Key result
A reduction in muscle contractile activity removes the metabolic and mechanical incentives that trigger myh7 gene expression, leading to decreased slow myosin expression.
Why the study?
While mechanisms underlying slow myosin expression during increased contractile activity are largely understood, far less is known about mechanisms causing decreased MYHC I(beta) expression under reduced contractile activity.
The review highlights that tonic muscle activity is essential for maintaining slow myosin (myh7) expression, and its reduction leads to decreased expression of this muscle tone gene.
This is the authors' abstract. We don't add key points for this paper.
One of the main gravity-determined functions of the locomotor system is to maintain an upright posture. According to the views developed in the scientific school of Prof. I.B. Kozlovskaya, these functions are provided by the tonic muscular system. Under the term “tonic system” I.B. Kozlovskaya meant all the structures and regulatory mechanisms able to maintain basal mechanical tension (tone) for a long time. In mammals, she assigned to the tonic system the slow-twitch muscle fibers with a predominant expression of the myosin heavy chain beta slow isoform, MYHC I(β), and all the neural mechanisms of their control. It is quite obvious that the muscle’s ability to maintain tonic tension for a long time depends on the intensity of slow-myosin expression. Therefore, it would not be a great exaggeration if we call the slow myosin gene myh7 the true muscle tone gene. In the recent years, it has generally become clear how, against the background of prolonged increased muscle contractile activity, an increase in the expression of the slow MYHC isoform and a decrease in the expression of fast MYHC isoforms are triggered. Far less is known about the mechanisms behind a decrease in the expression of MYHC I(β) caused by a decrease in muscle contractile activity. This phenomenon was observed after exposure to true (spaceflight) weightlessness, after bed-rest hypokinesia and “dry” immersion, and also when using a standard rodent hindlimb suspension (unloading) model. Numerous studies of the myosin phenotypic plasticity are mainly concentrated on the search for the mechanisms that link changes in the expression of myosin genes with the muscle contractile activity pattern. The data discussed in the review indicate that constant expression of slow myosin is controlled by tonic activity and, in turn, is a prerequisite for maintaining such an activity. When this activity is considerably reduced or stopped, the metabolic and mechanical incentives, which trigger the signaling pathways of myh7 gene expression, disappear. Exactly this phenomenon is in the focus of this work.
Tonic activity may sustain myh7 expression; leaves open whether modulating it affects cardiac myosin phenotypes in humans.
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Shenkman et al. (2021) conducted a review in Decreased muscle contractile activity. Decreased muscle contractile activity was evaluated on myh7 gene expression. A reduction in muscle contractile activity removes the metabolic and mechanical incentives that trigger myh7 gene expression, leading to decreased slow myosin expression.
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