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Disproportionate loss of thin filaments in human soleus muscle after 17‐day bed rest
Author(s) -
Riley Danny A.,
Bain James L.W.,
Thompson Joyce L.,
Fitts Robert H.,
Widrick Jeffrey J.,
Trappe Scott W.,
Trappe Todd A.,
Costill David L.
Publication year - 1998
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199810)21:10<1280::aid-mus6>3.0.co;2-7
Subject(s) - bed rest , rest (music) , soleus muscle , human muscle , chemistry , biophysics , medicine , physical medicine and rehabilitation , endocrinology , skeletal muscle , biology
Previously we reported that, after 17‐day bed rest unloading of 8 humans, soleus slow fibers atrophied and exhibited increased velocity of shortening without fast myosin expression. The present ultrastructural study examined fibers from the same muscle biopsies to determine whether decreased myofilament packing density accounted for the observed speeding. Quantitation was by computer‐assisted morphometry of electron micrographs. Filament densities were normalized for sarcomere length, because density depends directly on length. Thick filament density was unchanged by bed rest. Thin filaments/μm 2 decreased 16–23%. Glycogen filled the I band sites vacated by filaments. The percentage decrease in thin filaments (Y) correlated significantly ( P < 0.05) with the percentage increase in velocity (X), (Y = 0.1X + 20%, R 2 = 0.62). An interpretation is that fewer filaments increases thick to thin filament spacing and causes earlier cross‐bridge detachment and faster cycling. Increased velocity helps maintain power (force × velocity) as atrophy lowers force. Atrophic muscles may be prone to sarcomere reloading damage because force/μm 2 was near normal, and force per thin filament increased an estimated 30%. © 1998 John Wiley & Sons, Inc. Muscle Nerve 21:1280–1289, 1998.