Sami Mansfield: My new favorite exercise oncology word is myokines

Quoting William Wallace‘s post:

“The muscle-brain connection: The role of exercise-induced myokines in combatting aging-delated disease(s).

Last week, I made a post on myokines – signaling molecules secreted by muscles in response to exercise, and their impact on multiple different organ systems. This post is meant to highlight how exercise modalities influence myokine release and, by extension, their potential to mitigate aging-related cognitive decline and muscle dysfunction.

Physical exercise has long been recognized for its myriad health benefits, including its protective effects against sarcopenia and neurodegenerative diseases. The secret behind exercise’s systemic benefits lies in part in myokines, which serve as messengers in the muscle-brain crosstalk.

Myokines are a diverse group of peptides and proteins with the ability to facilitate communication between skeletal muscles and various organs, including the brain. They are highly important in processes such as neuroprotection, inflammation modulation, and the regulation of energy metabolism. Specific myokines released in response to exercise include: brain-derived neurotrophic factor (BDNF) and insulin-like growth factor 1 (IGF-1), vascular endothelial growth factor (VEGF), cathepsin B (CATB), irisin, Interleukin-6 (IL-6) etc.

Different forms of exercise )e.g., aerobic exercise, resistance exercise, and combined exercise) affect myokine secretion (and all somewhat differently). Aerobic exercise emerges as a particularly potent stimulator of a broad array of myokines, reinforcing its role in enhancing both cognitive functions and muscle health during aging.

The differential impacts of these exercise types on myokine levels suggests potential importance of tailored exercise prescriptions to maximize health benefits, especially among aging populations.”