Regular exercise enhances mitochondrial function by promoting healthy mitochondrial remodeling, but the underlying mechanisms are not thoroughly understood. An emerging hypothesis suggests that, in addition to anabolic events such as mitochondria biogenesis, the selective degradation of dysfunctional mitochondria (i.e., mitophagy) also is a key component of exercise-mediated adaptations in striated muscle, which eventually leads to better mitochondrial functions.
Mitophagy is a key component in exercise-induced adaptations at the mitochondrial reticulum in both skeletal muscle and heart.
Department of 1Pharmacology,
2Center for Skeletal Muscle Research at the Robert M. Berne Cardiovascular Research Center,
3Departments of Medicine, and
4Molecular Physiology and Biological Biophysics, School of Medicine, University of Virginia, Charlottesville, VA
Address for correspondence: Zhen Yan, Ph.D., Center for Skeletal Muscle Research at the Robert M. Berne Cardiovascular Research Center, School of Medicine, University of Virginia, 409 Lane Road, MR4-6031A, Charlottesville, VA 22908 (E-mail: firstname.lastname@example.org).
Accepted for publication: March 19, 2019.
Editor: Marni D. Boppart, Sc.D., FACSM.
Online date: April 15, 2019