February 9, 2012

We all know that exercise is good for our bodies, and when we hear people talking about it in the media, the benefits are discussed in big-picture terms. A recent paper describes the effects of exercise at the cellular level, and gives me new motivation to get my ass in gear. Well, after I finish this heart-shaped Dunkin’ Donut (don’t give me that smug look…you know it’s delicious).

Autophagy is the process in which a cell metabolizes its own organelles and proteins. Autophagy takes place in the lysosome at a normal rate to rid the cell of old organelles, but is induced at higher rates in response to cellular stress to allow the cell to adjust to changing nutritional needs. A recent study finds that exercise can induce autophagy in muscle cells. In this paper, He and colleagues tracked autophagy in mice after they ran on treadmills. As seen in the images above, the number of autophagosomes (green dots) in the tibialis anterior muscle was higher in mice after 80 minutes of exercise (right), compared to before the exercise (left). Mice with a genetic mutation that prevented exercise-induced autophagy had lower endurance for exercise and had altered glucose metabolism. These fascinating findings provide us with a cellular understanding of how exercise prolongs life and protects our bodies from diseases such as diabetes and cancer.

He, C., Bassik, M., Moresi, V., Sun, K., Wei, Y., Zou, Z., An, Z., Loh, J., Fisher, J., Sun, Q., Korsmeyer, S., Packer, M., May, H., Hill, J., Virgin, H., Gilpin, C., Xiao, G., Bassel-Duby, R., Scherer, P., & Levine, B. (2012). Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis Nature, 481 (7382), 511-515 DOI: 10.1038/nature10758
Adapted by permission from Macmillan Publishers Ltd, copyright ©2012