The pulmonary circulation and exercise responses in the elderly

Abstract

Aging is associated with a progressive deterioration in the structure and function of the pulmonary circulation. Remodeling of the pulmonary vasculature occurs from maturity to senescence that is characterized by an increase in pulmonary vascular stiffness, pulmonary vascular pressures, and pulmonary vascular resistance along with increased heterogeneity of alveolar ventilation and pulmonary perfusion and decreased pulmonary capillary blood volume and membrane diffusing capacity that is consistent with a reduction in alveolar-capillary surface area. In theory, the aforementioned age-related changes in the pulmonary circulation may conspire to make elderly individuals more susceptible to gas exchange abnormalities during exercise. However, despite the erosion in ventilatory reserve with aging, the healthy older adult appears able to maintain alveolar ventilation at a level that allows maintenance of arterial blood gases within normal limits, even during heavy exercise. This ability to maintain adequate gas exchange likely occurs because age-related reductions in the maximal metabolic demand of exercise occur at a rate equal to or greater than the rate of deterioration in ventilatory reserve. A more prominent aspect of aging is the loss of lung elastic recoil that is associated with a modest reduction in the expiratory boundary of the maximal flow-volume envelope. This in turn increases the severity of expiratory airflow limitation and induces dynamic lung hyperinflation during exercise. The consequences of this age-associated decrease in elastic recoil on the pulmonary circulation are speculative, but an age-associated decline in elastic recoil may influence pulmonary vascular resistance and cardiac output, in addition to its impact on the work and oxygen cost of breathing.

Figure 1

Cross-sectional data obtained in our laboratory showing the age-associated change in diffusion capacity of the lung for carbon monoxide (DLCO) in 105 healthy non-smokers. Linear regression beyond the age of 20 results in an annual decrease of 0.15 mL/min/mmHg/year [y =−0.1451 (age) +33.543].

Figure 2

Overview of the age-associated changes in the pulmonary vasculature and gas exchange at rest, and their effect on the response to exercise in the healthy older adult.

Figure 3

Pulmonary arterial pressure (Ppa) and pulmonary wedge pressure (Ppw) at rest and in response to exercise in young (<50 years of age, open squares) and old (>50 years of age, closed squares). Based on data obtained from Emirgil et al, Kovacs et al, and Reeves et al.

Figure 4

Diffusion capacity of the lung for carbon monoxide (DLCO) obtained by rebreathing at rest and during exercise relative to cardiac output in young highly trained adults (open circles, n =8) and older, healthy adults of average fitness (closed squares, n =7). DLCO is reduced at rest in older adults but increases in a linear fashion with progressive exercise similar to that in young adults. Reprinted by permission of Oxford University Press.

Figure 5

Alveolar (PAO₂) and arterial (PaO₂) oxygen tensions during progressive exercise in young, untrained adults (open diamonds, only peak exercise response shown); young, endurance-trained athletes (open circles); and older subjects of average fitness (closed circles). From Johnson.

Figure 6

Ventilatory response to exercise in young, untrained adults (A) and older active adults (B) matched for exercise capacity. Tidal-breathing exercise flow-volume loops are plotted at increasing exercise intensity according to measured end-expiratory lung volume with the maximal volitional flow-volume loop. Additional mean gas exchange parameters are given for both groups. From Johnson.