bluuebunny/crossref_metadata_2025_split huggingface dataset:
VO2max Can Be Accurately Predicted in American Football Athletes from Treadmill Exercise Time
Authors: Crouse Stephen F. , Tolson Homer , Martin Steven E. , Green John S. , Bramhall J P. , Hedrick Phil , Lytle Jason R. 
Published: June 2021

IntroductionPrediction models for estimating maximal oxygen uptake (VO2max) from treadmill exercise time are lacking for American‐style football (ASF) athletes. Models developed from non‐athletes have not been tested in ASF players.PurposeWe proposed to develop a model to estimate VO2max from exercise treadmill time in ASF athletes, and compare our Football model against the Foster (AHJ, 1984) and Bruce (AHJ, 1973) prediction equations.MethodsBetween 2003 and 2017, 472 collegiate ASF athletes (age 18 ± 1 yr, height = 186.1 ± 8.2 cm, weight 101.8 ± 20.4 kg) underwent treadmill exercise to maximal voluntary exhaustion (Bruce protocol) with VO2 measured (M‐VO2max) by means of an automated metabolic gas analysis system. Treadmill exercise time in minutes (T), as used in the Foster and Bruce equations, was used to predict M‐VO2max. For cross‐validation purposes, the 472 participants were randomly divided into Validation and Cross‐validation groups, n=236 for each group, using a random number generator. Linear regression was used to identify the predictive power (r2) in both groups. Independent t‐tests (with a Bonferroni adjusted α) and repeated measures ANOVA were used to test for differences between the two groups, and for differences among M‐VO2max, Foster, Bruce, and our Football estimates of VO2max. An α = 0.05 was used for all statistical tests.ResultsThe Validation and Cross‐validation groups were not statistically different on any variable measured (p range = 0.454 to 0.941). Equations to estimate VO2max (mlO2.kg−1.min−1) were: Validation group VO2max = 4.012 * T −4.628 (r2 = .678, .001, SEE=4.07); Cross‐validation group VO2max = 4.025 * T – 4.693 (r2 = .661, .001, SEE‐4.16). These equations had a cross‐validation coefficient = 0.813 and a double cross‐validation coefficient = 0.823. Since no measured variables were different between the two validation groups, all athletes were combined to yield our final prediction equation: Football VO2max = 4.017 * T – 4.644 (r2 = 0.670, .001, SEE = 4.11). Estimated Football VO2max was not different from M‐VO2max (mean difference −0.002, p = 0.989). Foster and Bruce VO2max estimates were significantly different from M‐VO2max (mean difference −0.975, p = 0.001 and 1.995, p = 0.001, respectively) and from Football VO2max (p = 0.001).ConclusionVO2max of collegiate ASF athletes can be accurately estimated by our Football prediction equation using maximal treadmill exercise time as the predictor variable.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Assessment of Activity Monitor Placement During Free‐Living Conditions
Authors: Molesky Monroe J. , Vusich John , Montoye Alexander HK. 
Published: June 2021

Despite the popularity of consumer‐based physical activity monitors (AMs), many of these AMs have little data examining their comparability when worn on different body locations.PURPOSEOur study's purpose was to determine placement‐related differences of a popularly available AM for estimating steps, Calories (kcals), distance traveled, active minutes, and sleep time in a free‐living setting.METHODSParticipants (n=48) aged 18–28 years completed an unstructured, free‐living protocol in which participants wore two identical AMs (the Fitbit Flex or Fitbit Flex2), one on the non‐dominant (ND) wrist and one on the dominant (D) wrist, for five days. Participants were given the AMs early Monday morning and then instructed to return them Friday afternoon. Participants were instructed to wear the AMs 24 hours per day during all of their regular daily activities excluding contact sports and water‐based activities. Data were averaged across the three full days (Tuesday‐Thursday) and compared between wrists using paired t‐tests for each of the five recorded variables (steps, kcals, distance traveled, active minutes, and sleep time). Additionally, mean absolute difference (MAD) and mean absolute percent difference (MAPD) were calculated to assess differences between wrists.RESULTSThe AMs had varied results in recording steps, kcals, distance traveled, active minutes, and sleep time in the comparison of the ND and D wrist locations. For all variables, estimates from the ND wrist were higher than the D wrist. AM step differences were significantly different with MAD of 664.7 steps/day (MAPD of 6.7%; p<0.001), kcals had an MAD of 53.4 kcals/day (MAPD of 2.1%; p<0.001), distance had MAD of 0.3 miles/day (MAPD of 6.8%; p<0.001), and active minutes had an MAD of 7.3 minutes/day (MAPD of 36.5%; p<0.001). Participant sleep duration trended toward statistical significance (p=0.22) with an MAD of 23.8 minutes/day (MAPD of 5.9%) between wrists.CONCLUSIONData collected from AMs placed on the ND and D wrists were not equivalent. While differences for some variables were relatively small, others were substantial. Caution is warranted when wearing AMs on different wrists despite the seemingly all purpose and multi‐locational nature of AMs. Future research should investigate other AM placements and optimum conditions for use.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Skeletal myofiber VEGF‐A‐targeted gene deletion induces mitochondrial, structural and contractile alterations in mouse diaphragm
Authors: Cannon Daniel T. , Rodewohl Lukas , Adams Volker , Breen Ellen C. , Bowen T Scott 
Published: June 2021

Respiratory muscle weakness is a hallmark of COPD, heart failure, and critical illness. Vascular endothelial growth factor (VEGF) may be an important therapeutic target in chronic cardiopulmonary disease as it is essential for neovascularization and vessel repair following trauma. We hypothesized that respiratory muscle, which is required to persistently function, would exhibit impaired mitochondrial, structural, and contractile function in skeletal myofiber VEGF gene deleted mice.We measured diaphragm biochemistry, structure, and contractile function in adult mice with conditional deletion of the VEGF‐A gene in skeletal myofibers (SkmVEGF−/−). Male SkmVEGF−/− mice (n=12) were compared to wild type (WT) controls (n=13) – both on a C57BL/6J background. Fiber bundles were isolated and electrically stimulated in vitro to evaluate force‐frequency and fatigue profiles. Mitochondrial O2 consumption and H2O2 flux (index of mitochondrial ROS) were simultaneously measured in saponin‐permeabilized fiber bundles (Oroboros, Innsbruck, AT). Fiber structure and biochemistry were measured using standard techniques (IHC, Western, ELISA).Diaphragm VEGF protein was lower in SkmVEGF−/− than WT mice (1.5±0.2 vs. 3.0±0.4 pg/total protein, p<0.05). Compared to WT mice, the force‐frequency relationship was depressed in SkmVEGF−/− (F[7,161]=15.0, p<0.05), with maximal specific force reduced by ~10 % (24±1 vs. 21±1 N/cm2; p<0.05). However, fatigue resistance tended to be greater following SkmVEGF−/− (F[2,115]=3.3, p=0.06). Fiber type proportions were unchanged, but type I fiber cross‐sectional area was reduced in SkmVEGF−/− (653±45 vs 493±53 μm2; p<0.05). Compared to WT, sarcomeric actin protein expression was reduced by ~30% in SkmVEGF−/− (p<0.05) while myosin heavy chain, MAFbx, MuRF1, PGC1α, and HIF1α protein remained unchanged (p>0.05). Mitochondrial respiration was not different between SkmVEGF−/− and WT (F[1,80]=0.9, p>0.05) in each of the respiratory states. However, H2O2 flux was reduced in SkmVEGF−/− (F[1,75]=14.6, p<0.05).Skeletal myofiber‐specific VEGF deletion contributed to diaphragm weakness, but tended to improve fatigue resistance in this highly oxidative muscle. Reductions in oxidative fiber size, sarcomeric actin protein content, and ROS generation following VEGF gene deletion may contribute to protecting mitochondrial respiratory function in the diaphragm. The adaptations may be part of compensatory mechanisms mitigating larger deficits in force generation and fatigue resistance.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
O‐GlcNAc Transferase is Required to Maintain Satellite Cell Viability
Authors: Daughtry Morgan , Geisler Hannah , Fisher Taylor , Luo Jing , Shi Hao , Gerrard David 
Published: June 2021

O‐GlcNAcylation is the addition and removal of UDP‐GlcNAc to proteins by O‐GlcNAc transferase (OGT) and O‐GlcNAcase (OGA), respectively. This process functions as a nutrient sensing pathway because UDP‐GlcNAc, synthesized in the hexosamine biosynthetic pathway, fluctuates with nutrient levels available to the cell. Although previous studies have established the critical role of OGT in metabolism in a variety of cell types, the role of OGT in satellite cells (SCs) remains unknown. In this study, we generated SC‐specific OGT knock‐out (cKO) mice to investigate the functional role of OGT in SC homeostasis. Initially we subjected WT and cKO muscle to cardiotoxin‐induced injury to assess SC regenerative capacity during muscle regeneration. Compared to WT mice, the cKO mice experienced severely impaired regenerative myogenesis. To investigate whether OGT deficiency induced lack of regeneration was caused by changes in SC intrinsic properties, we traced SCs cycling and self‐renewal in vivo by monitoring the turnover rate of green fluorescent protein (GFP) intensity using a H2B‐GFP lineage tracing strategy. Flow cytometry analysis of the GFP labeling revealed that cKO SCs possessed a higher percentage of GFP‐retained subpopulation than WT SCs after a 10‐week chase period, indicating that SCs lacking OGT had impaired self‐renewal. We then assessed SC proliferative capacity in vitro using clone assay and observed SCs from cKO mice had significantly reduced clone size compared to their WT counterparts. Morphologically, cKO SCs exhibited larger cell size and increased complexity compared to WT SCs, suggesting the lack of proliferation may be caused by the impairment of SC's ability to divide. Taken together, our findings suggest that OGT, and thus O‐GlcNAc signaling, plays a critical role in SC self‐renewal, proliferation, and tissue repair through mediating nutrient sensitive cell division.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
AMP Deaminase 3 Knockout Does Not Reduce Mitochondrial Content Loss in Denervation Induced Inactivity
Authors: Verhoeven Nicolas A. , Brault Jeffrey J. 
Published: June 2021

Muscle atrophy leads to decrements in muscle function, partly attributable to reductions in mitochondrial content. One controller of mitochondrial content is AMP‐activated protein kinase (AMPK), which when bound by AMP stimulates PGC‐1α leading to mitochondrial biogenesis, keeping mitochondrial content elevated. AMP Deaminase 1 is the dominant isoform of AMPD in skeletal muscle, yet AMP Deaminase 3 (AMPD3) is robustly upregulated during atrophy conditions in skeletal muscle, and degrades AMP (AMP à IMP + NH3). The purpose of this study is to determine if loss of AMPD3 gene will reduce mitochondrial content loss typically seen with atrophy.MethodsWhole body AMPD3 knock out mice on a C57BL6 strain background were surgically denervated on the left hind limb by removal of ~2 mm of the sciatic nerve. A sham surgery was performed on the right hind limb. Two weeks later, mice were weighed, and extensor digitorum longus (EDL) muscles were collected, weighed, and analyzed for citrate synthase enzyme activity as a measure of mitochondrial content. ANOVA analyses were made between three genotypes (Wild Type ‐ WT, AMPD3 heterozygous ‐ HET, and AMPD3 knockout ‐ KO) of 12 week old littermate female mice (n = 5–8).ResultsBody weights were not significantly different among genotypes (22.9 ± 0.7 g WT, 22.3 ± 0.4 HET, 22.0 ± 1.0 KO)(p = .74). Likewise, non‐denervated EDL muscle weights were not significantly different among genotypes (8.75 ± 0.2 mg WT, 8.47 ± 0.2 HET, 8.77 ± 0.3 KO)(p = 0.67). As expected, surgical denervation for two weeks led to substantial muscle atrophy versus innervated muscle (22.07 ± 1.42% WT, 23.69 ± 4.84 HET, 19.2 ± 3.67 KO), which was not different among genotypes (p = 0.68). Finally, citrate synthase activity in innervated EDL was not significantly different among genotypes (10.27 ± 0.36 WT, 9.3 ± 0.77 HET, 8.93 ± 0.38 KO)(p = 0.16). The decrease in citrate synthase activity due to denervation was not significantly different between wild type and heterozygous, but there was a trend for heterozygous group to have less activity (20.32 ± 2.02% WT, 4.38 ± 5.83 HET)(p = 0.059).ConclusionThese data suggest AMPD3 does not affect mitochondrial content loss in this atrophy model. However, since AMPD3 was not present during development in our AMPD3 knockout mice, we cannot exclude compensation from other AMPD isoforms. Therefore, future research should investigate either inducible muscle specific AMPD3 knockouts or loss of both AMPD1 and AMPD3.Support or Funding InformationNIH R01 AR 070200This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Heat Stroke Triggers Electrocardiographic (ECG) Abnormalities in a Conscious Rat Model
Authors: Mayer Thomas Andrew , Leon Lisa 
Published: June 2021

Heat stroke (HS) is a potentially fatal injury that affects thousands of individuals every year. Multiple organs, including the heart, may be damaged as a result of HS. We showed previously that HS rats exhibit tachycardia, elevated cardiac Troponin I, and histological cardiac damage. Several observational studies and numerous case reports have described electrocardiogram (ECG) abnormalities among human HS patients, but these abnormalities have not been thoroughly investigated in animal HS models. This study identified the type of ECG abnormalities elicited in HS rats. Adult male Fisher 344 rats weighing 278.1±3.9 grams were previously implanted with radiotelemetry for continuous recording of core temperature (Tc), heart rate (HR), blood pressure, and Lead II ECG. After surgical recovery, rats were passively heated at an ambient temperature of 39°C until Tc reached 42.0±0.1°C (TcMax). Injury severity was classified as mild, moderate, or severe based on Tc responses during 24‐h of recovery. Baseline ECG recordings prior to heat exposure were normal. Severe and moderate rats had higher HR than mild rats at TcMax (mild 567±5; moderate 608±4; severe 611±15 bpm; p<0.05). Amplitude of the R wave during 1‐h of recovery was less for severe than mild and moderate rats (mild 1.58±0.12; moderate 1.60±0.10; severe 1.20±0.11 mV; p<0.05). ST depression was frequently observed prior to and shortly after TcMax and worsened with increasing injury severity. ST elevation was noted in two severe rats. ECG recordings taken the day after HS demonstrated an absence of T waves among severe rats and some moderate rats. These results demonstrate that ECG abnormalities occur as HS injury progresses and persist throughout acute recovery, which may be indicative of damage or dysfunction of the heart. Importantly, two rats died within 24‐h of HS recovery; one had extensive morphological ECG alterations whereas the other had a normal ECG, suggesting that cardiovascular dysfunction does not solely determine mortality but may contribute. In conclusion, ECG recordings should be monitored after HS for assessment of injury severity and potential cardiovascular dysfunction. Author views are 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.
Blocking Peripheral Beta‐Adrenergic Receptors Reduces Induction of Skeletal Muscle Thermogenesis
Authors: Gorrell Erin , Mull Sarah , Novak Colleen 
Published: June 2021

Obesity is a worldwide trend that is cause for concern due to its detrimental effects on numerous health factors and increased risk of mortality. The propensity for obesity, although influenced by diet, is also worsened by sedentary lifestyle. Indeed, individuals' daily activity levels and activity energy expenditure predict weight gain and obesity. Increased energy expenditure, whether deliberate or spontaneous, is associated with leanness and reduced risk for obesity. With respect to increasing energy expenditure through thermogenesis, previous investigation has focused largely on browning of white adipose and brown adipose tissue thermogenesis, with much less attention paid to mechanisms mediating thermogenesis in skeletal muscle. Here, we investigated the effects of contextually induced muscle thermogenesis in rats through exposure to predator odor in rats. We hypothesize that thermogenesis in skeletal muscle is mediated by the sympathetic nervous system (SNS), specifically through activation of muscle β‐adrenergic receptors. To test this, we examined the effects of nadolol, a peripherally acting β‐adrenergic antagonist, on predator odor‐induced thermogenesis. IPTT‐300 transponders from Bio Medic Data Systems were surgically implanted in the left and right gastrocnemius muscles of male rats (N=13). Rats were exposed to each of four conditions (2×2): nadolol or saline vehicle, each with and without predator odor (1.5″×2″ towel with ferret odor) or control stimulus; muscle temperatures were measured over 120 minutes. Predator odor significantly induced muscle thermogenesis in vehicle‐treated animals. The mixed β‐adrenergic antagonist nadolol significantly reduced predator odor‐induced thermogenesis. This demonstrates that predator odor‐induced skeletal muscle thermogenesis is mediated, at least in part, by β‐adrenergic receptor activation, likely stemming from sympathetic nerve activation. Our previous work has demonstrated that this thermogenic induction is accompanied by enhanced energy expenditure. With the focus on muscle, rather than adipose thermogenesis, we establish a pathway that expands the understanding of energy balance, its mechanisms, and possible treatments. Going forward, induction of muscle thermogenesis may be applied to the treatment of obesity.Support or Funding InformationNIH NIDDK R15‐DK‐097644 and R15‐DK‐108668 to CMNThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Kappa opioid receptor activation in the Preoptic Area (POA) contributes to the impairment of brown adipose tissue activation in rats on a high fat diet (HFD)
Authors: Madden Christopher J. 
Published: June 2021

We have recently demonstrated that cold‐evoked activation of brown adipose tissue is inhibited in rats maintained on a high fat diet for at least eight weeks. Activation of neurons in the external lateral parabrachial nucleus is a necessary relay in the afferent pathway for cold‐evoked increases in BAT thermogenesis and BAT sympathetic nerve activity. In order to assess whether there was an impaired activation of the cold afferent pathway, the present study examined the expression of the immediate early gene, fos, in the external lateral parabrachial nucleus of cold exposed rats maintained on either a control diet or a HFD. Contrary to the hypothesis, there was no difference in HFD rats compared to control diet rats, in the number of neurons in the external lateral parabrachial nucleus which expressed fos in response to cold‐exposure. However, there was an increase in the number of neurons expressing fos in the dorsal lateral parabrachial nucleus (LPBd) of HFD rats compared to control diet rats. This is interesting since the LPBd is an area that has been shown to inhibit cold‐evoked activation of BAT SNA. Furthermore, many of the dorsal lateral parabrachial neurons that were activated in the HFD rats during cold exposure contained preprodynorphin. Preprodynorphin cells in the LPBd project to the preoptic area and can produce the kappa opioid receptor agonist dynorphin. These observations led to my hypothesis that activation of kappa opioid receptor (KOR) in the POA contributes to the inhibition of BAT thermogenesis during HFD. Therefore, the present study tested the hypothesis that selective blockade of KOR, in the POA would reverse the impairment of cooling‐evoked BAT SNA in HFD rats, but fail to increase BAT SNA in control diet rats. Nanoinjection of the KOR antagonist, norBNI, in the POA reversed the HFD‐induced impairment of cold evoked BAT SNA and thermogenesis. In contrast, injection of norBNI in rats on a control diet did not increase BAT SNA or BAT thermogenesis. These data suggest that there is an aberrant activation of a dynorphin input from the LPBd to the POA in rats on a high fat diet. Activation of this pathway in HFD‐induced obesity may help to explain the weight reducing effects of KOR antagonists such as naltrexone.Support or Funding Information1 R01 DK112198‐01A1This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
High Mobility Group Box 1 Neutralization in the Brain Prevents Inflammation, Sympathoexcitation and Hypertension
Authors: Sriramula Srinivas , Nair Anand R. , Francis Joseph 
Published: June 2021

High mobility group box 1 (HMGB1) is a nuclear protein, that once translocated to cytoplasm, can act as a chemoattractant and a proinflammatory mediator. Post‐translationally modified HMGB1 can interact with different receptors, such as toll‐like receptor 4 (TLR4) and chemokine receptor CXC receptor 4 (CXCR4), to induce acute and chronic inflammation. We have previously showed that central TLR4 blockade delayed progression of hypertension and improved cardiac function. However, the involvement of HMGB1 and its interaction with TLR4 in the pathogenesis of hypertension has not been fully explored. Therefore, in this study, we investigated the role of HMGB1 in mediating hypertension, inflammation and sympathoexcitation. We hypothesized that blockade of HMGB1 prevents the development of hypertension. Chronic angiotensin II (AngII) infusion (200 ng/kg/min, SC, 14 days) significantly increased mean arterial pressure (telemetry) in male Sprague‐Dawley rats compared to saline‐infused controls (163 ±5 vs. 105 ±4 mmHg, n=7, p<0.01). AngII‐infusion significantly increased HMGB1 levels in the plasma (21 ±3 vs.15 ±2 ng/ml, p<0.01) and cerebrospinal fluid (34±3 vs. 21±1 ng/ml, p<0.01), and elevated HMGB1 protein expression (2.5 fold, n=6, p<0.01 vs. Control) in the brain hypothalamic paraventricular nucleus (PVN). Intracerebroventricular infusion of neutralizing monoclonal anti‐HMGB1 antibody (10 μg/kg/day) attenuated AngII‐induced hypertension (120 ±2 mmHg, p<0.01 vs. AngII). Furthermore, AngII‐infusion significantly increased expression of TNF, IL‐1, IL‐6, TLR4, CXCR4, and NF‐kB in the PVN, which was prevented by HMGB1 neutralization. AngII infusion resulted in sympathoexcitation, as indicated by increased plasma norepinephrine levels (1602 ±53 vs. 549 ±25 pg/ml, P<0.01 vs. Control), but this increase was blunted by HMGB1 neutralization (720 ±25 pg/ml, P<0.05 vs. AngII). Taken together, these data suggest that neutralization of HMGB1 in the brain reduces inflammation and decreases sympathoexcitation, thereby preventing the development of AngII‐induced hypertension.Support or Funding InformationThe American Heart Association, 15SDG25720021 (SS), 16GRNT30510012 (JF)This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.