Neuromotor control in chronic obstructive pulmonary disease

Abstract

Neuromotor control of skeletal muscles, including respiratory muscles, is ultimately dependent on the structure and function of the motor units (motoneurons and the muscle fibers they innervate) comprising the muscle. In most muscles, considerable diversity of contractile and fatigue properties exists across motor units, allowing a range of motor behaviors. In diseases such as chronic obstructive pulmonary disease (COPD), there may be disproportional primary (disease related) or secondary effects (related to treatment or other concomitant factors) on the size and contractility of specific muscle fiber types that would influence the relative contribution of different motor units. For example, with COPD there is a disproportionate atrophy of type IIx and/or IIb fibers that comprise more fatigable motor units. Thus fatigue resistance may appear to improve, while overall motor performance (e.g., 6-min walk test) and endurance (e.g., reduced aerobic exercise capacity) are diminished. There are many coexisting factors that might also influence motor performance. For example, in COPD patients, there may be concomitant hypoxia and/or hypercapnia, physical inactivity and unloading of muscles, and corticosteroid treatment, all of which may disproportionately affect specific muscle fiber types, thereby influencing neuromotor control. Future studies should address how plasticity in motor units can be harnessed to mitigate the functional impact of COPD-induced changes.