occlusion does not impair RH responses. In addition, in young healthy humans, RH responses are preserved following continuous hypoxia throughout occlusion.Support or Funding InformationUniversity of Dayton‐ Research Council Grant‐In‐Aid; University Honors Berry Summer Thesis Program
Blunted Arterial Blood Pressure Responses to Whole‐Body Cold Stress in Individuals with Multiple Sclerosis
Authors: Allen Dustin Ryan , Huang Mu Ryan , Frohman Elliot M , Davis Scott L 
Published: November 2023

Multiple sclerosis (MS) is a neurological disease in which demyelination disrupts signal transmission and/or integration within the central nervous system. Reduced resting MSNA has been previously reported in MS patients (Keller et al., 2014). The aim of this study was to test the hypothesis that individuals with MS will have blunted sympathetic‐mediated responses to a whole‐body cold stress stimulus compared to healthy controls (CON). Ten subjects with relapsing‐remitting MS (age, 35±7 years old; height: 163±9 cm; weight: 64±12 kg; BSA: 1.7±0.2 m2) and 4 healthy controls (31±5 years old; height: 168±6 cm; weight: 66±14 kg; BSA: 1.7±0.2 m2) participated in the study. Subjects were instrumented with a tube‐lined water perfusion suit in which they were exposed to a thermoneutral (34 °C circulating water) condition for a baseline period of 10 minutes, followed by a 3‐minute whole‐body cold stress (5 °C circulating water) condition. Skin blood flow (laser‐Doppler flowmetry), beat‐to‐beat arterial pressure (photoplethysmography), heart rate (ECG), and mean skin temperature were continuously measured. Cutaneous vascular conductance was calculated from the ratio of laser‐Doppler flux to mean arterial pressure (CVC) and normalized to maximal responses obtained by local heating at 42 °C following cooling (%CVCmax). Mean arterial pressures (MAP) were derived during the final minute of baseline and cooling. There were no differences in ΔLDF flux (CON: −2.83±3.76; MS: −3.73±4.29, p=0.72), ΔCVC (CON: −0.05± 0.06; MS: −0.05±0.06, p=0.89), and Δ%CVCmax (CON: −2.43±3.75; MS: −0.24, p=0.12) from baseline to cooling. However, there was a significant difference in ΔMAP between groups (CON: 12.17±9.70; MS: −0.99±7.00, p=0.01). While cutaneous vasoconstrictor responsiveness was similar between groups, these data suggest individuals with MS exhibit reduced sympathetic‐mediated changes in blood pressure in response to a whole body cold stress.Support or Funding InformationProject funded by NIH grant (R15 HL117224) and National Multiple Sclerosis Society grants (RG4043A and RG4696A)
Parkin‐Mediated Mitophagy in Skeletal Muscle with Aging and Exercise
Authors: Chen Chris , Hood David 
Published: November 2023

In skeletal muscle, the progressive age‐related loss of muscle mass and strength is known as sarcopenia. Alterations in skeletal muscle mitochondria are considered to be a contributing factor in this process. When mitochondria are no longer able to sustain the energetic requirements of the cell, selective autophagy (mitophagy) pathways are induced to promote the clearance of damaged mitochondria. In aged muscle, dysfunctional mitochondria generate increased amounts of reactive oxygen species (ROS) and can impair quality control mechanisms that facilitate their removal. It remains unclear if mitophagy mediates this reduced response in aged muscle. Parkin is an ubiquitin ligase involved in mitophagy, but little is known about its function with aging. To evaluate mitophagic signaling in aged muscle, young (3 months) and aged (18 months) Parkin deficient (KO) mice and wild‐type (WT) animals were assigned to three groups: control, acute exercise, or acute exercise plus 2 hours of recovery. Muscle mass was reduced by 46% and 65% respectively in aged Parkin KO and WT mice when compared to their young counterparts. Furthermore, aged WT animals displayed a 25% decrease in whole muscle cytochrome c oxidase activity. This was accompanied by a 40% reduction in State 3 (active) intermyofibrillar mitochondrial respiration in aged WT animals. In response to exercise, both aged Parkin KO and WT mice exhibited ~30% declines in running performance, and increased lactic acidosis by 2.1‐ and 1.4‐fold, respectively. Interestingly, basal mitophagy flux and subsarcolemmal mitochondrial localization of LC3II, p62 and ubiquitin were augmented in both young and aged Parkin KO muscle. Acute exercise increased mitochondrial flux in young animals, but reduced flux in older muscle. Our findings indicate that the expression of mitophagy proteins and their localization to mitochondria are not decreased in aged muscle, even in the absence of Parkin. However, attenuation of exercise‐induced mitophagy in response to aging may contribute to mitochondrial accumulation and dysfunction in aged muscle.Support or Funding InformationSupported by NSERC.
Differential Agonistic Activities of Angiotensin Peptide Analogs
Authors: Speth Robert C , Sturchler Emmanuel , McDonald Patricia 
Published: November 2023

Biased agonism of angiotensin (Ang) peptides may differentiate beneficial from pathophysiological actions of the renin‐angiotensin system. To assess the potential for biased agonism a series of Ang peptides modified at the amino terminal, or carboxy terminal (with Isoleucine8), or with D amino acid substitutions were evaluated for their ability to increase cytoplasmic calcium levels, or to alter cellular impedence using the CellKey system to measure agonism, and also to cause desensitization. The most potent analogs for increasing cytoplasmic calcium were 71 to 2 times more potent (EC50 values) in the calcium assay relative to the CellKey assay in the order N‐Methylaspartate1 Ang II, Gly1 Ang II, D‐Arginine1 Ang III, Sarcosine0, Sarcosine1 Ang II, D‐Alanine1 Ang II, and Ang II. Less potent Ang peptides had potency ratios of calcium activation to CellKey activation of ~ 1 to 0.07. Isoleucine (Ile)8 substituted Ang II analogs had extremely weak ability to increase cytoplasmic calcium and moderately weak ability to alter impedence in the CellKey assay with potency ratios of 0.06 to 0.24. The ability of these Ang peptides to cause loss of responsiveness to a subsequent challenge with Ang II in the CellKey assay largely paralleled their potency, with N‐Methylaspartate1 Ang II, Gly1 Ang II,, Sarcosine0, Sarcosine1 Ang II,, and Ang II being most potent at causing desensitization (EC50 values ~ 1 nM). D‐Arginine1 Ang III, D‐Alanine1 Ang II, D‐Aspartate1 Ang II L‐beta Aspartate1 Ang II had lower potencies to cause desensitization, ~ 3 to 20 fold less potent. Interestingly two of the Ile8 substituted Ang peptides; D‐Alanine1, Ile8 Ang II and D‐beta Aspartate1, Ile8 Ang II displayed abilities to desensitize the response to Ang II with 24 and 47 nM potencies. Since the CellKey system measures an integrated cellular response resulting from both G protein as well as beta‐arrestin signaling, these data are consistent with possible differential agonism of these Ang peptide analogs. These data are consistent with previously noted biased agonistic effects of Ile8 containing analogs of Ang II. Since the most well characterized biased agonist for Ang II receptors, Sarcosine1, Ile4, Ile8 Ang II has a micromolar EC50, D‐Alanine1, Ile8 Ang II and D‐beta Aspartate1, Ile8 Ang II might represent more efficacious beta arrestin biased agonists.Support or Funding InformationR.C. Speth: NIH HL‐113905; Cardiovascular Neuroscience Research Fund, Nova Southeastern University; President's Faculty Research Development Grant, Nova Southeastern University.