Influences of electromechanical events in defining skeletal muscle properties

Abstract

Inactivity of the cat soleus muscle was induced via spinal cord isolation (SI), and the cats were maintained for 4 months. The soleus was electrically stimulated while lengthening (SI-L) or shortening (SI-S) during a simulated step cycle or during isometric (SI-I) contractions. For the SI, SI-S, SI-L, and SI-I groups, the soleus weights were 33, 55, 55, and 64% of the control, respectively, and the maximum tetanic tensions were 15, 30, 36, and 44% of the control, respectively. The specific tension was lower in all SI groups than in the control. Absolute forces at stimulation frequencies of 5-200 Hz were smaller in all SI groups than in the control. The SI-I group tended to have higher values for all force-related parameters than the other SI groups. Fatigue resistance was similar among all groups. The isometric twitch time-to-peak tension was shorter, and the frequency of the stimulation-tension response was shifted to the right in all SI groups with respect to the control. Maximum shortening velocities were 70, 59, and 73% faster for the SI, SI-S, and SI-L groups and similar to the control for the SI-I group. Inactivity resulted in an increased percentage of faster myosin heavy chains (MHCs) that was blunted in the SI-I and SI-L groups but not in the SI-S group. Pure type I MHC fibers atrophied by 80, 59, 58, and 47% in the SI, SI-S, SI-L, and SI-I groups. The data from the SI group quantify the contribution of activity-independent factors in maintaining the mechanical and phenotypic properties of the cat soleus. Relative to a fast-fatigable muscle, these results suggest that only 25% of the slowness (type I MHC) and none of the resistance to fatigue of the soleus muscle are dependent on activity-related factors. Short, daily bouts of electromechanical activation ameliorated several of these adaptations, with the isometric contractions being the most effective countermeasure. The clinical implications of these findings for rehabilitation strategies are discussed.

Muscle and bone plasticity after spinal cord injury: Review of adaptations to disuse and to electrical muscle stimulation

“…Even after brief periods of training, calcium dynamics in paralyzed muscle may begin to adapt [35]. These findings are consistent with animal studies, which have demonstrated that electrical stimulation (in concert with loading) prevents atrophy [45] and may prevent muscle fiber transformation [27,46]. Numerous studies have suggested that the dramatic training effects observed in electrically stimulated paralyzed muscle largely depend on the stimulation parameters used.…”

Focal adhesion kinase signaling is decreased 56 days following spinal cord injury in rat gastrocnemius

“…27 In addition, overexpression of FAK is associated with an increase in markers of an oxidative muscle phenotype. 9 There is a slow oxidative to fast glycolytic fiber type change following SCI, 19,28,29 and the loss of type 1 muscle fibers after SCI may be linked to or share common mechanisms with decreases in FAK expression and signaling. This agrees with previous data that shows cytomegalovirus-mediated FAK +FRNK overexpression into the rat soleus is associated with a decrease in type 1/2 muscle fiber hybrids and an increase in type 2 muscle fiber compared with overexpression with FAK alone.…”

Spastic Tail Muscles Recover From Myofiber Atrophy and Myosin Heavy Chain Transformations in Chronic Spinal Rats

“…It is also well documented that after SCI (in animals and humans), cauda equina injuries (in humans), and spinal isolation (in animals), reflex-generated exercise or direct electrical stimulation of muscle nerves induces recovery from myofiber atrophy in both primarily slow and primarily fast muscles and also opposes transformations in myofiber types toward faster isoforms (Dupont-Versteegden et al 1998;Hartkopp et al 2003;Kern et al 2004;Murphy et al 1999;Roy et al 1999Roy et al , 2002aShields and Dudley-Javoroski 2006). Thus the recovery of myofiber sizes and proportions in chronic spinal rats with long-term spasticity resembles the effects of training interventions that provide muscle activity after CNS lesions in animals and humans.…”

“…It is well documented that in the absence of muscle activity, myofibers often transform robustly toward faster, more fatigable types and undergo considerable atrophy (Roy et al 2002a). Early after spinal cord transection and after long-term spinal isolation in our rats, reduced muscle activity results in a similar atrophy and decrease in type I myofiber type proportions as seen in our results.…”

“…Interestingly, exercise or muscle activity induced by electrical stimulation attenuates or reverses such detrimental changes in muscle properties after SCI (Dupont-Versteegden et al 1998;Hartkopp et al 2003;Kern et al 2004;Murphy et al 1999;Roy et al 1992Roy et al , 1999Roy et al , 2002aShields and DudleyJavoroski 2006). That is, generating muscle activity after SCI interrupts the slow-to-fast myofiber transformations and atrophy, and ultimately assists in preserving the normal muscle contractile properties.…”