Muscle function and protein metabolism following initiation of
eccentric contraction-induced injury.
Lowe, Dawn A., Gordon L. Warren, Christopher P. Ingalls, and R. B.
Armstrong.
Muscle Biology Laboratory, Texas A&M University, College
Station, Texas 77843-4243
APStracts 2:0261A, 1995.
This study was designed to determine the relationship between skeletal
muscle function and protein metabolism following initiation of
eccentric contraction-induced injury. Mouse anterior crural muscles
were injured in vivo, then either immediately, or 3, 6, 24, 48, 72,
120, or 336 h following injury, muscles were isolated and studied for
indices of muscle function, injury, phagocyte infiltration, and
protein metabolism. A group of mice were administered anti
-polymorphonuclear cell and anti-macrophage antisera in an attempt to
reduce phagocytic infiltration into injured muscle. Force production
in extensor digitorum longus muscles was reduced 55% immediately
following injury induction and did not recover significantly until
120 h post-injury (28% below baseline). However, rates of protein
degradation were not elevated until 48 h post-injury (60% above
normal) and were not correlated with the changes in force production
(r = -0.37; p = 0.24). Phagocytic infiltration was evident 24-120 h
post-injury and was correlated with the elevated protein degradation
rates (r = 0.75; p < 0.01). Protein synthesis rates began to
increase about 48 h after injury was induced and were elevated by 83%
5 days post-injury. Fourteen days after injury, muscle protein
degradation and synthesis rates had returned to normal, as well as
specific force production, and phagocytic infiltration was not
detected. However, muscle mass, protein content, and absolute force
production were lower than normal. Antisera-treated mice were
rendered neutropenic but there was no difference in any variable
measured between muscles from these mice and muscles from normal
mice.
Received 7 April 1995; accepted in final form 26 May 1995.
APS Manuscript Number A379-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 July 1995.