Glycative stress and skeletal muscle dysfunctions: as an inducer of "Exercise-Resistance."

Abstract

Skeletal muscle, the largest tissue in the body, is often overlooked for its role as a locomotor organ, however over the past few decades it has been revealed that it also has an important role as a metabolic organ. In recent years, its role as an endocrine organ that controls the homeostatic functions of organs throughout the body mediated by myokine secretion has come under close scrutiny. Skeletal muscle is indispensable for our daily life activities, and in order to maintain its function, it is necessary to understand the factors that deteriorate muscle function and establish a countermeasure. Glycative stress has recently received attention as a factor that impairs skeletal muscle function. Accumulation of advanced glycation end products (AGEs) in skeletal muscle impairs contractile function and myogenic potential. Furthermore, AGEs in the blood elicit inflammatory signals through binding to RAGE (Receptor for AGEs) expressed on muscle cells, resulting in muscle proteolysis. Habitual exercise is important to mitigate the negative effects of such glycative stress on skeletal muscle. On the other hand, it is known that the beneficial effects of exercise vary among individuals. The state in which the effects of exercise are difficult to obtain is called "exercise-resistance," and we hypothesize that glycative stress may be one of the causes of exercise-resistance. In this paper, we will discuss the possibility of glycative stress as an inducer of exercise resistance and summarize its impacts on skeletal muscle.