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.
Highlights
Under physiological conditions, striated muscle generates force and heat
Physiologists have long perceived that a change in body temperature affects the mechanical properties of skeletal and cardiac muscles, such as active force generation and shortening velocity
We briefly review the effects of temperature on the mechanical properties of skeletal and cardiac muscles in the range between ∼36 and ∼40◦C, and discuss how striated muscle works efficiently at/around body temperature
Summary
Specialty section: This article was submitted to Striated Muscle Physiology, a section of the journal Frontiers in Physiology. 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. 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
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