Activity-induced fiber regeneration in rat soleus muscle

Abstract

In an attempt to understand why muscle recovery is limited following atrophy due to limb immobilization, satellite cell activity and muscle fiber regeneration were analyzed in rat soleus muscles. Adult rat hindlimbs were immobilized in plaster casts for a period of two to ten weeks. Soleus muscles were examined by electron microscopy for evidence of fiber degeneration or regeneration, and to quantify satellite cell nuclei. Immunocytochemical localization of embryonic myosin was used to identify regenerating myofibers. Soleus muscle wet weight to body weight ratios for the casted muscles significantly decreased over the 10-week immobilization period. The casted muscles displayed ultrastructural evidence of minor fiber damage, including myofibrillar atrophy, Z-disc disruption, and abnormal triadic junctions. No ultrastructural evidence of regeneration was seen in the casted animals. The number of satellite cells in the casted muscles significantly decreased from 6.4% to 3.3% by eight to 10 weeks of immobilization. Approximately 1.0% of extrafusal fibers in the control soleus muscles appeared to be regenerating since they expressed embryonic myosin and were of a small diameter, while in casted muscles, only 0.1% of the fibers were embryonic myosin-positive. Following release from immobilization, a reappearance of embryonic myosin-positive fibers was noted within four days of renewed activity. In contrast to control muscles, embryonic myosin-positive fibers in the recovery muscles included both small and large diameter fibers. Subtle changes in functional activity influence muscle damage and subsequent myofiber regeneration. Reduced activity reduces muscle fiber regeneration, while increased activity, as seen by increased hindlimb weight bearing and return to normal activity following immobilization, increase regenerating fibers and also the expression of embryonic myosin in adult fibers.

Morphological effects of two protocols of passive stretch over the immobilized rat soleus muscle

“…Some studies have reported that hypokinesia produces marked changes in skeletal muscle fibres (Baranska et al 1983(Baranska et al , 1997Flynn & Max, 1985;Wanek & Snow, 2000). The degenerative process, and atrophy in particular, depends on the duration of hypokinesia as well as on the position of immobilization and the type of muscle evaluated (Williams & Goldspink, 1978;Baker & Matsumoto, 1988;Williams, 1988Williams, , 1990.…”

Fitness and physical activity in youth with type 1 diabetes mellitus in good or poor glycemic control

“…Myopathy plays a significant role in childhood as the impairment in skeletal muscle growth results in remodeling of the muscle that can negatively impact the long-term physical and metabolic properties of the tissue. In contrast, adult skeletal muscle is capable of returning to its prestimulus state upon removal of the atrophic stimulus (2)(3)(4)(5). This indicates that developing muscle may be more vulnerable to myopathic effects compared to fully developed (mature) skeletal muscle tissue.…”

Effects of type 1 diabetes mellitus on skeletal muscle: clinical observations and physiological mechanisms

“…This adaptability of muscle is not limited solely to hypertrophy. Atrophic stimuli, such as casting or various disease states, result in a decrease in muscle mass, strength, and progenitor cell number (7)(8)(9). It is important to note that atrophic stimuli placed on adolescent muscle results in a rapid and irreversible remodeling process (7,8).…”

“…It is important to note that atrophic stimuli placed on adolescent muscle results in a rapid and irreversible remodeling process (7,8). In contrast to adolescent muscle, however, removal of the atrophic stimulus from adult skeletal muscle returns it to a preatrophy state, including its capacity for myofiber regeneration (7,9). Two very important points are gleaned from these studies: (i) adolescent muscle and adult muscle may respond differently to similar stimuli; and (ii) atrophic stimuli, such as poorly controlled T1DM, placed on developing muscle may lead to a lifetime of reduced physical and metabolic capacities.…”