Length-associated changes in muscle
Gossman, M.R., Sahrmann, S.A., & Rose, S.J. (1982). Review of length-associated changes in muscle: Experimental evidence and clinical implications. Physical Therapy, 62, 1799-1808.
Movement dysfunction that may be caused by length-associated changes in muscle is a problem of people treated by physical therapists. The purpose of this article is to review the literature related to length-associated changes in muscle. An analysis of length-associated changes in animal and human studies is presented. The methods used to produce the changes in animals are discussed, and the clinical implications of the length-associated changes in muscle are suggested.
Effects of shortening
Baker, J.H. & Matsumoto, D.E. (1988), Adaptation of skeletal muscle to immobilization in a shortened position. Muscle & Nerve, 11, 231-44.
This study determined the morphological changes and adaptations that occur following immobilization of rat soleus and gastrocnemius muscles when the ankle joint is placed in complete plantar flexion for 2, 5, 7, 14, 21, and 28 days by means of plaster casts. Previous studies of such shortened muscles have shown that the number of sarcomeres in series is reduced, but how the sarcomeres are reduced has not been determined. We observed that the fibers in the mid-belly region of the muscles demonstrated a progressive degenerative process over the first few weeks. Myofibrils across the entire width of the affected fibers underwent dissolution. However, by 4 weeks new myofibrils were being formed, and sarcomere lengths appeared normal. Portions of the fibers near the tendon underwent segmental necrosis. These findings are similar to the response of the soleus and gastrocnemius muscles to tenotomy and are clinically relevant to orthopedic procedures that maintain muscles in shortened conditions for prolonged periods.
Lieber, R.L., & Friden, J. (2002). Spasticity causes a fundamental rearrangement of muscle-joint interaction. Muscle Nerve, 25, 265-70.
Sarcomere length was measured in flexor carpi ulnaris (FCU) muscles from patients with severely spastic wrist flexion contractures (n = 6), as well as from patients with radial nerve injury and a normally innervated FCU (n = 12). Spastic FCU muscles had extremely long sarcomere lengths with the wrist fully flexed (3.48 +/- 0.44 microm) compared to the FCU muscles of patients with radial nerve injury (2.41 +/- 0.31 microm). In three of the patients with spastic wrist flexion contractures, the slope of the FCU sarcomere length-joint angle relationship was measured and found to be, essentially, normal (0.017 +/- 0.005 microm/degree, n = 3) suggesting that serial sarcomere number (and therefore muscle fiber length) was unchanged in spite of the dramatic absolute sarcomere length change. These results indicate that spasticity results in a major alteration of normal muscle-joint anatomical relationships that has not previously been recognized to our knowledge. We hypothesize that the results are explained either by the inability of muscle fibers to add serial sarcomeres in response to growth, or the selective loss of FCU muscle length secondary to the central nervous system lesion.
Robinson, G.A., Enoka, R.M., & Stuart, D.G. (1991). Immobilization-induced changes in motor unit force and fatigability in the cat. Muscle & Nerve, 14, 563-73.
The purpose of this study was to examine the effects of 3 weeks of immobilization on the mechanical properties of motor units in a cat hindlimb muscle. The muscle, tibialis posterior, was immobilized in a shortened position. Motor units were classified as type FF, F(int), FR, or S. Force, axonal conduction velocity, fatigability, and proportions of motor unit types were compared in control and immobilized muscles. All properties exhibited some change after immobilization, including slower axonal conduction velocities, greater twitch forces, slower twitch contraction times, and greater tetanic forces. In addition, most motor units were less fatigable after immobilization. The number of motor units that could not be included in one of the four classification categories increased significantly after immobilization; these units exhibited normal axon conductivity but failed to produce measurable force or associated EMG. Short-term immobilization induced a variety of physiological adaptations in neuromuscular processes that varied with motor unit type.
Williams, P.E. (1988): Effect of intermittent stretch on immobilised muscle. Annals of the Rheumatic Diseases, 47, 1014-6.
When muscle is immobilised in a shortened position there is a reduction in fibre length and an increase in the proportion of connective tissue. This results in reduced muscle compliance and a loss of range of joint motion. Experiments have been carried out to determine whether short periods of stretch are effective in preventing these changes. The soleus muscle of the mouse was immobilised in a shortened position for a period of 10 days by means of a plaster cast. Every two days the cast was removed and the muscle passively stretched for a 15 minute period. It was found that this treatment prevented the connective tissue changes but did not prevent the reduction in muscle fibre length, which in itself resulted in considerable loss of range of motion.
Williams, P.E., Catanese, T., Lucey, E.G., & Goldspink, G. (1988). The importance of stretch and contractile activity in the prevention of connective tissue accumulation in muscle. Journal of Anatomy, 158, 109-14.
The loss of serial sarcomeres which results when muscles are immobilised in a shortened position is accompanied by an increase in the proportion of collagen and an increased muscle stiffness. In order to determine whether it is lack of stretch or lack of contractile activity which is the main factor involved in these changes experiments were carried out using different combinations of immobilisation and electrical stimulation. It was found that the connective tissue accumulation that occurs in inactive muscles can be prevented either by passive stretch or by active stimulation. It was also shown that in muscle that is working over a reduced range there is, as in muscle immobilised in the shortened position, a reduction in serial sarcomeres. In this case, however, there is no concomitant increase in connective tissue, again indicating that contractile activity is important for the maintenance of normal muscle compliance.
Effects of lengthening
Goldspink, G. et al. (1992). Gene expression skeletal muscle in response to stretch and force generation. American Journal of Physiology,262, R356-R363.
Striated muscle is a tissue in which gene expression is influenced to a large extent by mechanical signals. This includes the regulation of gene expression-associated muscle fiber phenotype determination, which depends on which protein isoform genes are transcribed, as well as muscle fiber mass accretion, which appears to involve some translational regulation. Although muscle synthesizes a set of highly specialized proteins it has a remarkable ability to adapt by expressing different isoforms of the same protein so that it acquires the appropriate contractile characteristics. Our work has focused on the myosin heavy chain (HC) genes as these encode the myosin cross bridge, which is responsible for muscle intrinsic velocity of contraction and economy of force development.
RNA analyses after cast immobilization of the limb with the muscle in the lengthened or shortened position and/or with electrical stimulation were used to determine the effects of altered mechanical signals on gene transcription. When the soleus muscle was immobilized in the shortened position in the young animal it did not fully differentiate into a slow postural-type muscle. Even in the adult, the soleus muscle if deprived of stretch and contractile activity switches back to transcribing the fast myosin HC gene. The converse was true when the fast rabbit tibialis anterior was subjected to immobilization in the lengthened position and/or electrical stimulation. Both stretch alone and stimulation alone caused repression of the fast type and activation of the slow myosin genes. The reprogramming of the fast muscle was more complete when the stretch was combined with stimulation.
Williams, P., Watt, P., Bicik, V., & Goldspink, G. (1986). Effect of stretch combined with electrical stimulation on the type of sarcomeres produced at the end of muscle fibers. Experimental Neurology, 93,500-509.
Stretching a muscle results in a rapid addition of sarcomeres at the ends of the muscle fibers. The effect of a pattern of electrical stimulation resembling that of a slow motoneuron on the newly formed muscle tissue in a stretched, fast-contracting muscle was investigated. We found that after a period as short as 4 days, the type of sarcomeres which were added on to the ends of the existing myofibrils differed from those in the middle regions of the experimental muscles: there was a much higher proportion of type I and type IIA sarcomeres in the stretch-stimulated ends. This study showed that reprogramming of the synthesis of fiber type-specific contractile proteins can be achieved and detected within a very short time by using electrical stimulation combined with stretch.
Tardieu, C., Lespargot. A., Tabary, C., & Bret, M.D. (1988). For how long must the soleus muscle be stretched each day to prevent contracture? Developmental Medicine and Child Neurology, 30, 3-10.
The extent to which treatment of passive muscle contracture could be minimized without loss of efficiency was studied. Soleus muscle contracture was measured by the difference between the ankle angles at which minimal and maximal resistance occurred during slow dorsiflexion of the ankle. This examination was done twice, at the beginning and end of a seven-month observation period. During the observation period, also, the ankle angles were measured throughout a 24-hour period in the ordinary life of the child. The number of hours per 24-hour period during which the soleus muscle was stretched above a minimal threshold length was calculated. The major finding was that there was no progressive contracture when the soleus was stretched for at least six hours a day (the same time as in non-handicapped children). On the other hand, there was progressive contracture when the stretching time was as short as two hours. Two of the cases examined illustrated the possible causes of success or failure of night splints. These results provide new guidelines for the continuous treatment of children with cerebral palsy.