Abstract
Mitochondrial dysfunction is common to many organ system disorders, including skeletal muscle. Aging muscle and diseases of muscle are often accompanied by defective mitochondrial ATP production. This manuscript will focus on the pre-clinical evidence supporting the use of regular exercise to improve defective mitochondrial metabolism and function in skeletal muscle, through the stimulation of mitochondrial turnover. Examples from aging muscle, muscle-specific mutations and cancer cachexia will be discussed. We will also examine the effects of exercise on the important mitochondrial regulators PGC-1α, and Parkin, and summarize the effects of exercise to reverse mitochondrial dysfunction (e.g., ROS production, apoptotic susceptibility, cardiolipin synthesis) in muscle pathology. This paper will illustrate the breadth and benefits of exercise to serve as “mitochondrial medicine” with age and disease.
Highlights
Mitochondria are the principal organelles tasked with the provision of cellular energy in the form of adenosine triphosphate (ATP), which is supplied in equilibrium with the energy demands placed on the cell
As mitochondrial quality control is highly dynamic and relies on the convergence of multiple processes to regulate the function of the organelle network, the development of therapeutic interventions that adequately address all aspects of mitochondrial remodeling remains a challenge to identify
The metabolic nature of skeletal muscle, and the relative proportion of body mass that it comprises, make muscle a unique tissue to study in the context of various diseases
Summary
Reviewed by: Zsolt Radak, Semmelweis University, Hungary Cristina Mammucari, University of Padua, Italy. Mitochondrial dysfunction is common to many organ system disorders, including skeletal muscle. Aging muscle and diseases of muscle are often accompanied by defective mitochondrial ATP production. This manuscript will focus on the pre-clinical evidence supporting the use of regular exercise to improve defective mitochondrial metabolism and function in skeletal muscle, through the stimulation of mitochondrial turnover. Examples from aging muscle, muscle-specific mutations and cancer cachexia will be discussed. We will examine the effects of exercise on the important mitochondrial regulators PGC-1α, and Parkin, and summarize the effects of exercise to reverse mitochondrial dysfunction (e.g., ROS production, apoptotic susceptibility, cardiolipin synthesis) in muscle pathology. This paper will illustrate the breadth and benefits of exercise to serve as “mitochondrial medicine” with age and disease
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