title: In vivo (31)P NMR spectroscopy assessment of skeletal muscle bioenergetics after spinal cord contusion in rats.
abstract: OBJECTIVE
  Muscle paralysis after spinal cord injury leads to muscle atrophy, enhanced muscle fatigue, and increased energy demands for functional activities. Phosphorus magnetic resonance spectroscopy ((31)P-MRS) offers a unique non-invasive alternative of measuring energy metabolism in skeletal muscle and is especially suitable for longitudinal investigations. We determined the impact of spinal cord contusion on in vivo muscle bioenergetics of the rat hind limb muscle using (31)P-MRS.
  
  
  METHODS
  A moderate spinal cord contusion injury (cSCI) was induced at the T8-T10 thoracic spinal segments. (31)P-MRS measurements were performed weekly in the rat hind limb muscles for 3 weeks. Spectra were acquired in a Bruker 11 T/470 MHz spectrometer using a 31P surface coil. The sciatic nerve was electrically stimulated by subcutaneous needle electrodes. Spectra were acquired at rest (5 min), during stimulation (6 min), and recovery (20 min). Phosphocreatine (PCr) depletion rates and the pseudo first-order rate constant for PCr recovery (k PCr) were determined. The maximal rate of PCr resynthesis, the in vivo maximum oxidative capacity (V max) and oxidative adenosine triphosphate (ATP) synthesis rate (Q max) were subsequently calculated.
  
  
  RESULTS
  One week after cSCI, there was a decline in the resting total creatine of the paralyzed muscle. There was a significant reduction (~24 %) in k PCr measures of the paralyzed muscle, maximum in vivo mitochondrial capacity (V max) and the maximum oxidative ATP synthesis rate (Q max) at 1 week post-cSCI. During exercise, the PCr depletion rates in the paralyzed muscle one week after injury were rapid and to a greater extent than in a healthy muscle.
  
  
  CONCLUSIONS
  Using in vivo MRS assessments, we reveal an acute oxidative metabolic defect in the paralyzed hind limb muscle. These altered muscle bioenergetics might contribute to the host of motor dysfunctions seen after cSCI.
authors.affiliation: Department of Integrative Biology and Physiology, University of California in Los Angeles, 621 Charles E Young Dr, Los Angeles, CA, 90048, USA, pshahucla@gmail.com.
authors.forename: Prithvi K
authors.initials: PK
authors.lastname: Shah
authors.forename: Fan
authors.initials: F
authors.lastname: Ye
authors.forename: Min
authors.initials: M
authors.lastname: Liu
authors.forename: Arun
authors.initials: A
authors.lastname: Jayaraman
authors.forename: Celine
authors.initials: C
authors.lastname: Baligand
authors.forename: Glenn
authors.initials: G
authors.lastname: Walter
authors.forename: Krista
authors.initials: K
authors.lastname: Vandenborne
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D005260:Female; D009682:Magnetic Resonance Spectroscopy; D018482:Muscle, Skeletal / Q000378:metabolism* / Q000503:physiopathology; D010085:Oxidative Phosphorylation; D010725:Phosphocreatine / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013119:Spinal Cord Injuries / Q000378:metabolism*
chemical_list: D010725:Phosphocreatine; D000255:Adenosine Triphosphate