Estradiol effect on anterior crural muscles:tibial bone
relationship and susceptibility to injury.
Warren, Gordon L., Dawn A. Lowe, Cindi L. Inman, Otto M. Orr, Harry A.
Hogan, Susan A. Bloomfield, and R. B. Armstrong.
Muscle Biology Laboratory and Department of Mechanical Engineering,
Texas A&M University, College Station, Texas 77843
APStracts 3:0067A, 1996.
The study's objective was to determine if estradiol (E2) deficiency
alters the functional relationship of muscle to bone and causes a
differential increase in injury susceptibility. Ovariectomized, six
week-old mice were administered E2 (40 [mu]g/day/kg) (n = 8) or the
oil vehicle (n = 8) for 21 days. The anterior crural muscles of the
left hindlimb were then stimulated to produce 150 maximal in vivo
eccentric contractions. In vitro functional measurements were then
made on the EDL muscle and tibia from both the exercised and
unexercised legs. The maximal isometric torque produced by the
anterior crural muscles prior to the eccentric contraction protocol
and the unexercised EDL maximal isometric tetanic force (Po) were
higher in E2-treated mice by 18 and 14%, respectively (p /=
0.59). No evidence for increased injury susceptibility was found in
either tissue from E2-deficient mice. In fact, the decrement in Po
was only 36.9 +/- 3.8 % in exercised EDL muscles from E2-deficient
mice compared with 50.6 +/- 4.2 % in exercised muscles from E2
-treated mice (p = 0.03). Tibia stiffness was 3.9% higher in bones
from exercised legs than in bones from unexercised legs (72.64 +/-
2.77 vs. 69.95 +/- 2.66 N/mm; p = 0.05) with ultimate load showing a
similar trend (p = 0.07); no effect of E2 status was observed on
these differences (p >/= 0.53). In conclusion, the functional
relationship of bone to muscle and the susceptibility to injury in
bone are not altered by the presence of E2 in ovariectomized mice;
however, E2 does increase injury susceptibility in the EDL muscle.
Received 19 July 1995; accepted in final form 22 December 1995.
APS Manuscript Number A787-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 February 96