Muscle Changes During Atrophy

Abstract

Muscle atrophy typically is a direct effect of protein degradation induced by a diversity of pathophysiologic states such as disuse, immobilization, denervation, aging, sepsis, cachexia, glucocorticoid treatment, hereditary muscular disorders, cancer, diabetes and obesity, kidney and heart failure, and others. Muscle atrophy is defined by changes in the muscles, consisting in shrinkage of myofibers, changes in the types of fiber and myosin isoforms, and a net loss of cytoplasm, organelles and overall a protein loss. Although in the literature there are extensive studies in a range of animal models, the paucity of human data is a reality. This chapter is focused on various aspects of muscle wasting and describes the transitions of myofiber types during the progression of muscle atrophy in several pathological states. Clinical conditions associated with muscle atrophy have been grouped based on the fast-to-slow or slow-to-fast fiber-type shifts. We have also summarized the ultrastructural and histochemical features characteristic for muscle atrophy in clinical and experimental models for aging, cancer, diabetes and obesity, and heart failure and arrhythmia.

Keywords: Clinical conditions; Fiber-type shift; Immunohistochemistry markers; Molecular alterations; Muscle atrophy.