Myonuclear domains in muscle adaptation and disease

• Published in: Muscle & nerve 1999-10, Vol.22 (10), p.1350-1360
• Main Authors: Allen, David L., Roy, Roland R., Edgerton, V. Reggie
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological; Aging - physiology; Animals; apoptosis; Apoptosis - physiology; Biological and medical sciences; fiber size; Fundamental and applied biological sciences. Psychology; Humans; Hypertrophy; Life Sciences (General); Muscle Fibers, Skeletal - physiology; muscle plasticity; Muscle, Skeletal - pathology; Muscle, Skeletal - physiology; Muscle, Skeletal - physiopathology; Muscular Atrophy - physiopathology; Muscular Diseases - physiopathology; myofibers; space flight; Space life sciences; Striated muscle. Tendons; Vertebrates: osteoarticular system, musculoskeletal system
• ISSN: 0148-639X; 1097-4598
• DOI: 10.1002/(SICI)1097-4598(199910)22:10<1350::AID-MUS3>3.0.CO;2-8

Adult skeletal muscle fibers are among the few cell types that are truly multinucleated. Recently, evidence has accumulated supporting a role for the modulation of myonuclear number during muscle remodeling in response to injury, adaptation, and disease. These studies have demonstrated that muscle hypertrophy is associated with, and is dependent on, the addition of newly formed myonuclei via the fusion of myogenic cells to the adult myofiber, whereas muscle atrophy and disease appear to be associated with the loss of myonuclei, possibly through apoptotic-like mechanisms. Moreover, these studies also have demonstrated that myonuclear domain size, i. e., the amount of cytoplasm per myonucleus, is unchanged following the acute phase of hypertrophy but is reduced following atrophy. Together these data demonstrate that modulation of myonuclear number or myonuclear domain size (or both) is a mechanism contributing to the remodeling of adult skeletal muscle in response to alterations in the level of normal neuromuscular activity. Copyright 1999 John Wiley & Sons, Inc.