title: 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.
authors.affiliation: Brain Research Institute, University of California at Los Angeles, 1320 Gonda Neuroscience and Genetics Building, Box 951761, Los Angeles, California 90095-1761, USA. rrr@ucla.edu
authors.forename: Roland R
authors.initials: RR
authors.lastname: Roy
authors.forename: Hui
authors.initials: H
authors.lastname: Zhong
authors.forename: John A
authors.initials: JA
authors.lastname: Hodgson
authors.forename: Elena J
authors.initials: EJ
authors.lastname: Grossman
authors.forename: Boonclaire
authors.initials: B
authors.lastname: Siengthai
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Talmadge
authors.forename: V Reggie
authors.initials: VR
authors.lastname: Edgerton
mesh_terms: D000818:Animals; D000252:Calcium-Transporting ATPases / Q000032:analysis; D002415:Cats; D048429:Cell Size / Q000502:physiology; D004558:Electric Stimulation; D005260:Female; D007537:Isometric Contraction / Q000502:physiology*; D018656:Muscle Fibers, Fast-Twitch / Q000737:chemistry / Q000166:cytology / Q000502:physiology; D018657:Muscle Fibers, Slow-Twitch / Q000737:chemistry / Q000166:cytology / Q000502:physiology; D018482:Muscle, Skeletal / Q000166:cytology / Q000502:physiology*; D018995:Myosin Heavy Chains / Q000032:analysis; D009929:Organ Size; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases
chemical_list: D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D018995:Myosin Heavy Chains; D000252:Calcium-Transporting ATPases