Cardiopulmonary response to exercise in health and disease

Abstract

Exercise leads to increased metabolic request and this represents a challenge for the cardiopulmonary system, which must guarantee O2 and CO2 transfer and exchange. Ventilation (VE) and circulation are responsible for gas transfer, whereas gas exchange is due to both pulmonary and cellular diffusion.

At rest, muscle work is limited to that of the heart and the respiratory and bowel muscles. During exercise limb muscles work is added and leads to an increase in adenosine triphosphate (ATP) request and oxygen consumption (V’O2) and carbon dioxide production (V’CO2). As the exercise intensifies, the aerobic metabolism can not supply all the ATP quantity requested. Consequently, the anaerobic metabolism takes over, leading to increased lactic acid output.

In healthy sedentary subjects, who perform a maximal exercise, VE values range from 5-10 L/min at rest to 80-100 L/min at peak of exercise. Cardiac output (CO) increases linearly as external work increases, from 4-6 L/min at rest to 20 L/min at peak of exercise. In healthy sedentary subjects the factors which lead to exercise limitation are reaching the maximal CO, and consequently the maximal capacity of gas transfer to tissues, and depletion of glycogen stocks.

In heart and respiratory diseases, the cardiopulmonary exercise test (CPET) provides an overall assessment of functional capacity and allows to evaluate disease severity, prognosis and therapeutic interventions. Both in respiratory and cardiac patients exercise intolerance reflects integrated abnormalities of the ventilatory, cardiovascular, peripheral muscle, and neurosecretory systems. The CPET is able to identify which dysfunctional component impacts exercise capacity to the greatest extent.