Modelling the respiratory control system in human subjects for excercise conditions

摘要

A model is a very helpful tool to describe, interpret and explain the behaviour of a highly complex system such as the human respiratory system. The research work presented in this thesis is concerned with the development of a nonlinear dynamic simulation model of the respiratory control system in human subjects for exercise conditions. Modelling the respiratory system is not a new activity but the development of a general model that takes into account the conditions above the lactate threshold has not been attempted previously because of a number of problems that arise for these particular operating conditions. Many variables become increasingly non linear in terms of their temporal pattern and magnitudes. Also metabolic acidosis, which is negligible below the lactate threshold, cannot be neglected for exercise conditions that take the system above the lactate threshold. The current work has established a general model that applies for exercise conditions below and above the lactate threshold. The model takes into account the factor of metabolic acidosis, which is calculated by estimating the production and consumption of lactate in body tissues and its kinetics in the blood. The slow component increase of muscle energetics and O2 extraction is also considered. Well established algorithms are employed to estimate the O2 and CO2 dissociation curves and the Siggaard-Andersen nomogram is used to calculate blood pH. The model is able to reproduce the main features of the system response in terms of ventilation and pulmonary gas exchange during moderate and heavy exercise. It is also able to reproduce the characteristics of several blood quantities including arterial gas partial pressures, arterial O2 and CO2 concentrations, mixed-venous and arterial pH and also lactate and bicarbonate concentrations. Potential applications of the model include describing the contribution of haemoglobin to performance in exercise conditions, estimating how cardiac output should change during heavy exercise, describing the effect of acidosis, and describing the changes of body CO2 stores during exercise. Assumptions, limitations and procedures for testing and evaluating the model are discussed, along with suggestions for further developments that could lead to possible improvements of the model and thus to an extension of the range of problems to which the model could be applied.