Impedance Spectroscopy Measurements of Ionomer Film Oxygen Transport Resistivity in Operating Low-Pt PEM Fuel Cell

The work presents a model for local impedance of low-Pt proton exchange membrane fuel cells (PEMFCs), including cathode pore size distribution and O2 transport along pores and through a thin ionomer film covering Pt/C agglomerates. The model was applied to fit the local impedance spectra of low-Pt fuel cells operated at current densities from 100 to 800 mA cm−2 and recorded by a segmented cell system. Assuming an ionomer film thickness of 10 nm, the fitting returned the product of the dimensionless Henry’s constant of oxygen dissolution in ionomer KH by the oxygen diffusivity DN in the ionomer (KHDN). This parameter allowed us to determine the fundamental O2 transport resistivity RN through the ionomer film in the working electrode under conditions relevant to the realistic operation of PEMFCs. The results show that variation of the operating current density does not affect RN, which remains nearly constant at ≃0.4 s cm−1.

Oxygen - Mitochondrial fuel as a missing link in depressive pathophysiology

Major depressive disorder (MDD) causes enormous individual suffering and socioeconomic costs. Biochemical mechanisms leading to MDD are poorly understood and therapy success is not satisfactory. At present, there is evidence of low-grade inflammation, oxidative stress, and most interestingly, a disturbed energy metabolism in MDD and other mental health diseases. Mitochondria play a central part in energy production and stress signaling. Mitochondrial electron transport chain uses molecular oxygen (O2) as final electron acceptor during adenosine triphosphate production attributing a crucial role to an intact O2 supply. Adaptation to altered O2 availability by the highly conserved hypoxic response is essential for maintaining allostasis. Previous research confirmed the role of O2 metabolism in the pathophysiology of MDD. In this perspective article, we compile the evidence linking O2 transport, O2 homeostasis, and mitochondrial energy metabolism to MDD. Furthermore, we hypothesize that inflammation and oxidative stress-related alterations in O2 transport might lead to a hypoxic response, which explains changes in O2 homeostasis and energy metabolism in MDD. Our forthcoming studies will investigate the interplay between energy metabolism and O2 homeostasis in MDD that aim to improve the overall understanding of the pathophysiology of MDD and to guide medical and psychological diagnostics towards a holistic strategy.

Physiological insight into the evolution of complex phenotypes: aerobic performance and the O2 transport pathway of vertebrates

ABSTRACT Evolutionary physiology strives to understand how the function and integration of physiological systems influence the way in which organisms evolve. Studies of the O2 transport pathway – the integrated physiological system that transports O2 from the environment to mitochondria – are well suited to this endeavour. We consider the mechanistic underpinnings across the O2 pathway for the evolution of aerobic capacity, focusing on studies of artificial selection and naturally selected divergence among wild populations of mammals and fish. We show that evolved changes in aerobic capacity do not require concerted changes across the O2 pathway and can arise quickly from changes in one or a subset of pathway steps. Population divergence in aerobic capacity can be associated with the evolution of plasticity in response to environmental variation or activity. In some cases, initial evolutionary divergence of aerobic capacity arose exclusively from increased capacities for O2 diffusion and/or utilization in active O2-consuming tissues (muscle), which may often constitute first steps in adaptation. However, continued selection leading to greater divergence in aerobic capacity is often associated with increased capacities for circulatory and pulmonary O2 transport. Increases in tissue O2 diffusing capacity may augment the adaptive benefit of increasing circulatory O2 transport owing to their interactive influence on tissue O2 extraction. Theoretical modelling of the O2 pathway suggests that O2 pathway steps with a disproportionately large influence over aerobic capacity have been more likely to evolve, but more work is needed to appreciate the extent to which such physiological principles can predict evolutionary outcomes.

Physiology and Pathophysiology of Oxygen Sensitivity

Oxygen is an essential requirement for metabolism in mammals and many other animals. Therefore, pathways that sense a reduction in available oxygen are critical for organism survival. Higher mammals developed specialized organs to detect and respond to changes in O2 content to maintain gas homeostasis by balancing oxygen demand and supply. Here, we summarize the various oxygen sensors that have been identified in mammals (carotid body, aortic bodies, and astrocytes), by what mechanisms they detect oxygen and the cellular and molecular aspects of their function on control of respiratory and circulatory O2 transport that contribute to maintaining normal physiology. Finally, we discuss how dysregulation of oxygen availability leads to elevated signalling sensitivity in these systems and may contribute to the pathogenesis of chronic cardiovascular and respiratory diseases and many other disorders. Hence, too little oxygen, too much oxygen, and a malfunctioning sensitivity of receptors/sensors can create major pathophysiological problems for the organism.

Genetically and chemically tuned haemoglobin–albumin trimers with superior O2 transport efficiency

Haemoglobin (Hb)–albumin (HSA) trimers were synthesized using five distinct Hb variants in which the structures were genetically and chemically tuned as an artificial O2 carrier used for a red blood...

Progress in Ce0.8Gd0.2O2−δ protective layers for improving the CO2 stability of Ba0.5Sr0.5Co0.8Fe0.2O3−δ O2-transport membranes

A promising way of overcoming BSCF limitations in real operation conditions are CGO protective layers deposited by RF magnetron sputtering, as they show an improvement in the oxygen permeation flux when using pure CO2 as sweep gas.

Left Ventricular Assist Device Support Complicates the Exercise Physiology of Oxygen Transport and Uptake in Heart Failure

Low-output forward flow and impaired maximal exercise oxygen uptake (VO2 max) are hallmarks of patients in advanced heart failure. The continuous-flow left ventricular assist device is a cutting-edge therapy proven to increase forward flow, yet this therapy does not yield consistent improvements in VO2 max. The science of how adjustable artificial forward flow impacts the exercise physiology of heart failure and physical O2 transport between the central and peripheral systems is unclear. This review focuses on the exercise physiology of axial continuous-flow left ventricular assist device support and the impact that pump speed has on the interactive convective and diffusive components of whole-body physical O2 transport and VO2.