Whole skeletal muscle transplantation: Mechanisms responsible for functional deficits

Abstract

One aspect of tissue engineering of skeletal muscle involves the transposition and transplantation of whole muscles to treat muscles damaged by injury or disease. The transposition of whole muscles has been used for many decades, but since 1970, the development of techniques for microneurovascular repair has allowed the transplantation of muscles invariably result in structural and functional deficits. The deficits are of the greatest magnitude during the first month, and then a gradual recovery results in the stabilization of structural and functional variables between 90 and 120 days. In stabilized vascularized grafts ranging from 1 to 3 g in rats to 90 g in dogs, the major deficits are ∼25% decrease in muscle mass and in most grafts ∼40% decrease in maximum force. The decrease in power is more complex because it depends on both the average shortening force and the velocity of shortening. As a consequence, the deficit in maximum power may be either greater or less than the deficit in maximum force. Tenotomy and repair are the major factors responsible for the deficits. Although the data are limited, skeletal muscle grafts appear to respond to training stimuli in a manner no different from that of control muscles. The training stimuli include traditional methods of endurance and strength training, as well as chronic electrical stimulation. Transposed and transplanted muscles develop sufficient force and power to function effectively to: maintain posture; move limbs; sustain the patency of sphincters; partially restore symmetry in the face; or serve as, or drive, assist devices in parallel or in series with the heart.