Function of specialized regulatory proteins and signaling pathways in exercise-induced muscle mitochondrial biogenesis

AbstractSkeletal muscle mitochondrial content and function are regulated by a number of specialized molecular pathways that remain to be fully defined. Although a number of proteins have been identified to be important for the maintenance of mitochondria in quiescent muscle, the requirement for these appears to decrease with the activation of multiple overlapping signaling events that are triggered by exercise. This makes exercise a valuable therapeutic tool for the treatment of mitochondrially based metabolic disorders. In this review, we summarize some of the traditional and more recently appreciated pathways that are involved in mitochondrial biogenesis in muscle, particularly during exercise

Exercise, Muscle, and Mitochondria: Signaling Mechanisms, Health Consequences and New Challenges for the Future

Habitual physical activity has long been heralded as a laudable lifestyle behaviour, which can improve overall health and help stave off many major chronic diseases. In spite of substantial scientific evidence and public awareness about the importance of incorporating physical activity into our daily lives, the majority of the North American society remains insufficiently active, failing to meet the minimum requirements set forth by global health authorities. According to the World Health Organization, physical inactivity is now regarded as the 4th leading risk factor for premature death worldwide(1). In fact, recent research suggests that physical inactivity is responsible for approximately 6-10% of the world’s major noncommunicable diseases(2). These pathological conditions - which include cardiovascular disease, type 2 diabetes, and various types of cancers - account for nearly one third of all deaths that occur annually throughout the world, indicating just how important physical activity is in preventing the onset of disease

Recent advances in mitochondrial turnover during chronic muscle disuse

Chronic muscle disuse, such as that resulting from immobilization, denervation, or prolonged physical inactivity, produces atrophy and a loss of mitochondria, yet the molecular relationship between these events is not fully understood. In this review we attempt to identify the key regulatory steps mediating the loss of muscle mass and the decline in mitochondrial content and function. An understanding of common intracellular signaling pathways may provide much-needed insight into the possible therapeutic targets for treatments that will maintain aerobic energy metabolism and preserve muscle mass during disuse conditions