Exercise physiology in COPD

Multiple mechanisms contribute to exercise limitation in chronic obstructive pulmonary disease (COPD). The ability to increase ventilation during exercise is reduced; the more advanced the disease, the more impaired the exercise tolerance is. However, factors other than ventilatory limitation play an important role in reducing the exercise capacity in COPD. Data implicating peripheral muscle atrophy and muscle weakness as cofactors have been reported in individuals with advanced disease. At this stage daily activities are curtailed to avoid exertional respiratory discomfort. Recent studies have demonstrated that the muscle aerobic capacity of stable hypoxemic COPD patients is impaired; oxygen uptake (V′O 2) kinetics and 31P magnetic resonance spectroscopy studies have shown that these patients rely heavily on non-aerobic energy sources even during moderate, sustained workloads. Finally, early occurrence of metabolic acidosis has been demonstrated in patients with mild to severe COPD during exercise. Inadequate tissue oxygenation appears to result from a defect in peripheral oxygen utilization rather than from a reduction in O 2 bulk flow. Peripheral factors may include: a) impaired diffusive conductance for O 2 between red cells and mitochondria; b) heterogeneous distribution of O 2 bulk flow within the exercising muscle fibers; c) inertia of the oxidative processes at the cellular level; d) changes in distribution of muscle fibers, e) reduction in muscle aerobic enzymes; and f) poor nutritional status. Since muscle dysfunction has an important role in the development of exercise intolerance, physical rehabilitation is more and more used as part of the treatment of COPD. The aim of this review is to briefly discuss current views on the mechanisms responsible for the reduced ability to exercise and the rationale for exercise rehabilitation in COPD patients.