Abstract
Whereas the negative effects of aging and smoking on pulmonary function are undisputed, the potential favorable effects of physical activity on the aging process of the otherwise healthy lung remain controversial. This question is of particular clinical relevance when reduced pulmonary function compromises aerobic exercise capacity (maximal oxygen consumption) and thus contributes to an increased risk of morbidity and mortality. Here, we discuss whether and when the aging-related decline in pulmonary function limits maximal oxygen consumption and whether, how, and to what extent regular physical activity can slow down this aging process and preserve pulmonary function and maximal oxygen consumption. Age-dependent effects of reduced pulmonary function (i.e., FEV1, the volume that has been exhaled after the first second of forced expiration) on maximal oxygen consumption have been observed in several cross-sectional and longitudinal studies. Complex interactions between aging-related cellular and molecular processes affecting the lung, and structural and functional deterioration of the cardiovascular and respiratory systems account for the concomitant decline in pulmonary function and maximal oxygen consumption. Consequently, if long-term regular physical activity mitigates some of the aging-related decline in pulmonary function (i.e., FEV1 decline), this could also prevent a steep fall in maximal oxygen consumption. In contrast to earlier research findings, recent large-scale longitudinal studies provide growing evidence for the beneficial effects of physical activity on FEV1. Although further confirmation of those effects is required, these findings provide powerful arguments to start and/or maintain regular physical activity.
Highlights
Physical activity (PA) is defined as “any bodily movement produced by skeletal muscles that requires energy expenditure” [1] and includes physical exercise that is defined as planned, structured, repeated, and goal-directed PA
Whether it can slow down the aging-related decline in pulmonary function, commonly measured via the forced expiratory volume in 1 s (FEV1), is still debated. FEV1 decline starts from the fourth decade of life with a median rate of 43.5 and 30.5 mL per year for men and women, respectively [2]. FEV1 is an easy to assess variable, which has been traditionally used as a surrogate measure of maximum ventilatory capacity that was shown to represent an important predictor of dyspnea, leg effort, and aerobic capacity, irrespective of the degree of airflow limitation [3]
The latter has been attributed to impaired muscle metabolism, at least partly related to mitochondrial dysfunction, which favors the development of sarcopenia [17]
Summary
Current knowledge indicates a role for physical activity to slow down the age-related deterioration of pulmonary function and associated aerobic capacity in otherwise healthy individuals. These findings provide a further powerful argument to start and/or maintain regular physical activity
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