During the first 25 years of life, the lungs and the respiratory system undergo a phase of growth and maturation until maximal function is reached. Throughout the remainder of life, aging is associated with a progressive decline in lung performance. Normal aging of the respiratory system is attributed to structural changes of the chest wall (rib calcification, osteoporosis, vertebral fractures, narrowing of intervertebral disk spaces, increased dorsal kyphosis, “barrel chest” etc ), of the lung parenchyma (dilatation of alveoli, enfargement of airspaces, decrease in gas-exchange surface area and loss of supporting tissue for pelipheral airways) and of the respiratory muscles (decrease in muscle mass, decrease in the number of muscle fibres type II and motor units, alterations in neuromuscular junctions, decreased synthesis of myosin and decline in mitochondrial respiratory chain function). Age-related structural changes result in various functional alterations, such as increased chest wall stiffness, decreased lung elastic recoil and increased lung compliance, gas-trapping, hyperinflation and reduction of respiratory muscle strengrh. Furthermore, forced expiratory volume in one second (FEV1), vital capacity and expiratory flows at low lung volumes decline with a characteristic pattern in the flow-volume loop, indicating small airway dysfunction. Low ventilation-perfusion ratio (VA/Q) zones emerge as a result of premature closing of dependent airways and lead to an increase in VA/Q heterogeneity. Carbon monoxide diffusion decreases with age, reflecting a loss in surface area. Despite these extensive functional derangements, the respiratory system remains capable of maintaining adequate gas exchange at rest and on exertion, during the entire human lifespan, with only a mild decrease in arterial oxygen tension (PaO2) but without change in arterial carbon dioxide tension (PaCO2). However, aging tends to diminish the reserve of the respiratory system in cases of acute disease. In addition, the age-related diminished physical activity and the consequent deconditioning, the decreased sensitivity of respiratory centres to hypoxia/hypercapnia and the diminished ability to perceive added resistive and elastic loads, all may result in a blunted ventilatory response under various life-threatening clinical conditions (such as acute respiratory failure, heart failure and hydrostatic pulmonary edema, infection or bronchoconstriction) and therefore, lesser awareness of the disease and delayed diagnosis with possibly hazardous consequences. Pneumon 2000, 13 (2): 108-122