How Exercise Renews Muscle Cells Discovered – Mitophagy

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Exercise was found to make muscles and cells healthier by sending damaged muscle mitochondria for cellular recycling, a mechanism called mitophagy .
Nature Communications published this study explaining the cellular mechanism through which exercise helps keep the body, particularly muscles, healthy and strong. Researchers say bodily health is determined not by whether the blood is healthy, but by muscle volume and exercise capacity.
Exercise Improves Muscle Health by Renewing Mitochondria, the Cellular Powerhouses
Mitochondria are organelles serving as energy stations in cells that perform aerobic respiration. In humans, they occur in all cells except red blood cells. Simply put, mitochondria turn food into energy, converting proteins, fats and sugar into the energy the body needs to live.
How Does Exercise Affect Muscle Mitochondria?
Exercise was found to trigger mitophagy in mice. Mitophagydescribes the destruction and cellular recycling of damaged or dysfunctional mitochondria, generally after stress. It can therefore be considered a muscle-cell-mitochondria-specific form of autophagy .
To show how exercise stimulates mitophagy, researcher Yan and colleagues added a special mitochondrial reporter gene to mouse skeletal muscle. pMitoTimer is the gene that makes muscle cells appear green under a fluorescence microscope when healthy and red if damaged or broken down by lysosomes, the cell’s recycling system.
After mice ran on a small treadmill for 90 minutes, mitochondrial stress and some mitophagy signs appeared six hours later. Researchers explained that exercise activated a kinase enzyme called AMPK, which switched on another kinase, Ulk1. These chemical reactions were important in controlling removal of nonfunctional mitochondria.
Regular exercise therefore helps remove damaged, nonfunctional mitochondria from skeletal muscle. This mechanism can be seen as a biological interpretation of “working iron stays bright” —like a heavily used but regularly maintained machine lasting longer and working more efficiently…
Mice whose Ulk1 gene was deleted, preventing mitophagy, gained no metabolic benefit despite running as much as normal mice. These findings directly support exercise-induced mitophagy and demonstrate its importance.
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Sources
Ampk phosphorylation of Ulk1 is required for targeting of mitochondria to lysosomes in exercise-induced mitophagy.
Nature Communications. 15 September 2017
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