O2 Demand Research Articles

Effects of structural remodelling on gill physiology.

The complex relationships between the structure and function of fish gills have been of interest to comparative physiologists for many years. Morphological plasticity of the gill provides a dynamic mechanism to reversibly alter its structure in response to changes in the conditions experienced by the fish. The best known example of gill remodelling is the growth or retraction of cell masses between the lamellae, a rapid process that alters the lamellar surface area that is exposed to the water (i.e. the functional lamellar surface area). Decreases in environmental O2 availability and/or increases in metabolic O2 demand stimulate uncovering of the lamellae, presumably to increase the capacity for O2 uptake. This review addresses four questions about gill remodelling: (1) what types of reversible morphological changes occur; (2) how do these changes affect physiological function from the gill to the whole animal; (3) what factors regulate reversible gill plasticity; and (4) is remodelling phylogenetically widespread among fishes? We address these questions by surveying the current state of knowledge of gill remodelling in fishes, with a focus on identifying gaps in our understanding that future research should consider.

The distribution of particulate organic matter in the heterogeneous soil matrix - Balancing between aerobic respiration and denitrification

Denitrification, a key process in soil nitrogen cycling, occurs predominantly within microbial hotspots, such as those around particulate organic matter (POM), where denitrifiers use nitrate as an alternative electron acceptor. For accurate prediction of dinitrogen (N2) and nitrous oxide (N2O) emissions from denitrification, a precise quantification of these microscale hotspots is required. The distribution of POM is of crucial importance in this context, as the local oxygen (O2) balance is governed not only by its high O2 demand but also by the local O2 availability.Employing a unique combination of X-ray CT imaging, microscale O2 measurements, and 15N labeling, we were able to quantify hotspots of aerobic respiration and denitrification. We analyzed greenhouse gas (GHG) fluxes, soil oxygen supply, and the distribution of POM in intact soil samples from grassland and cropland under different moisture conditions. Our findings reveal that both proximal and distal POM, identified through X-ray CT imaging, contribute to GHG emissions. The distal POM, i.e. POM at distant locations to air-filled pores, emerged as a primary driver of denitrification within structured soils of both land uses. Thus, the higher denitrification rates in the grassland could be attributed to the higher content of distal POM. Conversely, despite possessing compacted areas that could favor denitrification, the cropland had only small amounts of distal POM to stimulate denitrification in it. This underlines the complex interaction between soil structural heterogeneity, organic carbon supply, and microbial hotspot formation and thus contributes to a better understanding of soil-related GHG emissions.In summary, our study provides a holistic understanding of soil-borne greenhouse gas emissions and emphasizes the need to refine predictive models for soil denitrification and N2O emissions by incorporating the microscale distribution of POM.

CALCULATION OF CO2 AND O2 NEEDS AS WELL AS CO2 ABSORPTION AND O2 PRODUCING IN ZONE 5 GREEN OPEN SPACES YOGYAKARTA STATE UNIVERSITY

Carbon dioxide (CO2) produced by smoke can produce humans if there are no trees or green open spaces that can absorb CO2 and emissions resulting from human activities. Therefore, efforts to reduce air pollution such as CO2 gas in the campus environment, especially Zone 5 of Yogyakarta State University are ways to build green open spaces. This study suggests to calculate the amount of CO2 emitted and the amount of O2 needed in Zone 5 of Yogyakarta State University that emits emissions from vehicles that are channeled and breathed by humans equipped with functions that absorb CO2 and produce O2. The estimation results show that total CO2 emissions in Zone 5 of Yogyakarta State University in 2019 were 7,479,066 tons / year while the demand for O2 in Zone 5 of Yogyakarta State University in 2019 was 6,763,027 tons / year. So the ability of green open space to absorb CO2 is 3.070,1308 tons/ year and the ability to produce O2 is 131,807 tons / year

Oxygen supersaturation adds resistance to a cnidarian: Symbiodiniaceae holobiont under moderate warming in experimental settings

Ocean warming reduces O2 solubility and increases organismal O2 demand, endangering marine life. Coastal ecosystems, however, experience O2 supersaturation during peak daytime temperatures due to metabolic cycles. Recent discoveries show that this environmental supersaturation can reduce the vulnerability of tropical species to warming by satisfying their oxygen requirements. To test whether this also occurs within the cnidarian holobiont, we elevated internal O2 in Cassiopea andromeda at nighttime (i.e. holobiont respiration prevails on Symbiodniaceae O2 production) relying on bell pulsation for ventilation, then experimentally subjected them to thermal stress (+1°C day-1). Though ecologically unrealistic, this approach verified our hypothesis and eliminated confounding factors. Holobionts were exposed to either constant levels of 100% air saturation (100AS) or nighttime supersaturation (NSS; where 100% air saturation transitioned to O2 supersaturation at nighttime). At sublethal temperatures, supersaturation mitigated reductions in holobiont size of ~ 10.37% (-33.418% ± 0.345 under 100AS vs -23.039% ± 0.687 under NSS). Supersaturation alleviated chlorophyll-a loss by 42.73% until 34°C, when counteraction of this process could not be sustained due to excessive thermal stress. Supersaturation also enriched potentially beneficial bacterial taxa of the microbiome and selected a more consistent bacterial community. Although modest, the detected effects show that a O2 surplus increased the resistance of the holobionts to thermal stress.

Linking red blood cell functional phenotypes to environmental tolerance in high-altitude adapted deer mice

Oxygen (O2) is essential for vertebrate life, and complex cardio-respiratory systems have evolved to transport the gas from the environment to each individual cell. Even short disruptions of this O2 flux can have deleterious effects that are linked to numerous disease states. Animals that have adapted to hypoxic environments, such as deer mice ( Peromyscus maniculatus) native to high altitude, can provide valuable insight into naturally evolved solutions to O2 deprivation. Previous work has shown that high-altitude deer mice have evolved a higher hemoglobin O2 affnity and other coordinated changes across the O2 transport cascade that enable higher metabolic rates in hypoxia. Red blood cells (RBC) are the functional unit of O2 and carbon dioxide transport in the blood and play central roles in matching O2 supply and demand in the microcirculation by releasing signaling molecules such as ATP and gasotransmitters; but how these cellular mechanisms respond to hypoxic environments has not been studied. We hypothesized that high-altitude adaptation in deer mice has improved the function of RBCs for cardiovascular gas transport in hypoxia. Lab-raised breeding colonies of deer-mice were established from wild mice caught at low altitude (~400 m in the Great Plains of Nebraska) and at high altitude (~4300 m in the Rocky Mountains of Colorado). Using a common-garden experimental design, third-generation deer mice from high- and low-altitude populations were acclimated to warm normoxia (21°C, 21 kPa O2) or cold hypobaric hypoxia (5°C, 12 kPa O2) for 8 weeks. Blood samples were collected for measurements of hematocrit, hemoglobin concentration, RBC volume, plasma erythropoietin concentration, RBC contents of membrane transport and channel proteins (anion exchanger, aquaporin 1 and rhesus associated glycoprotein) by immunocytochemistry and western blotting, and carbonic anhydrase activity using biochemical techniques. The release of ATP from RBCs was measured in tonometers at decreasing levels of O2 by luminometry, and the vascular sensitivity to ATP was determined by wire myography on second-order mesenteric arteries. Finally, bone marrow samples were collected from the femurs to measure gene expression levels in the erythropoietic tissue. Our experimental design allowed us to examine the interactive effects of cold hypoxic environments on RBC phenotype, by untangling environmentally-induced plasticity from the signatures of adaptation that are unique to high-altitude natives. This work is providing a better understanding of how RBC function participates in matching cardiovascular O2 supply and demand in extreme hypoxia, which has important applications in animal and human health. This work was supported by a NSERC Canada Banting Postdoctoral Fellowship to TSH and a Discovery Grant to GRS. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

The Arterial Baroreflex Buffers Muscle Metaboreflex-Induced Coronary Vasoconstriction

The ability to increase cardiac output and thereby skeletal muscle blood flow during dynamic exercise is paramount to maintaining exercise workload. Increases in cardiac output are driven via increases in heart rate, ventricular function, and central blood volume mobilization which raises arterial blood pressure, in part, due to activation of the muscle metaboreflex. The increase in cardiac sympathetic tone also activates coronary vascular alpha-adrenergic receptors which restrains increases in coronary blood flow which limits increases in ventricular function. During submaximal dynamic exercise, the muscle metaboreflex acts primarily to raise cardiac output with little net peripheral vasoconstriction. However, after sinoaortic baroreceptor denervation (SAD), the muscle metaboreflex causes increases in both cardiac output and total peripheral resistance indicating that the baroreflex buffers the muscle metaboreflex mainly via restraint of peripheral vasoconstriction. To what degree the arterial baroreflex restrains muscle metaboreflex-induced coronary vasoconstriction is unknown. Therefore, we utilized our chronically instrumented canine model to evaluate if SAD would significantly impact muscle metaboreflex-induced coronary vasoconstriction. Canines were chronically instrumented to measure cardiac output, left circumflex coronary artery blood flow, hindlimb blood flow and arterial blood pressure. During steady-state mild treadmill exercise (3.2 kph, 0% grade) the muscle metaboreflex was activated via partial inflation of vascular occluders placed distal to the hindlimb blood flow probe. Metaboreflex activation caused substantial increases in cardiac output, heart rate, cardiac power, coronary blood flow, and arterial blood pressure. Assessment of coronary vasodilation was performed via linear regression of the relationship between coronary vascular conductance (CVC; coronary blood flow/mean arterial pressure) vs. cardiac power (CP, an index of O2 demand). Experiments were performed at least 2 weeks after chronic bilateral SAD. Muscle metaboreflex activation after SAD caused a significantly greater pressor response driven by increases in both cardiac output and total peripheral resistance. Furthermore, after SAD the slope of the CVC-CP relationship was significantly lower during muscle metaboreflex activation (0.072 ml/min/mmHg/Watt, control vs 0.033 ml/min/mmHg/Watt, SAD; p<0.05) We conclude that the arterial baroreflex buffers the muscle metaboreflex and restrains the reflex coronary vasoconstriction. This baroreflex-induced restraint of metaboreflex mediated coronary vasoconstriction potentially limits metaboreflex-induced reductions myocardial oxygen delivery. Augmented coronary vasoconstriction with metaboreflex activation after SAD likely contributes to the smaller role of cardiac output in mediating the rise in arterial blood pressure after SAD, and provides further evidence that baroreflex buffering of metaboreflex responses improves cardiac function. Thus, reduced baroreflex function in heart failure may contribute to the accentuated metaboreflex coronary vasoconstriction which impairs ventricular performance during exercise in heart failure. This work was supported by the National Heart, Lung and, Blood Institute grants HL-055473, HL-126706. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Targeting hypoxia signaling pathways in angiogenesis.

Oxygen (O2) supply is constantly maintained by the vascular network for a proper tissue oxygenation. Hypoxia is the result of an increased O2 demand and/or decreased supply and is common in both physiological conditions and human diseases. Angiogenesis is one of the adaptive responses to hypoxia and is mainly regulated by the hypoxia-inducible factors, HIFs. These heterodimeric transcription factors are composed of one of three O2-dependent α subunits (HIF-1, HIF-2, and HIF-3) and a constitutively expressed O2-insensitive subunit (HIF-1β). Among them HIF-1α is the most characterized and its activity is tightly controlled. Under hypoxia, its intracellular accumulation triggers the transcription of several genes, involved in cell survival/proliferation, autophagy, apoptosis, cell metabolism, and angiogenesis. HIF pathway is also modulated by specific microRNAs (miRNAs), thus resulting in the variation of several cellular responses, including alteration of the angiogenic process. The pro-angiogenic activity of HIF-1α is not restricted to endothelial cells, as it also affects the behavior of other cell types, including tumor and inflammatory/immune cells. In this context, exosomes play a crucial role in cell-cell communication by transferring bio-active cargos such as mRNAs, miRNAs, and proteins (e.g., VEGFA mRNA, miR210, HIF-1α). This minireview will provide a synopsis of the multiple factors able to modulate hypoxia-induced angiogenesis especially in the tumor microenvironment context. Targeting hypoxia signaling pathways by up-to-date approaches may be relevant in the design of therapeutic strategies in those pathologies where angiogenesis is dysregulated.

Effects of manipulating Kingfish (Seriola lalandi) routine oxygen demand and supply on ventricular and skeletal muscle mitochondrial function

SummaryYellowtail kingfish (Seriola lalandi) are a highly active marine species, with increasing value in commercial aquaculture. While practices which manipulate oxygen (O2) dynamics through metabolic demand and environmental O2 supply have been shown to impact juvenile growth rate in fish development, there has been no work exploring the effects of O2 at the subcellular level. In addition, manipulation of O2 supply or demand via changes in environmental factors such as O2 levels or salinity, may impact whole animal performance. Still, there has been little work exploring the physiological effects at a subcellular level. Mitochondria (mt) consume O2 and are pivotal in central metabolism, directly impacting growth, and dictating whole animal performance. Here we explore the effects of manipulating O2 demand and supply on mt in yellowtail kingfish ventricle and skeletal muscle by exposure to chronic hyperoxia (200% [O2], 35 ppt) and to hypoosmotic conditions (100% [O2], 17.5 ppt). Chronic exposure to hypoosmotic conditions resulted in greater overall biomass, while it lowered relative ventricular mass compared to control fish. Mitochondrial respiratory flux for most measures remained consistent with control fish, with the exception of cytochrome c oxidase (COX) respiration. Chronic hyperoxia had no impact on overall morphology, and no significant effect on ventricle mt respiration, yet increased COX activity in skeletal muscle. These data indicate that lowering routine mt O2 demands in S. lalandi with hypoosmotic conditions has more impact than increasing O2 availability, and that this may enhance biomass output while maintaining mt integrity.

Effect of Eccentric Cycling on Oxygen Uptake and Hemodynamics in Patients With Pulmonary Vascular Disease: A Randomized Controlled Crossover Trial

BackgroundEccentric cycling exercise (ECC) allows training at low metabolic costs and may therefore be valuable for patients with precapillary pulmonary hypertension (PH) due to pulmonary vascular disease (PVD). Research QuestionThe aim of this study was to compare the ventilatory and circulatory responses to ECC versus conventional cycling (CON) in patients with PVD. Study Design and MethodsThis was a randomized controlled crossover trial in which patients diagnosed with PVD, defined as either pulmonary arterial or chronic thromboembolic PH (PAH/CTEPH), performed CON and ECC cycling tests at identical submaximal work-rates, following stepwise incremental protocols. Oxygen uptake (V’O2) and additional cardiorespiratory responses were measured breath-by-breath by ergospirometry. Hemodynamic parameters such as systolic pulmonary artery pressure (sPAP) and tricuspid annular plain systolic excursion (TAPSE) were measured by echocardiography. Results33 patients (19 PAH, 14 CTEPH, 13 females, 50±15 years) were included. At identical work-rates during ECC compared to CON, V’O2 was significantly lower by - 200 ml/min (-40%, 95CI: -272 to -129, p<0.01), minute ventilation by -5.5 l/min (-30%, 95CI: -9.2 to -3.1, p<0.01), and sPAP by -12 mmHg (-20%, 95CI: -20 to -4 p<0.01). Right ventricular–arterial coupling, as measured by TAPSE/sPAP, was 0.11 mm/mmHg higher (+31%, 95CI: 0.04 to 0.18, p<0.01). No adverse events occurred. InterpretationThe current study supports the hypothesis that ECC is a feasible and well-tolerated exercise modality for PVD patients, with lower O2 demand and a reduced load on the right ventricle. Future studies should investigate whether ECC improves exercise capacity, muscle force and possibly hemodynamics during prolonged rehabilitation programs in patients with PVD.

Isotope effects of O2 consumption in a deep lake as means for understanding partitioning of O2 demand among microorganisms, particles, and sediment

AbstractThe isotopic ratio 18O/16O of dissolved O2 in aquatic systems is affected by the preferential biological uptake of 16O (ε). Studies over the past six decades reveal that during incubation experiments, the isotopic effect of microorganism respiration (εorganism) varies in the range of −18‰ to −22‰. In contrast, natural variations in the deep‐ocean O2 concentration and δ18O levels show a considerably weaker effect (~ −10‰). The differences between these observations have been explained to result from either O2 uptake by sediments or organic particles that, due to diffusion‐limited respiration, are expected to weakly fractionate oxygen isotopes, by mixing processes or by weak fractionation at low temperatures. To gain better insight, we studied oxygen demand and δ18O in the deep, cold hypolimnion of Lake Stechlin between 2018 and 2021 as well as in various laboratory incubations. Our incubation results demonstrate an εorganism of about −24‰. Simple model calculations demonstrate a sediment O2 demand isotope effect (εSOD) of about −8.4‰, and a variated water‐column O2 demand isotope effect (εWOD) which is lower than εorganism, ranging from −13.9‰ in 2019 to −23‰ in 2021. Accompanying experiments indicate that the lower magnitude of εWOD may be related to respiration at organic particles lending to a weaker fractionation effect. Thus, variations in εWOD may reflect a changing partitioning of hypolimnion oxygen uptake between suspended particles and their containing microorganisms. Based on own incubation experiments with Daphnia carcasses, we discuss how possible changes of particle rigidity might influence εWOD.

Evolved changes in phenotype across skeletal muscles in deer mice native to high altitude.

The cold and hypoxic conditions at high altitude necessitate high metabolic O2 demands to support thermogenesis while hypoxia reduces O2 availability. Skeletal muscles play key roles in thermogenesis, but our appreciation of muscle plasticity and adaptation at high altitude has been hindered by past emphasis on only a small number of muscles. We examined this issue in deer mice (Peromyscus maniculatus). Mice derived from both high-altitude and low-altitude populations were born and raised in captivity and then acclimated as adults to normoxia or hypobaric hypoxia (12 kPa O2 for 6-8 wk). Maximal activities of citrate synthase (CS), cytochrome c oxidase (COX), β-hydroxyacyl-CoA dehydrogenase (HOAD), hexokinase (HK), pyruvate kinase (PK), and lactate dehydrogenase (LDH) were measured in 20 muscles involved in shivering, locomotion, body posture, ventilation, and mastication. Principal components analysis revealed an overall difference in muscle phenotype between populations but no effect of hypoxia acclimation. High-altitude mice had greater activities of mitochondrial enzymes and/or lower activities of PK or LDH across many (but not all) respiratory, limb, core and mastication muscles compared with low-altitude mice. In contrast, chronic hypoxia had very few effects across muscles. Further examination of CS in the gastrocnemius showed that population differences in enzyme activity stemmed from differences in protein abundance and mRNA expression but not from population differences in CS amino acid sequence. Overall, our results suggest that evolved increases in oxidative capacity across many skeletal muscles, at least partially driven by differences in transcriptional regulation, may contribute to high-altitude adaptation in deer mice.NEW & NOTEWORTHY Most previous studies of muscle plasticity and adaptation in high-altitude environments have focused on a very limited number of skeletal muscles. Comparing high-altitude versus low-altitude populations of deer mice, we show that a large number of muscles involved in shivering, locomotion, body posture, ventilation, and mastication exhibit greater mitochondrial enzyme activities in the high-altitude population. Therefore, evolved increases in mitochondrial oxidative capacity across skeletal muscles contribute to high-altitude adaptation.

Capillary oxygen regulates demand–supply coupling by triggering connexin40-mediated conduction: Rethinking the metabolic hypothesis

Coupling red blood cell (RBC) supply to O2 demand is an intricate process requiring O2 sensing, generation of a stimulus, and signal transduction that alters upstream arteriolar tone. Although actively debated, this process has been theorized to be induced by hypoxia and to involve activation of endothelial inwardly rectifying K+ channels (KIR) 2.1 by elevated extracellular K+ to trigger conducted hyperpolarization via connexin40 (Cx40) gap junctions to upstream resistors. This concept was tested in resting healthy skeletal muscle of Cx40-/- and endothelial KIR2.1-/- mice using state-of-the-art live animal imaging where the local tissue O2 environment was manipulated using a custom gas chamber. Second-by-second capillary RBC flow responses were recorded as O2 was altered. A stepwise drop in PO2 at the muscle surface increased RBC supply in capillaries of control animals while elevated O2 elicited the opposite response; capillaries were confirmed to express Cx40. The RBC flow responses were rapid and tightly coupled to O2; computer simulations did not support hypoxia as a driving factor. In contrast, RBC flow responses were significantly diminished in Cx40-/- mice. Endothelial KIR2.1-/- mice, on the other hand, reacted normally to O2 changes, even when the O2 challenge was targeted to a smaller area of tissue with fewer capillaries. Conclusively, microvascular O2 responses depend on coordinated electrical signaling via Cx40 gap junctions, and endothelial KIR2.1 channels do not initiate the event. These findings reconceptualize the paradigm of blood flow regulation in skeletal muscle and how O2 triggers this process in capillaries independent of extracellular K+.

Muscle metaboreflex stimulates the cardiac sympathetic afferent reflex causing positive feedback amplification of sympathetic activity: effect of heart failure.

Exercise intolerance is a hallmark symptom of heart failure and to a large extent stems from reductions in cardiac output that occur due to the inherent ventricular dysfunction coupled with enhanced muscle metaboreflex-induced functional coronary vasoconstriction, which limits increases in coronary blood flow. This creates a further mismatch between O2 delivery and O2 demand, which may activate the cardiac sympathetic afferent reflex (CSAR), causing amplification of the already increased sympathetic activity in a positive-feedback fashion. We used our chronically instrumented conscious canine model to evaluate if chronic ablation of afferents responsible for the CSAR would attenuate the gain of muscle metaboreflex before and after induction of heart failure. After afferent ablation, the gain of the muscle metaboreflex control of mean arterial pressure was significantly reduced before (-239.5 ± 16 to -95.2 ± 8 mmHg/L/min) and after the induction of heart failure (-185.6 ± 14 to -95.7 ± 12 mmHg/L/min). Similar results were observed for the strength (gain) of muscle metaboreflex control of heart rate, cardiac output, and ventricular contractility. Thus, we conclude that the CSAR contributes significantly to the strength of the muscle metaboreflex in normal animals with heart failure serving as an effective positive-feedback amplifier thereby further increasing sympathetic activity.NEW & NOTEWORTHY The powerful pressor responses from the CSAR arise via O2 delivery versus O2 demand imbalance. Muscle metaboreflex activation (MMA) simultaneously elicits coronary vasoconstriction (which is augmented in heart failure) and profound increases in cardiac work thereby upsetting oxygen balance. Whether MMA activates the CSAR thereby amplifying MMA responses is unknown. We observed that removal of the CSAR afferents attenuated the strength of the muscle metaboreflex in normal and subjects with heart failure.

Synthesis of bioactive hemoglobin-based oxygen carrier nanoparticles via metal-phenolic complexation

The transfusion of donor red blood cells (RBCs) is seriously hampered by important drawbacks that include limited availability and portability, the requirement of being stored in refrigerated conditions, a short shelf life or the need for RBC group typing and crossmatching. Thus, hemoglobin (Hb)-based oxygen (O2) carriers (HBOCs) which make use of the main component of RBCs and the responsible protein for O2 transport, hold a lot of promise in modern transfusion and emergency medicine. Despite the great progress achieved, it is still difficult to create HBOCs with a high Hb content to attain the high O2 demands of our body. Herein a metal–phenolic self-assembly approach that can be conducted in water and in one step to prepare nanoparticles (NPs) fully made of Hb (Hb-NPs) is presented. In particular, by combining Hb with polyethylene glycol, tannic acid (TA) and manganese ions, spherical Hb-NPs with a uniform size around 350–525 nm are obtained. The functionality of the Hb-NPs is preserved as shown by their ability to bind and release O2 over multiple rounds. The binding mechanism of TA and Hb is thoroughly investigated by UV–vis absorption and fluorescence spectroscopy. The binding site number, apparent binding constant at two different temperatures and the corresponding thermodynamic parameters are identified. The results demonstrate that the TA-Hb interaction takes place through a static mechanism in a spontaneous process as shown by the decrease in Gibbs free energy. The associated increase in entropy suggests that the TA-Hb binding is dominated by hydrophobic interactions.

Increased inflammatory proteins in patients with severe obesity is associated with persistent myocardial dysfunction one year after bariatric surgery. The FatWest study

Abstract Background Over half of patients with severe obesity have subclinical cardiac dysfunction and about 40% maintain impaired left ventricular (LV) mechanics one year after bariatric surgery despite impressive weight reduction. Purpose To investigate whether measurement of serum markers of chronic inflammation before bariatric surgery can help identify patients with persistent postoperative cardiac dysfunction. Methods In the prospective FatWest (Bariatric Surgery on the West Coast of Norway) study 75 patients with severe obesity (44±9 years, 72% women, body mass index [BMI] 41.5±4.7 kg/m², 56% with hypertension) underwent echocardiography before and 1 year after Roux-en-Y gastric bypass surgery. We assessed LV mechanics in the radial and longitudinal direction by the midwall shortening (MWS) and global longitudinal strain (GLS). Myocardial oxygen (O2) demand was derived from the LV mass-wall stress-heart rate product. Inflammation was assessed by high-sensitive C-reactive protein, serum amyloid A and calprotectin in biobank samples. Results Preoperatively, patients with low MWS (45% of the group) had increased high-sensitive C-reactive protein, total calprotectin, and several amyloid A isoforms, and patients with high myocardial O2 demand (20%) had high total calprotectin (all p&amp;lt;0.05). In the whole study population, bariatric surgery induced a significant improvement in both BMI (12.6±3.7 kg/m²), GLS (4.74±5.20%), myocardial O2 demand and inflammatory proteins (Figure A, all p&amp;lt;0.001). However, there were no significant improvement in MWS, and 33% of patients still had low MWS at the 1-year control. In logistic regression analyses, after adjustment for sex, BMI and hypertension, increased preoperative serum total calprotectin was independently associated with high myocardial O2 demand both pre- and postoperatively (Nagelkerke R² 0.47 and 0.51, p&amp;lt;0.05). In similar analyses, higher preoperative serum total amyloid A was related to low MWS and high myocardial O2 demand 1 year after surgery (Nagelkerke R² 0.55 and 0.51, p&amp;lt;0.05). A simple preoperative risk score based on sex, hypertension, biplane ejection fraction, and serum total amyloid A above 4.0 mg/ml predicted low 1-year MWS with 79% sensitivity and 75% specificity at a value of 1.75 in Receiver Operating Characteristic (ROC) analysis (AUC 0.80, p&amp;lt;0.001) (Figure B). Low GLS was not predicted by inflammatory biomarkers at any timepoint. Conclusion Increased serum concentration of inflammatory proteins in patients with severe obesity is linked to persistently elevated myocardial O2 demand and impaired LV midwall mechanics 1 year after bariatric surgery.Figure AFigure B

Hypoxia-Induced Signaling in Gut and Liver Pathobiology.

Oxygen (O2) is essential for cellular metabolism and biochemical reactions. When the demand for O2 exceeds the supply, hypoxia occurs. Hypoxia-inducible factors (HIFs) are essential to activate adaptive and survival responses following hypoxic stress. In the gut (intestines) and liver, the presence of oxygen gradients or physiologic hypoxia is necessary to maintain normal homeostasis. While physiologic hypoxia is beneficial and aids in normal functions, pathological hypoxia is harmful as it exacerbates inflammatory responses and tissue dysfunction and is a hallmark of many cancers. In this review, we discuss the role of gut and liver hypoxia-induced signaling, primarily focusing on HIFs, in the physiology and pathobiology of gut and liver diseases. Additionally, we examine the function of HIFs in various cell types during gut and liver diseases, beyond intestinal epithelial and hepatocyte HIFs. This review highlights the importance of understanding hypoxia-induced signaling in the pathogenesis of gut and liver diseases and emphasizes the potential of HIFs as therapeutic targets.

Climate, Oxygen, and the Future of Marine Biodiversity.

The ocean enabled the diversification of life on Earth by adding O2 to the atmosphere, yet marine species remain most subject to O2 limitation. Human industrialization is intensifying the aerobic challenges to marine ecosystems by depleting the ocean's O2 inventory through the global addition of heat and local addition of nutrients. Historical observations reveal an ∼2% decline in upper-ocean O2 and accelerating reports of coastal mass mortality events. The dynamic balance of O2 supply and demand provides a unifying framework for understanding these phenomena across scales from the global ocean to individual organisms. Using this framework, we synthesize recent advances in forecasting O2 loss and its impacts on marine biogeography, biodiversity, and biogeochemistry. We also highlight three outstanding uncertainties: how long-term global climate change intensifies ocean weather events in which simultaneous heat and hypoxia create metabolic storms, how differential species O2 sensitivities alter the structure of ecological communities, and how global O2 loss intersects with coastal eutrophication. Projecting these interacting impacts on future marine ecosystems requires integration of climate dynamics, biogeochemistry, physiology, and ecology, evaluated with an eye on Earth history. Reducing global and local impacts of warming and O2 loss will be essential if humankind is to preserve the health and biodiversity of the future ocean.

Complete mineralization of 2,4-dichlorophenoxyacetic acid in a reduction and oxidation Synergistic Platform (ROSP)

Emissions of 2,4-dichlorophenoxyactic acid (2,4-D), one of the most widely used herbicides, pose serious risks to human and ecosystem health. Although biodegradation and abiotic chemical methods are available for 2,4-D removal, continuous treatment systems for 2,4-D removal are rare. We evaluated a Reduction and Oxidation Synergistic Platform (ROSP) that sequentially links an H2-based membrane catalyst-film reactor (H2-MCfR) and an O2-based membrane biofilm reactor (O2-MBfR). In continuous operation of the ROSP, 50 μM (or 11 ppm) of 2,4-D was completely mineralized with a total HRT of 12 h, yielding an effluent concentration < 0.2 μM 2,4-D (or < 44 ppb). In the H2-MCfR, over 80% of the influent 2,4-D was reductively hydrodechlorinated to phenoxyacetic acid (POA). The produced POA was the primary substrate supporting the co-oxidation of 2,4-D in the O2-MBfR. The biofilm community structure and genes encoding enzymes for POA and 2,4-D co-oxidation were identified through shallow metagenomic sequencing of the biofilm DNA samples. The dominant bacterial genus, Variovorax, and various mono-/dioxygenase-encoding genes related to aromatic ring hydrolysis, hydroxylation, and ring cleavage were associated with the removal of 2,4-D. In summary, reductive-dehalogenation products from the H2-MCfR become the primary substrate to enable the co-oxidation of the halogenated organic pollutants in the O2-MBfR, which does not require the addition of other organic materials. Therefore, the ROSP eliminates the need for an added organic substrate, which greatly reduces the demand for O2 and minimizes CO2 emissions.

Muscle oxygen saturation rates coincide with lactate-based exercise thresholds.

Monitoring muscle metabolic activity via blood lactate is a useful tool for understanding the physiological response to a given exercise intensity. Recent indications suggest that skeletal muscle oxygen saturation (SmO2), an index of the balance between local O2 supply and demand, may describe and predict endurance performance outcomes. We tested the hypothesis that SmO2 rate is tightly related to blood lactate concentration across exercise intensities, and that deflections in SmO2 rate wouldcoincide with established blood lactate thresholds (i.e., lactate thresholds 1 and 2). Ten elite male soccer players completed an incremental running protocol to exhaustion using 3-min work to 30s rest intervals. Blood lactate samples were collected during rest and SmO2 was collected continuously via near-infrared spectroscopy from the right and left vastus lateralis, left biceps femoris and the left gastrocnemius. Muscle O2 saturation rate (%/min) was quantified after the initial 60s of each 3-min segment. The SmO2 rate was significantly correlated with blood lactate concentrations for all muscle sites; RVL, r = -0.974; LVL, r = -0.969; LG, r = -0.942; LHAM, r = -0.907. Breakpoints in SmO2 rate were not significantly different from LT1 or LT2 at any muscle sites (P > 0.05). Bland-Altman analysis showed speed threshold estimates via SmO2 rate and lactate are similar at LT2, but slightly greater for SmO2 rate at LT1. Muscle O2 saturation rate appears to provide actionable information about maximal metabolic steady state and is consistent with bioenergetic reliance on oxygen and its involvement in the attainment of metabolic steady state.

Techno-Economic Assessment of PEM Electrolysis for O2 Supply in Activated Sludge Systems—A Simulation Study Based on the BSM2 Wastewater Treatment Plant

The conversion of renewable energy into hydrogen (H2) by power-to-gas technologies involving electrolysis is seen today as a key element in the transition to a sustainable energy sector. Wastewater treatment plants (WWTP) could be integrated into future green H2 networks as users of oxygen (O2) produced alongside H2 in water electrolysis. In WWTPs, O2 is required for biological treatment steps, e.g., in activated sludge (AS) systems. However, the production costs of electrolysis O2 should be competitive with those of conventional O2 production processes. In this study, mathematical models of a polymer electrolyte membrane electrolyser (PEME) plant and the WWTP of the Benchmark Simulation Model No. 2 (BSM2) were used to simulate electrolysis O2 supply to an AS system and estimate net costs of production (NCP) for produced O2 via a techno-economic assessment (TEA). Assuming that produced H2 is sold to a nearby industry, NCPs for O2 were calculated for two different PEME plant dimensions, four alternatives regarding electricity supply and costs, and three sets of assumptions regarding system performance and market conditions. The analyses were performed for 2020 as a reference year and 2030 based on forecasts of relevant data. Results of the dimensioning of the PEME show the O2 demand of a municipal WWTP with an installed capacity of 80,000 population equivalents (PE), such as the one of the BSM2, can be covered for more than 99% of the simulated period by either a 6.4 MW PEME operated for 4073 full load hours or a 4.8 MW PEME operated for 6259 full load hours. Investment costs for the PEME stacks and the operational costs for electricity make up most of the NCP of electrolysis O2. The projected decrease in PEME stack costs and renewable energy prices in favourable market conditions can result in a competitive NCP for electrolysis O2 in 2030. The approach described in this study can be applied to analyse O2 supply to biological wastewater treatment in WWTPs with different characteristics, in processes different from AS, and under different assumptions regarding economic conditions.