Muscle fiber type-2 atrophy

One endurance-related measure uses either the number of repetitions that can be performed at 20, 25, or 50% of maximum peak torque or force. The units used to reflect endurance in this case are number of repetitions at a specified torque or force level. One difficulty with this definition has been described previously, that is, the issue of relative vs. absolute muscle endurance. Rothstein and Rose [1982] demonstrated that elderly subjects with selected muscle fiber type atrophy were able to maintain 50% of their peak torque longer than young subjects. However, if a high force level is required to perform the task, then the younger subject would have more endurance in that particular activity [Rothstein, 1982]. Another difficulty is that the repetition method can be used only for dynamic activities. If isometric activities are involved, then the time an activity can be sustained at a specified force or torque level is measured. Why have different units of endurance Time could be used in both cases. Furthermore, the issue of absolute vs. relative muscle endurance becomes irrelevant if the demands of the task are measured. 

The histopathological features of muscle samples from patients with myotonic dystrophy are not particularly distinctive. Early changes appear to be a selective atrophy of type 1 fibers, and hypertrophy of type 2 fibers, but the biochemical and/or physiological basis of these possibly related phenomena is not known. The incidence of degenerating fibers increases with age, although the presence of internally nucleated muscle fibers in early stages of the disease suggests that the muscle retains... 

Figure 16. Werdnig-Hoffman disease most muscle fibers show severe atrophy with some type 1 (dark) fibers showing hypertrophy.

Biopsy findings show disseminated muscle fiber atrophy which is confined to type 2 fibers, in many instances with type 2B (glycolytic) fibers most affected (Figure 23). Muscle necrosis is not seen, though at ultrastructural level focal myofibrillar disruption and myofilament loss may be evident. The muscle atrophy seems to be due to decreased protein synthesis, and at high doses, to increased catabolism. The reason for the selective effect on phasic, glycolytic fibers is not clear since, although steroids interfere with carbohydrate metabolism and oxidative capacity, there seems to be no overall effect on ATP levels. Nevertheless it has been... 

Primary hyperparathyroidism occurs as a result of hyperplasia or the occurrence of adenoma. Secondary hyperparathyroidism may result from renal failure because of the associated phosphate retention, resistance to the metabolic actions of PTH, or impaired vitamin D metabolism. The last-mentioned factor is primarily responsible for the development of osteomalacia. Muscle symptoms are much more common in patients with osteomalacia than in primary hyperparathyroidism. Muscle biopsy has revealed disseminated atrophy, sometimes confined to type 2 fibers, but in other cases involving both fiber types. Clinical features of osteomalacic myopathy are proximal limb weakness and associated bone pain the condition responds well to treatment with vitamin D. 

Ansved T, Odergren T, Borg K. Muscle fiber atrophy in leg muscles after botulinum toxin type A treatment of cervical dystonia. Neurology 1997 48(5) 1440-2. 

Figures 1.1-1.3) and (b) type-2 muscle fiber atrophy (Figure 1.4), and other less frequently seen atrophies, including vacuolar atrophies. Conceptu-... 

In an individual patient the cause of type-2 fiber atrophy can be multifactorial. For example, possibilities are (a) in arthritic muscle atrophy, in which the commonly associated muscle-fiber atrophy is typically type-2 fiber atrophy [46], but whether the mechanism(s) is, speculatively, related to hypofunc-tion/disuse, or a putative pain reflex decreasing LMN function, and/or, in rheumatoid arthritis, a concomitant dysimmune mechanism (b) in HIV the atrophy could be dysschwannian dysimmune neuropathic, dysneuronal neuropathotoxic, cachectic, or possibly viral-myotoxic, or a combination of these. 

Mendell JR, Engel WK. (1971) The fine structure of type n muscle fiber atrophy. Neurology 21, 358-365. 

Type-2 muscle fiber atrophy can be cansed by varions abnormalities, snch as cachexia, hypoactivity (disnse), glncocorticoid excess, hyperparathyroidism, a manifestation of recent pan-deinnervation [51, 52] or pan-dysinnervation, or npper-motor-nenron abnormality (for extensive discnssion, see Chapter 1). 

Vignette 1. Type-2 muscle-fiber atrophy, neoplasm-related cachectic atrophy, plus sensory-motor neuropathy... 

Proximal muscle weakness in an elderly patient associated with a normal electromyogram (EMG) can be caused by type-2 muscle fiber atrophy, which is diagnosable only on muscle biopsy. One should seek an identifiable cause, such as cachexia, disuse, glucocorticoid toxicity, a "remote" neoplasm, hyperparathyroidism, subtle denervation, or supra-segmental central nervous system (CNS) abnormality. This mainly-sensory nerve neuropathy can cause slowed sensory nerve conductions, if involving large diameter fiber, small diameter ones. 

---