Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Mitochondrial physiology

As the knowledge base and importance of mitochondrial physiology to evolution, health and disease expands, the necessity for harmonizing the terminology concerning mitochondrial respiratory states and rates has become increasingly apparent. The chemiosmotic theory establishes the mechanism of energy transformation and coupling in oxidative phosphorylation. The unifying concept of the protonmotive force provides the framework for developing a consistent theoretical foundation of mitochondrial physiology and bioenergetics. We follow the latest SI guidelines and those of the International Union of Pure and Applied Chemistry (IUPAC) on terminology in physical chemistry, extended by considerations of open systems and thermodynamics of irreversible processes. The concept-driven constructive terminology incorporates the meaning of each quantity and aligns concepts and symbols with the nomenclature of classical bioenergetics. We endeavour to provide a balanced view of mitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes. Uniform standards for evaluation of respiratory states and rates will ultimately contribute to reproducibility between laboratories and thus support the development of data repositories of mitochondrial respiratory function in species, tissues, and cells. Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery

Does an Acute COPD Crisis Modify the Cardiorespiratory and Ventilatory Adjustments to Exercise in Horses?

The present study was conducted to understand better the mechanisms leading to the decrease in exercise capacity observed in horses suffering from chronic obstructive pulmonary disease (COPD). Five COPD horses were submitted to a standardized submaximal treadmill exercise test while they were in clinical remission or in acute crisis. Respiratory airflow, O2 and CO2 fractions in the respired gas, pleural pressure changes and heart rate were recorded, and arterial and mixed venous blood were analyzed for gas tensions, hemoglobin, and plasma lactate concentrations. O2 consumption, CO2 production, expired minute ventilation, tidal volume, alveolar ventilation, cardiac output, total pulmonary resistance, and mechanical work of breathing were calculated. The results showed that, when submaximally exercised, COPD horses in crisis were significantly more hypoxemic and hypercapnic and that their total pulmonary resistance and mechanical work of breathing were significantly higher and their expired minute ventilation significantly lower than when they were in remission. However, their O2 consumption remained unchanged, which was probably due to the occurrence of compensatory mechanisms, i.e., higher heart rate, cardiac output, and hemoglobin concentration. Last, their net anaerobic metabolism seemed to be more important