Key result
Airway smooth muscle plasticity is facilitated by myosin filament evanescence and lengthening, allowing muscles to develop nearly the same force across a 3-fold range of lengths.
This review summarizes evidence supporting the plasticity of airway smooth muscle, highlighting that functional range is accommodated by plastic alterations in myofilaments.
Supports myosin filament plasticity in smooth muscle; leaves open relevance to vascular tone regulation.
At a similar meeting 10 years ago, we proposed (i) that the long functional range of some smooth muscles is accommodated by plastic alterations that place more myofilaments in series at longer lengths, (ii) that this plasticity is facilitated by myosin filament evanescence, with filaments dissociating partially during relaxation and reforming upon activation, and (iii) that filament lengthening during the rise of activation would cause velocity to fall. Since that meeting, we have accumulated a substantial body of evidence to support these proposals, as follows: (i) muscles develop nearly the same force when adapted to a range of lengths that can vary by 3-fold; (ii) other physiological parameters including shortening velocity, maximum power, compliance, ATPase rate, and thick-filament mass increase by about 2/3 for a doubling of muscle length; (iii) thick-filament density increases substantially during the rise of activation; and (iv) velocity falls as force rises during the rise of tetanic force, and when correction is made for differences in activation, velocity and force vary exactly in inverse proportion. This review explains the rationale for the different experimental measurements and their interpretation.
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Lincoln E. Ford (2005) conducted a review in Airway smooth muscle plasticity. Airway smooth muscle plasticity is facilitated by myosin filament evanescence and lengthening, allowing muscles to develop nearly the same force across a 3-fold range of lengths.
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