Effect of activation on force velocity properties of muscles during cyclical length changes


Meeting Abstract

P1-73  Monday, Jan. 4 15:30  Effect of activation on force velocity properties of muscles during cyclical length changes. TAHIR, U*; NISHIKAWA, KC; Northern Arizona University ut5@nau.edu

The sliding filament theory was proposed over 50 years ago and remains largely unchanged despite the fact that it fails to predict a number of important muscle properties. These properties enable muscles to change their force output in response to changes in load, length and velocity instantaneously without input from the nervous system. The force velocity relationship (FVR) describes how muscle force decreases with increasing shortening velocity, up to maximum shortening velocity, Vmax, and how muscle force increases with increasing stretch velocity. The FVR is typically attributed to the attachment and detachment kinetics of the cross bridges, but is often only studied in supra-maximally activated muscles in after-loaded isotonic contractions. This relationship can also be obtained from experiments in which muscles experience cyclical length changes demonstrating history dependent properties. The goal of the present study was to use work loop experiments to investigate how the FVR of muscles varies with activation. Soleus muscles from mice were isolated and attached to a force lever that measured muscle force and length during imposed length changes. Muscles were stretched and shortened cyclically over a range of lengths from ±2% to ±10% of optimum muscle length and activation levels of 100% to 0% of maximum activation. Force velocity curves were constructed from the data at all activation levels. Though seldom studied, passive muscles also display a force-velocity relationship. The curves were scaled to maximum activation to compare their shapes at different activation levels. Preliminary data suggest that force velocity curves from active muscles scale linearly with activation. The shape of the force-velocity curve differs between passive and active muscles, suggesting that a mechanism other than the cross bridges may contribute to the FVR in passive muscles.

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