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Journal of Applied Physiology, Vol 52, Issue 5 1113-1118, Copyright © 1982 by American Physiological Society
ARTICLES |
F. W. Booth
The immobilization of limbs resulted in atrophy of those muscles that are fixed either at or less than resting length. The loss in protein in these muscles can be described by a first-order equation. Decreases in protein synthesis rate in muscles of immobilized limbs occur during the first 6 h of immobilization, and this decrease probably played a role in initiating muscular atrophy. After weeks of immobilization, muscles composed predominately of slow-twitch fibers took on properties characteristic of fast twitch muscles. The EMG activity of muscles in immobilized limbs was reduced to 5--15% of control levels. Insulin responsiveness for 2-deoxyglucose uptake into the soleus muscle of a limb is decreased at the 24th h of limb immobilization. Muscles of immobilized limbs have either no change or a decrease in resting membrane potential, an increase in extrajunctional acetylcholine receptors of lesser magnitude than the increase that occurred in denervated muscle, and no change in acetylcholinesterase activity in neuromuscular junctions. Immobilizing muscles at stretched lengths prevented the decrease in nerve afterhyperpolarization that was seen in muscles immobilized at shortened positions. These observations suggested that metabolic changes in muscles have a retrograde trophic influence on motor nerves. The model of limb immobilization permits the study of many fundamental problems concerned with mechanisms by which a muscle adapts so that it can meet the requirements of the external environment.
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