Abstract
Muscles convert chemical energy to mechanical work. Mechanical performance of a muscle is often assessed by the muscle’s ability to shorten and generate power over a range of loads or forces, characterized by the force–velocity and force–power relationships. The hyperbolic force–velocity relationship of muscle, for a long time, has been regarded as a pure empirical description of the force–velocity data. Connections between mechanical manifestation in terms of force–velocity properties and the kinetics of the crossbridge cycle have only been established recently. In this review, we describe how the model of Huxley’s crossbridge kinetics can be transformed to the hyperbolic Hill equation, and link the changes in force–velocity properties to molecular events within the crossbridge cycle driven by ATP hydrolysis. This allows us to reinterpret some findings from previous studies on experimental interventions that altered the force–velocity relationship and gain further insight into the molecular mechanisms of muscle contraction under physiological and pathophysiological conditions.
Highlights
INTRODUCTIONAn activated muscle is able to exert force or carry a load while shortening. The velocity of shortening decreases as the load or force on the muscle increases
Data from Hill’s (1938) study suggested that the mechanics of muscle contraction could be linked to the muscle’s energy metabolism, because the same hyperbolic force–velocity relationship could be derived from heat measurements and the constant a was derived from the thermal constant of shortening heat—α (Hill, 1938)
Mechanical manifestation of muscle activation captured in the force–velocity relationship is a window through which the molecular events of the crossbridge cycle can be observed
Summary
An activated muscle is able to exert force or carry a load while shortening. The velocity of shortening decreases as the load or force on the muscle increases. The following discussion focuses on interventions that alter the force–velocity curvature It has been shown in earlier discussions that changes in the arrangement of sarcomeres, partial activation, and internal loads do not fundamentally alter the force–velocity relationship, because after normalization of force and velocity, the force–velocity curvature remains the same. Observations from many studies comparing the force–velocity relationships in fast and slow muscles, revealed that fast muscles, besides having higher Vmax, have less curvature (lower values for Fmax/a; Katz, 1939; Close, 1964; Woledge, 1968; Cecchi et al, 1978; Lännergren, 1978; Luff, 1981; Lännergren et al, 1982; Ranatunga, 1982; Brooks and Faulkner, 1988; Stienen et al, 1988; Barclay et al, 1993; Wahr and Metzger, 1998; Gilliver et al, 2009) This means that fast muscles possess a greater power output than slow muscles do, by having a faster shortening velocity, and by having less curvature in their force–velocity curves. The improvement in energetic efficiency may come as a result of fewer negatively strained bridges
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