title: Fatigue vs. shortening-induced deactivation in striated muscle.
abstract: Fatigue and shortening-induced deactivation, two conditions that both lead to reversible depression of the mechanical performance of striated muscle are briefly reviewed. Fatigue. Isolated fibres from frog skeletal muscle (1-3 degrees C) that are stimulated to produce a 1 s fused tetanus at 15 s intervals are brought into a state of myofibrillar fatigue, (tetanic force reduced to 70-75% of the control) that is attributable to reduced performance of the myofibrils with no significant change in activation of the contractile system. A more intense stimulation programme (a single stimulus applied at 1-2 s intervals) reduces the tetanic force below 70% of the rested-state level. Under these conditions, failure of activation becomes increasingly important as a cause of the force decline. Deficient inward spread of activation is likely to account for at least part of the force decline after a period of intense fatiguing stimulation. Shortening-induced deactivation. Striated muscle that is allowed to shorten during activity loses some of its capacity to produce force, full restoration of the contractile strength being attained 1-2 s after the shortening phase. The depressant effect of shortening is demonstrable in skinned preparations as well as in intact muscle fibres and the magnitude of the effect is dependent on the state of activation of the muscle fibre when the movement occurs. The experimental evidence supports the view that sliding of the thick and thin filaments during activity reduces the affinity for calcium at the regulatory sites on the thin filament, leading to a transitory deactivation of the contractile system.
authors.affiliation: Department of Pharmacology, University of Lund, Sweden.
authors.forename: K A
authors.initials: KA
authors.lastname: Edman
mesh_terms: D000818:Animals; D006801:Humans; D009119:Muscle Contraction / Q000502:physiology*; D018763:Muscle Fatigue / Q000502:physiology*; D009132:Muscles / Q000502:physiology* / Q000648:ultrastructure; D009210:Myofibrils / Q000502:physiology