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1 Department of Anatomy and Cell Biology, University of British Columbia, Vancouver, BC, Canada; The UBC McDonald Research Laboratories / The iCAPTURE Centre, St. Paul's Hospital / Providence Health Care, Vancouver, BC, Canada
2 Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; The UBC McDonald Research Laboratories / The iCAPTURE Centre, St. Paul's Hospital / Providence Health Care, Vancouver, BC, Canada
3 Department of Medicine, University of British Columbia, Vancouver, BC, Canada; The UBC McDonald Research Laboratories / The iCAPTURE Centre, St. Paul's Hospital / Providence Health Care, Vancouver, BC, Canada
4 Krannert Institute of Cardiology, Indiana University, Indianapolis, IN, USA
5 Department of Physiology, University of Manitoba, Winnipeg, MB, Canada
6 Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; Department of Pharmacology and Therapeutics, University of British Columbia, Vancouver, BC, Canada; The UBC McDonald Research Laboratories / The iCAPTURE Centre, St. Paul's Hospital / Providence Health Care, Vancouver, BC, Canada
* To whom correspondence should be addressed. E-mail: cseow{at}interchange.ubc.ca.
Airway smooth muscle is able to adapt and maintain a nearly constant maximal force generation over a large length range. This implies that a fixed filament lattice such as that found in striated muscle may not exist in this tissue, and that plastic remodeling of its cytoskeletal and contractile filaments may be involved in the process of length adaptation that optimizes contractile filament overlap. Here we show that isometric force produced by airway smooth muscle was independent of muscle length over a 2-fold length change; cell cross-sectional area was inversely proportional to cell length, implying that the cell volume was conserved at different lengths; shortening velocity and myosin filament density varied similarly to length change: increased by 69.4%±5.7(SE) and 76.0%±9.8 respectively for a 100% increase in cell length. Muscle power output, ATPase rate and myosin filament density also have the same dependence on muscle cell length: increased by 35.4%±6.7, 34.6%±3.4, and 35.6%±10.6 respectively for a 50% increase in cell length. The data can be explained by a model where additional contractile units containing myosin filaments are formed and placed in series with existing contractile units when the muscle is adapted at a longer length.
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