Role of exercise in improving skeletal muscle mitochondrial respiratory capacity and dynamics

The American College of Sports Medicine (ACSM) characterizes exercise as a specialized form of physical activity that is intentionally planned, structured, repetitive, and aimed at enhancing or sustaining physical fitness. Exercise elicits adaptations in skeletal muscle, largely attributed to its remarkable plasticity. These training-induced adaptations manifest as alterations in contractile proteins and function, metabolic regulation, transcriptional responses, epigenetic modifications, intracellular signaling pathways, and mitochondrial function. Thus, physical activity activates transcription factors that enhance mitochondrial biogenesis, leading to increased mitochondrial content and changes in composition, such as the protein-to-lipid ratio and protein import machinery components. Mitochondrial dynamics involve processes like fusion (combining mitochondria) and fission (dividing a mitochondrion into two), which are crucial for maintaining functional mitochondria. Research led by our group found that both acute and chronic exercise improve mitochondrial respiratory capacity in mouse skeletal muscle, though there were no significant changes in membrane potential or the redox state of CoQ.
In this study we would like to further investigate the mitochondrial adaptations in skeletal muscle following acute and chronic exercise. The present research aims to identify the key mitochondrial adaptations responsible for the increased mitochondrial respiratory capacity in skeletal muscle during acute and chronic exercise.
The specific objectives are:
a) To investigate the protein content of mitochondrial proteins within the oxidative phosphorylation that contribute to the observed increase in mitochondrial respiration during acute exercise
b) To explore mitochondrial dynamics by studying key proteins and assess potential mitochondrial supercomplexes formation formed during acute and chronic exercise and their impact on enhancing mitochondrial oxygen consumption.