Changes in the force–velocity relationship of fatigued muscle: implications for power production and possible causes
This review was presented at The Journal of Physiology Symposium on Modern views on muscle physiology and pathophysiology: Progress along the trail blazed by Professor Richard HT Edwards, which took place at the Joint Meeting of the Scandinavian and German Physiological Societies, Copenhagen, Denmark, 27 March 2010. It was commissioned by the Editorial Board and reflects the views of the author.
Abstract
Slowing of the contractile properties of skeletal muscle is one of the characteristic features of fatigue. First studied as a slowing of relaxation from an isometric contraction, it has become apparent that this slowing is indicative of functional changes in muscle responsible for a major loss of power with all its functional repercussions. There are three factors contributing to the loss of power in mammalian muscle at physiological temperatures, a decrease in isometric force, which mainly indicates a reduction in the number of active cross bridges, a slowing of the maximum velocity of unloaded shortening and an increased curvature of the force–velocity relationship. This latter change is a major cause of loss of power but is poorly understood. It is probably associated with an increase in the proportion of cross bridges in the low force state but there are no clear candidates for the metabolic changes that are responsible for this shift in cross bridge states. The possibility is discussed that the reduction in activating calcium that occurs with metabolically depleted muscle, alters the distribution of cross bridge states, affecting both shortening velocity and curvature.
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