Soleus fiber force and maximal shortening velocity after 14 days of
intermittent and non-weight bearing.
Widrick, Jeffrey J., Jill J. Bangart, Miloslav Karhanek, and Robert H.
Fitts.
Department of Biology, Marquette University, Milwaukee, WI
53201
APStracts 2:0496A, 1995.
This study examined the effectiveness of intermittent weight bearing
as a countermeasure to non-weight bearing induced alterations in
soleus type I fiber force (in mN), tension (force/fiber cross
-sectional area, or P0, in kN x m-2), and maximal unloaded shortening
velocity (V0, in fiber length x s-1). Adult rats were assigned to one
of the following groups: normal weight-bearing (WB), 14 d of hindlimb
non-weight bearing (NWB), and 14 d of hindlimb non-weight bearing
with intermittent weight bearing treatments (IWB). The IWB treatment
consisted of four 10 min periods of standing weight bearing each d.
Single chemically permeabilized soleus fiber segments were mounted
between a force transducer and position motor and studied at maximal
Ca2+ activation afterwhich type I fiber myosin heavy chain
composition was confirmed by SDS-PAGE. NWB resulted in a loss in
relative soleus mass (-45%), with type I fibers displaying reductions
in diameter (-28%) and peak isometric force (-55%) and an increase in
V0 (+33%). In addition, NWB induced a 16% reduction in type I fiber
P0, a 41% reduction in type I fiber peak elastic modulus (E0, defined
as (delta force/delta length) x (fiber length/fiber cross-sectional
area)), and a significant increase in the P0/E0 ratio. In comparison
to NWB, IWB reduced the loss of relative soleus mass (by 22%) and
attenuated alterations in type I fiber diameter (by 36%), peak force
(by 29%), and V0 (by 48%) but had no significant effect on P0, E0, or
the P0/E0 ratio. These results indicate that a modest restoration of
weight bearing activity during 14 d of NWB is sufficient to attenuate
type I fiber atrophy and to partially restore type I peak isometric
force and V0 to WB levels. However, the NWB induced reductions in P0
and E0, which we hypothesize to be due to a decline in the number and
stiffness of cross-bridges, respectively, are considerably less
responsive to this countermeasure treatment.
Received 20 March 1995; accepted in final form 27 October 1995.
APS Manuscript Number A300-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 November 95