title: Is spinal cord isolation a good model of muscle disuse?
abstract: The patterns of normal daily activity that are required to maintain normal skeletal muscle properties remain unknown. The present study was designed to determine whether spinal cord isolation can be used as a reliable experimental model of neuromuscular inactivity, that is, as a baseline for the absence of activity. Electromyograms (EMGs) were recorded from selected hindlimb muscles of unanesthetized rats over 24-hour periods before and 7, 30, 60, and 90 days after surgical isolation of the lumbar spinal cord. Our data indicate that some rat slow muscle fibers pre-surgery were activated for less than 3 hours per day. Spinal cord isolation (SI) reduced the mean daily integrated EMG (IEMG) and daily EMG duration in the primary slow extensor muscle (soleus) to <1% of control, and in the primary fast extensor muscles [medial gastrocnemius (MG) and vastus lateralis (VL)] to <2% of control. These parameters were decreased to <8% and 3% of control, respectively, in a primary fast flexor muscle, the tibialis anterior (TA). From 30 to 90 days post-SI, the mean amplitudes of the spontaneous EMG bursts were relatively normal in the soleus, increased approximately 2-fold in the MG and VL, and increased approximately 4-fold in the TA. Some evidence of the normal antagonistic flexor-extensor relationship was apparent in the brief periods of recorded activity post-SI. These results indicate that SI eliminates nearly all of the normal EMG activity in the hindlimb muscles in the presence of relatively normal muscle innervation and functional intraspinal neural circuitry.
authors.affiliation: Brain Research Institute, University of California Los Angeles, 1320 Gonda Neuroscience and Genetics Building, Box 951761, Los Angeles, California 90095-1761, USA. rrr@ucla.edu
authors.forename: R R
authors.initials: RR
authors.lastname: Roy
authors.forename: H
authors.initials: H
authors.lastname: Zhong
authors.forename: N
authors.initials: N
authors.lastname: Khalili
authors.forename: S J
authors.initials: SJ
authors.lastname: Kim
authors.forename: N
authors.initials: N
authors.lastname: Higuchi
authors.forename: R J
authors.initials: RJ
authors.lastname: Monti
authors.forename: E
authors.initials: E
authors.lastname: Grossman
authors.forename: J A
authors.initials: JA
authors.lastname: Hodgson
authors.forename: V R
authors.initials: VR
authors.lastname: Edgerton
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000818:Animals; D004195:Disease Models, Animal; D018450:Disease Progression; D004576:Electromyography; D005260:Female; D009119:Muscle Contraction / Q000502:physiology; D018656:Muscle Fibers, Fast-Twitch / Q000502:physiology; D018657:Muscle Fibers, Slow-Twitch / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation* / Q000503:physiopathology*; D020966:Muscular Disorders, Atrophic / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D019051:Rhizotomy / Q000379:methods*; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D013126:Spinal Nerve Roots / Q000293:injuries / Q000502:physiology / Q000503:physiopathology*