Abstract
In response to exercise, the oxidative capacity of mitochondria within skeletal muscle increases through the coordinated expression of mitochondrial proteins in a process termed mitochondrial biogenesis. Controlling the expression of mitochondrial proteins are transcription factors—a group of proteins that regulate messenger RNA transcription from DNA in the nucleus and mitochondria. To fulfil other functions or to limit gene expression, transcription factors are often localised away from DNA to different subcellular compartments and undergo rapid movement or accumulation only when required. Although many transcription factors involved in exercise-induced mitochondrial biogenesis have been identified, numerous conflicting findings and gaps exist within our knowledge of their subcellular movement. This review aims to summarise and provide a critical analysis of the published literature regarding the exercise-induced movement of transcription factors involved in mitochondria biogenesis in skeletal muscle.
Highlights
As a result of their bacterial origin, mitochondria cannot be created de novo and are instead made through mitochondrial biogenesis—a process most commonly defined as the synthesis of new components of the mitochondrial reticulum [12]
This review aims to summarise the current knowledge and provide a critical analysis of the exercise-induced movement of transcription factors involved in mitochondrial biogenesis in human skeletal muscle
The activity of AMPK is further upregulated by the reactive oxygen species (ROS) nitric oxide (NO−), a relationship that has been demonstrated by immunoblotting of in vitro rat myotubules [168,169]
Summary
Skeletal muscle comprises approximately 40% of an average human’s total mass [1]. The primary role of skeletal muscle is the conversion of chemical energy into mechanical movement, which can range from walking to world-class sporting performance. An inner mitochondrial membrane (IMM) forms the folded cristae—a structure important for energy generation that separates the IMS from the encapsulated interior matrix [5]. Larger molecules and proteins can move into the IMS through association with the translocase of the outer membrane (TOM) complex and into the matrix. Intermyofibrillar mitochondria (IMF), which comprise the remaining 90% of the total mitochondrial volume, are smaller and capable of compacting between myofibrils—the contractile filaments composed of the motor proteins actin and myosin [10]. Both mitochondrial populations are discrete, mapping of. While not as crucial for providing energy to myofibrils, SS mitochondria still play a vital role in exercise by heavily regulating calcium homeostasis and muscle contraction [10]
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