Atrophy and degeneration in skeletal muscle

SUMMARY1. Isometric contractions of motor units have been studied in selfreinnervated soleus and flexor digitorum longus muscles, the motor nerves of which had been transacted 6 months earlier.2. The distributions of motor unit tetanic tensions in both muscles were skewed towards large values and showed greater variance than normal: there were motor units which produced more tension and others which developed less tension than in control muscles. Mean tensions of motor units are compared with those of the controls.3. The variance of times to peak of motor units in both muscles was significantly smaller than normal.4. Conduction velocities of axons were slower than normal above the point of nerve section. A number of axons did not functionally cross this point and those that did conducted slowly below the neuroma.5. Many of the correlations seen in normal muscle between axon conduction velocity, motor unit tetanic tension, twitch time to peak and ratio of twitch to tetanic tension were demonstrated in reinnervated muscle.6. We suggest that the pattern of motor unit organization in selfreinnervated muscle can in part be due to random regrowth of axons but is largely produced by specific processes related to axon size which are not identical in fast and slow muscle.

Section: Introductioncontrasting

confidence: 40%

Isometric contractions of motor units in self‐reinnervated fast and slow twitch muscles of the cat

Bagust¹,

Lewis²

1974

“…Tower (1935) denervated cat interosseous muscle and showed that initially there was simple atrophy, the reduction in fibre diameter resulting from a loss of myofibrils and other intracellular structures. Later degeneration (or more strictly, necrosis) occurred, involving disruption of normal muscle fibre organization, eventually with loss of nuclei and destruction of fibres.…”

Section: Introductionmentioning

confidence: 43%

Effects of chronic electrical stimulation on contractile properties of long‐term denervated rat skeletal muscle.

Al-Amood¹,

Lewis²,

Schmalbruch³

1991

SUMMARY1. The contractile properties of fast-twitch (extensor digitorum longus or EDL) and slow-twitch (soleus) muscles in the rat were followed for periods of between 4 and 10 months after denervation. The effects of chronic electrical stimulation during the last 3-8 weeks of denervation were investigated.2. The fall in tetanic tension that follows axotomy ended after about 4 months' denervation. The equilibrium tension was about 0 75 % of control tension in EDL and 0 2-0{3 % in soleus.3. The low tension in soleus was due partly to the small diameter of the muscle fibres (atrophy) and partly to their necrosis that resulted in an 8-fold fall in specific tension (the force per unit cross-sectional area). Similar but less extreme changes occurred in EDL.4. It is speculated that the final level of tension reached by unstimulated denervated muscles is an equilibrium between decrease in force due to atrophy and necrosis and increase due to regeneration. Differences between the final tension levels in soleus and EDL cannot be accounted for quantitatively by known differences in atrophy alone. Therefore, the rate of necrosis in soleus and of regeneration in EDL may be higher.5. Chronic stimulation of long-term denervated muscle increased force generation by about 7-fold in EDL and between 20 and 55 times in soleus. The final tension reached was between 4 and 5 % of normal in both muscles. Specific tension of fibres was almost completely restored by stimulation and the number of fibres was normal. The failure to recover full tension was largely due to failure to reverse denervation atrophy completely.6. Twitch contraction and relaxation times were identical in denervatedstimulated soleus and EDL. There was no evidence for dependence on duration of stimulation or tension of the muscle. The normalized maximum rate of rise of tetanic tension remained higher in EDL than soleus. MIS 900144 I S. AL-AMOOD. D. M. LEW'IS AND H. SCHMALBRUCH

“…Muscle atrophy may be prevented or at least delayed by electrical stimulation, but only reinnervation can lead to functional and morphological recovery. Early experiments (Tower, 1935;Gutmann, 1945) showed that long-term denervation may cause degeneration and even necrosis of muscle fibres; rabbit muscles denervated for 20 months contained no cross-striated fibres, but structurally normal muscle fibres reappeared 6 months after reinnervation (Gutmann, 1945).…”

Section: Introductionmentioning

confidence: 44%

Morphology of long‐term denervated rat soleus muscle and the effect of chronic electrical stimulation.

Schmalbruch

Al-Amood

Lewis

1991

127

109

SUMMARY1. Rat soleus muscles were denervated for 6-10 months; some of these were chronically stimulated for the last 3-8 weeks before recording. The muscles were fixed at physiological lengths and embedded in epoxy resin.2. Sections for light microscopy were stained with p-phenylenediamine. Denervation reduced the mean cross-sectional area of fibres to 3% of controls (peak at 20 ,tm2). The cross-sectional areas of the stimulated fibres had a peak at 70 ,um2. In light micrographs of denervated muscles, the total number of fibres appeared to be reduced; however not all fibres could be identified (see paragraph (3)).3. In the electron microscope, many fibres showed disarrayed myofilaments. Few fibres had more or less normal cross-striations. Muscle fibres as small as 1 ,tm in diameter were seen. The smallest fibres did not contain myofilaments. Some unequivocally necrotic fibres were seen.4. Most stimulated denervated fibres showed an almost normal sarcomere pattern. Scattered throughout the muscle were single fibres as small as 2 ,tm in diameter, but these were well organized and could be recognized in the light microscope. Few fibres were necrotic. Often fibres were serially arranged. Satellite cells were prominent.5. It is concluded that in long-term denervated rat soleus the original fibres are lost and those seen are the result of repeated cycles of regeneration and necrosis. Stimulation maintains the sarcomeres and probably prevents secondary degeneration and necrosis.