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• W3176985710 abstract "ViewpointCommentaries on Viewpoint: Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered modelsPublished Online:18 Jun 2021https://doi.org/10.1152/japplphysiol.00327.2021MoreSectionsPDF (178 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Role of carnosine in the acid-base control of musclesJoão Pedro Assis Moreira,12 Thais Melo Marques,12 Ludmila Dias dos Santos Leal,12 Paula Souza Alves Santos,12 Joao Pedro de Souza Ferreira,12 Raul Dominguez,13 and Sandro Fernandes da Silva12.Author Affiliations1Grupo de estudo e pesquisa em respostas neuromusculares, Universidade Federal de Lavras, Lavras, Brazil.2Programa de Pós-Graduação em Nutrição e Saúde Universidade Federal de Lavras, Lavras, Brazil.3Departamento de Motricidad Humana y Rendimiento Deportivo, Universidad de Sevilla, Sevilla, Spain.to the editor: We read Rubin’s recent Viewpoint very carefully (1). The hypothesis of the role of bicarbonate in acid-base balance was established at the very first stage (1). However, considering bicarbonate as the only muscle buffer system may be a limited interpretation of the whole system. Currently, carnosine, a dipeptide formed by β-alanine and L-carnosine and found in high concentrations in skeletal muscle (∼20–30 g·kg−1), presents several physiological functions, with the most prominent being the regulation of acid-base balance (2). This is achieved due to carnosine’s pKa (6.83), which makes it an important physiological buffer during high-intensity exercise (3). Therefore, carnosine acts as a Ca2+ launcher to the sarcolemma, facilitating the formation of cross bridges through which it captures an H+ ion that it transports to the extracellular space (3). However, in skeletal muscle, the highest concentration of carnosine is in type II fibers, which makes it an important muscle buffer (4). Given that β-alanine supplementation is a limiting factor in carnosine synthesis, sports science has been trying to examine the role of carnosine, which is administered chronically, ranging in dosage from 4 to 6.4 g·day−1 and an administration of 4 to 10 wk (5). Various studies have pointed to an improvement in the buffering capacity of the muscles and an increase in power and anaerobic efforts, which highlights the important role of carnosine (5). Therefore, science should consider the important role that carnosine plays in acid-base control.REFERENCES1. Rubin DM. Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models. J Appl Physiol (1985). doi:10.1152/japplphysiol.00042.2021.Link | ISI | Google Scholar2. Matthews JJ, Artioli GG, Turner MD, Sale C. The physiological roles of carnosine and β-alanine in exercising human skeletal muscle. Med Sci Sports Exerc 51: 2098–2108, 2019. doi:10.1249/MSS.0000000000002033.Crossref | PubMed | ISI | Google Scholar3. Swietach P, Youm J-B, Saegusa N, Leem C-H, Spitzer KW, Vaughan-Jones RD. Coupled Ca2+/H+ transport by cytoplasmic buffers regulates local Ca2+ and H+ ion signaling. Proc Natl Acad Sci USA 110: E2064–E2073, 2013. doi:10.1073/pnas.1222433110.Crossref | PubMed | ISI | Google Scholar4. Blancquaert L, Everaert I, Missinne M, Baguet A, Stegen S, Volkaert A, Petrovic M, Vervaet C, Achten E, De Maeyer M, De Henauw S, Derave W. Effects of histidine and β-alanine supplementation on human muscle carnosine storage. Med Sci Sports Exerc 49: 602–609, 2017. doi:10.1249/MSS.0000000000001213.Crossref | PubMed | ISI | Google Scholar5. Saunders B, Elliott-Sale K, Artioli GG, Swinton PA, Dolan E, Roschel H, Sale C, Gualano B. β-Alanine supplementation to improve exercise capacity and performance: a systematic review and meta-analysis. Br. J. Sports Med. 51: 658–669, 2017. doi:10.1136/bjsports-2016-096396.Crossref | PubMed | ISI | Google ScholarREFERENCES1. Rubin DM. Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models. J Appl Physiol (1985). doi:10.1152/japplphysiol.00042.2021.Link | ISI | Google Scholar2. Matthews JJ, Artioli GG, Turner MD, Sale C. The physiological roles of carnosine and β-alanine in exercising human skeletal muscle. Med Sci Sports Exerc 51: 2098–2108, 2019. doi:10.1249/MSS.0000000000002033.Crossref | PubMed | ISI | Google Scholar3. Swietach P, Youm J-B, Saegusa N, Leem C-H, Spitzer KW, Vaughan-Jones RD. Coupled Ca2+/H+ transport by cytoplasmic buffers regulates local Ca2+ and H+ ion signaling. Proc Natl Acad Sci USA 110: E2064–E2073, 2013. doi:10.1073/pnas.1222433110.Crossref | PubMed | ISI | Google Scholar4. Blancquaert L, Everaert I, Missinne M, Baguet A, Stegen S, Volkaert A, Petrovic M, Vervaet C, Achten E, De Maeyer M, De Henauw S, Derave W. Effects of histidine and β-alanine supplementation on human muscle carnosine storage. Med Sci Sports Exerc 49: 602–609, 2017. doi:10.1249/MSS.0000000000001213.Crossref | PubMed | ISI | Google Scholar5. Saunders B, Elliott-Sale K, Artioli GG, Swinton PA, Dolan E, Roschel H, Sale C, Gualano B. β-Alanine supplementation to improve exercise capacity and performance: a systematic review and meta-analysis. Br. J. Sports Med. 51: 658–669, 2017. doi:10.1136/bjsports-2016-096396.Crossref | PubMed | ISI | Google ScholarCommentary on Viewpoint: Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered modelsDavid A. Story.Author AffiliationsDepartment of Critical Care, The University of Melbourne, Melbourne, Victoria, Australia.to the editor: For the critical care disciplines of Anesthesiology, Emergency Medicine, and Intensive Care, applied physiology is a scientific foundation of clinical practice. Analyzing acid-base physiology and pathophysiology is a part of assessing and managing high-risk, deteriorating, and critically ill patients (1, 2). Change is a central feature in acid-base analysis. Base-excess is the most effective approach to separate changes in bicarbonate and PCO2, providing a single metric for (nonrespiratory) metabolic changes (1, 3). As Rubin outlined (4), the Stewart approach (5) provides further insights. One barrier to bringing Stewart to a patient’s bedside is the mathematical complexity of this approach (5). Solutions to this barrier use simplified physiological models of Stewart’s work (1, 2, 4).When combined with base-excess as a measure of overall metabolic acid-base status, the simplified Stewart approaches provide detailed quantitative analyses (1, 2). These simplified Stewart approaches (2, 3) focus on quantifying the acid-base effects of key plasma chemistry elements, namely, sodium, chloride, and albumin, and potentially pathophysiological elements including lactate and unmeasured ions. Insights include: 1) hyperchloremic acidosis and hypochloremic alkalosis are relative phenomena partly dependent on plasma sodium concentration and subsequent strong-ion-difference; and 2) hypoalbuminemia is common among critical care patients (4) causing alkalosis that can mask the severity of coexisting acidosis (1, 2).The simplified Stewart approaches integrate acid-base physiology and routine plasma clinical chemistry, providing greater insights into both what changes have occurred and why they occurred. The qualitative bicarbonate-centered strategies (3, 4) are less integrated with general plasma chemistry and less able to identify specific components and changes of acid-base disorders.REFERENCES1. Berend K. Diagnostic use of base excess in acid-base disorders. N Engl J Med 378: 1419–1428, 2018. doi:10.1056/NEJMra1711860.Crossref | ISI | Google Scholar2. Story DA. Stewart acid-base: a simplified bedside approach. Anesth Analg 123: 511–515, 2016. doi:10.1213/ANE.0000000000001261.Crossref | PubMed | ISI | Google Scholar3. Story DA. Bench-to-bedside review: a brief history of clinical acid-base. Crit Care 8: 253–258, 2004. doi:10.1186/cc2861.Crossref | PubMed | ISI | Google Scholar4. Rubin DM. Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models. J Appl Physiol (1985). doi:10.1152/japplphysiol.00042.2021.Link | ISI | Google Scholar5. Stewart PA. Independent and dependent variables of acid-base control. Respir Physiol 33: 9–26, 1978. doi:10.1016/0034-5687(78)90079-8. Crossref | PubMed | Google ScholarREFERENCES1. Berend K. Diagnostic use of base excess in acid-base disorders. N Engl J Med 378: 1419–1428, 2018. doi:10.1056/NEJMra1711860.Crossref | ISI | Google Scholar2. Story DA. Stewart acid-base: a simplified bedside approach. Anesth Analg 123: 511–515, 2016. doi:10.1213/ANE.0000000000001261.Crossref | PubMed | ISI | Google Scholar3. Story DA. Bench-to-bedside review: a brief history of clinical acid-base. Crit Care 8: 253–258, 2004. doi:10.1186/cc2861.Crossref | PubMed | ISI | Google Scholar4. Rubin DM. Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models. J Appl Physiol (1985). doi:10.1152/japplphysiol.00042.2021.Link | ISI | Google Scholar5. Stewart PA. Independent and dependent variables of acid-base control. Respir Physiol 33: 9–26, 1978. doi:10.1016/0034-5687(78)90079-8. Crossref | PubMed | Google ScholarCommentary on Viewpoint: Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered modelsHarry B. Rossiter and Richard M. Effros.Author AffiliationsDivision of Respiratory and Critical Care Physiology and Medicine, The Lundquist Institute for Biomedical Innovation at Harbor-UCLA Medical Center, Torrance, California.to the editor: Of all of the variables used to evaluate the acid-base status, concentrations of H+ and OH− in plasma are by far the lowest, averaging ∼625,000 times less than those of HCO3−. It is consequently impractical, and possibly misleading, to represent H+ on the conventional “Gamblegram,” stacked histograms of ion concentrations. This discrepancy in the magnitudes of ionic concentrations is troublesome to Stewart’s approach (1), who suggested that H+ and pH should not be used as proper measures of acidity. This erroneous conclusion is related in part to a common failure of physiologists to recognize that the free energy differences between two solutions containing the same solute must be calculated from the ratios rather than the differences of the corresponding concentrations. This explains why differences in H+ concentrations of only 60 nmol/L across a mitochondrial membrane, and a transmembrane potential of 140 mV, can store much of the free energy produced in the cell (2), including all that is needed to maintain much greater differences in sodium concentrations of 100 mmol/L between the extracellular and intracellular compartments. Although the objective to consider all acid-base pairs in the Gamblegram of a clinical fluid is commendable, and is useful for quantifying electroneutrality and the presence of unknown ions (1), the approach may increase analytical errors since the measurement error of the primary variables exceeds the mean values of the minor constituents (3–5).REFERENCES1. Rubin DM. Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models. J Appl Physiol (1985). doi:10.1152/japplphysiol.00042.2021.Link | ISI | Google Scholar2. Mitchell P. Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism. Nature 191: 144–148, 1961. doi:10.1038/191144a0. Crossref | PubMed | ISI | Google Scholar3. Constable PD. Total weak acid concentration and effective dissociation constant of nonvolatile buffers in human plasma. J Appl Physiol (1985) 91: 1364–1371, 2001. doi:10.1152/jappl.2001.91.3.1364. Link | ISI | Google Scholar4. Schück O, Matousovic K. Relation between pH and the strong ion difference (SID) in body fluids. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 149: 69–73, 2005. doi:10.5507/bp.2005.007. Crossref | PubMed | Google Scholar5. Kurtz I, Kraut J, Ornekian V, Nguyen MK. Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches. Am J Physiol Renal Physiol 294: F1009–F1031, 2008. doi:10.1152/ajprenal.00475.2007. Link | ISI | Google ScholarREFERENCES1. Rubin DM. Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models. J Appl Physiol (1985). doi:10.1152/japplphysiol.00042.2021.Link | ISI | Google Scholar2. Mitchell P. Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism. Nature 191: 144–148, 1961. doi:10.1038/191144a0. Crossref | PubMed | ISI | Google Scholar3. Constable PD. Total weak acid concentration and effective dissociation constant of nonvolatile buffers in human plasma. J Appl Physiol (1985) 91: 1364–1371, 2001. doi:10.1152/jappl.2001.91.3.1364. Link | ISI | Google Scholar4. Schück O, Matousovic K. Relation between pH and the strong ion difference (SID) in body fluids. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub 149: 69–73, 2005. doi:10.5507/bp.2005.007. Crossref | PubMed | Google Scholar5. Kurtz I, Kraut J, Ornekian V, Nguyen MK. Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches. Am J Physiol Renal Physiol 294: F1009–F1031, 2008. doi:10.1152/ajprenal.00475.2007. Link | ISI | Google ScholarWhy still criticize Stewart?Johan M. van Schalkwyk.Author AffiliationsDepartment of Anaesthesiology, University of Auckland, Auckland, New Zealand.to the editor: The Viewpoint by Rubin (1) revisits the longstanding dispute between proponents of the Stewart approach to acid-base and “traditional acid-base physiologists” espousing a “bicarbonate-centered” approach (2, 3).As Karl Popper noted, the value of a scientific model depends on how well it withstands robust criticism (4). Such criticism should naturally be applied in an even-handed way to competing models. I believe that Rubin largely does this, in contrast to prior, perhaps more polemical analysis (2, 3), where absence of five of the relevant six equilibrium equations from the bicarbonate-centered approach is accommodated by empiric rules for “acute” or “chronic” acid-base disorders and self-justifying invocation of “buffers.”There are stark contrasts between Stewart proponents and critics. The latter deny Stewart’s variables are “independent”—but it is clear that this view is predicated on neglect of the obvious fact that species like H+ and HCO3− participate in multiple equilibria, whereas Stewart’s “independent” variables, [weak acid], partial pressure of CO2, and strong ion difference, each feature in just one of six equations. The second, related insight is causal: tradition disallows “independent” variables by forbidding causality outside experimentation—but this approach ignores the modern approach to causality and counterfactuals (5).The 21st century may be a good time to abandon not only the anachronism of using a single, insufficient equation to model a complex system but also oversimplified views of causality.REFERENCES1. Rubin DM. Stewart's approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models. J Appl Physiol (1985). doi:10.1152/japplphysiol.00042.2021.Link | ISI | Google Scholar2. Doberer D, Funk G-C, Kirchner K, Schneeweiss B. A critique of Stewart's approach: the chemical mechanism of dilutional acidosis. Intensive Care Med 35: 2173–2180, 2009. doi:10.1007/s00134-009-1528-y.Crossref | PubMed | ISI | Google Scholar3. Kurtz I, Kraut J, Ornekian V, Nguyen MK. Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches. Am J Physiol Renal Physiol 294: F1009–F1031, 2008. doi:10.1152/ajprenal.00475.2007.Link | ISI | Google Scholar4. Popper K. The Logic of Scientific Discovery. London, New York: Routledge, 1959.Google Scholar5. Pearl J. Causality: Models, Reasoning, and Inference. Cambridge, UK: Cambridge University Press, 2000.Google ScholarREFERENCES1. Rubin DM. Stewart's approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models. J Appl Physiol (1985). doi:10.1152/japplphysiol.00042.2021.Link | ISI | Google Scholar2. Doberer D, Funk G-C, Kirchner K, Schneeweiss B. A critique of Stewart's approach: the chemical mechanism of dilutional acidosis. Intensive Care Med 35: 2173–2180, 2009. doi:10.1007/s00134-009-1528-y.Crossref | PubMed | ISI | Google Scholar3. Kurtz I, Kraut J, Ornekian V, Nguyen MK. Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches. Am J Physiol Renal Physiol 294: F1009–F1031, 2008. doi:10.1152/ajprenal.00475.2007.Link | ISI | Google Scholar4. Popper K. The Logic of Scientific Discovery. London, New York: Routledge, 1959.Google Scholar5. Pearl J. Causality: Models, Reasoning, and Inference. Cambridge, UK: Cambridge University Press, 2000.Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Related ArticlesStewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models 18 Jun 2021Journal of Applied PhysiologyLast Word on Viewpoint: Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered models 18 Jun 2021Journal of Applied PhysiologyCited ByLast Word on Viewpoint: Stewart’s approach to quantitative acid-base physiology should replace traditional bicarbonate-centered modelsDavid M. Rubin18 June 2021 | Journal of Applied Physiology, Vol. 130, No. 6 More from this issue > Volume 130Issue 6June 2021Pages 2022-2023 Crossmark Copyright & PermissionsCopyright © 2021 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00327.2021PubMed34142891History Accepted 11 May 2021 Published online 18 June 2021 Published in print 1 June 2021 Metrics" @default.
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