Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
31,222
result(s) for
"Respiration - physiology"
Sort by:
The science of the lungs and respiratory system
\"How does oxygen reach our cells? What does our body do with the carbon dioxide it produces? Each breath we take demonstrates the marvel of the human lungs and respiratory system. This accessible book gives inquisitive readers an inside look at this essential bodily function. Engaging graphics and concise language create a reader-friendly experience that will attract even those who are reluctant to study science materials. Fun, easy-to-follow flowcharts summarize key concepts at the end of each chapter, ensuring that readers are able to visualize and retain essential information. This unique, visually rich approach to learning will make this book stand out in any library\" -- From publisher.
Book
Menstrual cycle influence on skeletal muscle mitochondrial respiration in humans
The menstrual cycle influences function in various tissues in the body. We sought to determine if menstrual cycle phase could influence mitochondrial function in skeletal muscle in females. Twenty‐nine females with regular menstrual cycles were randomized to have a vastus lateralis muscle biopsy during either the early follicular or luteal phase. High‐resolution respirometry was used to determine mitochondrial respiration on permeabilized muscle fibers. Glutamate/malate LEAK respiration was significantly higher during the luteal phase compared to the early follicular phase. Glutamate/malate/succinate LEAK respiration was the same during both menstrual cycle phases, as was maximal coupled and uncoupled respiration. There were no differences in fatty acid‐supported respiration. The fatty acid‐supported coupling efficiency ratios of 1‐OcM (octanoylcarnitine/malate) LEAK over maximal coupled respiration and 1‐OcM LEAK over maximal uncoupled respiration were both significantly higher in mitochondria from the early follicular phase than in the luteal phase. Mitochondrial H2O2 emission (glutamate/malate/succinate supported) was significantly increased in muscle from the early follicular phase. We detected no differences in mitochondrial content using citrate synthase activity between phases of the menstrual cycle. Collectively, our observations demonstrate a limited influence of the menstrual cycle on certain measures of submaximal respiration, coupling efficiencies, and H2O2 emission. The influence of the menstrual cycle was examined and found to influence elements of mitochondrial respiration and hydrogen peroxide release but not maximal respiration or citrate synthase activity.
Journal Article
What happens when I yawn?
Introduces yawning, discussing the causes and actions involved in the reflex.
Book
Mitochondrial ATP fuels ABC transporter-mediated drug efflux in cancer chemoresistance
Chemotherapy remains the standard of care for most cancers worldwide, however development of chemoresistance due to the presence of the drug-effluxing ATP binding cassette (ABC) transporters remains a significant problem. The development of safe and effective means to overcome chemoresistance is critical for achieving durable remissions in many cancer patients. We have investigated the energetic demands of ABC transporters in the context of the metabolic adaptations of chemoresistant cancer cells. Here we show that ABC transporters use mitochondrial-derived ATP as a source of energy to efflux drugs out of cancer cells. We further demonstrate that the loss of methylation-controlled J protein (MCJ) (also named DnaJC15), an endogenous negative regulator of mitochondrial respiration, in chemoresistant cancer cells boosts their ability to produce ATP from mitochondria and fuel ABC transporters. We have developed MCJ mimetics that can attenuate mitochondrial respiration and safely overcome chemoresistance in vitro and in vivo. Administration of MCJ mimetics in combination with standard chemotherapeutic drugs could therefore become an alternative strategy for treatment of multiple cancers.
Drug efflux through ABC transporters is a common mechanism leading to chemoresistance in cancer. Here, the authors show that mitochondrial respiration provides ATP to allow ABC transporters activity so mitochondrial respiration inhibition overcomes chemoresistance in preclinical cancer models.
Journal Article
Training-Induced Changes in Mitochondrial Content and Respiratory Function in Human Skeletal Muscle
A sedentary lifestyle has been linked to a number of metabolic disorders that have been associated with sub-optimal mitochondrial characteristics and an increased risk of premature death. Endurance training can induce an increase in mitochondrial content and/or mitochondrial functional qualities, which are associated with improved health and well-being and longer life expectancy. It is therefore important to better define how manipulating key parameters of an endurance training intervention can influence the content and functionality of the mitochondrial pool. This review focuses on mitochondrial changes taking place following a series of exercise sessions (training-induced mitochondrial adaptations), providing an in-depth analysis of the effects of exercise intensity and training volume on changes in mitochondrial protein synthesis, mitochondrial content and mitochondrial respiratory function. We provide evidence that manipulation of different exercise training variables promotes specific and diverse mitochondrial adaptations. Specifically, we report that training volume may be a critical factor affecting changes in mitochondrial content, whereas relative exercise intensity is an important determinant of changes in mitochondrial respiratory function. As a consequence, a dissociation between training-induced changes in mitochondrial content and mitochondrial respiratory function is often observed. We also provide evidence that exercise-induced changes are not necessarily predictive of training-induced adaptations, we propose possible explanations for the above discrepancies and suggestions for future research.
Journal Article
Convergence in the temperature response of leaf respiration across biomes and plant functional types
Plant respiration constitutes a massive carbon flux to the atmosphere, and a major control on the evolution of the global carbon cycle. It therefore has the potential to modulate levels of climate change due to the human burning of fossil fuels. Neither current physiological nor terrestrial biosphere models adequately describe its short-term temperature response, and even minor differences in the shape of the response curve can significantly impact estimates of ecosystem carbon release and/or storage. Given this, it is critical to establish whether there are predictable patterns in the shape of the respiration–temperature response curve, and thus in the intrinsic temperature sensitivity of respiration across the globe. Analyzing measurements in a comprehensive database for 231 species spanning 7 biomes, we demonstrate that temperature-dependent increases in leaf respiration do not follow a commonly used exponential function. Instead, we find a decelerating function as leaves warm, reflecting a declining sensitivity to higher temperatures that is remarkably uniform across all biomes and plant functional types. Such convergence in the temperature sensitivity of leaf respiration suggests that there are universally applicable controls on the temperature response of plant energy metabolism, such that a single new function can predict the temperature dependence of leaf respiration for global vegetation. This simple function enables straightforward description of plant respiration in the land-surface components of coupled earth system models. Our cross-biome analyses shows significant implications for such fluxes in cold climates, generally projecting lower values compared with previous estimates.
Journal Article
Skeletal muscle PGC-1α1 reroutes kynurenine metabolism to increase energy efficiency and fatigue-resistance
The coactivator PGC-1α1 is activated by exercise training in skeletal muscle and promotes fatigue-resistance. In exercised muscle, PGC-1α1 enhances the expression of kynurenine aminotransferases (Kats), which convert kynurenine into kynurenic acid. This reduces kynurenine-associated neurotoxicity and generates glutamate as a byproduct. Here, we show that PGC-1α1 elevates aspartate and glutamate levels and increases the expression of glycolysis and malate-aspartate shuttle (MAS) genes. These interconnected processes improve energy utilization and transfer fuel-derived electrons to mitochondrial respiration. This PGC-1α1-dependent mechanism allows trained muscle to use kynurenine metabolism to increase the bioenergetic efficiency of glucose oxidation. Kat inhibition with carbidopa impairs aspartate biosynthesis, mitochondrial respiration, and reduces exercise performance and muscle force in mice. Our findings show that PGC-1α1 activates the MAS in skeletal muscle, supported by kynurenine catabolism, as part of the adaptations to endurance exercise. This crosstalk between kynurenine metabolism and the MAS may have important physiological and clinical implications.
PGC-1α is activated by exercise and promotes resistance to fatigue in muscles. Here, the authors show that PGC-1α activates the malate-aspartate shuttle, and allows muscle to utilise kynurenine, leading to more efficient glucose oxidation and mitochondrial respiration.
Journal Article
Exercise modality‐dependent mitochondrial respiratory capacity in satellite cells and conditioned serum‐induced responses in cultured myotubes
Exercise‐induced mitochondrial adaptations contribute to muscle function and metabolic health. We aimed to investigate the association of moderate‐intensity swimming (MOD) and high‐intensity interval training (HIIT) with mitochondrial function in skeletal muscle cells treated with exercise‐conditioned serum. Male ICR mice (7–8 weeks old) were assigned to the Sedentary, MOD or HIIT group. The MOD group underwent five sessions of 60 min. The HIIT group performed weighted high‐intensity swimming intervals. This study assessed mitochondrial enzyme activity in the plantaris muscle, mitochondrial respiratory capacity in isolated satellite cells, and mitochondrial function in C2C12 myotubes treated with exercise‐derived serum. Serum was obtained immediately and 24 h postexercise to assess acute effects and chronic adaptations, respectively. The MOD and HIIT groups demonstrated significantly increased muscle citrate synthase and cytochrome c oxidase activities compared with the Sedentary group, but with no significant differences between the MOD and HIIT groups. Satellite cells exhibited higher basal respiration, ATP production and maximal respiratory capacity in the MOD group than in the Sedentary and HIIT groups. Acute serum notably improved maximal mitochondrial respiration in cultured C2C12 myotubes in the HIIT group, whereas serum from chronic training improved those parameters but demonstrated no modality‐specific effects. MOD enhances mitochondrial respiratory function in satellite cells, probably owing to sustained aerobic metabolic signalling, whereas HIIT produces a potent but transient systemic response that acutely boosts mitochondrial function in muscle cells. The differential effects of exercise modalities emphasize the importance of timing and exercise modality in driving specific mitochondrial adaptations, thereby providing valuable insights for tailored exercise prescriptions for optimizing metabolic health. What is the central question of this study? How do different exercise modalities differentially regulate mitochondrial function in skeletal muscle, satellite cells and systemically, via exercise‐conditioned serum? Additionally, how does the timing of serum collection (acute vs. chronic) influence mitochondrial adaptations in cultured muscle cells? What is the main finding and its importance? Exercise modality differentially influences mitochondrial adaptations in skeletal muscle, satellite cells and systemic endocrine signalling via serum factors. Chronic and acute exercise exert distinct effects on mitochondrial respiration, suggesting that both training frequency and intensity modulate metabolic adaptations. These findings highlight the complex interplay between direct muscular adaptations and systemic exerkine‐mediated signalling, providing valuable insights for optimizing exercise interventions.
Journal Article
Equilibration of adenylates in the mitochondrial intermembrane space maintains respiration and regulates cytosolic metabolism
Adenylate kinase (AK) uses one each of Mg-complexed and free adenylates as substrates in both directions of its reaction. It is very active in the mitochondrial intermembrane space (IMS), but is absent from the mitochondrial matrix where low [ADP] upon intensive respiration limits the respiratory rate. AK activity in the IMS is linked to ATP/ADP exchange across the inner mitochondrial membrane by using ATP (imported from the matrix) and AMP as substrates, the latter provided by apyrase and other AMP-generating reactions. The ADP formed by AK is exported to the matrix (in exchange for ATP), providing a mechanism for regeneration of ADP during respiration. From the AK equilibrium, and taking pH values characteristic of subcellular compartments, [Mg2+] in the IMS is calculated as 0.4–0.5 mM and in the cytosol as 0.2–0.3 mM, whereas the MgATP:MgADP ratio in the IMS and cytosol is 6–9 and 10–15, respectively. These represent optimal conditions for transport of adenylates (via the maintenance of an ATPfree:ADPfree ratio close to 1) and mitochondrial respiratory rates (via the maintenance of submillimolar [ADPfree] in the IMS). This, in turn, has important consequences for mitochondrial and cytosolic metabolism, including regulation of the protein phosphorylation rate (via changes in the MgATP:AMPfree ratio) and allosteric regulation of mitochondrial and cytosolic enzymes. Metabolomic consequences are discussed in connection with the calculation of metabolic fluxes from subcompartmental distributions of total adenylates and Mg2+.
Journal Article
Respiration of Microbiota-Derived 1,2-propanediol Drives Salmonella Expansion during Colitis
Intestinal inflammation caused by Salmonella enterica serovar Typhimurium increases the availability of electron acceptors that fuel a respiratory growth of the pathogen in the intestinal lumen. Here we show that one of the carbon sources driving this respiratory expansion in the mouse model is 1,2-propanediol, a microbial fermentation product. 1,2-propanediol utilization required intestinal inflammation induced by virulence factors of the pathogen. S. Typhimurium used both aerobic and anaerobic respiration to consume 1,2-propanediol and expand in the murine large intestine. 1,2-propanediol-utilization did not confer a benefit in germ-free mice, but the pdu genes conferred a fitness advantage upon S. Typhimurium in mice mono-associated with Bacteroides fragilis or Bacteroides thetaiotaomicron. Collectively, our data suggest that intestinal inflammation enables S. Typhimurium to sidestep nutritional competition by respiring a microbiota-derived fermentation product.
Journal Article