1. The purpose of this study was to determine the role of motor unit remodelling in the deficit that develops in the maximum isometric tetanic force (F.) of whole medial gastrocnemius (MGN) muscles in old compared with adult rats. The F. values and morphological data were determined for MGN muscles and eighty-two single motor units in muscles of adult (10-12 months) and sixty-two units in those of old (24-26 months) F344 rats. During an unfused tetanus, fast and slow (S) motor units were identified by the presence and absence of sag, respectively. Fast-fatigable (FF) and fast-fatigue-resistant (FR) units were classified by fatigue indices less than or greater than 0 50, respectively.2. For old rats, whole MGN muscle F. was 29% less than the value of 11 2 N measured for adult rats. The deficit in whole muscle F. of old rats resulted from equivalent decreases in the number of motor units, 16 % smaller than the adult value of ninety-seven, and in the mean motor unit Fo value, 14 % less than the adult value of 117 mN.3. With ageing, little motor unit remodelling occurred in FR units, whereas the S and FF motor units demonstrated dramatic, but opposing, changes. For S units, the number of units remained constant, but the number of fibres per motor unit increased 3-fold from 57 to 165. In contrast, the number of FF units decreased by 34% and the number of fibres per motor unit of the remaining units decreased to 86% of the adult value of 333. The agerelated remodelling of motor units appeared to involve denervation of fast muscle fibres with reinnervation of denervated fibres by axonal sprouting from slow fibres.
We developed an apparatus to quantify the biomechanical behavior of the dorsi- and plantarflexor muscles of the ankle of an anesthetized mouse. When the dorsi- or plantarflexor muscle group is activated by electrical stimulation of either the peroneal or tibial nerve, the apparatus measures the moment developed about the ankle during isometric, isovelocity shortening, or isovelocity lengthening contractions. Displacements may be performed over the full 105 degrees range of ankle motion with an angular resolution of 0.09 degrees. Bidirectional isovelocity ramps in ankle angle up to 1,100 degrees/s are possible and are equivalent to maximum velocities of 2.3 fiber lengths/s (Lf/s) for the fibers in tibialis anterior muscle and 11.9 Lf/s for those in gastrocnemius muscle. During single contractions of the dorsi- and plantarflexor muscle groups at 37 degrees C and with both knee and ankle joint at 90 degrees neutral position, the isometric tetanic force developed was 1.4 and 3.3 N, power output at 2.2 Lf/s was 3.1 and 5.9 mW, and power absorption at 0.5 Lf/s was 4.9 and 9.0 mW, respectively. These values are in reasonable agreement with data from the same muscle groups tested in situ. We conclude that the apparatus provides valid measurements of force and power of the dorsi- and plantarflexor muscle groups.
The functional properties of latissimus dorsi (LTD) muscles were evaluated 160 to 180 days after tenotomy and repair, when grafts had stabilized. Our hypothesis was that, compared with control LTD muscles, LTD grafts would develop less absolute force and power but that the specific force and normalized power would not differ. Expressed as a percentage of the value for control LTD muscles, values for grafts were 67% for muscle mass, 74% for mean single fiber cross-sectional area, 56% for maximum absolute isometric tetanic force, 64% for maximum absolute average force during shortening, and 70% for maximum absolute power. Compared with control LTD muscles, grafts showed no significant differences either in the number of fibers in the total muscle cross section or in the optimum velocity for the development of power. When force and power of grafts were normalized for total fiber cross-sectional area and mass, respectively, only the value for maximum specific force (84% of control value) was significant. The mechanisms responsible for the decrease in specific force after tenotomy and repair are not known. In contrast to the deficit in maximum specific force, the 30% deficit in maximum absolute power of grafts compared with control LTD muscles was explained completely by the 33% smaller muscle mass.
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 approximately 25% decrease in muscle mass and in most grafts approximately 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.
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