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Bioenergetics
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
However, peak blood lactate concentrations during intermittent high-intensity exercise can occur before the last bout, and peak muscle lactate concentrations can occur within 2 min of the initiation of intense exercise (119, 140, 149, 238, 239). It is the muscle lactic acid concentrations that appear to be the limiting factor during exercise and not the blood lactate concentration. The post-exercise lag time in peak blood lactate concentration results from a cellular transport mechanism for lactate (146), the monocarboxylate transporters. Although diffusion contributes to lactate initial removal (and uptake), movement into and out of the cell is facilitated by monocarboxylate transport proteins (MCT) (25). The MCTs are a family of proton-linked plasma membrane transporters that can transport molecules having one carboxylate group (monocarboxylates), such as lactate and pyruvate, across the cell membrane (107). MCTs are expressed in cells of nearly every type of tissue (216). In muscle, MCT1 is responsible for enhanced uptake, while MCT4 is responsible for facilitated removal of cellular lactate against a concentration gradient. Although various types of training can increase MCTs, it is believed that endurance training primarily enhances the expression of MCT1 and that anaerobic training, including strength training, enhances the expression of MCT4 (25, 279) and these alterations may be fiber-type specific (279).
Biochemistry of Buffering Capacity and Ingestion of Buffers In Exercise and Athletic Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Bryan Saunders, Guilherme G. Artioli, Eimear Dolan, Rebecca L. Jones, Joseph Matthews, Craig Sale
Lactate supplementation has been purported as a strategy for increasing extracellular buffering capacity. Following ingestion of sodium or calcium lactate, the lactate is absorbed in the intestine, preferentially in the jejunum (47), entering the bloodstream and increasing blood lactate concentration. The lactate can subsequently be oxidized or used as a metabolic substrate in gluconeogenesis (69, 76), processes that consume H+, subsequently altering acid–base balance. The increased lactate can also be taken up by the tissue for oxidation (54) or by hepatocytes for conversion into glucose (1). The transport of lactate into tissues is facilitated by the monocarboxylate transporters 1 and 4, which co-transport with H+ in a 1:1 ratio (59), thereby resulting in a net loss of H+ in blood, increasing blood pH, and sparing blood bicarbonate, which may be useful during high-intensity exercise.
Effect of Short-Chain Fatty Acids Produced by Probiotics
Published in Marcela Albuquerque Cavalcanti de Albuquerque, Alejandra de Moreno de LeBlanc, Jean Guy LeBlanc, Raquel Bedani, Lactic Acid Bacteria, 2020
Milena Fernandes da Silva, Meire dos Santos Falcão de Lima, Attilio Converti
Among the non-GPCR mechanisms of SCFA transport across the apical membrane, we can mention: (a) the electroneutral cotransport with H+ via monocarboxylate transporter 1 (MCT1, also referred to as SLC16A1) that may occur for a given SCFA, depending on the transmembrane concentration gradient, in either influx or efflux direction; (b) the electroneutral H+/monocarboxylate symport via monocarboxylate transporter 4 (MCT4, also referred to as SLC16A3); and (c) the electrogenic transport via sodium-coupled monocarboxylate transporters 1 (SMCT1 or SLC5A8) and 2 (SMCT2 or SLC5A12), with Na+ influx and monocarboxylate substrates leading to depolarization (Sivaprakasam et al. 2018) (Figure 2).
Targeting glucose metabolism to develop anticancer treatments and therapeutic patents
Published in Expert Opinion on Therapeutic Patents, 2022
Yan Zhou, Yizhen Guo, Kin Yip Tam
As the final product of glycolysis, pyruvate stands at the intersection of two fate pathways, which can be simplified as [7]: (1) reversible conversion to lactate by the lactate dehydrogenase (LDH) in cytosol, and (2) transport into mitochondrial TCA cycle where it will be oxidized to acetyl-CoA and CO2 by pyruvate dehydrogenase (PDH) which can be negatively modulated by pyruvate dehydrogenase kinases (PDKs) upregulation. The hypoxia-inducible factor-1α (HIF1α), which commonly presents in solid cancer, is reported to induce the overexpression of PDK and LDH [8]. Since the reversible reactions catalyzed by LDH led to the formation of lactic acid, cancer cells often overexpressed monocarboxylate transporters (MCTs) to prevent intercellular acidification [9]. Targeting LDH has recently emerged as one of the most promising anticancer strategies.
Innovations and revolutions in reducing retinal ganglion cell loss in glaucoma
Published in Expert Review of Ophthalmology, 2021
Mary Kelada, Daniel Hill, Timothy E. Yap, Haider Manzar, M. Francesca Cordeiro
The field of retinal bioenergetic research has gained increasing interest in glaucoma, with energy insufficiency at the optic nerve head having been suggested to play a role in the pathogenesis of glaucoma [62]. Recently, the expansion of energy input mechanisms of retinal cells has been described as a potential neuroprotective method. Monocarboxylate transporters (MCTs) act to transport lactate, pyruvate, and ketones across cell membranes. Harun-Or-Rashid et al. [63] demonstrated that the reduction of murine retinal levels of MCT2 using AAV2-cre lead to a significant reduction in visual evoked potential and ATP production. The same research group also demonstrated that virally induced overexpression of MCT2 in DBA/2 J (D2) glaucoma models, as well as murine magnetic bead models of OHT, increased RGC density and axon numbers compared to untreated mice [63]. MCT2 overexpression was also demonstrated to increase mitochondrial function (represented by succinate dehydrogenase activity) in both glaucoma models, compared to untreated control mice [63]. The findings of this preclinical study offer promising insight into the potential use of metabolic interventions as neuroprotective mechanisms.
Nanocarriers for brain specific delivery of anti-retro viral drugs: challenges and achievements
Published in Journal of Drug Targeting, 2018
Nila Mary Varghese, Venkatachalam Senthil, Shailendra K. Saxena
Monocarboxylate transporters are a family of integral membrane transport proteins, which facilitates the diffusion of monocarboxylates such as pyruvate, lactates and ketone bodies. About 14 members of the family have been recognised wherein four isoforms (MCT1-MCT4) are functionally characterised in the brain capillary endothelial vasculature, neurons and astrocytes [84]. In the study by Tsuji et al. [85] the acid form of the 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase inhibitors were transported across the BBB using the MCT. The study was done in in vitro and in vivo conditions and also concluded that the lactone and dicarboxylic forms of the inhibitors were unable to gain entry to the brain making use of this transporter system [85,86]. Another study done by Lee et al. [87] concluded that MCT1 is the transporter involved in the transcytosis of 4-phenylbutyrate across the BBB, through internal carotid artery perfusion in vivo and intravenous injection.