The physiological response to physical exercise is now recognized as an important tool which can aid the diagnosis and treatment of cardiovascular diseases. This is due to the fact that several mechanisms are needed to accommodate a higher cardiac output and a higher oxygen delivery to tissues. The aim of the present work is to provide a fully closed loop cardiorespiratory simulator reproducing the main physiological mechanisms which arise during aerobic exercise. The simulator also provides a representation of the impairments of these mechanisms in heart failure condition and their effect on limiting exercise capacity. The simulator consists of a cardiovascular model including the left and right heart, pulmonary and systemic circulations. This latter is split into exercising and non-exercising regions and is controlled by the baroreflex and metabolic mechanisms. In addition, the simulator includes a respiratory model reproducing the gas exchange in lungs and tissues, the ventilation control and the effects of its mechanics on the cardiovascular system. The simulator was tested and compared to the data in the literature at three different workloads whilst cycling (25, 49 and 73 watts). The results show that the simulator is able to reproduce the response to exercise in terms of: heart rate (from 67 to 134 bpm), cardiac output (from 5.3 to 10.2 l/min), leg blood flow (from 0.7 to 3.0 l/min), peripheral resistance (from 0.9 to 0.5 mmHg/(cm(3)/s)), central arteriovenous oxygen difference (from 4.5 to 10.8 ml/d1) and ventilation (6.1-25.5 l/min). The simulator was further adapted to reproduce the main impairments observed in heart failure condition, such as reduced sensitivity of baroreflex and metabolic controls, lower perfusion to the exercising regions (from 0.6 to 1.4 l/min) and hyperventilation (from 9.2 to 40.2 l/min). The simulator we developed is a useful tool for the description of the basic physiological mechanisms operating during exercise. It can reproduce how these mechanisms interact and how their impairments could limit exercise performance in heart failure condition. The simulator can thus be used in the future as a test bench for different therapeutic strategies aimed at improving exercise performance in cardiopathic subjects.
A Model of the Cardiorespiratory Response to Aerobic Exercise in Healthy and Heart Failure Conditions
Fresiello Libera;Ferrari Gianfranco
2016
Abstract
The physiological response to physical exercise is now recognized as an important tool which can aid the diagnosis and treatment of cardiovascular diseases. This is due to the fact that several mechanisms are needed to accommodate a higher cardiac output and a higher oxygen delivery to tissues. The aim of the present work is to provide a fully closed loop cardiorespiratory simulator reproducing the main physiological mechanisms which arise during aerobic exercise. The simulator also provides a representation of the impairments of these mechanisms in heart failure condition and their effect on limiting exercise capacity. The simulator consists of a cardiovascular model including the left and right heart, pulmonary and systemic circulations. This latter is split into exercising and non-exercising regions and is controlled by the baroreflex and metabolic mechanisms. In addition, the simulator includes a respiratory model reproducing the gas exchange in lungs and tissues, the ventilation control and the effects of its mechanics on the cardiovascular system. The simulator was tested and compared to the data in the literature at three different workloads whilst cycling (25, 49 and 73 watts). The results show that the simulator is able to reproduce the response to exercise in terms of: heart rate (from 67 to 134 bpm), cardiac output (from 5.3 to 10.2 l/min), leg blood flow (from 0.7 to 3.0 l/min), peripheral resistance (from 0.9 to 0.5 mmHg/(cm(3)/s)), central arteriovenous oxygen difference (from 4.5 to 10.8 ml/d1) and ventilation (6.1-25.5 l/min). The simulator was further adapted to reproduce the main impairments observed in heart failure condition, such as reduced sensitivity of baroreflex and metabolic controls, lower perfusion to the exercising regions (from 0.6 to 1.4 l/min) and hyperventilation (from 9.2 to 40.2 l/min). The simulator we developed is a useful tool for the description of the basic physiological mechanisms operating during exercise. It can reproduce how these mechanisms interact and how their impairments could limit exercise performance in heart failure condition. The simulator can thus be used in the future as a test bench for different therapeutic strategies aimed at improving exercise performance in cardiopathic subjects.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.