Exercise is a good thing — it keeps the body and mind fit, maintains healthy weight, and reduces the risk of diabetes, heart disease and cancer. These facts are known to all of us and even as we strive to incorporate activity and exercise in our busy lives, now there is more reason than before.
In a recent article published in Nature, postdoctoral researcher at UT Southwestern Medical Center Congcong He and colleagues showed that exercise boosts autophagy in mammals. Autophagy is the cell's recycling system; using the lysosomal machinery, the cell degrades its own intracellular components and is essential for maintaining cellular homeostasis. Under normal conditions, each cell is a basal level of autophagy. However, under conditions of stress, such as nutrient deprivation, the rate of autophagy is increased to conserve nutrients and to recycle cellular components. Autophagy is also known to protect the cells from infections, cancer and other diseases.
In their study, the researchers found that in mice that were fed, exercise increased the rate of autophagy in skeletal and cardiac muscle tissue. Furthermore, they found that mutations in the BCL2 gene prevented the exercise-induced increase in autophagy. The BCL2 gene plays a role in many cancers and therefore, this link between BCL2 and exercise-induced autophagy is crucial for understanding the relationship between exercise, genes and diseases. The paper also outlines what biochemical pathways are activated in response to exercise and how the autophagy pathway may be activated.
These results present very exciting prospects for understanding how exercise is beneficial to us. But there is more to this research — by identifying the link between exercise, autophagy and BCL2, the scientists have opened up a whole new way of looking at metabolism, disease, genetics and exercise. While we look out for new and exciting results along this vein, let's remember to stay active!
- Explaining Exercise (Science, 2012)
- UT Southwestern Medical Center: Health benefits of exercise may depend on cellular degradation, researchers report