Sarcopenia is defined as the age-related loss of skeletal muscle strength, power, and size. Understanding the fundamental mechanisms whereby sarcopenia occurs is an area of research that has received much attention due to the aging population. Skeletal muscle tissue is used for locomotion and acts as a major site aiding the regulation of metabolism. Myokines are cytokines released from skeletal muscle tissue that act in an autocrine, paracrine, or endocrine manner. Myokines have been termed the ‘exercise factor’ or ‘work factor’ that scientists have long thought communicate between skeletal muscle and various physiological systems, including muscle-to-muscle cross-talk. One area of research that has been underexplored is the effect that myokines may have in an autocrine manner on skeletal muscle tissue itself. Although the myokine role in skeletal muscle hypertrophy and atrophy has been somewhat elucidated in rodent models, relatively little research has been performed in human models to understand the role myokines have on anabolic and catabolic metabolism in an autocrine manner. This review will provide an overview of myokine function within a biological context, some molecular pathways involved in skeletal muscle anabolism, a mechanistic understanding of myokine autocrine action, key evidence in relation to skeletal muscle satellite cell interaction with myokines, how myokines may be involved in skeletal muscle regeneration, and an outline of some key myokines that have the potential to act in an anabolic fashion within skeletal muscle. The review will then emphasize some important areas of research that are needed to understand the role of myokines in maintaining or improving skeletal muscle mass within an aging context.
Cornish et al. (Wed,) studied this question.