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Force recovery after activated shortening in whole skeletal muscle: transient and steady-state aspects of force depression

Force recovery after activated shortening in whole skeletal muscle: transient and steady-state... The depression of isometric force after active shortening is a well-accepted characteristic of skeletal muscle, yet its mechanisms remain unknown. Although traditionally analyzed at steady state, transient phenomena caused, at least in part, by cross-bridge kinetics may provide novel insight into the mechanisms associated with force depression (FD). To identify the transient aspects of FD and its relation to shortening speed, shortening amplitude, and muscle mechanical work, in situ experiments were conducted in soleus muscle-tendon units of anesthetized cats. The period immediately after shortening, in which force recovers toward steady state, was fit by using an exponential recovery function ( R 2 > 0.99). Statistical analyses revealed that steady-state FD (FD ss ) increased with shortening amplitude and mechanical work. This FD ss increase was always accompanied by a significant decrease in force recovery rate. Furthermore, a significant reduction in stiffness was observed after all activated shortenings, presumably because of a reduced proportion of attached cross bridges. These results were interpreted with respect to the two most prominent proposed mechanisms of force depression: sarcomere length nonuniformity theory (7, 32) and a stress-induced inhibition of cross-bridge binding in the newly formed actin-myosin overlap zone (14, 28). We hypothesized that the latter could describe both steady-state and transient aspects of FD using a single scalar variable, the mechanical work done during shortening. As either excursion (overlap) or force (stress) is increased, mechanical work increases, and cross-bridge attachment would become more inhibited, as supported by this study in which an increase in mechanical work resulted in a slower recovery to a more depressed steady-state force. shortening-induced depression; mechanical work; stress-induced cross-bridge inhibition; sarcomere length nonuniformity; rate of force redevelopment Address for reprint requests and other correspondence: D. T. Corr, The McCaig Centre for Joint Injury & Arthritis Research, Heritage Medical Research Bldg., Univ. of Calgary, 3300 Hospital Dr. N.W., Calgary, AB T2N 4N1, Canada (E-mail: dcorr@ucalgary.ca ) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Applied Physiology The American Physiological Society

Force recovery after activated shortening in whole skeletal muscle: transient and steady-state aspects of force depression

Corr, David T.; Herzog, Walter
Journal of Applied Physiology , Volume 99 (1): 252 – Jul 1, 2005
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Publisher
The American Physiological Society
Copyright
Copyright © 2011 the American Physiological Society
ISSN
8750-7587
eISSN
1522-1601
DOI
10.1152/japplphysiol.00509.2004
pmid
15746298
Publisher site
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Abstract

The depression of isometric force after active shortening is a well-accepted characteristic of skeletal muscle, yet its mechanisms remain unknown. Although traditionally analyzed at steady state, transient phenomena caused, at least in part, by cross-bridge kinetics may provide novel insight into the mechanisms associated with force depression (FD). To identify the transient aspects of FD and its relation to shortening speed, shortening amplitude, and muscle mechanical work, in situ experiments were conducted in soleus muscle-tendon units of anesthetized cats. The period immediately after shortening, in which force recovers toward steady state, was fit by using an exponential recovery function ( R 2 > 0.99). Statistical analyses revealed that steady-state FD (FD ss ) increased with shortening amplitude and mechanical work. This FD ss increase was always accompanied by a significant decrease in force recovery rate. Furthermore, a significant reduction in stiffness was observed after all activated shortenings, presumably because of a reduced proportion of attached cross bridges. These results were interpreted with respect to the two most prominent proposed mechanisms of force depression: sarcomere length nonuniformity theory (7, 32) and a stress-induced inhibition of cross-bridge binding in the newly formed actin-myosin overlap zone (14, 28). We hypothesized that the latter could describe both steady-state and transient aspects of FD using a single scalar variable, the mechanical work done during shortening. As either excursion (overlap) or force (stress) is increased, mechanical work increases, and cross-bridge attachment would become more inhibited, as supported by this study in which an increase in mechanical work resulted in a slower recovery to a more depressed steady-state force. shortening-induced depression; mechanical work; stress-induced cross-bridge inhibition; sarcomere length nonuniformity; rate of force redevelopment Address for reprint requests and other correspondence: D. T. Corr, The McCaig Centre for Joint Injury & Arthritis Research, Heritage Medical Research Bldg., Univ. of Calgary, 3300 Hospital Dr. N.W., Calgary, AB T2N 4N1, Canada (E-mail: dcorr@ucalgary.ca )

Journal

Journal of Applied Physiology – The American Physiological Society

Published: Jul 1, 2005

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