Thermal Activation of Thin Filaments in Striated Muscle

Abstract

In skeletal and cardiac muscles, contraction is triggered by an increase in the intracellular Ca²⁺ concentration. During Ca²⁺ transients, Ca²⁺-binding to troponin C shifts the "on-off" equilibrium of the thin filament state toward the "on" sate, promoting actomyosin interaction. Likewise, recent studies have revealed that the thin filament state is under the influence of temperature; viz., an increase in temperature increases active force production. In this short review, we discuss the effects of temperature on the contractile performance of mammalian striated muscle at/around body temperature, focusing especially on the temperature-dependent shift of the "on-off" equilibrium of the thin filament state.

Keywords: Ca2+ sensitivity; actomyosin; cardiac muscle; skeletal muscle; temperature; tropomyosin; troponin.

FIGURE 1

Schematic showing the effects of altered temperature on functional properties of mammalian striated muscle. (A) Top: relationship of temperature vs. endo-systolic pressure in mammalian hearts. Inset: time-course of ventricular pressure at different temperatures. Blue, gray, and red lines indicate hypothermic, physiological, and hyperthermic conditions, respectively. Middle: relationship of temperature vs. Ca²⁺ transients (left) and twitch force (right) in intact muscles. Blue, gray, and red lines indicate hypothermic, physiological, and hyperthermic conditions, respectively. Bottom: relationship of temperature vs. Ca²⁺ sensitivity (left) and maximal force (right) in skinned muscles. (B) Effects of rapid cooling (left; shown in blue bar) or rapid heating (right; shown in red bar) on [Ca²⁺]_i (top) and force (bottom) in intact cardiomyocytes. Rapid cooling increases both [Ca²⁺]_i and force, while rapid heating increases force with little or no influence on [Ca²⁺]_i. (C) Effects of a change in temperature on thin filaments. Increasing temperature 1) enhances Ca²⁺ binding to TnC (see top graph) and 2) induces Ca²⁺-independent thermal activation of thin filaments via partial dissociation of the Tn–Tm complex from actin (see bottom graph), thereby coordinately acting to increase the fraction of the “on” state of thin filaments. See text for details.