Relevant bibliographies by topics / Lactate output

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  2. Dissertations / Theses
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Academic literature on the topic 'Lactate output'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Lactate output"

1

Nielsen, H. B., M. A. Febbraio, P. Ott, P. Krustrup, and N. H. Secher. "Hepatic lactate uptake versus leg lactate output during exercise in humans." Journal of Applied Physiology 103, no. 4 (2007): 1227–33. http://dx.doi.org/10.1152/japplphysiol.00027.2007.

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The exponential rise in blood lactate with exercise intensity may be influenced by hepatic lactate uptake. We compared muscle-derived lactate to the hepatic elimination during 2 h prolonged cycling (62 ± 4% of maximal O2 uptake, V̇o2max) followed by incremental exercise in seven healthy men. Hepatic blood flow was assessed by indocyanine green dye elimination and leg blood flow by thermodilution. During prolonged exercise, the hepatic glucose output was lower than the leg glucose uptake (3.8 ± 0.5 vs. 6.5 ± 0.6 mmol/min; mean ± SE) and at an arterial lactate of 2.0 ± 0.2 mM, the leg lactate ou
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Morris, David Michael, and Rebecca Susan Shafer. "Comparison of Power Outputs During Time Trialing and Power Outputs Eliciting Metabolic Variables in Cycle Ergometry." International Journal of Sport Nutrition and Exercise Metabolism 20, no. 2 (2010): 115–21. http://dx.doi.org/10.1123/ijsnem.20.2.115.

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The authors sought to compare power output at blood lactate threshold, maximal lactate steady state, and pH threshold with the average power output during a simulated 20-km time trial assessed during cycle ergometry. Participants (N = 13) were trained male and female cyclists and triathletes, all permanent residents at moderate altitude (1,525–2,225 m). Testing was performed at 1,525 or 1,860 m altitude. Power outputs were determined during a simulated 20-km time trial (PTT), at blood pH threshold (PpHT), at maximal lactate steady state (PMLSS), and at blood lactate threshold determined by 2 m
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Mo, F. M., and H. J. Ballard. "Intracellular lactate controls adenosine output from dog gracilis muscle during moderate systemic hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 1 (1997): H318—H324. http://dx.doi.org/10.1152/ajpheart.1997.272.1.h318.

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The influence of systemic hypoxia on lactate and adenosine output from isolated constant-flow-perfused gracilis muscle was determined in anesthetized dogs. The lactate transport inhibitor alpha-cyano-4-hydroxycinnamic acid (CHCA) was employed to distinguish the direct effects of hypoxia on adenosine output from the effects produced indirectly by a change in lactate concentration. Reduction of arterial PO2 from 135 +/- 4 to 39 +/- 2 mmHg raised arterial lactate from 1.26 +/- 0.32 to 2.22 +/- 0.45 mM but decreased venoarterial lactate difference from 0.53 +/- 0.09 to -0.13 +/- 0.19 mM, indicatin
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Burton, Michael T., and Joseph M. Santin. "A direct excitatory action of lactate ions in the central respiratory network of bullfrogs, Lithobates catesbeianus." Journal of Experimental Biology 223, no. 24 (2020): jeb235705. http://dx.doi.org/10.1242/jeb.235705.

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ABSTRACTChemoreceptors that detect O2 and CO2/pH regulate ventilation. However, recent work shows that lactate ions activate arterial chemoreceptors independent of pH to stimulate breathing. Although lactate rises in the central nervous system (CNS) during metabolic challenges, the ability of lactate ions to enhance ventilation by directly targeting the central respiratory network remains unclear. To address this possibility, we isolated the amphibian brainstem–spinal cord and found that small increases in CNS lactate stimulate motor output that causes breathing. In addition, lactate potentiat
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Wasserman, D. H., J. L. Johnson, J. L. Bupp, D. B. Lacy, and D. P. Bracy. "Regulation of gluconeogenesis during rest and exercise in the depancreatized dog." American Journal of Physiology-Endocrinology and Metabolism 265, no. 1 (1993): E51—E60. http://dx.doi.org/10.1152/ajpendo.1993.265.1.e51.

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To assess the mechanism of the accelerated gluconeogenesis in the insulin-deficient state, chronically catheterized (carotid artery, portal vein, hepatic vein, vena cava) normal (C; n = 9) and depancreatized (PX; n = 7) dogs were studied during rest (40 min) and moderate exercise (150 min). Tracers ([14C]alanine, [3H]glucose) and dye were infused to measure determinants of gluconeogenesis in the gut and liver. Arterial levels, net gut output, hepatic load, and net hepatic uptake of alanine were similar in C and PX at rest. During exercise, alanine levels fell in C but rose approximately 100% i
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Weber, J. M., W. S. Parkhouse, G. P. Dobson, J. C. Harman, D. H. Snow, and P. W. Hochachka. "Lactate kinetics in exercising Thoroughbred horses: regulation of turnover rate in plasma." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 6 (1987): R896—R903. http://dx.doi.org/10.1152/ajpregu.1987.253.6.r896.

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Plasma lactate turnover rate of Thoroughbred racehorses was measured by bolus injection of [U-14C]lactate at rest and two levels of submaximal treadmill exercise (3-4 m/s trot, 6% incline, and 6.5 m/s horizontal canter). Our goals were 1) to determine the relative effects of changes in cardiac output and in plasma lactate concentration on turnover rate [using cardiac output data from Weber et al. (28)] and 2) to assess the importance of lactate as a metabolic fuel in a trained animal athlete. Lactate turnover rates were 9.3 mumol.min-1.kg-1 (rest), 75.9 mumol.min-1.kg-1 at the beginning of the
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Yang, Woo-Hwi, Hyuntae Park, Marijke Grau, and Oliver Heine. "Decreased Blood Glucose and Lactate: Is a Useful Indicator of Recovery Ability in Athletes?" International Journal of Environmental Research and Public Health 17, no. 15 (2020): 5470. http://dx.doi.org/10.3390/ijerph17155470.

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During low-intensity exercise stages of the lactate threshold test, blood lactate concentrations gradually diminish due to the predominant utilization of total fat oxidation. However, it is unclear why blood glucose is also reduced in well-trained athletes who also exhibit decreased lactate concentrations. This review focuses on decreased glucose and lactate concentrations at low-exercise intensity performed in well-trained athletes. During low-intensity exercise, the accrued resting lactate may predominantly be transported via blood from the muscle cell to the liver/kidney. Accordingly, there
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Clow, Angela, Vivette Glover, M. W. Weg, et al. "Urinary Catecholamine Metabolite and Tribulin Output During Lactate Infusion." British Journal of Psychiatry 152, no. 1 (1988): 122–26. http://dx.doi.org/10.1192/bjp.152.1.122.

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Urinary output of homovanillic acid and 4-hydroxy-3-methoxymandelic acid was decreased both in patients with panic attacks and in normal controls during lactate infusion, whereas that of tribulin (an endogenous monoamine oxidase inhibitor and benzodiazepine receptor binding inhibitor) was increased. There was no change in urinary excretion of any of these compounds during saline infusion. These findings provide further evidence of a link between tribulin output and stress and anxiety in man and point to its possible in vivo action as a monoamine oxidase inhibitor.
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Owen, Valerie M. "Japan — Regulation of output current of L-lactate sensors." Biosensors and Bioelectronics 10, no. 9-10 (1995): v. http://dx.doi.org/10.1016/0956-5663(95)99234-c.

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Perret, Claudio, and Kathrin Hartmann. "Heart Rate-based Lactate Minimum Test in Running and Cycling." International Journal of Sports Medicine 42, no. 09 (2021): 812–17. http://dx.doi.org/10.1055/a-1342-7744.

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AbstractThe heart rate-based lactate minimum test is a highly reproducible exercise test. However, the relation between lactate minimum determined by this test and maximal lactate steady state in running and cycling is still unclear. Twelve endurance-trained men performed this test in running and cycling. Exercise intensity at maximal lactate steady state was determined by performing several constant heart rate endurance tests for both exercise modes. Heart rate, power output, lactate concentration, oxygen uptake and rating of perceived exertion at lactate minimum, maximal lactate steady state
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Dissertations / Theses on the topic "Lactate output"

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Mancini, Wendy F. "Power output and lactate concentration following repeated 10 s intervals using varying recovery patterns." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61140.

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Blood lactate concentration and mean power output were examined over a series of maximal intermittent exercise bouts with varying recovery patterns. Thirteen elite male cyclists completed four randomly assigned experimental conditions. Each exercise/recovery condition consisted of twelve 10 s maximal exercise bouts on a Monark cycle ergometer. Four different recovery patterns (30, 60, 90 and 120 s) followed the repeated 10 s all-out efforts. Results revealed that the mean power output averaged over the 12 trials was 12.7, 13.0, 13.2 and 13.4 W/kg, for the 30, 60, 90 and 120 s conditions, respe
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Bentley, David J. "Measurement of peak power output and the lactate threshold : significance for endurance cycling performance." Thesis, University of Bath, 2002. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250852.

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Nielsen, Corey Michael. "The Effect of Normobaric Hypoxia on Power Output During Multiple Wingate Anaerobic Tests." Kent State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=kent1490258656616795.

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Püschel, Gerhard P., Ursula Hespeling, Martin Oppermann, and Peter Dieter. "Increase in prostanoid formation in rat liver macrophages (Kupffer cells) by human anaphylatoxin C3a." Universität Potsdam, 1993. http://opus.kobv.de/ubp/volltexte/2008/1671/.

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Human anaphylatoxin C3a increases glycogenolysis in perfused rat liver. This action is inhibited by prostanoid synthesis inhibitors and prostanoid antagonists. Because prostanoids but not anaphylatoxin C3a can increase glycogenolysis in hepatocytes, it has been proposed that prostanoid formation in nonparenchymal cells represents an important step in the C3a-dependent increase in hepatic glycogenolysis. This study shows that (a) human anaphylatoxin C3a (0.1 to 10 mug/ml) dose-dependently increased prostaglandin D2, thromboxane B, and prostaglandin F2alpha formation in rat liver macrophages (Ku
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Püschel, Gerhard P., Martin Oppermann, Waldemar Muschol, Otto Götze, and Kurt Jungermann. "Increase of glucose and lactate output and decrease of flow by human anaphylatoxin C3a but not C5a in perfused rat liver." Universität Potsdam, 1989. http://opus.kobv.de/ubp/volltexte/2008/1673/.

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The complement fragments C3a and C5a were purified from zymosan-activated human serum by column chromatographic procedures after the bulk of the proteins had been removed by acidic polyethylene glycol precipitation. In the isolated in situ perfused rat liver C3a increased glucose and lactate output and reduced flow. Its effects were enhanced in the presence of the carboxypeptidase inhibitor DL-mercaptomethyl-3-guanidinoethylthio-propanoic acid (MERGETPA) and abolished by preincubation of the anaphylatoxin with carboxypeptidase B or with Fab fragments of an anti-C3a monoclonal antibody. The C3a
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Muschol, Waldemar, Gerhard Püschel, Martina Hülsmann, and Kurt Jungermann. "Eicosanoid-mediated increase in glucose and lactate output as well as decrease and redistribution of flow by complement-activated rat serum in perfused rat liver." Universität Potsdam, 1991. http://opus.kobv.de/ubp/volltexte/2010/4589/.

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Rat serum, in which the complement sytem had been activated by incubation with zymosan, increased the glucose and lactate output, and reduced and redistributed the flow in isolated perfused rat liver clearly more than the control serum. Heat inactivation of the rat serum prior to zymosan incubation abolished this difference. Metabolic and hemodynamic alterations caused by the activated serum were dose dependent. They were almost completely inhibited by the cyclooxygenase inhibitor indomethacin and by the thromboxane antagonist 4-[2-(4-chlorobenzenesulfonamide)-ethyl]-benzene-acetica cid (BM 13
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Carlsson, Magnus. "Physiological demands of competitive elite cross-country skiing." Doctoral thesis, Högskolan Dalarna, Idrotts- och hälsovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-102878.

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Introduction Researchers have, for decades, contributed to an increased collective understanding of the physiological demands in cross-country skiing; however, almost all of these studies have used either non-elite subjects and/or performances that emulate cross-country skiing. To establish the physiological demands of cross-country skiing, it is important to relate the investigated physiological variables to the competitive performance of elite skiers. The overall aim of this doctoral thesis was, therefore, to investigate the external validity of physiological test variables to determine the
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Carlsson, Tomas. "The importance of body-mass exponent optimization for evaluation of performance capability in cross-country skiing." Doctoral thesis, Högskolan Dalarna, Idrotts- och hälsovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-102872.

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Introduction Performance in cross-country skiing is influenced by the skier’s ability to continuously produce propelling forces and force magnitude in relation to the net external forces. A surrogate indicator of the “power supply” in cross-country skiing would be a physiological variable that reflects an important performance-related capability, whereas the body mass itself is an indicator of the “power demand” experienced by the skier. To adequately evaluate an elite skier’s performance capability, it is essential to establish the optimal ratio between the physiological variable and body mas
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Manselin, Tom, and Olof Södergård. "Six weeks of high intensity interval training with hyperoxia or normoxia in trained cyclists : A polarized and periodized training approach." Thesis, Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:gih:diva-4262.

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Aim The main aim of this study was to investigate the longitudinal effects on cycling performance using a polarized and periodized scheme that was highly supervised and controlled. The second aim was to investigate the effect of using Hyperoxia. The questions used to address the aim were: (1) How does overall performance change after a six-week training intervention? (2) What is the time-course and pattern of performance changes to the training scheme? (3) How does the performance change within the groups?   Method Nineteen male and female cyclists started the study (13 male and 6 female), how
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Books on the topic "Lactate output"

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Buchanan, Mark Kevin. The effects of pedal frequency on VO₂ and work output: At lactate threshold (LT), fixed blood lactate concentrations of 2 and 4 mM and at max in competitive cyclists. 1985.

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The effects of pedal frequency on VO₂ and work output at lactate threshold (LT), fixed blood lactate concentrations of 2 and 4 mM and at max in competitive cyclists. 1985.

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The effects of pedal frequency on VOb2s and work output: At lactate threshold (LT), fixed blood lactate concentrations of 2 and 4 mM and at max in competitive cyclists. 1985.

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4

Jakob, Stephan M., and Jukka Takala. Oxygen transport in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0137.

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Adequate oxygen delivery is crucial for organ survival. The main determinants of oxygen delivery are cardiac output, haemoglobin concentration, and arterial oxygen saturation. The adequacy of oxygen delivery also depends on oxygen consumption, which may vary widely. Mixed venous oxygen saturation reflects the amount of oxygen not extracted by the tissues, and therefore provides useful information on the relationship between oxygen delivery and oxygen needs. If not in balance, tissue hypoxia may ensue and arterial lactate concentration increases. This occurs at higher oxygen delivery rates in a
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Kipnis, Eric, and Benoit Vallet. Tissue perfusion monitoring in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0138.

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Resuscitation endpoints have shifted away from restoring normal values of routinely assessed haemodynamic parameters (central venous pressure, mean arterial pressure, cardiac output) towards optimizing parameters that reflect adequate tissue perfusion. Tissue perfusion-based endpoints have changed outcomes, particularly in sepsis. Tissue perfusion can be explored by monitoring the end result of perfusion, namely tissue oxygenation, metabolic markers, and tissue blood flow. Tissue oxygenation can be directly monitored locally through invasive electrodes or non-invasively using light absorbance
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Book chapters on the topic "Lactate output"

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Donker, A. J. M., P. M. ter Wee, J. J. Weening, and J. M. Wilmink. "Vitamine B1 deficiëntie kan leiden tot een lactaat-acidose en een ‘high output failure’." In Nierziekten en milieu intérieur – een werkboek. Bohn Stafleu van Loghum, 1996. http://dx.doi.org/10.1007/978-90-313-6387-2_53.

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Waldmann, Carl, Andrew Rhodes, Neil Soni, and Jonathan Handy. "Tissue perfusion monitoring." In Oxford Desk Reference: Critical Care. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198723561.003.0008.

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Over the past few years, the haemodynamic management of critically ill patients is moving from the stabilization of microcirculatory parameters (such as arterial pressure, heart rate, or cardiac output) to resaturation and maintenance of tissue perfusion parameters. This change of paradigm is necessary as we now know that normalization of microcirculatory parameters does not necessarily mean normal tissue perfusion. For that reason, in this edition we include a chapter dedicated to tissue perfusion monitoring. This includes discussion on mixed venous oxygen saturation (including physiology, equivalence of mixed venous oxygen saturation and central venous oxygen saturation, interpretation, and use as a therapeutic or prognostic target), pCO<sub>2</sub> arterial-venous gap (physiology, interpretation, and use as therapeutic target), lactate concentration (metabolism of glucose to lactate, lactate and shock, parameters of tissue hypoperfusion and tissue hypoxia, persistent hyperlactataemia, and practical approach), and the videoscopy of microcirculation (describing a definition and physiological background, haemodynamic coherence, techniques and technologies, and clinical applications).
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Ravikumar, Nakul, Geoffrey R. Sheinfeld, and William T. McGee. "Hemodynamic Perspectives in Anemia." In Hemodynamics [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99725.

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Oxygen delivery in normal physiologic states is determined by cardiac output, hemoglobin, oxygen saturation, and to a lesser extent, dissolved oxygen in the blood. Compensatory mechanisms such as an increase in stroke volume, heart rate, and re-distribution of blood flow helps in scenarios with increased oxygen demand. In cases of acute hemodynamic decompensation, this pre-existing physiologic relation between oxygen delivery and oxygen consumption is altered, resulting in tissue hypoxia and resultant anaerobic metabolism. A persistent state of sub-critical O2 delivery correlates with increased mortality. Oxygen consumption itself is usually independent of delivery unless a critical threshold is unmet. We can use various parameters such as serum lactate, oxygen extraction, and central venous oxygen saturation to determine this pathology. A basic understanding of this physiology will help better tailor therapy to improve outcomes in critically ill patients.
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